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Surgery > GI & Nutritional Disorders > Flashcards

GI & Nutritional Disorders Flashcards

1
Q

What are the 6 primary risk factors for cholelithiasis?

A
  1. Fat
  2. Fair
  3. Female
  4. Forty
  5. Fertile
  6. Flatus (esp burping)
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2
Q

What are the clinical manifestations of cholelithiasis?

A
  1. Biliary colic- episodic, abrupt RUQ pain that resolves slowly
  2. Nausea possible
  3. Precipitated by fatty foods & large meals
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3
Q

What is the test of choice for diagnosing cholelithiasis?

A

Ultrasound

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4
Q

What is the treatment for cholelithiasis?

A
  1. Asymptotic- observation

2. Elective cholecystectomy in symptomatic patients (usually laparoscopic)

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5
Q

What drains internal hemorrhoids?

A

Superior rectal vein to the portal system

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6
Q

What drains external hemorrhoids?

A

Inferior rectal vein to the vena cava

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7
Q

What are some risk factors for hemorrhoids?

A 
Increase venous pressure 
Cirrhosis 
Portal HTN
Straining during defecation 
Pregnancy
Obesity 
Prolonged sitting
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8
Q

What are the clinical manifestations of internal hemorrhoids?

A

Intermittent rectal bleeding, hematochezia, purple nodules with prolapse

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9
Q

What are the clinical manifestations of external hemorrhoids?

A

Perianal pain (aggravated by defecation), +/- tender/palpable mass

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10
Q

Name 3 treatment options for hemorrhoids (from most conservative to least)

A
  1. Increase fiber in diet, increase fluids, warm sitz baths, and topical rectal corticosteroids for pruritus and discomfort
  2. If failed #1 or if you have debilitating pain, strangulation, or they are stage 4- rubber band ligation
  3. Hemorrhoidectomy
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11
Q

What are the clinical manifestations of anal fissures?

A

SEVERE rectal pain, especially with BMs- causes pt to withhold

Can lead to constipation and bright red blood per rectum

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12
Q

How do you treat anal fissures?

A
  • about 80% resolve spontaneously
  • supportive measures: warm sitz baths, analgesics, increase fiber, increase water, stool softeners, laxatives, mineral oil
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13
Q

What is a perianal abscess? Fistula?

A
  1. Abscess- bacterial infection of anal ducts/glands and fluid accumulation. If fluid drains to outside of skin you can get…
  2. Fistula- open tract between 2 epithelium-lined areas, seen especially with deeper abscesses
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14
Q

What are the clinical manifestations of perianal abscess?

A

Redness, tenderness, swelling/mass around anus, pain is worse with sitting, coughing, and defecation

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15
Q

How do you treat perianal abscess?

A

I&D followed by WASH

W: warm water cleansing
A: analgesics
S: sitz baths
H: high fiber diet

(For fistulas- small tracks: fistulotomy)

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16
Q

Where do indirect inguinal hernias occur?

A

LATERAL to inferior epigastric artery

Travel through deep and superficial inguinal rings

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17
Q

Where do direct inguinal hernias originate and terminate?

A

Originate- MEDIAL to epigastric vessels within Hesselbach’s triangle (RIP: rectus abdominis, inferior epigastric, pouparts ligament/inguinal ligament)

Terminate- may protrude through superficial inguinal ring, does NOT reach scrotum

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18
Q

What are the clinical manifestations of inguinal hernias?

A
  1. Swelling or fullness, enlarges with increased intra-abdominal pressure and standing (may develop scrotal swelling)
  2. Incarcerated: painful enlargement of irreducible hernia (+/- N/V)
  3. Strangulated: ischemic with systemic toxicity, severe/painful BM (EMERGENCY)
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19
Q

Who is most likely to get a femoral hernia?

A

Women

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20
Q

Who’s most at risk for incisional (ventral) hernias?

A

Patients who have undergone operation with vertical incision

Obese patients

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21
Q

What are the main causes of ventral hernias?

A
  1. Weakness of surgical wounds
  2. Increased intra-abdominal pressure due to chronic cough, constipation, urinary obstruction (BPH), pregnancy, or ascites
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22
Q

What population is most often associated with umbilical hernias? How are they managed?

A

Children, usually resolve by 2

Kids > 5 you will do surgical repair to avoid incarceration/strangulation

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23
Q

What is the main cause of LBO?

A

Malignancy

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24
Q

Abdominal DDX

Abrupt onset?

A

Acute event

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25
Q

Abdominal DDX

Chronic constipation and BM straining?

A

Diverticulitis or carcinoma

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26
Q

Abdominal DDX

Changes in stool caliber?

A

Carcinoma

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27
Q

Abdominal DDX

Recurrent LLQ pain over several years?

A

Diverticulitis or diverticular stricture

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28
Q

Imaging for suspected LBO?

A

CT is preferred if obstruction suspected- contrast enhanced!

Can also do X-ray (with or without contrast)

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29
Q

How do you treat a LBO?

A
  1. Initial- volume resuscitation, pre-op abx, timely surgical consultation, consider NG
  2. Surgical emergency- closed loop obstruction, bowel ischemia, volvulus
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30
Q

What’s the most common area for diverticula to develop?

A

Sigmoid colon

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31
Q

What’s the likely age of onset for diverticular disease?

A

> 40

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32
Q

What is the main cause of lower GI bleeding?

A

Diverticulosis

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33
Q

What is associated with diverticulosis?

A

Low fiber diet, constipation, obesity

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34
Q

How is diverticulitis defined?

A

Inflamed diverticula secondary to obstruction or infection (fecaliths)

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35
Q

Fever, LLQ pain, and N/V/D/constipation/and bloating are commonly associated with what?

A

Diverticulitis

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36
Q

How do you diagnose diverticulitis?

A

CT scan!

High WBCs

Positive guaic

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37
Q

How do you treat diverticulosis?

Diverticulitis?

A
  1. Diverticulosis: increase fiber (+/- supplements)

2. Diverticulitis: clear liquid diet, abx (Cipro or Bactrim + Flagyl)

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38
Q

What is defined by the twisting of bowel at its mesenteric attachment site?

A

Volvulus

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39
Q

Where is a volvulus most likely to occur?

A

Sigmoid colon & cecum

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40
Q

How is a volvulus treated?

A

Endoscopic decompression

2nd line- surgical correction

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41
Q

Most common etiology of a SBO?

