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EOR Exam - Family Medicine > Gastrointestinal Part 2 > Flashcards

Gastrointestinal Part 2 Flashcards

1
Q

Define gastritis and gastropathy.

A

Gastritis: superficial inflammation/irritation of stomach mucosa with mucosal injury
Gastropathy: mucosal injury without evidence of inflammation

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2
Q

List factors that protect against injury to the layers of the GI tract wall.

A

mucus, bicarb, mucosal blood flow, prostaglandins, alkaline state, hydrophobic layer, epithelial renewal

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3
Q

What is the most common cause of gastritis?

A

H Pylori

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4
Q

What are the most common sequelae of H Pylori infection?

A

peptic ulcer, gastric adenocarcinoma,

gastric lymphoma

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5
Q

Other than the most common, list other causes of gastritis.

A

NSAIDs (PG inhibition), acute stress in critically ill patients, ETOH.

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6
Q

What is the role of prostaglandins in protecting the GI tract lining?

A

PGs inhibit acid secretion and stimulate mucus and bicarb secretion.

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7
Q

What S/S are associated with gastritis?

A

Most patients are asymptomatic. If S/S –> upper GI bleed, epigastric pain, N/V, anorexia, dyspepsia, abdominal pain

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8
Q

What is the gold standard for diagnosing gastritis and related issues?

A

Endoscopy

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9
Q

What non-invasive test is commonly used to evaluate for H Pylori?

A

Urea breath test

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10
Q

Describe the treatment for gastritis.

A

H. Pylori: clarithromycin + amoxycillin + PPI –> metronidazole if PCN allergy
Not H Pylori: PPIs, H2RAs, Sucralfate

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11
Q

What is the most common cause of gastroenteritis?

A

Salmonella –> 8-48 hours after ingestion

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12
Q

State the S/S of gastroenteritis.

A

N/V, fever, abdominal cramping, bloody diarrhea

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13
Q

What is used to diagnose gastroenteritis?

A

Stool culture

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14
Q

What is the treatment of gastroenteritis?

A

Supportive care in most –> self-limiting

Bactrom, ampicillin, Cipro options in severely ill or patients with SCD, or are malnourished.

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15
Q

Differentiate gastritis from gastroenteritis.

A

Gastritis: inflammation of the stomach lining specifically, and not always caused by infection.
Gastroenteritis: inflammation of the stomach and bowel, caused by an infection.

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16
Q

Define GERD

A

transient relaxation of LES –> gastric acid reflux –> esophageal mucosal injury

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17
Q

Define pyrosis and regurgitation as typical symptoms of GERD.

A

Pyr: heartburn –> usually 30-60 min post-prandial
Reg: water brash or sour taste in mouth

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18
Q

What complaints associated with GERD are cause for alarm?

A

dysphagia, odynophagia, weight loss, bleeding

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19
Q

What are potential complications of GERD?

A

esophagitis, esophagus stricture, barrett’s esophagus, esophageal adenocarcinoma, Barrett’s esophagus.

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20
Q

Define Barrett’s esophagus.

A

Esophageal squamous epithelium replaced by precancerous metaplastic columnar cells from the
cardia of the stomach.

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21
Q

When is endoscopy indicated in the evaluation of GERD?

A

New onset in patient > age 45, recuurent symptoms, failure to respond to therapy, indication of more serious condition –> anemia, dysphagia, recurrent vomiting.

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22
Q

What are the indications for esophageal manometry of 24 hour pH monitoring in the evaluation of GERD?

A

Manometry –> done if normal endoscopy

pH monitoring –> gold standard test but not usually done

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23
Q

Describe the hierarchy of therapeutics for GERD from mild to severe.

A

Lifestyle changes + OTC antacids and H2RAs –> Px PPIs –> Px PPI at night + Px H2RA during the day for severe overnight symptoms –> Nissen fundoplication if refractory.

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24
Q

What are risk factors for GERD?

