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LOL REDO GI II BC NO WAY > McgOWan 2 > Flashcards

McgOWan 2 Flashcards

1
Q

What are the 4 causes of diarrhea in general?

A

infectious, malabsorption disorder, inflammatory disorder, medication induced

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2
Q

What is the definition of diarrhea? (timing)

A

either: 3 or more loose/watery stools per day OR decrease in consistency and increase in frequency of BMs of individual

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3
Q

What is the timing of acute, subacute, and chronic diarrhea?

A

acute: less than 2 weeks; subacute: 15 days-4 weeks; chronic: >4 weeks

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4
Q

A greasy malodorous stool may suggest what?

A

a malabsorption disorder

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5
Q

Stool containing blood or pus may suggest what?

A

inflammatory disorder

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6
Q

watery stool may suggest what?

A

a secretory process

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7
Q

The presence of abdominal pain with diarrhea could suggest what?

A

irritable bowel syndrome or inflammatory bowel disease

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8
Q

When evaluating a patient with diarrhea, what lab/chemistry is important to look at and why?

A

the electrolytes; the patient could lose bicarbonate and potassium (hypokalemia); the patient could be dehydrated

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9
Q

what stool studies would you obtain in a patient with diarrhea? and what do they tell you?

A

stool culture; C. Diff toxin; Fecal lactoferrin (indicates intestinal inflammation; fecal calprotectin (correlates with histologic inflammation)

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10
Q

What is in your DDx for non-infectious diarrhea?

A

antibiotic associated diarrhea

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11
Q

What are the characteristics associated with antibiotic associated diarrhea? (4)

A

usually mild/self-limited; non-inflammatory; watery; occurs during the period of antibiotic exposure (resolves spontaneously after discontinuation of the antibiotic)

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12
Q

What are the diagnostics used for abx associated diarrhea?

A

it does not require any specific laboratory evaluation or treatment; if stool examination is done however: reveals no fecal leukocytes, and stool cultures reveal no pathogens

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13
Q

What are the three most common causes of chronic diarrhea?

A

medications, IBS, or lactose intolerance

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14
Q

How do you obtain/calculate the osmotic gap?

A

you obtain stool electrolytes: osmotic vs. secretory

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15
Q

What stool/”fecal” diagnostic test do you get to check for malabsorption?

A

qualitative staining for fat (sudan stain) or fecal elastase (low)

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16
Q

What stool/ “fecal” tests suggests IBD?

A

leukocytes, calprotectin, lactoferrin

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17
Q

There are 2 different types of chronic diarrhea- what are they?

A

secretory or osmotic

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18
Q

How is osmotic diarrhea different from secretory diarrhea?

A

Osmotic: increased stool osmotic gap and diarrhea gets better with fasting; secretory: normal stool osmotic gap and diarrhea does not get better with fasting

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19
Q

What are the protozoans most commonly associated with chronic diarrhea?

A

Giardia and E. histolytica

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20
Q

what are the intestinal nematodes most commonly associated with chronic diarrhea?

A

strongyloidiasis stercoralis (endemic regions + eosinophilia)

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21
Q

what are the bacterial infections most commonly associated with chronic diarrhea?

A

C difficile

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22
Q

In immunocompromised patients/AIDS- what are the most common viral causes of chronic diarrhea?

A

CMV and HIV

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23
Q

in immunocompromised patients/ AIDS- what are the most common bacterial causes of chronic diarrhea?

A

clostridium difficile, mycobacterium avium complex

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24
Q

in immunocompromised patients/ AIDS- what are the most common protozoal causes of chronic diarrhea?

A

cryptosporidium

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25
Q

What are 6 DDx considerations for chronic osmotic diarrhea?

A

medications, IBS, lactase deficiency/intolerance, chronic infections, malabsorptive conditions, pseudodiarrhea/overflow (stool) incontinence/ fecal impaction

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26
Q

What associated symptoms of chronic diarrhea are not consistent with the 3 most common causes and warrant further evaluation? (4)

A

nocturnal diarrhea, weight loss, anemia, or positive results on fecal occult blood test (FOBT)

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27
Q

What are 5 medications that are known to cause chronic diarrhea?

A

metformin, cholinesterase inhibitors, SSRIs, NSAIDs, allopurinol

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28
Q

What is occurring in IBS and what is the result of this?

A

visceral hyperalgesia to mechanoreceptor stimuli–> altered colonic and small intestine motility at rest and in response to stress, cholinergic drugs, cholecystokinin; enhanced visceral sensation (lower pain threshold in response to gut distention)

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29
Q

when might IBS present?

A

post-infectious (after an episode of gastroenteritis)

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30
Q

What 3 things characterize IBS?