A

Post-surgical adhesions

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42
Q

Other causes of SBOs?

A

Incarcerated hernias, Crohns, malignancy, and intussuception

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43
Q

Different types of SBO include…

A
  1. Closed loop- lumen is occluded at 2 points, which can reduce blood supply (causing strangulation, necrosis, and peritonitis)
  2. Open loop
  3. Complete v. Partial
  4. Distal v. Partial (distal has more distention and less vomiting)
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44
Q

What are the clinical manifestations of a SBO (think CAVO)?

A
  1. Cramping abdominal pain
  2. Abdominal distention: +/- dehydration and electrolyte imbalance
  3. Vomiting: may be bilious if proximal, N/V usually follows pain
  4. Obstipation: late finding, diarrhea first!
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45
Q

_________ (hypoactive/hyperactive) bowel sounds are heard in the early phases of a SBO and _________(hypoactive/hyperactive) sounds are heard in the late phases.

A

Hyperactive…Hypoactive

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46
Q

How is a SBO diagnosed?

A

Abdominal X-ray

Will see air-fluid levels in step ladder pattern and dilated bowel loops

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47
Q

How is a SBO managed?

A
  1. Nonstrangulated: NPO, IV fluids, bowel decompression (NG suction)
  2. Strangulated: surgical intervention
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48
Q

What are the RFs for pancreatic carcinoma?

A

Smoking, >60, chronic pancreatitis, EtOH, DM, male, obesity, A.A.

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49
Q

Histology of pancreatic carcinoma…

A

MC: Ductal Adenocarcinoma

-70% found in head of pancreas

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50
Q

What are the clinical manifestations of pancreatic carcinoma?

A

Usually have mets by time of presentation (regional lymph nodes and liver)

  1. Abdominal pain radiating to back- may be relieved by sitting up and leaning forward
  2. PAINLESS JAUNDICE (80%)- 2ry to common bile duct obstruction. WEIGHT LOSS in 75% of cases
  3. Pruritus due to increased bile salts on skin, anorexia, acholic stools, dark urine
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51
Q

What is Courvoisiers sign?

A

PE finding in Pancreatic Cancer

Palpable, nontender, distended gallbladder associated with jaundice

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52
Q

How is pancreatic cancer diagnosed?

A

CT scan 1st choice!

ERCP is most sensitive

Labs: tumor markers CA 19-9 and CEA

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53
Q

What is a Whipple Procedure?

A

For treating pancreatic cancer-

Radical pancreaticoduodenal resection, done if cancer is confined to head/duodenal area

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54
Q

What is Meckel’s Diverticulum?

A

Persistent portion of embryonic yolk stalk

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55
Q

What is the Rule of 2s and what does it apply to?

A

Applies to Meckel’s Diverticulum

2% of population 
2 feet from ileocecal valve 
2% symptomatic 
2 inches in length 
2 types of ectopic tissue- gastric or pancreatic 
2 years- MC age at presentation 
2 times more common in boys
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56
Q

Clinical manifestations:

  1. Usually asymptomatic
  2. Painless rectal bleeding/ulceration (peri umbilical and radiates to RLQ)
  3. Can cause: intussuception, volvulus, or obstruction. May cause diverticulitis in adults

Of…

A

Meckel’s Diverticulum

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57
Q

How do you diagnose Meckel’s Diverticulum?

A

Meckel’s scan looks for ectopic gastric tissue in ileal area

Management: surgical excision if symptomatic

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58
Q

What lab findings are associated with anorexia nervosa?

A

Leukocytosis, leukopenia, anemia, hypokalemia, increased BUN (dehydration), hypothyroidism

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59
Q

How long does it take the stomach to empty clears? Light meal?

A

Clears- 2h

Light meal- at least 6h

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60
Q

____ (percentage) amount of total body water is intracellular and _____ (percentage) is extracellular

A 
Intracellular= 2/3
Extracellular= 1/3
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61
Q

Of the extracellular portion of total body water about ____ (fraction) is interstitial and ____ (fraction) is intravascular

A 
Interstitial= 3/4
Intravascular= 1/4
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62
Q

TBW= 0.6 X Body weight (kg)

A

Do I need to know this???

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63
Q

Calculating maintenance fluid requirements…

A

Hourly: 4-2-1 Rule

4cc/kg/hr for 1st 10kg
2cc/kg/hr for 2nd 10kg
1cc/kg/hr for remaining kgs

For 70kg person that would be 110cc/hr

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64
Q

Third-spacing occurs when too much fluid moves from intravascular space to interstitial space. Usually happens around POD __ (number). Can get a very large UOP at this time.

A

3

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65
Q

What are the 5 W’s of post-op fever and what POD does each represent?

*early fever is normal, later fever is more concerning for infection

A 
Day 1= Wind (Atelectasis) 
Day 3= Water (UTI)
Day 5= Wound (Surgical site infection) 
Day 7= Walking (DVT)
Day ≥ 9= Wonder (Drugs)
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66
Q

Atelectasis will most likely be bilateral. A unilateral infiltrate will most likely be _______.

A

Pneumonia

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67
Q

What is Virchow’s Triad?

A

Explains 3 categories thought to contribute to thrombosis:

  1. Stasis
  2. Hypercoaguability
  3. Vessel damage
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68
Q

_____ is #1 cause of post-op infection

A

Wound infection= 40%

UTI= 29%

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69
Q

Normal daily water loss…

A 
Urine= 1200-1500cc
Respiratory= 500-700cc 
Sweat= 200-400cc
Feces= 100-200cc
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70
Q

Typical maintenance fluid for an adult is…

A

D5 1/2 NS with 20 mEq of KCl (5% dextrose solution in 1/2 normal saline solution with 20 mEq of KCl)

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71
Q

___% of total body weight= blood volume

A

Approximately 7%

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72
Q

Minimal urine output for an adult on maintenance fluid is ____ cc/kg/hr

A

0.5cc/kg/hr (for 75kg adult that is about 35cc/hr)

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73
Q

Nutritional Requirements:

Protein= \_\_\_\_ g/kg/day
Calories= \_\_\_\_\_ kcal/kg/day
A

Protein= 1 g/kg/day

Calories= 35 kcal/kg/day

  • For surgical patient you need to be mindful of Vitamins A, C, and zinc
  • *Albumin level is a good indicator of overall nutrition
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74
Q

Heartburn that is retrosternal and postprandial (30-60 min after eating) is associated with what condition?

