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Step 1 Smart Book > GI > Flashcards

GI Flashcards

1
Q

Patient with ulcerative colitis experiences abdominal pain and distention, fever, diarrhea, signs of shock - what are you worried about?

A

Toxic megacolon

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2
Q

What do we use to diagnose toxic megacolon?

A

Plain abdominal X-ray

Barium enema and colonoscopy are contraindicated because they may cause rupture

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3
Q

Is toxic megacolon seen more often in ulcerative colitis or Crohn’s?

A

Ulcerative colitis

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4
Q

Spared rectum - ulcerative colitis or Crohn’s?

A

Crohn’s

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5
Q

Transmural inflammation - ulcerative colitis or Crohn’s?

A

Crohn’s

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6
Q

Continuous mucosal damage - ulcerative colitis or Crohn’s?

A

Ulcerative colitis

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7
Q

What happens if the angle between the SMA and aorta becomes more acute?

A

Superior mesenteric artery syndrome

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8
Q

At what level does the SMA leave the aorta?

A

L1

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9
Q

What part of the duodenum becomes entrapped in superior mesenteric artery syndrome?

A

Transverse portion of the duodenum

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10
Q

Two immunoglobulin monomers + J chain + secretory component = ?

A

Secretory form of IgA

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11
Q

Where do we find secretory form of IgA

A

Tears, saliva, mucus, colostrum

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12
Q

What is colostrum?

A

First breast milk fed to an infant

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13
Q

What acid-base disturbance can Mallory-Weiss lead to?

A

Metabolic alkalosis from loss of H+ in the repeated episodes of vomiting

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14
Q

Abdominal X-ray shows air in the gallbladder and biliary tree - what does this make you suspicious of?

A

Gallstone ileus - a large gallstone causes the formation of a cholecystenteric fistula between gallbladder and adjoining gut tissue; the gallstone is able to pass through the fistula and the fistula then allows gas from the small bowel to enter the gallbladder

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15
Q

What happens to the gallstone in gallstone ileus?

A

Typically goes through the fistula but then gets stuck at the ileocecal valve

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16
Q

Imperforate anus (abnormal development of anorectal structures) is most commonly associated with what other developmental defects?

A

Urogenital tract anomalies

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17
Q

Contrast the different mediators of the body’s immune defense against localized vs. hematogenous infection by candida.

A

Localized - T cells vs. hematogenous - neutrophils

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18
Q

Esophageal biopsy showing moderately differentiated tumor cells with keratin nests and pearls - squamous cell or adenocarcinoma of the esophagus?

A

Squamous cell

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19
Q

What are 3 major risk factors for squamous cell carcinoma?

A

EtOH, smoking, consumption of foods with nitrosamines

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20
Q

Describe what happens in base excision repair.

A
  1. Glycosylases remove the defective base
  2. Endonuclease and then lyase cleave and remove the corresponding sugar-phosphate
  3. DNA polymerase replaces the missing nucleotide
  4. Ligase reconnects the DNA strand
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21
Q

What do you see on histology of squamous cell carcinoma of esophagus?

A

Keratin pearls

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22
Q

Presentation: colicky abdominal pain, constipation, irritability, headaches, works at a battery manufacturing plant - diagnosis?

A

Lead poisoning

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23
Q

Essential fructosuria is a benign disorder resulting from a defect/deficiency in what enzyme?

A

Fructokinase

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24
Q

What is the difference between metaplasia and ectopy?

A

Ectopy is the result of congenital malformation vs. metaplasia occurs during adult life

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25
Q

What is ectopy?

A

Microscopically and functionally normal cells/tissues found in an abnormal location due to embryonal maldevelopment

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26
Q

What’s the difference between gastric erosion vs. ulcer?

A

Erosion - mucosal defects that do not fully extend through the muscularis mucosa (i.e. limited to the mucosa layer)

Ulcer - mucosal defects that penetrate through the mucosal layer and extend into the submucosa

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27
Q

When an ulcer penetrates the posterior duodenal wall, it is likely to erode into what artery?

A

Gastroduodenal

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28
Q

What does it mean that the lac operon in E. coli (codes for proteins for lactose metabolism) is polycistronic?