A

altered bowel habits (constipation, diarrhea, alternating); abdominal pain (crampy, lower); Absence of detectable organic pathology (diagnosis of exclusion)

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31
Q

What are some associated findings seen in patients with IBS?

A

pasty stools, ribbony or pencil-thin stools, heartburn, bloating, back pain, weakness, faintness, palpitations, and urinary frequency

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32
Q

How do you make the diagnosis of IBS?

A

considered chronic is symptoms more than 6 months (symptoms for at least 3 months is when you can consider it); it is a clinical diagnosis; utilize the ROME criteria; rule out other things with sigmoidoscopy and barium radiographs

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33
Q

how do you treat IBS?

A

low foodmap diet (avoid fatty foods and caffeine); patients presenting with IBS to a physician have an increased frequency of psychological disturbances (depression, hysteria, OCD)

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34
Q

What are the alarm features associated with chronic diarrhea?

A

acute onset, nocturnal diarrhea, severe constipation or diarrhea, hematochezia/ FOBT; weight loss, fever, FH of cancer/IBD/celiac

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35
Q

What causes secondary lactase deficiency?

A

GI disorders that affect the proximal small intestine mucosa–> crohn dx, celiac dx, and viral gastroenteritis

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36
Q

How is the diagnosis of lactase deficiency confirmed?

A

diagnosis confirmed by hydrogen breath test

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37
Q

Patients who chose to restrict or eliminate milk products may have increased risk of what?

A

osteoporosis

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38
Q

What is C. diff?

A

an anaerobic, gram-positive, spore-forming bacillus

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39
Q

what toxins are associated with c. diff?

A

cytotoxin (A&B) (exotoxin mediated)

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40
Q

Who is at high risk of c. diff infection? (5)

A

elderly/debilitated/immunocompromised; hospitalized for more than 3 days; those on multiple abx or prolonged abx; PPI use; those with IBD

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41
Q

what antibiotics most commonly cause c. diff?

A

ampicillin, clindamycin, third-generation cephalosporins, fluoroquinolones

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42
Q

How does c. diff present?

A

mild to moderate greenish, foul-smelling watery diarrhea 5-15 times per day; not typically bloody: only if associated with IBD [UC]

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43
Q

how do you diagnose c. diff?

A

stool for C. diff toxins (PCR); leukocytosis (>15k); flexible sigmoidoscopy with biopsy

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44
Q

what does a flexible sigmoidoscopy with biopsy show in a patient with c. diff?

A

pseudomembranous colitis: yellow adherent plaques; biopsy shows: epithelial ulceration with classic “volcanic” exudate of fibrin and neutrophils

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45
Q

How do you treat c. diff (medication wise)?

A

PO/IV metronidazole; PO vancomycin, fidaxomicin, fecal transplant

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46
Q

What are the complications associated with c. diff?

A

toxic megacolon/hemodynamic instability–> perforation–> death

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47
Q

What could cause malabsorption syndromes?

A

small bowel mucosal disorders

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48
Q

what are 5 examples of small bowel mucosal disorders that lead to malabsorption?

A

crohn disease, celiac sprue, lactase deficiency, whipple disease, and small bowel resections (short bowel syndrome or bile salt malabsorption)

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49
Q

What are the characteristics of malabsorptive syndromes? (4)

A

weight loss, osmotic diarrhea, steatorrhea, nutritional deficiency

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50
Q

Significant diarrhea without weight loss is not likely to be due to what?

A

malabsorption

51
Q

What is the effect of gluten in diet of a celiac?

A

diffuse damage to the proximal small intestinal mucosa with malabsorption of nutrients

52
Q

What is the humoral immune response seen in celiac disease?

A

antibodies to gluten, tissue transglutaminase (tTG)

53
Q

what happens when a celiac takes gluten out of their diet?

A

levels of all antibodies become undetectable after 3-12 months of dietary gluten withdrawal

54
Q

What does an endoscopy with duodenal biopsy show in a patient with celiac’s disease?

A

atrophy or scalloping of the duodenal folds may be observed; histology shows hypertrophy of the intestinal crypts and blunting or complete loss of intestinal villi

55
Q

What screening is recommended in all patients with celiac’s?

A

dual-energy x-ray densitometry scanning is recommended in all patients with celiacs to screen for osteoporosis (secondary prevention)

56
Q

Where are bile salts reabsorbed?

A

in the terminal ileum

57
Q

what can lead to insufficient intraluminal bile salts?

A

resection or disease of this area (e.g. crohn disease)

58
Q

How does bile salt malabsorption present?

A

mild steatorrhea, minimal weight loss, gaseous distention and flatulence, large greasy foul smelling stools

59
Q

what is common in bile salt malabsorption? (complications)

A

impaired absorption of fat-soluble vitamins (ADEK)

60
Q

what does impaired absorption of fat-soluble vitamins (ADEK) result in?

