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CGRN > Disease, Disorders, Dysfunctions, Anomalies And Traumas > Flashcards

Disease, Disorders, Dysfunctions, Anomalies And Traumas Flashcards

1
Q

What is Gastroesophageal Reflux Disease (GERD)

A

It develops with gastric or duodenal contents flow back into the esophagus

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2
Q

Is it normal for adults and children to have some amount of reflux after eating

A

Yes

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3
Q

When is reflux considered a pathological condition

A

When it causes undesirable symptoms, such as pain or respiratory distress

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4
Q

When should someone be aggressively investigated for the possibility of GERD

A

All patients with:
1. Chronic cough
2. Recurrent pneumonia
3. And asthma

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5
Q

When do patients have symptomatic GERD

A

They have an incompetent LES
The LES does not have enough intraluminal pressure to prevent reflux

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6
Q

What is the main cause for GERD

A

Dysfunction of the LES -

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7
Q

What are causes for GERD

A
  1. Dysfunction of the LES
  2. Motility disorder
  3. Pyloric stenosis
  4. Intestinal malrotation
  5. Obesity
  6. Pregnancy - because of the increase in intraabdominal pressure (usually resolves after delivery)
  7. Smoking
  8. Scleroderma
  9. Diabetes
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8
Q

What are the most common signs and symptoms of GERD

A
  1. Pyrosis (heartburn). 7. Chest pain
  2. Dyspepsia (epigastric pain). 8. Belching up sour contents
  3. Regurgitation. 9. Globus sensation (feeling of having a lump in your throat)
  4. Dysphagia (difficulty swallowing). 10. Sore throat or hoarseness
  5. Odynophagia (painful swallowing) 11. Nausea
  6. Persistent cough. 12. Asthma
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9
Q

How is GERD diagnosed

A
  1. Upper GI Endoscopy
  2. Barium swallow
  3. Motility studies
  4. 24-hour pH studies
  5. Bernstein test
  6. Gastric emptying scintigraphy
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10
Q

How is an Upper GI endoscopy used to diagnose GERD

A
  1. Can determine the presence and extent of esophagitis or Barrett’s esophagus, as well as anatomical disorders
  2. Symptoms can be present without evidence of esophagitis
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11
Q

How is a barium swallow used to diagnose GERD

A
  1. Will demonstrate reflux, but will not evaluate frequency or association with other symptoms
  2. Valuable tool for anatomical disorders
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12
Q

How are motility studies used in the diagnosis of GERD

A
  1. May be used if a motility disorder is suspected
  2. Used as an adjunct, but cannot confirm diagnosis
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13
Q

How are 24-hour pH studies used to diagnose GERD

A
  1. Thought to be the most accurate test for reflux
  2. Determines the frequency of reflux episodes and their relationship to other symptoms
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14
Q

How is a Bernstein test used in the diagnosis of GERD

A
  1. May be used to differentiate between cardiac and noncardiac chest pain
  2. Nasogastric tube is positioned about 5cm above the GE junction
  3. Out of the patient’s view, solutions of 0.1N hydrochloric acid and normal saline are alternatively dripped in
  4. The aim is to reproduce the chest pain
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15
Q

How is a Gastric emptying scintigraphy test used to diagnose GERD

A
  1. Nuclear medicine scan to evaluate how food moves through the stomach and GI tract
  2. Can determine if there is either accelerated or delayed gastric emptying
  3. Used for evaluation of abdominal pain, early satiety, and as a preoperative evaluation
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16
Q

What are the treatment options for GERD

A
  1. Medical management
  2. Drug therapy
  3. Surgery
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17
Q

What are the three objectives for the treatment of GERD

A
  1. Relieving symptoms
  2. Healing damaged mucosa
  3. Prevention complications
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18
Q

What is the first line of treatment for GERD

A

Behavior modification and lifestyle changes

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19
Q

What are some examples of behavior modification and lifestyle changes that can help in the treatment for GERD

A
  1. Making dietary modifications by avoiding foods and beverages that lower the LES pressure
  2. Losing weight
  3. Avoiding tight fitting garments
  4. Elevating the head of the bed on blocks
  5. Stopping smoking
  6. Avoiding food or drink 2 to 3 hours prior to bedtime
  7. Avoiding overeating and greasy, fatty foods
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20
Q

What are the drug therapy options for the treatment of GERD

A
  1. Histamine type 2 receptor antagonist (H2 blockers) - famotidine (Pepcid, Pepcid AC)
  2. Proton pump inhibitors (PPIs) - omeprazole, Esomeprazole magnesium, Rabeprazole, Lansoprazole or Dexlansoprazole
  3. Antacids may provide temporary relief
  4. Prokinetic agents, such as metoclopramide increase motility and strengthen the LES, but side effects should me monitored
  5. Sucralfate - (carafate)
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21
Q

When is surgery an option for treatment of GERD

A

Considered for patients who:
1. Are debilitated by severe esophagitis
2. Are refractory to medical management
3. Are subject to episodes of aspiration pneumonia
4. Have Barrett’s esophagus

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22
Q

What are the surgical options for the treatment of GERD

A
  1. Laparoscopic
  2. Open Nissen fundoplication, which creates a gastric wrap, tightening the LES
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23
Q

What is the incidence of pediatric patients developing GERD

A
  1. Most common up to 6 months of age, but may continue to 18 months of age
  2. Generally self-limiting
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24
Q

What causes GERD in pediatric patients

A

Lack of muscle control in infants

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25
Q

What are signs and symptoms of GERD in pediatric patients

A
  1. Recurrent vomiting
  2. Failure to thrive
  3. Aspiration
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26
Q

How is GERD diagnosed in pediatric patients

A

The same ways as with adults

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27
Q

How is GERD treated in pediatric patients

A
  1. Smaller more frequent meals
    - infants - changing feeding schedules, trying solid food (with doctor approval)
    - children - serving several small meals throughout the day, rather than three large meals
  2. Thicken formula with dry rice cereal
  3. Avoid active play after eating
  4. Position in elevated prone position
  5. Provide medications
    • anticholinergics
    • H2 blockers
  6. Consider surgery - Nissen fundoplication
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28
Q

What are potential complications of GERD

A
  1. Surgery
    • up to 15% of infants with GERD undergo surgery; most often the Nissen fundoplication
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29
Q

What are esophageal tumors

A
  1. May be benign or cancerous
  2. Squamous cell carcinoma and adenocarcinoma account for more than 95% of esophageal tumors
  3. Adenocarcinoma occurs in about 5% of cases of Barrett’s esophagus
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30
Q

What is the survival rate in cancerous esophageal tumors

A

3%

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31
Q

What is the reason for palliative care treatment in esophageal tumors

A

It is intended to restore normal swallowing

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32
Q

What causes esophageal tumors

A
  1. Chronic irritation of the mucosa predisposes patients to esophageal cancer
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33
Q

What are causes of chronic irritations that can lead to esophageal cancer

A
  1. Caustic ingestion
  2. Chronic esophagitis and strictures
  3. Excessive smoking or consumption of alcohol
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34
Q

What are signs and symptoms of esophageal tumors

A
  1. Dysphagia and odynophagia
  2. Substernal chest pain radiating to the back
  3. Anorexia and weight loss
  4. Hoarseness and cough
  5. Supraclavicular lymphadenopathy
  6. Hepatomegaly
  7. Obstruction with pneumonitis
  8. Blood loss is usually slow and steady rather than by acute hemorrhage
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35
Q

How are esophageal tumors diagnosed

A
  1. Barium swallow
  2. Endoscopy, biopsy, and brush cytology
  3. CT scan, MRI or PET scan
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36
Q

What is the treatment for esophageal tumors

A
  1. Surgery
  2. Radiation and chemotherapy
  3. Photodynamic therapy
  4. Prosthesis
  5. Psychological support
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37
Q

What type of surgery is considered for esophageal tumors

A

Includes esophageal resection with anastomosis to stomach, or may require colonic interposition

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38
Q

When is radiation and chemotherapy used in the treatment for esophageal tumors

A
  1. Often done prior to surgery in an attempt to shrink the tumor
  2. Radiation - when done post surgery may cause stricture formation
  3. Often done as palliation
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39
Q

When is photodynamic therapy (PDT) used in treatment for esophageal tumors

A

May be used to treat advanced tumors

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40
Q

What type of prosthesis is used in the treatment of esophageal tumors

A

Stent placement

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41
Q

What are diverticula in relation to the esophagus

A

Outpouchings of one or more layers of the esophageal wall

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42
Q

What are risk factors of developing diverticula of the esophagus

A
  1. Esophageal pressure
  2. Motor abnormalities
  3. Extrinsic inflammation
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43
Q

How many types of esophageal diverticula are there

A

3

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44
Q

What are signs and symptoms of esophageal diverticula

A
  1. More often then not patients are asymptomatic
  2. Some patients experience
    - difficulty swallowing - occurs in less than 5% of patient
    - feeling like food is caught in the throat
    - regurgitating food when bending over, lying down, or standing up
    - pain when swallowing
    - chronic cough
    - bad breath
    - chest or neck pain
    - weight loss
    - vocal changes (Boyce’s sign - a gurgling sound when air passes through the diverticulum)
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45
Q

What are the three types of esophageal diverticula

A
  1. Zenker’s
  2. Traction
  3. Epiphrenic
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46
Q

What is Zenker’s diverticulum

A

Located immediately above the UES and associated with a dysfunctional UES
Occurs at the junction of the hypopharynx and the esophagus in an area known as Killian’s triangle

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47
Q

Who is more likely to develop Zenker’s diverticulum

A

Usually found in men over the age of 50

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48
Q

What are signs and symptoms associated with Zenker’s diverticulum

A
  1. Cervical dysphagia
  2. Halitosis
  3. Aspiration pneumonia
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49
Q

How is Zenker’s diverticulum diagnosed

A

Includes:
1. Barium swallow
2. EGD
3. Manometry

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50
Q

What are potential complications of Zenker’s diverticulum

A
  1. Malnourishment caused by poor oral intake
  2. Aspiration pneumonia
  3. Perforation of the diverticulum - leading to severe inflammation of the mediastinum with possibly fatal sequelae
  4. Most common life-threatening complication is aspiration
  5. Other complications include:
    - massive bleeding from the mucosa or from fistulization into a major vessel
    - esophageal obstruction
    - fistulization into the trachea
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51
Q

What is treatment for Zenker’s diverticulum

A
  1. Except in the cases of disabling respiration pneumonia, the condition is left untreated
  2. Elevate head of the bed on blocks
  3. Do not eat or drink 3-4 hours before bedtime
  4. Surgery - most common method of surgical intervention is diverticulectomy
    • for small diverticulum may be treated simply with a myotomy (cutting the cricopharyngeal muscle under local anesthesia
    • or a combination of both surgeries
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52
Q

Where do traction diverticula occur in the esophagus

A

Located in the mid-esophagus

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53
Q

What are causes of traction diverticula

A
  1. Evidence suggests that they may be caused by an esophageal motor dysfunction
    • spasm
    • achalasia
    • LES hypertension
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54
Q

What are signs and symptoms of a traction diverticulum

A

May cause no signs or symptoms

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55
Q

How are traction diverticulum diagnosed

A
  1. Barium swallow
  2. Upper GI endoscopy
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56
Q

How are traction diverticulum treated

A
  1. The diverticula are usually small and require no therapy
  2. Occasionally an underlying abnormality requires a long myotomy
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57
Q

Where are epiphrenic diverticula located

A

Immediately above the LES often on the anterior wall of the esophagus

Very rare - occurring at a rate of 1 in 500,000 annually

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58
Q

What causes epiphrenic diverticula

A
  1. May be discoordination between esophageal contraction and LES relaxation
  2. Another casual theory is a combination of esophageal obstruction, functional or mechanical dysfunction and a point of weakness in the muscularis propria
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59
Q

What are signs and symptoms of epiphrenic diverticula

A

May regurgitate large amounts of fluid, usually at night while lying down

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60
Q

How are epiphrenic diverticula diagnosed

A
  1. Barium swallow
  2. Chest radiograph
  3. Endoscopy
  4. Manometry
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61
Q

What are potential complications of epiphrenic diverticula

A

Large diverticula can results in:
1. Severe dysphagia
2. Regurgitation
3. Food retention
4. The risk of aspiration pneumonia

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62
Q

What is the treatment for epiphrenic diverticula

A
  1. Elevate the head of the bed
  2. No food or drink 3-4 hours prior to bedtime
  3. Surgery - surgical intervention would include diverticulectomy and long myotomy to treat the motility disorder
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63
Q

What is an intramural diverticula

A

An obscure condition characterized by numerous small intramural Outpouchings that probably represent dilated ducts of submucosa glands

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64
Q

Where do intramural diverticula occur

A

Intramurally along the body of the esophagus

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65
Q

What are risk factors of getting intramural diverticula

A

Associated with:
1. Strictures
2. Esophageal dysmotility
3. Infection

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66
Q

What are symptoms of intramural esophageal diverticula

A

The symptoms are thought to be associated with symptoms of gastroesophageal reflux

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67
Q

What is the treatment for intramural esophageal diverticula

A

It is generally treated by treating the coexisting conditions such as stricture or infection

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68
Q

What are strictures of the esophagus

A

Abnormal formation of fibrous tissue that is usually at the lower end of the esophagus and may or may not be circumferential

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69
Q

What are the causes of esophageal strictures

A

Usually complications of:
1. Caustic injuries
2. Surgical procedures
3. Prolonged and severe reflux
4. GERD
5. Tumors
6. Scar tissue
7. Candidiasis

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70
Q

What are signs and symptoms of esophageal strictures

A
  1. Dysphagia - the most common clinical feature
  2. Regurgitation of food contents
  3. Cough at night
  4. Dehydration
  5. Weight loss
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71
Q

How are esophageal strictures diagnosed

A
  1. Barium swallow
  2. Upper GI Endoscopy
    • to rule out malignancy as the cause:
      -multiple biopsies and brush exfoliative cytological examination are mandatory
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72
Q

What is the treatment for esophageal strictures

A
  1. Change in dietary habits
  2. Medications that control acid production
  3. Dilation:
    • with weighted tungsten bougies -aka Maloney or Hurst dilators
    • hydrostatic balloon dilators
    • graduated plastic Savary-Gilliard or American dilators
    • mercury-weighted bougies may still be used in some proactive settings
    • many patients require follow-up with further dilation at variable intervals
  4. Surgery
  5. A long narrow stricture seen more often in children may be treated surgically by colon interposition
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73
Q

What is achalasia

A

The muscles of the esophagus fail to relax during swallowing, causing food to remain in the esophagus for long periods of time

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74
Q

What are causes of achalasia

A

A defect of peristalsis in the esophageal body and elevated LES pressure

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75
Q

What are symptoms of achalasia

A
  1. Dysphagia - to solids and liquids
  2. Chest pain
  3. Cough
  4. Nausea and vomiting of undigested food
  5. Weight loss
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76
Q

How is achalasia diagnosed

A
  1. Barium swallow
  2. Esophageal manometry - determines the lack of contraction - peristalsis may be absent with very high LES pressures
  3. EGD to rule out abnormal growths and/or scarring - it may be difficult to pass the scope through the LES
  4. Radiographic examination
    • on x-ray films the esophagus appears dilated with a narrow “bird beak” at the distal end
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77
Q

How is achalasia treated

A

Treatment is aimed at relaxing the contraction of the sphincter between the stomach and esophagus
1. Botulinum toxin injection
2. Drugs such as nitrates or calcium channel blockers may not be very effective but are used in patients who cannot be dilated or have surgery, to reduce the LES pressure
3. Achalasia balloon dilation
4. Heller’s myotomy - surgery to cut the muscle between the stomach and esophagus
5. A newer treatment is Peroral endoscopic myotomy (POEM) - a submucosal tunnel is created by the endoscopist, followed by a myotomy of the circular muscle of the lower esophagus
6. Rarely, a transhiatal esophagectomy may be recommended

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78
Q

What are potential complications of achalasia

A
  1. Retention and stasis in the esophagus
  2. Esophagitis
  3. Aspiration of esophageal contents
  4. Bronchopneumonia
  5. Prevalence of esophageal carcinoma is higher than normal
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79
Q

What is nutcracker (jackhammer) esophagus

A

When swallowing contractions are too powerful

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80
Q

What are causes of nutcracker (jackhammer) esophagus

A

GERD

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81
Q

What are signs and symptoms of nutcracker (jackhammer) esophagus

A
  1. Chest pain
  2. Dysphagia
  3. Heartburn
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82
Q

How is nutcracker (jackhammer) esophagus diagnosed

A
  1. Esophageal manometry - defined manometrically as peristalsis with contractile amplitude that is two to three times the normal value
  2. Upper GI endoscopy to rule out abnormal growths or scars
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83
Q

What is the treatment for nutcracker (jackhammer) esophagus

A
  1. Anti-reflux therapy
  2. Drugs such as nitrates or calcium channel blockers provide relief for some patients, but overall not very effective
  3. Tricyclic antidepressants - lower sensation of pain
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84
Q

What is Diffuse Esophageal Spasm

A

When the esophagus contracts in an uncoordinated way

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85
Q

What causes diffuse esophageal spasm

A

Disruption or damage to nerves coordinating the muscles of the esophagus

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86
Q

What are signs and symptoms of diffuse esophageal spasm

A
  1. Chest pain - mimics angina pectoris
  2. Dysphagia - may be present with both solids and liquids and is most severe when the patient ingests extremely hot or cold foods
  3. Heartburn
  4. In most cases the distal two-thirds of the esophagus shows a muscular thickening
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87
Q

How is diffuse esophageal spasm diagnosed

A
  1. Barium swallow - May show isolated, uncoordinated movements of the lower two-thirds of the esophagus - the entire two-thirds of the esophagus may contract as a unit, propelling barium both retrograde and into the stomach
  2. Esophageal manometry - may reveal a simultaneous high-amplitude and abnormally long contraction in the lower two-thirds of the esophagus
  3. Upper GI endoscopy
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88
Q

What are potential complications of diffuse esophageal spasm

A

Formation of strictures or squamous cell carcinoma

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89
Q

What is the treatment for diffuse esophageal spasm

A
  1. Botulinum toxin
  2. Drugs to relax the muscle
  3. Myotomy
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90
Q

What are esophageal webs

A
  1. Thin circumferential mucosal shelves within the esophagus mucosa and submucosa only
  2. Generally occur in the upper esophagus
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91
Q

What causes esophageal webs

A
  1. GERD
  2. Consider idiopathic causes
  3. Possibly iron deficiency anemia - in middle aged women is known as Paterson-Kelly or Plummer-Vinson syndrome
    • in these cases the web seems to regress spontaneously with treatment of the iron-deficiency anemia
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92
Q

What are symptoms of esophageal webs

A

Intermittent dysphagia

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93
Q

How are esophageal webs diagnosed

A
  1. Barium swallow
  2. Upper GI endoscopy - although it can provide diagnosis it usually ruptures the web
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94
Q

What are potential complications of esophageal webs

A

With Paterson-Kelly or Plummer-Vinson syndrome is also associated with an increased incidence of postcricoid carcinoma

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95
Q

How are esophageal webs treated

A

1.If the obstruction remains after endoscopy, bougie-nage with Maloney dilators may be used
2. In rare cases, a patient may require dilation with a pneumatic balloon
3. If symptoms recur, further dilation may be necessary

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96
Q

What are esophageal rings

A
  1. Also known as Schatzki’s rings or B-rings
  2. They are usually thicker than webs
  3. Circumferential shelves within the esophageal mucosa, submucosa, and muscle
  4. Rings usually appear in the lower esophagus and at the GE junction
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97
Q

What causes esophageal rings

A

GERD

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98
Q

What are signs and symptoms of esophageal rings

A
  1. They are more likely to cause symptoms than webs
  2. Progressive dysphagia is the most common
  3. Food impaction - which is often associated with eating food rapidly
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99
Q

How are esophageal rings diagnosed

A
  1. Barium swallow
  2. Upper GI endoscopy with biopsy to rule out malignancy
    • needed to rule out the presence of a peptic stricture
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100
Q

What is the most common complication of esophageal rings

A
  1. Food impaction that requires endoscopic removal
  2. Dilation follows at a later time due to the inflammation caused by the food impaction
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101
Q

What is the treatment for esophageal rings

A
  1. Most require dilation at variable intervals using:
    • Maloney dilation
    • pneumatic balloon dilators
    • graduated wire-guided dilators
  2. Steroid injection into the ring
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102
Q

What are foreign body obstructions of the esophagus

A
  1. The most common site of acute foreign-body obstruction
  2. Ingestion of nondigestible object or an object too large to pass the digestive tract
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103
Q

What are risk factors of foreign body obstructions of the esophagus

A
  1. The majority of foreign body ingestions occur in children with coins being the most frequently ingested
  2. In adults, the most frequently observed foreign body is meat
  3. Most foreign bodies pass spontaneously into the stomach through the GI tract
  4. Individuals with mental illness may be at risk for ingesting other foreign objects; removal of which may require endoscopy or surgical intervention
  5. If a pill is swallowed with little or no fluid intake with the patient in supine position or just before going to bed, it can remain in the esophagus, eroding esophageal tissue and causing an ulcer
    • substances known to damage the esophagus are - doxycycline, tetracycline, clindamycin, potassium chloride, ferrous sulfate, quinidine, aspirin, NSAIDs, and vitamin A
  6. If small alkaline batteries are swallowed, they must be retrieved as soon as possible, and any sign of perforation should be treated surgically because the local corrosive effects may be fatal
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104
Q

What are signs and symptoms of a foreign body obstruction of the esophagus

A
  1. Pain
  2. Dysphagia
  3. Odynophagia
  4. Inability to swallow own secretions
  5. In pediatric patients, a chronic foreign body (where a foreign object has been in the esophagus for 1-12 months) presents itself as a recurrent cough or abdominal pain
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105
Q

How are foreign body obstructions of the esophagus diagnosed

A
  1. Plain film chest x-ray - may provide information on the location and size of the obstruction
  2. Upper GI endoscopy
  3. note - barium swallow may result in aspiration and hinder endoscopic removal
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106
Q

What are potential complications of a foreign body obstruction of the esophagus

A
  1. Esophageal ulceration
  2. Perforation or penetration of the aorta or its branches followed by hemorrhage
  3. The risk of perforation can be minimized by the use of overtubes and hoods that cover objects as they are being withdrawn
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107
Q

What is the treatment for foreign body obstructions of the esophagus

A
  1. Smooth muscle relaxant - glucagon or sublingual nitroglycerin may relax the LES in adults and allow objects to pass
    - not a very common practice anymore
  2. Endoscopic removal
  3. Surgery
  4. Treatment for damage to the esophagus from medication involves stopping the medication, relieving odynphagia, providing adequate nutrition and watching for complications
    - in 3-6 weeks the patients symptoms should be relieved
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108
Q

What are caustic injuries to the esophagus

A

Accidental or deliberate ingestion of highly alkaline or acid compounds that may cause injury to the esophagus

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109
Q

What are causes for caustic injuries to the esophagus

A
  1. Highly alkaline compounds, such as lye, drain cleaners, and bleaches, typically cause more damage than acidic compounds
  2. Highly acidic compounds typically include toilet bowel cleaners and battery fluids
  3. Ingestion of highly acidic or highly alkaline compounds, causing burns to the mucosa
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110
Q

What is the prognosis for caustic injuries of the esophagus

A
  1. Dependent on degree, depth, and extent of injury or damage
  2. May result in stricture formation
  3. Increased risk for squamous cell carcinoma
  4. Dilation may be required in the future for second-degree injury
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111
Q

What are signs and symptoms of caustic injuries to the esophagus

A
  1. Odynophagia (most common)
  2. Dysphagia
  3. Chest pain
  4. Drooling
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112
Q

How long can it take for symptoms to completely manifest

A

It can take up to 14 days for symptoms to fulling manifest due to the necrotizing process of the esophageal tissue

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113
Q

How is a caustic injury of the esophagus diagnosed

A
  1. X-rays of the neck, chest and abdomen to rule out perforation or pneumonia
  2. Endoscopy - to document the extent of the injury, unless there is evidence of a perforation or extensive necrosis
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114
Q

When is an endoscopy performed after a caustic injury to the esophagus

A

12-24 hours after ingestion, since tissue damage is usually not immediate

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115
Q

How many stages of esophageal burns are there

A

3

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116
Q

What are signs of a first-degree burn of the esophagus

A
  1. Hyperemia and edema of the mucosa
  2. Damage is limited to the mucosa
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117
Q

What are signs of a second-degree burn of the esophagus

A

Exudate, erosions, and shallow ulcers destructive of the mucosa and submucosa with penetration of the injury into the muscle layers

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118
Q

What are signs of a third-degree burn of the esophagus

A

Deep ulceration, circumferential necrosis, often the presence of black coagulum, and full-thickness injury with extension into the pleura and mediastinum

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119
Q

What is the treatment for caustic injuries of the esophagus

A

It depends on the product ingested and extent of damage, but patients should always be kept NPO

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120
Q

What is the treatment for Alkaline caustic injuries to the esophagus

A
  1. Nasogastric (NG) tube may be placed
  2. Vital signs monitored and supported
  3. Intake and output (I&O) monitored
  4. Endotracheal tube for laryngeal edema or respiratory distress
  5. Medications include corticosteroids and antibiotics (H2 blockers and PPIs)
  6. Parenteral feeding
  7. Surgery with colonic interposition for patients who deteriorate despite intensive therapy, esophagectomy may be required for third-degree injury
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121
Q

What is the treatment for Acidic caustic injuries of the esophagus

A
  1. Administer large volumes of milk and water following the ingestion to dilute acid
  2. Nasogastric (NG) tube may be placed
  3. Vital signs monitored and supported
  4. Intake and output (I&O) monitored
  5. Endotracheal tube for laryngeal edema or respiratory distress
  6. Medications include corticosteroids and antibiotics (H2 blockers and PPIs)
  7. Parenteral feeding
  8. Surgery with colonic interposition for patients who deteriorate despite intensive therapy, esophagectomy may be required in third degree injury
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122
Q

What are potential complications of caustic injuries to the esophagus

A
  1. Formation of strictures
  2. Squamous cell carcinoma
  3. Post-corrosive complications can be fatal due to perforation or tracheal necrosis
  4. Fistula formation
  5. Pneumonia
  6. Anemia

All can prolong hospital stay and be another cause of mortality

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123
Q

What is esophageal atresia

A
  1. During embryonic development, the trachea and esophagus develop as one tube, separating into two distinct tubes. In congenital defect, the esophagus forms improperly
  2. Fistula - separation is incomplete where the upper esophagus attaches to the trachea and there continues to be a communication between the two tubes
  3. Atresia - the remain portion of the upper or lower esophagus ends in a blind sac
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124
Q

What causes esophageal atresia

A

Congenital defect

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125
Q

What are signs and symptoms of esophageal atresia

A
  1. Fistula results in aspiration on first feeding of the neonate
  2. Atresia without tracheal connection results in aspiration
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126
Q

How is esophageal atresia diagnosed

A
  1. Prenatal ultrasound
  2. Cinematoradiography (the filming of motion pictures through a fluoroscope or X-ray machine)
  3. Post-party nasogastric tube (NGT) placement
  4. X-ray
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127
Q

What is the treatment for esophageal atresia

A

Includes surgery, followed by progressive dilatation as the child grows

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128
Q

What is Barrett’s esophagus

A
  1. Epithelial metaplasia in which normal squamous epithelium is replaced by one or more of the following types of columnar epithelium: a distinctive, specialized columnar epithelium; a junctional type of epithelium; and/or gastric fundus
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129
Q

What are risk factors for Barrett’s esophagus

A
  1. 20% of patients with esophageal reflux develops Barrett’s esophagus
    Reasons for screening for Barrett’s
  2. Chronic GERD
  3. Hiatal hernia
  4. Age greater than or equal to 50 years
  5. Male gender
  6. White race
  7. Central obesity
  8. Cigarette smoking
  9. A confirmed history of Barrett’s esophagus or esophageal adenocarcinoma in a first-degree relative
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130
Q

What causes Barrett’s esophagus

A
  1. Replacement of normal squamous cells of the esophagus with columnar cells of the stomach (precancerous adenocarcinoma )
  2. Result of years of GERD with stomach contents refluxed into the esophagus
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131
Q

What are signs and symptoms of Barrett’s esophagus

A

Barrett’s esophagus usually shows no signs; symptoms are usually that of GERD
1. Chronic heartburn
2. Dysphagia
3. Regurgitation of stomach contents
4. Bitter or sour taste in the mouth
5. Nausea in the morning

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132
Q

How is Barrett’s esophagus diagnosed

A

By upper GI endoscopy with biopsy

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133
Q

What is the treatment for Barrett’s esophagus

A
  1. Controlling acid reflux
  2. Endoscopic mucosal resection
  3. Ablation therapies

Low grade dysplasia is usually managed conservatively
High grade dysplasia options include
1. Endoscopic therapy
2. Surgery
3. Intensive surveillance until biopsy reveals adenocarcinoma

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134
Q

What are potential complications of Barrett’s esophagus

A

The prevalence of adenocarcinoma in Barrett’s patients is greater than the general population
It is the only known precursor to adenocarcinoma

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135
Q

Wha is a bronchoesophageal esophageal fistula

A

An abnormal passage between the bronchus and the esophagus

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136
Q

What is a tracheoesophageal fistula

A

An abnormal passage between the trachea and the esophagus

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137
Q

What are risk factors / causes of bronchoesophageal or tracheoesophageal fistulas

A

Usually cancer but may be caused by a benign inflammatory process such as infectious esophagitis or trauma

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138
Q

What are signs and symptoms of bronchoesophageal or tracheoesophageal fistulas

A
  1. Chronic cough
  2. Fever
  3. Recurrent pulmonary infection
  4. May or may not have dysphagia
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139
Q

How are bronchoesophageal or tracheoesophageal fistulas diagnosed

A

By contrast tests such as barium swallow, CT scan or MRI

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140
Q

What are the treatment options for bronchoesophageal or tracheoesophageal fistulas

A

Surgery to remove necrotic tissue and to close the fistula

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141
Q

What is an aortoesophageal fistula

A

An abnormal passage between the aorta and the esophagus

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142
Q

What causes aortoesophageal fistulas

A

May develop when:
1. An ingested foreign body lodges in the region above the aortic arch
2. A tumor extends through the wall of the esophagus

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143
Q

What are signs and symptoms of aortoesophageal fistulas

A
  1. Minor bleeding as an erosion connects the aorta and esophagus
  2. Massive bleeding can occur at any time and almost always causes death
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144
Q

How is an aortoesophageal fistula diagnosed

A

An upper GI endoscopy
Contrast tests such as barium swallow, CT scan or MRI

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145
Q

What is the treatment for an aortoesophageal fistula

A

Surgery to remove necrotic and irreversibly damaged tissue and to close the fistula

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146
Q

What is a complication of aortoesophageal fistula

A

Massive bleeding may begin at any time and almost always causes death

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147
Q

What are esophageal varices

A
  1. Abnormal, enlarged, or dilated veins in the lower part of the esophagus. Can occur in other parts of the GI tract, including the stomach and hemorrhoidal plexus
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148
Q

How are esophageal varices classified

A

Based on the size on a scale of I-IV
Classes III and IV have the greatest risk for bleeding

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149
Q

What is the prognosis for esophageal varices

A
  1. After an episode of esophageal bleeding, a patient has a 60% chance of a rebleed within a year
  2. Hemorrhage has a mortality of at least 20% at 6 weeks
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150
Q

What are the causes of esophageal varices

A
  1. Related to portal hypertension
  2. Most often associated with alcoholic cirrhosis
  3. May also be seen in:
    • Chronic hepatitis
    • Portal vein thrombosis
    • Primary biliary cirrhosis
    • Biliary atresia
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151
Q

What is portal hypertension

A
  1. Fibrotic liver changes and hepatic vein obstruction are associated with portal hypertension due to resistance of blood flow
  2. In addition, there is intrahepatic vasoconstriction
  3. The pressure is transmitted to pre-existing collateral circulation, which results in dilatation of the submucosal esophageal veins
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152
Q

What are signs and symptoms of esophageal varices

A
  1. Varices are usually asymptomatic
  2. Bleeding is painless and life-threatening
  3. Bleeding presents with classic upper GI bleed symptoms, resulting in:
    - Voluminous hematemesis
    - Symptoms of hypovolemia
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153
Q

How are esophageal varices diagnosed

A
  1. Upper GI endoscopy
  2. Esophageal capsule study
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154
Q

What is the treatment for esophageal varices

A

Based on three phases
1. Prevent variceal hemorrhage
2. Control acute hemorrhage
3. Endoscopic treatment with EVL

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155
Q

In treatment for esophageal varices; what are ways to prevent variceal hemorrhage

A
  1. Cessation of alcohol consumption
  2. Use of non selective beta blockers such as nadolol or propranolol
  3. Prophylactic endoscopic variceal ligation (EVL)
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156
Q

In treatment for esophageal varices how do you control acute hemorrhage

A
  1. Treat shock first - replacement of blood and fluid lost
  2. Correction of concurrent coagulopathy with fresh frozen plasma (FFP)
  3. Airway maintenance
  4. Pharmacological agents, including octreotide, which decrease portal pressure
  5. Transjugular intrahepatic portosystemic shunts (TIPS)
  6. Balloon tamponade should only be used for a maximum of 24 hours due to complications of necrosis and perforation
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157
Q

In treatment for esophageal varices what is endoscopic treatment with EVL

A
  1. Antibiotics to reduce the chances of infection
  2. Complications include:
    • Perforation
    • Mediastinitis
    • Rebleeding
    • Stricture formation
    • Ulcerations
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158
Q

What are different esophageal infections

A
  1. Candidiasis
  2. Herpetic esophagitis
  3. Cytomegalovirus infection
  4. HIV esophagitis
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159
Q

What are contributing factors of getting candidiasis of the esophagus

A
  1. Diabetes
  2. Malignancy and chemotherapy
  3. HIV
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160
Q

What are causes of esophageal candidiasis

A
  1. Organism: fungus - Monilia albicans
  2. Rare that healthy individuals are found with this infection
  3. Risk factors
    • poor immune system
    • diabetes
    • cancer
    • antibiotic use
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161
Q

What are signs and symptoms of esophageal candidiasis

A
  1. Dysphagia
  2. Odynophagia
  3. Severe infection can destroy the nerves, causing motility disorders
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162
Q

How is esophageal candidiasis diagnosed

A
  1. Endoscopy shows whitish plaques with a normal mucosal pattern between plaques
  2. Barium swallow is not definitive
  3. Definitive diagnosis is by demonstration of mycelial forms in tissue samples obtained from a biopsy or cytology brushing
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163
Q

What is the treatment for esophageal candidiasis

A
  1. Fluconazole
  2. Itraconazole suspension
  3. Voriconazole
  4. Amphotericin B
  5. Caspofungin
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164
Q

What are possible complications of esophageal candidiasis

A
  1. Yeast dissemination
  2. Hemorrhage
  3. Perforation (rare)
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165
Q

What are contributing factors of Herpetic esophagitis

A
  1. Lymphoma
  2. Leukemia
  3. Immunocompromised condition
  4. HIV infection
  5. Organ transplantation
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166
Q

What causes herpetic esophagitis

A

The Herpes simplex virus (HSV)

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167
Q

What are signs and symptoms of Herpetic esophagitis

A
  1. Dysphagia
  2. Odynophagia
  3. Nausea
  4. Chest pain
  5. Heartburn
  6. Fever
  7. Multiple small, deep ulcers on endoscopy (in the back of the mouth and throat)
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168
Q

How is Herpetic esophagitis diagnosed

A
  1. Virus tissue culture
  2. Characteristic cellular changes on cytology or biopsy
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169
Q

What are potential complications of herpetic esophagitis

A

Spontaneous esophageal perforation has been reported in cases of esophageal HSV

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170
Q

What is the treatment for herpetic esophagitis

A
  1. Topical anesthesia
  2. Antacids
  3. Soft diet
  4. Medication
    • acyclovir
    • famciclovir
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171
Q

What is cytomegalovirus (CMV) infection

A

May appear as a spectrum of lesions in the esophagus ranging from superficial mucosal inflammation to giant ulcerations

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172
Q

What causes cytomegalovirus infection

A

Organism - cytomegalovirus (CMV)

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173
Q

Who is at risk for getting cytomegalovirus infection

A
  1. Organ transplant patients
  2. Those undergoing long-term renal dialysis
  3. HIV or AIDS patients
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174
Q

What are signs and symptoms of cytomegalovirus infection

A
  1. Dysphagia
  2. Odynophagia
  3. Retrosternal pain
  4. Nausea and vomiting
  5. Abdominal pain
  6. Fever
  7. Diarrhea
  8. Weight loss
  9. Chest pain
  10. Hemoptysis
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175
Q

How is cytomegalovirus infection of the esophagus diagnosed

A
  1. Endoscopy - biopsy shows cytomegalovirus inclusion bodies in the cytoplasm or nucleus of these cells
    • appear as a spectrum of lesions in the esophagus, ranging from superficial mucosal inflammation to giant ulcerations
    • biopsy should be sent for viral culture; cytology brushings are sent for stain to detect infected cells
  2. Double contrast barium swallow
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176
Q

What is the treatment for cytomegalovirus esophagitis

A

Symptomatic relief:
1. Viscous lidocaine (Xylocaine)
2. H2 blockers
3. Antacids
4. Sucralfate

Antiviral medications
1. Ganciclovir
2. Valganciclovir (Valcyte)
3. Cidofovir (Vistide)
4. Foscarnet (Foscavir)

In some cases, combination therapy of two or more drugs may be necessary

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177
Q

What is a contributing factor to HIV esophagitis

A
  1. Immune deficiency
  2. May be present in patients who are HIV positive
  3. Usually is secondary to one of the other infectious esophagitis types, such as infections with Candida, HSV or CMV
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178
Q

What causes HIV esophagitis

A

Organism - human immunodeficiency virus (HIV)

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179
Q

What are signs and symptoms of HIV esophagitis

A
  1. Dysphagia
  2. Odynophagia
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180
Q

How is HIV esophagitis diagnosed

A

EGD with tissue culture to differentiate between HIV and CMV ulcers

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181
Q

What is the treatment for HIV esophagitis

A

Steroids
Antiviral medications

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182
Q

What is Crohn’s esophagitis

A

Crohn’s disease can produce inflammation anywhere in the GI tract
Inflammation isolated to the esophagus can occur but is usually associated with disease elsewhere in the GI tract

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183
Q

What is Eosinophilic esophagitis

A

A chronic, allergic, inflammatory disease characterized by excessive histamine production and mast cell degradation
It is usually found in the upper GI tract

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184
Q

What are contributing factors to Eosinophilic esophagitis

A

Occurs in people who are highly allergic and have multiple food allergies, allergic rhinitis, asthma and eczema

Is is associated with a heightened immune response, causing inflammation and luminal narrowing in the esophagus

Can occur secondary to Eosinophilic gastritis

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185
Q

What are signs and symptoms of Eosinophilic esophagitis

A
  1. Dysphagia for solid foods
  2. Episodes of food impaction
  3. Heartburn
  4. Aphthous ulcers in the mouth are often associated with this disease
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186
Q

How is Eosinophilic esophagitis diagnosed

A
  1. Barium swallow
  2. Endoscopy with biopsy
    - the esophageal appearance shows circular rings, linear furrows, whitish papules, and plaques
    - diagnosis is made by identifying eosinophil count >10 per high-power field on microscopic examination of biopsies
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187
Q

What are potential complications of Eosinophilic esophagitis

A
  1. Narrowing of the esophagus by scarring or stricture
  2. Barrett’s esophagus
  3. Failure to thrive
  4. Nausea and vomiting in children; food impaction in adults
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188
Q

What is the treatment for Eosinophilic esophagitis

A

Aimed at stopping the allergic response and identifying and avoiding allergy triggers

  1. H2 blockers
  2. Mast cell stabilizer
    • Montelukast sodium
    • Cromolyn sodium
    • Topical corticosteroid inhaler
  3. PPIs
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189
Q

What is a Mallory-Weiss tear

A

A mucosal tear at the GE junction

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190
Q

What causes a Mallory-Weiss tear

A

Associated with prolonged, forceful vomiting; trauma; childbirth; or complications of EGD

Patients who have a Mallory-Weiss tear often have a history of alcohol abuse

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191
Q

What are symptoms of a Mallory-Weiss tear

A

Prolonged emesis or dry heaves

Followed by vomiting bright red blood

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192
Q

How are Mallory-Weiss tears diagnosed

A

Can be diagnosed and treated during an upper endoscopy

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193
Q

What are complications of a Mallory-Weiss tear

A

In severe cases, they can cause severe bleeding

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194
Q

What is the treatment for a Mallory-Weiss tear

A
  1. Generally treated conservatively because bleeding stops spontaneously
  2. Profuse bleeding may be controlled endoscopically with a coagulating contact probe or by placing several clips to close the tear
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195
Q

What is an Upper GI tract perforation

A
  1. An artificial hole or perforation in the upper GI tract
  2. Can occur in the esophagus, stomach, or duodenum
  3. Can be the result of:
    • blunt trauma
    • increased intraesophageal pressure
    • underlying pathology
    • ingestion of a foreign body
    • mechanical trauma during endoscopy (more common during therapeutic procedures)
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196
Q

What are risk factors for perforation during endoscopy

A
  1. Anterior cervical osteophytes
  2. Strictures
  3. Zenker’s diverticulum
  4. Ischemia
  5. Neoplasm or malignancy
  6. Caustic ingestion
  7. Uncooperative patient
  8. Ulcer disease
  9. Biopsies of ulcerated lesions
  10. Impaction in hiatal hernia sac
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197
Q

What are potential causes for perforation during upper GI endoscopy

A
  1. Instrument trauma 2. Complication from:
    - all types of dilators - ulcer disease
    - electrocautery. - anomaly in anatomy
    - biopsy or EMR. - previous injury or disease process
    - Retroduodenal perforations can occur with sphincterotomy
    - gastric mucosal stripping and duodenal perforations (with push
    Enteroscopy and use of overtubes)
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198
Q

What are signs and symptoms of perforation of the esophagus

A

Pain is the most consistent sign of an upper GI perforation - the type of pain and other signs are determined by the site of perforation

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199
Q

What are signs and symptoms of cervical esophagus perforation

A
  1. Dysphagia
  2. Crepitus and stiffening of the neck
  3. Neck and throat pain aggravated by swallowing or movement of spine
  4. May experience
    • fever
    • tenderness on the affected area
    • neck swelling
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200
Q

What are signs and symptoms of thoracic esophageal perforation

A
  1. Substernal and epigastric pain that increases with respiration and movement of trunk
  2. Shortness of breath
  3. Cyanosis
  4. Pleural effusion
  5. Back pain may be present
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201
Q

What are signs and symptoms of distal esophageal perforation, near the diaphragm

A
  1. Shoulder pain
  2. Dyspnea
  3. Severe back and abdominal pain
  4. Tachycardia
  5. Cyanosis
  6. Diaphoresis
  7. Hypotension
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202
Q

What are signs and symptoms of Boerhaave’s syndrome (spontaneous, non traumatic rupture of the esophagus)

A
  1. Dysphagia following a vomiting episode
  2. Severe chest and abdominal pain
  3. Appears acutely ill
  4. Hypotension
  5. Fever
  6. Subcutaneous emphysema
  7. Unilateral absence of breath sounds
  8. Pleural effusion
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203
Q

What are signs and symptoms of gastric perforation

A
  1. Severe back and abdominal pain
  2. Tachycardia
  3. Cyanosis
  4. Diaphoresis
  5. Hypotension
  6. Drop in temperature, followed by high fever
  7. Prolonged distention following gastroscopy
  8. Disappearance of liver dullness on percussion due to free air in the abdomen
  9. Indications of leaking gastric contents, causing peritonitis
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204
Q

What are signs and symptoms of duodenal perforation

A
  1. Initially, vital signs are stable
  2. Experiences brief period of improvement, then sudden local or generalized pain
  3. Peritonitis
  4. Rigid abdomen
  5. High fever
  6. Hypotension
  7. Tachycardia
  8. Severe pain inhibiting abdominal movement
  9. Inability to breathe deeply
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205
Q

How are upper GI perforations diagnosed

A
  1. Esophagram using Gastrografin is the mainstay for esophageal perforation
  2. Signs and symptoms
  3. Surgical consultation is needed
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206
Q

What is the treatment for upper GI perforation

A
  1. Symptomatic treatment and close observation if perforation is suspected
  2. Medical management - small perforations that are noted early may be medically managed
  3. Conservative management is contraindicated if: major leak is apparent; perforation occurs through an ulcer or tumor
  4. Surgery - depends on the type
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207
Q

What is the medical management for someone with an upper GI perforation

A
  1. Nasogastric or pharyngeal suction placement
  2. Parenteral nutrition
  3. Broad spectrum antibiotics
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208
Q

What are the different types of surgeries used in treatment for upper GI perforation

A
  1. Cervical perforation - may be sutured and patient treated with antibiotics
  2. Intrathoracic perforations - often need surgery
  3. Small gastric perforations - can be managed conservatively
  4. Anterior gastric perforations with peritoneal signs and free air - require surgical intervention
  5. Perforations from sphincterotomy - may require stent placement
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209
Q

What are complications of upper GI perforations

A
  1. Dysphagia
  2. Hematemesis
  3. Melena
  4. Dyspnea
  5. Marked chest pain
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210
Q

What are acid peptic disorders of the stomach (also known as Peptic ulcer disease PUD)