A

One mRNA codes for several proteins (in this case, it encodes genes z, y, and z which are beta-galactosidase, permease, and beta-galactoside transacetylase respectively)

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29
Q

What should you think of if a hospitalized patient on broad spectrum antibiotics suddenly develops white/yellow membrane like plaques on the colonic mucosa accompanied with loose stools, low grade fever, and leukocytosis?

A

C. difficil overgrowth

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30
Q

Gastroenteritis caused by oxidase positive, gram negative, comma shaped rod that can survive on alkaline media - organism?

A

Vibrio cholerae

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31
Q

What is the mechanism of action of Ribavirin?

A

Thought to be multifactorial but ultimately leads to interference with the duplication of viral genetic material:

  1. Lethal hypermutation (since it is a nucleoside analog)
  2. Inhibition of RNA polymerase
  3. Inhibition of inosine monophosphate dehydrogenase (depletes GTP)
  4. Enhancing Th1 response
  5. Inhibition of RNA guanylyltransferase and methyltransferase resulting in defective 5’ cap
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32
Q

Which cells does Shigella invade?

A

M cells in the Peyer’s patches

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33
Q

What are the 3 main causes of HIV-associated esophagitis?

A

Candida, CMV, HSV-1

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34
Q

What would you see on stool microscopy with vibrio?

A

Just mucus and epithelium because vibrio does not invade the mucosa or cause enterocyte death

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35
Q

What would you likely need to supplement in a patient who has a gastrojejunostomy?

A

Iron because you have now bypassed the duodenum and proximal jejunum where iron is typically absorbed

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36
Q

What part of the immunoglobulin do macrophages and neutrophils bind?

A

Fc portion

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37
Q

What down regulates gastric acid secretion after a meal?

A

Intestinal influences (colon and ileum release peptide YY on ECL and inhibit histamine release which would stimulate gastrin)

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38
Q

Presentation: pruritus, rash, flushing, abdominal cramps, lots of mast cells on small intestine biopsy - diagnosis?

A

Mastocytosis - gastric hypersecretion from mast cell proliferation which leads to lots of histamine release

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39
Q

What is the first event in the pathogenesis of acute appendicitis?

A

Obstruction of the lumen

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40
Q

Is Meckel’s diverticulum a true or false diverticulum?

A

True

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41
Q

What GI side effect can opioids have?

A

Contraction of smooth muscles in the Sphincter of Oddi leading to increased pressures in the bile duct and gall bladder

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42
Q

How does secretory IgA defend against bacteria?

A

Binds to pili and other outer membrane proteins that mediate bacterial adherence and penetration through the mucosa

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43
Q

What mutation is required for the first step in the emergence of small adenomatous polyps from normal colonic mucosa?

A

APC

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44
Q

False diverticula are also called what?

A

Pulsion diverticula - created by herniation through weak spots in the colonic muscular layer

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45
Q

Upon lactose challenge, what are the significant findings in lactase-deficient individuals?

A
  1. Increased stool osmotic gap
  2. Increased breath hydrogen content
  3. Decreased stool pH
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46
Q

What is polyethylene glycol?

A

Osmotic laxative

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47
Q

What molecule is involved in mediating the accumulation of pus?

A

IL-8 because it induces chemotaxis and phagocytosis in neutrophils

48
Q

What is a pancreatic pseudocyst?

A

Common complication of acute pancreatitis in which there is a collection of fluid rich in enzymes and inflammatory debris with walls consisting of granulation tissue and fibrosis

49
Q

Dietary lipids are primarily absorbed where?

A

Jejunum

50
Q

What hormone stimulates the release of bicarbonate rich secretions from the pancreas?

A

Secretin

51
Q

Where is secretin produced?

A

Duodenum

52
Q

Hyperammonemia in hepatic encephalopathy results in depletion of what 2 things?

A

Alpha-ketoglutarate and glutamate

53
Q

Where is the esophagus located on CT?

A

Between the trachea and the vertebral bodies in the superior thorax

54
Q

Retroperitoneal hematoma in a stable patient is likely to occur due to injury to what organ?

A

Pancreas

55
Q

What organisms are most common in intraabdominal infections?

A

Typically polymicrobial but most commonly contain Bacteroides and E. coli

56
Q

What is the most effective treatment for patients with peptic ulcer disease?

A

Get rid of the H. pylori infection with antibiotics

56
Q

Why is the minimal infectious dose for vibrio normally so high?