A

GERD

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75
Q

Most common cause of noncardiac chest pain is _____?

A

GERD

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76
Q

How is GERD diagnosed?

A

Usually clinically based on history.

ENDOSCOPY is used if symptoms persist/with complications

24h pH monitoring used if symptoms persistent

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77
Q

What foods should be avoided with GERD dx?

A

fatty/spicy, citrus, chocolate, caffeinated products, peppermint, alcohol

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78
Q

What pharmacological agents can treat GERD?

A
  1. Antacids
  2. H2 recetor antagonists
  3. PPIs (moderate to severe dz)
  4. Nissen fundoplication if refractory
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79
Q

2 key electrolyte abnormalities we worry about with persistent vomiting are…?

A
  1. Hypokalemia

2. Metabolic alkalosis

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80
Q

3 most common causes of N/V are?

A
  1. Gastroenteritis
  2. Drugs
  3. Toxins
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81
Q

Bilious vomiting is often a sign of a ____?

A

Bowel obstruction

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82
Q

Vomiting partially digested food a few hours after eating is a sign of ____?
(HINT: common after abdominal surgery and in diabetics)

A

Gastroparesis or Ileus

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83
Q

Mild to moderate nausea for many days with accompanying: jaundice, anorexia, and malaise may be a sign of ____?

A

Hepatitis

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84
Q

N/V Red Flags include:

A
  1. Signs of hypovolemia
  2. HA, stiff neck, mental status change
  3. Peritoneal signs
  4. Distended, tympanitic abdomen
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85
Q

Drugs for vomiting include:

A
  1. Motion sickness: Scopolamine, antihistamines
  2. Mild-moderate: Metoclopramide (Reglan), Promethazine (Phenergan)–> Dopamine blockers
  3. Severe/Refractory: Odansetron (Zofran)–> 5-HT3 antagonists, serotonin receptor blockers
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86
Q

What are the main causes of esophagitis and how is it diagnosed?

A

MC: GERD, infections in immunocompromised (Candida, CMV, HSV)

Dx: Upper Endoscopy

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87
Q

____ is defined by increased LES pressure. MC in 5th decade.

A

Achalasia

no inhibitory nitric oxide= increased tone

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88
Q

What is the gold standard for diagnosing achalasia?

A

Esophageal manometry

esophagram shows the bird’s beak appearance of LES

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89
Q

Achalasia results in dysphagia to BOTH ___ & ___

A

Solids and Liquids

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90
Q

A corkscrew appearance on an esophagram suggests a diagnosis of ______

A

Diffuse esophageal spasm

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91
Q

Achalasia is treated with what medications?

A

Botox injections, nitrates, calcium channel blockers

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92
Q

A pharyngoesophageal pouch that causes dysphagia, regurgitation of undigested food, feeling as if there is a lump in neck, and halitosis is associated with what diagnosis?

A

Zenker’s Diverticulum

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93
Q

How is Zenker’s Diverticulum treated?

A
  • Diverticulectomy

- Cricopharyngeal myotomy

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94
Q

Full thickness rupture of the distal esophagus, associated with repeated and forceful vomiting is known as _____ Syndrome?

A

Boerhaave Syndrome

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95
Q

How is Boerhaave Syndrome diagnosed?

A
  1. Chest CT/CXR: pneumomediastinum, left-sided hydropneumothorax
  2. Contrast esophagram
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96
Q

Vomiting with hematemesis after an EtOH binge with hydrophobia is known as _____ Syndrome?

A

Mallory-Weiss Syndrome

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97
Q

How is Mallory-Weiss Syndrome diagnosed?

A

Upper Endoscopy (see superficial, longitudinal mucosal erosions)

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98
Q

Dilation of gastroesophageal veins as a complication of portal vein HTN is known as ______?

A

Esophageal varices

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99
Q

Main cause of esophageal varices in adults is ____?

A

Cirrhosis

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100
Q

The primary clinical manifestation of esophageal varices is ______?

A

Upper GI bleeds

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101
Q

How are esophageal varices diagnosed?

A

Upper Endoscopy- enlarged veins

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102
Q

How are esophageal varices treated?

A
  1. Endoscopic Intervention- ligation
  2. Pharmacologic Vasoconstrictors- Octreotide
  3. Surgical Decompression- TIPS
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103
Q

What medications are used to prevent rebleeds in patients with esophageal varices?

A
  1. Nonselective beta blockers (NOT used in acute bleeds because it blunts cardiac output)
  2. Isosorbide (long acting nitrate)
104
Q

Protrusion of the upper portion of the stomach into the chest cavity due to a diaphragm tear or weakness is known as a ____ hernia?

A

Hiatal

105
Q

A type 1 hiatal hernia is also known as a _____ hernia and is the _____ (most/least) common type.

A

Sliding, Most

106
Q

A type 2 hiatal hernia is also known as a _____ hernia.

A

Rolling
(fundus of stomach protrudes through diaphragm- may lead to strangulation)

Treatment- surgical repair of the defect

107
Q

_____ is the MC cause of esophageal cancer worldwide and occurs in the _____ (portion) of the esophagus.

A

Squamous cell, upper 1/3

108
Q

RFs for squamous cell esophageal cancer are?

A

Tobacco/EtOH use, exposure to noxious stimuli, increased incidence in A.A.

109
Q

______ type of esophageal cancer is MC in younger patients, obese, and caucasians. Occurs in the ____ (portion) of the esophagus.

A

Adenocarcinoma, lower 1/3

adenocarcinoma can be a complication of GERD, leading to Barrett’s esophagus

110
Q

Clinical manifestations of esophageal cancer include:

A
  1. Dysphagia to solid food and eventually fluids, odynophagia
  2. Weight loss and chest pain
  3. Hypercalcemia in patients with squamous cell
111
Q

How is esophageal cancer diagnosed? Treated?

A

Upper Endoscopy with biopsy

Treatment- resection, radiation, chemo (depending on stage)

112
Q

What is the primary agent responsible for gastritis?

A

H. pylori

113
Q

NSAIDs/Aspirin can cause irritation of what organ?

A

Stomach (Gastritis)

114
Q

How is gastritis diagnosed?

A

Endoscopy

115
Q

What are the top 2 causes of PUD (peptic ulcer disease)?

A
  1. H. pylori
  2. NSAIDs
    (Zollinger-Ellison Syndrome- gastrin producing tumor)
116
Q

Dyspepsia that is worse at night is associated with what condition?

