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Adv. Health Assessment (Spring 2024) > Exam 2 Gastrointestinal Diseases > Flashcards

Exam 2 Gastrointestinal Diseases Flashcards

1
Q

What symptoms are presented with esophageal disease?

A

Dysphagia

Heartburn

Regurgitation - the effortless movement of gastric content up to the pharynx, not necessarily vomiting

Chest pain

Odynophagia- pain with swallowing

Globus sensation- lump in the throat

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2
Q

What is Achalasia?

A

Motility disorder where the esophageal outflow obstruction d/t inadequate relaxation of the lower esophageal sphincter (LES).

Essentially, the distal end of the esophagus is dilated and food accumulates there and drains into the LES very slowly.

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3
Q

What is the normal resting tone of the LES?

A

29 mmHg

LES hypertension is greater than 29 mmHg
LES hypotension is less than 29 mmHg

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4
Q

Signs and Symptoms ofAchalasia.

A

Dysphagia (both solids/liquids)
Regurgitation (high risk of aspiration, sleep upright)
Heartburn
Chest pain

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5
Q

Prolonged achalasia is correlated to high incidences of _____ cancer.

A

Esophageal

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6
Q

What are treatments for achalasia to relieve obstruction (drugs and procedures)?

A

Relieves obstruction… not peristalsis

Nitrates, CCB - LOW doses

Botox - Relax LES

Pneumatic (balloon) dilation

Heller myotomy - cutting smooth muscle at the distal portion of the esophagus and the top portion of the fundus, laparoscopic procedure.

Per oral endoscopic myotomy (POEM)

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7
Q

Anesthesia concerns for achalasia

A

Aspiration➔ RSI or awake intubation

POEM – NPO up to 48 hours

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8
Q

What does a Distal Esophageal Spasm mimic?

A

Mimics anginal pain - patients often think they are having a heart attack

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9
Q

What is used to dx distal esophageal spasm?

A

Esophagram- a series of x-ray pictures of the esophagus taken after a patient drinks a liquid containing barium sulfate.

A distal esophageal spasm x-ray will show a corkscrew-like or rosary bead-like appearance.

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10
Q

What are treatments for esophageal spasms?

A

Nitroglycerin (0.4 mg)
Trazodone (25-50 mg)
Imipramine (antidepressants)
Sildenafil (Phosphodiesterase Inhibitors)

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11
Q

What is an esophageal diverticula?

What 3 regions of the esophagus can have a diverticulum?

A

Esophageal wall outpouching.

  1. Pharyngoesophageal (Zenker’s diverticulum)-picture below.
  2. Mid-esophageal
  3. Epiphrenic (supradiaphragmatic diverticulum)
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12
Q

What are the signs and symptoms of esophageal diverticula?

What is the treatment for esophageal diverticula?

A

Bad Breath
Dysphagia - the bigger the diverticulum, the more compression on the esophagus, and the worse the dysphagia.

Diverticula removal
(or drink a beer- won’t be on the test)

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13
Q

Anesthesia considerations for esophageal diverticula.

A

Aspiration risk

No cricoid pressure - increase the risk of displacing contents in the diverticulum.

Intubate w/ head elevated

Avoid NGT - increase the risk of perforating the diverticulum.

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14
Q

What is a hiatal hernia?

What are the two different types of hiatal hernias?

A

A condition where part of the stomach enters the thoracic cavity through the esophageal hiatus (diaphragm).

  1. Sliding hiatal hernia
    - Gastroesophageal (GE) junction and fundus
    slideupward
  2. Paraesophageal hernia
    - GE junction doesn’t move
    - Pouch of the stomach herniates next to the GE junction through esophageal hiatus
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15
Q

How are hiatal hernias repaired?

A

Hiatal hernias are not generally repaired.
Most patients are asymptomatic.

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16
Q

What kind of cells make up esophageal tumors?

What are the signs and symptoms of esophageal tumors?

Treatment for esophageal tumors?

A

Squamous cells (mid esophagus) or adenocarcinomas (distal esophagus)

S/S:
Progressive dysphagia - tumor causing compression
Malnourishment
Dehydration
Significant weight loss
Pancytopenia
Lung injury (post-chemo and radiation)

Treatment: Esophagectomy, chemotherapy, or radiation(cut, poison, and burn)

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17
Q

What is GERD?

A

Reflux causes esophageal mucosal injury or at extraesophageal sites (pharynx or larynx).

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18
Q

How does our body prevent reflux?