A

bleeding tendencies, osteoporosis, and hypocalcemia

61
Q

What type of diarrhea does bile salt malformation cause?

A

watery secretory diarrhea

62
Q

How do you treat bile salt malabsorption?

A

treat the underlying cause; therapeutic trial with a bile acid-binding resin such as cholestyramine

63
Q

What is whipple disease and what causes it?

A

a rare multi-system disease; infections with the gram positive bacillus, not acid fast, Tropheryma whipplei

64
Q

How does whipple disease present?

A

weight loss, malabsorption, (hypoalbuminemia–> peripheral edema), chronic diarrhea, fever, hypotension, LAD, arthralgias, dementia, lethargy, nystagmus

65
Q

How do you diagnose whipple disease?

A

endoscopy with duodenal biopsy: periodic acid schiff (PAS)- positive macrophages with characteristic bacillus

66
Q

what is the treatment for whipple disease?

A

goal is to prevent progression; antibiotic therapy–> prolonged treatment for at least 1 year is required; drugs that cross the BBB are preferred

67
Q

what is the prognosis of untreated whipple disease?

A

it is fatal

68
Q

What is overflow diarrhea? and who is at risk?

A

severe constipation–> only contents that get by is liquid; elderly/nursing home patients

69
Q

how do you make the diagnosis of overflow diarrhea?

A

if there is fecal impaction that is readily detectable by rectal examination

70
Q

what is pseudo-diarrhea?

A

frequent passage of small volumes of stool

71
Q

what is pseudo-diarrhea often associated with?

A

rectal urgency, tenesmus, or a feeling of incomplete evacuation; accompanies IBS or proctitis

72
Q

What are the complications associated with constipation?

A

fecal impaction and stercoral ulcers

73
Q

What is the clinical presentation of fecal impaction?

A

decreased appetite, nausea and vomiting, abdominal pain and distention, there may be paradoxical diarrhea as liquid stool leaks around the impacted feces: overflow incontinence

74
Q

how do you diagnose fecal impaction?

A

DRE: firm feces are palpable in rectal vault

75
Q

What are the complications associated with chronic laxative use?

A

melanosis coli: a benign hyperpigmentation of the colon

76
Q

What are the risk factors for AAA?

A

atherosclerosis, male sex, smoking, age, HTN, FH

77
Q

What does aneurysmal pain usually mean?

A

it is usually a harbinger of rupture and represents a medical emergency

78
Q

How do you diagnose an AAA?

A

abdominal ultrasound

79
Q

How do you prevent AAA/ who should get this screening?

A

abdominal ultrasound in male sex, 65-75 years who have ever smoked; or siblings/offspring of persons with AAA

80
Q

What is the management of an AAA?

A

monitor yearly: the risk of rupture increases with the size of the aneurysm –> aneurysms >5 cm in diameter

81
Q

How does an AAA rupture present?

A

without any prior warning, is always life threatening; acute pain and hypotension–> requires and emergency operation

82
Q

How does an aortic dissection present?

A

creates a false lumen (seen on CT), atypical “tearing” chest pain, widen mediastinum, vital signs abnormal

83
Q

How is appendicitis initiated?

A

by obstruction of the appendix by a fecalith, inflammation, foreign body, or neoplasm

84
Q

Besides surgery, how do you treat appendicitis?

A

broad-spectrum antibiotics with gram-negative and anaerobic coverage

85
Q

What are the complications associated with appendicitis?

A

gangrene; perforation leading to abscess usually in the pelvis or suppurative peritonitis (secondary peritonitis)

86
Q

what are some atypical presentations of appendicitis?

A

elderly–> minimal vague symptoms; pregnancy: random areas due to displacement of appendix due to uterus

87
Q

What are the risk factors for ectopic pregnancy?

A

pelvic inflammatory disease, ruptured appendix, and prior tubal surgery

88
Q

How do you diagnose an ectopic pregnancy?

A

positive pregnancy test: failure of serum beta-hCG to double every 48 hours; no intrauterine pregnancy on transvaginal ultrasound with elevated serum beta-hCG

89
Q

What is ovarian torsion associated with?

A

ovarian enlargement

90
Q

Which side do 70% of ovarian torsions occur on? Why?

A

right side: increased length of utero-ovarian ligament on right; the sigmoid on left limits space

91
Q

How do ovarian torsions present?

A

sudden onset, severe, unilateral, lower abdominal pain that may develop after episodes of exertion

92
Q

What is acute colonic-pseudo obstruction (OGILVIE syndrome)

A

spontaneous massive dilation of cecum or right colon; without mechanical obstruction

93
Q

Who usually develops OGILVIE syndrome?