A

PUD

117
Q

Pain that is worse 2-5h after meals along with nocturnal symptoms are classically associated with _____ (gastric, duodenal) ulcers while pain 1-2h after meals and weight loss is associated with _____ ulcers.

A
  1. Duodenal

2. Gastric

118
Q

What is the main cause of an UPPER GI bleed?

A

PUD

119
Q

How is PUD diagnosed?

A

Endoscopy

-biopsy to rule out malignancy if GU present

120
Q

What are 3 ways to test for H. pylori?

A
  1. Endoscopy with biopsy
  2. Urea breath test- if Endo can’t be done, can also confirm eradication after therapy
  3. H. pylori stool antigen
121
Q

How is H. pylori eradicated (hint: triple therapy)?

A

CAP

Clarithromycin + Amoxicillin + PPI (Flagyl if PCN allergic)

122
Q

______ (drug) is good for preventing NSAID induced ulcers but should be avoided in premenopausal women because it is abortifacent & causes cervical ripening

A

Misoprostol (Cytotec)

123
Q

_____ (DU/GU) are more common in younger patients: 30-55y and _____ (DU/GU) are more common in older patients: 55-70y.

A
  1. DU

2. GU

124
Q

_________ Syndrome is caused by gastrin-secreting neuroendocrine tumors.

Clinical Manifestations?

A

Zollinger-Ellison

CM- multiple peptic ulcers, refractory ulcers, diarrhea

125
Q

How is ZES diagnosed?

Treated?

A
  1. Fasting gastrin level
  2. Secretin test- increased gastrin levels seen with this test (usually gastrin release is inhibited by secretin)

Treatment-

  1. Surgical resection of tumor
  2. If metastatic then PPIs and surgical resection (usually liver and abdominal LN are MC sites for METS)
126
Q

_______ is MC cause of gastric carcinoma.

The most important RF is _______.

A

Adenocarcinoma

RF- H. pylori

127
Q

Clinical manifestations of gastric carcinoma include:

A

Dyspepsia, weight loss, early satiety, iron deficiency anemia (bleeding)

128
Q

How is gastric carcinoma diagnosed?

Treated?

A

Upper Endoscopy with Biopsy

Poor prognosis :( Gastrectomy, radiation & chemo

129
Q

Dark urine & light colored stools are only seen with elevated _________.

A

Direct bilirubin

-Because there is excess direct bilirubin and it gets excreted in urine

130
Q

Some Info…

  1. PREHEPATIC PHASE: Bilirubin is produced from heme metabolism. Heme is degraded by macrophages primarily in the liver and spleen. Unconjugated (indirect) bilirubin is not soluble in water and is sent to the liver for conjugation and excretion!
  2. INTRAHEPATIC PHASE: Unconjugated bilirubin is conjugated in hepatocytes with a sugar via the enzyme UGT. It is now water soluble (for bile excretion).
  3. POSTHEPATIC PHASE: Transported to be stored in the gallbladder or intestine. In the intestine, conjugated bilirubin is converted to urobilinogen which can go through 3 main pathways:
    - Oxidation into stercobilin (gives stool brown color)
    - Some converted in kidney and excreted (giving urine its color)
    - Some is recycled back to the LIVER & BILE for reuse (enterohepatic circulation)
A

Learning is so fun : x

131
Q

Jaundice is not a disease but a sign of disease. Occurs when bilirubin levels > 2.5mg/dL

Etiologies include:

A
  • increased bilirubin production (ex- hemolysis), decreased hepatic bilirubin uptake, impaired conjugation, biliary obstruction, hepatitis
  • increased bilirubin without increased LFTs–> suspect familial bilirubin disorders
132
Q

What are the 3 D’s of Dubin-Johnson Syndrome?

A

Dubin, Direct bilirubinemia, Dark liver

133
Q

What is Crigler-Najjar Syndrome and how is it treated?

A

Hereditary unconjugated hyperbilirubinemia

Type 1 more severe (no UGT activity)- see neonatal jaundice with severe progression in the 2nd week leading to kernicterus

DX- Isolated indirect hyperbilirubinemia with normal LFTs

Treatment:

  1. Type 1- phototherapy and liver transplant (definitive)
  2. Type 2- usually not needed. Phenobarbital can increase UGT activity
134
Q

What is Gilbert’s Syndrome?

A

Relatively common, hereditary indirect hyperbilirubinemia (reduced UGT activity)

-May develop transient episodes of jaundice during periods of stress, fasting, ETOH, or illness

NO TREATMENT NEEDED :)

135
Q

____ (ALT/AST) is more sensitive for liver disease.

A

ALT

136
Q

Cholestasis (when flow of bile from liver stops or slows) is measured by an increase in _____ and ______.

A

Alkaline phosphatase & GGT

  • Also increase in bilirubin is greater than increase in ALT and AST
  • *If ALP goes up and NOT GGT then look for sources other than the liver (bone, gut)
137
Q

PT (prothrombin time) depends on synthesis of coagulation factors (vitamin K dependent). It is an early indicator of severe LIVER INJURY/PROGNOSIS

A

Albumin is a useful marker of overall liver protein synthesis. Levels decrease with liver failure.

138
Q

Would AST or ALT be higher in alcohol hepatitis?

A

AST (S= Scotch)

139
Q

Gallstones located in the common bile duct is associated with ________.

A

Choledocholithiasis

140
Q

Acute pancreatitis and acute cholangitis are complications of _______.

A

Choledocholithiasis

141
Q

What are the 3 elements of Charcot’s Triad (associated with acute cholangitis)?

A
  1. RUQ
  2. Fever
  3. Jaundice
142
Q

How is choledocholithiasis diagnosed?

A
  1. Transabdominal ultrasound

2. ERCP- Test of choice!! (diagnostic and therapeutic)

143
Q

Biliary tract infection secondary to obstruction is known as _______.

A

Acute cholangitis

*E. coli ascending from duodenum is the most common cause!

144
Q

What is Reynold’s Pentad (associated with acute cholangitis)?

A
  1. Charcot’s Triad PLUS
  2. Shock
  3. Altered mental status
145
Q

How is acute cholangitis diagnosed?

A
  1. Labs= leukocytosis and cholestasis findings (increase in alk phos, ggt, and bilirubin).
  2. US or CT scan may show dilation of the common bile duct.
  3. GOLD STANDARD= Cholangiography
146
Q

How is acute cholangitis treated?