A

LES

LES pressure (29 mmHg) - patients with significant GERD have an LES pressure of 13 mmHg

Crural diaphragm

GE junction

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19
Q

What causes GE junction/LES incompetence?

A

Transient LES relaxation
LES hypotension ( <29 mmHg)
Anatomic distortion of GE junction - hernia

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20
Q

S/S of Gerd.

Complications of GERD.

A

S/S:
Heartburn
Regurgitation
Dysphagia
Chest pain - the bigger the hernia, the bigger the chest pain

Complications:
Esophagitis
Laryngopharyngeal reflux variant- can lead to a chronic cough
Recurrent pulmonary aspiration

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21
Q

GERD treatment:

A

Lifestyle Modification - Avoid fried food, acidic food, EtOH, and peppermint. Reduce LES tone

PPIs > H2 antagonists

Nissen Fundoplication - Surgery where the top of the stomach is wrapped around the lower esophagus. This reinforces the LES, making it less likely that acid will back up in the esophagus.

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22
Q

Anesthesia concerns for GERD.

A

Aspiration Risk
Perform RSI w/ cricoid pressure

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23
Q

What can be given to mitigate aspiration risk for GERD?

A

Cimetidine and Ranitidine
Famotidine > Cimetidine

PPIs - given during the day of surgery

Sodium citrate + metoclopramide - raise the pH of stomach acid (pH 2.5). This will be given to DM, morbidly obese, and pregnant pts d/t decreased emptying.

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24
Q

What is peptic ulcer disease (PUD)?

What do a lot of patients complain of?

A

Ulcers in the mucosal lining ofthe stomach or duodenum.

A lot of patients complain of burning epigastric pain. Exacerbated when the patient is fasting.

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25
Q

What is the number one cause of peptic ulcer disease?

A

Helicobacter Pylori (H. Pylori) - reduce the duodenal mucosa’s production of bicarbonate.

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26
Q

What is a Gastric Ulcer?

What is it caused by?

A

Form of Peptic Ulcer Disease, where the ulcer is the stomach.

NSAIDs (most common)
H. pylori + NSAIDs use

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27
Q

What are peptic ulcer disease risk factors for death?

A

Peritonitis - from perforation
Perforation
Sepsis
Dehydration
Bleeding

28
Q

What is the mortality rate of patients with PUD if there are complications with bleeding?

A

Mortality 10% to 20%

29
Q

What is the percent risk of perforation with untreated duodenal ulceration?

A

10%
If there is perforation there will be sudden and severe epigastric pain.

30
Q

What is a gastric outlet obstruction (GOO)?

Signs and Symptoms.

Anesthesia considerations.

A

A clinical syndrome characterized by epigastric abdominal pain and postprandial vomiting due to mechanical obstruction. Acute or slow development.

S/S: vomiting, dehydration, and hypochloremic alkalosis.

Anesthesia Consideration: GOO is considered as a full stomach, NGT suction, IV antisecretory drugs (ex: PPIs)

31
Q

PUDTreatment

A

Antacids
OTC for symptomatic relief of dyspepsia/indigestion
Aluminum/magnesium hydroxide (TUMS)
Calcium carbonate

H2 Receptor Antagonists
Inhibits basal and stimulated HCL secretion
Cimetidine, ranitidine, famotidine, and nizatidine 4-6 weeks

PPIs
Inhibits all phases of gastric acid secretion
Omeprazole, pantoprazole

Prostaglandin Analogues
Misoprostol will Maintain mucosal integrity

Cytoprotective agents
Sucralfate or Peptobismol will create a physicochemical barrier to protect the mucosa

32
Q

Treatment of H. Pylori.

A

Triple combination therapy - 14 days
PPI + 2 ABX (Clarithromycin and amoxicillin or metronidazole)

Surgery will correct the immediate problem such as hemorrhage, perforation, and obstruction.

33
Q

What is Dumping Syndrome?

A

Emptying hyperosmolar gastric contents into the proximal small bowel from the release of vasoactive GI hormones (histamine, bradykinin, NO).

34
Q

When can Dumping Syndrome occur?

A

Early – 15-30 mins post-prandial
Crampy abdominal pain, syncope, palpitations, epigastric discomfort, nausea, tachycardia, dizziness, diaphoresis, and diarrhea. C SPENT DDD

Late – 1-3 hours post-prandial
Vasomotor symptoms secondary to hypoglycemia d/t excessive insulin release

35
Q

What are treatments for Dumping Syndrome?

A

Dietary modification

Octreotide therapy- works by reducing the secretion of hormones that cause rapid movement of food through the digestive system.