A

An imbalance in the acid and peptic activity of gastric juices

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211
Q

What are risk factors of developing peptic ulcer disease

A
  1. Helicobacter pylori (H. Pylori0 infection
  2. Chronic use of salicylates and nonsteroidal anti inflammatory drugs (NSAIDs)
  3. Family history of gastric ulcers
  4. Cigarette smoking
  5. Excessive acid production from Gastrinomas (gastrin-secreting tumors) seen in Zollinger-Ellison syndrome
  6. High-dose and prolonged use of corticosteroids, bisphosphonates, potassium chloride, and some chemotherapeutic agents
  7. The role of emotional and physical stress and personality type in the development of gastric ulcers remains controversial
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212
Q

What are causes of peptic ulcer disease

A
  1. Strong link between H. Pylori and ulcer disease
  2. Inflammation, erosions, or ulcers occur when the normal balance between the factors that protect the gastric mucosa and the factors that can promote gastric injury is upset
  3. Causes may be chemical, mechanical, infectious, or ischemic
  4. Protective factors
  5. Injurious factors
  6. Decreased pyloric sphincter pressure
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213
Q

What are protective factors that can cause peptic ulcer disease

A
  1. Intact gastric epithelium
  2. Bicarbonate and mucus secretion
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214
Q

What are injurious factors that cause peptic ulcer disease

A
  1. Gastric acid
  2. Bile acids
  3. Pepsin
  4. Ingested substances
  5. Bacterial infection
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215
Q

How can decreased pyloric sphincter pressure cause peptic ulcer disease

A
  1. May permit reflux of duodenal material into the stomach that can disrupt the gastric mucosal barrier
  2. Continued disruption may lead to erosion and perforation, resulting in peritonitis
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216
Q

What are signs and symptoms of Peptic ulcer disease

A
  1. Pain and/or burning - sometimes relieved temporarily by eating
  2. Nausea and vomiting
  3. Appetite changes
  4. Hemorrhaging, in more severe cases
  5. Abdominal pain that is localized to the epigastrium and does not radiate
  6. Presence of pain that awakens the person from sleep, which is the most discriminating (although in exact) symptom
  7. Complaints of black or bloody stool
  8. Vomit that resembles coffee grounds or contains blood
  9. Sharp, severe, and continuous upper abdominal pain (sometimes radiating to the back)
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217
Q

How is Peptic ulcer disease diagnosed

A
  1. Upper GI series with barium or a water-soluble contrast such as Gastrografin
  2. CT scan for evaluation of abdominal pain or EGD
  3. Lesions
    • Prepyloric ulcers are usually benign
    • gastric ulcers are potentially malignant and require tissue biopsy. 1:100 gastric lesions are malignant
  4. Rapid urease biopsy to rule out H. Pylori
    • serum antibodies useful only for the first episode of illness
    • future testing will show antibodies present whether or not the ulcer is present
  5. Differential diagnosis to rule out:
    • Zollinger- Ellison syndrome (gastric acid hypersecretion)
    • unrecognized malignancy
    • Crohn’s disease
    • Tuberculosis (TB)
    • Lymphoma
    • Immunodeficiency
    • CMV
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218
Q

What is the treatment for Peptic ulcer disease

A
  1. Drug therapy
  2. Diet
  3. Surgery
  4. Follow-up
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219
Q

What is the drug therapy treatment for Peptic Ulcer disease

A
  1. PPIs
  2. H2 blockers
  3. Sucralfate - forms a protective gel over the ulcer
  4. Antacids - neutralize gastric acid, enhance mucosa barrier, and heighten tone of the LES
  5. Prostaglandins - have antisecretory and cytoprotective effects
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220
Q

What is the dietary treatment for peptic ulcer disease

A
  1. The effectiveness of diet on ulcer healing is unknown
  2. Foods known to increase acid secretion include milk and milk products, alcoholic and caffeinated beverages, and decaffeinated coffee
  3. Encourage patients to avoid foods that cause symptoms
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221
Q

What is the surgical treatment for peptic ulcer disease

A
  1. Rare for benign peptic disease, as most patients can be managed medically
  2. May be done for:
    • refractory ulcers
    • uncontrolled hemorrhage
  3. Gastric PUD surgery - emergency gastric surgery is required for uncontrolled hemorrhage from a gastric ulcer
    • surgical options include vagotomy with pyloroplasty, Billroth I (gastroduodenostomy and hemigastrectomy), Billroth II (gastrojejunostomy), total gastrectomy ( esophagojejunostomy) or gastric resection (antrectomy)
    • complications include- dumping syndrome, hypoglycemic symptoms, nutrient deficiency states, weight loss, diarrhea, and recurrent ulceration
    • the risk of gastric carcinoma may be increased after certain types of surgery for PUD
  4. Duodenal PUD surgery- if emergency surgery is required to treat complications from duodenal ulcer; options may consist of a truncal vagotomy and drainage (pyloroplasty or gastrojejunostomy), a selective vagotomy and drainage or a highly selective vagotomy
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222
Q

What is the follow-up treatment for peptic ulcer disease

A
  1. Repeat EGD in about 8 weeks to document healing is often done
  2. Ulcers refractory to medical management are rare and noncompliance is the most common cause
  3. If ulcers remain with compliance to medical management, a repeat EGD with biopsy is indicated
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223
Q

What are potential complications of peptic ulcer disease

A
  1. Hemorrhage
    • occurs in approximately 15% of patients with an ulcer
    • in some cases life threatening hemorrhage is the first sign of ulcer
  2. Perforation - less common and tends to occur in the lesser curvature of the stomach
  3. Penetration - similar to perforation, except the ulcer crater extends into an adjacent organ, most commonly the liver
  4. Obstruction - can result from impaired antral motility caused by inflammation of the ulcer
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224
Q

What is gastric cancer

A

One of the most common types of cancers in the world
It’s incidence varies with geographic region
Over the last few decades, the incidence of gastric cancer has rapidly declined due to the discover of H. Pylori, use of refrigeration for food storage, frequent use of antibiotics to treat infections, and reduction of other dietary and environmental risk factors

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225
Q

What are risk factors of developing gastric carcinoma

A
  1. Families with type A blood
  2. Males more than females
  3. Risk increases with age
  4. Persons with diets high in starch, nitrates, pickled vegetables, salted fish, and meat
  5. Having certain conditions such as:
    • adenomatous polyps
    • Menetrier’s disease (hypoproteinemic hypertrophic gastropathy)
    • common variable immune deficiency (CVID)
    • Peutz-Jeghers syndrome (PJS) or Li-Fraumeni syndrome (LFS)
    • Gastric ulcers
    • Previous gastric surgery
    • Achlorhydria
    • Pernicious anemia
    • Chronic Atrophic gastritis
    • intestinal metaplasia
    • H. Pylori infection ]
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226
Q

What are different types of gastric carcinoma

A
  1. 90-95% adenocarcinoma
  2. 5-10% lymphoma, leiomyomas, carcinoid, metastatic disease to the stomach
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227
Q

Where do gastric carcinomas develop most often

A
  1. Most develop in the antrum or along the lesser curvature
  2. Greater curvature lesions are considered malignant until proven otherwise
  3. Cancers that develop from gastric atrophy are usually found in the upper stomach
  4. Metastatic lesions originate primarily in the liver or lungs
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228
Q

What is the prognosis for gastric carcinomas

A
  1. Early gastric cancer that is limited to the mucosa or submucosa - 5 year survival rate is 95%
  2. Superficial spreading without deep invasion - 5 year survival rate is 95%
  3. Without metastatic disease after a partial gastrectomy with removal of localized lymph nodes that are negative - 5 year survival rate is 50%
  4. Linitis plastica, or “leather bottle” stomach, which is a submucosal tumor that spreads diffusely - worst prognosis
  5. At presentation, 65% of gastric cancers in the U.S. are at an advanced stage
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229
Q

What are the most common causes of gastric carcinomas

A
  1. Gastric surgery that results in achlorhydria
  2. Pernicious anemia
  3. Gastric atrophy
  4. Intestinal metaplasia
  5. Adenomatous polyps
  6. H. Pylori
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230
Q

What are signs and symptoms of Gastric carcinoma

A
  1. Unexplained weight loss, early satiety, or anorexia
  2. Anemia
  3. Abdominal or epigastric mass
  4. Gastric outlet obstruction, including nausea and vomiting
  5. Ascites
  6. Enlarged lymph nodes in supraclavicular area
  7. Epigastric discomfort
  8. Vomiting
  9. Occult blood
  10. Low hematocrit or hypoalbuminemia
  11. Gross hematemesis is rare
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231
Q

How can gastric cancer metastasize

A
  1. Direct extension to the greater and lesser omentum, liver, pancreas, diaphragm, spleen, transverse colon, mesocyclone, biliary tract, and the duodenum
  2. Through the lymphatics to local perigastric nodes; regional to celiac, common hepatic, left gastric, or splenic nodes; distant to supraclavicular, left axillary, or umbilical nodes
  3. Through hematogenous to the liver, pulmonary system, bone or central nervous system (brain)
  4. Within the perineum to the pelvis (ovary or rectum) or general dissemination
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232
Q

How are gastric carcinomas diagnosed

A
  1. Double contrast upper GI films
  2. Computerized tomography (CT) scan
  3. Endoscopy with biopsy and brush cytology
  4. Blood test
    • low hemoglobin and hematocrit
    • hypoalbuminemia
  5. EUS is currently the gold standard test to evaluate the gastric cancer extension locally
    • an abdominal CT scan is used to identify distant metastasis and may be ordered to determine the spread of the tumor
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233
Q

What is the treatment for gastric carcinomas

A
  1. Surgery - largely palliative for control of bleeding and/or removal of obstruction
    • total gastrectomy - for negative margins if needed
    • esophagogastrectomy - for tumors localized in the cardia and gastroesophageal junction
    • subtotal gastrectomy - for tumors located in the distal stomach
  2. Chemotherapy - adjuvant (postoperative), neoadjuvant (preoperative) and combined modality or multi modality therapy
  3. Radiation
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234
Q

What are gastric polyps

A
  1. Discreet stomach tumors
  2. Relatively uncommon
  3. Can be single or multiple
  4. Generally found in antrum or lesser curvature
  5. Usually occur after age 55 years (seldom seen in younger people)
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235
Q

What are the different types of gastric polyps

A
  1. Hyperplastic (regenerative) polyps
  2. Fundic gland polyps
  3. Adenomatous polyps
  4. Gatstrointestinal stromal tumors (GISTs)
  5. Hamartomatous polyps
  6. Inflammatory fibroid polyps
  7. Neuroendocrine tumors
  8. Leiomyomas - smooth muscle tumors
  9. Adenomyomas (histomas) - which are benign but abnormal mixture of tissue
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236
Q

What are Hyperplastic (regenerative) polyps

A
  1. Are commonly associated with chronic inflammatory disorders such as:
    • chronic gastritis
    • H. Pylori gastritis
    • pernicious anemia
    • chemical gastritis
  2. Usually located in the antrum, body, fundus and cardia
  3. Consist of normal gastric epithelium and are the most common
  4. Usually benign, but the risk of malignancy increases if the polyp is greater than 1cm and pedunculated
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237
Q

What are fundic gland polyps

A
  1. Mostly benign polyps located in the gastric corpus
  2. Long-term use of proton-pump inhibitors (PPIs) is associated with increase risk for these polyps
  3. They are sporadic and are also seen in 20% to 100% of patients diagnosed with familial adenomatous polyposis (FAP) and in 11% of patients diagnosed with MUTYH-associated polyposis (MAP)
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238
Q

What are adenomatous polyps

A
  1. Also called raised intraepithelial neoplasia
  2. Are precursors to gastric cancer
  3. Histologically they are similar to colon adenomatous and are commonly associated with chronic Atrophic gastritis and intestinal metaplasia
  4. Polyps that are greater than 2cm pose a risk for neoplasia
  5. They are also linked to FAP
  6. They are typically isolated and found in the antrum but can be located anywhere in the stomach
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239
Q

What are Gastrointestinal stromal tumors (GISTs)

A
  1. Rare connective tissue tumors ( a subset of GI mesenchymal tumors)
  2. Histologically they are classified as:
    • Leiomyoma
    • Leiomyosarcoma
    • Leiomyoblastoma
    • Schwannoma
  3. They usually develop in the muscularis propria layer of the intestinal wall
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240
Q

What are Hamartomatous polyps

A
  1. Typically mucosal-based are are derived from three embryonic layers
  2. They are rare and commonly associated with certain syndromes:
    • hereditary mixed polyposis syndrome (HMPS)
    • juvenile polyposis syndrome (JPS)
    • Cobden syndrome
    • PJS
  3. These polyps are usually benign with abnormal mixtures of tissue indigenous to the organ
  4. Some have an increased risk of cancer
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241
Q

What are inflammatory fibroid polyps

A
  1. Commonly referred to as Vanek’s tumors and are very uncommon
  2. Typically, patients do not have any symptoms
  3. These polyps have been associated with gastric outlet obstruction or bleeding
  4. They arise in the submucosa and are usually non-Neoplastic
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242
Q

What are neuroendocrine tumors

A
  1. Divided into four types and derived from enterochromaffin-like cells
  2. Type 1 - is the most common form
  3. Type 1 and 2 are associated with hypergastrinemia and are usually located in the fundus and body of the stomach
  4. Type 3 is usually solitary and found throughout the stomach
  5. Type 4 is sporadic and may arise anywhere in the stomach
  6. Type 4 is the most aggressive form with the worst prognosis
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243
Q

What are the most common causes of gastric polyps

A
  1. Achlorhydria - absence of free hydrochloric acid in the stomach
  2. Pernicious anemia
  3. Gastric cancer after gastric resection
  4. Atrophic gastritis
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244
Q

What are signs and symptoms of gastric polyps

A
  1. Gastric polyps are asymptomatic and usually found incidentally
  2. Unless a polyp bleeds, is usually causes no symptoms
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245
Q

How are gastric polyps diagnosed

A
  1. Upper GI series, MRI, ultrasonography, angiography, CT scan
  2. Endoscopy with biopsy and cytology
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246
Q

What is the treatment for gastric polyps

A

Endoscopic polypectomy
Gastrectomy

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247
Q

What is Gastritis

A

Inflammation of the gastric mucosa

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248
Q

How is gastritis classified

A

There are several classification systems
1. The Sydney system combines the morphological, topographical, and etiological information for the classification
- Location of gastritis: antrum, fundus, body, cardia, focal or diffuse
- Type of gastritis - acute, chronic, lymphocytic, granulomatous, Eosinophilic, etc.
- Grading the presence or activity of the following:
H. Pylori
Glandular atrophy
Intestinal metaplasia of the epithelium
Neutrophilic infiltrates of the lamina propria, pits, or surface epithelium; and then the
Type and pattern of inflammation (chronic, active, or both)

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249
Q

What is acute (erosive or hemorrhagic) gastritis

A
  1. Mucosal damage occurs
  2. May be associated with a serious illness, alcoholism, localized gastric trauma, or gastrectomy
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250
Q

What is chronic (nonerosive, nonspecific) gastritis or NNG

A
  1. May have gradual blood loss that goes unnoticed over a period of years
  2. Superficial - pathological changes limited to upper one-third of mucosa
  3. Atrophic - involves the full thickness of the mucosa, atrophy of gastric glands, with loss of chief and parietal cells
  4. Gastric atrophy - little inflammation is noted, but there is marked or total gland loss and mucosa is thinned
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251
Q

What are some specific forms of gastritis

A
  1. Menetrier disease
  2. Eosinophilic gastritis
  3. Sarcoidosis
  4. And certain infections, but they are less common
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252
Q

What are risk factors for gastritis

A
  1. Irritant such as gastric acid, bile reflux, or medications
  2. Impairment of the natural protective mechanism
  3. Most commonly caused by H. Pylori infection
  4. Damage to the stomach lining
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253
Q

What are risk factors for acute gastritis

A

Serious or life threatening illness, alcoholism, localized gastric trauma, gastrectomy

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254
Q

What are risk factors for chronic gastritis

A

Common in adults and may be associated with non infectious and infectious causes
1. Non infectious
- normal aging, chemical gastropathy (linked to irritants), uremic gastropathy, chronic noninfectious granulomatous gastritis (linked to Crohn’s disease and sarcoidosis), lymphocytic gastritis, Eosinophilic gastritis, radiation injury to the stomach, graft-versus-host disease and ischemic gastritis.
- chronic gastritis may also occur due to drug therapy, autoimmunity, and allergic reactions
2. Infectious
- H. Pylori infection; Helicobacter Heilmannii infection; viruses (cytomegalovirus CMV, herpes virus) and parasites (strongyloides, schistosoma, and diphyllobothrium lantum

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255
Q

What are signs and symptoms of gastritis

A
  1. Abdominal pain
  2. Nausea and vomiting
  3. Gastric bleeding
    • may test positive for occult blood in stool, have flecks of blood in vomitus or exhibit chronic anemia
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256
Q

How is gastritis diagnosed

A
  1. Hemoccult may be positive
  2. Endoscopy - most effective tool in diagnosing gastritis in patients with acute GI bleed
  3. Gastric biopsies may be obtained to determine etiology
  4. In rare instances such as severe gastritis and recurrent gastric ulcers; serum gastrin and a gastric analysis may be ordered to determine the cause
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257
Q

What is the treatment for gastritis

A

Depends on signs and symptoms
1. Medications
- antacids
- Sucralfate
- H2 blockers
- PPIs
- Prostaglandins
- Antibiotics, if a bacterial infection is found
2. Elimination of contributing factors, where possible
- irritating medications
- smoking
- heavy alcohol consumption
- H. pylori

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258
Q

What are stress ulcers

A
  1. Mucosal erosions associated with a serious illness
  2. They are commonly found in the fundus and the body of the stomach but can develop in the antrum, duodenum, or distal esophagus
  3. Cushing’s ulcers may be located in the esophagus, stomach, or duodenum
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259
Q

What is the prognosis for people with stress ulcers

A

With hemorrhage, the mortality rate is about 50%

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260
Q

What are causes and risk factors of stress ulcers

A
  1. Severe trauma, ongoing sepsis or serious illness
  2. Burn injuries - Curling’s ulcer, primarily located in the duodenum
  3. Intracranial trauma - Cushing’s ulcer
    • may be located in the esophagus, stomach, or duodenum
    • tend to be deep and full thickness
    • more prone to perforation than gastric mucosal ulcerations induced by trauma and sepsis
  4. Chronic ingestion of drugs or substances that irritate the gastric mucosa (NSAIDs or ethanol)
  5. Being treated for illnesses such as environmental electrical injuries, stroke complications, or liver failure
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261
Q

What are signs and symptoms of stress ulcers

A
  1. Massive GI bleed
  2. Occurs 3 to 7 days after initial injury, but can be up to 21 days
  3. Rarely cause classic ulcer symptoms before bleeding begins
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262
Q

What are potential complications of stress ulcers

A
  1. Deeper and more distal stress ulcerations can deteriorate the submucosa and cause severe hemorrhaging
  2. Perforation is a rare complication
  3. Cushing’s ulcers tend to be deep, full thickness ulcers and therefore are more prone to perforation than gastric mucosal ulcerations induced by trauma or sepsis
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263
Q

How are stress ulcers diagnosed

A

Endoscopy

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264
Q

What is the treatment for stress ulcers

A
  1. Control bleeding
  2. Correct shock
  3. Treat underlying disorder
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265
Q

What is Dieulafoy’s lesion

A
  1. A dilated, aberrant, submucosal artery that erodes the mucosa in the absence of an ulcer
  2. It is an important etiology of acute upper GI bleeding
  3. About 70% of the lesions occur in the stomach, 6cm from the gastroesophageal junction along the lesser curvature
  4. Other common locations include the duodenum, the distal stomach, and the esophagus
  5. These lesions are responsible for 1.5% of acute upper GI bleeding
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266
Q

What are symptoms of Dieulafoy’s lesion

A

Acute, profuse bleeding, which results in
- hematemesis
- melena
- or hematochezia

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267
Q

How is Dieulafoy’s lesion diagnosed

A
  1. EGD is usually preferred for diagnosis due to the presentation
  2. Diagnostic accuracy increases when EGD is performed within 24 hours of the bleed
  3. Endoscopic biopsies are contraindicated because of the risk of severe bleeding from the exposed artery
  4. If the endoscopy is nondiagnostic, interventional angiography maybe required to establish the diagnosis and treat the vessel in the setting of acute bleeding
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268
Q

What are potential complications of Dieulafoy’s lesion

A

Bleeding can be massive, life-threatening, and recurrent

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269
Q

What is the treatment for Dieulafoy’s lesion

A

Standard treatments include:
1. Endoscopic hemostasis using hemoclips, band ligation, injection therapies, epinephrine injection, ablation therapy, heater probe, electrocoagulation, or Argon plasma coagulation (APC)
2. PPIs IV
3. Volume resuscitations

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270
Q

What are gastric varices

A
  1. Abnormally dilated and tortuous veins in the stomach
  2. Related to portal hypertension
  3. Two-thirds of patients with esophageal varices may also have gastric varices
  4. Less common sites of varices due to gastrointestinal bleed are the duodenum, ileum, colon, and rectum
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271
Q

What is the prognosis for people with gastric varices

A

Poor

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272
Q

What are potential complications of gastric varices

A
  1. Risk of bleeding from gastric varices is directly related to the size of the varix and liver dysfunction
  2. Frequency of bleeding in gastric varices is similar to that of large esophageal varices
  3. Risk of bleeding can be as high as 75% in patients with advanced disease
  4. The chance of recurrent variceal bleeding is common
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273
Q

What are causes of gastric varices

A

Portal hypertension resulting from cirrhosis, may lead to the development of collateral circulation with formation of varices that carry blood away from the portal circulation

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274
Q

How are gastric varices diagnosed

A
  1. Medical history
  2. An upper Endoscopy
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275
Q

What is the treatment for gastric varices

A
  1. Stabilization
  2. Stopping acute variceal bleeding using two methods:
    • endoscopic schlerotherapy using a sclerosant and/or
    • endoscopic variceal ligation using a rubber-band ligation
  3. Tamponade - with a Sengstaken-Blakemore tube, Lipton-Nachlas tube, or Minnesota tube
  4. Surgical shunting procedure - TIPS
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276
Q

What is a hiatal hernia

A

When part of the stomach protrudes through the diaphragm and into the thoracic cavity

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277
Q

Who is more likely to have a hiatal hernia

A
  1. A common disorder
  2. More frequent over 40 years of age
  3. More frequent in female
  4. People who are overweight
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278
Q

How is a hiatal hernia designated

A

By size - small or large

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279
Q

What are the different types of hiatal hernias

A
  1. Sliding - stomach and esophagus slide up into the chest (most common)
  2. Paraesophageal - part of the stomach moves into the chest next to the esophagus
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280
Q

What are Cameron lesions in relation to hiatal hernias

A
  1. Linear gastric ulcers that may occur where the stomach slides back and fourth through the diaphragmatic hiatus
  2. May be a cause of iron deficiency anemia
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281
Q

What is a cause of hiatal hernia

A

Often associated with a weakening of the LES from causes such as:
1. Injury
2. Congenitally large hiatus
3. Persistent and intense pressure on the surrounding muscles

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282
Q

What are signs and symptoms of hiatal hernias

A

Often associated with esophageal reflux
1. Small hiatal hernia usually causes no symptoms
2. Large hiatal hernia is often associated with:
- esophageal reflux
- belching
- heartburn
- dysphagia
- chest or abdominal pain
- feeling especially full after meals
3. With a rolling hernia patients may have a feeling of fullness and discomfort after meals but reflux is not common

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283
Q

How are hiatal hernias diagnosed

A
  1. Chest x-ray
  2. Barium swallow
  3. Upper GI endoscopy
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284
Q

What is the treatment for hiatal hernias

A

The same as for GERD

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285
Q

What are potential complications of hiatal hernias

A
  1. Reflux esophagitis
  2. Heartburn
  3. Acid regurgitation
  4. Water brash
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286
Q

What is infantile hypertrophic pyloric stenosis

A
  1. The second most common disorder requiring surgery in the first few months of life (inguinal hernia is the first)
  2. Occurs in 1:500 births
  3. Boys affected 4-5 times more than girls
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287
Q

What are potential causes of infantile hypertrophic pyloric stenosis

A
  1. May be familial
  2. Seen more often in preterm infants
  3. Environmental conditions and genetic susceptibility may influence the likelihood of developing
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288
Q

What are symptoms of infantile hypertrophic pyloric stenosis

A
  1. The first symptoms of pyloric stenosis usually occur at 3-6 weeks of age and rarely occur after 12 weeks of age
  2. Have a history of nonbilious vomiting, which becomes projectile
  3. In infants diagnosed with IHPS, the hypertrophied pylorus is palpable, and they may look dehydrated, very thin and weak
  4. Dehydration
  5. Electrolyte imbalance
  6. Metabolic alkalosis with hypokalemia
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289
Q

How is infantile hypertrophic pyloric stenosis diagnosed

A
  1. GI series shows a narrowed antrum and pylorus
  2. Abdominal ultrasound
  3. Barium swallow
  4. Upper endoscopy
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290
Q

What is the treatment for infantile hypertrophic pyloric stenosis

A

1.The treatment of choice is a Ramstedt pyloromyotomy even though laparoscopic pyloromyotomy has been used
2. Non-surgical treatments are still being researched

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291
Q

What are potential complications of infantile hypertrophic pyloric stenosis

A

1.Occasionally dysphagia or symptoms of postprandial vomiting and nausea
2. May become dehydrated, have electrolyte disturbances and commonly are in metabolic alkalosis with hypokalemia

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292
Q

What are other congenital abnormalities of the stomach

A
  1. Gastric, antral and pyloric atresias
  2. Pyloric or antral membranes
  3. Microgastria
  4. Gastric duplication
  5. Neonatal perforation of the gastric wall
  6. Gastric diverticula
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293
Q

What are gastric, antral and pyloric atresias

A

When the stomach ends blindly or is totally occluded by two apparent membranes connected by a strand of each mucosa and submucosa

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294
Q

What is pyloric or antral membranes

A

May produce no obstructive symptoms until late in life

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295
Q

What is microgastria

A

Also called hypoplasia, a rare condition with limited life expectancy, in which the stomach never becomes differentiated from the primitive foregut into a true fundus, body, and pylorus

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296
Q

What is gastric duplication

A

A rare condition in which a distinct mass lesion that contains all layers of the gastric wall develops in the stomach

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297
Q

What is neonatal perforation of the gastric wall

A

A rare condition associated with prematurity, peptic ulceration, and distal small intestinal obstruction

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298
Q

What is gastric diverticula

A
  1. Most of which are congenital
  2. Located high on the posterior wall of the stomach, below the GE junction
  3. Prepyloric diverticula, which are relatively rare, are usually associated with previous peptic ulceration
  4. Occasionally, gastric diverticula may cause dyspepsia or symptoms of postprandial vomiting and nausea
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299
Q

What are gastric motor dysfunctions

A

Range from both excessively slow and excessively rapid; both can be debilitating

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300
Q

In what order are things emptied from the stomach

A

Carbohydrates first
Then proteins
Finally fats

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301
Q

What is gastroparesis

A

Excessively slow stomach emptying

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302
Q

What is dumping syndrome

A

Excessively fast stomach emptying

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303
Q

What are risk factors to getting gastric motor dysfunction

A
  1. After vagotomy and pyloroplasty
  2. In patients with mechanical obstructions
  3. Acute metabolic disorders
  4. Inflammatory diseases
  5. Long-standing diabetes mellitus
  6. A side effect of certain medications
  7. Serious dysfunction may be idiopathic, as in antral tachygastria
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304
Q

What is antral tachygastria

A

When an aberrant pacemaker in the antrum cycles 3-4 times faster that the usual pacemaker area in the gastric body

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305
Q

What causes dumping syndrome

A

May be related to rapid fluid shifts from plasma to the intestinal lumen as a result of the rapid introduction of hyperosmolar solutions into the jejunum and the release of numerous hormones and vasoactive intestinal polypeptides into the bloodstream

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306
Q

What are symptoms of dumping syndrome

A

Early - 30 minutes after the start of a meal Later -30-90 minutes after the meal - may result from reactive hypoglycemia
1. Anxiety 1. Weakness
2. Weakness. 2. Diaphoresis
3. Dizziness 3. Tachycardia
4. Tachycardia with a pounding pulse. 4. Sometimes a decreased level of consciousness may be experienced
5. Diaphoresis
6. Flushing
7. Abdominal cramps
8. Diarrhea

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307
Q

What is the treatment gastric motor dysfunction

A

Based on the cause
1. Gastric muscle stimulants may be helpful in delayed gastric emptying
2. Both, dumping syndrome and delayed gastric emptying may be improved with dietary changes
- no liquids during meals
- six small meals per day
- high protein, high fat, low carbohydrates food choices

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308
Q

What parasitic organisms can cause infectious gastritis

A

Occurs rarely
1. Cryptosporidiosis
2. Anisakiasis
3. Strongyloidiasis
4. Giardiasis

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309
Q

What fungi can cause infectious gastritis

A
  1. Candidiasis
  2. Mucormycosis
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310
Q

What viruses can cause infectious gastritis

A

CMV
Rare because viruses don’t survive in a pH less that 3.0

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311
Q

What bacteria can cause infectious gastritis

A

H. Pylori

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312
Q

Who is at risk for developing infectious gastritis

A

Immunocompromised patients
1. Those with HIV or AIDS
2. Organ transplant recipients
3. Those undergoing chemotherapy

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313
Q

What is H. Pylori

A

It lives in the mucous lining of the stomach causing 60-80% of all gastric ulcers and 90% duodenal ulcers

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314
Q

What causes an H. Pylori infection

A
  1. The infection does not cause the ulcer itself, but it makes the mucosa more susceptible to gastritis and ulcers
  2. 95% of duodenal ulcers have H. Pylori and gastritis
  3. Lower socioeconomic status and household crowding are risk factors for H. Pylori
  4. Likely the transmission is from person-person through oral-oral and fecal-oral routes
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315
Q

What are signs and symptoms of an H. Pylori infection

A

All gastritis symptoms
1. Epigastric pain
2. Possible nausea and vomiting
3. Bloating and burning pain

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316
Q

How is H. Pylori infection diagnosed

A

Noninvasive
1. Serology for antibody or antigen testing
2. A fecal antigen test
3. Carbon13 or Carbon14 urea breath testing

Invasive
1. Biopsy during EGD for either rapid urease testing or histology
2. Culture is considered the gold standard but is usually prohibited by cost and time

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317
Q

What are potential complications of H. Pylori infection

A
  1. Chronic gastritis and peptic ulcer disease
  2. Patients have a higher rate of gastric cancer - is associated with a higher risk of gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma
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318
Q

What is the treatment for infectious gastritis

A
  1. Medication is organism specific, plus includes ulcer treatment
  2. Combination treatment can include:
    - stomach-coating agent, such as Pepto-Bismol
    - antibiotics
    • Metroniadazole (Flagyl)
    • Tetracycline and amoxicillin
    • Clarithromycin
  3. PPIs, such as Prilosec or Prevacid
  4. H2 blockers, such as Zantac or Tagamet HB
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319
Q

What is a gastric outlet obstruction

A

Obstruction of the pyloric sphincter at the outlet of the stomach, blocking the flow of gastric contents into the duodenum

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320
Q

What are causes of a gastric outlet obstruction

A
  1. Neoplastic disease
  2. Foreign body
  3. Pyloric stenosis due to inflammation or ulcer disease
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321
Q

What are signs and symptoms of a gastric outlet obstruction

A
  1. Vomiting of partially digested gastric contents
  2. Feeling of fullness only relieved by vomiting
  3. Anorexia, occurring in two-thirds of patients
  4. May have weight loss
  5. Pain aggravated by eating
  6. Abdominal tenderness or distention
  7. Metabolic alkalosis secondary to prolonged vomiting
  8. Succussion splash
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322
Q

How is a gastric outlet obstruction diagnosed

A
  1. Endoscopy
  2. Abdominal x-ray
  3. Nuclear scanning
  4. Upper GI series
  5. Barium studies
  6. A saline load test to confirm gastric retention and to rule out atony as the cause
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323
Q

What are potential complications of a gastric outlet obstruction

A
  1. Anemia
  2. Prolonged vomiting may lead to an electrolyte imbalance such as hypokalemia or metabolic alkalosis
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324
Q

What is the treatment for a gastric outlet obstruction

A
  1. Restoration of fluids and electrolytes
  2. Decompression of the stomach and correction of nutritional deficiencies
  3. Balloon dilatation of the pylorus
  4. Surgery may be necessary if the cause of the obstruction cannot be treated through endoscopic measures
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325
Q

What is a caustic injury of the of the stomach

A

The oropharynx and esophagus are most often damaged by caustic substance ingestion, but in 20-30% of patients with an esophageal injury, also have a gastric injury

The severity of the injury depends on the nature, concentration and quantity of the caustic agent ingested and the duration of tissue contact

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326
Q

What causes a caustic injury of the stomach

A
  1. Ingestion of highly acid or alkaline substance may cause tissue damage on contact
  2. Severity depends on the caustic substance and duration of tissue contact
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327
Q

What damage can be caused by ingestion of alkaline agents

A

The oropharynx, hypopharynx and esophagus are most frequently injured by ingestion of alkaline agents
Contact with strong alkaline agents causes liquefactive necrosis, which is the complete destruction of entire cells and their membranes

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328
Q

What damage can be caused by ingestion of acidic agents

A

In the case of acid ingestion, the caustic agent tends to pass rapidly through the esophagus, this producing shallow burns
Contact with strong acids promote coagulation necrosis and the formation of a firm, protective eschar, which limits the depth, penetration and injury produced by the acid
In the stomach, acids usually collect in the antrum, where the most severe damage occurs

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329
Q

What are signs and symptoms of a caustic injury to the stomach

A
  1. Epigastric pain
  2. Retching
  3. Emesis of tissue, blood, or coffee-ground appearing material
  4. The severity of tissue injury ranges from diffuse gastritis to hemorrhagic ulceration and necrosis leading to perforation of the stomach
  5. Gastric perforation, in turn may lead to mediastinitis, peritonitis and shock
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330
Q

How are caustic injuries of the stomach diagnosed

A
  1. Chest x-ray to evaluate for aspiration pneumonia or perforation
  2. Cautious endoscopy
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331
Q

What are potential complications of a caustic injury to the stomach

A
  1. Tissue injury may lead to severe gastritis, perforation, peritonitis, and shock
  2. Stricture formation is a common late complication, usually apparent by 8 weeks
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332
Q

What is the treatment for caustic injuries to the stomach

A
  1. Determined by caustic substance ingested
  2. NPO
  3. Emergency surgery, which may be necessary in the event of perforation, peritonitis, mediastinitis, or severe hemorrhage
  4. Dilation, if stricture develops
  5. Partial or total gastrostomy in the case of severe gastric burns or antral and pyloric stenosis
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333
Q

What is a bezoar

A

Concretions of foreign material in the stomach; including:
1. Phytobezoars
2. Trichobezoars
3. Lactobezoars
4. Pharmacobezoars

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334
Q

What is a phytobezoar

A
  1. Plant or vegetable material
  2. Most commonly seen in males over 30 years of age
  3. May be seen with gastrectomy, especially those with a vagotomy
  4. May be associated with hypochlorhydria, diminished antral motility, and incomplete mastication
  5. People with diabetes and gastroparesis are at risk of developing bezoars
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335
Q

What is a pharmacobezoars

A
  1. Concretions of medications that occur due to changes in the GI tract anatomy or problems with motility
  2. Can be composed of drugs that are difficult to dissolve such as enteric-coated or extended-release drugs, sucralfate or sodium alginate
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336
Q

What are trichobezoars

A
  1. Hair that has been chewed
  2. Most commonly seen in females under the age of 30 years
  3. Cab resemble a solid mass when it becomes matted together and they can also assume the shape of the stomach
  4. The most common type of bezoar found in the pediatric population
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337
Q

What are Lactobezoars

A
  1. Milk curds
  2. Occur in infants, but are seldom seen since the advent of premixed formulas
  3. Form as a result of infants ingesting a powdered formula diluted with an inadequate amount of water
  4. Continuous drip feeding of preterm infants seems to be the most important predisposing factor
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338
Q

What are signs and symptoms of bezoars

A
  1. Fullness
  2. Epigastric pain
  3. Nausea and vomiting
  4. Palpable mass
  5. Anorexia
  6. Bleeding due to ulceration
  7. Weight loss
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339
Q

How are bezoars diagnosed

A
  1. EGD - best technique
  2. Plain x-ray films of the abdomen or an upper GI series may show signs of an abdominal mass
  3. Pharmacobezoars are rare and may be difficult to diagnose
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340
Q

What are potential complications of bezoars

A

Can result in:
1. Anorexia
2. Vomiting
3. Ulceration
4. Bleeding
5. Perforation
6. Constipation
7. Obstipation
8. Small bowel obstruction

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341
Q

What is the treatment for bezoars

A
  1. Endoscopic removal - fragmentation with forceps, wire snare, jet spray or laser may be used
  2. Metroclopramide may be given to for several days after fragmentation to increase peristalsis and aid passage of the material
  3. Enzymes - can result in gastric perforation especially if the bezoar caused ulceration of gastric tissue
    • papain
    • acetylcysteine
    • Cellulase
  4. Gastrostomy - especially for trichobezoars
  5. Infants with Lactobezoars
    • gastric lavage with saline
    • hydration
    • withhold feeding 48 hours
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342
Q

What is acute gastroenteritis

A

Inflammation of the lining of the stomach and intestines

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343
Q

What are contributing factors to acute gastroenteritis

A
  1. Ingestion of contaminated food
    • incubation and colonization occurs in 6 to 24 hours
    • Enterotoxin ( a toxin that specifically affects the cells of the intestinal mucosa) is produced after colonization
    • secretion of enterotoxins create the body’s reaction, causing the secretion of water and electrolytes
  2. Bacterial invasion causes inflammation and ulceration, creating bloody diarrhea
  3. Viral gastroenteritis, commonly known as the stomach flu, is usually self-limiting
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344
Q

What bacteria cause acute gastroenteritis

A
  1. Staphylococcus aureus (S. Aureus)
  2. Salmonella
  3. Campylobacter jejuni
  4. Clostridium difficile (C. Difficile)
  5. Escherichia coli (E. Coli)
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345
Q

What viruses cause acute gastroenteritis

A
  1. Norovirus
  2. Rotavirus
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346
Q

What are signs and symptoms of acute gastroenteritis

A
  1. Sudden onset nausea
  2. Diarrhea
    • often watery
    • bloody diarrhea more commonly seen with bacterial cause
  3. Malaise
  4. Myalgia
  5. Fever
  6. Dehydration
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347
Q

How is acute gastroenteritis diagnosed

A
  1. Complete history, including recent travel and ingested food
  2. Stool culture
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348
Q

What is the treatment for acute gastroenteritis

A
  1. Depends whether the case is viral or bacterial
  2. Antacids, sucralfate, and/or acid-blocking medications
  3. Antidiarrheals
  4. Medications for nausea and vomiting
  5. Replacement of fluids
  6. Antibiotics for bacterial cause
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349
Q

What are potential complications of acute gastroenteritis

A
  1. Chronic anemia
  2. Erosive mucosal damage
  3. Acute GI bleeding
  4. Dehydration
  5. Electrolyte imbalance in severe cases
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350
Q

What is Gastric Antral Vascular Ectasia (GAVE)

A
  1. Dilation and thrombosis of capillaries and veins in the antrum that radiate toward the pylorus
    • can be longitudinal, looking like watermelon stripes
    • can be in diffuse patterns
  2. Characterized by mucosal and submucosal vascular ectasia causing recurrent GI hemorrhage
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351
Q

What causes Gastric Antral Vascular Ectasia (GAVE)

A
  1. Specific cause is unknown
  2. Seen more frequently in patients with chronic liver disease
  3. More prevalent in females
  4. Has been associated with autoimmune diseases and rheumatological diseases such as multiple sclerosis
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352
Q

What are signs and symptoms of Gastric Antral Vascular Ectasia (GAVE)

A
  1. Iron deficiency anemia
  2. Hemoccult positive stool
  3. Typically, patient does not experience any abdominal pain
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353
Q

How is Gastric Antral Vascular Ectasia diagnosed

A

Endoscopy

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354
Q

What is the treatment for Gastric Antral Vascular Ectasia (GAVE)

A
  1. Avoid aspirin and NSAIDs due to mucosal irritation
  2. Coagulation therapy
    • heater probe
    • Argon Plasma Coagulation (APC)
    • Laser therapy
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355
Q

What is cirrhosis

A

Liver deterioration and malfunction due to chronic injury, resulting in:
1. Fibrosis - scarring that obliterates the architecture of the underlying tissue
2. Regenerative nodules - occur as a result of damaged tissue be rejuvenated

Outcome of progressive hepatic damage, either as a result of chronic inflammation or cholestasis
The anatomical hallmarks of this disorder are hepatic parenchymal inflammation and necrosis, nodular regeneration, loss of the centrilobular vein, and formation of new connective tissue (fibrosis)
This makes it increasingly difficult for the liver to carry out essential functions

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356
Q

What are the different classifications of cirrhosis of the liver

A
  1. Micronodular cirrhosis
  2. Macronodular cirrhosis
  3. Mixed cirrhosis
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357
Q

What is Micronodular cirrhosis

A

Regenerative nodules are uniform in size and less than 3 mm in diameter

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358
Q

What is Macronodular cirrhosis

A

Regenerative nodules are variable in size, but greater than 3mm in diameter

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359
Q

What is mixed cirrhosis

A

Both types of nodules are present in approximately equal proportions

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360
Q

What is the prognosis for cirrhosis of the liver

A

Although most well established cases are irreversible, the disease process may be haunted by managing the cause and treating complications

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361
Q

What are the causes of cirrhosis of the liver

A
  1. Alcoholic cirrhosis
  2. Nonalcoholic steatohepatitis (NASH)
  3. Immune-related bile duct injuries
  4. Postnecrotic cirrhosis
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362
Q

What is alcoholic cirrhosis

A
  1. Also known as Micronodular, portal, or Laennec’s cirrhosis
  2. Accounts for 50% of adult patients with adult cirrhosis
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363
Q

What is nonalcoholic steatohepatiits (NASH)

A

Etiology is unknown, but research points to the autoimmune system

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364
Q

What is Immune-related bile duct injuries

A
  1. Includes primary biliary cirrhosis and sclerosing cholangitis, which are diseases of uncertain etiology
  2. Primarily affects middle aged women
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365
Q

What is Postnecrotic cirrhosis

A
  1. Caused by hepatic necrosis
  2. May be related to hepatitis, infection, metabolic liver disease, and exposure to toxins
  3. Liver becomes small and distorted
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366
Q

What are symptoms of cirrhosis of the liver

A
  1. Ascites
  2. Caput medusae
  3. Cruveilhier Baumgarten syndrome
  4. Spider Angiomata or spider telangiectasia
  5. Gynecomastia and male pattern baldness
  6. Splenomegaly
  7. Jaundice
  8. Anorexia and weight loss
  9. Abdominal pain
  10. Bruising and bleeding
  11. Esophageal varices
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367
Q

What is ascites

A
  1. Develops as a consequence of increasing hydrostatic pressure
  2. The change in pressures within the splanchnic bed forces proteinaceous fluid to leak into the abdominal cavity, eventually leading to hypoalbuminemia
  3. The accumulation of fluid in the abdominal cavity reduces systemic volume and stimulates the production of aldosterone, a form of mineralocorticoid that further promotes fluid retention
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368
Q

What is Caput medusae

A
  1. A cardinal feature of portal hypertension that appears as engorged veins radiating from the umbilicus
  2. With the increased portal pressure, blood is shunted through the umbilical veins into the veins of the abdominal wall resembling the serpent hair of Medusa from Greek mythology
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369
Q

What is Cruveilhier Baumgarten syndrome

A
  1. A rare symptom of portal hypertension, which is a loud venous murmur heard over the epigastric area
  2. This murmur is caused by blood flow from the portal vein to the umbilical vein branches
  3. The murmur can be present even in the absence of Caput medusae
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370
Q

What are spider angiomata

A
  1. Also known as spider telangiectasia
  2. Swollen blood vessels under the skins surface, mainly on the face, arms and trunk
  3. Where small radiating vessels surround a central arteriole resembling a spider web
  4. Spider angiomata and also palmar erythema, may be caused by the liver’s decreased ability to degrade estradiol
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371
Q

Why can gynecomastia and male pattern baldness occur in patients with cirrhosis

A

Due to the enhanced conversion of androstenedione to estrone and estradiol

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372
Q

Why does splenomegaly occur in patients with cirrhosis

A

Believed to occur as a result of portal congestion tissue hyperplasia, and liver fibrosis

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373
Q

What is jaundice

A
  1. The yellow discoloration of skin, oral mucus membranes and sclera that is caused by an abnormal elevation of bilirubin attributed to the liver’s impaired excretory function
  2. The discoloration is usually detectable when serum bilirubin level is >or=2mg/dL (34mmol/L)
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374
Q

How is cirrhosis of the liver diagnosed

A
  1. Requires histological confirmation of altered hepatic architecture through biopsy examination
    - a liver biopsy is collected either by Percutaneous, Transjugular, laparoscopic, or radiographically guided fine needle aspiration (FNA) is useful in diagnosing cirrhosis
    - the simplest approach to staging cirrhosis is to categorize it according to compensated and decompensated stages
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375
Q

What is compensated cirrhosis

A

Patients typically have normal portal pressure and are generally asymptomatic or may report nonspecific symptoms such as poor appetite, easy fatigability, weakness, and weight loss