A
  1. ABX (monotherapy of ampicillin/sulbactam or Ceftriaxone + Flagyl or Fluoroquinolone + Flagyl)
  2. Common bile duct decompression/stone extraction via ERCP
147
Q

What is the primary cause of acute cholecystitis?

A

E. coli (also Klebsiella and Enterococci)

148
Q

What are the clinical manifestations of acute cholecystitis?

A
  1. CONTINUOUS RUQ/epigastric pain. May be associated with nausea and may be precipitated by fatty foods and large meals
149
Q

What are the PE findings for acute cholecystitis?

A
  1. Fever (often low-grade)
  2. Positive Murphy’s sign- acute RUQ pain/inspiratory arrest with palpation of the gallbladder
  3. Positive Boas sign- referred pain to the right shoulder/subscapular area (phrenic nerve irritation)
150
Q

How is acute cholecystitis diagnosed?

A
  1. US= test of choice! Thickened gallbladder (>3mm) , sludge, gallstones
  2. CT scan or AXR
  3. Labs= increase in WBCs, bilirubin, alk phos, and LFTs
  4. HIDA scan: Gold standard. Positive HIDA scan= nonvisualization of the gallbladder in cholecystitis
151
Q

How is acute cholecystitis managed?

A
  1. NPO, IV fluids, abx (ceftriaxone + flagyl)–> cholecystectomy (usually within 72 hours)
  2. Cholecystostomy (percutaneous drainage of gallbladder) if patient is nonoperative
  3. Pain control with NSAIDs or narcotics
152
Q

Acute acalculous cholecystitis most commonly occurs in the seriously ill (postop, ICU patients)

A

Secondary to: dehydration, prolonged fasting, TPN, gallbladder stasis, burns, DM…

Due to gallbladder sludge, not gallstones

153
Q

CHRONIC cholecystitis is associated with gallstones

A
  • Strawberry gallbladder: interior of gallbladder resembles a strawberry, secondary to cholesterol submucosal aggregation
  • Porcelain gallbladder: premalignant condition
154
Q

What is the MC cause of fulminant hepatitis (acute hepatic failure)?

A

Acetaminophen

-Also: drug reactions (rifampin, antiepileptics, abx), viral hep, Reye syndrome

155
Q

What are the clinical manifestations of acute hepatitis?

A
  1. Encephalopathy: vomiting, coma, AMS, seizures, asterixis (flapping tremor of hand with wrist extension)
  2. Coagulopathy: due to decreased hepatic production of coagulation factors (proteins)
  3. Hepatomegaly, jaundice
156
Q

How is acute hepatitis diagnosed?

A

Increased ammonia levels, PT/INR ≥ 1.5, increased LFTs, hypoglycemia

157
Q

How is acute hepatitis treated?

A
  1. Encephalopathy: Lactulose (neutralizes ammonia), ABX that decrease bacteria that produce ammonia in GI tract (neomycin), Protein restriction (reduced breakdown of protein into ammonia)
  2. Liver transplant- only definitive treatment
158
Q

What are some of the clinical manifestations of viral hepatitis?

A
  1. Prodromal phase: malaise, arthralgia, fatigue, URI sx, N/V, loss of appetite (Hep A assoc. with spiking fever)
  2. Icteric phase: jaundice
159
Q

Chronic hepatitis is when the disease lasts longer than _____.

A

6 months, may lead to end stage liver disease (ESLD) or hepatocellular carcinoma (HCC)

*10% of HBV cases become chronic and 80% of HCV cases become chronic

160
Q

Both AST and ALT are >500 if ____ (acute/chronic) and <500 if _____ (acute/chronic).

A

Acute, Chronic

161
Q

_______ malignancies are more commonly secondary to metastasis (lung, breast, etc)

A

Hepatic

162
Q

What are the RFs for hepatocellular carcinoma (HCC)?

Clinical manifestations?

A

RFs: Chronic viral hepatitis (B,C, & D), cirrhosis, aflatoxin B1 exposure

Clinical Manifestations: Malaise, weight loss, jaundice, abdominal pain, hepatosplenomegaly

163
Q

How is HCC diagnosed?

Treated?

A

DX:
1. US!! (also CT, MRI, hepatic angiogram)

  1. Increase in alpha-fetoprotein

Treatment:
Surgical resection if confined to a lobe & no cirrhosis

164
Q

Irreversible liver fibrosis with nodular regeneration secondary to chronic liver disease is known as _____.

A

Cirrhosis

165
Q

What causes cirrhosis?

A

ETOH (MC in US), chronic viral hepatitis, NAFLD (obesity, DM, hypertriglyceridemia), hemochromatosis, drug toxicity, etc.

166
Q

What do you find on a PE in a patient with cirrhosis?

A
  1. Ascites (decrease production of albumin and third spacing of fluid due to decreased oncotic pressure)
  2. Gynecomastia (liver can’t metabolize estrogen)
  3. Caput medusa, spider angioma, muscle wasting, bleeding, palmar erythema, jaundice, Dupuytren’s contractures
167
Q

Asterixis (flapping tremor), fetor hepaticus (“breath of the dead”), and increased ammonia levels are associated with _______.

A

Hepatic encephalopathy

168
Q

How is cirrhosis diagnosed?

A

US: determines liver size and evaluate for HCC with liver biopsy

169
Q

Management of encephalopathy, ascites, and pruritus includes?

A
  1. Encephalopathy: lactulose or neomycin- lactulose is converted into lactic acid and pulls ammonia into the gut, neomycin decrease the ammonia-producing flora
  2. Ascites: Na restriction and diurectics, paracentesis
  3. Pruritus: Cholestyramine (bile acid sequestrant that reduces bile salts in the skin leading to less irritation)
  4. LIVER TRANSPLANT IS DEFINITIVE
170
Q

What are the 2 primary causes of acute pancreatitis?

A

Gallstones and ETOH

*Also scorpion bite and mumps in children

171
Q

Constant, boring epigastric pain that radiates to the back and relieved by leaning forward is associated with ______.

A

Acute pancreatitis

172
Q

Cullen’s sign (periumbilical ecchymosis) and Grey Turner (flank ecchymosis) are associated with _____.

A

Acute pancreatitis

173
Q

What laboratory values are associated with acute pancreatitis?

A

Leukocytosis, increased glucose & bilirubin & triglycerides

  1. Lipase! (more specific than amylase)
  2. Increased ALT is highly specific for gallstone pancreatitis
  3. Hypocalcemia (necrotic fat binds to calcium)
174
Q

What is the test of choice for acute pancreatitis?