A

It has high sensitivity to gastric acid - any condition that increases gastric pH will lower the minimum infective dose for the bug

56
Q

If a patient has alternating episodes of diarrhea and constipation, how do you differentiate between Crohn’s and IBD?

A

Crohn’s is more likely to have fistulas and abscesses

56
Q

What type of colonic tumor appears as a cauliflower-like mass on colonoscopy?

A

Villous adenoma

56
Q

What is the diagnosis for uncoordinated contractions of the esophagus and what work up needs to be done?

A

Diffuse esophageal spasms - need to do a cardiac work up to rule out angina pectoris

56
Q

Mutations of what genes are responsible for Lynch syndrome?

A

DNA mismatch repair genes

56
Q

How do we diagnose strongyloides infection?

A

Rhabditiform larva in the stool

56
Q

In what cellular layer do we find the intrinsic factor secreting parietal cells?

A

Upper glandular layer (beneath the superficial layer of the lamina propria)

56
Q

What is the most common location for colon adenocarcinoma?

A

Rectosigmoid colon

56
Q

Presentation: severe heartburn, fingertip ulcerations, multiple telangiectasias - diagnosis?

A

CREST syndrome = calcinosis, Raynaud syndrome, esophageal dysmotility, sclerodactyly, telangiectasia

56
Q

What is responsible for the esophageal dysmotility in CREST syndrome?

A

Atrophy and fibrous replacement of esophageal muscles

56
Q

What are carcinoid tumors derived from?

A

Enterochromaffin cells of intestinal mucosa

68
Q

Appendix biopsy shows nests/sheets of uniform cells with eosinophilic cytoplasm oval-to-round stippled nuclei - diagnosis?

A

Carcinoid tumor

69
Q

What do you see on histology in patients with lactase deficiency?

A

Normal intestinal mucosa

70
Q

Compared to sporadic colorectal carcinoma, how would you describe colitis associated carcinoma?

A
  1. Affects younger patients
  2. Progress from flat and non-polyploid dysplasia
  3. Histologically appear mucinous and/or have signet ring morphology
  4. Develop early p53 mutations and late APC gene mutations
  5. Be distributed within the proximal colon
  6. Be multifocal in nature
71
Q

Bilious vomiting after the first 24 hours of life is a sign of what?

A

Some kind of obstruction below the second part of the duodenum

72
Q

What causes intestinal atresia distal to the duodenum?

A

Vascular accidents in utero

73
Q

Which cytokines have anti-inflammatory effects?

A

IL-10 and TGF-beta

74
Q

question 9

A

come back to this

75
Q

If a drug inhibits gastric acid secretion in response to all 3 stimuli (histamine, ACh, gastrin), then it likely acts where?

A

H/K ATPase pump on parietal cell membrane

76
Q

What does 99mmTc-pertechnetate scan in the right lower abdominal quadrant indicate?

A

Meckel diverticulum - it detects the presence of gastric mucosa

77
Q

What is the difference in antibodies produced between the killed vaccine vs. the live attenuated vaccine for polio?

A

Live attenuated - more IgA vs. Killed - not as good at stimulating mucosal surfaces

78
Q

Describe the mechanism of diphenyoxylate.

A

Anti-diarrhea drug that works by binding to mu opiate receptors in the GI tract and slowing motility

79
Q

What does gross morphology show for signet-ring carcinomas in the stomach?

A

Diffuse infiltrative growth within the stomach wall

80
Q

Which picornavirus is the most acid-labile?

A

Rhinovirus (makes sense because the rest of them are enteroviruses so they are able to handle the acidic environment of the stomach)

81
Q

What strain of E. coli is unable to ferment sorbitol/produce glucuronidase?

A

EHEC O157:H7

82
Q

Describe the toxin produced by EHEC.

A

Shiga-like toxin that inactivates the 60S ribosomal subunit in human cells leading to an inhibition of protein synthesis and eventual cell death

83
Q

What do the toxins produced by C. difficile do?

A

Toxin A - attracts neutrophils causing mucosal inflammation while Toxin B - causes actin depolymerization and loss of cellular cytoskeleton integrity

84
Q

What are the 2 most common causes of acute pancreatitis?

A

Gallstones and alcoholism

85
Q

How can hypertriglyceridemia cause acute pancreatitis?

A

High levels of circulating triglycerides can lead to increased production of free fatty acids within the pancreatic capillaries by pancreatic lipase. If the concentration of free fatty acids exceeds the binding capacity of albumin, then it can lead to direct injury to the pancreatic acinar cells.