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376
Q

What is decompensated cirrhosis

A

Patients are at a higher risk if death due to severe associated complications such as bleeding varices, ascites hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome

Clinical features include ascites, Caput medusae, Cruveilhier Baumgarten syndrome, hormonal imbalance, splenomegaly, and jaundice

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377
Q

What is the treatment for cirrhosis

A

Shunting procedures with the purpose of directing blood flow around the liver and away from collateral vessels, however some blood is still sent to the liver

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378
Q

What are potential complications of cirrhosis

A
  1. Portal hypertension
  2. Hepatocellular carcinoma
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379
Q

What is portal hypertension

A
  1. It leads to the development of collateral vessels that bypass the liver
  2. Because of this bypass, toxins that are normally removed by the liver are instead introduced into the general circulation
  3. The collateral vessels become enlarged, convoluted (varices) and can develop in the esophagus, stomach, abdominal wall, and rectum
  4. The varices are fragile and can bleed with occasional fatal results
  5. Portal hypertension also can lead to ascites, and splenomegaly, a condition that further predisposes the patient to bleeding and infection
  6. Occurs when liver blockage leads to increased portal vein resistance and back flow, causing increased pressure within the portal vein
  7. 75% of blood flow to the liver is from the portal vein, so collateral circulation develops to relive hypertension and redirect blood flow
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380
Q

What are signs and symptoms of portal hypertension

A
  1. Varices
  2. Hemorrhoids
  3. Dilated veins in the umbilical region
  4. Splenomegaly
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381
Q

How is portal hypertension diagnosed

A
  1. Assessing portal hypertension in liver cirrhosis is done by measuring the hepatic vein pressure gradient (HVPG) an estimate of the difference in pressure between the portal vein and the inferior vena cava
  2. This technique is safer and less invasive than direct measurement of portal pressure
  3. HVPG >4mmHg is considered portal hypertension, and higher scores are associated with more severe clinical manifestations and increased risk for complications
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382
Q

What are potential complications of portal hypertension

A

It progresses to the eventual development of such complications as:
1. Ascites
2. Hepatic encephalopathy
3. Variceal hemorrhage
4. Spontaneous bacterial peritonitis
5. Hepatorenal syndrome
6. Portal hypertensive gastropathy
7. Hepatic hydrothorax
8. Hepatopulmonary syndrome
9. Portopulmonary hypertension
10. Cirrhosis cardiomyopathy

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383
Q

What is the treatment for portal hypertension

A
  1. A Transjugular intrahepatic portosystemic shunt (TIPS) is currently the most efficient treatment for portal hypertension
  2. It creates a connection between a branch of hepatic vein and a branch of portal vein (usually the right branch) to improve blood flow and decrease portal hypertension
  3. During the procedure a needle catheter is inserted via the Transjugular vein and passed into the hepatic vein
  4. The needle is advanced through the liver parenchyma to the portal vein
  5. Finally, an intrahepatic metal stent is deployed to make the connection between the hepatic vein and the portal vein
  6. This procedure is less invasive compared to previously used open surgical shunt procedures
  7. One of the most common complication of a TIPS procedure is hepatic encephalopathy
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384
Q

What are causes for varices

A
  1. Increased pressure within the portal venous system caused by both fibrotic liver changes and hepatic vein obstruction caused by liver disease
  2. As blood enters the liver through the portal vein, the connective tissue and liver nodules compress the blood vessels and cause resistance
  3. This resistance forces blood into the collateral vessels that may be formed in the esophagus, umbilical area, duodenum, abdomen, or rectum, causing distention and producing varices
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385
Q

What are signs and symptoms of varices

A

Spontaneous bleeding that can become a life-threatening event

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386
Q

What are causes for ascites

A
  1. Occurs when fibrotic tissue associated with cirrhosis prohibits blood from leaving the liver
  2. The liver begins to expand beyond its normal capacity
  3. Fluid, mostly plasma, leaks through the liver’s surface into the peritoneal cavity
  4. Portal hypertension secondary to cirrhosis is the most common cause of ascites, accounting for most cases
  5. Other causes are cancer (malignant-related ascites), cardiac ascites with a history of CHF, acute hemorrhagic pancreatitis or ruptured pancreatic duct in chronic pancreatitis and trauma
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387
Q

What are signs and symptoms of ascites

A
  1. Sodium retention
  2. Renal function abnormalities
  3. Local splanchnic capillary pressure changes that cause a fluid shift to the abdominal cavity
  4. Increased waist size and weight
  5. Severe cases cause abdominal distention and discomfort
  6. The swollen abdomen may put pressure on the lungs leading to dyspnea and sometimes may lead to anorexia with increased pressure on the stomach
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388
Q

How is ascites diagnosed

A
  1. Physical examination
  2. Ultrasonography
  3. CT scan
  4. Paracentesis helps with fluid sampling for laboratory analysis
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389
Q

What are potential complications of ascites

A
  1. Spontaneous bacterial peritonitis
    • symptoms include:
      • abdominal tenderness
      • fever
      • confusion
      • disorientation
      • drowsiness
    • treatment is antibiotics
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390
Q

What is the treatment for ascites

A
  1. Sodium restriction diet (2g/day)
  2. Diuretics
  3. Bed rest
  4. Paracentesis - done only to relieve acute respiratory or abdominal distress or for diagnostic purposes
  5. TIPS

Grade 1 ascites
1. No treatment required
Grade 2 ascites
1. Dietary modification
2. Administration of diuretics
Grade 3 ascites
1. Large volume Paracentesis (LVP)
2. Administration of albumin

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391
Q

What is hepatorenal syndrome

A
  1. A functional form of renal failure linked to severe liver disease
  2. A progressive failure that occurs in patients with significant liver disease, especially liver cirrhosis
  3. Toxins build up due to kidney failure and contribute to the liver damage
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392
Q

What is the prognosis for someone with hepatorenal syndrome

A

Mortality rate is greater than 90%

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393
Q

What are the risk factors and cause for hepatorenal syndrome

A
  1. Most likely starts with subclinical renal dysfunction caused by decreased perfusion of the kidneys in patients with severe liver disease
  2. The exact cause is unknown but is attributed to the increase in nitric oxide release due to portal hypertension
  3. Nitric oxide causes vasodilation of splanchnic circulation that subsequently reduces circulatory blood volume
  4. The kidney’s juxtaglomerular apparatus responds to the low volume activating the renin-angiotensin-aldosterone mechanism, creating vasoconstriction and reduced blood flow to the kidneys
  5. As a result, glomerular filtration rate, sodium excretion, and mean arterial pressure decline
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394
Q

What are signs and symptoms of hepatorenal syndrome

A
  1. Progressive azotemia
  2. Urine volume less than 500ml/ day
  3. Concentrated urine
  4. Urinary sodium concentration less than 10mEq/L
  5. There are two form of Hepatorenal syndrome Type 1 and Type 2
  6. Type 1 symptoms
    • decreased urination, edema, azotemia, hepatic encephalopathy, associated with rapid progression to kidney failure
    • creative level rises to >2.5mg/dL in less than 2 weeks. There is also a reduction in urine output to <500ml/day
  7. Type 2 symptoms
    • is less severe and associated with slow progressive kidney failure
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395
Q

How is hepatorenal syndrome diagnosed

A

Urinalysis

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396
Q

What is the treatment for hepatorenal syndrome

A
  1. High-calorie, low-protein, low sodium diet
  2. Dialysis may be helpful with patients with reversible forms of liver disease or while on the liver transplant wait list
  3. In appropriate candidates, liver transplantation will cure hepatorenal syndrome
  4. Management of HRS includes the identification, removal and treatment of any factors know to precipitate renal failure
  5. The short-term treatment includes:
    • albumin is the most effective plasma expander use for HRS
    • vasoconstrictors such as vasopressin (vasostrict and pitressin), norepinephrine (Levophed), midodrine (orvaten) and octreotide (sandostatin)
  6. The combination of albumin, norepinephrine, midodrine, and octreotide is effective as a regimen
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397
Q

What is hepatic encephalopathy

A
  1. Neuropsychiatric complication of chronic liver disease related to accumulation of large amounts of ammonia within the brain tissue
  2. One of the liver’s main function is to convert nitrogen containing compounds into urea to be excreted safely by the kidneys
  3. In patients with liver cirrhosis this conversion process is severely impaired
  4. The liver’s inability to metabolize ammonia increases ammonia in the blood and the concentration in the brain
  5. Also called portosystemic encephalopathy (PSE), Gamma-amino butyric acid (GABA)
  6. An inhibitory neurotransmitter, may play a role in hepatic encephalopathy development
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398
Q

What are causes and risk factors for hepatic encephalopathy

A
  1. Under normal conditions, ammonia is produced by the breakdown of protein in the bowel and is metabolized in the liver to form urea
  2. In patient with portal hypertension or severe liver disease, blood cannot pass into liver, so ammonia enters the systemic circulation and flows to the brain
  3. May arise as a complication of liver cirrhosis and advanced hepatic dysfunction
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399
Q

What are signs and symptoms of hepatic encephalopathy

A

Progresses in four stages
1. Mild confusion
2. Confusion
3. Severe confusion
4. No reaction to stimuli

Sleep pattern disturbances such as insomnia or hypersomnia are early symptoms
Neuropsychiatric signs and symptoms are seen in the advanced stages of the disorder and include hand-flapping tremors (asterixis), hyperactive deep tendon reflexes, and transient decerebrate posturing

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400
Q

How is hepatic encephalopathy diagnosed

A
  1. Thorough history
  2. CBC, liver function tests, ammonia levels and electroencephalogram
  3. CT scan and MRI are used to exclude other brain conditions such as tumors
  4. Treatment is based on severity
    - Minimal
    - Grade I
    - Grade II
    - Grade III
    - Grade IV
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401
Q

In the staging of hepatic encephalopathy what is evident at a minimal stage

A
  1. Psychometric or neuropsychological alterations of tests exploring psychomotor speed/executive functions without evidence of mental change
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402
Q

In the staging of hepatic encephalopathy what is evident at the Grade I stage

A
  1. Changes in behavior, mild confusion, slurred speech, disordered sleep
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403
Q

In the staging of hepatic encephalopathy what is evident at the Grade III stage

A
  1. Marked confusion (stupor), incoherent speech, sleeping but arousable, bizarre behavior
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404
Q

In the staging of hepatic encephalopathy what is evident at the Grade IV stage

A
  1. Coma; unresponsive to pain
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405
Q

What is the treatment for hepatic encephalopathy

A
  1. Correct pH and electrolyte imbalances
  2. Restrict dietary protein 1.2-1.5g/kg/day and total intake to 35-40kcal/kg/day
  3. Watch for signs of GI bleeding, because intestinal blood breakdown also results in ammonia production
  4. Lowering blood ammonia concentrations with medications such as Lactulose or lactitol - both are available in enema form for those that cannot tolerate the oral form
  5. Administering antibiotics such as rifaximin (Xifaxan) or neomycin to reduce GI bacterial load known to be responsible for toxin production
  6. Correcting hypokalemia, as hypokalemia increases renal ammonia production

Those with minimal hepatic encephalopathy without signs of showing advanced stages would benefit from lactulose or lactitol

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406
Q

What is hepatitis

A
  1. An inflammation of the liver
  2. May be acute or chronic
  3. Most prevalent type is caused by a virus
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407
Q

What are the viral types of hepatitis

A
  1. Hepatitis A (HAV)
  2. Hepatitis B (HBV)
  3. Hepatitis C ( HCV)
  4. Hepatitis D (HDV)
  5. Hepatitis E (HEV)
  6. Hepatitis G (HGV)
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408
Q

What are the non-viral types of hepatitis

A
  1. Alcoholic hepatitis
  2. Drug-induced hepatitis
  3. Autoimmune hepatitis
  4. NASH
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409
Q

What are the general signs and symptoms of hepatitis

A

Occurs when the disease prevents the liver from functioning normally, causing problems with digestion due to lack of bile and the regulation of blood

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410
Q

What is hepatitis A

A

A member of the genus Hepatovirus in the family Picornaviridae
1. The most common type
2. Transmitted by fecal-oral route
3. Onset is abrupt
4. Immunization is available
5. The incubation period is 15-50 day, during which patients are considered infectious
6. The hosts immune response causes the liver injury

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411
Q

What are risk factors for getting hepatitis A

A

Transmitted from person to person by the fecal-oral route or by contaminated food and water

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412
Q

What are signs and symptoms of hepatitis A

A
  1. Nausea and vomiting
  2. Abdominal pain
  3. Fever
  4. Malaise
  5. After several days, infected patients may manifest dark colored urine, acholic stools, jaundice, sclera icterus, pruritus, hepatomegaly, skin rashes and arthralgia
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413
Q

What are the potential complications of Hepatitis A

A

Fulminant hepatic failure associated with HAV infection is rare but can occur among individuals with underlying liver disease

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414
Q

What is the treatment for hepatitis A

A
  1. A period of rest from strenuous activity
  2. Usually self-limiting and treatment is supportive care
  3. Recovery is expected within 3-months, although relapse is possible after 6-12 months from onset
  4. Patients infected by HAV become immune to the virus
  5. In the US the vaccine is given to all children at 1 year or between 2 and 18years if not given between 12-23 months
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415
Q

For what population is the Hepatitis A vaccine recommended

A
  1. People traveling to or working in countries with intermediate or high rates of HAV infection
  2. Men who have sex with men
  3. People who use recreational drugs, both injectable and non injectable
  4. People who have risk of exposure based on their occupation such as working in a research laboratory
  5. People with chronic liver disease and clotting factor disorders
  6. People in close contact, during the first 60 days following the arrival in the US, with an international adoptee from a country with intermediate to high HAV infection incidence
  7. People who have direct contact with or recent exposure to someone in HAV
  8. Vaccines available - Havrix, vaqta, and twinrx ( a combination Hep A and Hep B vaccine
  9. Immune globulin GamaSTAN S/D can provide up to 2 months of protection and are available for
    • older than 40 years or younger than 12 months
    • immunocompromised and not responsive to the hepatitis A vaccine
    • allergic to the vaccines
    • suffering from a chronic medical condition such as chronic liver disease who are unable to wait for the second dose of the vaccine
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416
Q

What is the prognosis for Hepatitis A

A
  1. Most patients recover uneventfully after
  2. Most patients have no permanent liver damage
  3. HAV does not progress to chronic hepatitis
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417
Q

What is hepatitis B (HBV)

A
  1. DNA virus
  2. Transmitted via blood or sexual contact
  3. Major route is through perinatal infection of infants born to carriers of virus
  4. Immunization is available
  5. Onset slower than Hepatitis A
  6. A member of Hepadnavirus family
  7. The vein attaches itself to the hepatocyte membrane and penetrates the cells’ nuclei for replication via reverse transcriptase
  8. Some replicated viruses are then released, while some are recycled to repeat the replication process
  9. The host’s cytotoxic T lymphocyte response induces severe inflammatory liver disease
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418
Q

Who is at risk for getting Hepatitis B

A

Those who:
1. Use recreational injectable drugs
2. Have multiple sexual partners or men who have sex with men
3. Have household contacts with unvaccinated individuals with chronic HBV infection
4. Are developmentally disabled and living in long-term facilities
5. Are incarcerated
6. Work with patients who are HBV positive
7. Are on hemodialysis
8. Have HCV infection
9. Travel to countries where HBV is endemic
10. Have chronic liver disease, HIV or diabetes

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419
Q

What are signs and symptoms of Hepatitis B

A

Early symptoms are similar to an allergic reaction or serum sickness-like syndrome
Following this prodromal period signs and symptoms associated with acute infection are
1. Fever, Fatigue (malaise), loss of appetite (anorexia), nausea and/or vomiting, jaundice, sclera icterus, dark urine, alcoholic stool, abdominal pain, myalgia, and arthralgia
2. Symptoms can last from 1 week to 1 month

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420
Q

How is Hepatitis B diagnosed

A
  1. Serology - Hepatitis B surface antigen (HBsAg) and hepatitis B surface antibody (antiHBs)
  2. These markers are used to screen asymptomatic individuals and diagnose HBV infection
  3. In acute infection HBsAg becomes detectable around 1-10 weeks after exposure
  4. The level subsequently drops to an undetectable level at 4-6months, denoting recovery
  5. In most patients, the disappearance of HBsAg is followed by the appearance of anti-HBs, a marker indicating long-term immunity
  6. HBsAg that persists for more than 6 months implies chronic infection
  7. Other useful markers include hepatitis B core antigen, hepatitis b core antibody, isolated anti-HBc, hepatitis B e antigen and Hepatitis B e antibody
  8. Alanine and aspartate aminotransferases are also elevated
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421
Q

What are potential complications of Hepatitis B

A
  1. Liver damage (cirrhosis)
  2. Hepatocellular carcinoma (HCC)
  3. Fulminant hepatic failure
  4. Chronic hepatitis - an inflammatory reaction of the liver that lasts more than 6 month and develops in less than 5% of adult patient with HBV infection
  5. Mild hepatitis has a protracted course
    • cirrhosis is rare in patient with mild hepatitis but the incidence of hepatocellular carcinoma is increased after the age of 50
      -symptoms are usually mild if any and no therapy is needed
  6. Moderate to severe hepatitis, which is uncommon in patients with HBV infection
    • is associated with higher levels of serum tranaminases, along with mild hyperbilirubinemia and more severe portal and periorbital inflammation with erosion of the limiting plate of peripheral hepatocytes (piecemeal necrosis)
      - in more severe cases, necrosis may span the lobules (bridging the necrosis) or multilobular collapse may be stating a progressive process that leads to fibrosis, scar formation and cirrhosis
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422
Q

What is the treatment for Hepatitis B

A
  1. Usually supportive
  2. Includes 1 to 2 weeks of rest from strenuous activity
  3. If episode is severe, may require antiviral medication or even liver transplant
  4. Goal is to decrease serum HBV DNA levels in the blood; lessening infectivity; decreasing the level of hepatic inflammation; and preventing or slowing the development of cirrhosis, liver failure, and liver cancer
  5. Nutritionally balanced diet
  6. IV hydration and electrolyte management, if necessary
  7. Subcutaneous vitamin K and fresh frozen plasma in some cases
  8. Medications used sparingly and alcohol avoidance
  9. Liver transplantation as an option, although the risk of damage to the transplanted organ from HBV is high
  10. Antiviral for chronic HBV infection
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423
Q

What antivirals are used in the treatment for Hepatitis B

A
  1. Nucleoside analogs or pegylated interferon (PegINF)
  2. Nucleoside analogs like tenofovir (Vemlidy, Viread) and entecavir (Baraclude) are recommended as initial treatment because of their potent antiviral activity and the drug resistance is less likely to occur
  3. Other nucleoside analogs currently available are lamivudine (Epivir-HBV, Epivir) and adefovir (Hepsera)
  4. Lamivudine is associated with a high drug resistance
  5. Adefovir’s effect in viral suppression is slow and increased doses may lead to nephrotoxicity
  6. PegINF is also an initial treatment option for HBV infection, but it has been found to cause further liver damage as a result of necroinflammation and is associated with more side effects
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424
Q

Who is the Hepatitis B vaccine recommended for

A
  1. All neonates
  2. Individuals without HBV infection who live, travel to, or work in intermediate or high endemic areas
  3. People who are high risk, including those who are in sexual, household, and needle-sharing contact with HBV carriers, individuals in a setting with high HBV prevalence such as prisons and facilities for people who are developmentally disabled, and health care and public safety workers
  4. People with healthy disorders such as end-stage renal disease, chronic liver disease, HIV infection, HBV infection and diabetes
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425
Q

What is the prognosis for those with Hepatitis B infection

A
  1. 95% of adults recover uneventfully
  2. 10% develop chronic hepatitis - 0.1% of these patients die due to fulminant hepatic failure
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426
Q

What is Hepatitis C

A
  1. Formally called non-A, non-B hepatitis
  2. Transmission is through contact with contaminated blood, such as IV drug use, blood transfusions or sexual contact
  3. Can be carried without symptoms for 15 to 20 years
  4. It is estimated that 2.4million people in the US are living with HCV infection
  5. The incidence of acute HVC infection has been increasing
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427
Q

Who is at risk for getting Hepatitis C

A
  1. The leading cause for hepatitis C transmission is sharing needles of recreational injectable drugs
  2. Other methods of transmission are needle-stick injury to health care workers and transmission by infected mother to baby
  3. Sharing personal articles such as razors and toothbrushes, sexual contact with an infected person, and getting a tattoo in an unregulated setting are less common methods of HCV spread
  4. In the past, HCV was commonly transmitted by blood transfusion and organ transplantation
    - in the US widespread screening of blood supply has all but eliminated this source of infection
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428
Q

What are signs and symptoms of Hepatitis C

A
  1. The majority of patients with acute HCV infection are asymptomatic
  2. For some, mild and flu-like symptoms may occur within 2 weeks to 6 months after exposure
    • these symptoms may include fatigue, sore muscles, joint pain, fever, anorexia, nausea, abdominal pain, itching, dark urine, and jaundice
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429
Q

How is Hepatitis C diagnosed

A
  1. The HCV antibody test is a serology test
  2. A reactive result may indicate an active infection or that the patient has past exposure to HCV that has been resolved
  3. A positive HCV RNA test (a qualitative test that uses a process called polymerase chain reaction (PCR)) or transcription-mediated amplification (TMA) confirms chronic HCV infection
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430
Q

What are potential complications of Hepatitis C

A
  1. 75-85% of acute cases of HCV infection progress to chronic HCV infection, and 10-20% of these patients develop cirrhosis
  2. Also associated with extra-hepatic disease
    • the most important of these is cryoglobulinemia
      • this immune-related disease can cause kidney failure and a rash on the lower legs
  3. Alcohol consumption increases the risk of developing cirrhosis and accelerates the time to cirrhosis
  4. People who have HCV infection and cirrhosis are at a markedly increased risk of developing liver cancer
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431
Q

What is the treatment for Hepatitis C

A
  1. 15-25% of infected patients are able to clear HCV in their bodies without treatment
    - however reinfection is possible, even in those whose infection was cleared with treatment
  2. The selection of treatment is based on prior treatment history, and includes exposure and prior response to therapy
    • there is a difference in establishing the treatment plan for treatment-naive patients versus for treatment-experienced patients
  3. Direct-acting antivirals have 4 classes
    • no structural proteins 3/4A (NS3/4A) protease inhibitors, NS%B nucleoside polymerase inhibitors, NS5B non-nucleoside polymerase inhibitors, NS5A inhibitors
  4. Interferon-free regimens
    • Epclusa (sofosbuvir, velpatasvir), Harvoni (ledipasvir, sofosbuvir), Sovaldi(sofosbuvir), Vosevi (sofosbuvir, velpatasvir, voxilaprevir), Daklinza (daclatasvir)
  5. Patients with decompensated cirrhosis or a MELD score >10 should be evaluated for liver transplantation prior to initiation of therapy
  6. Development of a Hepatitis C vaccine is underway
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432
Q

What is the prognosis for patients with Hepatitis C

A
  1. 90% of patients will develop chronic hepatitis
  2. 20% are at risk for development of cirrhosis
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433
Q

What is Hepatitis D

A
  1. Simple parasite the preys on the hepatitis B virus either as a co-infection or a super-infection
  2. Endemic in nature
  3. In general, tends to increase virulence and severity of HBV
  4. 5% of HBV sufferers also have the HDV form
  5. Also referred to as hepatitis delta virus or delta agent
  6. For HDV to complete virion assembly and secretion, the patient must also be infected with Hepatitis B virus, so patient with HDV infection are always dually infected with HBV and HDV
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434
Q

Who is at risk for developing Hepatitis D

A
  1. It’s endemic in Italy and other Mediterranean countries and several regions of South America
  2. In nonendemic areas such as North America and northern Europe, HDV is transmitted primarily by serum as is found mainly in children who have had multiple transfusions, men who have sex with men and people who use recreational drugs
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435
Q

What are signs and symptoms of Hepatitis D

A

Acute HDV infection. Chronic HDV infection
1. Fatigue 1. Have few symptoms for several years before severe chronic liver complications
2. Anorexia Develop
3. Nausea and vomiting 2. Weakness
4. Right upper quadrant pain. 3. Fatigue
5. Acholic stool. 4. Weight loss
6. Dark urine 5. Abdominal swelling
7. Jaundice 6. Edema , pruritus, and jaundice

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436
Q

How is Hepatitis D diagnosed

A

Made with high tigers of IgG and IgM anti-HDV
Detection of HDV RNA confirms the diagnosis
Additional tests may include elastography and liver biopsy

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437
Q

What are potential complications of Hepatitis D

A

Although rare HDV infection can lead to acute liver failure
Chronic HDV infection may lead to cirrhosis, liver failure, and liver cancer

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438
Q

What is the treatment for Hepatitis D

A

1.Specific treatment is not established
2.Fulminant hepatitis related to HDV and HBV infection has been reverse by focarnet sodium (Foscavir) in some patients
3.The success rate of interferon Alfa (IFNa) is low, built is currently the only drug approved for chronic HDV infection
4. There is no vaccination available for HDV
5. Protection against HBV, which is required for HDV replication is an important measure in preventing HDV infection

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439
Q

What is the prognosis for Hepatitis D

A
  1. As a coinfection, the HBV is usually eliminated and chronic hepatitis does not ensue
  2. Superinfection with HDV often leads to rapidly progressive liver damage
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440
Q

What is Hepatitis E

A
  1. The causative agent for hepatitis E infection is the hepatitis E virus (HEV) in the genus Hepevirus in the family Hepeviridae
  2. There are 5 known genotypes of HEV, 4 of which are associated with human infection
  3. It is found worldwide, but the disease is most common in East and South Asia
  4. The incubation period for HEV infection is 15-60 days
  5. In chronic HEV infection, the disease continues to be detectable in blood or stool for longer than 6 months
  6. Incubation period is 6 to 8 weeks
  7. Usually only lasts a couple of weeks
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441
Q

Who is at risk for developing hepatitis E

A
  1. Transmission of HEV can be fecal-oral
  2. Consumption of raw or undercooked, meat
  3. Blood transfusion
  4. Mother-to-child
  5. Chronic HEV infection almost exclusively occurs among patients who are immunocompromised
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442
Q

What are signs and symptoms of Hepatitis E

A
  1. A self-limiting and primarily asymptomatic or mildly symptomatic
  2. Symptoms may include jaundice, malaise, anorexia, nausea and vomiting, joint pain, pruritus, skin rashes and elevated AST/ALT
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443
Q

What are potential complications of Hepatitis G virus

A

Acute hepatic failure associated with HEV infection is a potential complication, although this is rare in the US 0.4%

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444
Q

What is the treatment for Hepatitis E

A
  1. Preventative measures for HEV infection include avoiding food from a setting where preparation is questionable and avoiding eating raw or undercooked meat, especially deer, wild boar, and pig liver sausage
  2. The treatment of acute HEV infection is mainly supportive, although a liver transplant may be necessary with fulminant hepatic failure
  3. The antiviral ribavirin (Rebetol, Ribasphere, Virazole) is recommended for chronic HEV infection, along with reduction of immunosuppressive therapy
  4. Blood level monitoring is essential to prevent drug toxicity
  5. Ribavirin is teratogenic and should not be used for women who are pregnant
  6. For patients who do not respond to Ribavirin therapy Peginterferon and sofosbuvir may be considered
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445
Q

What is Hepatitis G

A
  1. Referred to as GB virus C (GBV-C), was identified in 1995
  2. The virus is a single-strand RNA belonging to the Flaviviridae family
  3. People are usually infected with HBV and/or HCV
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446
Q

What are the risk factors of getting Hepatitis G

A

Blood and sexual contact are the most likely mode of transmission

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447
Q

What are signs and symptoms of Hepatitis G

A

Most individuals with GBV-C are asymptomatic and the incubation period is unknown

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448
Q

How is Hepatitis G diagnosed

A
  1. Associated with elevated liver enzymes
  2. A detectable HGV RNA by reverse transcriptase PCR indicates GBV-C infection
  3. There is no serologic test available for GBV-C
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449
Q

What are potential complications of Hepatitis G

A
  1. Most of GBV-C infections are cleared, although, in some patients, it can become chronic
  2. Patient with HCV infection are often co-infected with GBV-C, and a higher GBV-C infection incidence is associated with B-cell non-Hodgkin’s lymphoma
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450
Q

What is the treatment for Hepatitis G

A
  1. Bed rest
  2. Avoiding alcohol
  3. Eating a well-balanced diet
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451
Q

What is the prognosis for those with Hepatitis G

A

Has not been proven to lead to cirrhosis or acute liver failure

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452
Q

What is alcoholic hepatitis

A

Inflammation of the liver that is the result of alcohol use

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453
Q

What are risk factors for alcoholic hepatitis

A
  1. Heavy consumption of alcohol - >3.5oz daily for 20 years or more
  2. However sex (being female), obesity, genetics, race and ethnicity( African American, and Hispanic), and binge drinking are also identified as other risk factors affecting those who consume less alcohol
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454
Q

What are signs and symptoms of alcoholic hepatitis

A
  1. Right upper quadrant abdominal pain
  2. Fever
  3. Vomiting
  4. Anorexia
  5. Dark urine
  6. Unlike other forms of hepatitis patients do not present with jaundice
  7. Physical signs include an enlarged and tender liver, splenomegaly, signs of chronic alcohol misuse and cirrhosis and mental status abnormalities
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455
Q

How is alcoholic hepatitis diagnosed

A
  1. Biopsy of the liver in patients with a history of alcoholism may show scattered fatty deposition, hepatocyte degeneration and necrosis, peri cellular fibrosis and inflammation, cholestasis and cirrhosis
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456
Q

What are complications of alcoholic hepatitis

A
  1. Considered a precirrhotic lesion
  2. If not reversed, alcoholic hepatitis can be deadly with significant short-term mortality
  3. Patient who are untreated are at a higher risk of dying 1 month from the onset of signs and symptoms
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457
Q

What is the treatment for alcoholic hepatitis

A
  1. Alcohol abstinence
  2. Corticosteroid
  3. Pentoxifylline (Pentoxil)
  4. Nutrition supplementation
  5. Liver transplantation
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458
Q

In the treatment for alcoholic hepatitis what is the importance of alcohol abstinence

A

Critical to improve the outcome of treatment and prognosis

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459
Q

In the treatment for alcoholic hepatitis what is the importance of corticosteroids

A
  1. A first line drug used to reduce liver inflammation associated with alcoholic hepatitis
  2. This drug increases the survival rate for patients with severe alcoholic hepatitis, although it is linked to side effect such as:
    • increased fungal infection risk
    • hyperglycemia
    • weight gain
    • electrolyte imbalance
  3. Corticosteroids are not recommended for patients with:
    • coexisting sepsis
    • acute pancreatitis
    • GI bleeding
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460
Q

In the treatment for alcoholic hepatitis wrath is the importance of Pentoxifylline (Pentoxil)

A
  1. An alternative drug that also has a beneficial effect for patients with alcoholic hepatitis who do not respond to corticosteroids
  2. Although Pentoxifylline’s exact action is not clearly understood, the drug may have a protective mechanism to prevent hepatorenal syndrome
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461
Q

In the treatment for alcoholic hepatitis what is the importance of nutritional supplementation

A

Should be considered especially in patients with alcoholic hepatitis who are prone to protein-calorie malnutrition

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462
Q

In the treatment for alcoholic hepatitis what is the importance of liver transplantation

A

1.Before being considered for transplantation patients are required to satisfy the criterion of at least six months of alcohol abstinence
2. Other barriers include a shortage of donor organs, sociocultural factors and public option regarding the self-inflicted nature of alcoholic hepatitis

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463
Q

What is toxic (drug induced) hepatitis

A
  1. An inflammation of the liver that is caused by a drug or toxic substance
464
Q

Who is at risk for developing toxic (drug-induced) hepatitis

A

Drugs and toxic substances can cause a wide range of hepatic injuries
1. A predictable dose-related hepatotoxic reaction such as that produced by acetaminophen (Tylenol), carbon tetrachloride and methotrexate
2. An unpredictable non-dose-related viral-like hepatitis, with or without cholestasis, which is produced by such drugs as:
- isoniazid (Laniazid)
- flurazepam
- methyldopa
3. Cholestasis related to the use of anabolic steroids, birth control pills and haloperidol

465
Q

How is Toxic (drug-induced) hepatitis diagnosed and what are the symptoms

A

Clinical presentation ranges from asymptomatic persons with transaminase elevations to patients who develop fulminant hepatic failure

466
Q

What are complications of Toxic (drug-induced) hepatitis

A

Patients who ingest massive doses of acetaminophen are at risk for fulminant hepatic failure

467
Q

What is the treatment for toxic (drug-inducing) hepatitis

A
  1. Most patients recover within 1 to 2 weeks of discontinuing the offending agent
  2. For acetaminophen toxicity, appropriate therapy must be instituted within 24 hours of ingestion, including ipecac-induced emesis and administration of N-acetylcysteine in a loading dose, followed by the maintenance doses until plasma acetaminophen falls below hepatotoxic levels
468
Q

What is the prognosis for patients with toxic(drug-induced) hepatitis

A

Most patients recover within 1-2 weeks after discontinuing the offending drug

469
Q

What is autoimmune hepatitis

A
  1. The body’s immune system attacks the liver cells and causes inflammation
  2. Believed to be the result of an environmental agent that causes an abnormal T-cell response that specifically targets the liver, causing inflammation, elevation of antibodies, and hypergammaglobulinemia
470
Q

Who is at risk for developing autoimmune hepatitis

A

Affects genetically susceptible individuals
Affects more women than men

471
Q

What is the most common sign and symptom of autoimmune hepatitis

A

Fatigue

472
Q

What are potential complications of autoimmune hepatitis

A

May result in cirrhosis and fulminant hepatic failure

473
Q

What is the treatment for autoimmune hepatitis

A
  1. Prednisone is the drug of choice for initial treatment
  2. However due to prednisone’s side effects, Azathioprine (Imuran, Azasan) is more favored as a long-term maintenance drug, especially during remission
  3. In patient who are unable to tolerate azathioprine, mycophenolate mofetil (Cellcept) may be used an an alternative
  4. Daily doses of corticosteroid therapy, with or without azathioprine
  5. Medications are given for a period put out 10 to 20 years
474
Q

What is the prognosis for autoimmune hepatitis

A

Favorable with treatment

475
Q

What is Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH)

A

Non alcoholic fatty liver disease (NAFLD)
1. The accumulation of fat in the liver (hepatic steatosis) that is not associated with alcohol exposure and shows no evidence of liver inflammation

Nonalcoholic steatohepatitis (NASH)
1. Is non alcoholic fatty liver disease with evidence of liver inflammation

NAFLD includes a range of conditions from Type 1 to Type 4 with Types 3 and 4 being considered NASH

476
Q

What are risk factors to developing NASH

A
  1. Obesity
  2. Type 2 diabetes
  3. Hyperlipidemia
  4. Fat accumulates in the liver when the liver cannot degrade or export the lipids
  5. The diagnosis of NASH will likely increase as millions of American adults are overweight or obese and the incidence of obesity has increased throughout the world
477
Q

What are signs and symptoms of NASH

A
  1. Fatigue
  2. Vague right upper quadrant pain
  3. Weight loss
  4. Weakness

The advanced stages of NASH
1. Lack of appetite
2. Nausea
3. Varices
4. Loss of interest in sex
5. Ascites
6. Itching
7. Edema and encephalopathy

478
Q

How is NAFLD and NASH diagnosed

A

NAFLD
1. Ultrasonography

NASH
1. Liver biopsy

479
Q

What is a potential complication of NASH

A

Can develop into cirrhosis

480
Q

What is the treatment for NAFLD and NASH

A
  1. Remove the cause of the fatty infiltration of the liver and remove exposure to factors that may worsen the condition
  2. Weigh loss (even if slightly overweight)
  3. Control of blood sugar
  4. Low-fat diet
  5. Aerobic exercise
  6. Vitamin E and pioglitazone (Actos) continue to show good results in reducing disease activity
  7. Bariatric surgery is an option for selected patients; usually young adults <40-50 years of age
  8. Peroxisome proliferator-activator receptors (PPARs) farsenoid X receptor (i.e. obeticholic acid (OCAI), glucagon-like peptide (GLP-1), lipid-altering agents such as steatoryl-CoA desaturate (SCD), SCD-1 inhibitor (Aramchol), and statins (HMG-CoA reductive inhibitors)
  9. Further studies are needed to fully confirm their efficacy
481
Q

What is fulminant hepatic failure

A
  1. Also referred to as acute liver failure
  2. A loss of liver function that has developed over a period of less than 26 weeks in a patient without cirrhosis or pre-existing liver disease
482
Q

What are risk factors of developing fulminant hepatic failure

A
  1. Acetaminophen toxicity. 11. HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome
  2. Idiosyncratic drug reactions 12. Malignant infiltration of the liver
  3. Viral hepatitis 13. Partial hepatectomy
  4. Alcoholic hepatitis 14. Toxin exposure (including mushroom poisoning)
  5. Autoimmune hepatitis 15. Sepsis
  6. Wilson’s disease 16. Heat stroke
  7. Ischemic hepatopathy 17. Hemophagocytic
  8. Budd-Chiari syndrome 18. Lymphohistiocytosis (primarily in children)
  9. SOS
  10. Acute fatty liver of pregnancy
483
Q

What are signs and symptoms of fulminant hepatic failure

A

Nonspecific symptoms
1. Jaundice
2. Right upper quadrant pain
3. Fatigue
4. Malaise
5. Anorexia
6. Nausea and vomiting

484
Q

How is fulminant hepatic failure diagnosed

A

The defining characteristics are:
1. Encephalopathy
2. Abnormal prothrombin time (INR >or= 1.5)

485
Q

What are potential complications of fulminant hepatic failure

A

In its progressive stages patients may develop:
1. Ascites
2. Coagulopathy
3. GI bleeding infection
4. Cerebral edema resulting in seizures and mental status changes such as lethargy, confusion and eventually coma

486
Q

What is the treatment for fulminant hepatic failure

A

Liver transplantation is the only treatment

Care options
1. Initial fluid resuscitation
2. A vasopressor and norepinephrine may be required
3. A proton-pump-inhibitor or histamine 2 blocker is given prophylactically
4. Antibiotic prophylaxis
5. An intake of 60g of protein per day
6. Mannitol is given

Routine lactulose for encephalopathy secondary to acute liver failure is no longer recommended, as the drug does not improve overall outcomes and causes bowel distention that results in technical difficulties during liver transplantation

487
Q

In the treatment for fulminant hepatic failure what is the importance of fluid resuscitation

A
  1. Using normal saline is important with hemodynamic derangements
  2. Half normal saline with 75mEq/L of sodium bicarbonate can be used for patient with acidosis
  3. Overhydration should be avoided to prevent worsening cerebral edema
488
Q

In the treatment for fulminant hepatic failure why would vasopressin and norepinephrine be used

A

It may be required for patients with poor response to fluid resuscitation

489
Q

In the treatment for fulminant hepatic failure why would a proton-pump-inhibitor or histamine 2 blocker be used

A

They are given prophylactically to prevent bleeding in the GI tract, a common site of bleeding in fulminant hepatic failure

490
Q

In the treatment of fulminant hepatic failure why would an antibiotic be used

A
  1. Antibiotic prophylaxis remains controversial and is only recommended when there is evidence of active infection or clinical deterioration
  2. Piperacillin/tazobactam (Zosyn) or fluorquinolones are drugs of choice
  3. Aminoglycosides are avoided due to their nephrotoxic effects
491
Q

In the treatment for fulminant hepatic failure why is it important to have an intake of 60g of protein per day

A

To prevent catabolism of protein stores in the body
Severe protein restriction should be avoided

492
Q

In the treatment for fulminant hepatic failure why would Mannitol be given

A
  1. 0.5 to 1.0g/kg is given to patients with increased intracranial pressure (ICP) to achieve an ICP <25mmHg and a cerebral perfusion pressure >50mmHg
493
Q

What is Budd-Chiari Syndrome

A

A rare condition characterized by an obstruction of the hepatic venous outflow tract at the level of the small hepatic veins, large hepatic veins, and suprahepatic segment of the inferior vena cava

494
Q

What are risk factors of developing Budd-Chiari Syndrome

A
  1. Malignancy
  2. Thrombogenic disorders
  3. Inflammatory disorders
  4. Other risk factors such as hormone disorders
495
Q

What are signs and symptoms of Bud-Chiari syndrome

A
  1. In the classic form BCS is a nearly complete obstruction of flow cause by the acute formation of a clot at the opening or an acute phlebitis of the hepatic veins into the inferior vena cava
  2. This sudden event is followed by the onset of hepatomegaly, pain, ascites and liver failure
496
Q

How is Budd-Chiari Syndrome diagnosed

A

Usually established by:
1. Doppler ultrasonography
2. CT scan
3. Magnetic resonance imaging (MRI)

497
Q

What are potential complications for Budd-Chiari syndrome

A

The course of BCS is unpredictable
1. In some patients, complete spontaneous remission occurs with or without remitting aggravation of liver insufficiency or portal hypertension
2. In other patients secondary BCS is related to invasion or compression of the veins by a lesion

498
Q

What is the treatment for Budd-Chiari syndrome

A

Treatment is based on cause
1. Anticoagulation and thrombolytic therapy are possible treatments
2. Angioplasty with or without stenting is an option
3. If angioplasty fails or is impossible, Transjugular intrahepatic portosystemic shunting (TIPS) may be performed
4. Liver transplant may increase survival in the most severe cases

499
Q

What are benign hepatic tumors

A
  1. Most are hemangiomas that consist of blood vessels
  2. Focal nodular hyperplasia
  3. Hepatic adenoma
  4. Idiopathic noncirrhotic portal hypertension
  5. Regenerative nodules
500
Q

What causes benign hepatic tumors

A

History of:
1. Cirrhosis
2. Hepatitis B
3. Hepatitis C
4. Alcohol
5. Androgen therapy
6. Exposure to hepatotoxic chemicals

501
Q

What are signs and symptoms of benign hepatic tumors

A

Most patients are asymptomatic

502
Q

How are benign hepatic tumors diagnosed

A
  1. Ultrasound
  2. Often in incidental finding
503
Q

How are benign hepatic tumors treated

A

Most require no treatment

504
Q

What are malignant hepatic tumors

A
  1. More common than benign tumors
  2. Primary tumors originate in either hepatocytes or bile duct cells
  3. Include hepatocellular carcinoma (HCC), cholangiocarcinoma, and metastatic disease
505
Q

What are causes of malignant hepatic tumors

A

Predisposing factors include:
1. Cirrhosis
2. Hepatitis
3. Alcohol
4. Exposure to hepatotoxic chemicals

Primary tumors are less common than metastatic or secondary liver tumors, which often spread from the lungs, breasts, GI tract, thyroid, prostate, or skin

506
Q

What are signs and symptoms of malignant hepatic tumors

A

Most are asymptomatic until advanced stage

Abdominal pain can occur in ruptured and bleeding adenoma and HCC

507
Q

How are malignant hepatic tumors diagnosed

A
  1. CT scan
  2. MRI
  3. Hepatic angiography
  4. Needle biopsy examination
508
Q

What is the treatment for malignant hepatic tumors

A
  1. Treatment for very large tumors involves tumor excision to reduce the risk of tumor rupture and hemorrhage
  2. If the tumor obstructs the bile duct, a stent is placed
509
Q

What is the prognosis for people with malignant hepatic tumors

A

Poor

510
Q

What is Hepatocellular carcinoma

A
  1. The most common primary malignant tumor of the liver
  2. The third most common cause of cancer-related death in the world and seventh in the US
  3. The incidence of HCC increases progressively with age in all populations and is rare in children
511
Q

What are the risk factors of developing Hepatocellular Carcinoma

A
  1. Hepatitis B
  2. Hepatitis C
  3. Cirrhosis
  4. Repeated exposure to environmental toxins such as:
    • aflatoxin (from contaminated corn, soybeans, and peanuts)
    • chewing betel nut
    • microcystin (from contaminated pond-ditch water)
  5. Other important factors include tobacco, and alcohol misuse, diabetes mellitus, obesity, NAFLD, hemochromatosis, alpha-1 antitrypsin deficiency, acute intermittent porphyria, Cholelithiasis, and cholecystectomy
512
Q

What are signs and symptoms of Hepatocellular carcinoma

A
  1. Most patients are asymptomatic until the disease is well advanced
  2. Symptoms are similar to all liver failure diagnoses including:
    • abdominal pain, weight loss, weakness, nausea, and vomiting
  3. Physical signs include:
    • hepatomegaly, hepatic bruit, ascites, splenomegaly, jaundice, wasting, and fever
  4. Paraneoplastic manifestations include:
    • hypoglycemia, polycythemia, hypercalcemia, sex hormone changes, portal hypertension, watery diarrhea, porphyria, neuropathy, osteoarthritis, and carcinoid syndrome
513
Q

How is Hepatocellular carcinoma diagnosed

A
  1. Screening of individuals in high-risk groups for liver cancer using ultrasound and assessing serum levels of alpha fetoprotein (AFP), des-y-carboxy prothrombin, or a-l-fucosidase are essential steps to finding small tumors and applying curative procedures
  2. CT scan, MRI, hepatic angiography, and needle biopsy
  3. Large elevations in serum AFP are virtually diagnostic for primary hepatocellular carcinoma
514
Q

What are the potential complications of Hepatocellular carcinoma

A

Prognosis is grim if the patient has a large tumor or has any evidence of metastatic disease