A

obesity, pregnancy, diabetes, hiatal hernia, connective tissue disorders

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25
Q

What lifestyle modifications are recommended for treatment of GERD?

A

Elevated HOB at night, avoid laying down after meals, eat small meals, smoke cessation, weight loss, diet –> avoid fat, spicy, citrus, chocolate, caffeine, ETOH

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26
Q

What anatomical landmark differentiates upper GI bleeding from lower GI bleeding?

A

ligament of Treitz

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27
Q

Other than visible blood in stool or emesis, describe S/S that can present secondary to blood loss.

A

Syncope, fatigue, weakness

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28
Q

State the most common cause of upper GI bleed and list other causes.

A

Most common = peptic ulcer disease

Other: erosive esophagitis, duodenitis, varices, Mallory Weiss tear, vascular malformations

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29
Q

Patients on what medications are at 2-3 x higher risk of GI bleed?

A

ASA, PGY12 inhibitors, Vitamin K antagonists

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30
Q

What is the gold standard for evaluation of a suspected acute upper GI bleed?

A

Endoscopy

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31
Q

Differentiate pharmacologic therapy for an upper GI bleed when the suspected cause is esophageal varices vs not esophageal varices.

A

Varices: PPI –> 80 bolus follwed by 72 hour infusion

No varices: Ocreotide –> 25-50 mcg followed by infusion

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32
Q

What is used to reduce the risk of upper GI bleeding in a patient that must be on an NSAID or anti-coagulant medication?

A

PPI plus their NSAID/anti-coagulant

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33
Q

Define hemorrhoids.

A

enlarged venous plexus that increases with increased venous pressure

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34
Q

Define the 4 stages of internal hemorrhoids.

A

1: confined to anal canal, may bleed with defecation
2: protrude from anus but reduce spontaneously
3: require manual reduction after bowel movement
4: chronically protrude and risk strangulation

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35
Q

What are the most common S/S of external and internal hemorrhoids?

A

Ext: perianal pain
Int: intermittent rectal bleeding

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36
Q

Describe treatment of hemorrhoids.

A

Stage 1 and 2: high fiber diet, inc fluids, sitz bath, suppositories, hydrocortisone for itching/pain.
Stage 3 and 4: after failing conservative therapy –> injection, band ligation, sclerotherapy

37
Q

Define hiatal hernia.

A

Protrusion of the stomach through the diaphragm via the esophageal hiatus

38
Q

Differentiate between sliding (type 1) and rolling (tyoe 2) hiatal hernias.

A

1: GE junction and stomach slide into mediastinum –> treat like GERD.
2: fundus of stomach protrudes through diaphragm with GE junction remaining in place –> surgical repair.

39
Q

Differentiate between ulcerative colitis and Crohn’s in terms of the areas affected and the depth of the lesions.

A

UC: Affects only colon with rectum always involved and lesions limited to mucosal & submucosal layers.
Crohn’s: Can affect any part of GI tract and lesions are transmural.

40
Q

What part of the GI tract is most commonly affected by Crohn’s?

A

Terminal ileum –> LRQ pain.

41
Q

Differentiate the common S/S of UC from Crohn’s.

A

UC: Colicky LLQ pain with bloody diarrhea.

Crohn’s: Colicky LRQ pain with weight loss and non-bloody diarrhea.

42
Q

Differentiate Crohn’s from UC in terms of complications from each disease.

A

UC: colon cancer, toxic megacolon, primary sclerosing cholangitis.
Crohn’s: perianal disease (fistulas, abscesses, etc.), plus iron and B12 deficiency.

43
Q

T/F: Smoking increases risk of complications from Crohn’s and Ulcerative Colitis.

A

False: Smoking worsens Crohn’s but actually improves UC.

44
Q

Differentiate Crohn’s from UC in terms of findings on colonoscopy.

A

UC: uniform inflammation in rectum and colon –> “sandpaper appearance”.
Crohn’s: Skip lesions –> “cobblestone appearance”

45
Q

Differentiate Crohn’s from UC in terms of findings on barium studies.