86
Q

What mutation facilitates the growth of adenomas by causing uncontrolled cell proliferation?

A

K-ras

87
Q

What is a necessary cofactor in the synthesis of delta-aminolevulinic acid?

A

Pyridoxal phosphate

88
Q

What does a duodenal ulcer in the distal duodenum suggest?

A

Zollinger Ellison syndrome (peptic ulcer syndrome tends to present in the first portion of the duodenum)

89
Q

The longitudinal mucosal tears in Mallory Weiss syndrome are secondary to?

A

Rapid increase of intraabdominal and intraluminal gastric pressure (i.e. during retching and vomiting)

90
Q

How many calories does 1 g of protein or carbohydrate yield?

A

4

91
Q

How many calories does 1 g of fat yield?

A

9

92
Q

How many calories does 1 g of ethanol yield?

A

7

93
Q

Compression of the splenic artery most affects which branch?

A

Short gastric - has the worst anastomoses of all the branches of the splenic artery

94
Q

How does chronic mesenteric ischemia present?

A

Epigastric or periumbilical pain 30-40 minutes after eating because more blood is needed for the digestion and absorption of nutrients

95
Q

Patients with Barrett’s esophagus have an increased risk of which cancer?

A

Esophageal adenocarcinoma

96
Q

What is the primary pathophysiologic mechanism for GERD?

A

Gastroesophageal junction incompetence

97
Q

When a patient is suspected to have H. pylori, where should you biopsy?

A

The prepyloric area because the organism is typically found in the greatest concentration in the gastric antrum

98
Q

Is B12 a fat or water soluble vitamin?

A

Water soluble

99
Q

Presentation: Baby with poor feeding, weakness, complete loss of extremity muscle tone, and eats honey. Diagnosis?

A

Infant botulism

100
Q

What test can be used to diagnose infant botulism?

A

Test stool for bacterial toxins

101
Q

Presentation: Progressive weight loss, jaundice, anorexia, enlarged but non tender gall bladder. Diagnosis?

A

Pancreatic adenocarcinoma

102
Q

What are the major risk factors for pancreatic cancer?

A

Old age, smoking, diabetes, chronic pancreatitis, genetic predisposition

103
Q

AST:ALT > 2 is indicative of what?

A

Alcohol hepatitis

104
Q

What do you see in terms of the mean corpuscular volume with chronic alcohol abuse?

A

Macrocytosis - either related to B12/folate deficiency or just from direct toxicity of alcohol on the marrow

105
Q

What happens to lactose in the body?

A

Catabolized into glucose and galactose by an intestinal brush border disaccharidase (lactase)

106
Q

What is galactosyl beta-1,4-glucose?

A

Lactose

107
Q

What prevents overgrowth of C. diff?

A

Intestinal biomass (the normal flora)

108
Q

Are villous or tubular adenomas more likely to progress to adenocarcinoma?

A

Villous

109
Q

What enzyme deficiency is the second most common cause of SCID (after X linked inheritance)?

A

Adenosine deaminase - enzyme necessary for the elimination of excess adenosine within cells

110
Q

What layer should be biopsied in Hirschsprung disease?

A

Submucosal (Meissner) and myenteric (Auerbach) autonomic plexi are absent in the affected segment of the bowel in Hirschsprung disease

111
Q

Where do most anal fissures occur?

A

Posterior midline distal to the dentate line because posterior anal canal is relatively poorly perfused

112
Q

Why are patients with Crohn’s disease at increased risk for gallstones?

A

Increased biliary acid wasting (bile acids are not reabsorbed as well in the ileum when it is affected by Crohn’s) leads to less bile acid in the bile relative to cholesterol causing cholesterol to precipitate and form stones

113
Q

Why are patients with Crohn’s disease at increased risk for kidney stones?

A

Impaired bile acid absorption in the terminal ileum leads to loss of bile acids in the feces –> fat malabsorption –> lipids end up binding calcium –> calcium doesn’t bind oxalate –> oxalate precipitates as kidney stones

114
Q

Histology of chalky white lesions in the mesentery show fat cell destruction and calcium deposition - suggestive of?

A

Acute pancreatitis

115
Q

Abnormal rotation and fixation of what leads to intestinal malrotation?

A

Midgut

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