515
Q

What is the treatment for Hepatocellular carcinoma

A
  1. For patients with a localized mass without lymph node, bile duct, or blood vessel involvement or distal metastases, up to 80% of the liver may be resected
    • curative procedures include lobe resection and liver transplantation
  2. Alcohol injection or Radiofrequency ablation, chemoembolization and chemotherapy
  3. Pain may be relieved with chemotherapeutic liver perfusion via the hepatic artery
  4. Ligation or occlusion of the hepatic artery may temporarily slow cell growth and activity
  5. If the tumor obstructs the bile duct, endoscopic or transhepatic insertion of a biliary decompression catheter or stent may provide some relief
516
Q

What is Wilson’s disease

A
  1. A rare autosomal-recessive disorder that is characterized by defective excretion of copper in bile
  2. 50% of all patients have symptoms before age 15 years
  3. All family members should be screened
517
Q

What are risk factors to getting Wilson’s disease

A
  1. Linked to a mutation in the ATP7B gene acquired genetically from both parents in autosomal recessive pattern
  2. This gene plays an important role in the transport of copper from the liver to other parts of the body
518
Q

What are signs and symptoms of Wilson’s disease

A
  1. Excessive amounts of copper accumulate in the brain, liver, kidneys, and corneas (Kayser-Fleischer ring), causing:
    • tissue necrosis, hepatic disease and potentially liver failure
  2. Physical signs
  3. Hepatic disorders
  4. Neurologic symptoms
  5. Psychiatric disorders
  6. Other disorders
519
Q

What are physical signs of Wilson’s disease

A
  1. Characteristic rusty brown ring of pigment around the periphery of the cornea called a Kayser-Fleischer ring and a bluish discoloration on the fingernails (lunulae ceruleae
520
Q

What are hepatic disorders that can occur in patients with Wilsons disease

A
  1. Jaundice
  2. Ascites
  3. Asymptomatic hepatomegaly
  4. Isolated splenomegaly
  5. Persistently elevated aspartate transaminase (AST) and alanin transaminase (ALT)
  6. Acute or chronic hepatitis
  7. Fatty liver
  8. Cirrhosis
521
Q

What are Neurologic symptoms of Wilson’s disease

A
  1. Dysarthria
  2. Ataxia
  3. Tremors
  4. Parkinsonism
  5. Drooling
  6. Seizures
  7. Urinary incontinence
  8. Autonomic dysfunction
  9. Abnormal involuntary body movements such as dystonia, risus sardonicus, chorea, athetosis, hyperreflexia, and myoclonia
522
Q

What are psychiatric disorders associated with Wilson’s disease

A
  1. Depression
  2. Bipolar disorder
  3. Schizophrenia
  4. Dementia
523
Q

What are other disorders associated with Wilson’s disease

A
  1. Renal abnormalities
  2. Ocular sunflower cataracts
  3. Pancreatitis
  4. Hypoparathyroidism
  5. Menstrual irregularities
  6. Cardiomyopathy
  7. Skeletal abnormalities such as premature osteoporosis and arthritis
524
Q

How is Wilson’s disease diagnosed

A

By a combination of diagnostic tests such as:
1. Blood and urine tests
2. Eye exam
3. Liver biopsy and genetic testing

Once a diagnosis is confirmed, all first-degree relatives should be screened for the disease

525
Q

What are potential complications of Wilson’s disease

A

Without treatment patients will invariably succumb to liver disease or neurological complications

526
Q

What is the treatment for Wilson’s disease

A
  1. Requires a lifelong therapy with chelating agents
    • Penicillamine (cuprimine, depen)
    • trientine (syprine) is also an effective treatment and is indicated especially for patients who are intolerant of Penicillamine
    • both drugs are chelators and promote excretion of copper into urine
  2. Zinc which interferes with absorption of copper, is sometimes used as maintenance therapy and has minimal side effects
    • zinc appear preferable for pre-symptomatic children under age 3
  3. Liver transplantation is the only option for patients with acute liver failure or those with decompensated liver disease unresponsive to medical therapy
  4. Patient should avoid the intake of high concentrations of copper in foods (shellfish, nuts, chocolate, mushrooms, and organ meats) and water (well water or water transported in copper pipes)
  5. Copper containing cookware should not be used to cook or store food
  6. A water-filtering system that filters out copper is advisable
527
Q

What is prophyria

A

A hereditary or acquired enzyme defect in which the biosynthesis of heme in either the bone marrow or liver leads to an overproduction of porphyrins or their precursors

528
Q

What are the different types of porphyria

A
  1. Acute intermittent porphyria (AIP)
  2. Hereditary coproporphyria (HCP)
  3. Variegate porphyria (VP)
  4. Delta-aminolevulinic acid (ALA) dehydratase (ALAD) porphyria (ADP)

The most common form of hepatic porphyria is porphyria cutanea tarda (PCT)

529
Q

What is acute intermittent porphyria (AIP)

A
  1. An autosomal-dominant inherited disease that usually occurs as episodes over the course of several hours or a few days
  2. The most common symptom is severe abdominal pain, nausea, vomiting, constipation or diarrhea, and abdominal distention
  3. Ileus and urinary retention, peripheral neuropathy, psychiatric symptoms (paranoia, and hallucination) and coma can also occur
  4. Porphyrins may be normal or slightly elevated in stool and plasma
  5. The erythrocyte porphobilinogen deaminase (PBGD) in blood is approximately half the normal level
530
Q

What is Hereditary coproporphyria (HCP)

A
  1. An autosomal-dominant inherited disease characterized by large amounts of coproporphyrin III in the feces and the urine
  2. Protoporphyrin is also mildly elevated in the feces
  3. Patients develop photosensitivity
531
Q

What is Variegate porphyria (VP)

A
  1. An autosomal-dominant disease characterized by large amounts of protoporphyrin and copoporphyrin III in the feces
  2. Plasma porphyrin and plasma fluorescence are also elevated
  3. VP is most common in the South African white population
  4. It can produce photosensitivity
532
Q

What is Delta-aminolevulinic acid (ALA) dehydratase (ALAD) porphyria (ADP)

A
  1. An autosomal-recessive inherited disease and a rare form of acute hepatic porphyria
  2. It’s clinical features are indistinguishable from other forms of acute porphyrias
  3. Urine detection of delta-aminolevulinic acid and molecular genetic testing are used to confirm the diagnosis
533
Q

What are causes of porphyria

A

Hereditary or acquired enzyme defect in which the biosynthesis of heme leads to overproduction of porphyrins

534
Q

What are signs and symptoms of porphyria

A

Can be classified as either erythropoietic or hepatic, however categorizing porphyrias based on their distinctive clinical features is more useful in establishing a diagnosis and selecting the appropriate treatment
1. Chronic skin lesions
2. Poor healing
3. Increased hair growth
4. Mild liver disease with fatty infiltration
5. No acute abdominal or neuropsychiatric attacks
6. Blistering cutaneous porphyrias
7. Acute no blistering cutaneous porphyrias
8. Acute hepatic porphyrias

535
Q

What are the symptoms with blistering cutaneous prophyrias

A

1.These causes chronic, blistering, cutaneous lesions on parts of the skin that are exposed to the sun
2. The most common porphyria under this category and the most common in adults is porphyria cutanea tarda (PCT

536
Q

What are the symptoms of acute nonblistering cutaneous porphyrias

A
  1. These cause photosensitivity
  2. The most common porphyria under this category is erythropoietic protoporphyria (EPP)
  3. It is the most common porphyria in children and the third most common porphyria in adults
537
Q

What are the symptoms of acute hepatic porphyrias

A
  1. These are characterized by neuropathic abdominal pain, autonomic changes such as tachycardia and hypertension, muscle weakness, sensory loss, and pain in the back, chest and extremities
  2. The four types of hepatic porphyrias include ADP, variegate porphyria (VP), hereditary coproporphyria (HCP), and acute intermittent porphyria (AIP)
538
Q

How is prophyria diagnosed

A

Based on the symptoms and types

539
Q

How is blistering cutaneous porphyria diagnosed

A
  1. The initial screening test is total plasma or urine porphyrins
  2. Additional tests include fractionation and fluorescence screen
540
Q

How is acute nonblistering cutaneous porphyrias diagnosed

A
  1. Screening tests include erythrocyte total protoporphyrin and measurement of metal-free and zinc protoporphyrin
541
Q

How is acute hepatic porphyrias diagnosed

A
  1. The initial test is a spot urine porphobilinogen (PBG)
  2. Additional tests to determine the specific type of porphyria under this category include urine ALA, plasma and fecal porphyrins, erythrocyte ALAD activity, lead level and urine organic acids
542
Q

What is the treatment for porphyria

A

The treatment depends on the symptoms and type of porphyria

543
Q

What is the treatment for blistering cutaneous porphyrias

A
  1. Phlebotomy or low-dose hydroxychloroquine (Plaquenil)
  2. Generally sun exposure should be avoided
544
Q

What is the treatment for acute nonblistering cutaneous porphyrias

A

Avoiding sun exposure is also important

545
Q

What is the treatment for acute hepatic porphyrias

A
  1. Even in the absence of biomedical confirmation, hemin (Panhematin), a drug that inhibits delta-aminolevulinic acid synthetase and limits the rate of the porphyrin/heme biosynthetic pathway, should be considered early in the diagnosis for patients with known prophyria to reduce risk of prolonged complications (nerve damage) and death
546
Q

What is hemochromatosis

A
  1. Genetic defect of iron metabolism causing an excessive iron in tissues
  2. Consists of three classifications
    • hereditary hemochromatosis
    • secondary iron overload
    • miscellaneous disorders
547
Q

What is hereditary hemochromatosis

A
  1. A recessively-inherited gene disorder often affecting people of north European descent
  2. It is caused by a mutation of the homeostatic iron regulator (HFE) gene that causes problems with iron metabolism and is characterized by excessive tissue iron deposition
  3. Screening to detect early disease and prevent complications is recommended in first-degree relatives of patient with HFE gene-related hereditary hemochromatosis
  4. There are four main categories of pathophysiological mechanisms of hereditary hemochromatosis
    • increased absorption of dietary iron in the upper intestines
    • decreased expression of the iron regulatory hormone hepcidin
    • altered function of HFE protein
    • tissue injury and fibrogenesis induced by iron
548
Q

What is secondary iron overload

A
  1. Also known as secondary hemochromatosis
  2. Typically seen in patients with hemoglobinopathies (sickle cell disease, thalassemia, sideroblastic anemia), congenital hemolytic anemias, myelodysplasia, excessive oral iron intake, increased iron absorption, and repeated blood transfusions (significant tissue deposition of iron is seen with >40 units transfused)
  3. Risk factors for secondary iron overload include alcoholism, family history of diabetes, heart disease, liver disease, and excessive intake of dietary iron especially when taken with vitamin C supplements
549
Q

What are miscellaneous disorders

A
  1. Refer to other disorders that are also associated with abnormal iron deposition such as congenital atransferrinemia and aceruloplasminemia
  2. Miscellaneous iron overload disorders are rare conditions
550
Q

What are symptoms of hemochromatosis

A
  1. Can be asymptomatic, frequently with no physical findings, although most patients have hepatomegaly
  2. Symptomatic patients will have complaints of weakness, malaise, loss of libido, weight loss, changes in skin colon, right upper quadrant abdominal pain, and arthralgias
  3. Physical findings can present as hepatomegaly, splenomegaly, ascites, arthritis, swollen joints, chondrocalcinosis, cardiomyopathy, congestive heart failure, increased skin pigmentation, hypothyroidism, porphyria cutanea tarda, testicular atrophy, or any sign of liver failure
  4. Hemochromatosis is sometimes called “bronze diabetes” because clinical findings usually include hyperglycemia and darkening of the skin
551
Q

How is hereditary hemochromatosis diagnosed

A
  1. Early diagnosis is crucial in preventing complications
  2. Lab tests that show increased iron stores, demonstrated by an elevated serum ferritin and serum iron concentration and by transferrin saturation
  3. Plain x-ray films of the hands that show chondrocalcinosis, sclerosis of subchondral cyst formation
  4. CT scans of the liver that show marked increases in density
  5. Liver biopsy, which is recommended for diagnosis, staging the degree of liver disease, and identifying the prognosis
    • biopsy of the liver also permits estimation of tissue irons by histochemical staining and chemical analysis of hepatic iron concentration
  6. Genetic testing that can detect gene mutations associated with the disorder
552
Q

How is secondary iron overload diagnosed

A
  1. Measuring serum ferritin, serum iron, and transferrin saturation; fasting serum iron and iron binding capacity
  2. Additionally, genetic testing along with a thorough history may be done to rule out hereditary hemochromatosis
553
Q

How are atansferrinemia and aceruloplasmineia diagnosed

A

Established by detailed history and genetic testing

554
Q

What are potential complications of hemochromatosis

A
  1. Iron accumulation in the organs may lead to liver cirrhosis and hepatocellular carcinoma
  2. Although hemochromatosis is generally not common in infants, if present , it can lead to the need for a liver transplant
555
Q

What is the treatment for hemochromatosis

A
  1. Phlebotomy is a treatment modality that can reduce iron overload - 200-250mg of iron are removed with every 500ml of whole blood
    - patients may tolerate removal of 0.5-2 units per week, depending on age, sex, BMI, and presence of cardiopulmonary disease
    - as maintenance, most patients require a 500 ml phlebotomy every 2-4 months
    - patients are encouraged to keep hydrated and avoid strenuous exercise 24 hours after phlebotomy to prevent hypovolemia
  2. For patients who are poor candidates for phlebotomy - for example patients with moderate to severe anemia, symptomatic hypovolemia, or aceruloplasminemia - chelating agents can help decrease iron blood levels
    -ex: Deferoxamine mesylate (Desferal), Deferasirox (Jadenu, Exjade, Jadenu Sprinkle), Deferiprone (Ferriprox)
  3. Erythrocytaphereis can remove larger quantities of iron than phlebotomy, but the procedure is associated with higher cost and technician time consumption
  4. Moderate consumption of iron-containing foods is allowed for patients who undergo phlebotomy, although dietary and nutritional supplements with iron and vitamin C should be avoided
    - fresh fruits and veggies are encouraged, except citrus fruits and juices
  5. Alcohol consumption should be limited because ethanol can increase iron absorption, and some red wines have high iron content
    - patients who consume large quantities of alcohol are more likely to develop hepatocellular carcinoma and cirrhosis
  6. Bacteria commonly found in seafood, including listeria monocytogenes, yersinia enterocolitica, and vibrio vulnificus thrive in a high-iron environment
    • patients with the disorder should avoid uncooked seafood to prevent bacterial infection
556
Q

What is Alpha-1 antitrypsin deficiency (AAT)

A
  1. An autosomal-recessive inherited disorder that can result in lung and liver disease
  2. In the US approximately 80,000 -100,000 people have severe AAT deficiency
  3. The disorder is thought to be as common as cystic fibrosis but is still under-recognized despite the availability of extensive educational evidence-based practice
557
Q

What are risk factors for developing Alpha-1 antitrypsin (AAT) deficiency

A
  1. The result of an inherited genetic mutation in the SERPINA 1 gene
  2. The most common phenotype is PIMM, which is associated with normal circulating levels of AAT
  3. The homozygous PiZZ phenotype, and most likely the heterozygous PiMZ phenotype play an important role in the development if this disease
558
Q

What are symptoms of Alpha-1 antitrypsin deficiency (AAT)

A
  1. Associated with pulmonary symptoms such as early emphysema
  2. Hepatic disorders such as cirrhosis
  3. Skin diseases such as panniculitis
  4. In the liver, pathological polymerization of AAT is thought to be the cause of AAT accumulation in the hepatocytes, which causes liver injury
559
Q

How is Alpha-1 antitrypsin deficiency (AAT) diagnosed

A
  1. Severe AAT deficiency is diagnosed by AAT serum level < 11mmol/L and phenotyping
  2. Isoelectric focusing, a phenotype test, is the gold standard for identifying AAT variants
560
Q

What are potential complications of Alpha-1 antitrypsin deficiency (AAT)

A

Long term outcomes vary
Affected patient May develop cirrhosis

561
Q

What is the treatment for Alpha-1 antitrypsin deficiency (AAT)

A
  1. Medical therapies and supportive care for specific symptoms
  2. For patients with lung problems, augmentation therapy helps in preventing lung disease progression
    • augmentation therapy is an intravenous AAT replacement that increases AAT protein blood level
  3. In the US there are five available alpha-1-proteinase inhibitors (human) for augmentation therapy
    • Prolastin-C, Aralast NP, Zemaira and Glassia
  4. Liver transplantation may be performed if liver failure develops
562
Q

What is Intrahepatic biliary dysplasia (IHBD)

A
  1. Also known as Alagille syndrome
  2. Incorporates a combination of anomalies that occur in conjunction which chronic cholestasis
  3. Is a unique, autosomal-dominant liver disease that occurs in approximately 1 in 70,000 live births
563
Q

What are symptoms of Intrahepatic biliary dysplasia

A
  1. Patients with IHBD display characteristic
    • facial features
    • vertebral malformations
    • delayed physical, mental, and sexual development
    • and various cardiac anomalies, most often peripheral pulmonic stenosis
  2. Liver changes are progressive
    • with a decrease in the number of portal zones
    • followed by bile plugging of small interlobular bile ducts
    • hepatocytes and small canaliculi
    • then leading to absence or decrease in portal bile ducts and collapsed portal bile ducts
  3. Infants and children with IHBD frequently have cholestatic jaundice in the neonatal period, often accompanied by failure to thrive, prematurity, or small size for gestational age
    • the liver is enlarged and firm or hard on palpation
    • Most infants and children with IHBD are more affected by their cardiac abnormalities than by their liver disease
564
Q

How is intrahepatic biliary dysplasia diagnosed

A
  1. Detailed history
  2. Liver biopsy
  3. Liver function tests
  4. Eye examination
  5. X-ray
  6. Abdominal ultrasound

The diagnosis is confirmed by genetic testing

565
Q

What are potential complications of intrahepatic biliary dysplasia

A
  1. The overall life expectancy for children with IHBD is unknown but depends on several factors including:
    • the severity of scarring in the liver
    • whether heart or lung problems develop
    • the patient’s nutritional status
  2. Adults with IHBD lead normal lives
566
Q

What is the treatment for intrahepatic biliary dysplasia

A
  1. Symptomatic and supportive care
    - including good nutrition and fat-soluble vitamin supplementation
    - Cholestyramine and phenobarbital may be given to relieve pruritus as a result of cholestasis
  2. Liver transplantation is considered when cirrhosis and liver failure develop
567
Q

What is biliary atresia

A

A bile duct disorder that results in rapid and progressive scarring, leading to obstruction of the flow of bile though the extrahepatic bile duct system
The overall incidence is low, about 1 in 10,000 live births

568
Q

What are symptoms of biliary atresia

A

Biliary atresia is suspected when the infants jaundice persists for >3 weeks after birth

569
Q

How is biliary atresia diagnosed

A
  1. Blood tests to measure bilirubin and liver function
  2. Ultrasound
  3. Hepatobiliary scan
  4. Liver biopsy
570
Q

What are potential complications of biliary atresia

A

Infants with biliary atresia have the inability to digest and absorb nutrition
This leads to poor growth and vitamin (A,D,E and K) deficiencies

571
Q

What is the treatment for biliary atresia

A
  1. No procedure has yet been developed to correct biliary atresia, except for liver transplantation
  2. Upon diagnosis the Kasai procedure (hepatoportoenterostomy (HPE)) is performed
  3. HPE creates a roux-en-Y loop, using a length of the infant’s small intestine, which is then anastomosed to the hilum of the liver, creating a duct into the distal bowel and restoring bile flow
  4. The goal of the Kasai procedure is to allow excretion of bile from the liver into the intestine
  5. However, some patients have poor response to the procedure because of obstructed intrahepatic and extrahepatic bile ducts
  6. The Kasai procedure is often not effective in restoring bile flow for infants over 2 months of age, so early diagnosis is critical
  7. Unfortunately; despite bile flow, the Kasai procedure is not a cure for biliary atresia
    - liver damage often continues leading to cirrhosis and the need for transplantation
    Biliary atresia is the most common indication for liver transplantation in young children
572
Q

What is neonatal hepatitis

A

Inflammation of the liver that occurs only in early infancy, usually between 1 and 2 months of age

573
Q

What are risk factors of developing neonatal hepatitis

A
  1. Some infants with neonatal hepatitis were infected by a virus that caused the inflammation before or shortly after birth
  2. While the remaining infants have no identifiable virus
  3. These viruses include cytomegalovirus (CMV), rubella, and hepatitis A, B, or C
574
Q

What are potential complications of neonatal hepatitis

A
  1. Caused by rubella or CMV may lead to cirrhosis and may be accompanied by mental retardation
  2. Caused by Hepatitis A usually resolves within 6 months
  3. Cases that are the result of the hepatitis B or C viruses will most likely result in chronic liver disease
575
Q

What is the treatment for neonatal hepatitis

A
  1. There is no specific treatment for neonatal hepatitis
  2. Attention to healthy nutrition and growth and development is essential to the long-term prognosis
  3. Infants who develop cirrhosis may require liver transplantation
576
Q

What is Gilbert syndrome

A
  1. A relatively common and benign congenital disorder
  2. It is estimated that from 3-7% of Americans have Gilbert syndrome
577
Q

What are the risk factors of developing Gilbert syndrome

A

The disorder occurs more frequently in males and is probably hereditary

578
Q

What are symptoms of Gilbert syndrome

A
  1. Characterized by a mild, fluctuating increase in serum bilirubin
  2. There are rarely significant symptoms but occasionally jaundice may occur
  3. Except for elevated serum bilirubin, liver test and cholangiography are normal
579
Q

How is Gilbert syndrome diagnosed

A
  1. By documenting the persistence of an increased serum bilirubin when other liver function tests are repeatedly normal
  2. A liver biopsy may occasionally be necessary to rule out other liver disease
580
Q

What is the treatment for Gilbert Syndrome

A

There is no treatment necessary for Gilbert syndrome and it will not interfere with a normal lifestyle

581
Q

What is the MELD score for liver transplantation and how is it calculated

A
  1. Model for End-stage Liver Disease; in 2016 it was updated to the MELDS-Na score
    The following information is needed:
    Plasma bilirubin (mg/dL)
    INR
    Plasma creatinine (mg/dL)
    Serum sodium
582
Q

What is the PELD score for liver transplantation and how is it calculated

A
  1. Pediatric End Stage Liver Disease - for liver transplant candidates under 12 years

Age at listing
Serum albumin (g/dL)
Total bilirubin (mg/dL)
INR
Growth failure (based on gender, height and weight)

583
Q

Do you want a higher or lower MELD or PELD score

A

The higher the score the higher the mortality rate
UNOs prioritizes patients with higher scores

584
Q

What is Cholelithiasis

A
  1. The presence of stones or calculi in the gallbladder
  2. Commonly referred to as gallstones
  3. Most common disease affecting the biliary system
585
Q

What are the different types of gallstones

A
  1. Cholesterol stones
  2. Pigment stones
586
Q

What are cholesterol stones

A
  1. Include both pure cholesterol stones and mixed stones
  2. These make up about 80% of all gallstones
  3. Usually yellow-green in color and are made primarily of hardened cholesterol, although they also contain calcium salts, bile acids, fatty acids, protein and phospholipids
  4. Associated with either the hepatic production of bile that is supersaturated with cholesterol or reduced bile-salt secretion
  5. When cholesterol is no longer soluble in this supersaturated system, it forms crystal nucleates that grow and cluster with each other and with other bile constituents to firm recognizable stones in the gallbladder
587
Q

What are pigment stones

A
  1. Less common than cholesterol stones
  2. They include black pigment stones made up of bilirubin polymers and inorganic calcium salts
  3. Brown pigment stones composed principally of calcium bilirubinate and organic fatty-acid salts of calcium
588
Q

When do gallstones cause a problem

A
  1. Gallstones move around in the gallbladder as it empties and refills, if they remain in one place they may be asymptomatic
  2. Stones that move to the neck, cystic duct, or common duct may obstruct these passages, resulting in mucosal irritation and subsequent bacterial invasion
  3. Stones also may pass through the biliary ducts causing pain, or they may obstruct the flow of bile if they become lodged there
  4. It is possible for small stones to be located in any part of the biliary system without causing distress or to pass into the duodenum and be discharged in the stool
  5. Gallstones can be as small as a grain of sand or as large as a golf ball
589
Q

What are the risk factors of developing cholesterol gallstones

A
  1. Being over 60 years of age
  2. Being female
  3. Pregnancy or use of oral contraceptives
  4. Hormone therapy
  5. Being of Mexican American , Native American, or European decent
  6. Ileal disease (Crohn’s disease), resection or bypass
  7. Certain forms of hyperlipidemia
  8. Obesity
  9. Rapid weight loss, weight reduction diets, or bariatric surgery
  10. Increased blood triglycerides
  11. Gallbladder stasis
  12. Spinal cord injury
  13. Diabetes, hemolytic anemia, or sickle cell disease
  14. Fasting
590
Q

What are risk factors for developing pigment stones

A
  1. Increasing age
  2. Chronic hemolysis, such as sickle cell disease or thalassemia
  3. Alcoholism or alcoholic cirrhosis
  4. Biliary infection, usually Escherichia coli (E. Coli) or parasitic infestation such as Clonorchis sine sis or Ascaris lumbricoides
  5. Total parental nutrition (TPN)
  6. Vagotomy
  7. Periampullary diverticula
  8. Gallbladder stasis

The prevalence of pigment stones is not influenced by gender

591
Q

What are symptoms of gallstones

A

Gallstones are asymptomatic in at least 50% of patients

In symptomatic patients, the severity, extent and nature of symptoms vary considerably

  1. Steady pain, often stems from gallbladder distention or spasms of the spincter of Oddi or ductal muscles
    - also known as biliary colic
    - usually occurs 3-6 hours after the heaviest meals of the day frequently during early hours of the night
    - radiates toward other parts of the abdomen or back and sometimes to the scapula, the middle of the back or tip of the right shoulder
  2. Nausea and vomiting may occur and pain relieved by vomiting
  3. Vague symptoms of upper abdominal discomfort
  4. Increased eructation (belching) and dyspepsia
  5. Some also have fevers, chills , result from a common duct stone, acute Cholecystitis or associated pancreatitis
  6. In children mild to moderate jaundice is a common symptom
  7. Because the diagnosis of Cholelithiasis is seldom considered in children the delay between onset and diagnosis is 1 to 5 years
592
Q

How are gallstones diagnosed

A
  1. Ultrasonography is the most effective diagnostic technique
    - can diagnose stones as small as 2mm
  2. CT scan
  3. MRC - magnetic resonance cholangiogram
  4. MRCP - magnetic resonance cholangiopancreatography
  5. Cholescintigraphy (hepatobiliary (HIDA) scan)
  6. Transabdominal or endoscopic ultrasonography
  7. Blood tests (liver and pancreas enzymes)
  8. Oral cholecystogram (OCG)
  9. ERCP - endoscopic retrograde cholangiopancreatography
  10. Examination of duodenal bile for cholesterol crystals or bilirubinate granules
593
Q

What are potential complications of gallstones (Cholelithiasis)

A
  1. Cholcystitis 12. 2-10% of cholecystectomy patients experience postcholecystecomy syndrome
  2. Cholangitis
  3. Abscess or fistula formation
  4. Perforation of the gallbladder
  5. Gangrene
  6. Pancreatitis
  7. Sepsis
  8. Jaundice
  9. Liver disease
  10. Hepatic damage
  11. Has also been linked to gallbladder cancer
594
Q

What is post-cholecystectomy syndrome

A
  1. Abdominal pain or dyspepsia in patients who have had a cholecystectomy
  2. Pain cannot be attributed to the surgical procedure
  3. Most common in women between 40-49
  4. Causes: residual biliary tract disease, nonbiliary digestive disease, nonspecific digestion dysfunction, psychiatric disorders
  5. Treatment is determined by specific diagnosis
  6. Retained common bile duct stones are not uncommon following cholecystectomy
    • may be removed by endoscopic introduction of a basket or balloon into the CBD by a second surgical procedure or through non operative manipulation of a basket inserted through a T-tube
595
Q

What is the treatment for Cholelithiasis (Gallstones)

A
  1. Noninterventional “expectant” management is preferred for asymptomatic patients because neither medical dissolution therapy nor elective cholecystectomy is warranted in such cases
  2. Management of patients with minor symptoms include: pain relief and dietary control to reduce fat intake
    - small frequent meals can sometimes help to prevent future attacks
  3. In children, cholecystectomy is probably indicated, regardless of the severity of symptoms
  4. Surgery is the treatment of choice for most symptomatic patients - cholecystectomy
    • prognosis is generally good but may vary depending on the patient’s age, sex and the presence of complicating conditions
  5. Other techniques used for the dissolution or removal of cholesterol stones including:
    - oral dissolution therapy
    - contact dissolution therapy
    - extracorporeal shock-wave lithotripsy (ESWL)
    - disadvantages of these therapies is the recurrence of gallstones after ending therapy
  6. No medial intervention options exist for pigment stones; surgery is the only option
596
Q

What is oral dissolution therapy used for in the treatment of gallstones

A
  1. Drugs made from bile acid that are used to dissolve cholesterol stones
  2. Ursodeoxycholic acid (Ursodiol) and Chenodeoxycholic acid (Chenodiol) work best for small cholesterol stones
  3. Recurrence rate of stone formation is high; so oral dissolution therapy is usually reserved for patients that cannot tolerate surgery
597
Q

What is contact dissolution therapy used in treatment for Cholelithiasis (gallstones)

A

This treatment consists of a continuous infusion of methyl tert-butyl ether into the gallbladder to dissolve stones

598
Q

What is Extracorporeal shock-wave lithotripsy (ESWL) used in treatment for Cholelithiasis (gallstones)

A
  1. Biliary lithotripsy, which involves fragmentation of gallstones by use of extracorporeal acoustic shock waves,
  2. It is often combined with dissolution therapy
  3. The treatment method can be done on an outpatient basis
  4. Patients have less pain, a shorter recovery period and less chance of infection than those who have cholecystectomies
599
Q

What is choledocholithiasis

A
  1. Presence of stones in the common hepatic duct or intrahepatic ductal system or common bile duct
  2. The obstruction of flow of bile into the duodenum
600
Q

What causes choledocholithiasis

A
  1. Stone formation in the CBD can still happen after the gallbladder is removed
    - a few people form stones in the CBD - primary stones (always pigment stones)
  2. Pigment stones can also be secondary stones, meaning they were formed in the gallbladder and traveled to the CBD
  3. Cholesterol stones found in the duct are always secondary stones
  4. About 40% of all CBD stones are pigment stones
601
Q

What are signs and symptoms of choledocholithiasis

A

Patients may have no symptoms or may present with a combination of the following:
1. Biliary colic, with constant epigastric or right upper quadrant pain or tenderness
2. Obstructive jaundice and pruritus
3. Cholangitis, with fevers, chills and jaundice (known as Charcot’s triad)
4. Loss of appetite, nausea, and vomiting
5. Acute gallstone pancreatitis, manifested by severe abdominal pain that radiates into the back

602
Q

How is choledocholithiasis diagnosed

A

Differential diagnosis may require:
1. Lab tests (bilirubin, complete blood count, pancreatic enzymes, liver enzymes)
2. Ultrasonography
3. Abdominal CT scan
4. Radioisotope imaging
5. OCG
6. ERCP
7. MRCP
8. Percutaneous transhepatic cholangiography (PTC)
9. Endoscopic ultrasound (EUS)
10. MRC, which although highly specific to identifying choledocholithiasis, lack therapeutic options

603
Q

What are complications of choledocholithiasis

A
  1. Cholangitis
  2. Cirrhosis with hepatic failure
  3. Portal hypertension
  4. Hepatic abscess formation
  5. Gallstone pancreatitis
604
Q

What is the treatment for choledocholithiasis

A
  1. NPO
  2. IV hydration and electrolyte replacement
  3. Analgesia should be provided
  4. NG tube suction may be used
  5. Antibiotics may be prescribed if there is evidence of sepsis or cholangitis
  6. Therapeutic ERCP is the preferred method of treatment
    • A sphincterotomy at the sphincter of Oddi and stone removal can be done
    • large stones can be broken up using mechanical, electro hydraulic or laser lithotripsy before removal
  7. The CBD may be explored surgically through a choledochotomy
605
Q

What is Cholecystitis

A
  1. Acute or chronic inflammation that causes painful distention of the gallbladder
  2. Of patients that require surgery for gallbladder disease 10-20% have Cholecystitis
  3. In the pediatric population it is most often chronic and associated with gallstones
  4. In 25-30% of children, jaundice and fever are seen and are more common in young infants
  5. Can occur without evidence or presence of gallstones
    • rare in adults but can occur frequently in children
    • the cause is unknown but has been associated with immediate postoperative states, trauma or burns
    • usually presents with fever, abdominal pain and jaundice
    • a lap chole is the surgical treatment of choice for Cholecystitis
606
Q

What is acute calculous Cholecystitis

A
  1. More than 90% of the time Cholecystitis is associated with a gallstone that is impacted in the cystic duct
  2. The obstructed gallbladder becomes distended, and the walls become edematous, ischemic and inflamed
  3. Secondary infections with enteric organisms may compound inflammation, leading to cholangitis and sepsis
607
Q

What are risk factors to developing acute calculous Cholecystitis

A

Predisposing factors include:
1. Older age
2. Ethnicity (especially persons of Italian, Jewish or Chinese descent)
3. Obesity
4. A sedentary lifestyle
5. Pregnancy
6. Hemolytic anemias
7. Insulin-dependent diabetes mellitus

608
Q

What are signs and symptoms of Acute Calculous Cholecystitis

A

Similar to those of Cholelithiasis:
1. Acute abdominal pain, usually mid epigastric or localized to the right upper quadrant, with radiation to the shoulders and back
2. Nausea, vomiting and anorexia
3. Fever, headache, and leukocytosis
4. Tachycardia and tachypnea
5. Tenderness, guarding, and rebound tenderness in the right upper quadrant
6. Intolerance of fatty foods and heavy meals

609
Q

How is Acute Calculous Cholecystitis diagnosed

A

To confirm the diagnosis, the physician may order blood tests, ultrasonography, and radioisotope imaging

610
Q

What are potential complications of Acute Calculous Cholecystitis

A
  1. Perforation with subsequent peritonitis
  2. Cholecystenteric fistula
  3. Gallstone ileus - a form of intermittent or permanent intestinal obstruction caused the impaction of a large gallstone that has entered the intestine through a Cholecystenteric fistula
    - most often found in the ileum because of the relatively small diameter compared to the rest of the intestine
    - gallstone ileus requires an emergency laparotomy
611
Q

What is the treatment for Acute Calculous Cholecystitis

A
  1. NG suctioning
  2. IV fluid and electrolyte replacement
  3. Analgesia
  4. Antibiotics should be given in cases of severe illness, sepsis, or complications
  5. Early cholecystectomy is the preferred treatment approach

If cholecystectomy is contraindicated than an operative or Percutaneous cholecystostomy may be performed
- the gallbladder is evacuated of stones and infected bile, and a catheter drains outside the body

Temporary or short-term biliary decompression can also be accomplished using ERCP to place a Nasobiliary catheter(NBC) or internal stent above the impacted stone

612
Q

What is Acalculous Cholecystitis

A

Cholecystitis in the absence of stones

Relatively rare

613
Q

What are risk factors to developing Acalculous Cholecystitis

A

Usually occurs in otherwise severely ill, hospitalized patients; conditions include:
1. Intercurrent illnesses such as: bacterial enteric infections
2. Parasitic infections
3. Hospitalization
4. Mechanical ventilation with positive end-expiratory pressure (PEEP)

614
Q

What intercurrent illness are risk factors to developing Acalculous Cholecystitis

A

Bacterial enteric infections
1. Typhoid fever
2. Shigellosis
3. E. Col infection
4. Viral gastroenteritis
5. Scarlet fever
6. Respiratory infections
7. Pneumonia
8. Human immunodeficiency virus (HIV) infection
9. Hepatitis A infection

615
Q

What parasitic infestations are risk factors to developing Acalculous Cholecystitis

A

Giardia or Ascaris found in the gallbladders of some patients

616
Q

What are hospitalizations reasons that are risk factors for developing Acalculous Cholecystitis

A

Burns
Trauma
Major surgery

617
Q

Why is mechanical ventilation with positive end-expiratory pressure (PEEP) a risk factor for developing acalculous Cholecystitis

A

Most patients requiring PEEP have been receiving TPN for longer than 3 months
The pathogenesis of Cholecystitis may result from the absence of oral intake associated with gallbladder stasis, sludge formation, and increased biliary pressure caused by narcotic drugs that increase the tone at the sphincter of Oddi

618
Q

What are symptoms of Acalculous Cholecystitis

A
  1. An acute onset of abdominal pain on the right side
  2. Abdominal tenderness and guarding
  3. Vomiting and nausea
619
Q

How is Acalculous Cholecystitis diagnosed

A
  1. Abdominal CT scan or abdominal ultrasonography
  2. Laboratory blood tests (CBC, liver function test)
  3. Blood cultures should be performed
620
Q

What are potential complications of Acalculous Cholecystitis

A

The incidence of gangrene, necrosis and perforation is high
Mortality may be as high as 50%

621
Q

What is the treatment for Acalculous Cholecystitis

A

Urgent cholecystectomy or cholecystostomy
Patients should also be treated with antibiotics to cover enteric organisms and enterococcus and other supportive measures should be taken as needed
High-risk surgical patients may receive an endoscopic gallbladder stent placement as a palliative treatment until a cholecystectomy can be performed

622
Q

What is emphysematous Cholecystitis

A

The gallbladder walls and bile ducts contain gas that has been produced by infective organisms
- such as E. Coli, Clostridium and other anaerobes

623
Q

What are risk factors to developing emphysematous Cholecystitis

A

Males older than 60 years of age with a history of type II diabetes mellitus

624
Q

What are symptoms of emphysematous Cholecystitis

A

Fever and right upper quadrant pain that often radiates to the back

625
Q

What are potential complications of emphysematous Cholecystitis

A

Gallbladder gangrene and perforation

626
Q

What is the treatment for emphysematous Cholecystitis

A

Acute cholecystectomy

627
Q

What is cholangitis

A

An uncommon bacterial infection of the bile duct that is often associated with choledocholithiasis or with obstruction of the hepatic or common bile duct by strictures, cysts, fistulas, neoplasm or parasites

Equally seen in females and males who are age 50 or older

Widespread inflammation may cause fibrosis and stenosis of the common bile duct

628
Q

What are risk factors to developing cholangitis

A

An impacted stone in the biliary system, resulting in bile stasis
1. Obstructive tumors, including pancreatic cancer, cholangiocarcinoma, ampullary cancer, and porta hepatis tumors or metastasis
2. Parasitic infections, including Ascaris lumbricoides infections
3. Benign or malignant strictures or stenosis
4. Endoscopic manipulation of the CBD
5. Choledochocele
6. Extrinsic compression by the pancreas
7. Sclerosing cholangitis (from biliary sclerosis)
8. AIDS colangiopathy
9. Choledocholithiasis, ERCP

629
Q

What are symptoms of cholangitis

A

A transient, self-limited illness that is characterized by a fever spike, chills, dark urine, and abdominal pain

630
Q

What are potential complications of cholangitis

A

In some patients the illness is devastating, consistent with profound toxic sepsis with shock and impaired mental function

The prognosis for these patients is poor

631
Q

What is the treatment for cholangitis

A
  1. A medical and surgical emergency
  2. Stabilized with IV hydration and antibiotics
  3. Which should be followed by prompt surgical or endoscopic decompression of the CBD
  4. If the CBD is explored to remove retained stones, a T-tube is inserted to provide a means of decompressing the biliary ducts
  5. The tube can be removed 3 weeks after surgery
  6. Retained stones can be removed by inserting a basket through the T-tube or by endoscopically introducing a basket or balloon for extraction
  7. Large stones that are difficult to remove may be fragmented by a mechanical lithotripter basket and the fragments pulled out by a balloon
632
Q

What is Primary Sclerosing Cholangitis (PSC)

A

An inflammatory process that results in multiple strictures of the bile ducts, causing a chronic cholestatic liver disease

633
Q

What are risk factors to developing primary sclerosing cholangiits

A
  1. The etiology is unknown
  2. 75-90% of patients with PSC have inflammatory bowel disease, Crohn’s disease or ulcerative colitis
    - but only 5% of patients with IBD develop PSC
  3. Has no correlation with UC exacerbations or remissions
  4. Men are affected twice as often as women, and the average age of diagnosis is 40
634
Q

What are symptoms of Primary Sclerosing Cholangitis

A
  1. Progressive fatigue
  2. Jaundice
  3. Pruritus
  4. Abdominal pain
  5. Elevated serum alkaline phosphatase
635
Q

How is primary sclerosing cholangitis diagnosed

A
  1. ERCP - may show strictured areas in the intrahepatic and extrahepatic ducts, with areas of dilatation between the strictures, giving a beaded appearance to the ducts
  2. PTC
  3. MRCP
  4. Liver biopsy
636
Q

What are potential complications of primary sclerosing cholangitis

A

In patients requiring liver transplantation for advanced stages of PCS
- progression to cirrhosis and portal hypertension is expected and death occurs from liver failure

637
Q

What is the treatment for primary sclerosing cholangitis

A
  1. Subclinical PSC requires no treatment
  2. If pruritus occurs, it can be treated with bile-salt binding agents such as Cholestyramine
  3. To bypass tight strictures, surgery or endoscopic balloon dilatation and/or placement of biliary stents may be required
  4. Liver transplant may be the only viable treatment in the advanced stages of the disease and is the third most common reason for transplant in the US
  5. Patients with PCS may require more than one liver transplant
638
Q

What is cholangiocarcinoma

A

Cancer of the biliary system
It may involve the gallbladder or less often the bile ducts

639
Q

What is gallbladder cancer

A
  1. Accounts for approximately 3% of all cancers
  2. 80% of gallbladder cancers are adenocarcinomas
  3. The remaining are squamous cell carcinomas, adenocanthomas and others
  4. Benign tumors are rare
  5. Most patients have evidence of local or metastatic spread, often through lymph nodes, at the time of diagnosis
640
Q

What are risk factors to developing gallbladder cancer

A
  1. Occurs more frequently in women than men
  2. The incidence peaks at age 70 years
  3. Approximately 80% of patients with gallbladder cancer also have gallstones
641
Q

What are symptoms of gallbladder cancer

A

Usually present with vague abdominal symptoms
1. Nausea and vomiting
2. Substantial weight loss
3. Anorexia
4. Fat intolerance
5. Jaundice
6. Right upper quadrant pain
7. If palpable a RUQ mass can be felt
8. The lesion is almost always incurable

642
Q

How is gallbladder cancer diagnosed

A
  1. Abdominal ultrasound
  2. Carcinoembryonic antigen (CEA) assay
  3. CT scan
  4. Cholecystogram
  5. Cholangiogram
  6. PTC
  7. EUS
  8. ERCP
  9. Possibly MRI
  10. Rarely diagnosed preoperatively because signs and symptoms are similar to those for cancer of the liver, cancer of the pancreas, and obstructive Cholelithiasis
643
Q

What are potential complications of gallbladder cancer

A

Resection, radiotherapy and chemotherapy seem to do nothing to prolong survival

644
Q

What is the treatment for gallbladder cancer

A
  1. Medical treatment should be supportive and symptomatic, with the goals of comfort and short-term rehabilitation
  2. If surgery is performed the average postoperative survival time is only 8 months
  3. Cholecystectomy is indicated only for patients with small, localized tumors
  4. If the lesion is inoperable, an internal bile drainage system may be inserted to permit flow of bile directly from the liver into the intestine
    - the objective is to relieve symptoms and prolong the quality and length of life
  5. To minimize malnutrition and dehydration, the patients may be given antiemetics or small sips of carbonated beverages to control nausea
  6. Vitamin and mineral replacements
  7. Small frequent meals; small amount of pain medications before meals
  8. If necessary tube feeding
  9. In the terminal stages of the disease, skin care, pain relief, and emotional support are of vital importance
645
Q

What is bile duct cancer

A

1.Cancer of the extrahepatic biliary tree
2. Adenocarcinoma is the most common form of extrahepatic bile duct cancer
3. Benign neoplasms are relatively rare

646
Q

What are risk factors to developing bile duct cancer

A
  1. Associated with gallstones in only 30% of patients
  2. May also be associated with longstanding UC, Crohn’s disease, PSC and/or congenital dilatation of the bile ducts
647
Q

What are symptoms of bile duct cancer

A
  1. Patients present with painless obstructive jaundice
  2. A serious symptom that represents a probable clinical presentation of bile duct carcinoma
  3. Later, pruritus, nausea, vomiting, weight loss, and intermittent or steady RUQ pain may develop
  4. Serum alkaline phosphatase is always elevated
648
Q

How is bile duct cancer diagnosed

A

Most often diagnosed during a laparotomy for other biliary tract disease

  1. Ultrasonography (endoscopic or laparoscopic)
  2. MRI
  3. MRCP
  4. Magnetic resonance angiography (MRA)
  5. Cholangiography
  6. Positron emission tomography (PET) scan
  7. CT scan - may be used to visualize dilated intrahepatic bile ducts
  8. PTC or ERCP are used preoperatively to define the level and cause of the obstruction
649
Q

What are potential complications of bile duct cancer

A

Most patients have localized extension or metastatic disease at the time of diagnosis

