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GI 1 Flashcards

1
Q

What are 3 key diagnostic labs in lactase-deficient individuals?

A

increased stool osmotic gap, increased breath hydrogen content, and decreased stool pH upon lactose challenge

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2
Q

Why is stool pH lowered in pts with lactose intolerance?

A

undigested lactose accumulates in the GI lumen, leading to osmotic diarrhea; bacterial fermentation of lactose produces short-chain FAs and excess hydrogen which acidifies stool and lowers pH

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3
Q

How is lactose intolerance confirmed with lactose intolerance test?

A

oral administration of 50g of lactose, with blood levels measured at 0. 60, and 120 minutes; if blood glucose increases <20mg/dL and the individual experiences Sx, the Dx of lactose intolerance is confirmed

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4
Q

How does lowering the cut-off affect sensitivity, TPs, FPs, PPV, and FN of a test?

A 
sensitivity: increase
TP: increase
FP: larger increase
PPV: decrease
FN: decrease
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5
Q

Which structures does the ventral pancreatic bud give rise to?

A

uncinate process, inferior/posterior portion of pancreas head, and major pancreatic duct of Wirsung

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6
Q

How does pancreas divisum present?

A

pancreatic ductal systems remain separate with accessory duct draining majority of pancreas

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7
Q

What is the MOA of VIP?

A

it causes relaxation of the GI smooth msucle, inhibition of gastric H+ secretion, and stimulation of pancreatic bicarbonate and chloride secretion

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8
Q

What is a VIPoma?

A

pancreatic islet cell tumor that leads to excess VIP secretion, resulting in pancreatic cholera, aka WDHA syndrome (Watery Diarrhea, Hypokalemia, Achlorhydria)

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9
Q

What is the MOA of CCK?

A

It causes increased secretion of pancreatic enzymes and bicarbonate, gallbladder contraction, and gastric emptying. It is produced by the I-cells of the proximal small bowel mucosa in response to FAs and monoglycerides

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10
Q

What is the MOA of secretin?

A

secretin is produced by duodenal S-cells in response to duodenal acidity and fatty acids and it increases pancreatic and biliary bicarbonate secretion and decreases gastric acid secretion

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11
Q

What is the MOA of gastrin?

A

it is produced by G-cells in the stomach mucosa and stimulates gastric acid production and growth of the gastric mucosa - it classically causes intractable peptic ulcer disease

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12
Q

What are two manifestations of glucagonoma?

A

secondary DM and mecrolytic migratory erythema of the skin

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13
Q

What is used to Tx the Sx of VIPoma?

A

somatostatin/octreotide

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14
Q

What is the central event in the pathogenesis of acute necrotizing pancreatitis?

A

abnormal activation of trypsinogen

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15
Q

What are some other pancreatic enzymes that trypsin can activate and what does activation of these lead to?

A

elastase, chymotrypsin, and phospholipase
activation leads to:
-pancreatic autodigestion (proteases)
-vascular damage and hemorrhage Ielastase)
-fat necrosis (lipase and phospholipase)

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16
Q

Does lipase require activation by trypsin?

A

no

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17
Q

Why do aneurysms most commonly occur at vessel branch points?

A

there is no medial layer of blood vessels at branch points which makes them a naturally weak area

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18
Q

What structures are in close relation to the second part of the duodenum?

A

head of the pancreas; ampulla of Vater is in the 2nd part of the duodenum

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19
Q

What structures are in close relation to the 3rd part of the duodenum and why are these structures at risk?

A

uncinate process of the pancreas and the superior mesenteric artery and vein - they are at high risk for direct invasion by a tumor in the 3rd part of the duodenum

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20
Q

What separates the duodenum from the jejunum?

A

ligament of Treitz

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21
Q

Which part of the duodenum courses horizontally across the abdominal aorta and IVC at the level of the 3rd lumbar vertebra?

A

third part of duodenum

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22
Q

What is the MOA of vancomycin?

A

it binds to D-alanyl-D-alanine termini in cell wall peptide precursors and prevents the formation of peptidoglycan

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23
Q

What is the MOA of vanco resistance?

A

a change in the peptide precursor structure that alters the vancomycin-binding site from D-alanyl-D-alanine terminus to a D-alanine-D-lactate terminus

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24
Q

What are the two modes of penicillin resistance?

