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General GI disorders + infections Flashcards

1
Q

What clinical findings suggest inflammatory diarrhea?

A

mucus or blood in the stool

fever

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2
Q

What microscopic exam findings indicate inflammatory diarrhea?

A

leukocytes on microscopic exam

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3
Q

What are the major causes of noninflammatory diarrhea?

A

vibrio cholerae, enterotoxigenic E coli, clostridium perfringens, bacillus cerus, staph aureus, rotavirus, norovirus, giardia lamblia, cryptosporidium

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4
Q

What are the major causes of of inflammatory diarrhea?

A

shigella, salmonella, campylobacter jejuni, enterohemorrhagic E. coli, enteropathogenic E. coli, yersinia enterocolitica, clostridioides difficile, entamoeba histolytica

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5
Q

What type of diarrhea is caused by: vibrio cholerae

A

noninflammatory diarrhea

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6
Q

What type of diarrhea is caused by: enterotoxigenic escherichia coli

A

noninflammatory diarrhea

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7
Q

What type of diarrhea is caused by: clostridium perfringens

A

noninflammatory diarrhea

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8
Q

What type of diarrhea is caused by: bacillus cerus

A

noninflammatory diarrhea

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9
Q

What type of diarrhea is caused by: staph aureus

A

noninflammatory diarrhea

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10
Q

What type of diarrhea is caused by: rotavirus

A

noninflammatory diarrhea

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11
Q

What type of diarrhea is caused by: noroviruses

A

noninflammatory diarrhea

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12
Q

What type of diarrhea is caused by: shigella spp.

A

inflammatory diarrhea

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13
Q

What type of diarrhea is caused by: salmonella spp.

A

inflammatory diarrhea

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14
Q

What type of diarrhea is caused by: enterohemorrhagic E. coli

A

inflammatory diarrhea

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15
Q

What type of diarrhea is caused by: enteropathogenic E. coli

A

inflammatory diarrhea

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16
Q

What are the most common bacterial causes of foodborne illnesses? Parasitic? Viral?

A

bacterial: campylobacter spp., salmonella enterica
parasite: giardia lamblia
viral: norovirus

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17
Q

What is the most common etiology of traveler’s diarrhea?

A

enterotoxigenic E. coli

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18
Q

What is the shape and gram stain of vibrio cholerae?

A

curved (“comma” shaped) gram-negative rods

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19
Q

How is vibrio cholerae spread?

A

contaminated water under conditions of poor sanitation, marine crustaceans

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20
Q

What are the virulence factors of vibrio cholerae?

A

toxin co-regulated pili –> bacterial aggregation

cholera toxin (A-B toxin) –> ADP-ribosylation leads to cAMP accumulation and activation of CFTR –> increased choloride scretion and decreased sodium uptake –> secretory diarrhea

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21
Q

What is the clinical presentation of vibrio cholerae infection?

A

severe dehydrate that can cause death following ingestion of contaminated water or seafood

“rice-water” stool

can lead to hypovolemia, shock, and death

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22
Q

What is the treatment for vibrio cholerae infection?

A

rapid replacement of fluids and electrolytes, antibiotics to shorten duration of symptoms

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23
Q

What is the virulence factor associated with enterotoxigenic E. coli (ETEC)?

A

heat labile toxin –> leads to CFTR chloride secretion and watery stools

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24
Q

What is clostridium perfringens (shape, gram stain)? What are the symptoms of infection?

A

anerobic gram-positive bacilius

causes food poisoning associated with contaminated meat/poultry/legumes

diarrhea, abdominal cramping, gas gangrean when inoculated into tissues

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25
Q

What is the shape/gram stain of bacillus cerus? What is the virulence factor(s)?

A

gram-positive rod

heat labile-type toxin, enterotoxin (leads to watery diarrhea and vomiting respectively)

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26
Q

Which infection is associated with reheating of rice?

A

bacillus cereus

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27
Q

What is rotavirus? What are the symptoms of infection?

A

double-stranded RNA virus

leads to severe diarrhea requiring oral rehydration

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28
Q

What are noroviruses? What is their presentation? Diagnosis?