A

significantly ill patients (ICU)

94
Q

How do you diagnose OGILVIE syndrome?

A

x-ray or CT demonstrate colonic dilation confined to the cecum and proximal colon; the upper limit of normal for cecal size is 9mm;

95
Q

what is associated with an increased risk of colonic perforation in OGILVIE syndrome?

A

a cecal diameter greater than 10-12 cm is associated with an increased risk of colonic perforation

96
Q

How should you manage OGILVIE syndrome?

A

cecal size should be assessed by abdominal radiographs every 12 hours; conservative is the appropriate first step for mild cases; a nasogastric tube and rectal tube should be placed; all drugs that reduce intestinal motility should be discontinued; NO ORAL LAXATIVES

97
Q

How do you treat OGILVIE patients who are not improving?

A

patients with a cecal dilation greater than 12 cm: neostigmine, colonoscopic decompression, surgery

98
Q

Where’s meckel’s diverticulitis located?

A

on the anti-mesenteric border of the ileum

99
Q

what is meckel’s diverticulitis?

A

remnant of the vitelline duct

100
Q

how does meckel’s diverticulum present?

A

RLQ pain

101
Q

what 3 things mimic appendicitis?

A

crohn disease, peptic ulcer disease (gastric tissue) and meckel’s diverticulitis

102
Q

How do you diagnose meckel’s diverticulitis?

A

angiography: seeing vitelline artery aupplying the diverticulum; Meckel’s scan:Technetium-99m scan- nuclear medicine

103
Q

how do you treat meckel’s diverticulitis?

A

surgical resection, PPIs, and NGT for obstructions

104
Q

what are the complications associated with meckel’s diverticulitis?

A

intestinal obstruction (intussusception or volvulus), SBO, perforation, or diverticular inflammation

105
Q

Where does diverticulitis typically present?

A

LLQ

106
Q

how do you diagnose diverticulitis?

A

CT with contrast

107
Q

what is contraindicated in a patient with diverticulitis?

A

endoscopy (sigmoidscopy or colonoscopy) or barium enema bc risk of perforation

108
Q

how should you treat someone with diverticulitis?

A

empiric therapy: Inpatient: IV fluids, NPO, antibiotics for 7-10 days; outpatients: abx, clear liquid diet–> low residue diet

109
Q

what are the complications associated with diverticulitis?

A

abscess, perforation, fistula, liver abscess, stricture

110
Q

what is an acute mesenteric ischemia?

A

inadequate blood flow through the mesenteric vessels–> ischemia and gangrene of the bowel wall (superior mesenteric artery); life threatening

111
Q

how does acute mesenteric ischmia present?

A

periumbilical pain out of proportion “gut attack”

112
Q

how do you diagnose an acute mesenteric ischemia?

A

abdominal plain x-ray shows bowel distention, air-fluid levels, thumbprinting (submucosal edema); CT angiography of abd and pelvis with IV contrast is test of choice

113
Q

what causes chronic mesenteric ischemia?

A

long standing atherosclerotic disease; gradual reduction in flow to the intestines

114
Q

how does chronic mesenteric ischemia present?

A

abdominal angina- dull crampy periumbilical pain 15-30 minutes after a meal and lasting several hours; patients will have food fear; weight loss

115
Q

how do you treat chronic mesenteric ischemia?

A

possible bypass graft surgery

116
Q

what are three causes of adhesions?

A

multiple abdominal surgeries, diverticulitis, and crohn disease

117
Q

what is the microbiology associated with peritonitis?

A

mixed flora in which gram-negative bacilli and anaerobes predominate

118
Q

what antibiotics should be given to someone with secondary peitonitis?

A

fluroquinolone or third-generation cephalosporin plus metronidazole

119
Q

toxic megacolon is a complication of what two diseases?

A

IBD: UC; and C. diff

120
Q

how does toxic megacolon present?

A

vital sign changes: tachycardia, tachypnea, fever, hypotension; abdominal pain and distention

121
Q

how do you diagnose toxic megacolon?

A

clinical; abdominal x-ray or CT with contrast; ENDOSCOPY (sigmoidscopy or colonoscopy) or barium enema is contraindicated bc of risk of perforation

122
Q

how do you treat toxic megacolon?

A

IVF, antibiotics, stop narcotics/anticholinergics/antidiarrheals, colonic decompression

123
Q

where might a volvulus occur?

A

sigmoid: pregnancy or older patients (due to constipation)
cecum: young adults

124
Q

how do you diagnose a volvulus?

A

abdominal plain x-ray shows: bent coffee bean sign”

barium enema shows: “bird’s beak” shape

LOL REDO GI II BC NO WAY (2 decks)

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