A

Abdominal CT!!

*Abdominal US is used to rule out gallstones, bile duct dilation, ascites, pseudocysts

175
Q

How is acute pancreatitis managed?

A

90% recover with supportive measures like NPO, IV fluids, analgesia (abx NOT used routinely)

176
Q

What criteria is used to determine prognosis of acute pancreatitis?

A

Ransons Criteria (APACHE score also used)

  • takes into account glucose, age, LDH, AST, and WBC
  • If score is ≥3 then pancreatitis is likely (on a scale of 0-8)
177
Q

Chronic ______ can lead to exocrine and sometimes endocrine dysfunction

A

Pancreatitis

178
Q

MC of chronic pancreatitis in adults is _______.

MC in children is _______.

A

Adults- ETOH

Children- CF

179
Q

Triad of calcifications, steatorrhea, and DM is a hallmark of _______.

A

Chronic pancreatitis

180
Q

How is chronic pancreatitis diagnosed?

A

AXR- calcified pancreas

Amylase and lipase usually not elevated

181
Q

How is chronic pancreatitis treated?

A
  1. Oral pancreatic enzyme replacement
  2. ETOH abstinence
  3. Pain control
182
Q

Acute dilation of the cecum and right hemicolon (mostly in men > 60) is known as _______.

A

Ogilvie’s Syndrome

183
Q

Clinical manifestations of Celiac Disease include:

A
  • Malabsorption- diarrhea

- Dermatitis Herpetiformis- papulovesicular rash on extensor surfaces, neck, trunk, and scalp

184
Q

How is celiac disease diagnosed?

A
  • positive endomysial IgA Ab & transglutaminase Ab

- Small bowel biopsy for definitive diagnosis

185
Q

How is lactose intolerance diagnosed?

A

Hydrogen breath test

186
Q

What is the MC cause of appendicitis?

A

Fecalith

187
Q

What are the clinical manifestations of appendicitis?

A

Anorexia, periumbilical/epigastric pain followed by…
-RLQ pain, nausea and vomiting (vomiting usually occurs after the pain)

-MC 10y-30y

188
Q

What do you find on a PE exam with appendicitis?

A
  • Rebound tenderness, rigidity, and guarding
    1. Rovsing sign: RLQ pain with LLQ palpation
    2. Obturator sign: RLQ pain with internal and external hip rotation with flexed knee
    3. Psoas sign: RLQ pain with leg raise against resistance
    4. McBurney’s point tenderness: point 1/3 the distance from the ASIS & navel
189
Q

How is appendicitis diagnosed?

A
  1. CT scan, US, Leukocytosis
190
Q

What is the hallmark symptom of irritable bowel syndrome?

A

Abdominal pain with altered defecation/bowel habits (diarrhea, constipation, or alternation between the 2)

  • Pain often relieved with defecation
  • MC in late teens-early 20s in Women

(Rome IV Criteria for diagnosing- p.158 PPP)

191
Q

How is IBS managed?

A
  1. Lifestyle Changes- smoking cessation, low fat/unprocessed food diet
  2. Diarrhea- Anticholinergics/spasm (Dicyclomine), antidiarrheal (Loperamide)
  3. Constipation- prokinetics, bulk-forming laxatives (Benefiber), saline (Milk of Mag) or osmotic laxatives (Miralax, Golytely)
192
Q

What are the clinical manifestations of chronic mesenteric ischemia?

A

Chronic, dull abdominal pain WORSE AFTER MEALS, weight loss

193
Q

How is chronic mesenteric ischemia diagnosed?

Managed?

A

Dx- Angiogram, Colonoscopy- muscle atrophy with loss of villi

Management- bowel rest. Surgical revascularization

194
Q

What is a common site for acute mesenteric ischemia?

A

Splenic flexure- less collateral blood perfusion

195
Q

What are the causes of acute mesenteric ischemia?

A

MC occlusion- embolus (A fib, MI), thrombus (atherosclerosis)

Shock (decreased blood flow) and cocaine (vasospasm) are also causes

196
Q

What are the clinical manifestations of acute mesenteric ischemia?

A

SEVERE abdominal pain out of proportion to physical findings- usually poorly localized

197
Q

How is acute mesenteric ischemia diagnosed?

Managed?

A

Dx- Angiogram is definitive

Managed- surgical revascularization or resection if bowel is not salvageable

198
Q

Where is ischemic colitis most likely to occur?

A

“Watershed” areas with decreased collaterals (splenic flexure & rectosigmoid junction)

199
Q

What are the clinical manifestations of ischemic colitis?

Diagnosed? Managed?

A

LLQ pain with tenderness, BLOODY DIARRHEA (due to sloughing of the colon)

Dx- Colonoscopy

Management- restore perfusion and observe for signs of perforation

200
Q

Extreme colon dilation > 6cm + signs of systemic toxicity is associate with what condition?

A

Toxic Megacolon

201
Q

What are some causes of toxic megacolon?

A

UC, Crohns, Pseudomembranous colitis, infections, radiation, ischemia

202
Q

What are the clinical manifestations of toxic megacolon?

A

Fever, abdominal pain, diarrhea, nausea, vomiting, rectal bleeding, tenesmus, electrolyte disorders

203
Q

What are PE findings for toxic megacolon?

A

Abdominal tenderness, rigiditiy, tachycardia, dehydration, hypotension, AMS

204
Q

How is toxic megacolon diagnosed?

Managed?

A

Dx- AXR, Colon > 6CM!!!

Management- bowel decompression, bowel rest, NG tube, broad spectrum ABX, electrolyte repletion

205
Q

What is the etiology of IBD (UC and Crohns)?

A

Idiopathic- most likely immune reaction to GI tract flora

MC- Caucasians 15-35y

206
Q

A little about UC…

A
  1. Where–> limited to colon (begins in RECTUM), involves mucosa and submucosa only
  2. What–> Abdominal pain: LLQ, colicky, Urgency, BLOODY DIARRHEA (Hematochezia)
  3. Dx–> Colonoscopy (UNIFORM INFLAMMATION), pseudopolyps
    - Barium studies: “Stovepipe sign” (loss of haustral markings)
    - Labs: +P-ANCA
  4. Treatment–> Surgery is curative
207
Q

A little about Crohns…

A
  1. Where–> Any segment of GI tract from mouth to anus, MC in TERMINAL ILEUM- RLQ pain, transmural
  2. What–> Abdominal pain: RLQ, crampy, weight loss common, diarrhea with NO visible blood
  3. Associations–> perianal disease: fistulas, strictures, abscesses, granulomas. Malabsorption- Fe & B12 deficiencies
  4. Dx–> Colonoscopy (SKIP LESIONS, cobblestone appearance)
    - Barium studies: “String Sign”
  5. Treatment–> Surgery is NONCURATIVE
208
Q

How are UC and Crohns diagnosed in acute disease?

