General GI disorders + infections Flashcards
1
Q
What clinical findings suggest inflammatory diarrhea?
A
mucus or blood in the stool
fever
2
Q
What microscopic exam findings indicate inflammatory diarrhea?
A
leukocytes on microscopic exam
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
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
5
Q
What type of diarrhea is caused by: vibrio cholerae
A
noninflammatory diarrhea
6
Q
What type of diarrhea is caused by: enterotoxigenic escherichia coli
A
noninflammatory diarrhea
7
Q
What type of diarrhea is caused by: clostridium perfringens
A
noninflammatory diarrhea
8
Q
What type of diarrhea is caused by: bacillus cerus
A
noninflammatory diarrhea
9
Q
What type of diarrhea is caused by: staph aureus
A
noninflammatory diarrhea
10
Q
What type of diarrhea is caused by: rotavirus
A
noninflammatory diarrhea
11
Q
What type of diarrhea is caused by: noroviruses
A
noninflammatory diarrhea
12
Q
What type of diarrhea is caused by: shigella spp.
A
inflammatory diarrhea
13
Q
What type of diarrhea is caused by: salmonella spp.
A
inflammatory diarrhea
14
Q
What type of diarrhea is caused by: enterohemorrhagic E. coli
A
inflammatory diarrhea
15
Q
What type of diarrhea is caused by: enteropathogenic E. coli
A
inflammatory diarrhea
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
17
Q
What is the most common etiology of traveler’s diarrhea?
A
enterotoxigenic E. coli
18
Q
What is the shape and gram stain of vibrio cholerae?
A
curved (“comma” shaped) gram-negative rods
19
Q
How is vibrio cholerae spread?
A
contaminated water under conditions of poor sanitation, marine crustaceans
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
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
22
Q
What is the treatment for vibrio cholerae infection?
A
rapid replacement of fluids and electrolytes, antibiotics to shorten duration of symptoms
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
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
25
What is the shape/gram stain of bacillus cerus? What is the virulence factor(s)?
gram-positive rod
heat labile-type toxin, enterotoxin (leads to watery diarrhea and vomiting respectively)
26
Which infection is associated with reheating of rice?
bacillus cereus
27
What is rotavirus? What are the symptoms of infection?
double-stranded RNA virus
leads to severe diarrhea requiring oral rehydration
28
What are noroviruses? What is their presentation? Diagnosis?
viruses acquired by fecal-oral transmission or through contaminated food/water
nausea, vomiting, diarrhea, fever
diagnosed by enzyme-linked immunosorbent or PCR assays
29
How is giardia lamblia transmitted?
fecal-orally --\> usually in cyst form in environment
30
How is cryptosporidium spp. acquired?
fecal-orally from domestic animals, often more severe in immunocompromised patients
31
What is the presentation of enterohemorrhagic E. coli (EHEC) infection?
bloody diarrhea, crampy abdominal pain without fever
associated with hemolytic-uremic syndrome
32
What are the 5 "F"s of shigella transmission?
fingers, food, flies, feces, fomites
33
What is the pathogenicity of shigella?
transmission through intestinal M cells with a type III secretion system
34
What is the clinical presentation of shigella infection?
mild, watery diarrhea or more extreme diarrhea with blood and pus
fever present
35
What is the shape and gram stain of campylobacter jejuni?
"sea-gull" shaped gram negative rod
36
What is the pathogenicity of C. difficile?
two toxins (A and B) that inactivate Rho GTPases leading to cell death and loss of barrier function
37
What is the clinical presentation of clostridioides infection?
diarrhea with variable severity and can include pseudomembrane formation
onset after antibiotic use
38
What form(s) are entamoebia histolytica in in GI infections?
trophozoites dwell in lumen and wall --\> change into cysts after leaving the gut
39
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) vibrio cholerae
40
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
c) prominent nausea and vomiting
41
All of the following cause an inflammatory diarrhea EXCEPT:
a) salmonella enterica
b) shigella flexneri
c) campylobacter jejuni
d) vibrio cholerae
e) entamoeba histolytica
d) vibrio cholerae
42
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
c) campylobacter jejuni
43
What is primary vs. secondary peritonitis?
primary = no inciting event, essentially only occurs with ascites
secondary = bacterial contamination through spillage of intestinal flora
44
What are intraperitoneal abscesses?
localized/confined (walled off) infection within the peritoneal space
includes diverticular and periappendiceal abscesses
45
What are visceral abscesses?
localized infections within organs
includes liver, splenic, perinephric, renal, pancreatic, and tubovarian abscesses
46
What are the most common pathogens of primary peritonitis?
E. coli, klebsiella, strep pneumo, enterococci
rarely anaerobes, rarely TB, gonorrhea, chlamydia
47
What is the pathogenesis of primary peritonitis?
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
What are the clinical manifestations of primary peritonitis?
fever, abdominal pain, nausea, vomiting, diarrhea, diffuse abdominal tenderness, rebound tenderness, hypoactive/absent bowel sounds
signs of liver disease/cirrhosis
49
How is primary peritonitis diagnosed?
