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UWORLD ABIM > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

GERD refractory to daily PPI

A
  • occurs in 10-40% of patients
  • next step: switch to different PPI OR maximize therapy w/ PPI BID* (*preferred)
  • consider GI referral
  • IF still not responding after BID PPI, do esophageal pH monitoring and impedance testing
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2
Q

clinical features of serum-sickness like reaction 2/2 HBV (initial and subsequent)

A

initial: fever, rash, symmetric polyarthralgias/arthritis
- rash and joint symptoms resolve in 2-3 weeks
- rash is pruritic, urticarial, WITHOUT mucosal involvement
- arthritis affects small joints predominantly, includes morning stiffness

followed by: jaundice, non-specific systemic complaints

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3
Q

pathophys of serum-sickness like reaction 2/2 HBV

A

accumulation of antigen-antibody or immune complexes leading to vascular and cellular inflammation

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4
Q

clinical features of HSV esophagitis in HIV patients

A

usually oral lesions with abrupt onset

odynophagia and substernal pain

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5
Q

diagnosis of HSV esophagitis in HIV patients

A

EGD: well-circumscribed shallow ulcers

biopsy: stains positive for HSV, viral culture

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6
Q

treatment of HSV esophagitis in HIV patients

A

acyclovir

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7
Q

Clinical Features and Diagnostic Findings of Menetrier’s Disease

A
  • GI symptoms: epigastric pain, nausea, vomiting, diarrhea
  • edema 2/2 hypoalbuminemia
  • significant weight loss

Endoscopy shows extreme enlargement of gastric folds in the fundus

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8
Q

What is Menetrier’s Disease

A
  • protein-losing hypertrophic gastropathy
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9
Q

Diagnosis of metaplastic (chronic) atrophic gastritis

A
  • diagnosis is confirmed by endoscopy
  • serum gastrin levels may be elevated (AMAG) due to hypochlorhydria. levels should be repeated along w/ gastric pH off PPI
  • serum gastrin levels >1000 pg / ML in both atrophic gastritis and Zollinger-Ellison Syndrome however gastric pH < 5.0 is diagnostic of ZE
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10
Q

metaplastic (chronic) atrophic gastritis: AMAG VS. EMAG

A

EMAG: (environmental)

  • 2/2 dietary carcinogens or H pylori
  • gastric mucosal changes in the antrum** > fundus
  • risk of gastric ulcers + cancer increased (more than in AMAG)

AMAG (autoimmune)

  • AD (autosomal dominant)
  • more common in women
  • more prone to pernicious anemia
  • associated with other autoimmune conditions (Hashimotos, vitiligo)
  • end-stage AMAG usually has metaplastic glands
  • AMAG has an increased risk of gastric carcinoid tumors (benign > malignant) due to increased gastrin
  • risk of gastric adenocarcinoma and esophageal SCC is also increase
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11
Q

Gastric pH that is diagnostic of ZE syndrome

A

< 5.0

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12
Q

Management of metaplastic (chronic) atrophic gastritis

A
  • treat the complications! ex. pernicious anemia, H pylori

- gastric cancer screening w/ EGD in high-risk patients (family hx, asian)

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13
Q

Clinical features of Candida esophagitis in HIV patients

A
  • involves entire esophagus
  • pain w/ solids>liquids
  • often associated with oral thrush (18% are not!)
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14
Q

Diagnostic findings of Candida esophagitis in HIV patients (EGD, biopsy, labs)

A

EGD: white exudate (cottage cheese)
Biopsy: pseudohyphae in mucosa
CD4 count < 100 or medication non-compliance

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15
Q

Treatment of Candida esophagitis in HIV patients

A
  • antifungal ex. fluconazole
  • empiric tx for 14-21 days
  • ** must be systemic, cannot give topical to HIV patients, only to non-HIV patients
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16
Q

You think an HIV patient has Candida esophagitis based on clinical features. Now what?