A

UC: flex sigmoidoscopy

Crohn: Upper GI series with small bowel follow through

209
Q

How are UC and Crohns treated?

A

Aminosalicylates (sulfasalazine, mesalamine), Corticosteroids, Immune modifying agents

210
Q

90% of colon polyps are ______ polyps and are a low risk for malignancy.

A

Hyperplastic polyps

211
Q

10% of colon polyps are ______ polyps and take 10-20y before becoming cancerous (esp if >1cm)

A

Adenomatous polyps

212
Q

What are the 3 types of adenomatous colon polyps?

A
  1. Tubular adenoma: nonpedunculated (MC and lowest risk of 3 types)
  2. Tubulovillous (mixture): intermediate risk
  3. Villous adenoma: tends to be sessile, HIGHEST RISK OF BECOMING CANCEROUS
213
Q

How does colorectal cancer develop?

A

Progression of adenomatous polyp into malignancy, MC site of metastatic spread is the LIVER

214
Q

RF for colorectal cancer include (3):

A
  1. Familial adenomatous polyposis (100% develop cancer by 40y)
  2. Lynch syndrome (40% risk of CRC development)
  3. Peutz-Jehgers (hamartomatous polyps, mucocutaneous hyperpigmentation)
215
Q

What are some clinical manifestations of CRC?

A
  • Iron deficiency anemia, rectal bleeding, abdominal pain, change in bowel habits
  • CRC MC cause of LBO in adults!
216
Q

How is CRC diagnosed?

A
  1. Colonoscopy with biopsy is test of choice!
  2. Barium enema: apple core lesion is classic
  3. Increase CEA
217
Q

How is CRC managed?

A
  1. Localized (Stage 1-3): surgical resection

2. Stage 3 & Metastatic: chemo is mainstay- 5FU

218
Q

Guidelines for colonoscopies for CRC screening

A
  1. Average risk: start at 50y, q10 years after
  2. 1st degree relative > 60y: start at 40, q10 years after
  3. 1st degree relative < 60y: start at 40 (or 10y before the age relative was diagnosed), q5 years after

**Colonoscopies done until 75 then individualized after

219
Q

CRC prognosis:

A

Preop CEA > 5, ulcerative growth patterns are associated with worse prognosis

220
Q

Autosomal recessive disorder of amino acid metabolism is known as _______.

A

Phenylketonuria- PKU

221
Q

Clinical manifestations of PKU are:

Dx:

Treatment:

A

Vomiting, mental delays, children often blonde & blue-eyed with fair skin.

Dx: Urine with musty (mousy) odor

Treatment: Lifetime dietary restriction of phenylalanine- milk, cheese, nuts, fish, chicken, meats, eggs, legumes, aspartame

222
Q

Vitamin A is found in kidney, liver, egg yolk, butter, and green leafy veggies. It contributes to vision, immune function, hematopoiesis, skin and cellular health.

Patients at risk for deficiency include:

A

ETOHics, patients with liver disease, fat free diets

223
Q

Visual changes such as night blindness & SQUAMOUS METAPLASIA/BITOT’S SPOTS (white spots on conjunctiva due to squamous metaplasia of corneal epithelium) are associated with what deficiency?

A

Vitamin A

224
Q

What populations are at risk for Vitamin C deficiency?

A

Those with diets lacking raw citrus fruits and green veggies, smokers, alcoholics, malnourished individuals, elderly

225
Q

Vitamin C deficiency is associated with SCURVY. What are the 3 H’s?

A

Hyperkeratosis

Hemorrhage- vascular fragility w/ recurrent hemorrhages in gums, skin, & joints. Impaired wound healing.

Hematologic- anemia, glossitis, malaise, weakness. Increased bleeding time.

226
Q

Fortified milk and sun exposure are great sources of _____.

A

Vitamin D

227
Q

Vitamin D deficiency can cause ______ in children and ______ in adults.

A

Rickets- softening of the bones leading to bowing deformities and fractures.

Osteomalacia- diffuse body pains, muscle weakness and fractures. Looser lines on X ray.

228
Q

____ is the mainstay of management of gastroenteritis.

A

Fluids- IV if needed but PO preferred.

-sports drinks, broths, IV saline, pedialyte

229
Q

____ diet is good when dealing with diarrhea.

A

BRAT

230
Q

Pepto-bismol (bismuth subsalicylate) should not be given to children with viral illness because of increased risk of ____ syndrome.

A

Reye

231
Q

_____ is an opioid agonist and is a good medication for non-invasive diarrhea (absent fever and no blood).

A

Loperamide (Immodium)

*Anticholinergics are another class of drugs for diarrhea that will inhibit GI motility and relax GI muscles

232
Q

_____ is given for N/V. It blocks serotonin receptors. It may cause diarrhea, constipation, and headache (also has some cardiac S/E).

A

Ondansetron (Zofran)

233
Q

_____ is given for N/V. It blocks dopamine receptors. It may cause QT prolongation, anticholinergic & antihistamine S/E (drowsiness!).

A

Promethazine (Phenergan)

Metoclopramide (Reglan)

234
Q

Extrapyramidal Sx (EPS) that may be brought on by dopamine blockers (for N/V) include:

A

Rigidity, bradykinesia, tremor, akathisia, dyskinesia (intermittent, sustained involuntary contractions including tongue protrusions, forced jaw opening, and facial grimacing)

235
Q

_____ is the MC overall cause of gastroenteritis in adults in N. America.

A

Norovirus

236
Q

Common causes of noninvasive (enterotoxin) infectious diarrhea include:
(Think voluminous, small intestine, no fecal WBCs or blood)

A
  1. Staph aureus- food contamination MC source
  2. Bacillus cereus- see above
  3. Vibrio cholerae & Vibrio parahemolyticus- leads to severe dehydration!
    - V.C.- think poor sanitation and overcrowding (esp. abroad)
    - V.P.- associated with raw shellfish (esp. Gulf of Mexico)
    * See copious watery diarrhea (grey “rice water stools”)
    * *Treatment: fluids, tetracyclines
  4. E. coli- MC cause TRAVELER’S DIARRHEA. Think unsanitary drinking water/ice.
    * Treatment: fluid replacement. If severe then fluoroquinolone.
  5. C. diff- Nosocomial/iatrogenic. Usually after abx (esp. CLINDAMYCIN) or chemo.
    * Presentation: Lymphocytosis, pseudomembranous colitis, & toxic megacolon
    * *Treatment: Flagyl 1st line for mild dz, Vancomycin PO 1st line for severe dz!
237
Q

Do not give ______ drugs with invasive diarrhea!