650
Q

What is the treatment for bile duct cancer

A
  1. Common surgical treatment may consist of removal of the duct a partial hepatectomy, the Whipple procedure, or liver transplantation
  2. Treatment options are based on the type and stage of the cancer, possible side effects the overall health of the patient, and the patients preferences
  3. Stent placement; often using permanent wall stent and surgical bypass
  4. Radiation therapy
  5. Chemotherapy
  6. Palliative and supportive care
  7. Although rare the most common pediatric neoplasm of the biliary tract is botryoid embryonal rhabdomyosarcoma
    - symptoms include pruritus, jaundice, RUQ, and epigastric abdominal pain, and sometimes a palpable mass
    -usually locally invasive; even with large surgical resection, radiation and drug therapy the prognosis is poor
651
Q

What are congenital anomalies of the gallbladder

A
  1. Agenesis, or congenital absence of the gallbladder - most likely occurs as a result of embryonic maldevelopment
  2. Anomalies of location (ectopic gallbladder) - which may occur anywhere in the abdomen and often requires cholecystectomy
  3. Anomalies of form - in which more than one cystic structure is found in the gallbladder, bilobed gallbladder, folded fundus, or Ladd’s bands across a normal gallbladder. If two organs exist and one is found to be diseased at the time of surgery; both should be removed
  4. Anomalies of fixation - occurs when the mesenteric, supporting structures of the gallbladder are elongated, thus leaving a normally functioning gallbladder to “float” below the inferior surface of the liver and occasionally into the pelvis
    - if the floating gallbladder twist, vascular occlusion, ischemic necrosis or perforation may occur, requiring cholecystectomy
652
Q

What are bile duct anomalies

A

Congenital anomalies of the hepatic and common bile duct
1. Anomalies of the extrahepatic duct configuration such as atresia, accessory ducts, abnormal lengths of ducts, variations in the junction of the cystic and hepatic ducts. Liver transplantation has greatly improved the survival rate of children with biliary atreasia
2. Cystic anomalies of the common bile duct, including cystic dilatation of the CBD (choledochal cyst) which makes up the majority of these anomalies; congenital Choledochocele; and congenital diverticulum of the CBD
- in patients with choledochal cyst, symptoms generally appear before the age of 10. Diagnosis is by ultrasound and the recommended treatment is Roux-en-Y choledochocystojejunostomy with cholecystostomy - complete excision of the cyst is recommended
3. Cystic dilatation of the intrahepatic ducts, called Caroli disease. This is a rare genetic disorder most often occurs in childhood or young adulthood. Symptoms include bile stasis, cholangitis and intrahepatic stone or abscess formation

653
Q

What is pancreatitis

A

1 An inflammatory condition of the pancreas that can result from obstruction of the pancreatic duct and from other mechanisms such as trauma, toxicity from alcohol, infections, and certain drugs

  1. It may be acute or chronic and represents a wide spectrum of severity and clinical presentations
  2. Many aspects of the pathogenesis of acute and chronic pancreatitis are poorly understood
  3. Therapy is often supportive and may be directed at a specific etiology or at morphological changes in the pancreatic duct (stricture,obstruction, disruption, stones)
654
Q

What are the different types of pancreatitis

A
  1. Acute pancreatitis
    • Necrotizing (severe) pancreatitis
    • Interstitial pancreatitis
    • Infected necrosis
  2. Chronic pancreatitis
655
Q

What are the three possible signs of acute pancreatitis

A

You only need to have two of the three to have acute pancreatitis

  1. Abdominal pain (often epigastric)
  2. Serum amylase or lipase level greater than three times the normal limit
  3. Radiologic imaging that is consistent with the diagnosis, CT scan or MRI
656
Q

What are anatomical signs of acute pancreatitis

A

A result of enzymatic digestion of the pancreatic parenchyma and peri pancreatic tissues by enzymes that are normally present in the pancreas in their inactive pro enzyme form

  1. Varying degrees of edema, necrosis hemorrhage and the release of harmful substances (cytokines) which can injure distant organs and lead to severe complications, including death
657
Q

What are risk factors and causes of acute pancreatitis

A
  1. 80% secondary to gallstones or alcohol misuse
  2. Abdominal trauma
  3. Hyperparathyroidism
  4. Hyperlipidemia
  5. Infections
  6. Certain drugs
  7. After ERCP
  8. Age, therapeutic endoscopic sphincterotomy, sphincter of Oddi dysfunction
  9. Prior history of post-ERCP pancreatitis
658
Q

What are signs and symptoms of acute pancreatitis

A
  1. Persistent severe pain in the midepigastrium, left chest, RUQ, shoulder and back
  2. Nausea and vomiting that persists for several hours
  3. Low-grade fever
  4. Abdominal swelling and tenderness
  5. Shock, hypovolemia, and hypertension
  6. Anorexia and excessive weight loss
  7. Hypocalcemia
  8. Hypoxia
  9. Very rarely, Grey’s Turner’s signs (a bluish flank discoloration) or Cullen’s sign (a bluish periumbilical discoloration) caused by blood tracking from the retroperitoneum to these sites
659
Q

How is acute pancreatitis diagnosed

A
  1. Epigastric abdominal pain
  2. Serum amylase greater than or equal to three-times the upper limit of normal
  3. Contrast CT scan demonstrates finding of acute pancreatitis
  4. MRI, MRCP
  5. Abdominal and/or endoscopic ultrasonography
  6. ERCP
660
Q

What is the treatment for acute pancreatitis

A
  1. Pain management, including:
    • rest to the pancreas
    • relief with analgesics
  2. Antibiotics are only given for severe acute pancreatitis, dilation of the CBD and an impacted stone on ultrasound
  3. GI rest by withholding of foods and fluids by mouth (NPO)
  4. Nasogastric suctioning - if there is significant vomiting
  5. Bed rest
  6. Electrolyte and fluid replacement
  7. Blood transfusions as required
  8. Insulin to control hyperglycemia or diabetes
  9. Full intensive care support, as appropriate, such as intubation and ventilation, renal dialysis, coagulation support, sedation, pressor support, and CT-guided fine needle aspiration of the pancreas if infected necrosis is suspected
  10. When the cause is gallstones -surgery (lap chole) is recommended during the same admission
  11. If there is evidence of biliary tract obstruction from stones or if the attack is severe, urgent ERCP is indicated with sphincterotomy as necessary
661
Q

What are potential complications of acute pancreatitis

A
  1. Secondary infection of pancreatic necrosis
  2. Pulmonary infections
  3. Pleural effusions
  4. Adult respiratory distress syndrome
  5. Multiple organ dysfunction syndrome (MODS)
  6. Renal failure
  7. Cardiac dysfunction
  8. “Third spacing”
  9. Coagulopathy
  10. Persistent hypotension
  11. Encephalopathy
  12. Liver failure
  13. Immunocompromise with opportunistic infections
  14. Ischemia of limbs and internal organs
  15. Malnutrition
662
Q

What is interstitial pancreatitis

A
  1. A milder form of acute pancreatitis that is characterized by pancreatic interstitial edema with intact pancreatic acini and ducts without necrosis
663
Q

What are potential complications of interstitial pancreatitis

A
  1. Mortality rate is lower than necrotizing pancreatitis
    • it however requires the same amount of intensive care when severe
  2. Large pseudocyst formation can follow
664
Q

What is necrotizing pancreatitis

A
  1. The most severe form of acute pancreatitis
  2. Diagnosed when there is >30% non enhancement of the pancreas on a contrast-enhanced CT scan
    • MRI is also useful in diagnosing severe condition
  3. The morphological findings include destruction of pancreatic tissue, blood vessels, and fat with extensive fluid accumulation in the retroperitoneum
665
Q

What is infected necrosis

A
  1. Also called an inflammatory mass
  2. This results when the collection of tissues resulting from necrotizing pancreatitis becomes infected
  3. Infected necrosis usually occurs 2-4 weeks during the course of necrotizing pancreatitis
  4. Stable patients are treated with antibiotics and maximum supportive care
  5. Surgical debridement is only considered for patients who are persistently ill or who have organ failure
  6. Develops in 30-70% of patients with acute necrotizing pancreatitis
  7. Accounts for more than 80% of deaths from acute pancreatitis
  8. Prevention of infection is critical
  9. Overall mortality rate is about 30%
666
Q

What are pseudocysts and organized necrosis

A
  1. Massive necrosis frequently leads to the formation of large pancreatic and peripancreatic collections of fluid, blood and necrotic debris, which are initially diffuse
  2. If the fluid collection persists beyond 4 weeks after the attack and becomes walled off by adjacent anatomical structures, it is called a pseudocyst
  3. If this contains significant debris, it is termed organized necrosis
667
Q

What are potential complications of acute pancreatitis that can occur more than 30 days after the initial attack

A

They are mostly in or around the pancreas and include:
1. Pseudocyst
2. Organized necrosis
3. Abscess
4. Pancreatic fistula
5. Duodenal and bile duct stricture

668
Q

What is chronic pancreatitis

A
  1. The persistent inflammation of chronic pancreatitis produces irreversible morphological changes by fibrosis and atrophy in the pancreas, resulting in endocrine and exocrine functional loss
  2. At least 90% of exocrine function must be lost before significant malabsorption is noticed and diabetes develops late in disease
669
Q

What are causes and risk factors of chronic pancreatitis

A
  1. Approximately 50 to 55% (75%) is associated with long-term, heavy alcohol use
  2. Worldwide it may also be the result of protein calorie malnutrition, cystic fibrosis, obstruction of the pancreatic duct by tumor, tropical pancreatitis, and familial pancreatitis
  3. Chronic pancreatitis is generally found in males who are between the ages of 40 and 50 years
  4. Hereditary pancreatitis, although rare, presents at a median age of 5 to 19 years
  5. Chronic obstructive pancreatitis can be caused by tumor, post-traumatic stricture, pancreatic calculi, tropical pancreatitis, and possibly by pancreas divisum
670
Q

What are the defining chronic characteristics of pancreatitis

A
  1. Strictures
  2. Clubbing
  3. Inadequate drainage
  4. Possible diminished cellular function
671
Q

What are signs and symptoms of chronic pancreatitis

A
  1. Epigastric subcostal or umbilical pain radiating to the back
    • predominant symptom
    • food intensifies pain
  2. Weight loss and malabsorption
  3. Steatorrhea
  4. Diabetes
  5. Obstructive jaundice from bile duct stricture
  6. Epigastric mass
672
Q

How do you diagnose chronic pancreatitis

A
  1. Family history
  2. Tests:
    • ERCP - ductal defect noted - identification of the extent of the disease, anatomy and presence of potentially correctable lesions.
    • MRCP
    • EUS or ultrasound - may be the most sensitive test for detecting early stages of chronic pancreatitis
    • CT scan
    • MRI
    • Secretin test
    • Pancreatography
673
Q

What is the treatment for chronic pancreatitis

A
  1. Non-surgical
  2. Abstinence from alcohol
  3. Acute and chronic pain relief
  4. Nutritional support
  5. Oral replacement of pancreatic enzymes when steatorrhea is detected
  6. Endoscopic intervention may reduce or eliminate the need for surgery
  7. Surgical intervention may be necessary in situations where symptoms such as pain and/or recurrent attacks of pancreatitis are uncontrolled
  8. Celiac plexus block to relieve chronic pain can be achieved percutaneously or by EUS
  9. Many chronic pancreatitis patients who are in permanent pain require the support of pain services and mental health professional
674
Q

What is pancreatitis in children

A
  1. Acute inflammation of the pancreas
  2. Chronic pancreatitis is rare in children
675
Q

What causes acute pancreatitis in children

A
  1. Biliary medication
  2. Systemic disease and trauma
  3. Congenital or acquired obstruction
  4. Drugs or toxins
  5. Metabolic or systemic disorders
  6. Infectious agents
  7. Hereditary or idiopathic conditions
  8. Hypercalcemia
  9. Biliary disorders
  10. An idiopathic cause
676
Q

What are known causes for acute pancreatitis in children

A
  1. Trauma to the pancreas, such as from motor vehicle accidents, sport injuries, falls and child abuse
  2. Drugs such as prednisone
  3. Viral infections - systemic disease such as sepsis, shock, and systemic lupus
677
Q

What are signs and symptoms of acute pancreatitis in children

A
  1. Severe abdominal pain
  2. Nausea and/or vomiting
  3. Fever
  4. Jaundice
  5. Ascites
  6. Pleural effusion
  7. A mild presentation may be confused with gastritis, where as a severe case may present as a small bowel obstruction
  8. Mid epigastric tenderness and/or pain with a sudden onset, increasing gradually and changing in severity
678
Q

How is pancreatitis in children diagnosed

A
  1. Serum and urine amylase and lipase
  2. Abdominal sonography
  3. CT scan
  4. ERCP for recurrent episodes to assess for congenital anomalies
  5. Ultrasound
679
Q

What is the treatment for pancreatitis in children

A
  1. Individualized based on symptomatology and severity of disease
680
Q

What is a potential complication of chronic pancreatitis

A

Addition to narcotics due to chronic pain

681
Q

What are types of pancreatic fluid collections

A
  1. Walled off pancreatic necrosis (WOPN)
  2. Pseudocyst
682
Q

What is walled-off pancreatic necrosis (WOPN)

A
  1. Previously called a pancreatic abscess
  2. Similar to a pseudocyst in that it results in injury to the pancreas
  3. In contrast, however, these are filled with solid debris and usually do not resolve on their own without endoscopic or operative intervention
683
Q

What is a pancreatic pseudocyst

A
  1. Called pseudocysts because they lack an epithelial layer typically present in “true cysts”
  2. An encapsulated sac lined by inflammatory cells and filled with fluid, pancreatic juice, inflammatory exudate, or sometimes blood
684
Q

What are the different types of pancreatic pseudocysts

A
  1. Communicating
  2. Non-communicating
  3. Directly communicates with the pancreatic duct
685
Q

What are causes and risk factors for developing pancreatic pseudocysts

A
  1. Injury to the pancreas
  2. Premalignant or malignant conditions
  3. Acute and chronic pancreatitis
    • 50% with acute
    • 20% with chronic
686
Q

What are signs and symptoms of pancreatic pseudocysts

A
  1. Most are small and asymptomatic
  2. Can be large and cause symptoms such as pain and fevers
  3. -Resistant intra-abdominal symptoms such as early satiety, nausea and vomiting, increase in cyst size and cyst-related adverse events such as biliary obstruction and infection
  4. That of acute and chronic pancreatitis
687
Q

How are pancreatic pseudocysts diagnosed

A
  1. Usually diagnosed 4 to 6 weeks after an attack of pancreatitis
  2. Abdominal ultrasound
  3. Endoscopic ultrasound
  4. CT scan
  5. ERCP
  6. MRI
688
Q

What is the treatment for pancreatic pseudocysts

A
  1. Approximately 60% resolve spontaneously
  2. Drainage
    • through ERCP, EUS or radiology
    • reserved for systemic pseudocyst, infection, or bleeding
  3. Urgent surgery is required if:
    • pseudocyst is infected
    • free pseudocyst rupture into the peritoneal cavity or chest
    • massive pseudocyst hemorrhage form a pseudoaneurysm within the cystic cavity
  4. Should be monitored carefully to make sure they don’t transform into a malignancy
  5. Fully-encapsulated fluid collections may require necrosectomy, but this is not indicated in acute fluid collections
689
Q

What is a potential complication of pancreatic pseudocysts

A

Recurrent episodes can evolve into chronic pancreatitis

690
Q

What are pancreatic fistulas

A
  1. Disruptions in the pancreatic duct with communication through the skin (external) or into other body structures (internal) such as the retroperitoneum
  2. The majority are external
691
Q

What can internal pancreatic fistulas cause

A
  1. Massive ascites
  2. Pleural effusion
  3. Pseudocysts
692
Q

What are causes and risk factors to developing pancreatic fistulas

A
  1. Trauma to the pancreatic duct
  2. External drainage of a pseudocyst
  3. Pancreatic surgery involving a ductal anastomosis
  4. Spontaneous pancreatic duct disruption as a complication of pancreatitis
693
Q

What are signs and symptoms of pancreatic fistulas

A

Clinically, external pancreatic fistulas should be suspected when clear fluid drains from the cutaneous fore-face of a high-risk patient

694
Q

How are pancreatic fistulas diagnosed

A

Confirmed when amylase content of drainage fluid is evaluated

695
Q

What is the treatment for pancreatic fistulas

A
  1. 75% close spontaneously within a few months
  2. 25% require surgery
  3. High output fistulas (greater than 200ml per day) should always be treated
  4. Medical treatment includes gut rest and octreotide (octapeptide of somatostatin) for suppression of pancreatic secretion
  5. If medical treatment fails, endoscopic therapy can be effective
  6. Surgery is reserved for complex fistulas, those with additional indications for surgery, or those not responding to less invasive treatment
696
Q

What are potential complications of pancreatic fistulas

A

Internal fistulas can cause:
1. Ascites (pancreaticoperitoneal fistula)
2. Pleural effusion (pancreaticopleural fistula)
3. Pseudocysts

697
Q

What is pancreatic cancer

A
  1. The fourth most common cancer-related cause of death in the United States
  2. The location of this small gland deep in the abdomen and its proximity to major organs and blood vessels contribute to the late diagnosis of this disease that is often with out symptoms (silent) until the disease is late stage
  3. As with all cancers, prognosis is stage-dependent. 90% of pancreatic tumors are solid malignant tumors and arise from the ductal epithelium, making exocrine tumors of the pancreas more common than those of endocrine origin
  4. 90% are adenocarcinomas
698
Q

What are causes and risk factors of pancreatic cancers

A
  1. Chronic pancreatitis
  2. Alcohol intake
  3. Diabetes
  4. Exposure to industrial carcinogens
  5. Heavy smoking
  6. High fat diet
  7. Genetic predisposition may have a role
    • may be present in up to 5% of patients diagnosed
    • a germline mutation of the p16 gene has been reported in families with pancreatic cancer and melanoma, as well as an excess of pancreatic cancer seen in families with the BRCA-2 (Breast cancer susceptibility gene-2) mutations
699
Q

What are signs and symptoms of pancreatic cancer

A
  1. May be site specific
    • Head. - Body or Tail
      • Dull mid epigastric pain. - Steady back pain or spinal pain
      • Weigh loss - Jaundice
      • Jaundice - Weight loss
      • Pruritus - Nausea and vomiting - Anorexia. - Abdominal mass
  2. Dark urine and light colored stools - occurs in 75% of cases
  3. Mental depression - occurs in 50-75% of cases
  4. Nausea, vomiting and weakness - occurs in 33% of cases
  5. Metastasis may result in liver symptoms
  6. Onset of diabetes
  7. Onset of steatorrhea
  8. Unexplained blood clots
700
Q

How is pancreatic cancer diagnosed

A
  1. ERCP
  2. Ultrasonography
  3. Radiography
  4. Nuclear scanning
  5. Angiography
  6. Tissue sampling is required for definitive diagnosis
  7. EUS to obtain fine needle aspirate to allow for tissue staging
  8. Abnormal liver enzymes
  9. Lab work - CA 19-9 tumor-associated antigen, are markers for this tumor
    • can be elevated in benign conditions, such as pancreatitis
    • a decrease in this tumor marker post surgery and chemo has been found to correlate with survival of pancreatic cancer patients
701
Q

What is the treatment for pancreatic cancer

A
  1. Curative for a very small number of patients
  2. More than 85% will require palliative and supportive care
  3. For operable cases, Whipple procedure is performed
  4. Endoscopy with stent placement to facilitate drainage
  5. Stenting of pancreatic ductal system, biliary system, and duodenum may be provided depending on tumor location
702
Q

What are pancreatic cystic tumors

A
  1. Can occur in head, body or tail; but are most commonly found in the head
  2. May contain fluid or mucous
  3. Range from benign to malignant and from very small to very large
703
Q

What are the different types of pancreatic cystic tumors

A

The dominant types
1. Serous cystadenoma
2. Cyst adenocarcinoma
3. Mucinous cystadenoma
4. Cystadenocarcinoma

Intraductal papillary mucinous neoplasm (IPMN) a variant that causes the ducts to dilate and fill with mucin
- carries a better prognosis than the more common pancreatic ductal adenocarcinoma

704
Q

How are pancreatic cystic tumors diagnosed

A
  1. May be indistinguishable from pseudocysts on CT scan, but the absence of a history of pancreatitis should raise suspicion
  2. FNA of cysts to determine pathology and cytology of the fluid content
705
Q

What is the treatment for pancreatic cystic tumors

A
  1. ERCP to allow for endoscopic drainage for symptomatic lesions
  2. Whipple procedure for cure
706
Q

What are endocrine tumors of the pancreas

A
  1. Classified on the basis of the predominant hormone they secrete
  2. Most secrete more than one hormone
707
Q

What are different types of islet cell tumors of the pancreas

A
  1. Gastrinoma islet cell tumor
  2. Insulinomas
  3. Glucagonoma
  4. Somatostatinoma
  5. VIPoma
708
Q

What are causes of a Gastrinoma islet cell tumor

A
  1. Zollinger-Ellison syndrome (ZES) - a rare Gastrinoma (or non-beta islet cell tumor of the pancreas) usually located in the pancreas and duodenum
  2. These tumors release an excess of the hormone gastrin into the circulation (hypergastrinemia)
  3. The hypergastrinemia is due to loss of the feedback inhibition of gastrin secretion, which then rises unchecked
  4. In turn this causes Atrophic gastritis and pernicious anemia, resulting in severe ulcers in the upper GI tract, predominantly in the distal duodenum and jejunum and often severe diarrhea
  5. Most frequently between the ages of 35 and 65 and is more common in men than in women
709
Q

What are the two types of gastrinoma islet cell tumors

A
  1. Sporadic - late in life and usually malignant
  2. Genetic - associated with multiple endocrine neoplasia type 1 (MEN1) syndrome and causes tumors or hyperplasia of the parathyroid, pancreatic Isley and pituitary glands
710
Q

What are signs and symptoms of Gastrinoma islet cell tumors

A
  1. Severe ulcers in distal duodenum or jejunum (PUD) related to hypersecretion of gastric acid
  2. Diarrhea and steatorrhea
  3. A history that suggests aggressive peptic ulcer disease (PUD) or gastroesophageal reflux disease (GERD) refractory to therapy or with recurrent complications
  4. Peptic ulcer disease with associated diarrhea
  5. Any feature that suggests the presence of MEN1 syndrome
711
Q

How are Gastrinoma islet cell tumors diagnosed

A
  1. Hypergastrinemia refers to an increased fasting serum gastrin level and is one of the characteristics of Zollinger-Ellison syndrome (ZES)
  2. Fasting serum gastrin level is elevated in a majority of patients with ZES
  3. If elevated, the fasting gastric pH should be checked to exclude achlorhydria
  4. Confirmatory diagnostic tests may include secretin infusion to stimulate gastrin levels further, when the fasting level is equivocal
  5. The best methods for determination of tumor site are CT scan, EUS, and octreotide nuclear scanning
712
Q

What are the potential complications of Gastrinoma islet cell tumors

A
  1. 1/3 of ZES patients have metastatic liver disease on presentation
    • progression of this disease is usually slow, with metastasis normally beginning in regional lymph nodes, then to the liver and later to the bone
  2. The extent of morbidity and mortality in patients with ZES is related principally to ulcer complication
    • fistulas, hemorrhage, or perforation
    • most patients experience complications of ulcer disease such as bleeding or perforation at some time during the course of their disease
713
Q

What is the treatment for Gastrinoma islet cell tumors

A
  1. Medical treatment of ZES is highly effective and involves long-term administration of PPIs- often at doses much larger than normally prescribed - which suppress acid production and promote healing
  2. For metastatic disease, chemo is promising
  3. When medical treatment fails, surgery may be recommended to remove the primary tumor if it can be located
  4. In patients who do not have MEN!, some gastrinomas can be completely resected with resultant cure
  5. If resection is possible, this is the optimal treatment
  6. Total gastrectomy to control acid section is very rarely needed
714
Q

What is an insulinoma

A
  1. The most common type of islet cell tumors
  2. Arises from beta cells
  3. 70-80% are benign
  4. Typically round, firm and encapsulated and is most frequently located in the body or tail of the pancreas
715
Q

What are signs and symptoms of insulinomas

A
  1. Hypoglycemia on fasting after exercise
  2. Overweight
  3. Insulin to glucose level is elevated
  4. May also experience neuropsychiatric manifestations, ranging from subtle personality changes to confusion, coma or seizure disorders
716
Q

What are glucagonomas

A
  1. Alpha islet cell tumor
  2. More than 50% are malignant
  3. Less common than insulinomas or gastrinomas
717
Q

What are signs and symptoms of glocagonomas

A
  1. Distinctive feature is necrolytic migratory erythema, a skin disorder, which appears as an erythematous area that develops a central blister and is followed by crusting, healing and sometimes bronze hyperpigmentation
  2. Most patients have diabetes
  3. Profound weight loss and anemia
718
Q

What are signs and symptoms of smoatostatinomas

A
  1. Consistent with the inhibitory effect of somatostatins on the secretion of gastrin, secretin, insulin, glucagon and cholecystokinin
  2. Include:
    • steatorrhea
    • mild diabetes mellitus
    • Cholelithiasis
    • weight loss
719
Q

What are VIPomas

A

Tumors that produce vasoactive intestinal peptide

720
Q

What are signs and symptoms of VIPomas

A
  1. Profuse watery diarrhea
  2. Hypokalemia
  3. Hypochlorhydria or achlorhydria
    • also known as the pancreatic cholera syndrome or Verner-Morrison syndrome
721
Q

What are potential complications of islet cell tumors

A

More than 50% of patients with a glucagonoma have metastases at the time of diagnosis

722
Q

What is the treatment for islet cell tumors

A
  1. The treatment of choice for most islet cell tumors is surgical excision
  2. Patients with metastatic disease may improve after surgical reduction of the tumor mass
  3. Streptozocin (Zanosar) has been shown to decrease tumor size and prolong survival
  4. A long-acting analog of somatostatin effectively controls symptoms in patients with several types of islet cell tumors
723
Q

What is pancreatic exocrine insufficiency

A
  1. Also referred to as exocrine pancreatic insufficiency (EPI)
  2. Problems with digestion result from a deficiency of the exocrine pancreatic enzymes needed to digest food
  3. Affects the pancreatic exocrine system, which produces amylase, protease, and lipase, and leads to pan-malabsorption and steatorrhea
724
Q

What are causes and risk factors to developing pancreatic exocrine insufficiency

A
  1. Results from chronic pancreatitis, leading to acinar loss
  2. Pancreatic duct obstruction should be excluded, since this may be a correctable cause
  3. Rare in children
    • most common causes
      • cystic fibrosis
      • Shwachman-Diamond syndrome
725
Q

What are signs and symptoms of pancreatic exocrine insufficiency

A
  1. Weight loss
  2. Most common clinical feature is stunted growth
  3. Leads to malabsorption and steatorrhea
726
Q

How are pancreatic exocrine insufficiency diagnosed

A
  1. Plain x-ray films - may show calcification of the pancreas
  2. CT scans are more sensitive
  3. 72-hour fecal fat analysis with stool fat output greater than 7% of intake is evidence of fat malabsorption
727
Q

What is the treatment for pancreatic exocrine insufficiency

A
  1. Oral enzyme preparations and concomitant acid suppression to improve delivery of sufficient enzyme into the small intestine
  2. Some patients may benefit from supplemental calcium, vitamin D, and other fat-soluble vitamins
728
Q

What is Cystic fibrosis

A
  1. Inherited disease of the secretory glands, including mucous and sweat
  2. Most common cause of pancreatic insufficiency in children
  3. Mainly effect lungs, pancreas, liver, intestines, sinuses, and sex organs
  4. Occurs in 1 out of every 3,000 newborns
729
Q

What are causes and risk factors to developing Cystic fibrosis

A

1 autosomal recessive disease of the exocrine glands
2. Incidence
- most common lethal genetic defect in the Caucasian population (1:2,500 births)
- less common in Asian Americans and African Americans
3. Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene are the cause of cystic fibrosis
4. The transcriptional regulation of CFTRs and underlying molecular mechanisms remain poorly understood
5. It is possible that alteration in a common intracellular mediator or inhibitor protein distal to the site of generation of cyclic adenosine monophosphate is likely to be the underlying abnormality in affected tissues of patients with cystic fibrosis

730
Q

Hat are signs and symptoms of Cystic Fibrosis

A
  1. Affects the pancreas, respiratory system, sweat glands, and reproductive system
  2. Poor fat and protein digestion, producing greasy foul smelling stools
  3. Weight loss despite an increased appetite
  4. Episodes of pneumonia or bronchitis with coughing, wheezing and noisy respirations
  5. Meconium ileus or intestinal obstruction
  6. Intussusception
  7. Rectal prolapse
  8. Constipation
  9. Biliary cirrhosis
  10. Diminished or absent pancreatic enzymes
  11. The production of thick, sticky dry mucus
731
Q

How is cystic fibrosis diagnosed

A
  1. Usually diagnosed in the first year of life
  2. Definitive diagnostic test is the sweat electrolyte test
    • quantitative pilocarpine iontophoresis shows elevated sodium and chloride levels in affected patients
    • may not be reliable in neonates and in individuals with edema
  3. DNA testing can be performed to identify patients with cystic fibrosis and carriers of the cystic fibrosis gene
732
Q

What are potential complications of cystic fibrosis

A
  1. A hallmark of cystic fibrosis is bacterial infection, and most people with the condition die from respiratory failure
  2. The airways show an increased viscoelasticity and the resulting mucus thickens over time, leads to bacterial overgrowth, and prevents mucus clearance
  3. Recognized as a poly microbial disease
  4. GI complications include; intestinal obstruction (Meconium ileus equivalent), intussusception, constipation and rectal prolapse
    - liver disease, esophageal varices, hyperglycemia, and diabetes may also be present
  5. Approximately 5-30% of patients with cystic fibrosis develop liver cirrhosis
  6. Infertility for both men and women
733
Q

What is the treatment for cystic fibrosis

A
  1. Managed by controlling respiratory complications and by aiding digestion through dietary regulations
  2. Supplements of vitamins A,D,E,and K; and pancreatic enzyme replacement
  3. The pancreatic exocrine dysfunction requires the patient to rely on oral pancreatic enzymes
  4. Gene therapy is promising
  5. Much of the morbidity and virtually all of the mortality beyond the neonatal period in patients with cystic fibrosis is attributable to chronic obstructive pulmonary disease (COPD)
  6. As of 2010 the survival rate is 37 years for women and 40 years for men
  7. The prolongation of life can be attributed largely to the development of pancreatic replacement therapy, use of antibiotics and vigorous pulmonary hygiene
734
Q

What is Shwachman-Diamond Syndrome

A
  1. Inherited exocrine pancreatic insufficiency
  2. The second most common cause of pancreatic insufficiency
735
Q

What are causes and risk factors of developing Shwachman-Diamond syndrome

A
  1. The suggested mode of inheritance is autosomal recessive
  2. Incidence is 1:10,000-20,000 births
736
Q

What are signs and symptoms of Shwachman-Diamond syndrome

A

Characteristics
1. Growth retardation - usually below to the 3rd percentile for height; but linear growth is maintained - as adults they rarely reach above the 25th percentile for height
2. Dental abnormalities
3. Metaphyseal dystopias (skeletal abnormalities)
4. Ichthyosis (skin is dry and scaly)

Signs and symptoms are those of pancreatic insufficiency
1. Malabsorption
2. Steatorrhea
3. Malnutrition
4. Failure to thrive
5. Vitamins A, D,E and K deficiencies
6. Hematological changes - neutropenia, thrombocytopenia and anemia

737
Q

How is Shwachman-Diamond syndrome diagnosed

A
  1. Confirmed by performing a secretin pancreozymin stimulation test, which results in a very low or absent pancreatic zymogen enzyme or an elevation in stool fat content
  2. Blood counts are performed twice weekly for 3 weeks as a confirmation of diagnosis
  3. A negative sweat test excludes cystic fibrosis
738
Q

What are potential complications of Shwachman-Diamond syndrome

A
  1. More susceptible to bacterial infections and predisposed to orthopedic complications
  2. They are at risk for aplastic anemia and leukemia, which contribute further to their morbidity and mortality
  3. There is a prevalent association of pancreatic insufficiency with hematopoietic manifestations and leukemia
739
Q

What is the treatment for Shwachman-Diamond syndrome

A
  1. Symptomatic and supportive
  2. Pancreatic enzyme replacement
  3. Fat soluble vitamins
  4. Antibiotics as needed due to increased susceptibility to infections
  5. Orthopedic and hematological needs monitored and treated as necessary
740
Q

What is pancreatic rest

A
  1. Also known as heterotropic pancreas
  2. Uncommon, ectopic pancreatic tissue that does not communicate with the pancreas
  3. Found as a polyp-like formation in the stomach or small intestine
741
Q

What causes pancreatic rest

A

A congenital anomaly

742
Q

What are signs and symptoms of pancreatic rest

A
  1. When symptomatic, the condition may produce ulceration, bleeding or clinical pancreatitis
  2. Often asymptomatic
  3. Epigastric pain
  4. Polyp-like formation found in the antrum during EGD
743
Q

How is pancreatic rest usually diagnosed

A

An incidental finding during an upper GI endoscopy

744
Q

What is the treatment for pancreatic rest

A
  1. Symptomatic lesions are treated with simple excision, which can be accomplished by endoscopic mucosectomy
745
Q

What is pancreatic divisum

A
  1. The most common congenital pancreatic anomaly occurring in approximately 10% of individuals
  2. Occurs when the two embryonic precursors of the pancreas - the ventral and the dorsal buds fail to fuse, resulting in separate dorsal and ventral pancreatic ducts
  3. The dorsal gland is drained by the duct of Santorini through the minor or accessory papilla into the duodenum, whereas the ventral gland is drained by an abnormally short duct of Wirsung and enters the duodenum through the major papilla together with the bile duct
  4. Occurs in 7% of the population
746
Q

What causes pancreatic divisum

A

A congenital anomaly

Associated with pancreatitis

747
Q

What are signs and symptoms of pancreatic divisum

A
  1. Associated with pancreatitis
  2. May be that both pancreas divisum and a stenosis accessory papilla must be present for clinically evident pancreatitis to occur
  3. Recurrent acute pancreatitis may attributable to pancreatic divisum when the pancreatic ducts appear normal but chronic pancreatitis may occur consequently and often affects both ducts
748
Q

How is pancreatic divisum diagnosed

A
  1. Pancreatography and EUS with recurrent pancreatitis
  2. On ERCP the major papilla is often difficult to cannulate, but on injection with contrast, the duct of Wirsung appears stunned and of small diameter
    - additionally there is rapid filling of small accessory ducts
    - if possible, the accessory duct should be cannulated, revealing a duct of Santorini running the entire length of the pancreas that is not in communication with the duct of Wirsung
  3. Pancreatic manometry and secretin ultrasound scanning is sometimes used if stenosis of the papilla is not demonstrated by MRCP
749
Q

What is the treatment for Pancreas divisum

A
  1. Main purpose is to dilate the minor papilla and promote drainage
  2. Endoscopic treatment options
    • sphincterotomy of minor papilla
    • dilatation of the minor papilla
    • stent placement within the minor papilla
750
Q

What is annular pancreas

A

Occurs when the embryonic dorsal and ventral glands fail to fuse, and part of the ventral pancreas encircles the duodenum, often resulting in duodenal obstruction

Most common anomaly obstructing the duodenum in infancy

751
Q

What are causes and risk factors that lead to the development of annular pancreas

A
  1. Congenital anomaly
  2. May be associated with:
    • Down syndrome
    • excess amniotic fluid in pregnancy
    • pancreatitis
752
Q

What are signs and symptoms of annular pancreas

A
  1. Nausea and vomiting
  2. Newborn does not eat enough and spits up more than usual
  3. May not cause symptoms until adulthood
    • at that time, presenting complaints include intermittent epigastric discomfort that is relieved by vomiting
753
Q

How is annular pancreas diagnosed

A
  1. Abdominal ultrasound
  2. Abdominal x-ray
  3. CT scan
  4. Upper GI series - shows a narrowing of the second portion of the duodenum
754
Q

What is the treatment for annular pancreas

A
  1. If symptomatic - surgical bypass is performed using a duodenojejunostomy
755
Q

What are potential complications of annular pancreas

A
  1. Obstructive jaundice
  2. Pancreatic cancer
  3. Pancreatitis
  4. Pepticular
  5. Intestinal perforation
756
Q

What are pathological conditions that can effect nutrient development in the small intestine

A
  1. Duodenal disease - deficiencies in iron and calcium absorption
  2. Jejunal disease - malabsorption of fats, proteins, and carbohydrates
  3. Ileal disease - B12 deficiency and bile salt malabsorption
757
Q

What are duodenal ulcers

A
  1. Peptic ulcers can develop in the lower esophagus, stomach, pylorus, duodenum or jejunum
  2. The yearly incidence of peptic ulcers is greater than 5 cases per 1000 people
  3. Most peptic ulcers are duodenal ulcers
  4. They occur when the protective mucosa of the duodenum cannot resist corrosion by above-normal hydrochloric acid levels
758
Q

What are causes and risk factors to developing duodenal ulcers

A
  1. Occur when the protective mucosa cannot resist corrosion by above normal levels of hydrochloric acids
  2. H. Pylori is present in almost all adults with duodenal ulcers - it penetrates the mucous layer of the duodenum
  3. Chronic use of NSAIDs
  4. Most common in men between the ages of 20 and 50 years of age
  5. In people with type O blood
  6. Has a round, punched-out appearance and is on average about 0.5cm across
759
Q

What are signs and symptoms of duodenal ulcers

A
  1. Gnawing or burning epigastric pain
    • 1 to 3 hours after a meal
    • awakens at night
  2. Heartburn
  3. Pain is exacerbated by:
    - fatty foods
    - acidic foods
    - alcohol
    - NSAIDS
  4. Almost 50% of patients with ulcers may present with bleeding
760
Q

How are duodenal ulcers diagnosed

A
  1. Upper GI x-rays
    - a double-contrast technique is more sensitive than a single-contrast technique
  2. EGD - may be more sensitive than radiography
  3. Testing for H. Pylori - with endoscopic biopsy or a C-urea breath test , or measurement of H. Pylori antibodies in the blood, or a stool antigen test
  4. In patients over the age of 50 with new-onset dyspepsia
  5. In patients at any age with alarm features that suggest significant structural disease or malignancy or for any patient with persistent dyspeptic symptoms
  6. Not recommended to evaluate benign-appearing uncomplicated duodenal ulcers identified on Radiographic imaging
761
Q

What are potential complications of duodenal ulcers

A

Erosion of the affected mucosa can lead to hemorrhage, perforation, and peritonitis

762
Q

What is the treatment for duodenal ulcers

A
  1. Eradication of H. Pylori
  2. Acid suppression
  3. Smoking cessation
  4. Decreasing alcohol intake
  5. Surgical intervention
    • necessary when complications occur, such as hemorrhage or perforation
    • procedures
      • suture ligation of bleeding vessel
      • simple omental patch closure of perforation
      • truncal vagotomy
      • highly selected vagotomy
      • truncal vagotomy and antrectomy
      • complementary gastrojejunostomy or antrectomy
      • antisecretory procedures
763
Q

What are small bowel infections

A

Infections that can affect the absorption of nutrients and results in diarrhea

764
Q

What types of bacteria and viruses effect the small intestine

A
  1. Enterotoxigenic bacteria
  2. Invasive bacteria
  3. Penetrating bacteria
  4. Viruses
765
Q

What enterotoxigenic bacteria infect the small intestine

A

Produces enterotoxins that stimulate the active secretion of electrolytes into the lumen of the proximal small intestine
1. Escherichia coli (E. Coli)
2. Vibrio cholerae (V. Cholerae)
3. Bacillus cereus (B. Cereus)
4. Clostridium perfingens
5. Staphylococcus aureus (S. Aureus)

766
Q

What invasive bacteria can infect the small intestine

A

Invasive bacteria invade and damage the intestinal mucosa of the distal small intestine and colon
1. Salmonella species
2. Shigella species
3. E. Coli
4. Clostridium difficile (C. Diff)
5. Vibro cholerae (V. Cholerae)
6. Vibro parahaemolyticus (V. Parahaemolyticus)
7. Staphylococcus aureus (S. Aureus)

767
Q

What penetrating bacteria can infect the small intestine

A

Invade the mucosa, usually in the distal small intestine, but do not produce extensive mucosal ulcerations
1. Yersinia enterocolitica
2. Salmonella Typhi

768
Q

What viruses can infect the small intestine

A
  1. Coronavirus
  2. Rotavirus
  3. Norwalk virus
  4. Adenovirus
769
Q

What are signs and symptoms of enterotoxigenic bacteria infection of the small bowel

A
  1. Produce toxins that cause secretion of electrolytes into the lumen of the proximal small bowel
    2.Produce watery, voluminous diarrhea that is not usually accompanied by fever, and fecal leukocytes are seldom present
770
Q

What are signs and symptoms of invasive bacteria infection of the small intestine

A
  1. Damage mucosa of distal small bowel
  2. Scant, bloody mucoid stools
  3. Fever
  4. Fecal polymorphonuclear leukocytes
771
Q

What are signs and symptoms of a penetrating bacteria infection of the small intestine

A
  1. Usually invade the distal small bowel, but do not produce extensive mucosal ulceration
  2. Extraintestinal symptoms such as:
    • sepsis
    • fever
    • fecal leukocytosis
772
Q

What are signs and symptoms of a virus infection of the small intestine

A
  1. Invades the mucosa
  2. Need a host to survive
  3. Malabsorption
  4. Diarrhea
773
Q

How are bacteria infections and viruses of the small intestine diagnosed

A

Medical history
1. Symptom pattern
2. Recent exposure to infected individuals or contaminated food or water
3. Recent foreign travel

Should be evaluated for fluid status and abdominal tenderness, and stools should be examined for the presence of fecal leukocytes

774
Q

What are potential complications of bacteria or viral infections of the small intestine

A

GI tract infections are a major cause of morbidity and mortality throughout the world

775
Q

What is the treatment for bacteria or virus infections of the small intestine

A
  1. In most cases, infectious diarrhea can be treated with rest and fluid replacement
    • Oral hydration solutions
    • IV fluids may be needed for patients with severe dehydration
  2. Generally, for both adults and children with acute infectious diarrhea, consumption of an unrestricted diet should continue
    • with additional fluids or oral rehydration solutions provided to replace increased stool water losses
  3. Bacterial infections - antibiotic treatment of specific infectious agent
  4. Viral infections - vaccinations - provide immunity to infection
    • antiviral drugs - selectively interfere with viral replication
    • antibiotics do not work in viruses
  5. Antidiarrheal medication is contraindicated
    • prolongs mucosal contact with infectious organisms
    • exacerbates intestinal stasis, gas, and abdominal pain
776
Q

What is the treatment for a bacteria infection of the small intestine if the bacteria is staphylococcus aureus

A

None
Self-limited

777
Q

What is the treatment for a bacteria infection of the small intestine when the bacteria agent is Toxigenic Escherichia coli
(Also called enterotoxigenic E. coli (ETEC))

A

Trimethoprim-sulfamethoxazole (cetraxal)

778
Q

What is the treatment for a bacteria infection of the small intestine when the bacteria is Vibrio cholerae

A
  1. Doxycycline (Oracea, Monodox, Doryx)
  2. Ciprofloxacin (Cipro)
  3. Trimethoprim-sulfamethoxazole
779
Q

What is the treatment for a bacteria infection of the small intestine when the bacteria is Clostridium botulinum

A
  1. Polyvalent antitoxin (Botulism Antitoxin Heptavalent (A,B,C,D,E,F,G) Equine))
  2. Penicillin
  3. Colonic lavage
780
Q

What is the treatment for bacteria infections of the small intestine when the bacteria is Clostridium perfringens

A

None

781
Q

What is the treatment for bacteria infections of the small intestine when the bacteria is Vibrio parahaemolyticus

A

Tetracycline (Sumycin, Actisite, Panmycin (oral))

782
Q

What is the treatment for bacteria infections of the small intestine when the bacteria is shigella

A

For severe infection
1. Ampicillin
2. Trimethoprim-sulfamethoxazole

783
Q

What is the treatment for bacteria infection of the small intestine when the bacteria is Salmonella

A

For debilitated patients
1. Ampicillin
2. Chloramphenicol (Chloracol)
3. Amoxicillin (Amoxicot, Amoxil, DisperMox, Moxatag, Trimox)
4. Trimethoprim-sulfamethoxazole
5. Cefotaxime (Claforan)
6. Ceftriaxone
7. Fluoroquinolones - either Ciprofloxacin or levofloxacin (Levaquin)

784
Q

What is the treatment for a bacteria infection of the small intestine when the bacteria is Clostidium difficile

A
  1. Metronidazole (Flagyl, Flagyl ER)
  2. Vancomycin (Vancocin)
785
Q

What are the parasitic diseases that affect the small intestine

A

Recognized by an elevated immunoglobulin E (IgE)
Once detected, can be traced to the parasitic infection

  1. Giardiasis
  2. Coccidiosis
  3. Cryptosporidiosis
  4. Strongyloidiasis
  5. Ascariasis
  6. Diphyllobothriasis
786
Q

What is Giardiasis

A
  1. Organism: Protozoa (Giardia duodenalis (also called G. Lambda or G. Intestinalis)
  2. Two forms - cysts and trophozoites
  3. Endemic to New York and to the Rocky Mountains, especially in Colorado
  4. May be present in as many as 20-30% of people in the developing world and in as many as 2-3% of people in the industrialized world
  5. The most frequently identified intestinal parasite in the United States
787
Q