36
Q

What is Ulcerative Colitis (UC)?

Signs and Symptoms.

A

A mucosal disease where there is continuous inflammation of the colon to the rectum.

Diarrhea
Rectal bleeding
Anorexia
Fever
Tenesmus - a continual urge to have a BM.
Passage of mucous
Crampy abdominal pain
N/V
Weight loss

DRAFT Pick Cam NeWton

37
Q

Complications of UC.

Treatment for UC.

A

Massive hemorrhage
Toxic megacolon - transverse colon is dilated (picture)
Obstruction
Perforation

Treatment: Total Proctocolectomy, removing colon and rectum.

38
Q

What is Crohn’s disease?

A

Acute or chronic bowel inflammation. (Terminal ileum/ cecal value is the area where there will be a presentation of Chron’s disease.)

In Crohn’s disease, there are healthy parts of the intestine mixed in between inflamed areas. Whereas in UC, there is continuous inflammation.

39
Q

What are the signs and symptoms of Crohn’s disease?

A

Weight loss
Inflammatory mass
Malnutrition
Postprandial pain - pain after eating
Steatorrhea - increases fat excretion in stool
Stricture formation - a type of abnormal narrowing in a passage in the body.
Bowel spasm

WIMPSSB

40
Q

Complications of Crohn’s disease.

Surgical Treatment.

A

Complications: Stricture, obstruction, abscess, or fistula

Surgical Treatments:
Small bowel resection d/t fistula or obstruction
Total proctocolectomy w/ end ileostomy

41
Q

Inflammatory Bowel Disease medical treatment.

A

Purine Analogs: Azathioprine and 6-mercaptopurine, 3-4 weeks to reach efficacy

Immunosuppressive: Methotrexate (inhibit DNA synthesis of UC/Crohn’s) and Cyclosporine (inhibit T-cell mediated responses).

Glucocorticoids to treat both UC and Crohn’s

Anti-inflammatory: 5-Acetylsalicylic acid (5-ASA)

ABX – Ciprofloxacin or metronidazole

42
Q

Where can carcinoid tumors originate from?

What can these tumors secrete?

A

Originate from the GI tract:
Foregut, midgut, and hindgut
<25% of carcinoid tumors originate in lung tissue (foregut)

Secrete GI peptides and/or vasoactive substances (insulin, histamine, serotonin)

43
Q

Which gut will have high serotonin secretion?

A

Midgut

44
Q

Likelihood of carcinoid syndrome in the
Foregut:
Midgut:
Hindgut:

A

Carcinoid Syndrome
Foregut: Atypical
Midgut: Typical
Hindgut: Rare

45
Q

How are carcinoid tumors without carcinoid syndromes usually found?

A

Found accidentally during an appendectomy. .

46
Q

Carcinoid tumors w/ systemic symptoms are d/t what secreted products?

A

GI peptides and /or vasoactive substances (insulin, histamine, serotonin)

Midgut carcinoids are more likely to produce mediators than foregut carcinoids.

Non-producing tumors can present as a mass or bowel obstruction.

47
Q

What common presentation will be present if there are carcinoid tumors in these locations?
Small Intestine:
Rectum:
Bronchus:
Thymus:

A

Small Intestine: Abdominal pain (51%) and Intestinal obstruction (31%)

Rectum: Bleeding (39%) and constipation (17%)

Bronchus: Asymptomatic

Thymus: Anterior Mediastinal Mass

48
Q

Patients with carcinoid syndrome will release _________ and _______ (vasoactive substances) into the systemic circulation.

What will be the signs of symptoms of Carcinoid Syndrome?

A

Patients with carcinoid syndrome will release Serotonin and Histamine (vasoactive substances) into the systemic circulation.

Flushing, diarrhea, hypotension, HTN, bronchoconstriction, wheezing.

49
Q

What are the signs and symptoms of a carcinoid crisis?

A

Intense flushing, diarrhea, abdominal pain, tachycardia, HTN or hypotension. Carcinoid Crisis may be fatal w/o treatment

50
Q

What can cause a carcinoid crisis?

What drugs may provoke mediator release?

What drugs do not provoke mediator release?

A

Spontaneous or provoked by stress, chemotherapy, biopsy, or drugs.

Succinylcholine, Atracurium, Epi, NE, Dop, Isoproterenol, Thiopental.

Propofol, Etomidate, Vecuronium, Cisatracurium, Fentanyl, Inhalation Anesthetics.

51
Q

Carcinoid Tumors medical treatment.