A
  • FIRST you do empiric treatment (PO antifungal like fluconazole) you ONLY do EGD if treatment fails in 72 hours.
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17
Q

Clinical features of CMV esophagitis in HIV patients

A
  • odynophagia and substernal pain
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18
Q

Diagnostic findings of CMV esophagitis in HIV patients

A

EGD: sharply demarcated, linear ulcers in the distal 1/3 of the esophagus

biopsy: intranuclear inclusions

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19
Q

Treatment of CMV esophagitis in HIV patients

A

IV ganciclovir

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20
Q

Complications of gastric bypass surgery (name 3)

A
  1. Stomal stenosis / outlet obstruction

2. Dumping Syndrome

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21
Q

Features, diagnosis and treatment of stomal stenosis/outlet obstruction (complication of gastric bypass surgery)

A
  • occurs at the gastro-jejunal anastamosis
  • 5-20% of patients
  • onset at 3-6 mos post-op
  • obstructive symptoms: N/V, abdo pain, GERD, dysphagia, inability to tolerate PO intake
  • diagnosis: endoscopy
  • treatment: endoscopic balloon dilation (usually require serial)
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22
Q

Features, diagnosis and treatment of Dumping Syndrome (complication of gastric bypass surgery)

A
  • 50% of patients
  • abdo pain, nausea, hypotension (osmotic fluid shift from plasma to bowel)
  • reflex tachycardia
  • management: avoid by replacing simple carbs with complex carbs, increasing fiber, increasing protein
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23
Q

Incidence and preventative ppx of cholelithiasis as a complication of gastric bypass surgery

A
  • 40% of patients

- decreased incidence with 6 mos of post op ppx: ursodeoxycholic acid

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24
Q

What is the difference in ICU GI bleeding risk on GI ppx vs. without?

A

1.5%-8.5% risk on GI ppx

15% without

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25
Q

Negative effects of using stress ulcer prophylaxis in ICU patients

A

nosocomial PNA (HCAP), c-diff infection

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26
Q

Options for stress ulcer ppx in ICU

A

PPI (preferred, cost effective)
H2RA
PO antacids

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27
Q

Indications for stress ulcer ppx in ICU patients

A
  • history of GI bleed in past year
  • evidence of coagulopathy
  • mechanical ventilation for over 48h
  • severe CNS injury
  • severe burns
  • combination of sepsis, ICU stay or corticosteroid use

DISCONTINUE once they leave ICU if no more indication!!!

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28
Q

Clinical Features of Dyspepsia

A

post-prandial fullness

early satiety

epigastric pain

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29
Q

Approach to dyspepsia

A

eliminate aggravating factors (NSAIDS, excessive EtOH)

IF typical GERD symptoms: tx with PPI trial

IF NO typical GERD symptoms: TEST for H Pylori, TREAT if positive, PPI trial if negative. If age >= 60, Endoscopy.

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30
Q

Clinical Features, Etiology of Factitious Diarrhea

A
  • 2/2 laxative abuse of addition of substances, ex. water to dilute to stool
  • may have nocturnal symptoms ,weight loss, orthostasis, hypoK, hyperMg (in laxative abuse)
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31
Q

Diagnosis of Factitious Diarrhea

A
  • diagnosis of exclusion
  • get a 24 hour stool specimen
  • osmolality <250 suggests water was added to the specimen, osmolality >400 suggests urine was added to specimen
  • osmotic gap = measured osmolality - 2*(Na + K)
  • osmolality 250-400 and osm gap <75 suggests SEcretory laxative use (SAline, SEnna, biSAcodyl)
  • osm gap >75 suggests laxative with UNmeasured solutes (mag sUlfate, lactUlose, sorbitol)
  • colonoscopy will show melanosis coli (black/brown discoloration of colonic mucosa)
  • EGD will be normal
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32
Q

Causes of Secretory Diarrhea

A

Crohn’s disease (*you will see positive fecal leukocytes)

Collagenous colitis (microscopic colitis)

Hyperthyroidism (**presents with increased stool frequency rather than volume)

VIPomas (neuroendocrine tumor in pancreas)

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33
Q

Celiac Disease- Intra-intestinal Manifestations

A

Diarrhea, abdominal pain, malabsorptive symptoms (weight loss, iron deficiency, B12/folate deficiency)

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34
Q

Celiac Disease (Extra-Intestinal Manifestations)

A

Osteoporosis, arthritis, neurological symptoms, infertility, increased AST/ALT (can occur with minimal/no intestinal symptoms), autoimmune disease association

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35
Q

Etiology and Risk Factors for Small-bowel Mesenteric Ischemia

A

Usually occurs 2/2 precipitating event (ex, a fib)

Variable age

Risk factors: atherosclerosis, embolic source, hypercoag.