A

Anti-motility (may cause toxicity)

238
Q

Invasive (infectious) diarrhea is associated with:

A

High fever, blood and fecal leukocytes, less voluminous (think large intestine), mucus

239
Q

Some examples of invasive diarrhea include:

A
  1. Campylobacter Enteritis- C. jejuni is MC cause of BACTERIAL ENTERITIS in US!
    * Sources: undercooked poultry, raw milk
    * *Sx: diarrhea–> first watery then bloody
    * **Treatment: fluids, Erythromycin if severe
  2. Shigella- fecal/oral contamination. Highly virulent!
    * Sx: Explosive, watery diarrhea–> mucoid and bloody!
    * *Dx: Fecal WBCs/RBCs. CBC–> WBC > 50,000; Sigmoidoscopy–> punctate areas of ulceration
    * **Treatment: Fluids; if severe- Bactrim is 1st line
  3. Salmonella- greater in summer months. MC source- poultry products, exotic pets (reptiles, turtles)
    * High risk groups: immunocompromised, sick cell dz, kids, old
    * *Treatment: fluids, if severe fluoroquinolones!
240
Q

______ is a cause of invasive diarrhea that is associated with daycare centers, contaminated water, undercooked ground beef, and unpasteurized milk.

A

Enterohemorrhagic E. coli

241
Q

Protozoan infections include:

A
  1. Giardia lamblia- contaminated water from remote streams/wells.
    * Sx: frothy, greasy, foul diarrhea (no blood or pus)
    * *Treatment: fluids and flagyl
  2. Amebiasis- MC seen in travelers to developing nations or in the immigrant population.
    * Sx: GI colitis, dysentery, amebic liver abscesses
    * *Dx: stool ova & parasites
    * **Treatment: fluids, Flagyl, Tinidazole
  3. Cryptosporidium- MC cause of chronic diarrhea in patients with AIDS (feco-oral transmission)
242
Q

Osmotic v. Secretory Diarrhea

A

See p. 171/ look up

243
Q

Whipple’s Disease is MC in _____ around contaminated soil. Symptoms include:

A

Farmers

  • Sx: malabsorption, weight loss, steatorrhea, rhythmic motion of eye muscles while chewing
  • *Dx: Duodenal bx- dilation of lacteals
  • **Treatment: Penicillin 1-2 years
244
Q

Some causes of slow colonic transit (constipation) include:

A

idiopathic, motor disorders (CRC, DM, hypothyroid), S/E of many drugs like opioids, verapamil, outlet delay (Hirschsprung’s dz)

245
Q

Medical interventions for constipation

A
  1. Fiber
  2. Bulk forming laxatives: Benefiber, Citrucel
  3. Osmotic laxatives: Miralax, Lactulose, Sorbitol, Milk of Mag/Mag Citrate
  4. Stimulant laxatives: Dulcolax, Senna
246
Q

What is the MC intestinal obstruction in infancy that increases with erythromycin use?

A

Pyloric Stenosis (rare >6 months!)

  • If seen in adults it’s associated with chronic ulcer disease
  • Sx: non-bilious vomiting/regurgitation- projectile, hypochloremic metabolic alkalosis from vomiting, olive-shaped hard pylorus
  • *Dx: US, Upper GI contrast- “string sign”
  • **Treatment: IV fluids, potassium repletion, pyloromyotomy is the definitive management.
247
Q

The most common cause of small bowel cancer is ____.

A

Carcinoid tumors- pretty rare

  • MC in 60-68y black males
  • *Intestinal obstruction is more common than perforation
  • **Dx: CT, AXR
  • ***Treatment: Surgical resection +/- chemo if METs
248
Q

Pancreatic pseudocysts are associated with ____ (acute/chronic) pancreatitis and are usually found _____ (within/outside) the pancreas.

A

Chronic, outside

*Dx: transabdominal US, contrast CT and/or MRI

249
Q

Bariatric surgery is indicated for patients between 21-55y with either a BMI ≥ ____ or a BMI > _____ with life-threatening comorbidities, and for whom supervised weight-reducing programs have failed.

A

40, 35

250
Q

Examples of restrictive bariatric procedures include:

A

-Adjustable gastric banding (AGB), sleeve gastrectomy, and vertical banded gastroplasty

251
Q

Examples of malabsorptive bariatric procedures include:

A

-Jejunal-ileal bypass or biliopancreatic diversion

252
Q

2 most common types of bariatric surgery are ______ and ______.

A
  1. AGB

2. Roux-en-Y Gastric Bypass (RYGB)- restrictive and malabsorptive

253
Q

Nutritional complications of gastric bypass include:

A

Anemia (iron and B12), calcium deficiency, electrolyte deficiencies, dehydration, protein malnutrition

254
Q

Some more about RYGB…

A
  • Creates a gastric pouch with a 30mL holding capacity
  • postoperatively patients may experience “dumping syndrome”–> abdominal cramps, N/V, flushing (esp. with sweets)
  • associated with 75-80% excess weight loss
  • associated with resolution of DM, HTN, OSA
255
Q

Some more about AGB…

A
  • placing a silicone band around upper portion of stomach
  • a catheter connects the band to an injection chamber, implanted subcutaneously (band is gradually inflated postoperatively to progressively narrow the gastric inlet)
  • NO intestines bypassed- no dumping syndrome
  • 30-40% excess weight loss within a year. Long-term weight loss is about 50-55%. DM improvements
256
Q

Which of the following typical findings would be revealed during a sigmoidoscopy on a patient with Crohn’s disease of the intestine?

A

Intermittent, longitudinal mucosal ulcers and fissures- Ulcerations tend to be linear with transverse fissures in Crohn’s disease. These skip lesions are common with Crohn’s disease.

Surgery (11 decks)

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