A

viruses acquired by fecal-oral transmission or through contaminated food/water

nausea, vomiting, diarrhea, fever

diagnosed by enzyme-linked immunosorbent or PCR assays

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29
Q

How is giardia lamblia transmitted?

A

fecal-orally –> usually in cyst form in environment

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30
Q

How is cryptosporidium spp. acquired?

A

fecal-orally from domestic animals, often more severe in immunocompromised patients

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31
Q

What is the presentation of enterohemorrhagic E. coli (EHEC) infection?

A

bloody diarrhea, crampy abdominal pain without fever

associated with hemolytic-uremic syndrome

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32
Q

What are the 5 “F”s of shigella transmission?

A

fingers, food, flies, feces, fomites

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33
Q

What is the pathogenicity of shigella?

A

transmission through intestinal M cells with a type III secretion system

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34
Q

What is the clinical presentation of shigella infection?

A

mild, watery diarrhea or more extreme diarrhea with blood and pus

fever present

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35
Q

What is the shape and gram stain of campylobacter jejuni?

A

“sea-gull” shaped gram negative rod

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36
Q

What is the pathogenicity of C. difficile?

A

two toxins (A and B) that inactivate Rho GTPases leading to cell death and loss of barrier function

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37
Q

What is the clinical presentation of clostridioides infection?

A

diarrhea with variable severity and can include pseudomembrane formation

onset after antibiotic use

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38
Q

What form(s) are entamoebia histolytica in in GI infections?

A

trophozoites dwell in lumen and wall –> change into cysts after leaving the gut

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39
Q

For which of the following does an ADP-ribosylating toxin play a crucial role in disease?

a) vibrio cholerae
b) campylobacter jejuni
c) salmonella enterica
d) clostridioides difficle
e) staphylococcus aureus

A

a) vibrio cholerae

40
Q

A patient of yours states that he has had diarrhea after attending a church picnic. Which of the following features would suggest staph aureus as the cause?

a) bloody diarrhea
b) large numbers of leukocytes in the stool
c) prominent nausea and vomiting
d) fever
e) symptoms lasting at least a week

A

c) prominent nausea and vomiting

41
Q

All of the following cause an inflammatory diarrhea EXCEPT:

a) salmonella enterica
b) shigella flexneri
c) campylobacter jejuni
d) vibrio cholerae
e) entamoeba histolytica

A

d) vibrio cholerae

42
Q

Guillain-Barre syndrome has been associated with which of the following?

a) salmonella enterica
b) shigella flexneri
c) campylobacter jejuni
d) vibrio cholerae
e) entamoeba histolytica

A

c) campylobacter jejuni

43
Q

What is primary vs. secondary peritonitis?

A

primary = no inciting event, essentially only occurs with ascites

secondary = bacterial contamination through spillage of intestinal flora

44
Q

What are intraperitoneal abscesses?

A

localized/confined (walled off) infection within the peritoneal space

includes diverticular and periappendiceal abscesses

45
Q

What are visceral abscesses?

A

localized infections within organs

includes liver, splenic, perinephric, renal, pancreatic, and tubovarian abscesses

46
Q

What are the most common pathogens of primary peritonitis?

A

E. coli, klebsiella, strep pneumo, enterococci

rarely anaerobes, rarely TB, gonorrhea, chlamydia

47
Q

What is the pathogenesis of primary peritonitis?

A

hematogenous, lymphatic, or transmural seeding of bacteria to the peritoneal fluid (ascitic fluid specifically)

liver disease prevents clearance of bacteria and seed into liver lymph into ascitic fluid

cirrhosis leads to complement deficiency and reduced immune activity

48
Q

What are the clinical manifestations of primary peritonitis?

A

fever, abdominal pain, nausea, vomiting, diarrhea, diffuse abdominal tenderness, rebound tenderness, hypoactive/absent bowel sounds

signs of liver disease/cirrhosis

49
Q

How is primary peritonitis diagnosed?

A

paracentesis with ascitic fluid that has > 250/mm3 of neutrophils

culture may or may not be positive (not necessary)

CT or ultrasound to rule out other causes of infection

50
Q

What is the treatment for primary peritonitis?