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36
Q

Clinical Presentation and Diagnosis of Small-bowel Mesenteric Ischemia

A

Severe pain out of proportion to physical exam (there is not significant abdominal tenderness on exam)

Patients appear severely ill

Hematochezia is a late complication

Diagnosis is made by CTA or MRA, or angiography

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37
Q

Etiology and Risk Factors for Colonic Ischemia

A

no precipitating event

2/2 hypovolemia/decreased effective blood volume to watershed areas

age >60 (most common form of ischemic bowel disease in the elderly)

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38
Q

Clinical Presentation and Diagnosis of Colonic Ischemia

A

Mild periumbilical / L-sided pain w/ abdominal tenderness on exam

Do NOT appear severely ill

Early hematochezia or bloody diarrhea

Diagnosis by CT scan w/ contrast AND colonoscopy

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39
Q

Frequency for colon cancer screening in patients at increased risk

  1. Family Hx of Adenomatous Polyps or CRC
    IF
    - 1 first degree relative age >60
    - >=2 first degree relatives any age
A

Age 40 OR 10 years prior to age of diagnosis, whichever is earlier. Repeat q5 years

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40
Q

Indications for colon cancer screening in patients at increased risk (Name 4)

A

FHx of adenomatous polyps or CRC

IBD - UC or Crohn’s (if colonic involvement)

Classic familial adenomatous polyposis

HNPCC (Lynch syndrome)

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41
Q

Frequency for colon cancer screening in patients at increased risk

  1. IBD: UC or Crohn’s (if there is colonic involvement)
A

Begin 8 years after onset. Repeat every 1-3 years.

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42
Q

Frequency for colon cancer screening in patients at increased risk

  1. Classic familial adenomatous polyposis
A

Begin at age 10-12

Repeat every year

43
Q

Frequency for colon cancer screening in patients at increased risk

  1. HNPCC (Lynch Syndrome)
A

Begin at age 20-25

Repeat every 1-2 years

44
Q

who is most affected by microscopic colitis?

A

disproportionally affects middle aged women

45
Q

What are the clinical findings of microscopic colitis?

A

clinical findings: watery, non-bloody diarrhea, fecal urgency/incontinence, abdominal pain, fatigue, wt loss, arthralgias, uveitis

46
Q

what are some triggers/ associations of microscopic colitis?

A

smoking, medications- NSAIDS, PPI, SSRIs, ranitidine

can be associated w/ autoimmune diseases (T1DM, thyroiditis)

47
Q

Diagnostic findings of microscopic colitis

A

Colonoscopy appears grossly normal.

Biopsy shows mononuclear lymphocytic infiltrates in the lamina propria

There are 2 histological subtypes:
collagenous: thick subepithelial collagen band

lymphocytic: intraepithelial lymphocytic infiltrates

48
Q

Management of microscopic colitis

A
  • first remove the trigger, can also give antidiarrheal medication
  • add budesonide if persistent symptoms
  • other options for persistent symptoms include cholestyramine, bismuth subsalicylate and TNF inhibitors
49
Q

variceal hemorrhage bleed algorithm

A

suspected variceal bleed –>

  1. place 2 large-bore IV catheters –>
    - volume resuscitation
    - IV octreotide
    - abx
    - ->
  2. urgent endoscopic therapy

IF no bleeding found: secondary ppx: BB and endoscopic band ligation in 1-2 weeks

IF continued bleed: balloon tamponade (temporary treatment) –> then TIPS/shunt

IF early re-bleed: repeat endoscopic therapy. IF recurrent –> TIPS/shunt

50
Q

Follow up colonoscopy recommendations after polypectomy FOR

small rectal hyperplastic polyps

A

10 years

51
Q

Follow up colonoscopy recommendations after polypectomy FOR

1 or 2 small (<1 cm) tubular adenomas

A

5 years

52
Q

Follow up colonoscopy recommendations after polypectomy FOR

3-10 adenomas OR any adenoma >1 cm OR adenoma with high-grade dysplasia OR villous features