A

UC: Stove pipe appearance (loss of haustra in colon)

Crohn’s: String sign (inflamed area narrows)

46
Q

Describe the serum lab findings used to help diagnose Crohn’s and UC.

A

p-ANCA and ASCA are not, by themselves, diagnostic of either disease. But they are used to differentiate between the two when IBD is suspected.
UC: more likely when p-ANCA is positive
Crohn’s: more likely when ASCA is positive

47
Q

T/F: The definitive cure for Crohn’s and UC is surgery.

A

False: Surgery is curative in UC but not curative in Crohn’s

48
Q

What findings are common to both Crohn’s andf UC?

A

Ankylising spondylitis, episclerirtis (reddening of eyes), fever, weight loss, fatigue, erythema nodosum, pyoderma gangreosum.

49
Q

What are the tests of choice in the diagnosis of acute disease in UC and Crohn’s?

A

UC: sigmoidoscopy

Crohn’s: Upper GI series with small bowel follow through

50
Q

T/F: Colonoscopy and barium enema are useful tests in definitive diagnosis of UC and Crohn’s.

A

False: Colonoscopy (perforation risk) and barium enema (toxic megacolon risk) are contraindicated in UC.

51
Q

What diet recommendations are indicated for management of Crohn’s disease?

A

Smoke cessation, B12, folate, and vitamin D supplementation.

52
Q

Describe the class and MOA of mesalamine and sulfasaline.

A

5-aminosalicylates –> ASA that gets to the intestines
Mesalamine: most active in terminal SI and colon –> best used for maintenance.
Sulfasaline: works primarily in colon but has a much higher AE profile.

53
Q

Describe the use of corticosteroids in UC and Crohn’s.

A

Used PO or topical for acute flares only.

54
Q

What is the most common cause of chronic abdominal pain in the US?

A

Irritable Bowel Syndrome (IBS)

55
Q

Define irritable bowel syndrome (IBS).

A

Combination of altered motility and hypersensitivity to intestinal distention often with psychological distress.

56
Q

What are common S/S associated with IBS?

A

Pain with altered bowel habits, post-prandial urgency and pain, relief after defecation.

57
Q

What S/S associated with IBS are cause for alarm?

A

Evidence of bleeding, anorexia, weight loss, fever, celiac sprue, dehydration, onset > age 45

58
Q

Describe the diagnostic process for IBS and important diseases in the differential.

A

Dx of exclusion –> r/o lactose intolerance, cholecystitis, chronic pancreatitis, bowel obstruction, celiac, carcinoma of pancreas/stomach

59
Q

What is the Rome IV criteria for diagnosing IBS?

A

Recurrent abdominal pain at least 1 day per week plus at least 2 of …

  • improvement with defecation
  • change in stool frequency
  • change in stool form/appearance
60
Q

What lifestyle changes are recommended to patients with IBS?

A

Smoking cessation, low fat and unprocessed foods, avoid beverages with sorbitol and fructose, avoid cruciferous vegetables, sleep, exercise

61
Q

What anti-depressant medication may be used to manage pain associated with IBS?

A

amitriptyline (TCA)

62
Q

Describe broadly the causes of jaundice.

A

Increased bilirubin (hemolysis), decreased hepatic bilirubin uptake, impaired conjugation, biliary obstruction, hepatitis

63
Q

Differentiate lab findings associated with pre-hepatic (hemolytic), post-hepatic (obstructive), and intra-hepatic (hepatocellular) causes of jaundice.

A

Pre: inc unconjugated bilirubin
Post: inc conjugated bilirubin, inc GGT and ALP
Intra: inc conjugated and unconjugated bilirubin, markedly increase AST and ALT

64
Q

Differentiate between ETOH hepatitis, acute hepatitis, and chronic hepatitis by AST and ALT findings.

A

ETOH: AST > ALT by more than 2:1 ratio
Acute: ALT > AST –> both levels > 1,000
Chronic: ALT > AST –> both levels < 500

65
Q

What bilirubin level is diagnostic and what does it mean if bilirubin is elevated with no rise in LFTs?