What are risk factors to developing Giardiasis

A
  1. Most often associated with ingestion of contaminated food or water
  2. The cysts are transmitted readily in eater or through contamination from a number of hosts, including domestic and wild animals
  3. A heavily infected host may pass thousands of cysts into the environment with as few as 10 cysts possibly resulting in infection
  4. Hosts may be without symptoms and become carriers
  5. After the cyst is ingested orally or nasally, it matures and, once in the stomach, releases trophozites
  6. These trophozites adhere to the wall of the proximal small intestine, causing an inflammatory response
  7. The incubation period lasts between 7-14 days, although cysts do not appear in the stool until one week after the development of symptoms
788
Q

What are signs and symptoms of Giardiasis

A

Adults
1. May be asymptomatic
2. May have: nonbloody diarrhea; malabsorption

Children
1. May range from asymptomatic to acute illness
2. May have: abdominal discomfort and distention
- non-bloody diarrhea
- headaches
- nausea and vomiting
Infants, children, the elderly, and immunocompromised patients are at high risk for infection

789
Q

How is Giardiasis diagnosed

A
  1. Examination of multiple fresh stool specimens for cysts
  2. Stool specimen for Giardia antigen (most reliable)
  3. Duodenal aspiration with small intestinal biopsy examination
  4. Serology testing is available
790
Q

What is the treatment for Giardiasis

A
  1. Adults
    - Metronidazole (Flagyl) in three divided doses each day for a week 250mg
    - Tinidazole (Tindimax) in one dose per day
    - Nitazoxanide (Alinia) tablet form
    - Paromomycin
    -Furazolidone (oral)
    -Quinacrine
  2. Pediatric
    -Nitzoxanide (Alinia) in a liquid suspension for one year and older, a tablet 12 years and older
    -Metronidazole - 5mg/kg for children given three times a day for 5 to 7 days
    -An alternative treatment for pediatric patients is Furazolidone
  3. For patients who are resistant to Metronidazole alone, a combine regimen of quinacrine and metronidazole for 2 weeks may be effective
  4. Recheck stool and/or duodenal aspirate 2 weeks post treatment
  5. Second course of treatment may be necessary
791
Q

What causes coccidiosis

A
  1. Organism: protozoans that multiply in small bowel, damaging mucosa
    • Cystoisospora belli (formally Isospora belli)
    • Isospora hominis (human coccidiosis)
    • Isospora natalensis (human parasite)
  2. It is endemic throughout the world but is rarely seen in the United States
  3. The parasite multiplies in the small intestine, causing mucosa damage
  4. It has occasionally been identified in travelers’ diarrhea
792
Q

What are signs and symptoms of coccidiosis

A

Appears in a few days to six months
1. Acute fulminant diarrhea
2. Chronic or intermittent diarrhea
3. Steatorrhea

793
Q

How is coccidiosis diagnosed

A
  1. Stool examination
  2. Small bowel biopsy
  3. Blood test for eosinophilia
794
Q

What is the treatment for coccidiosis

A
  1. Adults with a mild case - fluid and electrolyte replacement
  2. Children with severe diarrhea and malabsorption
    • temporary Parenteral nutrition
  3. In severe cases - sulfonamide Furazolidone (Furoxone) is drug of choice
795
Q

What causes Cryptosporidiosis

A

Organism - the protozoan parasite Cryptosporidium (Crypto)
1. Attack the small bowel and colon, but may be found in other parts of the GI and respiratory tract
2. Transmission
- occurs through the fecal-oral route
- water transmission has been reported
- between animals to humans
- rarely transmitted from human to human
3. Oocysts are ingested and become embedded in bowel wall to pass their life cycle
4. After 12 days, oocyst are passed in the stool
5. Immunocompromised patients are particularly susceptible - the beginning of the AIDS epidemic marked a noteworthy increase in its prevalence in humans
- more prominent in the elderly
- children in developing countries are also susceptible candidates and have a high morbidity from this infection

796
Q

What are signs and symptoms of Cryptosporidiosis

A
  1. The severity of the illness ranges from self-limited diarrheal episodes lasting from 3 days to 4 weeks to more severe symptoms in immunocompetent hosts, sometimes leading to death in immunocompromised individuals
  2. Onset is acute, with malaise and fever
  3. Followed by abdominal pain, diarrhea and vomiting
  4. Steatorrhea
  5. And occasionally milf rectal bleeding and non-specific proctitis
797
Q

How is Cryptosporidiosis diagnosed

A
  1. A serial stool examination for identification of acid-fast oocysts or intestinal biopsy examination
  2. The most accurate staining method for identification of the parasite is a three-step procedure that involves concentration evaluation using a sugar flotation technique, iodine staining, and a modified acid-fast stain
  3. Immunoassays or PCR-based assays may increase detection sensitivity
798
Q

What is the treatment for Cryptosporidiosis

A
  1. Correction of fluid and electrolyte imbalance
  2. Severe cases
    • Metronidiazole (Flagyl)
    • Nitazoxanide (Alinia)
    • Thiabendazole (Mintezol)
  3. For immunocompromised patient such as HIV-infected individuals, the approach is to maintain immune system function by using highly active antiretroviral therapy (HAART)
    - antibiotics to consider for immunocompromised patients include: paromomycin, azithromycin(Zithromax, Zmax) and nitazoxanide (NTZ) (Alinia),
  4. Has some resistance to antimicrobial drugs
799
Q

What causes Strongyloidiasis

A
  1. Occurs in warm, moist climates and is caused by the nematode Strongyloides stercoralis (S. Stericoralis) - American threadworm - a soil-transmitted helminth
  2. Filariform larvae are the infectious form, while rhabditiform larvae are noninfectious
  3. Infection cycle
    - human skin contact the larvae found in soil or other materials contaminated with human feces
    - larvae are swallowed and enter the duodenum where the adults attached to or penetrate the wall
  4. Multiple cycles of the same parasite may occur in a single host, thereby allowing some patients to harbor S. Stericoralis for 30-50 years
  5. Repeated auto infection may cause fatal hyper infection
  6. Endemic to: tropical and subtropical areas; in the US it occurs in the southeastern states
800
Q

What are signs and symptoms of Strongyloidiasis

A
  1. Most infected do not experience prominent symptoms
  2. Duodenitis
  3. Diarrhea
  4. Anorexia
  5. Nausea and vomiting
  6. Eosinophilia
  7. Fever
  8. Migratory, erythematous, macular eruptions over distal extremities (cutaneous lesion at the entry site in the perianal area or on feet)
  9. Productive or nonproductive cough
  10. Heavy worm burdens affect other organs:
    - pneumonitis
    - esophagitis
    - meningitis
    - gastritis
    - enterocolitis
    - hepatitis
    - myocarditis
    - intestinal obstruction
    - intestinal perforation
    - malabsorption and abdominal pain
    - shock
801
Q

How is Strongyloidiasis diagnosed

A
  1. Blood tests
  2. Stool examination - larvae first appear 3 to 4 weeks after dermal penetration
  3. GI series with small bowel follow through - duodenojejunal fluid aspirate
  4. Chest x-ray
  5. Eosinophilia is present, but may be absent in immunocompromised patients
  6. Serologic test vary in sensitivity
  7. The agar plate method is the most sensitive test to identify the larvae
802
Q

What are potential complications of Strongyloidiasis

A

In some patients, repeated auto-infection may produce an overwhelming fatal hyperinfective syndrome

803
Q

What is the treatment for Strongyloidiasis

A
  1. Fluid and electrolytes as needed
  2. Medication for 5 to 7 days
    - Ivermectin (stromectol) as 200mcg/kg orally for 2 day - safety of this drug in children less than 15kg or in pregnant women has not yet been determined
    - Abendazole is an alternative 400mg BID for 7 days - less effective
  3. Second course of treatment as needed
  4. Follow-up 1 to 2 weeks post therapy
    • stool examination - checking 3 samples can increase the identification rate to 50% and seven stool samples improve the identification rate to 100%
    • CBC to check for eosinophilia
    • serologies
804
Q

What causes Ascariasis

A
  1. Organism: the nematode (round worm) Ascaris lumbricoides
    • largest intestinal nematode
    • endemic to the US
      • especially in the South where it is as high as 90% in some areas - southeastern Appalachian range
      • in dry areas during the rainy months
  2. Cycle
    - transmission is through ingestion of eggs by the fecal-oral route
    - lifespan of 10 to 24 months
    - passed in stool
    - adult worms live in small bowel (usually jejunum or ileum) for 10-18 months
    - worms invade blood vessels and lymphatics, portal circulation, liver and lungs
    - the adult male measures 15-25 cm and is smaller than the female- which may be as large as 35cm
    - the mature female may produce up to 200,000 eggs daily
805
Q

What are signs and symptoms of Ascariasis

A

Reaction to larvae
1. High fever
2. Spasmodic coughing
3. Hemoptysis

Reaction to adult worm
1. Colicky mid epigastric pain
2. Abdominal distention and pain
3. Vomiting
4. Constipation
5. Obstruction
6. Loss of appetite

A rare reaction is pancreatitis with symptoms of biliary or pancreatic disease
Extraintestinal manifestations have been reported in as many as 50% of patients

806
Q

How is Ascariasis diagnosed

A
  1. Definitive diagnosis requires that the egg or the adult worm be identified in the stool
    • the worms and eggs are easy to identify
  2. The larvae reach the lungs via the pulmonary artery into the alveoli and bronchi
  3. The larvae develop into adult worms in the small bowel
  4. Lung involvement precedes intestinal phases by 8-10 weeks
  5. Eosinophils may be present during the pulmonary phase with Charot Leyden crystals, as well as larvae visualized in the sputum
  6. Live worms have been reported in sputum and vomitus
  7. Imaging - X-ray, Barium swallow, ultrasonography, CT scan, serology
807
Q

What are potential complications of Ascariasis

A
  1. The most common complication is partial or complete intestinal obstruction
    - more common in children
    - may occur in the appendix
  2. A hypersensitivity reaction in the lung may occur, causing self-limiting disease known as Loffler syndrome
  3. Extraintestinal conditions such as pancreatitis, may be serious problems
808
Q

What is the treatment for Ascariasis

A
  1. Albendazole (Albenza) as 400mg orally in a single dose
  2. Mebendazole (Emverm, Vermox) as 100mg orally BID for 3 days or 500mg as a single dose
  3. Ivermectin (Stromectol) as 150-200mcg/kg orally as a single dose - an alternative drug
    • safety in children and pregnant women is not yet established for ivermectin
  4. Pyrantel pamoate used in pregnant women
  5. Endoscopic or laparoscopic extraction
  6. Surgery for intestinal obstruction

Prognosis is usually good, but is dependent on the worm burden and the presence of complications

809
Q

What causes Diphylllobothriasis

A
  1. Organism - the fish tapeworm Diphyllobothrium latum
    • ingestion of infected raw fish
    • endemic in US in Northern Wisconsin, Michigan, and Minnesota
    • in Baltic countries, Northern Europe, northern Siberia, Asia, japan, and northern Manchuria
    • lives with its head attached to the small intestinal mucosa and grows into adulthood within 3 weeks, reaching up to 10mm in length
    • a single parasite may live within the host for years
810
Q

What are signs and symptoms of Diphyllobothriasis

A
  1. May be asymptomatic
  2. Vitamin B12 deficiency
  3. Abdominal pain
  4. Ataxia
  5. Paresthesia
  6. Nausea and vomiting
  7. Weigh loss
  8. Diarrhea
  9. Fatigue
811
Q

How is Diphyllobothriasis diagnosed

A
  1. Detection and identification of egg in stool (an egg with a cap on one end)
  2. Mild eosinophilia may occur
812
Q

What is the treatment for Diphyllobothriasis

A
  1. Niclosamide (Niclocide) as a 2gm single dose
  2. An alternative is Praziquantel (Biltricide) as 5-10mg/kg in a single dose
  3. Isoniazid (Laniazid)
  4. Follow-up stool exams should be done in 6-8 weeks
  5. Patients may pass a very long worm following treatment
  6. With proper treatment prognosis is excellent
  7. All fish should be thoroughly cooked or frozen for 24 hours to prevent the infection
813
Q

What is Crohn’s disease

A

Chronic inflammatory bowel disease (IBD)
1. Also known as regional enteritis, granulomatous colitis, or transmural colitis
2. One of two chronic IBDs - Crohn’s disease and ulcerative colitis

First documented in 1761 by Morgani
9 cases of inflammatory bowel disease were described in 1913 by Dalziel, a Scottish surgeon
Received the name of Crohn’s disease when later described in a detailed paper by Crohn, Ginzburg, and Oppenheimer

814
Q

What location does Crohn’s disease most commonly occur

A
  1. Can occur anywhere in the GI tract from mouth to anus
  2. Most commonly affects the terminal ileum
  3. Many patients also have cecum and/or right colonic involvement

30% of cases involve only the small intestine
40% of cases involve both the small intestine and the large intestine
25% involve only the colon

815
Q

How is Crohn’s disease characterized

A

By relapsing and remitting inflammation with periods of remission
The segmental inflammation and rectal sparing of Crohn’s disease are features that distinguish if from ulcerative colitis

816
Q

How would the lesions in Crohn’s disease be described

A
  1. May be continuous or asymmetric and patchy
  2. Can extend beyond the mucosal layer, penetrating deep into the submucosa, even to full thickness of the bowel wall
817
Q

What does inflammation look like in Crohn’s disease

A
  1. Spreads slowly and progressively
  2. Prone to periods of exacerbations
818
Q

What is the progression of Crohn’s disease

A
  1. Begins with lymphatic obstruction that causes edema
  2. Followed by:
    - inflammation
    - mucosal ulceration
    - stenosis due to the inflammation and chronic scarring of the mucosa
  3. As the disease progresses:
    - fibrosis occurs and serositis develops, causing diseased bowel loops to adhere to normal or other diseased loops
    - possible development of fistulae and abscesses
819
Q

Who is at risk for developing Crohn’s disease

A
  1. Higher in caucasians and persons of Jewish descent, but is becoming a worldwide disease in more industrialized countries
  2. In the US an incidence of 6-15 per 100,000 and a prevalence of 50-200 per 100,000
  3. The most common age of first occurrence is 15-30 years
  4. Occurs equally in males and females - in some surveys females predominate by as much as 1.6 to 1
  5. In western countries the incidence is from 6-10 per 100,000 people and the prevalence is 130 per 100,00 people
  6. There is a higher incidence in Caucasians than nonwhites and in urban than rural settings
  7. There is a lower incidence in Japan, South America and Africa
820
Q

What are causes for developing Crohn’s disease

A
  1. Remains unknown
  2. Current theories involve a multifactorial process leading to bowel inflammation
    • genetically predisposed individuals
    • dysregulated, inappropriate immune response
    • environmental insults which lead to alterations in the GI microbiota, including:
      • infection
      • antibiotic use
      • tobacco use
      • hygiene
      • Western diet
  3. Potential infectious agents include Myobacterium avium paratuberculosis (MAP) and the measles virus
  4. Genetic factors seem to be the single strongest risk factor for developing the disease
    • familial association with a positive history in 25% of people with the disease
    • chromosomes 16, 3, 7, and 12 have been linked to Crohn’s disease
    • NOD2 gene, also called CARD15, gene of chromosome 16, found in monocytes involved in immune response to pathogens is responsible for the increased susceptibility
      - immunologic factors suggest autoimmune phenomenon as a cause
  5. Stress may play a role in exacerbation of symptoms but is not an identified cause of illness
821
Q

How does the disease process of Crohn’s disease begin

A
  1. Lacteal blockage and lymphedema in the submucosa
  2. Peyer’s patches appear in the intestinal mucous membrane
  3. Lymphatic obstruction causes edema with inflammation, mucosal ulceration and possibly granulomas
  4. Typically, deep longitudinal “rake ulcers” appear in the bowel
  5. If deep ulcers appear between islands of edematous inflamed mucosa, the bowel wall takes on a cobblestone appearance
  6. As the disease progresses, fibrous is occurs and serositis develops, causing diseased bowel loops
  7. Perianal lesions may be present
822
Q

What are symptoms of Crohn’s disease during periods of acute inflammation

A
  1. Intermittent and colicky abdominal pain, particularly in the lower abdomen with diarrhea the next most frequent symptom
  2. People with involvement at the thoracic vertebra level T1 may present with RLQ
  3. Systemic symptoms may include low-grade fever, malaise, bloody diarrhea and malabsorption may be severe, leading to malnutrition and weight loss
  4. Growth failure or a decline in the rate of linear growth may be presenting symptom in children and adolescents
823
Q

What are chronic symptoms of Crohn’s disease

A

More persistent but less severe
1. Diarrhea
2. Abdominal pain
3. Steatorrhea
4. Anorexia
5. Weight loss
6. Nutritional deficiencies

824
Q

What are clinical symptoms of Crohn’s disease

A
  1. Fever
  2. Abdominal pain
  3. Diarrhea
  4. Weight loss
  5. Signs of malnutrition
  6. Abdominal mass
  7. Growth failure in children and adults
  8. Fatigue
  9. Abdominal distension
825
Q

What are signs and symptoms of Crohn’s disease when the disease process is ileocecal disease

A
  1. Right lower quadrant pain RLQ
  2. Diarrhea
  3. Fever
826
Q

What are signs and symptoms of Crohn’s disease when the disease process is colonic disease

A
  1. Bloody diarrhea
  2. Weight loss
  3. Fever
827
Q

What are signs and symptoms of Crohn’s disease when the disease process is perianal disease

A
  1. Pain
  2. Fistulae
  3. Edematous hemorrhoids
  4. Fissures
  5. Painful and swollen perianal skin tags
828
Q

What are signs and symptoms of Crohn’s disease when the disease process is rectal-vaginal fistulae

A
  1. Passing stool and/or flatus thru vagina
  2. Recurrent vaginal infections
829
Q

What are signs and symptoms of Crohn’s disease when the disease process is Enterovesival fistulae

A
  1. Recurrent urinary tract infections (UTI)
  2. Pneumaturia (passing air from the urethra with urination)
  3. Fecaluria
830
Q

What are extraintestinal signs and symptoms of Crohn’s disease

A

Occur in 43% of patients and may include:
1. Arthritis
2. Iritis
3. Spondylitis
4. Liver disease - primary sclerosing cholangitis
5. Renal disease
6. Skin lesions
7. Hematologic symptoms - hypercoagulability
8. Dermatologic symptoms - erythema nodosum and pyoderma gangrenous
9. Ophthalmic symptoms - sclera-conjunctivitis, uveitis, and episcleritis

831
Q

How is Crohn’s disease diagnosed

A

Based on clinical history and physical examination
1. Physical exam
2. Labs
3. Endoscopic exams
4. Ultrasonography
5. Computerized tomography (CT) scan

832
Q

How can a physical exam be helpful in diagnosing Crohn’s disease

A

Exam may reveal no findings or a right lower quadrant mass
The patient may be anemic, pale and febrile

833
Q

How can labs be used to help diagnose Crohn’s disease

A

May reveal:
1. Anemia
2. Increased erythrocyte sedimentation rate
3. C-reactive protein
4. Leukocytosis
5. Thrombocytosis
6. Hypoalbuminemia
7. Serologic markers in 60-70% of cases demonstrate an increase in the anti-saccharomyces cerevisiae antibodies (ASCA)
8. If the perinuclear antineutrophil cytoplasmic antibody (pANCA) is negative, the diagnosis is positive

834
Q

How do endoscopic exams help in diagnosing Crohn’s disease

A

Scope with biopsy to evaluate the histologic evidence of inflammation
1. Ileoscopy - colonoscopy to assess terminal ileus and colon
2. EGD - esophagus, stomach and upper small bowel
3. Double-balloon enteroscopy and barium contrast studies
- identify stricture, inflamed bowel loop, and enteroenteric fistulas
4. Histological exams of blood and tissue are commonly used
5. Colonoscopic exam may reveal aphthous ulcerations of the bowel with skipped areas
6. Terminal ileum should be biopsied
7. Capsule endoscopy may reveal ulcerations and strictures

835
Q

How can ultrasonography be used in diagnosing Crohn’s disease

A

Ultrasound may be useful in assessing undiagnosed right lower quadrant pain

836
Q

How can computerized tomography (CT) scan be used in diagnosing Crohn’s disease

A
  1. CT scan shows increased fat pad deposition and smudgy areas outside the bowel, as well as areas of bowel wall thickness
  2. An Upper GI series with small bowel follow through
  3. Magnetic resonance enterography (MRE)
    • detailed images of small bowel
    • evaluate fistulae or abscesses
837
Q

What other diseases are ruled out in the differential diagnosis of Crohn’s disease

A

Infectious diarrhea
1. C. Difficile
2. CMV
3. Giardia
4. Parasites
5. Other pathogens

Other diseases
1. Celiac disease
2. Autoimmune enteritis
3. IBS

838
Q

What are potential complications of Crohn’s disease

A

The development of fistulas
1. Occur in 20-40% of patients
2. Are usually enteroenteric or enterocutaneous
3. Occur between sites of perforation and adjacent organs

Perforation and obstruction
1. Perforation can lead to general peritonitis in rare situations
2. Localized abscesses occur near perforation sites in 15-20% of patients with Crohn’s disease

Malabsorption of bile acids and Vitamin B12
1. Common in disease of the ileum
Toxic mega colon with a presentation of colonic dilatation, fever, and leukocytosis
Long-standing Crohn’s disease may predispose patients to certain cancers
- adenocarcinoma of the colon and small intestine, most commonly in the ileum
- squamous cell carcinoma of the vulva and anal canal
- hodgkin’s and non-hodgkins lymphomas
Long-term data demonstrate that nearly all patients will develop structuring or penetrating complications over a 20-year course
- approximately half of patients will require surgical resection within 10 years of diagnosis, with a similar number of patients experiencing postoperative recurrence after 10 years

839
Q

What does treatment of Crohn’s disease involve

A
  1. Diet and nutrition
  2. Medications
  3. Induction
  4. Induction and maintenance
  5. Surgery
  6. Psychosocial support
840
Q

What is the dietary treatment for Crohn’s disease

A
  1. Diminish symptoms and nutrient replacement
  2. Diet during exacerbation to diminish symptoms
    - low in fiber and high in protein, calories, vitamins, and minerals to replace nutrient losses associated with the inflammatory process and provide sufficient nutrients to promote energy and nitrogen balance
    - small, frequent meals
    - lactose avoidance by patients who are lactose-intolerant
    - chemically defined elemental and polymeric diets, especially in patients whose disease is limited to the small intestine (shown to decrease disease activity in some studies)
    - liquid polymeric diets (may be better tolerated by patients
    - total Parenteral nutrition (TPN) for patients with severe disease or short bowel syndrome refractory to oral therapy or specialized enteral tube feeding
    - elemental diet - strictures or partial obstructions
  3. Dietary supplements - vitamins and minerals for specific deficiencies, such as:
    - vitamins A, B12, or D
    - Calcium, potassium or magnesium
841
Q

What types of medications are used in the treatment of Crohn’s disease

A
  1. Aminosalicylates - limited to mild disease
  2. Corticosteroids - used as induction medication
  3. Immunosuppressants - moderate to severe disease and maintenance, often used in combination with tangent inflammatory substance tumor necrosis factor (Anti-TNFs)
  4. Anti-TNF agents - moderate to severe disease and maintenance
  5. Anti-adhesion molecule therapy - moderate to severe disease and maintenance
  6. Antibiotics
  7. Antidiarrheals
  8. Bile acid sequestrants - decrease diarrhea due to bile salt wasting
842
Q

What aminosalicylates are used in the treatment of Crohn’s disease

A

Limited to mild disease
1. Sulfasalazine
2. Olsalazine
3. Mesalamine
4. Balsalazide

843
Q

What corticosteroids are used in the treatment of Crohn’s disease

A

Used as induction medication

Traditional
1. Hydrocortisone
2. Prednisolone
3. Prednisone

Minimal systemic effects
1. Budesonide

844
Q

What immunosuppressant are used in the treatment of Crohn’s disease

A

Moderate to severe disease and maintenance, often used in combination with target inflammatory substance tumor necrosis factor (Anti-TNFs)
1. Azathioprine
2. 6-Mercaptopurine
3. Methotrexate

845
Q

What Anti-TNF agents are used in the treatment of Crohn’s disease

A

Moderate to severe disease and maintenance
1. Adalimumab
2. Certolixumab
3. Infliximab.

846
Q

What anti-adhesion molecule therapy is used in the treatment of Crohn’s disease

A

Moderate to severe disease and maintenance
1. Natalizumab
2. Vedolizumab

847
Q

What antibiotics are used in the treatment for Crohn’s disease

A
  1. Metronidazole
  2. Ciprofloxacin
848
Q

What antidiarrheals are used in the treatment of Crohn’s disease

A
  1. Loperamide
  2. Atropine and diphenoxylate (Lomotil)
849
Q

What bile acid sequestrants are used in the treatment of Crohn’s disease

A

Decrease diarrhea due to bile salt wasting
1. Cholestyramine
2. Colestipol
3. Colesvelam

850
Q

How often is surgical intervention necessary for patients with Crohn’s disease

A
  1. Required in at least half of patients during their disease course
  2. Postoperative recurrence is high
  3. Reserved for patients who develop complications or have medically refractory disease
851
Q

What is the goal of surgical management of Crohn’s disease

A

Preserve intestinal length and function

852
Q

What is the purpose of surgical management for treatment of Crohn’s disease

A
  1. Alleviate symptoms
  2. Manage complications
  3. Improve quality of life
853
Q

What are indications for surgical management of Crohn’s disease

A
  1. Intestinal obstruction
  2. Intestinal perforation with fistula formation or abscess
  3. Free perforation
  4. GI bleed
  5. Neoplasm/cancer
  6. Growth retardation
  7. Urologic complications
  8. Perianal disease
854
Q

What are the procedures used in surgical management of Crohn’s disease

A
  1. Bowel resection
  2. Stricturoplasty
  3. Laparoscopic approach when possible
    - minimizes adhesions
    - smaller incisional scars
    - decreases postoperative ileus
    - decreases length of stay
    - decreases morbidity
855
Q

What type of psychological support and education should be given to patients with Crohn’s disease

A
  1. Encouraged to rest, reduce tension in their lives, and communicate their feelings about this chronic and often disabling disorders
  2. Education about the disease and its process and treatments should be provided
  3. Contact information for community agencies and support groups such as the Crohn’s and Colitis Foundation can be provided, and participation should be encouraged
  4. Depression is a common emotion experienced by patients with Crohn’s disease, therefore, the provision of emotional support is an important part of the treatment process
  5. Studies have shown that positive disease outcomes, including steroid-free remissions, decreased risk of major abdominal surgery and overall improvement of quality of life are all possible with mucosal healing
  6. Treatment models have changed from a “step-up” approach, where the treatment progresses in intensity as the disease worsens, to a more personalized format, in which there is earlier, more aggressive treatment for those patients who are found to be at risk for more complicated forms of Crohn’s disease
  7. Common self-management strategies
    - use of phone or computer apps to track symptoms, diet and exercise
    - anxiety and stress reduction, such as exercise, yoga, and planning for bowel accidents with extra clothing
  8. Adherence to treatment and follow up
  9. Tobacco use and cessation
856
Q

How often are their reoccurrences of Crohn’s disease after surgery

A
  1. During the first year the endoscopic recurrence rates are between 35 and 85% with 10 to 38% of the patients showing symptoms
  2. Three years post-operatively, the recurrence rates are 85% to 100%
857
Q

What is Meckel’s diverticulum

A
  1. Outpouching of the ileum
  2. Pouches are lined by typical ileal mucosa, but may contain ectopic gastric and/or pancreatic tissue
  3. Secretion of acid or pepsin from this ectopic tissue may cause ulceration and hemorrhage
  4. A congenital anomaly of the GI tract, resulting from incomplete separation of the fetal gut from the yolk sac
  5. This is a true diverticula of the intestine, with all layers of the intestinal wall affected
  6. The diverticulum range in size from 1-10 cm in length and 1-3cm in width and are located 30-90cm proximal to the ileoceal junction
858
Q

What are causes and risk factors to developing Meckel’s diverticulum

A
  1. Congenital anomaly of the GI tract
  2. Tissue left from the umbilical cord at birth
  3. Occurs in 2-3% of the general population
  4. Most frequent congenital anomaly of the GI tract
859
Q

What are signs and symptoms of Meckel’s diverticulum

A
  1. Majority of cases are asymptomatic
  2. Typically occurs during the first year of a child’s life, but can also occur into adulthood
  3. Can include:
    • GI bleeding seen in the stool - common symptom in children under 2 years old due to ulcers from stomach acid secretions
    • painless rectal bleeding - melanous stool
    • abdominal pain and cramping in epigastrium
    • tenderness near the umbilicus
    • obstruction of the bowels.
      • pain
      • bloating, diarrhea, constipation and vomiting
      • occurs due to volvulus or intussusception
    • diverticulitis can occur at any age, but is more common in older children
      - tumors are rare, but can occur in adults
860
Q

How is Meckel’s diverticulum diagnosed

A

Cannot be diagnosed by endoscopic or radiological contrast studies

  1. Meckel’s diverticulum scan with Tc-99m - allows diagnosis by administration of technetium, which is excreted by gastric mucosa, followed by a nuclear medicine scan to identify area of excretion
    • administration of cimetidine or ranitidine orally for several days before the scan or given IV before the scan increases the accuracy of this diagnostic tool by decreasing anion secretion from the gastric mucosa
    • Crohn’s disease or other inflammatory disorders can lead to false positive scans
  2. Colonoscopy
  3. Wireless capsule endoscopy
  4. Enteroclysis examination or Angiography
  5. Ultrasonography
  6. CT scan can provide a differential diagnosis between appendicitis, Cholecystitis, diverticulitis and salpingitis
  7. Small intestine follow through
861
Q

What are potential complications of Meckel’s diverticulum

A
  1. This Outpouching of the ileum is lined by typical ileal mucous membrane but may contain ectopic gastric and/or pancreatic tissue in its wall
  2. Secretion of acid or pepsin from this ectopic tissue may cause ulceration of adjacent ileal tissue, resulting in hemorrhage
  3. Hemorrhage usually occurs in children under 2 years of age and typically presents as painless passage of bright red blood from the rectum
  4. Intestinal obstruction may result from Meckel’s diverticulum, either from volvulus or intussusception
    • symptoms include: abdominal pain, bilious or recurrent vomiting, and/or passage of bright red or “currant jelly” stools
  5. Unusual complications in adults include development of carcinomas, such as carcinoids, sarcomas, and adenocarcinomas
  6. Other complications include development of enteroliths that may lodge in the diverticulum and result in vomiting, obstruction and bleeding
862
Q

What is the treatment for Meckel’s diverticulum

A
  1. Not always necessary if asymptomatic and discovered during surgery or tests for another condition
  2. Diverticulectomy with intestinal anastomosis
  3. Resection of the adjacent ileum
  4. Because there is low risk of complications of Meckel’s diverticulum in adults, the incidental finding of such a lesion may be left intact
  5. When Meckel’s diverticulum causes bleeding, surgical correction is required
  6. In the rare Littre hernia, Meckel’s diverticulum is a component of the hernia sac
    • difficult to diagnose, but the clinical picture includes localized pain over pre-existing hernia that is accompanied by intestinal obstruction, bleeding, perforation, fistula and malignancy
863
Q

What is Vitamin B12 deficiency

A
  1. In the stomach, protein-bound vitamin B12 is freed by the action of gastric pepsin
  2. The free B12 binds to two molecules of intrinsic factor, which is a glycoprotein secreted by gastric parietal cells
  3. This complex protects vitamin B12 from use by bacteria and from the formation of unabsorbable aggregates while it is in the small intestine
  4. In the ileum, the complex B12 and intrinsic factor binds to receptor sites on the brush border, thus facilitating B12 entry into the enterocytes
  5. After passage through the enterocytes, B12 is transported in the blood bound to transcobalamins, which deliver the vitamin to the tissue
  6. Intrinsic factor remains bound to the receptor site, where it may promote the uptake of more B12
  7. When the amount of ingested B12 is very large, absorption also occurs by diffusion, probably at all levels of the intestine
864
Q

What are risk factors to developing vitamin B12 deficiency

A
  1. May occur if any one of the steps of production, transport, or absorption is impaired
  2. Disorders or conditions that may result in vitamin B12 deficiency include gastrectomy, pancreatic insufficiency, Zollinger-Ellison syndrome, Crohn’s disease, bacterial overgrowth, ileal disease or resection, familial cobalamin malabsorption, or transcobalamin deficiency
  3. Additionally, infestation with the tapeworm diphyllobothrium latum may be a cause when a competitive situation for vitamin B12 occurs
865
Q

What are signs and symptoms of Vitamin B12 deficiency

A
  1. May be subtle, with the patient appearing with Neurologic findings such as degeneration of the spinal cord and progressive neuropathy, or there may be full-scale megaloblastic or pernicious anemia
866
Q

How is Vitamin B12 deficiency diagnosed

A

The source of vitamin B12 malabsorption may be pinpointed using the three-part Schilling test which traces the excretion of radiolabeled B12 in the urine with or without the addition of intrinsic factor or a broad-spectrum antibiotic

867
Q

What is the treatment for Vitamin B12 deficiency

A
  1. Treatment is directed at the underlying disease state
  2. Parenteral vitamin B12 intramuscularly may be required in cases of severe disease that includes gloss it is and peripheral neuropathy or in extensive ileal resection
868
Q

What is malabsorption syndrome

A
  1. Includes one or both:
    - abnormalities of mucosal transport
    - intraluminal digestion of one or more dietary constituents
  2. All nutrients are absorbed in the mucosa of the small intestine
  3. Small intestine disorders often affect the absorption of:
    - fat
    - protein
    - carbohydrates
    - vitamins and/or minerals
  4. The clinical significance of malabsorption depends on the site and extent of involvement
869
Q

What cause malabsorption syndromes

A
  1. Small bowel diseases
    - celiac sprue
    - tropical sprue
    - Whipple’s disease
    - Lactase deficiency
    - abetalipoproteinemia
  2. Small bowel syndrome
  3. Small bowel resection
  4. Pancreatic exocrine deficiency
  5. Bile acid insufficiency
  6. Lymphatic disorders
  7. Gastric hypersecretory states
  8. GIST tumors
  9. Small intestinal bacteria overgrowth (SIBO)
  10. Infection with Giardia lamblia and Strongyloidiasis
870
Q

What are signs and symptoms of malabsorption syndromes

A
  1. The primary symptom is chronic diarrhea
  2. Other symptoms may or may not be present, including:
    • weight loss and anorexia, despite a high caloric intake
    • physical weakness
    • abdominal bloating and cramping
    • chronic fatigue
871
Q

How are malabsorption syndromes diagnosed

A
  1. Blood and urine tests
  2. CT scan of the abdomen
  3. Hydrogen breath test
  4. Schilling test for vitamin B12 absorption
  5. Secretin stimulation test
  6. Small bowel biopsy - diagnose celiac disease, Whipple disease, abetalipoproteinemia or agammaglobulinemia
  7. Stool culture or culture of small intestine aspirate
  8. Quantitative stool fat test
  9. X-rays of the small bowel or other imaging tests
872
Q

What is the treatment for malabsorption disorders

A

Directed at the underlying disease

873
Q

What is Celiac disease

A
  1. Also known as celiac sprue or gluten-sensitive enteropathy
  2. Characterized by:
    • poor food absorption
    • intolerance of gluten, a protein found in wheat, oats, rye, barley and their products
  3. Malabsorption results from:
    - atrophy of the villi
    - decrease in the amount and activity of enzymes in the epithelium
  4. First describe by Gee in 1888 as “Celiac affliction”
  5. Dicke and colleagues found in 1950 that removing wheat from the diet caused signs and symptoms to disappear
  6. The term celiac disease should only be used when gluten is demonstrated to be the cause
874
Q

What is the likely incidence of celiac disease occurring

A
  1. Can occur at any age
  2. More common
    • age 8 to 24 months old after receiving gluten in the diet
    • clinical signs can disappear during adolescence
    • around 20 years of age
875
Q

What are risk factors to developing Celiac disease

A
  1. Being female
  2. Family history
  3. Northwestern European ancestry
  4. 1:133 people in the US have celiac disease
  5. Affects 1% of the world’s population
  6. Ireland, Italy, and the Netherlands have a high incident rate
876
Q

What causes celiac disease

A
  1. An inherited inflammatory autoimmune disease that affects the lining of the small intestine
  2. It most likely results from a combination of environmental factors and genetic predisposition
877
Q

What are signs and symptoms of celiac disease

A
  1. Abdominal pain, bloating gas or indigestion
  2. Constipation
  3. Decreased appetite (may also be increased or unchanged) without weight gain
  4. Diarrhea, either constant or off and on
  5. Lactose intolerance (common when the person is diagnosed, usually goes away after treatment)
  6. Nausea and vomiting
  7. Stools that are foul smelling, oily, or sticks to the toilet when flushed
  8. Unexplained weight loss (although can be overweight or of normal weight)
  9. Anemia
  10. Vitamin K deficiency
  11. Missed menstrual periods, infertility, or spontaneous miscarriages
  12. Weakness, fatigue, lack of energy
  13. Irritability’s uncooperativeness and/or apathy or depression
  14. Arthritis
878
Q

What are signs and symptoms of celiac disease in children

A
  1. Defects in the tooth enamel and changes in tooth color, canker sores and dermatitis herpetiformis
  2. Delayed puberty
  3. Diarrhea, constipation, or fatty or foul-smelling stools
  4. Nausea and vomiting
  5. Irritable and fussy behavior
  6. Poor weight gain
  7. Slowed growth and shorter than normal height for age, muscle wasting, delayed development, iron deficiency anemia, bone or joint pain and osteoporosis
879
Q

How is celiac disease diagnosed

A
  1. History and physical
  2. Blood tests
    - antibodies
    • anti-tissue transglutaminase antibodies (tTGA)
    • anti-endomysial antibodies
    • patients are NOT to begin a gluten-free diet prior to testing as this may provide a false negative test result
      - cholesterol - may be low
      - complete blood count for anemia
      - comprehensive metabolic panel
      - folate level
      - iron level
      - PTT
      - vitamin B12 level
      - vitamin D level
  3. Upper endoscopy
    - follow-up for positive antibody test
    - biopsy from the first part of the duodenum - villous atrophy with an increase in intraepithelial lymphocytes (IELs)
    - capsule endoscopy
  4. Genetic testing can be offered to family members of a person positive for celiac disease to determine who may be at risk for celiac disease
  5. Bone density test
  6. Diagnosis is complete if symptoms resolve within weeks following a gluten-free diet
880
Q

What are potential complications of Celiac disease

A
  1. In adults - an increased risk of malignant small intestine lymphoma and carcinoma of the esophagus and stomach
  2. In individuals who have had celiac disease for many years, osteoporosis, anemia, and infertility may occur
881
Q

What is the treatment for Celiac disease

A

Cannot be cured

  1. Lifelong elimination of gluten from the diet
  2. May need dietary supplements to correct deficiencies
  3. During acute exacerbation:
    - fluid and electrolyte replacement
    - corticosteroids
    - vitamin K
  4. Follow-up biopsy or blood test
    - may be ordered several months after treatment begins to assess effectiveness
    - normal results mean treatment is working and confirms diagnosis
  5. Follow with dietitian who specializes in celiac disease and the gluten-free diet
  6. Support group
  7. In cases of severe intestinal damage, a lactose-free diet may also be recommended until intestinal mucosa heals
  8. Consideration needs to be given to ensure medications prescribed to patients are gluten-free
  9. Possible adjunctive therapies under investigation include bacterial prolyl endopeptidases, development of a site-specific inhibitor of intestinal tissue transglutaminase (TTG), T-cell silencing, cytokine therapy, genetically modified wheat, and monoclonal antibodies
  10. Additional therapies in various trial stages include enzyme-based treatment with the intent to inhibit toxic potential of gluten, as well as antibody targets to both the disease and treat the symptoms
  11. Hookworm larvae have a potential role in treating gluten sensitivity through the anti-inflammatory proteins that the hookworms secrete
882
Q

What is Tropical sprue

A
  1. A malabsorption syndrome acquired in endemic tropical areas
  2. It’s characterized by progressively more severe alterations of the jejunum and ileum
  3. Histological changes associated with tropical sprue consist of lengthening of the crypt area, a broadening and shortening of the villi, epithelial cell changes and infiltration by chronic inflammatory cells
883
Q

What are risk factors to developing Tropical sprue

A
  1. Associated with an abnormal small intestinal bacterial flora, with the jejunum becoming contaminated with colonic bacteria
  2. Results in mucosal injury
  3. Bacterial contamination of the jejunum may occur during acute GI infection
884
Q

What are signs and symptoms of Tropical Sprue

A
  1. Chronic diarrhea
  2. Malaise
  3. Fatigue
  4. Weight loss associated with malabsorption of fat, carbohydrates (glucose and d-xylose), folate, and vitamin B12
885
Q

What is the treatment for tropical sprue

A
  1. Antibiotic treatment improves vitamin B12 malabsorption and serves to reduce intestinal bacteria
  2. However, vitamin B12 may not return to normal levels
  3. Treatment with folate and vitamin B12 may improve the epithelium in 3-6 days with an increase in mitotic activity, redevelopment of villi, and reversion of nuclear alterations
  4. D-xylose malabsorption may persist in greater than 50% of the patients, despite treatment with folate, vitamin B12, or antibiotics
  5. Steatorrhea is treated with a low-fat diet
886
Q

What is Whipple disease

A
  1. A rare bacterial infection primarily affecting the small intestine
  2. It is characterized by chronic diarrhea and progressive wasting
  3. It is also known as intestinal lipodystrophy
  4. Only about 700 cases have been reported, primarily in the US (many from the state of Connecticut), England, continental Europe, and South America
  5. First describe by George Whipple in 1907
887
Q

What are risk factors to developing Whipple disease

A
  1. The bacterium that causes the disease was isolated and identified as Tropheryma whipplei in 1992
  2. Transmission is believed to be the fecal-oral route, often from consuming bacteria-contaminated food or water, coupled with genetic immune system response defect that increases infectious tendency with exposure
  3. Whipple disease most often affects Caucasian men between the ages of 20 and 67
888
Q

What are signs and symptoms of developing Whipple disease

A

The most common signs and symptoms
1. Weight loss
2. Diarrhea
3. Arthralgias
4. Vague abdominal pain

Other symptoms
1. Bloating
2. Steatorrhea
3. Impaired intestinal absorption
4. Slight fever
5. Hyperpigmentation
6. Peripheral, mesenteric, periaortic and celiac lymphadenopathy
7. Occasionally splenomegaly
8. There may be central nervous system involvement, including signs of aging, dementia, ophthalmoplegia (paralysis of muscles around the eye) , myoclonus
9. Cardiac involvement with fibrinous pericarditis and endocarditis

889
Q

How is Whipple disease diagnosed

A
  1. Biopsy examination of the small intestine
    • shows lipid-filled macrophages and large cytoplasmic granules that stain a brilliant magnet with the periodic acid-Schiff (PAS) stain
    • the bacterium can be demonstrated on electron microscopy
890
Q

What are potential complications of Whipple disease

A
  1. Some Neurologic signs (dementia) may not reverse
  2. PAS positive macrophages may persist between 1 and 8 years
  3. Untreated, the disease can be fatal
891
Q

What is the treatment for Whipple disease

A
  1. Doxycycline (vibramycin, oracea) 200mg/day and hydroxychloroquine (plaquenil) 600mg/day for 12 months
    - followed by a lifetime treatment of doxycycline 200mg/day
  2. Chronic localized infections should be treated with doxycycline 200mg/day and hydroxychloroquine 60mg/day for 12-18 months
  3. During the acute phase, corticosteroids may be administered
  4. Patient with iron deficiency anemia need iron supplements
  5. Most extraintestinal manifestations and positive signs disappear within a year
892
Q

What is short bowel syndrome

A
  1. A malabsorptive disorder that occurs as a result of decreased functional mucosal surface are
  2. Malabsorption of macro- and micronutrients, fluid and electrolytes
  3. Severity of malabsorptive disturbances varies with:
    - age (if occurring in infancy or childhood)
    - length and location of resected bowel
    - condition of the remaining bowel
  4. Prognosis - good with 25% or more of small bowel with duodenum, proximal jejunum, and distal ileum intact
    • successful management of complex nutrition support can offer long term survival and a desirable quality of life
    • early and aggressive enteral feeding can reduce the need for Parenteral nutrition and prevent associated complications
893
Q

What is the most common cause of short bowel syndrome in infants

A
  1. Congenital anomalies ( jejunal and ileal atresia and gastrochisis)
  2. Necrotizing enterocolitis
  3. Volvulus with malrotation
  4. Small intestine resection due to long-segment Hirschsprung’s disease, omphalocele, Crohn’s disease and trauma
  5. Although rare, congenital short bowel may also be a cause of SBS in a small number of infants
894
Q

What are causes and risk factors of developing short bowel syndrome

A
  1. Radiation enteritis may lead to functional SBS if injury to small intestine mucosa is extensive
  2. Large resection of at least half of the small intestine
  3. Conditions affecting the small bowel
    - Crohn’s disease
    - Dysmotility disorders
    - Necrotizing enterocolitis
    - bowel trauma
    - bowel tumors
895
Q

What are signs and symptoms of short bowel syndrome with a total duodenal resection

A

Isolated duodenal resection is uncommon
1. Problems with absorption of proteins, fats, and fat soluble vitamins
2. May result in malabsorption of iron, folate, and calcium, possibly leading to anemia and osteopenia
3. Fat and lipid soluble vitamin malabsorption may occur in the absence of pancreatic and biliary secretions