A

antibiotic therapy –> broad spectrum until specific organisms are identified

liver transplant

51
Q

What are the major causes of secondary peritonitis?

A

perforation of GI (appendicitis, diverticulitis, peptic ulcer, neoplasm)

strangulation of bowel

pancreatitis, cholecystitis

52
Q

What organisms are associated with secondary peritonitis?

A

endogenous intestinal organisms –> mostly anaerobes, some gram-positive cocci

normally polymicrobial

53
Q

What is the pathogenesis of chemical peritonitis?

A

leakage of bile, gastric fluid, or pancreatic secretions leading to inflammation, necrosis –> increases susceptability to infection

54
Q

What are the local responses to secondary peritonitis? Systemic?

A

local: localized abscess, diffuse peritonitis
systemic: ileus, sepsis/septic shock, ARDS, acute renal failure

55
Q

How is secondary peritonitis diagnosed?

A

elevated WBC count with left shift

ileus on abdominal x-ray, “free air” on CXR, fluid on abdominal CT

56
Q

What is the treatment for secondary bacterial peritonitis?

A

broad-spectrum antibiotics

surgery to fix the leak/problem

percutaneous drainage

57
Q

What is CAPD peritonitis?

A

peritonitis of peritoneal dialysate, often by gram-positive bacteria from the skin

58
Q

What bacteria is associated with intraperitoneal abscess formation?

A

B. fragilis

often polymicrobial though

59
Q

What is the source of infection for this abscess: RLQ, pelvic abscesses

A

appendicitis

60
Q

What is the source of infection for this abscess: LLQ, pelvic abscesses

A

diverticulitis

61
Q

What is the source of infection for this abscess: lesser sac abscesses

A

pancreatitis

62
Q

What is the source of infection for this abscess: psos abscess

A

vertebral osteomyelitis

63
Q

What are pancreatic abscesses?

A

infections that wall off in the pancreas

often polymicrobial

64
Q

What is the pathogenesis of hepatic abscesses?

A

biliary spread (cholangitis)

portal spread

contiguous spread (cholecystitis)

hematogenous spread

traumatic spread

65
Q

What is the pathogenesis of acute appendicitis?

A

most often: obstruction of appendiceal lumen by hyperplasia (from inflammation) or by fecaliths, fibrosis, or neoplasms

obstructed lumen increases pressure and leads to necrosis and/or perforation and rupture

66
Q

What is the clinical presentation of acute appendicitis?

A

RLQ pain, anorexia, nausea, vomiting, fever, rebound tenderness, voluntary guarding, rigidity

67
Q

What is the treatment for acute appendicitis?

A

surgery (if ruptured)

broad spectrum antibiotics

68
Q

What is the treatment for diverticulitis?

A

maybe antibiotics (if systemic or high risk)

drainage and surgery (if large abscesses or complicated)

69
Q

Which area of the GI tract, if injured, is most likely to result in intraabdominal infection?

A

colon –> more microorganisms

70
Q

A 57 yo woman presents with abdominal pain and fever. On exam, she is febrile and tachycardic with a marked LLQ tenderness. What is the most likely diagnosis? How can you confirm your suspected diagnosis? Should she go immediately to the operating room for exploratory laprotomy?

A

diagnosis: complicated diverticulitis

imaging can help confirm diagnosis (CT scan)

treat with antibiotics and bowel rest, delay surgery if possible

71
Q

A patient with advanced liver disease and ascites awaiting transplant presents with fever, confusion, abdominal pain. Analysis of ascitic fluid shows increased neutrophils. A gram stain shows gram-negative bacilli, gram-positive cocci, and gram-positive bacilli. Is further evaluation needed? Is antibiotic therapy alone likely to cure infection?