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
What is the treatment for primary peritonitis?
antibiotic therapy --\> broad spectrum until specific organisms are identified
liver transplant
51
What are the major causes of secondary peritonitis?
perforation of GI (appendicitis, diverticulitis, peptic ulcer, neoplasm)
strangulation of bowel
pancreatitis, cholecystitis
52
What organisms are associated with secondary peritonitis?
endogenous intestinal organisms --\> mostly anaerobes, some gram-positive cocci
normally polymicrobial
53
What is the pathogenesis of chemical peritonitis?
leakage of bile, gastric fluid, or pancreatic secretions leading to inflammation, necrosis --\> increases susceptability to infection
54
What are the local responses to secondary peritonitis? Systemic?
local: localized abscess, diffuse peritonitis
systemic: ileus, sepsis/septic shock, ARDS, acute renal failure
55
How is secondary peritonitis diagnosed?
elevated WBC count with left shift
ileus on abdominal x-ray, "free air" on CXR, fluid on abdominal CT
56
What is the treatment for secondary bacterial peritonitis?
broad-spectrum antibiotics
surgery to fix the leak/problem
percutaneous drainage
57
What is CAPD peritonitis?
peritonitis of peritoneal dialysate, often by gram-positive bacteria from the skin
58
What bacteria is associated with intraperitoneal abscess formation?
B. fragilis
often polymicrobial though
59
What is the source of infection for this abscess: RLQ, pelvic abscesses
appendicitis
60
What is the source of infection for this abscess: LLQ, pelvic abscesses
diverticulitis
61
What is the source of infection for this abscess: lesser sac abscesses
pancreatitis
62
What is the source of infection for this abscess: psos abscess
vertebral osteomyelitis
63
What are pancreatic abscesses?
infections that wall off in the pancreas
often polymicrobial
64
What is the pathogenesis of hepatic abscesses?
biliary spread (cholangitis)
portal spread
contiguous spread (cholecystitis)
hematogenous spread
traumatic spread
65
What is the pathogenesis of acute appendicitis?
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
What is the clinical presentation of acute appendicitis?
RLQ pain, anorexia, nausea, vomiting, fever, rebound tenderness, voluntary guarding, rigidity
67
What is the treatment for acute appendicitis?
surgery (if ruptured)
broad spectrum antibiotics
68
What is the treatment for diverticulitis?
maybe antibiotics (if systemic or high risk)
drainage and surgery (if large abscesses or complicated)
69
Which area of the GI tract, if injured, is most likely to result in intraabdominal infection?
colon --\> more microorganisms
70
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?
diagnosis: complicated diverticulitis
imaging can help confirm diagnosis (CT scan)
treat with antibiotics and bowel rest, delay surgery if possible
71
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?
yes further evaluation is necessary
polymicrobial infection indicates a secondary cause of peritonitis --\> need evaluation for possible perforation
72
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
c) peritoneal fluid neutrophil count
73
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
e) acute perforated appendicitis
74
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
c) aerobic gram negative bacilli and anerobes
75
What are "functional" GI disorders generally?
GI disorders without a structural basis
76
What are the diagnostic criteria for IBS?
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
What is the treatment strategy for functional GI disorders?
treating prevailing symptoms (based on their MOA if possible)
78
What is the treatment for IBS?
pharmacologic and non-pharmacologic interventions
symptomatic treatment, CBT, peppermint oil
79
True or false: functional bowel disorders are predominately psychological disorders?
False
80
True or false: irritable bowel syndrome is a diagnosis of exclusion.
False
81
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
d) establishing a good MD-patient relationship
82
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) abdominal pain
83
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
e) A-C
84
What is IBS-C vs. IBS-D?
IBS-C is predominantly hard/lumpy stools with constipation
IBS-D is predominantly loose/watery stools with diarrhea
85
What imaging modalities are used to image the stomach, small bowel, and large bowel?
barium studies in fluoroscopy
CT and MRI
86
What imaging modalities are used for liver imaging?
ultrasound, CT, and MRI
87
What imaging modalities are used for the gallbladder?
ultrasound followed by MRI
88
What imaging modalities are used for pancreatic pathologies?
CT, MRI
89
What structures are hyperdense on CT imaging?
calcium, blood, solid tumor, contrast dye
## Footnote
*bright/white*
90
What structures are hypodense on CT?
simple fluids, solids, fat
## Footnote
*dark colored*
91
What does it mean for a structure to be enhancing on CT scans?
solid tumor/inflammation
92
What structures are anechoic (black) on ultrasound?
simple fluids
93
What structures are hypoechoic (dark) on ultrasound?
not simple fluid, masses
94
What structures are echogenic (bright) on ultrasound?
calcium, air, tumors
95
What do fluoroscopic studies of the GI tract assess for?
bowel motility/obstruction, mucosal abnormalities, masses, bowel perforations
96
What does an abdominal CT with IV and oral contrast used to evaluate for?
bowel obstruction/perforation, inflammation, tumor, abscesses
97
What does this imaging suggest?
Achalasia
## Footnote
*dilated esophagus, birds beak*