896
Q

What are signs and symptoms of short bowel syndrome with an extensive jejunal resection

A
  1. May lead to carbohydrate malabsorption due to the loss of the primary intestinal site of disaccharridase activity
  2. Problems with absorption of proteins, fats and fat soluble vitamins
  3. Undigested and malabsorbed carbohydrate contributes to osmotic diarrhea
  4. The duodenum and jejunum are also the primary site of absorption of proteins, fats, copper, and lipid-soluble vitamins
  5. Although resection of the ileum and preservation of the jejunum may initially cause fewer complications associated with fluid and nutrient absorption, the long-term capacity for adaptation is greater in the ileum after a proximal small intestine resection than in the jejunum after a distal small intestine resection
897
Q

What are signs and symptoms of short bowel syndrome when there is an extensive resection of the ileum

A
  1. Severe fluid and electrolyte malabsorption and imbalances due to the inability of the jejunum to compensate
  2. Bile salt malabsorption, causing diarrhea and steatorrhea
  3. Vitamin B12 deficiency
898
Q

Why is it important to preserve the ileocecal valve when resecting the small intestine

A
  1. Affects prognosis because the ileocecal valve performs functions that ultimately influence enteral feeing tolerance
  2. Regulates the flow of fluid and nutrients from the small intestine into the colon and the rate of small intestine transit
  3. Prevents migration of colonic bacterial flora into the small intestine
  4. Bacterial counts in the small intestine increase dramatically when the ileocecal valve is resected as a result of the migration of colonic flora
899
Q

What are general signs and symptoms of short bowel syndrome

A
  1. Diarrhea - may be loose, watery or foul smelling
  2. Malnutrition
  3. Weight loss
  4. Abdominal pain
  5. Abdominal distension
  6. Vomiting
  7. Fatigue
  8. Heartburn
900
Q

How is small bowel syndrome diagnosed

A
  1. Confirmed based on surgical records, upper GI and small bowel contrast imaging and EGD
  2. The serum level of citrulline is a quantitative biomarker to assess remaining functional absorptive capacity
  3. Evaluation for anemia and iron, Vitamin B12, and lactose absorption and tolerance provides a clear therapeutic guideline
901
Q

What is the treatment of small bowel syndrome

A
  1. Nutritional support
  2. Medications - symptom management
  3. Surgery
902
Q

What is the nutrition support treatment for short bowel syndrome

A
  1. Rehydration
  2. Enteral feedings
  3. Parenteral nutrition
  4. Vitamin and mineral supplements
  5. Special diet
    • small frequent meals
    • avoiding foods high in fat
    • avoiding foods that cause diarrhea, such as those high in sugar, protein and fiber
  6. Follow up with dietician specializing in nutrition support
903
Q

What is the medication treatment for short bowel syndrome

A

Symptom management
1. Antibiotics to reduce bacterial overgrowth
2. H2 blockers
3. Bile salt binders
4. Hypomotility agents

904
Q

What is the surgical treatment for short bowel syndrome

A

Goals
1. Increase absorptive ability of the small intestine
2. Prevent blockage
3. Preserve remaining length of the small intestine
4. Narrow any dilated segment of the small intestine
5. Slow the time it takes for food to travel through the small intestine
6. Lengthen the small intestine

Transplantation - performed for patients
1. When other treatments have failed
2. Who have life threatening complications from long-term Parenteral nutrition

905
Q

What is lactase deficiency

A
  1. Absence of or reduced activity of lactase, the enzyme that breaks down lactose in the intestinal mucosa
  2. Most common disorder of carbohydrate absorption
  3. Also called lactose intolerance
  4. Holzel first describe defective lactose absorption in infants in 1959
906
Q

What are causes and risk factors to developing lactose deficiency

A
  1. Deficiency in the brush border enzyme lactase, which leads to malabsorption of lactose
  2. Genetics and exposure
    - similar genetic backgrounds can have different tolerances to lactose based on exposure
    - patient can acquire tolerance from repeated exposure
  3. Secondary deficiency as a result of other small bowel diseases
    - celiac sprue
    - Crohn’s disease
    - viral, bacterial or radiation enteritis
  4. Congenital lactase deficiency is a rare disorder in which mucosal lactase levels are low at birth
907
Q

What are signs and symptoms of lactase deficiency

A

Usually occur following ingestion of milk or milk products
1. Abdominal cramping
2. Distention
3. Watery diarrhea
4. Flatulence
5. Nausea

908
Q

How is lactase deficiency diagnosed

A
  1. History and physical
  2. Hydrogen breath test (lactose tolerance test)
  3. Stool acidity test
  4. Relief of symptoms with lactose-free diet and reappearance of symptoms with lactose-free diet and reappearance do symptoms with reintroduction of lactose into the diet
909
Q

What is the treatment for lactase deficiency

A
  1. Restriction of milk and milk products
  2. Use of lactose enzyme (lactase supplements)
  3. Dietician consultation
910
Q

What are potential complications of lactase deficiency

A
  1. Vitamin D deficiency
  2. Calcium deficiency
911
Q

What is abetalipoproteinemia (ABL)

A
  1. A rare autosomal recessive disorder with a frequency <1 in 100,000 people
  2. Impairs the normal absorption of fat and certain vitamins from the diet
912
Q

What are risk factors to developing abetalipoproteinemia

A
  1. The fundamental biochemical defect is a complete absence of plasma apolipoprotein (apo) beta-lipoproteins, specifically chylomicrons a very-low density lipoprotein (VLDL) and low-density lipoprotein (LDL)
  2. A deficiency of microsomal triglyceride transfer protein (MTP) activity has been suggested to be the central cause of abetaliproteinemia
913
Q

What are signs and symptoms of abetalipoproteinemia

A
  1. Fat malabsorption, acanthocytosis and hypocholesterolemia in infants
  2. Later in life, deficiency in fat-soluble vitamins associated with development of atypical retinitis pigmentosa, coagulopathy, posterior column neuropathy and myopathy
  3. GI affectations: including diarrhea and fat soluble vitamin deficiency
  4. Hepatic symptoms of elevated serum transaminases with hepatomegaly and cirrhosis
  5. Hematologic symptoms including acanthocytosis
  6. Neurological changes of the central and peripheral nervous system and demyelination
  7. Muscle involvement of the striated and smooth muscle and myositis
  8. Ophthalmic changes of pigment are retinal degeneration, loss of night vision, loss of color vision, and complete loss of vision
914
Q

What is the treatment for abetalipoproteinemia

A
  1. Dietary modification and replacement of fat-soluble vitamins
  2. A low-fat diet improves the steatorrhea and allows absorption of other nutrients essential for growth and development
  3. High dose oral fat-soluble vitamin supplementation (high oral doses of combined vitamin A and E) introduced early in therapy may help clinical outcomes
915
Q

What is chronic intestinal pseudo-obstruction (CIPO)

A
  1. A rare disorder of GI motility
  2. The clinical syndrome mimics signs and symptoms of intestinal obstruction, but no mechanical obstruction is present on evaluation
  3. CIPO is thought to be a form of dysmotility where the muscles and nerves control peristalsis are affected, resulting in altered and inefficient movement of material through the GI tract
916
Q

What are risk factors to developing chronic intestinal pseudo-obstruction

A

May be related to a functional disturbance in the interstitial cells of Cajal
The condition may be congenital or may develop with age

917
Q

What are signs and symptoms of Chronic intestinal pseudo-obstruction

A
  1. Can manifest at any age
  2. Nausea, vomiting
  3. Distention, abdominal pain
  4. Inability to have a bowel movement
  5. Failure to thrive
918
Q

How is chronic intestinal pseudo-obstruction diagnosed

A
  1. Fluoroscopic studies (x-ray, barium contrast studies)
  2. Nuclear medicine studies
  3. CT scan
  4. Gastric emptying study
  5. Antroduodenal, esophageal and intestinal motility studies
  6. Laparoscopic biopsy
  7. A thyroid evaluation as well as tests for collagen and vascular diseases , may be done
  8. Additional testing may involve a deep biopsy of intestinal muscle
919
Q

What are potential complications of chronic intestinal pseudo-obstruction

A

Malnutrition with impaired growth and development in children may occur in the absence of prompt intervention
May die within a few months to years

920
Q

What is the treatment for chronic intestinal pseudo-obstruction

A

Generally supportive in nature
1. Nutrition - enteral feedings may be given via nasogastric, Nash jejunal, gastrostomy, or jejunostomy tube
- many children tolerated tube feedings only on an intermittent basis or not at all
- these children require Parenteral nutrition is required to meet nutritional needs
- diet should be low in fat and fiber and administered in frequent small feeding
2. Pharmacotherapy - use of motility agents may be effective in alleviating symptoms in some patients
3. Decompression - gastric and/or intestinal decompression may be necessary to maintain comfort
4. Surgery - palliative surgery in the form of decompression of the bowel and colectomy may be done

Future progress with small intestine transplantation may provide an alternative treatment option

921
Q

What are small intestine tumors

A
  1. May be benign or malignant
  2. Make up less than 5% of GI tumors
  3. Usually occur in patients over 50
922
Q

What are causes of tumors of the small intestine

A
  1. Primary or secondary lymphomas
  2. Primary cancer - most likely seen in the duodenum
  3. Secondary carcinomas - relatively common and most often arise as metastasis from the breast, bronchus, or malignant melanomas
  4. Peutz-Jeghers syndrome
    - tumors may be seen from the cardiac sphincter to the anus, but are regularly present in the small bowel
    - characterized by increased pigmentation on the face, hands, feet, oral cavity, and perianal and genital area
    - Hamartomas
  5. Alpha heavy chain disease
923
Q

What are hamartomas of the GI tract

A
  1. Occur in Peutz-Jeghers syndrome (PJS)
    • characterized by multiple GI hamartomatous polyps, as well as an increased risk of various neoplasms and melanocytic maculae’s of the lips, buccal mucosa, and digits
  2. A consistent feature is jejunal polyp identification with intussusception and bleeding as usual symptoms
  3. PJS is an inherited Mendelian-dominant syndrome
924
Q

What are lymphomas of the GI tract

A
  1. May be primary, with or without involvement of the adjacent mesenteric nodes, or secondary, having spread from elsewhere
  2. In primary small intestine lymphomas, patients present with abdominal pain or obstruction
  3. In secondary lymphomas, non-alimentary complaints usually precede involvement of the gut
925
Q

What is alpha heavy chain disease

A
  1. A proliferation of lymphoid tissue that involves the IgA secretory system, leading to the production of incomplete immunoglobulin molecules made up of IgA heavy chains
  2. Clinical features of alpha heavy chain disease include severe malabsorption syndrome and frequently finger clubbing
  3. Histopathological features include plasma cell proliferation in the small intestinal mucosa and in the nodes, followed by the development of overt malignant lymphoma in most cases
926
Q

What are primary carcinomas of the small intestine

A
  1. Most likely to occur in the duodenum or the jejunum and make up 30-50% of the small intestine tumors
  2. Virtually all are adenocarcinomas
  3. Predisposing factors are alcohol abuse, Crohn’s disease celiac disease, neurofibromatosis and pre-existing adenoma
  4. Symptoms include pain, vomiting, anorexia, malaise, and nausea
  5. Diagnosis is by barium x-ray
  6. Small intestine carcinomas are usually flat, stenosing, ulcerative or polypoid
927
Q

What are secondary carcinomas of the small intestine

A
  1. Relatively common as a site of metastasis
  2. They must often arise from the breast, bronchus or are metastatic malignant melanomas
928
Q

What are carcinoid tumors

A
  1. Often found by chance during appendectomy and occur most frequently in the ileum and appendix
  2. Those that metastasize to the liver may be associated with carcinoid syndrome
929
Q

What are signs and symptoms of small intestine tumors

A
  1. Small bowel obstruction
  2. Abdominal pain and/or vomiting
  3. GI bleeding
  4. Weight loss
  5. Distended, tympanic abdomen
  6. High-pitched bowel sounds
  7. Stool may contain occult blood
930
Q

How are small intestine tumors diagnosed

A
  1. Blood studies
  2. Upright plain x-ray of abdomen
  3. Barium contrast x-rays
  4. Endoscopy and biopsy examination for lesions in the proximal duodenum
  5. Ultrasonography or CT scan
  6. Selective arteriography if the celiac axis and superior mesenteric artery
  7. Video capsule endoscopy
931
Q

What is the treatment for small intestine tumors

A
  1. Most are treated surgically
    - even secondary metastatic tumors may require palliative surgery to relieve obstruction or bleeding
  2. Multiple enterotomies are usually required to remove large polyps
  3. Protocols for treatment of lymphomas may include surgical resection in addition to radiotherapy and chemotherapy
  4. Radiation and chemotherapy of other malignant small intestine tumors have been largely ineffective
932
Q

What is lymphangiectasia of the small intestine

A
  1. In adults is a disorder with dilated intestinal lacteals, causing a loss of lymph into the lumen of the small intestine
  2. It results in hypoproteinemia, hypogammaglobulinemia, hypoalbuminemia, and reduced number of circulating lymphocytes of lymphopenia
  3. There is a resultant impairment in the absorption of chylomicrons and such fat soluble vitamins and vitamin D
933
Q

What are risk factors to developing lymphangiectasia of the small intestine

A
  1. May occur as a primary congenital disorder or secondary to abdominal or retroperitoneal carcinoma, lymphoma, chronic pancreatitis, Crohn’s disease, Whipple disease, celiac disease, or congestive heart failure
934
Q

What are signs and symptoms of lymphangiectasia of the small intestine

A
  1. Patients present with malabsorption, as well as lymphocytopenia with hypogammaglobulinemia and evidence of protein-losing enteropathy
  2. There may be bilateral lower limb edema, sometimes with lymphedema, pleural effusion and chylous ascites and low serum proteins, particularly serum albumin
  3. “Yellow-nail Syndrome” has been described in primary intestinal lymphangiectasia with dystrophic ridging and loss of nail lunula
  4. Osteomalacia (marked softening of bone) associated with vitamin D deficiency has been noted, as well as tetany secondary to hypcalcemia
  5. GI symptoms may include diarrhea with steatorrhea, abdominal pain, distention, nausea and vomiting and GI bleeding
  6. There may be increased fecal loss of protein, manifested in increased fecal alpha-1-antitrypsin
  7. Iron deficiency anemia may be at times associated with occult small intestinal bleeding
935
Q

How is lymphangiectasia of the small intestine diagnosed

A
  1. Jejunal biopsy that indicates dilated lymphatic lacteals
  2. Endoscopy may reveal white opaque spots in the duodenum
  3. Double-balloon enteroscopy has been useful in evaluating malabsorption and finding in some patients may include yellow and white submucosal plaques - most likely lymphangiectasia
  4. Video capsule endoscopy and enteroscopy may reveal more extensive changes along the small intestine
  5. Measurement of GI clearance of alpha-1-antitrypsin and stool fat quantitation may be done
  6. Prothrombin time, serum calcium, and carotene levels may be determined to assess the degree of malabsorption and nutritional deficiency
  7. MRI can evaluate intestinal, mesenteric and thoracic duct changes
  8. CT scan may be performed
  9. Lymphangiography may be used in congenital cases
936
Q

What is the treatment for lymphangiectasia of the small intestine

A

Directed towards the underlying disease
1. Therapy includes a low-fat diet with medium-chain triglyceride supplementation that leads to portal venous rather than lacteal uptake
2. Management of lower limb edema, usually with elastic bandages or stockings, is important
3. Localized resection of involved areas of the small intestine may be done
4. Other therapies include tranexamic acid (Cyklokapron, Lysteda), an anti plasmid, in an effort to normalized immunoglobulin and lymphocyte numbers
5. Octreotide (Sandostatin) has been useful but the mechanism of action has yet to be determined

937
Q

What are lower GI tract perforations

A
  1. Spontaneous or mechanical artificial hole or perforation to the lower GI tract
938
Q

What patients are at a higher risk for a lower GI tract perforation

A
  1. Diverticular disease
  2. Ischemic colitis
  3. Adhesions
  4. Obstruction
  5. Carcinoma
  6. IBD
  7. Colonic strictures
  8. Radiation colitis
  9. Poorly prepped bowel
  10. Uncooperative during colonoscopy
939
Q

What causes lower GI tract perforations

A
  1. Mechanical trauma - related to manipulation of the scope during colonoscopy
  2. Pneumatic perforation - results from over-distension with insufflated air
  3. Polypectomy (two-time increase in risk)
    • predisposing factors that can increase the chance of perforation include:
      Large polyps
      Sessile polyps
      Removal of lipomas
      - perforations secondary to polypectomy can occur up to two weeks after procedure
  4. Thermal injury - during therapeutics
940
Q

What are the signs and symptoms of a lower GI tract perforation

A
  1. Initially may have little or no pain secondary to the effects of sedation, but as the sedation wears off the pain will progressively worsen
  2. Sudden severe abdominal pain that becomes generalized
  3. Signs of peritonitis - rigid abdomen and guarding
  4. Abdominal distension
  5. Pneumoperitoneum
  6. Tympany
  7. Liver dullness
  8. Malaise
  9. Sudden change in vital signs
  10. Fever
  11. Bloody or mucopurulent rectal drainage
941
Q

How are lower GI tract perforations diagnosed

A
  1. Hole in colon or omentum visualized during procedure
  2. A flat plate x-ray of the abdomen demonstrating free air in the abdominal cavity or under the diaphragm
942
Q

What is the treatment for lower GI tract perforation

A
  1. Surgical exploration
  2. Retroperitoneal perforation, which is usually a pneumatic perforation, can be treated conservatively
    • close observation
    • symptomatic treatment
    • broad spectrum antibiotics
943
Q

What are potential complications of lower GI tract perforations

A
  1. Postoperative complications
  2. Burns
944
Q

What are colon polyps

A
  1. Discrete tissue masses found in the lumen of the bowel
  2. Some polyps may be flat and not easily visualized
  3. They usually develop in the rectum, sigmoid, and the descending colon
  4. There is a greater incidence in the ascending colon or right colon
  5. May be pedunculated or sessile
  6. Removal of polyps reduces the incidence of cancer
945
Q

What is a pedunculated polyp

A

Polyps that are to the intestinal wall by a stem

946
Q

What is a sessile polyp

A

Broad-based and attached directly to the intestinal wall

947
Q

What are different types of polyps found in the colon

A
  1. Juvenile polyps
  2. Adenomatous polyps
  3. Hyperplastic polyps
  4. Inflammatory polyps
  5. Villous adenomas
  6. Flat adenomas
948
Q

What are characteristics of a juvenile polyps

A
  1. Also called retention polyps
  2. Usually single, friable and ulcerated
  3. Tend to bleed and prolapse
  4. Peak occurrence is between 5 to 6 years of age (75% are found in children under 10 years of age)
  5. Rarely found in infants, and uncommon after early adolescence
  6. Nearly all polyps found in children are benign
949
Q

What are characteristics of adenomatous polyps

A
  1. Most do not become cancerous; however, nearly all colon cancer arises from this type
  2. Malignant potential depends on size, number, and degree of atypia
  3. Frequency and time course to become malignant is not precisely clear, but is thought to take from 3 to 7 years
950
Q

What are characteristics of Hyperplastic polyps

A
  1. Usually less than 5mm in size
  2. Most often found in the sigmoid
  3. Are not of clinical concern, but are usually biopsied to rule out adenoma
951
Q

What are characteristics of inflammatory polyps

A
  1. Also called pseudopolyps
  2. Regenerative response to inflammation
  3. Often seen in IBD
  4. Minimal potential for malignancy
952
Q

What are characteristics of villous adenomas

A
  1. Large, sessile, and bulky polyps
  2. Cauliflower appearance
  3. Usually in a distal location
  4. 30-50% have a foci of carcinoma
  5. Seen more often in those over the age of 60 years
953
Q

What are characteristics of flat adenomas

A
  1. Minimally raised erythematous discoid plaques
  2. Have a high-grade atypia in more than 30%
  3. Often multiples and seen with other small carcinomas
954
Q

What are causes of developing polyps

A
  1. Genetics
  2. Lifestyle
  3. Aging
  4. Family history
955
Q

What are signs and symptoms of colon polyps

A
  1. Typically asymptomatic, but some patients may experience bleeding
  2. Changes in caliber of stool
956
Q

How are colon polyps diagnosed

A
  1. Flexible sigmoidoscopy
  2. Colonoscopy
  3. Barium enema
  4. CT scan
957
Q

What is the treatment for colon polyps

A
  1. Endoscopic removal
  2. Surgical excision
  3. Colon resection
  4. Monitor through surveillance colonoscopy
958
Q

What are potential complications of colon polyps

A
  1. Colon cancer
  2. Large intestinal blockage
  3. Perforation
959
Q

What are inherited disorders that put patients at a higher risk for polyps

A
  1. Familial adenomatous polyposis (FAP)
  2. Gardner syndrome
  3. Peutz-Jeghers syndrome (PJS)
  4. Hereditary non polyposis colorectal cancer (HNPCC, also called Lynch syndrome)
960
Q

What is Familial adenomatous polyposis (FAP)

A
  1. Also called familial polyposis coli
  2. Characterized by the development of hundreds of adenomatous polyps
  3. The average age for development in children is in their mid-teens
  4. Polyps are less than 0.5 cm in diameter and are evenly distributed throughout the colon
  5. An inherited autosomal dominant trait
  6. Incidence is 1:7000 to 1:22000
  7. No geographic or ethnic variations
961
Q

What are signs and symptoms of familial adenomatous polyposis

A

Nonspecific
1. Hematochezia
2. Diarrhea

962
Q

How is familial adenomatous polyposis diagnosed

A
  1. Digital rectal exam
  2. Colonoscopy
  3. Procto-sigmoidoscopy
  4. Barium enema
963
Q

What is the treatment for familial adenomatous polyposis

A
  1. Due to the high incidence of colon cancer, colectomy is recommended
  2. Surveillance of small intestines
964
Q

What is Gardner’s syndrome

A
  1. Characterized by polyposis
  2. Hereditary
  3. Less common than FAP
  4. Multiple adenomatous polyps appear along the colon or other parts of the GI tract
  5. Osteomas appear on the mandible, skull and long bones
965
Q

What are signs and symptoms of Gardner syndrome

A

Similar to FAP and thought to variable expressions of a single disease
1. Hematochezia
2. Diarrhea

966
Q

What is the treatment for Gardner syndrome

A

Polyps with Gardner syndrome tend to become cancerous in 10-15 years
1. Surgical intervention is recommended
2. Surveillance

967
Q

What is Peutz-Jeghers syndrome

A
  1. Inherited as an autosomal dominant trait caused by mutations in the STK11/LKB1 gene
  2. Characterized by polyposis - non cancerous growths called hamartomatous polyps (adenomatous)
  3. Children often develop melanin deposits (small, dark-colored spots) on their lips, around and inside the mouth, near the eyes and nostrils, and around the anus
  4. Melanin deposits fade into adulthood
  5. Associated with a high incidence of cancer development
    • GI tract - colon and pancreas
    • Gynecological - cervix, ovary and breast
968
Q

What are signs and symptoms of Peutz-Jeghers syndrome

A
  1. Abdominal pain caused by mechanical blockage or intussusception - most common symptom
  2. Chronic bleeding
    - rectal bleeding and abdominal pain secondary to polyps appear during the second decade of life
  3. Been associated with precocious puberty in girls and feminizing gonadal tumors in boys
  4. Hepatic cysts, and thyroid papillary adenocarcinoma
969
Q

How is Peutz-Jeghers syndrome diagnosed

A
  1. Average age of diagnosis is 23 for males and 26 for females
  2. Upper and lower endoscopy and small bowel capsule every two years throughout life
970
Q

What is the treatment for Peutz-Jeghers syndrome

A
  1. Symptom dependent
  2. Genetic testing
  3. Surveillance for associated cancers
    • increased risk of developing GI, pancreatic breast ovarian and cervical cancer
971
Q

What is Hereditary non-polyposis colorectal cancer (HNPCC)

A
  1. Also called Lynch syndrome
  2. A gene that produces colon cancer 2 to 3 decades before typically diagnosed
  3. Mean age at diagnosis is 44.6 years, whereas in the general population the mean age is 67 years or later
  4. Cancer arises in discrete adenomas, but polyposis does not occur
972
Q

What is the criteria for Hereditary non-polyposis colorectal cancer (Lynch syndrome)

A
  1. At least three relatives with colon cancer, one must be a first-degree relative of the other two
  2. Colorectal cancer involving two generations
  3. One or more of the cancers was diagnosed before age 50 years
973
Q

What are signs and symptoms of Hereditary non-polyposis of colorectal cancer (Lynch syndrome)

A
  1. Bleeding or blood in stools
  2. Change in caliber of stools
974
Q

What is the treatment for hereditary non-polyposis colorectal cancer (Lynch syndrome)

A
  1. Surveillance with colonoscopy
  2. Colon resection depending on findings
975
Q

How is hereditary non-polyposis colorectal cancer (Lynch syndrome) diagnosed

A
  1. Genetic testing
  2. Early screening via colonoscopy
    - 10 years earlier than the first-degree relative
976
Q

What is angiodysplasia

A
  1. Also known as arteriovenus malformations (AVMs)
  2. Vascular dilatations in the submucosa that consist of arterial, venous and capillary elements
  3. Often multiple dilatations
  4. Occur most frequently in the cecum and right colon, but may be found anywhere in the GI tract
  5. Most commonly found in the elderly
977
Q

What are causes and risk factors to developing Angiodysplasias

A
  1. Most are associated with normal aging - most common in patients over the age of 50 years
  2. Etiology remains uncertain
  3. Osler-Weber-Rendu syndrome
    • genetic disorder
    • also known as hereditary hemorrhagic telangiectasia
    • AVMs are found throughout the GI tract and often on the lips and mouth
  4. Chronic medical diseases such as chronic kidney disease and valvular heart disease
  5. Benign and malignant tumors
  6. Polyps
  7. Crohn’s disease
  8. NSAIDs
    9 those over the age of 60 with no history of GI bleeding may have colonic vascular ectasia (type found in the colon)
978
Q

What are signs and symptoms of angiodysplasia

A

Some people are asymptomatic

  1. GI bleeding - may be attributed to another coexisting disorder
  2. Blood loss ranges from occult to hemorrhage
  3. Not uncommon for a person to experience several bleeding episodes before the proper diagnosis is made
979
Q

How is angiodysplasia diagnosed

A
  1. Colonoscopy
  2. Selective mesenteric angiography during active bleeding is the most accurate differentiating diagnostic technique when determining origination of bleeding
    • such as diverticula versus Ectasia
980
Q

What are potential complications of angiodysplasia

A
  1. Bleeding from vascular ectasia may range from occult to torrential
  2. Chronic anemia
  3. Lethargy
981
Q

What is the treatment for angiodysplasia

A

Asymptomatic individuals require no treatment
1. The treatment of choice for symptomatic angiodysplasia is endoscopic treatment with bipolar electrocoagulation
2. Argon plasma coagulation (APC) is an alternate option
3. If electrocoagulation is not successful, resection of the bowel segment containing the lesion may be performed
4. Rebleeding can recur in patients who are treated surgically

982
Q

What is colitis

A
  1. An inflammation of the colon
983
Q

What are different types of colitis

A
  1. Ischemic colitis
  2. Necrotizing enterocolitis
  3. Ulcerative colitis
  4. Pseudomembranous colitis
  5. Crohn’s colitis
  6. Radiation enteritis
  7. Food protein-induced enterocolitis
984
Q

What is ischemic colitis

A
  1. Acute vascular insufficiency of the colon
  2. May occur in any part of the small or large bowel, but usually affects the descending colon near the splenic flexure or the sigmoid colon
    • portions of the colon that are supplied by the inferior mesenteric artery
985
Q

What are causes and risk factors to developing ischemic colitis

A
  1. Occlusive
  2. Nonocclusive
986
Q

What are occlusive causes for ischemic colitis

A

Mechanical obstruction of blood vessels that supply the bowel due to an embolus from an artificial mitral valve or surgical bypass

987
Q

What are nonocclusive causes of ischemic colitis

A

Related to severe derangement in the central circulation as a consequence of:
1. Congestive heart failure (CHF)
2. Myocardial infarction (MI)
3. Sepsis
4. Cardiac arrhythmia
5. Medications causing:
- thrombosis
- arterial constriction
- hypotensive agents

988
Q

What are signs and symptoms of ischemic colitis

A
  1. Abrupt onset of pain in the left iliac fossa
  2. Bloody diarrhea
  3. Low grade fever
  4. Abdominal distention
  5. Mild abdominal tenderness
989
Q

How is ischemic colitis diagnosed

A
  1. Sigmoidoscopy may reveal nonspecific colitis ulcerations and/or bluish nodules - must be done carefully
  2. Barium enema shows classic diagnostic sign of thumb printing in the affected area of bowel; resulting from localized elevation of the mucosa by submucosal hemorrhage
  3. Histology may reveal characteristic apoptosis (programmed cell death)
990
Q

What is the treatment for ischemic colitis

A
  1. Most patients recover spontaneously
  2. Minority of patients develop a bowel infarction and peritonitis requiring a surgical resection
    • segmental resection with either a primary anastomosis or temporary colostomy
  3. Follow up barium enema or colonoscopy should be done 6-8 weeks post-operative to rule out ischemic strictures
991
Q

What are potential complications of ischemic colitis

A
  1. Bowel infarction and peritonitis
    - require emergent attention
  2. Ischemic strictures may occur during healing
992
Q

What is necrotizing enterocolitis (NEC)

A

A disease of focal or diffuse ulceration of the GI tract that usually occurs in the distal small bowel and/or colon

993
Q

What are causes and risk factors to developing necrotizing enterocolitis (NEC)

A
  1. Occurs almost exclusively in the neonatal period
  2. No single etiological factor has been found to be responsible
  3. Three factors acting either individually or in concert have been associated with occurrence
    -these are:
    1. Formula feeding as opposed to breast-feeding
    2. Intestinal ischemia
    3. Mucosal or systemic invasion of enteric bacteria
  4. Immaturity due to prematurity or low birth weight, including an inefficient intestinal barrier, has also been implicated as a risk factor
    • an undeveloped mucosal barrier allows bacterial invasion into the intestinal wall
  5. Sepsis and hypoxia may also contribute to the condition
994
Q

What are signs and symptoms of necrotizing enterocolitis (NEC)

A

The classic signs:
1. Abdominal distention
2. Bilious vomiting
3. Bloody stools

Other systemic signs and symptoms include:
1. Hypothermia
2. Apnea
3. Tachycardia or Bradycardia

995
Q

How is necrotizing enterocolitis (NEC) diagnosed

A

1.Radiologic studies showing pneumatosis intestinalis (air within the intestinal wall or air in the hepatic portal venous system) and dilated bowel loops
2. Colonoscopy is contraindicated due to the risk of progression to perforation as a result of insufflating more air into the colon

996
Q

What are potential complications of necrotizing enterocolitis (NEC)

A

Infection may result from perforation

997
Q

What is the treatment for necrotizing enterocolitis (NEC)

A

Largely supportive
1. Nasogastric tube
2. IV fluid replacement
3. Broad spectrum antibiotic IV therapy
4. Surgical resection of gangrenous bowel - may be necessary in cases of perforation

998
Q

What is ulcerative colitis

A
  1. A chronic and recurrent inflammation affecting the mucosa and submucosa of the large intestine
  2. Diffuse ulceration and hemorrhage, as well as congestion and edema
  3. Crypt abscesses formation
  4. Healing causes granulation that causes the large bowel to narrow and shorten and lose its haustra
  5. Periods of remission and exacerbation
  6. Inflammation often originates in the lower colon and then spreads proximal
999
Q

What are differences between ulcerative colitis and Crohn’s disease

A

Ulcerative Colitis. Crohn’s disease
1. Continuous inflammation. 1. “Skips areas” or segmental areas of ulceration with normal tissue between
Ulcerations
2. Mucosal ulceration only. 2. Ulcerations typically affect all layers of the bowel wall
3. Most often seen in the left colon and. 3. Usually seen in the right colon, involving the terminal ileum, but may involve any
Rectosigmoid areas, but at times may. Area of the GI tract from the mouth to the anus
Involve the entire colon
4. Characterized by exacerbations and. 4. Often slow and progressive
Remissions
5. May cause a shortening effect on the. 5. Can narrow the lumen with stricture formation
Bowel
6. Inconsistent mucosal cobblestoning 6. Consistent mucosal cobblestoning effect with intermittent pattern of healthy and
Effect with no patches of healthy Diseased tissue visualized
Tissue visualized in the diseased
Section
7. Diarrhea is bloody and mucopurulent. 7. Diarrhea is watery and sometimes associated with steatorrhea
8. Pseudopolyps are common. 8. Pseudopolyps are rare
9. Inflammatory masses are rare. 9. Inflammatory masses are common

1000
Q

What are causes and risk factors to developing Ulcerative Colitis

A
  1. The exact cause is not known
  2. The incidence and prevalence have drastically and rapidly grown over the last 20 years
  3. Environmental and genetic factors created altered immune response that result in inflammation of the bowel mucosa
  4. Alterations in the T-cell and cytokine responses occur
1001
Q

What are signs and symptoms of Ulcerative colitis

A

The colon mucosa develops diffuse ulceration and hemorrhage with congestion, edema and exudative inflammation in the lamina propria and submucosa
Crypt abscesses form and become necrotic, leading to bloody mucoid stools. Periods of remission often alternated with exacerbations. As crypt abscesses heal, granulation tissue forms, causing the colon to narrow and shorten, and lose its haustra

  1. Bloody, mucopurulent diarrhea - the cardinal symptom and may come with urgency
  2. Abdominal cramping
  3. LLQ tenderness or tenesmus (painful rectal cramping)
  4. Distention
  5. Nausea and vomiting
  6. Fever
  7. Dehydration
  8. Lethargy
  9. Weight loss with malnutrition
  10. Anemia
  11. Constipation due to rectal spasm that interferes with passage of stool, particularly in elderly patients
  12. Atypically, the skin, joints, eyes and liver may also be affected
    - the patient may experience a skin rash or inflamed joints
1002
Q

What are signs and symptoms of ulcerative colitis in pediatric patients

A

Present with moderate signs of systemic illness
1. Abdominal pain
2. Diarrhea
3. Hematochezia
4. Cholangitis
5. Growth failure

1003
Q

How is ulcerative colitis diagnosed

A
  1. History and physical
  2. Stool studies to rule out pathogens for ova and parasites
  3. Blood tests, such as CBC, ESR, and electrolytes
  4. Endoscopic procedures
    • colonoscopy to determine the extent of the disease
    • may be active from the rectum to the cecum
    • findings consistent with UC include granularity and increased friability of the mucosa, ulceration, and pseudopolyps
    • biopsies are done for histological verification of the disease process
  5. CT scan reveals thickened bowel
  6. Barium enema may be ordered, but is contraindicated in patients with very active or fulminant colitis
    • findings are spicules of mucosa, strictures, and loss of haustral markings
  7. Serologic markers are helpful, revealing an elevation of perinuclear antineutrophil cytoplasmic antibody(pANCA) and anti-Saccharomyces cerevisiase antibody (ASCA). A combination of positive pANCA and negative ASCA are indicative of a positive predictive value
  8. An additional sign of extensive disease is hypoalbuminemia, severe diarrhea may cause such electrolyte imbalances as hypokalemia
1004
Q

What is the differential diagnosis for ulcerative colitis

A
  1. Large bowel involvement only
  2. Continuous involvement starts in the rectum and spreads proximally
  3. Diffuse ulceration and hemorrhage
  4. Congestion and edema of mucosa
  5. Purulent appearing exudate
  6. Involves mucosa layer only
1005
Q

What are potential minor local complications of ulcerative colitis

A
  1. Pseudopolyps
  2. Hemorrhoids
  3. Anal fissures
  4. Perianal or ischiorectal abscess
  5. Rectal prolapse
1006
Q

What are more serious local potential complications of ulcerative colitis

A
  1. Massive colonic hemorrhage
  2. Colonic strictures
  3. Colonic perforation
  4. Perianal disease
1007
Q

What is pouchitis or inflammation of an ileal pouch in relation to a potential complication for ulcerative colitis

A

After surgery for UC may occur, with symptoms similar to those seen with UC

Treatment with antibiotics and anti-inflammatory agents may be required

1008
Q

What are bone related complications of ulcerative colitis

A
  1. Arthritis - a frequent extraintestinal manifestation in patients with UC, correlates with disease activity
  2. Sacroiliitis and ankylosing spondylitis - shown to be higher in patients with UC
    • defined as inflammation of one or more vertebrae and sacroiliac joint
    • these conditions are rare and occur in patients with histocompatibility marker (HLA-B27)
    • these conditions follow a course independent of intestinal disease
  3. Osteoporosis - has been reported at increased incidence in patients with UC
1009
Q

What are potential liver complications of ulcerative colitis

A
  1. Minor elevations of serum transaminase or alkaline phosphatase levels are not uncommon in UC and may be secondary to hepatic steatosis
  2. The major chronic liver disease associated with UC is sclerosing cholangitis, which is generally progressive and independent of intestinal disease
    • this may occur before UC develops and is a part of an autoimmune process
    • it may progress to liver failure
1010
Q

What are potential ophthalmological complications of ulcerative colitis

A
  1. Uveitis - inflammation of the vascular middle layer of the eye)
  2. Episcleritis - reddened eye from inflammation between the conjunctiva and the sclera
  3. Conjunctivitis may occur in children with UC
1011
Q

What are potential hematological complications that may occur with ulcerative colitis

A

Hematological abnormalities may occur, including thromboembolic disease

1012
Q

What are potential dermatological complications that can occur in ulcerative colitis

A

Erythema nodosum and pyoderma gangrenosum ( a classic manifestation of extraintestinal activity) may occur

1013
Q

What is a potential renal complication of ulcerative colitis

A

Renal disease may occur

1014
Q

What is toxic megacolon in relation to a potential complication of ulcerative colitis

A
  1. An acute dilatation of the diseased colon (with colonic diameter of greater than 6-7cm) that is associated with systemic toxicity
  2. Is is the most severe and life-threatening complication of UC
    • mortality rates are higher in patients with UC perforation but may also be associated with any severe inflammatory conditions of the bowel, including Crohn’s disease, bacterial colitis, and amebiasis
  3. In some patients with UC toxic megacolon presents as the first attack, but it is relatively rare in young patients
1015
Q

What are the prominent symptoms of toxic megacolon

A
  1. Fever
  2. Elevated heart rate
  3. Abdominal pain
  4. Vomiting
  5. Dehydration
  6. Mental changes
  7. Electrolyte disturbance
  8. Hypotension
  9. Fatigue
  10. May experience a progressive decrease in frequency of stools, as well as, markedly hypoactive or absent bowel sounds resulting from a loss of colonic propulsive activity
  11. Leukocytosis
  12. Anemia
  13. Hypomagnesemia
  14. Hypoalbuminemia
1016
Q

How is toxic megacolon diagnosed

A

Plain x-ray films of the abdomen will reveal dilatation of the entire colon or only the transverse colon

1017
Q

What are potential catastrophic complications of toxic megacolon

A
  1. Colonic perforation
  2. Gram-negative sepsis
  3. Massive hemorrhage
1018
Q

Who is more likely to develop toxic megacolon

A
  1. Patients with pancolitis
    - they are moser apt to develop the condition early in the course of the disease, most often with the first episodes of colitis
    - early recognition of the condition with prompt intervention is key to a positive outcome is key
1019
Q

In relation to ulcerative colitis why is adenocarcinoma of the colon a potential complication

A
  1. Patients are at increased risk
  2. The risk of cancer is related to the extent of colon involvement and the duration of the disease
  3. The risk of developing cancer becomes greater 8-10 years after diagnosis and increases with time
  4. The cancers that develop are largely submucosal
  5. For surveillance purposes, it is recommended that colonoscopy be performed yearly after 10 years of disease identification
  6. If no dysplasia or adenoma is found on initial colonoscopy, monitoring should be done every 2 years
  7. Specimens for mucosal biopsy are taken every 5-10cm
  8. Ten areas should be sampled
1020
Q

What is the treatment for ulcerative colitis

A

Goal of therapy is to reduce inflammation and return to normal lifestyle

  1. Diet therapy
  2. Medication
  3. Surgery
1021
Q

What is the dietary treatment for ulcerative colitis

A
  1. In adults, avoidance of foods that appear to aggravate symptoms
  2. In children, nutritional therapy to correct nutritional deficiencies and provide supplemental calories, optimal healing, and growth requirements
  3. In those with strictures, fiber restriction
  4. In those with lactose intolerance, lactose avoidance
1022
Q

What is the drug therapy treatment for ulcerative colitis

A
  1. Anti-inflammatories
  2. Corticosteroids
  3. Immunosuppressive agents
  4. Biologicals
1023
Q

What anti-inflammatory medications are used in the treatment of ulcerative colitis

A
  1. Sulfasalazine (Azulfidine)
  2. Mesalamine (Asacol HD, Pentasa, Rowasa, Apriso, Delzicol, Lialda)
1024
Q

What corticosteroids are used in the treatment for ulcerative colitis

A
  1. Budesonide (Entocort EC, Uceris)
  2. Other steroids such as prednisone are used for acute exacerbation or flares
1025
Q

What immunosuppressive agents are used in the treatment for ulcerative colitis

A

Also called tumor necrosis factor (TNF) inhibitors
1. 6-Mercaptopurine
2. Azathioprine (Imuran)
3. Methotrexate (Trexall)
4. Cyclophosphamide (cytoxan)

1026
Q

What biological agents are used in the treatment for ulcerative colitis

A
  1. Infliximab (Remicaide)
  2. Adalimumab (Amjevita, Cytezo, Humira)
  3. Vedolizumab (entyvio)
  4. Golimumab (Simponi)
1027
Q

When is surgery a treatment option for ulcerative colitis

A

Bedrest, possibly in the hospital for acute exacerbation
1. Surgery is required in 20% of patients, during the course of disease
2. Includes treatment for conditions such as exxsanguinationing hemorrhage, perforation, documented or strongly suspected carcinoma, severe colitis with or without toxic megacolon, unresponsiveness to conventional maximal medication therapy, intractable symptoms or intolerable steroid side effects
3. In children growth failure is considered a form of intractability of the disease and therapy should be initiated prior to epiphyseal closing that occurs during puberty
4. Colectomy is a curative procedure
5. Emergency colectomy may be required in toxic megacolon
6. Surgery may be a total proctocolectomy with a permanent ileostomy; a one stage procedure

1028
Q

What is pseudomembranous colitis

A
  1. An acute inflammation of the bowel mucosa with the formation of pseudomembranous plaques overlying an area of superficial ulceration
  2. Also called pseudomembranous enterocolitis
  3. Antibiotic-associated colitis or diarrhea or C. Diff associated colitis or diarrhea
  4. Community-acquired C. Diff - associated diarrhea is reported at an estimated 450,000 cases reported
    • 12.1% is reported among hospitalized patients
  5. Any disturbance in the micro flora ecosystem within the colon can account for the increased incidence among hospitalized patients
1029
Q

What are causes and risk factors to developing pseudomembranous colitis

A
  1. Antibiotic associated - usually seen within 10 weeks after the start of antibiotics
  2. C. Diff associated - toxin or toxins produced by C. Diff
  3. Radiation enteritis
    - results of radiation for pelvic intra-abdominal or retroperitoneal malignancies
    - 5-15% of patients experience severe chronic damage
    - two types
    • acute - occurs during treatment as a result of functional changes at the cellular level
    • chronic - results from abnormalities in vascular or connective tissue appearing 3 months to 30 years post exposure
1030
Q

What are signs and symptoms of pseudomembranous colitis

A

Acute phase
1. Nausea
2. Cramping
3. Altered bowel habits
4. Diarrhea
5. Tenesmus (feeling the urge to defecate, even when bowels are empty)
6. Rectal emptying

Chronic phase
1. Proctocolitis
2. Bleeding
3. Strictures
4. Perforation
5. Fistula

1031
Q

How is pseudomembranous colitis diagnosed

A
  1. GI contrast with small bowel follow-through
  2. Large bowel biopsy
  3. Lactose hydrogen breath test
  4. Fecal fat collection
  5. Endoscopy to detect typical red edematous, fragile mucosa with yellow-white raised plaques that may extend from the rectosigmoid area to the proximal colon
  6. The most useful diagnostic test is the demonstration of toxins A and B in the stool, using either enzyme-linked immunosorbent assay (ELISA) or counterimmunoeclectrophoresis (CIE)
1032
Q

What are potential complications of pseudomembranous colitis

A
  1. Toxic megacolon
  2. Pneumoperitoneum
  3. Severe electrolyte imbalance
  4. Hypoalbuminemia
  5. Acute migratory poly arthritis
1033
Q

What is the treatment for pseudomembranous colitis

A

Usually self-limited; although diarrhea can last for 4-6 weeks
1. Adjust radiation exposure
2. Antiemetics
3. Bulk forming agents
- an agent that binds the C. Diff toxin such as Cholestyramine or Colestipol (Colestid)
4. Antidiarrheal agents
5. Drug therapy - including steroid enemas and 5-ASAs
- an agent that eradicates the organism all together such as Flagyl or oral vancomycin for 10 days
6. Dilation of strictures
7. Surgery for:
- complete obstruction
- uncontrolled bleeding
- perforation
- fistulas
8. C. Diff may recur in approximately 20% of patients following 7-14 days of therapy
- probiotics with Saccharomyces boulardii or lactobacillus rhamnosus may be used to prevent reinfection
9. The current treatment for intractable C Diff-associated diarrhea is fecal transplant therapy or fecal microbiota transplantation in which healthy donor stool is used to restore the flora of the colon that is resistant to C. Diff