A

3 years

53
Q

Follow up colonoscopy recommendations after polypectomy FOR

> 10 adenomas

A

1-2 years

consider underlying familial syndrome

54
Q

Follow up colonoscopy recommendations after polypectomy FOR

a) large (>2 cm) sessile polyp removed by piecemeal excision OR
b) polyp with adenocarcinoma (minimal invasion and >= 2 mm margin)

A

a) 2-6 mos

b) 2-3 mos

55
Q

Hyperplastic Polyposis Syndrome

A

5 or more proximal (up to sigmoid) hyperplastic polyps (at least 2 of which are >1 cm)

OR

any number of proximal hyperplastic polyps and family hx of a first degree relative with HPS

OR

> 30 hyperplastic polyps

56
Q

Lab findings of acute mesenteric ischemia

A

Leukocytosis

Elevated amylase and phosphate levels

Metabolic acidosis 2/2 elevated lactate

57
Q

Diagnostic findings of SBO (imaging)

A

Start with plain upright CXR and upright and supine abdominal films

  • will see multiple air-fluid levels with distended small-bowel loops.
  • if there is air in the colorectal area it usually rules out complete obstruction
  • Abdo CT w/ oral and IV contrast is preferred next step if plain films are not diagnostic
  • Water-soluble (Gastrografin) contrast study used with CT scan can assess for strangulation and be used for therapy.

small-bowel series are inferior to CT scan. only done if CT non-diagnostic

58
Q

How does gastrografin contrast help as a therapy for SBO?

A

It is hypertonic, draws water into the lumen of intestine to decrease wall edema, stimulate peristalsis and improve bowel function with faster symptom resolution. Presence of contrast in colon 4-24 hours after administration is good predictor of SBO resolution

59
Q

What percent of SBO patient require surgery?

A

approx 25%

60
Q

management of opioid-induced constipation (first-line and refractory treatment)

A

increasing fluid and dietary fiber intake and physical activity

if that does not work, can try pharmacotherapy, first with daily senna-docusate or an osmotic laxative ex. polyethylene glycol, lactulose

if refractory constipation despite the above, try subcutaneous methylnaltrexone (Relistor), peripherally acting opioid antagonist that does not cross the blood brain barrier- will not cause opiate withdrawal symptoms
- use w/ caution in pts with GI lesions like malignancy, PUD, diverticular disease, as you can get bowel perf

61
Q

Clinical features and etiology of diabetic diarrhea

A

painless, watery diarrhea, that can occur at night, assoc w/ fecal incontinence

  • can also have periods of normal BMs and constipation
  • etiology: multifactorial. largely due to autonomic neuropathy –> small bowel / colon hypomotility, increased intestinal fluid secretion, anorectal dysfunction
  • can co-exist with SIBO
  • in absence of SIBO, tx with antimotility agents (ex loperamide)
62
Q

Diagnosis of diabetic diarrhea

A

Diagnosis of exclusion

Workup includes stool studies, serum chemistries and endocrine studies, and endoscopic biopsy

63
Q

SIBO diagnosis and treatment

A

dx: carbohydrate breath test (ex. lactulose, glucose)
- can also do a jejunal aspirate and culture showing high bacterial concentrations - >100,000

tx: abx (rifaximin most commonly used, otherwise augmentin)
avoid antimotility agents like narcotics
dietary changes- high fat, low carb
pro-motility agents- ex metaclopromide

endoscopic/histopathologic studies usually non-revealing

64
Q

Definition of nonalcoholic fatty liver disease (NAFLD)

A

Hepatic steatosis on imaging or biopsy

Exclusion of significant alcohol use

Exclusion of other causes of fatty liver

65
Q

Clinical features of NAFLD

A
  • Mostly asymptomatic but can have non specific sx
  • Metabolic syndrome
  • +/- steatohepatitis (AST/ALT ratio <1)
  • Hyperechoic texture on u/s
66
Q

Treatment of NAFLD

A

Diet/exercise

Consider bariatric surgery if BMI >= 35

67
Q

Zenker’s Diverticulum- clinical presentation

A
  • results from esophageal motility abnormalities and defect in musculature of posterior hypopharynx
  • pharyngeal pouch, traps food/mucus/pills/sputum

presentation:

  • after age 60
  • months-years of transient oropharyngeal dysphagia, halitosis, gurgling in throat, regurg, neck mass, wt loss
  • recurrent asp pna
68
Q

Zenker’s Diverticulum-

diagnosis and treatment

A

dx: barium swallow/esophagram preferred
tx: surgery (or endoscopy in some skilled centers)

69
Q

Management of esophageal perforation, aka spontaneous esophageal rupture/Boerhaave syndrome

(stepwise algorithm after seeing mediastinal or free peritoneal air on CXR)

A

Get Chest CT or esophagram (w/ gastrografin)

IF there is a free perforation, first line tx is surgery, or endoscopic stent placement in some cases.

IF the perforation is contained, can do conservative management: NG suction, broad spec IV abx, TPN, abscesses & effusions require drainage

70
Q

Clinical presentation of Boerhaave syndrome/spontaneous esophageal rupture

A
  • vomiting/retching and chest/upper abdo pain w/ rapid progression to odynophagia, fever, dyspnea, septic shock

phys ex: subq emphysema

CXR- pneumomediastinum / pleural effusions

pl fluid analysis exudative w/ low pH, very high amylase >2500

71
Q

clinical presentation of primary sclerosing cholangitis (PSC)

A

asymptomatic or jaundice w/ fatigue and pruritis

72
Q

Lab findings in PSC

A

elevated ALP, bili, IgM

p-ANCA

73
Q

Imaging/biopsy findings in PSC

A

ultrasound is often normal

ERCP or MRCP:
Multifocal bile duct stricturing and dilation –> “beaded” appearance (of both intrahepatic and extrahepatic bile ducts)

Biopsy:
Fibrous obliteration of small bile ducts –> “onion skin”

74
Q

Management

A

Endoscopic dilation and stenting of strictures

Screening for cholangiocarcinoma and CRC

Liver transplant in advanced disease

75
Q

Colonoscopy screening recs for pts with PSC (1. with IBD, 2. Without IBD)

A

with IBD: every year

without IBD: every 5 years

76
Q

Biopsy findings in PBC

A

mononuclear cell-mediated destruction and/or periductal granulomatous inflammation of INTRAhepatic bile ducts

77
Q

Causes of intrahepatic cholestasis

A

PBC

drug toxicity

pregnancy

postop

infectious hepatitis- rare

78
Q

Causes of extrahepatic cholestasis

A

choledocholithiasis

PSC

malignant biliary obstruction

79
Q

Antimitochondrial antibodies are high in:

A

PBC

80
Q

Treatment of anal fissure

A

Topical nitroglycerin (improves blood flow, promotes wound healing)

conservative measures: adequate fluid and fiber intake, sitz baths, dry/clean area

Botox for refractory pts

81
Q

High-risk peptic ulcer features on endoscopy, and subsequent management

A
  • active arterial bleeding
  • nonbleeding visible vessel
  • adherent clot
  • oozing without visible vessel

management:

  • endoscopic hemostasis
  • IV PPI
  • CLD for 2 days
  • eradicate H pylori
  • risk reduction (stop/limit NSAIDs, anticoag, antiplatelets)
  • hospitalization for at least 3 days (b/c risk of rebleeding in 72h), discharge on twice-daily PPI for 2 weeks then daily.
82
Q

Intermediate-risk ulcer features on endoscopy and subsequent management

A
  • flat pigmented spot
management:
- once daily oral PPI
- CLD for 1 day
- eradicate H pylori
Risk reduction
(stop/limit NSAIDs, anticoag, antiplatelets)
- hospitalize for 1-2 days
83
Q

Low-risk ulcer features on endoscopy and subsequent management

A
  • clean base

management:

  • once daily oral PPI
  • regular diet
  • H pylori
  • risk reduction (stop/limit NSAIDs, anticoag, antiplatelets)
  • early disharge
84
Q

If pt presents with acute GI bleed 2/2 PUD, and gastric mucosal biopsy is negative for H Pylori, do you need further w/u of H Pylori?