A

yes further evaluation is necessary

polymicrobial infection indicates a secondary cause of peritonitis –> need evaluation for possible perforation

72
Q

A patient with cirrhosis and portal hypertension presents with encephalopathy and tense ascites. Which test is most likely to diagnose spontaneous bacterial peritonitis (SBP)?

a) CT scan of the abdomen
b) peripheral WBC count
c) peritoneal fluid neutrophil count
d) peritoneal fluid gram stain
e) peritoneal fluid culture

A

c) peritoneal fluid neutrophil count

73
Q

A 52 yo previously healthy male presents with abdominal pain, nausea, vomiting, fever. On abdominal exam, you identify RLQ tenderness, guarding, and rebound. Which of the following is the likely diagnosis?

a) spontaneous bacterial peritonitis
b) acute cholecystitis
c) pancreatic abscess
d) acute perforated diverticulitis
e) acute perforated appendicitis

A

e) acute perforated appendicitis

74
Q

CT scan confirms acute appendicitis, perforation, and peri-appendiceal abscess. Empiric antibiotic therapy should be directed against which microorganisms?

a) staph aureus
b) group A strep
c) aerobic gram negative bacilli and anerobes
d) non-tuberculosis mycobacteria
e) candida species

A

c) aerobic gram negative bacilli and anerobes

75
Q

What are “functional” GI disorders generally?

A

GI disorders without a structural basis

76
Q

What are the diagnostic criteria for IBS?

A

recurrent abdominal pain of at least 1 day per week in the last 3 months with 2 or more of the following:

  • pain/discomfort related to defecation
  • pain/discomfort associated with a change in stool frequency
  • pain/discomfort associated with a change in stool consistency
77
Q

What is the treatment strategy for functional GI disorders?

A

treating prevailing symptoms (based on their MOA if possible)

78
Q

What is the treatment for IBS?

A

pharmacologic and non-pharmacologic interventions

symptomatic treatment, CBT, peppermint oil

79
Q

True or false: functional bowel disorders are predominately psychological disorders?

A

False

80
Q

True or false: irritable bowel syndrome is a diagnosis of exclusion.

A

False

81
Q

Which of the following is the most important therapeutic intervention when treating patients with FGIDs?

a) choosing the correct pharmaceutical
b) psychiatric treatment
c) explaining to the patient that it is just in their head
d) establishing a good MD-patient relationship
e) dietary modifications

A

d) establishing a good MD-patient relationship

82
Q

Based on Rome IV, what is the essential criteria which needs to be present to make a diagnosis of IBS?

a) abdominal pain
b) changes in stool texture
c) changes in stool frequency
d) pain associated with defecation

A

a) abdominal pain

83
Q

Which of the following are potential therapies for patients with IBS-D?

a) alosetron
b) rifaximin
c) CBT
d) lubiprostone
e) A-C
f) all of the above

A

e) A-C

84
Q

What is IBS-C vs. IBS-D?

A

IBS-C is predominantly hard/lumpy stools with constipation

IBS-D is predominantly loose/watery stools with diarrhea

85
Q

What imaging modalities are used to image the stomach, small bowel, and large bowel?

A

barium studies in fluoroscopy

CT and MRI

86
Q

What imaging modalities are used for liver imaging?

A

ultrasound, CT, and MRI

87
Q

What imaging modalities are used for the gallbladder?

A

ultrasound followed by MRI

88
Q

What imaging modalities are used for pancreatic pathologies?

A

CT, MRI

89
Q

What structures are hyperdense on CT imaging?

A

calcium, blood, solid tumor, contrast dye

bright/white

90
Q

What structures are hypodense on CT?

A

simple fluids, solids, fat

dark colored

91
Q

What does it mean for a structure to be enhancing on CT scans?

A

solid tumor/inflammation

92
Q

What structures are anechoic (black) on ultrasound?

A

simple fluids

93
Q

What structures are hypoechoic (dark) on ultrasound?

A

not simple fluid, masses

94
Q

What structures are echogenic (bright) on ultrasound?

A

calcium, air, tumors

95
Q

What do fluoroscopic studies of the GI tract assess for?

A

bowel motility/obstruction, mucosal abnormalities, masses, bowel perforations

96
Q

What does an abdominal CT with IV and oral contrast used to evaluate for?

A

bowel obstruction/perforation, inflammation, tumor, abscesses

97
Q

What does this imaging suggest?

A

Achalasia

dilated esophagus, birds beak

GI (10 decks)

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