1034
Q

What is Crohn’s colitis

A

The disease can occur anywhere in the GI tract but when it is only located in the colon it is referred to as Crohn’s colitis

1035
Q

What are signs and symptoms of Crohn’s colitis

A
  1. May resemble UC, but the ulceration is often longitudinal and involves the full thickness of the bowel disease
  2. The disease is often segmental
1036
Q

How is Crohn’s colitis diagnosed

A

Colonoscopy

1037
Q

What are potential complications of Crohn’s colitis

A
  1. Stricture formation is common
  2. Fistulas are a frequent complication, especially in the perineum
1038
Q

What are treatment options for Crohn’s colitis

A

The same as Crohn’s in other parts of the GI tract

1039
Q

What is radiation enteritis

A
  1. Inflammation or damage of the intestinal lining usually caused by traditional therapy
  2. Many patients experience mild, acute symptoms during treatment, but some experience severe, chronic damage
1040
Q

What are risk factors to developing radiation enteritis

A

When radiation injury occurs to the GI tract, it is usually a result of radiotherapy for pelvic, intra-abdominal or retroperitoneal malignancies such as carcinoma of the cervix, prostate, bladder, testicle or ovary

1041
Q

What are signs and symptoms of radiation enteritis

A
  1. The acute phase of radiation enteritis occurs during treatment and is related to alterations in the epithelial cell function
    2.it is characterized by:
    - nausea
    - cramping
    - altered bowel habits
  2. If the colon is involved there may be acute proctocolitis with diarrhea, tenesmus, and rectal bleeding
  3. The chronic phase of radiation enteritis results from abnormalities in vascular and connective tissue
  4. Symptoms may appear 3 months to 30 years after radiation treatment
  5. When the colon and rectum are involved, proctocolitis, bleeding, strictures, perforation and fistula formation may result
1042
Q

How is radiation enteritis diagnosed

A
  1. Upper GI contrast study with small intestine follow-through
  2. Lactose breath hydrogen test
  3. Fecal fat collection
  4. Small intestine biopsy
1043
Q

What are potential complications of radiation enteritis

A

Chronic enteritis is often an intractable and progressive disease associated with significant morbidity and mortality

1044
Q

What is the treatment for radiation enteritis

A
  1. In the acute phase of radiation enteritis, the extent of injury can be controlled by altering the size and timing of radiation dosage and by using antiemetics, bulk forming agents, and antidiarrheal agents
  2. Medical management for radiation enteritis consists of administration of steroid enemas, sulfasalazine (Azulfidine) and transfusions for chronic bleeding
  3. Strictures can be dilated manually or by using a colonoscope
  4. Radiation proctitis is treated with argon plasma coagulation
    - most times it takes several return treatments for effective control of bleeding
  5. Surgery may be used selectively in patients with complete obstruction, uncontrolled bleeding, perforation, or fistulas
    • complications and disease progression following surgery are common
    • resection is recommended for localized disease, but bypass is preferred for more extensive disease
1045
Q

What is food protein-induced enterocolitis

A
  1. Sometimes referred to as cow’s milk protein-induced enterocolitis
  2. May be present soon after birth or up to 6 months of age
1046
Q

What are risk factors to developing food protein-induced enterocolitis

A
  1. The exact mechanism of the hypersensitivity reaction to cow’s milk and other food proteins is not known, and there is a wide spectrum of clinical presentation
  2. This syndrome has been found to occur even in breast-fed infants who are sensitized to cow’s milk protein through the mother’s diet
  3. Reactivity to soy proteins may occur in as many as 40% of those with cow’s milk protein-induced enterocolitis
1047
Q

What are signs and symptoms of food protein-induced enterocolitis

A

Classic manifestations include:
1. Vomiting
2. Diarrhea
3. Poor weight gain
4. Hematochezia
5. Irritability

1048
Q

How is food protein-induced enterocolitis diagnosed

A

Diagnosis made by:
1. Withdrawal and challenged with the offending protein
2. Supportive evidence can be gained by small intestine and/or rectosigmoid biopsies revealing increased plasma cell content of the lamina propria, along with eosinophilia

1049
Q

What is the treatment for food protein-induced enterocolitis

A

May involve:
1. Simply switching to a hypoallergenic formula or
2. If severe, total Parenteral nutrition with bowel rest, followed by slow reintroduction of feedings via a nasogastric tube using a synthetic elemental formula

1050
Q

What is irritable bowel syndrome

A
  1. Functional disorder of motility of the small and large intestines
  2. No evidence of anatomic abnormality
  3. The most common GI disorder in the US
  4. The most frequent reason for outpatient visits to GIs at about 3million office visits per year
  5. It ranks close to the common cold as a frequent cause of work absenteeism
1051
Q

What are causes and risk factors to developing irritable bowel syndrome

A
  1. Diet
  2. Stress
  3. Bowel habits
  4. The anatomical cause is unknown
  5. Thought to be a disturbance in the autonomic and enteric nervous systems of the gut and the gut-brain axis
  6. The results are abnormal motility and visceral hypersensitivity, and it has been suggested that these abnormalities are secondary to psychological disturbances
  7. Evidence regarding the role of immune activation in the etiology of IBS continues to increase
  8. More common in Jewish and white populations
  9. The female predominance that is found in adults doses not exist in children
  10. 75% of children with IBS, at least one parent or sibling has a functional GI disorder
  11. In Western countries, 6% of middle school and 14% of high school children are found to experience this condition
1052
Q

What are signs and symptoms of irritable bowel syndrome

A
  1. Chronic and intermittent pain and spasm
  2. Diarrhea, constipation, or both
    - diarrhea - accelerated transit time
    - constipation - delayed transit time
  3. Bloating, distention, and flatulence
  4. Symptoms vary in pattern and intensity
  5. Additional symptoms include increased straining, urgency, feeling of incomplete evacuation, appearance of mucus, and change in the caliber or appearance of stool
1053
Q

How is irritable bowel syndrome diagnosed

A
  1. Signs and symptoms
  2. Rule out IBD
  3. Endoscopic procedures
1054
Q

What are potential complications of irritable bowel syndrome

A

Functional complications
1. Although it is associated with severe discomfort, IBS is not related to other chronic or life-threatening conditions or with decreased longevity

1055
Q

What is the treatment for irritable bowel syndrome

A
  1. Sympathetic diagnosis and reassurance that organic causes have been ruled out, including thyroid disease, lactose intolerance, and fructose intolerance
  2. A high-fiber diet at 25-35 grams daily
  3. Anticholinergic agents to decrease abdominal pain such as diphenoxylate/atropine sulfate (Lomotil) and dicyclomine (Bentyl)
  4. Antidiarrheals such as loperamide (Imodium A-D)
  5. Laxatives
  6. Psychological support and drug therapy, which may include antidepressants aimed at decreasing anxiety that may be related to stress such as despiramine (Norpramin) or amitriptyline
  7. Addition of probiotics containing Bifidobacterium infantis such as Bifantis, Align, Florastor, Phillips Colon Health, or VSL#3
  8. Serotonin receptor agonists (5-HT4) to decrease colonic motility such as alosetron (Lotronex)
  9. Rifaximin (Xifaxan) for bacterial overgrowth
    10 Peppermint oil as an antispasmodic to relax intestinal smooth muscle. It is available in an enteric coated preparation (Colpermin)
1056
Q

What are chronic and recurrent abdominal pain syndromes

A
  1. Chronic Abdominal Pain (CAP) and recurrent abdominal pain (RAP) are common disorders in childhood and adolescence
  2. Apley first described CAP of either continuous abdominal pain or intermittent abdominal pain also called recurrent abdominal pain, occurring in school-age children, persisting for more Thant 3 months and affecting normal activity
1057
Q

What are risk factors to developing chronic and recurrent abdominal pain syndromes

A
  1. Thought to be a manifestations of IBS in pediatric patients
  2. Reported to occur in 10% of children and about 2% of adults, mostly female
  3. The etiology and pathogenesis of the pain with this syndrome is unknown; however, the prevailing viewpoint revolved around a disorder of GI motility and/or visceral hypersensitivity
1058
Q

What are signs and symptoms of chronic and recurrent abdominal pain syndromes

A

Children with chronic or recurrent abdominal pain experience the pain
1. With only occasional bloating, dyspepsia, and alteration of bowel patterns
2. Associated symptoms in children include headache, pallor, dizziness, and nausea

1059
Q

How is chronic and recurrent abdominal pain syndromes diagnosed

A

In most cases, only limited evaluation is indicated to rule out organic causes

1060
Q

What are potential complications of chronic and recurrent abdominal pain syndromes

A

Although IBS and chronic or recurrent abdominal pain may be associated with severe pain and discomfort, they do not predispose a patient to other chronic or life-threatening conditions, and there is no evidence that they interfere with longevity

1061
Q

What is the treatment for chronic and recurrent abdominal pain syndromes

A
  1. Careful counseling and explanation regarding the condition is key
  2. Emphasis on acknowledging the presence and severity of the pain is important for both the parent and child
  3. Use of a high-insoluble fiber diet is somewhat controversial but has been shown to be of some benefit
  4. There is no data to support the use of drug therapy in children with chronic or recurrent abdominal pain, and it may lead to hypochondriasis
  5. Consultation with a child psychologist may be beneficial if stress or maladaptive coping mechanisms are identified
1062
Q

What are parasitic infestations of the colon

A
  1. Amebiasis
  2. Trypanosomiasis
  3. Trichuriasis
1063
Q

What is Amebiasis

A
  1. A form of colitis caused by the protozoan Entamoeba histolytica
  2. In the US, E. Histolytica represents the third most frequently identified protozoan from human specimens
1064
Q

What are risk factors to developing amebiasis

A
  1. Transmitted primarily by fecal contamination of food or water but other modes of transmission include close interpersonal contact, venereal spread, and houseflies and cockroaches
  2. Ingested cysts form trophozoites in the small bowel, which are then released into the colon
  3. It may take only one cyst to cause infection in a susceptible host
  4. Approximately 50,000 cysts are produced annually in a patient with invasive E. Histolytica
  5. The amebae penetrate host tissues, causing necrosis without inflammation
  6. Lesions are located throughout the colon, most often in the cecum, ascending colon, and rectosigmoid colon areas
1065
Q

What are signs and symptoms of amebiasis in the colon

A

Carriers of E. Histolytica are often asymptomatic but symptoms include:
1. Amebic diarrhea, an afebrile illness that is usually intermittent and followed by constipation
2. Amebic dysentery, associated with headache, nausea and vomiting, fever and chills, tenesmus, abdominal cramps, and stools with a large amount of blood-tinged mucus
3. Amebic appendicitis, an obstruction of the appendix lumen
4. Ameboma, a large, mass-like lesion in the wall of the intestine, most often in the cecum
5. Visceral abscess, particularly a single abscess in the right lobe of the liver, which ruptures in a small number of cases

1066
Q

How is amebiasis diagnosed

A
  1. Demonstration of E. Histolytica trophozoites and cysts in the stool
  2. Sigmoidoscopy and indirect hemagglutination tigers may be useful diagnostic tools and barium enema may be helpful in diagnosing amebomas
  3. Additional serologic tests may be helpful. These include counter immunoelectrophoresis and agar gel diffusion
    • EIA is positive in 95% of patients with extraintestinal infection and 70% of patients with active infection
  4. Final diagnosis is passed on identifying the pathology or trophozoites on examination of the aspirated material
  5. In cases of suspected liver abscess, liver-spleen scan, abdominal ultrasonography, or CT scan, radiography, MRI, or Percutaneous needle aspiration may be used
  6. When there is liver involvement, patients have elevated alkaline phosphatase
1067
Q

What are potential complications of amebiasis

A
  1. Colon perforation
  2. Pleuropulmonary conditions
  3. Amebic brain abscesses claim a high mortality rate
1068
Q

What is the treatment for amebiasis

A
  1. Oral antiprotozoal, most often diiodohydroxyquinoline - also called iodoquinol (Yodoquin, Diquinol, Yodoquinol, Yodoxin) with or without Flagyl
  2. With appropriate treatment, response to therapy is often dramatic and prognosis is excellent
1069
Q

What is trypanosomiasis

A
  1. A chronic illness caused by the protozoan trypanosoma cruzi (T. Cruzi), which causes Chagas’ disease, also known as South American trypanosomiasis
  2. The parasite multiplies rapidly at the site of inoculation, producing a severe inflammatory reaction
  3. It may be disseminated through the bloodstream to any organ, particularly the heart, esophagus or colon
  4. At the site of infection, the parasite causes degeneration of the intramuscular autonomic nerve plexuses, resulting in megaesophagus, megacolon or dilatation of other tubular organs many years after the initial infection
  5. Symptomatic Chagas’ disease has been confined largely to rural areas of south and Central American but is has been found in all western hemisphere countries except Guyana, Surinam, and Canada
1070
Q

What are risk factors to developing trypanosomiasis

A
  1. Transmitted primarily by the bite of the reduviid bug, but may also be transmitted by damage to the placenta during birth, blood transfusion or contaminated food
1071
Q

What are signs and symptoms of trypanosomiasis

A
  1. Acute Chagas’ disease is most often seen in children under age 2
  2. Symptoms include:
    - anorexia
    - nausea and vomiting
    - generalized lymphadenopathy
    - diarrhea
    - unilateral conjunctivitis
    - edema of the face and eyelids
    - swelling of the lacrimal and submaxillary glands
    - hepatosplenomegaly
    - cardiac arrhythmias
    - congestive heart failure
    - frequently death
1072
Q

How is trypanosomiasis diagnosed

A

1.Identification of T. Cruzi in blood or tissue
2. Trypanosomes may be found in cerebrospinal fluid (CSF) cultures

1073
Q

What is the treatment for trypanosomiasis

A

For active infections:
1. Prolonged oral administration of nifurtimox (Lampit) or benznidazole (Radanil, Ro7-1051, Rochagan) is effective
2. Ultimately surgery may be required to correct the “mega syndromes” which include megaesophagus and megacolon
3. Treatment of the illness is unsatisfactory after a certain period of time

1074
Q

What is trichuriasis

A
  1. Caused by the nematode Trichuris trichiura
  2. Also known as whip worm because of the whip-like appearance of the parasite
  3. Whip worm is most often found in tropical areas or in areas of poor sanitation
  4. The life span of the adult worm can range from 1-8 years
  5. Each female worm can produce as many as 3,000-20,000 eggs
  6. 604-795 billion people are affected worldwide
1075
Q

What are risk factors to developing trichuriasis

A
  1. Transmission is fecal-oral
  2. The ingested eggs hatch in the duodenum
  3. When the larvae mature into adult worms, they migrate down the GI tract and accumulate in the cecum and ascending colon
1076
Q

What are signs and symptoms of trichuriasis

A

The majority of patients are asymptomatic
Heavy infestations may cause:
1. Dehydration
2. Weakness
3. Abdominal distention and cramping
4. Anorexia
5. Weight loss
6. Acute and chronic diarrhea
7. Bloody mucoid stools
8. Anemia
9. Occasionally rectal prolapse
10. There is usually low-grade eosinophilia

1077
Q

What are potential complications of trichuriasis

A

In children, chronic heavy infestation may be an important contributor to impairment of growth and development

1078
Q

How is trichuriasis diagnosed

A
  1. Requires identification of the characteristic eggs in the stools, or rarely, detection of the worms by sigmoidoscopy or colonoscopy
  2. The worms may be visualized hanging in the intestinal lumen or buried within the wall
1079
Q

What is the treatment for trichuriasis

A

Treatment is dependent on the type of the infection (T.b. Gambiense or T.b. Rhodesiense) and the stage of the disease
1. The recommended drug for first-stage T.b. Gambiense infection is pentamidine, which is widely available in the US

1080
Q

What is diverticular disease

A
  1. Diverticula are a herniation of the colonic mucosa through the muscular layer of the colon
  2. Formation of diverticula increases with age, as strength and elasticity of the colon decreases
  3. Occurs in 30-50% of adults over the age of 50 years
  4. 96% of the time occurs in the sigmoid colon
  5. More common in highly industrialized countries due to diets low in fiber
  6. Asian countries have traditionally seen lower incident rates
  7. In migrants from low-prevalence areas to westernized countries, diverticular disease incidence increases within 10 years
  8. May take the form of diverticulosis or diverticulitis
1081
Q

What is diverticulosis

A

Uncomplicated diverticular disease

1082
Q

What is diverticulitis

A
  1. An inflammation in the wall of the diverticulum at its apex and, rarely, at its neck.
  2. It occurs most often in the sigmoid colon and adjacent structures and may last for several weeks
1083
Q

What are risk factors to developing diverticular disease

A
  1. Hypertrophy of segments of the colon’s circular muscle
  2. Increased intraluminal, intracolonic pressure from uncoordinated peristalsis
  3. Age-related atrophy or weakness in the bowel muscles (rare in people younger than age 40)
  4. Chronic constipation and straining
  5. Lack of dietary fiber
  6. Obesity
  7. Inadequate luminal contents
1084
Q

What are signs and symptoms of diverticulosis

A
  1. Show no signs of infection, most are asymptomatic
  2. Approximately 20% of individuals with diverticulosis present with symptoms
  3. Symptoms include
    - bloating
    - excessive flatulence
    - irregular defecation
    - intermittent abdominal pain
1085
Q

What are signs and symptoms of diverticulitis

A
  1. Low-grade fever
  2. Localized or diffuse abdominal pain
  3. Nausea and vomiting
  4. Constipation
  5. Palpable sigmoid
  6. Mild leukocytosis (predominantly of polymophonuclear leukocytes)
  7. Obstipation

In children the most common type of diverticulum of the GI tract to become symptomatic is Meckel’s diverticulum

1086
Q

How is diverticulosis diagnosed

A

Confirmed by barium enema or colonoscopy

1087
Q

How is diverticulitis diagnosed

A
  1. Patient complaint of severe abdominal pain
  2. X-ray films
  3. Proctosigmoidoscopy and CT scan
  4. CT scan is preferred, as it will reveal abscess formation, perforation, bowel thickening and disease extent
  5. While blood cell count is an additional evaluative test
1088
Q

What are potential complications of diverticular disease

A
  1. Rupture of an inflamed diverticulum, with localized or generalized peritonitis
  2. Abscess formation around the diverticulum
  3. Edema or spasm related to inflammation
  4. Vesicocolonic fistula formation
  5. Erosion of an artery or vein with bleeding
  6. Colonic fibrosis and narrowing possibly leading to obstruction
  7. Patients may develop bacteremia and septicemia
  8. Repeated attacks of diverticulitis May cause abscesses
1089
Q

What is the treatment for diverticular disease

A
  1. Mildly symptomatic diverticular disease usually involves dietary management, most often in the form of a high-fiber diet and use of hydrophilic colloids or bulk-forming laxatives to help maintain a regular soft stool
  2. Acute attacks may require hospital admission, bed rest, IV antibiotics, bowel rest, and analgesics. Slow progression of diet from clear liquids to low fiber then to high fiber will follow bowel rest
  3. Colonic strictures, peritonitis, or septicemia may require surgical intervention in the form of a colon resection (one-stage) or a temporary diverting colostomy (two-stage procedure when continuity of bowel function is restored). Surgical mortality rates are 3%
  4. Abscesses may be treated using Percutaneous drainage
  5. Bleeding is treated through arteriography with injection of sclerosing agents to occlude the bleeding vessel, vasopressin (vasostrict), or vessel embolization. Mesalamine (5-aminosalicylic acid) may aid in decreasing diverticulitis attacks
1090
Q

What is acute diverticulitis

A
  1. Inflammation in the wall of the diverticulum at the apex, rarely at the neck
  2. More common in the sigmoid
  3. May last for several weeks
1091
Q

What are causes of acute diverticulitis

A
  1. Hypertrophy of segments of the colon’s circular muscle
  2. Increased intracolonic pressure
  3. Age related atrophy or weakness of the bowel muscles
  4. Chronic constipation
  5. Irregular, uncoordinated bowel movements
  6. Diet low in fiber
  7. Obesity
1092
Q

What are signs and symptoms of acute diverticulitis

A
  1. Fever
  2. Left lower quadrant (LLQ) pain
  3. Nausea and vomiting
  4. Constipation
  5. Palpable sigmoid
1093
Q

How is acute diverticulitis diagnosed

A
  1. Abdominal pain
  2. X-ray
  3. Sigmoidoscopy
  4. CT scan

Barium enema is NOT recommended as it can worsen the attack or cause perforation

1094
Q

What is the treatment for acute diverticulitis

A
  1. Bowel rest
  2. Broad spectrum antibiotics
  3. Pain management
  4. Surgery is recommended in 15-30% of patient with recurrent episodes
1095
Q

What are potential complications of acute diverticulitis

A
  1. Repeated attacks may lead to pericolic abscesses
  2. Rupture of an inflamed diverticulum
  3. Edema or spasm related to inflammation
  4. Vesicocolic fistula formation
  5. Erosion of an artery or a vein resulting in diverticular bleed
  6. Colonic fibrosis leading to stricture formation and obstruction
  7. Peritonitis
  8. Septicemia
1096
Q

what is colorectal cancer

A
  1. The third most common cancer type in adults in the US, after lung cancer in men and breast cancer in women
  2. It occurs most frequently in people between ages 50 and 80
  3. Incidence is 1 in 23 in the US and 16.1-32.2 per 100,000 people in Asian countries
  4. Approximately 95% of intestinal cancers are adenocarcinomas
  5. Types of adenocarcinomas include mucinous or colloid varieties
  6. In adults, mucinous tumors comprise 15% of colorectal carcinomas and as many as 40% in children
  7. African Americans have a higher incidence than other racial groups in the US
  8. Currently, the highest percentage of colorectal cancers in the US in Caucasians are located in the cecum and ascending colon (22% in males and 27% in females) and in the sigmoid colon (25% in males and 23% in females)
  9. Cancers of the colon in children tend to be more evenly distributed throughout the large intestine
  10. Metastasis usually involves the liver
1097
Q

What are causes and risk factors to colorectal cancer

A

Believed to be an acquired genetic disease caused by exposure to environmental carcinogens
Risk factors include
1. Lifestyle factors, including:
- low-fiber diet with high intake of fat and high-fat red meat and/or processed meats
- a sedentary lifestyle
- smoking
- being overweight or obese
- heavy alcohol use
2. Increasing age
3. Family history of colon or rectal cancer
4. Previous colon cancer
5. Personal history of adenomatous polyps
6. Familial adenomatous polyposis (FAP) or Gardner syndrome
7. UC for more than 7 years
8. Genital cancer or breast cancer (in women)
9. Genetic alterations in KRAS, APC, DCC, and TP53 genes in hereditary non polyposis colorectal cancer (HNPCC) or Lynch syndrome

1098
Q

What are different types of tests used for screening for colon cancer for those at average risk

A

Beginning at age 45

  1. Flexible sigmoidoscopy - done every 5 years and if positive a colonoscopy should be performed
  2. Fecal occult blood test (FOBT) - yearly and if positive a colonoscopy should be performed
  3. Colonoscopy - every 10 years, it provides an opportunity to visualize, sample and/or remove significant lesions
  4. Double contrast barium enema (DCBE) - every 5 years and colonoscopy should be done if positive
  5. CT colonography (Virtual colonoscopy) - every 5 years and colonoscopy should be done if positive
  6. Fecal ummunochemical test (FIT) - yearly colonoscopy should be done if positive
  7. Stool DNA (sDNA) test - every 3 years and colonoscopy should be done if positive
1099
Q

How often is screening necessary for those at high risk for colon cancer

A
  1. Small rectal Hyperplastic polyps - same as those as average risk colonoscopy
    - those with Hyperplastic polyposis syndrome are at an increased risk for adenomatous polyps and cancer and should be more intensive follow-up
  2. 1 or 2 small (less than 1cm) tubular adenomas with low-grade dysplasia - 5 years after the polyps are removed - colonoscopy
    - time between tests should be based on other factors, such as prior colonoscopy findings, family history, and patient and doctor preferences
  3. 3-10 adenomas, a large (1cm or greater) adenoma, or any adenomas with high-grade dysplasia or villous features - 3 years after the polyps are removed - colonoscopy
    - adenomas must have been completely removed. If colonoscopy is normal or shows only 1 or 2 small tubular adenomas with low-grade dysplasia, future colonoscopies can be done every 5 years
  4. More than 10 adenomas on a single exam - within 3 years after the polyps are removed - colonoscopy
    • doctor should consider the possibility of a genetic syndrome such as FAP, HNPCC, or lynch syndrome
  5. Sessile adenomas that are removed in pieces - 2-6 months after adenoma removed - colonoscopy
    - if the entire adenoma has been removed, further testing should be based on doctor’s judgement
  6. Diagnosed with colon or rectal cancer - time of colorectal surgery, or can be 3-6 months later if person doesn’t have cancer spread that can be removed - colonoscopy to view entire colon and remove all polyps
    -if the tumor presses on the colon or rectum and prevents colonoscopy, CT colonoscopy with IV contrast or double contrast barium enema may be done to look at the rest of the colon
  7. Had colon or rectal cancer removed by surgery - within 1 year after cancer resection or 1 year after colonoscopy to make sure the rest of the colon and rectum are clear - colonoscopy
    -if normal, repeat exam in 3 years. If 3-year follow up exam is normal then, repeat exam every 5 years. Time between tests may be shorter if polyps are found or there is reason to suspect HNPCC or other hereditary polyp syndromes. After low anterior resection for rectal cancer, exams of the rectum may be done every 3-6 months for the first 2-3 years to look for signs of recurrence
  8. Colorectal cancer or adenomatous polyps in any first degree relative before age 50 or in 2 or more first degree relatives at any age (if not hereditary syndrome) - age 40 or 10 years before the youngest case in the immediate family’s whichever is earlier - colonoscopy
    - every 5 years
  9. Colorectal cancer or adenomatous polyps in any first-degree relative age 50 or younger or in at least 2 second-degree relatives at any age - age 40 colonoscopy
    - same intervals as for those at average risk
  10. FAP - age 10-12 years - yearly flex sig to look for signs of FAP; counseling to consider genetic testing if it hasn’t been done
    - if genetic test is positive, removal of the colon (colectomy) should be considered
  11. HNPCC or Lynch syndrome or at an increased risk based on family history without genetic testing - age 20-25 years, or 10 years before the youngest case in the immediate family - colonoscopy every 1-2 years; counseling to consider genetic testing if it hasn’t been done
    - genetic testing should be offered to first-degree relatives of people found to have HNPCC or Lynch syndrome mutations by genetic tests. It should also be offered if 1 of the first 3 of the revised Bethesda Guidelines criteria is met
  12. Inflammatory bowel disease: chronic UC or Crohn’s - cancer risk begins to be significant 8 years after the onset of pancolitis (involvement of entire large intestine) or 12-13 years after the onset of left-sided colitis - colonoscopy every 1-2 years with biopsies for dysplasia
    - recommend referral to a center with experience in the surveillance and management of inflammatory bowel disease
1100
Q

What are signs and symptoms of colorectal cancer

A

Depends on the location
1. Right-sided tumor:
- Melanie stools
- dull abdominal pain referred to the upper abdomen and back
- anorexia and weight loss
- malaise, lethargy, weakness, and indigestion
2. Left-sided tumor
- a distinct change in bowel habits
- including difficulty passing stools
- abdominal distention
- ribbon or pencil-shaped stools
- constipation
- cramping
- flatulence
- a feeling of rectal pressure or incomplete stool evacuation

1101
Q

How is colorectal cancer diagnosed

A
  1. Stool test for occult blood
  2. Sigmoidoscopy or colonoscopy with biopsy examination and brush cytology
  3. Barium enema, usually with air contrast
  4. Upper GI series if small intestine involvement is suspected
  5. Possibly a serum carcinoembryonic antigen (CEA) test - less sensitive in children
1102
Q

What are potential complications of colorectal cancer

A
  1. Early detection of colon cancer is of primary importance because for patients with carcinoma limited to the bowel wall, the five year survival rate is 75%, compared to only 5% for patients with disseminated disease
  2. Large intestine tumors often show no signs or symptoms until they become rather large, thereby reducing the likelihood of early diagnosis and making surgery difficult
  3. Based on delayed recognition and types of tumors found in children; the prognosis for children with carcinoma of the colon is poor
1103
Q

How are colorectal tumors staged

A
  1. Duke’s classification recognizes four stages of tumor involvement
    - Class A - limited to the mucosa and submucosa
    - Class B - penetration of the entire bowel wall and serosa or pericolic fat
    - Class C - Class A and B, plus invasion of regional draining lymph node system
    - Class D - advanced and widespread regional metastasis
  2. The TNM classification describes the anatomical extent of the primary tumor depending on:
    - T: size, invasion depth, and surface spread of the tumor
    - N: extent of nodal involvement
    - M: presence or absence of metastasis
1104
Q

What are the surgical options for colorectal cancer

A

May be curative or palliative
1. Bowel resection and anastomosis
2. Or stoma formation (colostomy)
- single-barrel stoma - when the functioning proximal end of the bowel is brought through the abdominal wall, then folded in on itself and sutured to form a cuff
- double-barrel stoma - when both the active and inactive bowel ends are temporarily brought through the abdominal wall, thereby creating two stomas
- loop stoma - a temporary procedure formed by brining an intact bowel loop through the abdominal wall and making an incision in the top of the loop
3. The need for a temporary or permanent colostomy depends on the part of the colon involved and the extent of the disease
4. Surgery involves resection of the tumor and associated blood vessels, lymphatic channels, and affected structures as a unit
- sometimes the surgeon will irrigate the peritoneum with an anti Neoplastic agent and do a biopsy examination of the liver and abdominal lymph nodes
5. Conscientious ostomy care is required, with priority given to protecting the skin from corrosive enzymes controlling odor and fecal drainage, and providing emotional support and encouragement

1105
Q

What radiation and chemotherapy can be used for treatment of colorectal cancer

A
  1. Radiation therapy - for rectal cancer
  2. A fluorouracil (5-FU) and leucovorin combination for all patients with stage III is suggested
  3. Diets for patients with stage III should be a high-fiber, non-Western diet
  4. Patients with stage C tumors, adjuvant therapy has improved recurrence rates
  5. The standard of care for stage III colon adenocarcinoma after resection is chemotherapy and provides a 22% to 32% overall survival rate and a 30% reduction in recurrence
1106
Q

What are mechanical intestinal obstructions

A

Mechanical obstructions may result from congenital defects or acquired causes

1107
Q

What are causes and risk factors to developing mechanical intestinal obstructions

A
  1. Related to congenital defects, including:
    - atresia
    - stenosis
    - hernia
    - malrotation
    - Meconium ileus
  2. Hirschsprung’s disease (aganglionic megacolon)
    - a congenital absence of intramural ganglia of the anorectum and variable lengths of the distal colon
    - results in failure of relaxation of the contracted segment and internal sphincter, followed by obstructive symptoms
    - become apparent shortly after birth when the infant passes little Meconium and develops a distended colon
    • 2% of these patients have Down syndrome
1108
Q

What are signs and symptoms of a mechanical obstruction of the colon

A
  1. Small amount of stool in bowel movements
  2. Abdominal pain
  3. Abdominal distention
1109
Q

How are mechanical obstructions of the colon diagnosed

A
  1. Barium enema
  2. Anorectal manometry
  3. Confirmed by full thickness biopsy of rectal mucosa
1110
Q

What is the treatment for a mechanical obstruction of the colon

A

Surgical, involving removal of the aganglionic segment

1111
Q

What is a neurogenic obstruction (intestinal pseudo-obstruction) of the colon

A
  1. There is no mechanical blockage
  2. Instead this anomaly results from ineffective intestinal peristalsis
  3. Paralysis is usually incomplete
1112
Q

What are causes and risk factors of developing neurogenic obstruction of the colon

A
  1. Failure of the intestinal pump due to alteration of the enteric nervous system
  2. It may be primary, also known as chronic idiopathic intestinal pseudo-obstruction (CIP) and associated with generalized visceral neuropathy or it may be secondary and associated with identified smooth muscle, endocrine, neurological, or pharmacological causes
  3. Abdominal surgery may be a cause of neurological impairment of peristalsis (adynamic or paralytic ileus)
    - in such cases it is reversible, self-limited form of pseudo-obstruction that usually disappears 2-3 days after surgery
1113
Q

What are signs and symptoms of neurogenic obstruction of the colon

A
  1. Cachexia and variable degrees of abdominal distention
  2. Pain results from abdominal distention and heightens with increasing distention
1114
Q

How is a neurogenic obstruction of the colon diagnosed

A
  1. Paralytic ileus with dilated bowel loops present on x-ray
  2. Esophageal manometry shows poor peristalsis of the esophagus and incomplete relaxation of the lower esophageal sphincter
  3. Made by observation of abdominal distention, gastric aspiration, lack of flatus and constipation
1115
Q

What are potential complications of a neurogenic obstruction of the colon

A
  1. Inflammation within the myenteric ganglia may cause severe progressive neuropathic CIP in conjunction with autoimmune disease and circulating anti-enteric neuronal antibodies
  2. Paralytic ileus secondary to abdominal surgery may be prevented by maintaining fluid and electrolyte balance and by handling the bowel gently during surgery
    - it is treated by nasogastric suction and IV fluid administration to correct electrolyte imbalance
    - in some cases, rectal tube decompression or colonoscopic decompression may be performed
1116
Q

What is a vascular obstruction

A
  1. It occurs when emboli or atherosclerotic narrowing interrupts the blood supply to the bowl
  2. Another source of vascular obstruction is telangiectasia, in which capillaries and venules are dilated in the mucus membranes throughout the GI system
1117
Q

What are symptoms of an intestinal vascular obstruction

A
  1. Abdominal pain
  2. Vomiting
  3. Obstipation (intractable constipation)
  4. Failure to pass flatus
  5. Abdominal distention
1118
Q

How is an intestinal vascular obstruction diagnosed

A
  1. Taking a careful history and conducting a thorough physical examination
  2. Other tests may be ordered such as abdominal Radiographic examinations; a barium enema or swallow, blood tests to detect dehydration, tissue necrosis, and electrolyte imbalance
1119
Q

What are potential complications of intestinal vascular obstructions

A

It inhibits peristalsis and can lead to life threatening intestinal ischemia in as little as 40 minutes

1120
Q

What is the treatment for intestinal vascular obstruction

A
  1. Restoring bowel patency
  2. Regulating fluids and electrolytes, often intravenously. Correction and prevention of specific deficiencies of vitamins and mineral are often necessary
  3. Administering medications to control pain and nausea
  4. Using a nasogastric or intestinal tube to relieve abdominal distention
  5. Using a decompression gastrostomy or colostomy during periods of exacerbation
  6. A feeding jejunostomy placed endoscopically may allow for slow refeeding and tolerance of enteral nutrition without prolonged use of Parenteral nutrition that may be required in some patients, especially those with CIP
  7. After abdominal distention and compression have been controlled, surgical intervention may be necessary
  8. The type of surgery performed depends on the source of the obstruction but may include hernia reduction, adhesion division, intestinal bypass, lesion excision, or a diverting colostomy
  9. After the surgery the patient should be monitored for signs of recurrent obstruction or paralytic ileus
  10. Any abdominal drain should be monitored for patency and drainage amount
  11. Drug therapy using metoclopramide (reglan, metzolv) and erythromycin has been tried, with scattered reports of success
  12. A diet lower in fat, lactose, and fiber may help to prevent or control a recurrence of symptoms
1121
Q

What are anorectal disorders

A
  1. Hemorrhoids
  2. Fecal impaction
  3. Encopresis
  4. Anorectal abscess
  5. Fistula
  6. Fissure
  7. Rectal prolapse
1122
Q

What are hemorrhoids

A
  1. Vascular masses in the anal canal
  2. They are varicose dilatations of the radicals of the superior or inferior plexus of the hemorrhoidal veins
  3. Internal hemorrhoids bulge into the rectal lumen above the internal sphincter and the anorectal line
  4. External hemorrhoids are dilatations of the inferior hemorrhoidal plexus
    - they lie below the anorectal line and protrude below the external sphincter
  5. Affect 1 in 20 Americans usually affecting people age 50 and older
1123
Q

What are causes and risk factors to developing hemorrhoids

A
  1. Genetic predisposition
  2. Absence of valves in the portal venous system attributed to the erect human posture
  3. Conditions that cause transient or constant increased pressure or stasis within the rectal venous plexus including:
    - straining from constipation
    - frequent bowel movements (diarrhea)
    - rectal tumors
    - strictures
    - pregnancy
    - pelvic tumors
  4. Obesity
  5. Heavy lifting
  6. Prolonged sitting
  7. Vaginal child birth
  8. Primary internal hemorrhoids are rarely seen in pediatric patients but may be associated with portal vein obstruction
1124
Q

What are signs and symptoms of hemorrhoids

A
  1. Bright-red rectal bleeding - occasionally leading to iron deficiency anemia
  2. Rectal pain
  3. Sensation of a bulging mass on exertion
1125
Q

How are hemorrhoids diagnosed

A
  1. Visual examination
  2. Proctoscopy or anoscopy

Internal hemorrhoids are graded one to four depending on their degree of prolapse

1126
Q

What is the treatment for hemorrhoids

A

Medical interventions include:
1. High-fiber diet and adequate fluid intake if chronic dehydration is suspected
2. Comfort measures such as warm compresses; topical analgesic ointments; and Seitz baths, with or without salts in warm water or astringents (witch hazel)
3. Stool softeners (psyllium seed)
4. Hydrocortisone suppository or cream
5. Mesalamine (canasa) suppository to decrease inflammation
6. Benzocaine 20% spray or dibucaine 1% topical ointment
7. Injection sclerotherapy

Surgical intervention such as:
1. Rubber band ligation
2. Hemorrhoidectomy
3. Cryosurgery
4. Infrared photo coagulation or electrocautery
5. The first-line non medical therapy is rubber band ligation, which is superior to sclerotherapy

1127
Q

What is fecal impaction

A

Formation of a large, firm, immovable mass of stool that occurs when normal movement of feces is impaired
This allows the bowel to absorb more water that usual, thereby hardening the fecal matter and making it difficult to pass

1128
Q

What are causes and risk factors of fecal impaction

A
  1. Occurs when normal movement of feces is impaired
  2. Chronic severe dehydration
  3. Chronic constipation
  4. Inactivity
  5. Medications
  6. Anal disease that causes painful defecation
  7. Neurological problems
  8. Barium retention after radiological studies
  9. Relatively common in children, resulting from voluntary withholding stool subsequent to a painful bowel movement
1129
Q

What are signs and symptoms of fecal impaction

A
  1. Abdominal discomfort
  2. Sensation of rectal fullness
  3. Nausea and vomiting
  4. Headache
  5. Rectal pain
  6. Passing small amounts of watery, malformed stool
  7. A large, firm mass in the left lower quadrant
1130
Q

What are potential complications of fecal impaction

A

Intestinal or urinary tract perforation
Spontaneous perforation

1131
Q

What is the treatment for fecal impaction

A
  1. Oil retention enemas
  2. Digital disimpaction
  3. Laxative
1132
Q

What is encopresis

A

A condition of chronic constipation that results in involuntary leakage of feces after the developmental age of 4 years

1133
Q

What are risk factors to developing encopresis

A
  1. Not directly related to organic illness
  2. This is more common in boys than in girls
1134
Q

What are signs and symptoms of encopresis

A
  1. Chronic constipation with involuntary leakage, causing soiling
1135
Q

How is encopresis diagnosed

A

Made based on exclusion of organic causes of constipation and psychological disorders that may be associated with incontinence

1136
Q

What is the treatment for encopresis

A
  1. The use of non-habit-forming stool softeners and bowel habit retraining
  2. The goal of stool softening therapy should be to promote the passage of one to two large, loose bowl movements daily
  3. Maintenance of an empty rectal vault assists in the return of bowel tone and proper functioning
  4. Biofeedback training in combination with stool softening may be beneficial to help some patients speed their recovery
  5. Dietary therapy in pediatrics is rarely sufficient to overcome encopresis; however, it is used as an adjunctive therapy when stool softeners are weaned
1137
Q

What are anorectal abscesses

A
  1. Occur when infection causes localized accumulation of pus in the tissue space around the anorectum
  2. Incidence is high in patients with Crohn’s disease
1138
Q

What are causes and risk factors to developing anorectal abscesses

A
  1. Infection
  2. In children, pruritus, perianal cellulitis, and blood streaked stools may be caused by group A beta-hemolytic streptococci
  3. Patients with Crohn’s disease are particularly susceptible to abscess formation
  4. Other predisposing conditions include malignancy, radiation proctitis, leukemia, lymphoma, tuberculosis, actinomycosis and lymphogranuloma venereum
1139
Q

What are signs and symptoms of anorectal abscess

A
  1. Throbbing anorectal pain
  2. Fever
  3. Fatigue
  4. Purulent drainage
1140
Q

How is an anorectal abscess diagnosed

A
  1. Endosonography
  2. MRI
1141
Q

What is the treatment for anorectal abscesses

A
  1. Abscess drainage
  2. Antibiotics
  3. Analgesics
  4. Stool softeners
  5. Seitz baths
1142
Q

What are potential complications of anorectal abscesses

A
  1. Abscess extension
  2. Anorectal fistula
  3. Mortality may increase if not treated
1143
Q

What is an anorectal fistula

A
  1. A hollow, fibrous tract leading from the anal canal or rectum to the perianal skin
  2. The types of anorectal fistula are complete internal, blind internal (sinus), external (intrasphincteric and trans-sphincteric), branching (complex) and horseshoe
  3. Usually a primary drainage port drains into the perianal skin or rectal mucous membrane
1144
Q

What are causes and risk factors to developing an anorectal fistula

A

Often results from an anorectal abscess in the chronic phase

1145
Q

What are signs and symptoms of anorectal fistulas

A
  1. Drainage of blood, pus, mucous, and stool from the rectum
  2. Drainage of stool through the vagina in females
  3. Pruritus
  4. Pain
  5. Odor
  6. Presence of a palpable tract on rectal exam
1146
Q

How are anal rectal fistulas diagnosed

A
  1. Anoscopy
  2. Palpation of a tract
  3. Sigmoidoscopy
1147
Q

What is the treatment of an anorectal fistula

A
  1. Fistulectomy to repair superficial, straight fistulas or fistulotomy to correct deep fistulas
  2. Closure of fistulae with fibrin glue
  3. Placement of setons (temporary drains)
  4. Surgical creation of a rectal flap
1148
Q

What is an anal fissure

A
  1. A thin tear of the superficial anal mucosa
  2. It occurs most commonly in the distal anal canal, usually in the posterior midline
1149
Q

What are causes and risk factors for developing an anal fissure

A
  1. Most commonly trauma following passage of a large, hard stool
  2. Increased resting anal pressure
  3. If the fissure’s edges adhere immediately after defecation, thereby preventing pus drainage, the resulting edema and fibrosis of adjacent tissue may cause the development of a sentinel pile or take at the lower end of the fissure
1150
Q

What are signs and symptoms of an anal fissure

A
  1. Severe itching and burning
  2. Rectal bleeding -discharge of bright red blood on the toilet paper or in the bowl
  3. Acute, severe pain (tearing or burning sensation) after defecation - the pain may persist for hours
1151
Q

How are anal fissures diagnosed

A
  1. Inspection and anoscopy
  2. Digital rectal examination is extremely painful and should be avoided
  3. Sigmoidoscopy should be deferred until the symptoms abate
1152
Q

What is the treatment for anal fissures

A
  1. Analgesia
  2. Topical ointments (lidocaine plus hydrocortisone cream)
  3. Sitz baths
  4. Bulking agents
  5. Stool softeners
  6. An emollient suppository may provide some relief
  7. Surgical excision or lateral subcutaneous sphincterotomy (for internal sphincter) may be required for chronic fissures with 90% success rate
  8. Additional treatment includes topical nitrates (glycerol trinitrate), calcium channel blockers, and Botox
1153
Q

What is a rectal prolapse

A
  1. When the rectal mucosa (one or more layers) bulges through the anal orifice
  2. It can be partial or complete
  3. Among adults, females are more susceptible than males
  4. Rectal prolapse is uncommon in children and must be distinguished from a prolapsed rectal polyp
1154
Q

What are causes and risk factors to rectal prolapse

A
  1. Often a result of straining with defecation
  2. Result from increased intra-abdominal pressure when straining, relaxed anal sphincters and weak pelvic muscles, or tissue damage or trauma during childbirth
  3. In the elderly or debilitated patients, the cause is loss of sphincteric tone
  4. In pediatrics , both cystic fibrosis and previous imperforate anus repair have been associated with rectal prolapse
1155
Q

What are signs and symptoms of rectal prolapse

A
  1. Protruding rectal mass
  2. Mucus discharge
  3. Rectal bleeding
  4. Fecal incontinence
1156
Q

What is the treatment for rectal prolapse

A
  1. Reduction of prolapse either digitally or by surgery depending on the severity of the prolapse
  2. Avoidance of constipation and prolonged straining by taking non-habit-forming stool softeners titrated to a dose to maintain loose stool passage with a minimal amount of effort
  3. Injection treatment with a sclerosant may be used if simple measures are unsuccessful
  4. Surgery involves a combined procedure in which the rectum is fixed to the sacral hollow and the redundant sigmoid colon is removed
    - the extra-abdominal approach through the perineum to accomplish a rectosigmoidectomy is preferred for the elderly
    - if the prolapse is considered small or the patient is not medically stable for surgery, supportive garments can help

CGRN (9 decks)

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