A

Yes- can be false negative with acute bleed or meds (ppi/bismuth/abx), so you repeat urea breath test or stool test as outpatient after safely being off ppi for 1-2 weeks

85
Q

Threshold for hgb for blood transfusion in patients with GI bleed? (hemodynamically stable)

A

<7

86
Q

Clinical features of Gilbert’s Syndrome

A
  • asymptommatic or non-specific sx like generalized fatigue, icterus
  • elevated isolated unconjugated/indirect hyperbilirubinemia on repeated testing (6-12 mos after)
  • occurs due to decreased production <30% ofUDP- glucuronyl transferases, leading to decreased glucuronidation of bilirubin and hyperbilirubinemia
  • normal liver enzymes
  • no hemolysis
  • autosomal recessive, more prevalent in males
87
Q

What deficiencies and malabsorption results from ileal resection?

A

b12 deficiency

bile salt malabsorption (leading to malabsorption of fat and fat soluble vitamins)

88
Q

what kind of diarrhea results from ileal resection? and what is its pathophys of this diarrhea?

A

secretory

bile acids are not absorbed so they end up in colon, causing colonic stimulation

89
Q

how do you treat diarrhea resulting from ileal resection- what is the mechanism of this medication?

A

cholestyramine (binds the bile acids)

90
Q

What do you do when someone has typical biliary colic symptoms but they don’t have gallstones on imaging?

A

HIDA scan (also known as cholecystokinin cholescintigraphy) to identify biliary dyskinesia

91
Q

Diagnostic tests for Celiac Disease:

A

if clinically suspicious,

check:
tissue transglutaminase ab (IgA) - increased
anti-endomysial ab (IgA)- increased

IF negative- check IgA levels

if these serologies are positive you must still do endoscopy (small bowel enteroscopy) with biopsy. Can also do endoscopy w/ biopsy if all serologies are negative but very clinically suspicious.

Duodenal biopsy shows:
increased intraepithelial lymphocytes
flattening of the villi

Cutaneous biopsy showing dermatitis herpetiformis is also diagnostic

92
Q

Etiology of SIBO

A

anatomical abnormalities (surgery, strictures)

motility disorders (DM, scleroderma)

93
Q

What electrolyte abnormality can occur with chronic ppi use?

A

hypomagnesemia due to impaired intestinal magnesium absorption

94
Q

Risk factors for GI toxicity with NSAIDs

A

High risk:

  • history of complicated PUD
  • greater than 2 of following risk factors:
  • > 65 years of age
  • high dose NSAID therapy
  • previous hx of uncomplicated PUD
  • concurrent use of asa, corticosteroids or anticoag

moderate risk:
- 1-2 of above risk factors

low risk
- no risk factors

**high or moderate risk patients should switch to selective COX-2 inhibitor or combine the NSAIDs with PPI or misoprostol. they should be on lowest possible dose of NSAID

95
Q

which ppi is approved for prevention of NSAID induced ulcers in the US

A

lansoprazole is approved for prevention of NSAID-induced ulcers

96
Q

Most common infectious cause of malabsorption

A

Giardia lamblia

97
Q

Causes of persistent bowel symptoms in celiac sprue

A
  • poor dietary compliance/symptom recurrence
  • refractory sprue
  • EATL and ulcerative jejunoileitis
  • other co-existing conditions:
  • lactose intolerance
  • IBS
  • pancreatic insufficiency
  • microscopic colitis
  • SIBO
98
Q

Types of refractory celiac sprue

A

Type 1: no initial response to GFD for 12 mos

Type 2: Initial response but symptoms return regardless. This is assoc with poor prognosis and frequent progression to enteropathy-associated T cell lymphoma (EATL). Treatment involves steroids

99
Q

EATL and ulcerative jejunoileitis

A

This is due to aberrant T cell populations. presents with abdo pain, B symptoms, GI bleeding. Often intestinal obstruction or perf. No response to steroids

100
Q

onset of acute vs chronic radiation proctitis

A

acute: during or within 6 weeks of radiation therapy
chronic: 9-12 mos after therapy

101
Q

sigmoidoscopy findings of radiation proctitis

A

large, continuous areas of mucosal pallor with friability and telangiectasias

102
Q

Clinical presentation and diagnosis of schatzki ring

A

asymptomatic or dysphagia and/or reflux

dx: barium esophagram

103
Q

treatment of schatzki ring

A

dilation and acid suppression therapy

UWORLD ABIM (11 decks)

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