A

Serotonin blockers
5HT1 or 5HT2 - treat diarrhea
5HT3(ondansetron) – diarrhea and nausea; occasionally relieve the flushing

Histamine blockers- treat flushing

Somatostatin analogs (works great on 80% of patients)
Prevents crisis development
Lanreotide most commonly used, Subq for 4 weeks.
Octreotide-start 24-48 hours before surgery

Octreotide, histamine blockers, and ipratropium- treat or prevent Bronchoconstriction

52
Q

What are three protective mechanisms that prevent autodigestion of the pancreas?

A
  1. Packaging of proteases in precursor form
  2. Synthesis of protease inhibitors
  3. The low intra-pancreatic concentration of calcium
53
Q

What are the causes of pancreatitis?

A

Gallstones and ETOH abuse account for 60 to 80% of pancreatitis
AIDS
Hyperparathyroidism
Trauma

54
Q

Signs and Symptoms of Pancreatitis.

A

Mid-epigastric pain, N/V, abd distention (ileus)
Dyspnea, low-grade fever, tachycardia, hypotension
Shock d/t hypovolemia
Increased serum amylase and lipase

55
Q

Name the components of the Ranson Criteria for Acute Pancreatitis.
Age:
WBC count:
BUN:
AST:
Arterial PaO2:
Fluid deficit:
Blood glucose:
Lactate dehydrogenase:
Corrected [Calcium]:
Fall in Hct:
Metabolicacidosis with a base deficit:

A

Age: > 55 years
WBC count: > 16,000 cells/mm3
BUN: >16 mmol/L
AST: > 250 units/L
Arterial PaO2: < 60 mmHg
Fluid deficit: > 6 L
Blood glucose: > 200 mg/dL w/o a history of DM
Lactate dehydrogenase: > 350 IU/L
Corrected [Calcium]: < 8 mg/dL
Fall in Hct: >10%
Metabolicacidosis with a base deficit: > 4 mmol/L

56
Q

Mortality r/t number of Ranson criteria present in acute pancreatitis
0-2 criteria:
3-4 criteria:
5-6 criteria:
7-8 criteria:

A

0-2 criteria <5% mortality
3-4 criteria 20% mortality
5-6 criteria 40% mortality
7-8 criteria 100% mortality

57
Q

Complications of Acute Pancreatitis.

A

Shock will be the major risk factor for death

58
Q

Acute Pancreatitis Treatment

A

Aggressive IVF administration
Colloid replacement
NPO - prevent pancreas stimulation
Enteral/TPN
NGT suction
Pain management
Removal of gallstones

59
Q

What is Chronic Pancreatitis?

What is this caused by?

A

Persistent inflammation w/ irreversible damage. There will be a loss of exocrine and endocrine function.

Caused by Chronic ETOH abuse, CF, and hyperparathyroidism

60
Q

Signs of and symptoms of chronic pancreatitis.

Treatment.

A

Signs and symptoms
Post-prandial, epigastric pain
Thin, emaciated, steatorrhea
DM - end result of chronic pancreatitis

Treatment
Management of pain, manage diabetes and treat malabsorption

61
Q

What is the top cause of upper GIB?

A

Esophageal Varices

62
Q

What is the top cause of upper GIB, outside of esophageal varices?

What can cause lower GIB?

A

PUD (Duodenal 36% or Gastric Ulcer 24%)

Diverticulosis or tumors (10-20%)
Colonic Diverticulosis (42%)
Older Patients

“Focus on the big numbers”

63
Q

Signs and symptoms of upper GIB

A

Acute GIB will present with
Hypotension and tachycardia w/ blood loss >25% of total blood volume
Hct will initially appear normal.
Anemia after fluid resuscitation.

Orthostatic hypotension when Hct <30%

BUN >40 mg/dL

Esophageal variceal bleeding, malignancy

64
Q

Treatment for upper GIB.

Anesthetic consideration.

A

Treatment
Upper endoscopy to dx
Active bleeding with maintained airway use endoscopic coagulation or clipping

Anesthetic Considerations
Aspiration risk – ETT w/ RSI

65
Q

What is Lower GIB?

Causes of Lower GIB.

Treatment of Lower GIB.

A

Abrupt passage of bright red blood and clots via the rectum

Caused by diverticulosis, tumors, ischemic colitis, and infectious colitis caused by C diff.

Treatment
Sigmoidoscopy/colonoscopy to find the source of bleeding.
Angiography and embolic therapy
Surgery

Adv. Health Assessment (Spring 2024) (25 decks)

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