A

Bilirubin > 2.5 = diagnostic. If no rise in LFTs, suspect familial disorders or hemolysis.

66
Q

What are the most common causes of pancreatitis?

A

Acute: cholelithiasis
Chronic: ETOH
Other causes: hypertriglyceridemia, trauma, drugs, hypercalcemia, penetrating PUD

67
Q

What is the typical description of pain associated with pancreatitis?

A

Boring epigastric pain radiating to back that is relieved when leaning forward.

68
Q

What is the classic triad of chronic pancreatitis?

A

Calcifications, steatorrhea, DM

69
Q

What lab findings are indicative of pancreatitis?

A

Elevated amylase and lipase –> lipase more sensitive than amylase. Amylase increase is transient and will likely resolve in 48-72 hours.

70
Q

What is the imaging test of choice in the diagnosis of pancreatitis?

A

Abdominal CT

71
Q

What x-ray and US findings are consistent with pancreatitis?

A

x-ray: sentinel loop, colon cut-off sign

US: calcifications on pancreas

72
Q

What are the cornerstones of the management of pancreatitis?

A

NPO, IV fluids –> 90% resolve without further intervention.

73
Q

Describe the management of chronic pancreatitis.

A

PO pancreatic enzyme replacement, pain management, surgical removal of affected part of pancreas, ETOH cessation.

74
Q

What are the causes of peptic ulcer disease?

A

H/ Pylori (MC), NSAIDs, Zollinger-Ellison syndrome

75
Q

Differentiate S/S of duodenal ulcer from gastric ulcer.

A

Duodenal: pain improves with food intake
Gastric: pain worsens with food intake

76
Q

What is the gold-standard test for suspected PUD?

A

Endoscopy

77
Q

What testing is used to determine presence of H. Pylori?

A

Urea breath test - initial and confirm eradication
Stool antigen test - initial and confirm eradication
Serologic antibodies - initial but cannot confirm eradication

78
Q

What medications are used in the management of H. Pylori?

A

clarithromycin + amoxicillin + PPI

79
Q

What is the drug of choice for H. Pylori negative PUD?

A

PPI –> take 30 minutes before meals.

80
Q

Describe the best use of misoprostil for treating PUD.

A

Used to prevent NSAID related ulcers but does not treat an existing ulcer.

81
Q

What is the contraindication for use of misoprostil?

A

Pre-menopausal women –> abortifacent

82
Q

Describe use of magnesium containing and aluminum containing compounds for GI disorders.

A

Mg: used to treat constipation –> Mg is a laxative
AL: used to treat diarrhea

83
Q

Describe the prodromal and icteric phases of viral hepatitis.

A

Pro: malaise, arthralgia, fatigue, URI sx, anorexia, spiking fevers in Hep A
Ict: jaundice

84
Q

Describe fulminant hepatitis.

A

encephalopathy, coagulopathy, jaundice, edema, ascites, asterixis, hyperreflexia

85
Q

T/F: Hep A is the only viral hepatitis associated with spiking fevers.

A

True

86
Q

What is used for post-exposure prohylaxis against Hep A?

A

HAV immune globulin

87
Q

What are the most common causes of each type of viral hepatitis?

A 
A: fecal-oral
B: STI
C: IVDU
D: requires Hep B
E: fecal-oral associated with water-borne transmission
88
Q

Describe the relevance of HBsAG, HBsAb, and HBcAb testing for the diagnosis of Hep B.

A

HBsAG: 1st evidence of infection before symptoms –> positive for 6 months = chronic Hep B
HBsAb: Evidence of resolved infection or vaccination –> if not present after 6 months = chronic Hep B
HBcAb: IgM = acute infection and IgG = chronic or resolved infection

89
Q

What is the vaccine schedule for Heo B and when is it contraindicated?

A

Three doses at 0, 1, and 6 months

CI in allergy to baker’s yeast

EOR Exam - Family Medicine (15 decks)

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