A

1) production of B-lactamases

2) modification of penicillin binding proteins

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25
Q

What is the MOA of polymyxins?

A

they bind, disrupt, and interfere with the permeability of the cytoplasmic membrane

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26
Q

What is the MOA of tetracyclines?

A

it inhibits protein synthesis by binding the 30s ribosomal unit, preventing bacterial protein synthesis

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27
Q

What is the MOA of tetracycline resistance?

A

increased efflux of drug from within the bacterial cell via efflux pumps or production of protein that allows translation to take place in the presence of tetracycline

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28
Q

What do stool guaiac tests detect?

A

trace bleeding in the GI tract

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29
Q

How are GI ulcers defined?

A

breaches of the alimentary tract mucosa that extend through the muscularis mucosae into the submucosa

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30
Q

How are peptic ulcers defined?

A

They are chronic lesions in areas exposed to acid and peptic juices; the most common locations include the proximal duodenum, anral stomach, and gastroesophageal junction

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31
Q

Which type of peptic ulcers are rarely malignant?

A

duodenal ulcers

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32
Q

How many calories of energy are supplied by 1g of protein, carbohydrate, fat, or ethanol?

A

protein and carbohydrates: 4 cal

fat: 9 cal
ethanol: 7 cal

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33
Q

What do pts undergoing total gastrectomy require supplementation of?

A

lifelong B12 supplementation d/t poor B12 absorption that occurs with intrinsic factor deficiency

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34
Q

What results from an “apple-peel” atresia in utero, where an infant presents with bilious vomiting?

A

superior mesentaric artery atresia that manifests as a blind-ending proximal jejunum with absence of a long length of small bowel and dorsal mesentery; the terminal ileum distal to the atresia spirals around an ileocolic vessel

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35
Q

Why do pts with Crohn disease have an increased risk of presenting with calcium oxalate stones?

A

In a healthy bowel, calcium binds oxalate, producing insoluble calcium oxalate salts that are able to excrete oxalate. In Crohn, Ca2+ binds lipids instead, making it unavailable for complexing wiht oxalate. As a result, an increased amount of oxalate is absorbed, promoting the formation of urinary stones

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36
Q

What happens to bile acids in Crohn?

A

When the terminal ileum is inflamed, most bile acids are lost with feces which cases impaired fat absorption. The excess lipids in the bowel lumen bind Ca2+ ions and these soap complexes are excreted with the feces

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37
Q

How do opioid analgesics cause biliary colic? What should be used for pain control?

A

They cause contraction of smooth muscles in the sphincter of Oddi leading to increased pressures in the bile duct and gallbbladder
-NSAIDs like diclofenac or ketorolac should be used

38
Q

How is DNA base excision pair conducted for nitrates?

A
  • glycosylases remove the defective base
  • the corresponding sugar-phosphate is cleaved and removed by endonuclease, followed by lyase
  • DNA polymerase then replaces teh missing nucleotides
  • ligase reconnects the DNA strands
39
Q

what disorder is similar to the MOA of polyethylene glycol?

A

lactose intolerance d/t lactase deficiency leading to osmotic darrhea

40
Q

When are osmotic laxatives like polyethylene glycol given?

A

constipation in elderly pts, debilitated pts, and those on chronic opiate therapy

41
Q

How is trypsinogen activated into trypsin?

A

by enteropeptidase, an enzyme produced in teh duodenum

42
Q

What are clinical manifestations of enteropeptidase deficiency?

A

diarrhea, growth retardation, and hypoproteinemia

43
Q

What is a painful condition that causes lipase deficiency?

A

chornic pancreatitis

44
Q

What is the function of secretin

A

to secrete bicarb from the pancreas and gallbladder to neutralize the acidic pH entering the duodenum for proper funciton of pancreatic enzymes

45
Q

What are the two functions that make trypsin essential for protein digestion?

A
  1. it degrades complex peptides to dipeptides and amino acids
  2. it activates other proteases such as carboxypeptidase, elasetase, and chymotrypsin
46
Q

What test is used to screen for malabsorption?

A

Sudan III stain of stool which identifies fecal fat

47
Q

What is linkage equilibrium?

A

when a pair of alleles from two loci are inherited together in the same gamete (haplotype) more or less often than would be expected by random chance alone given their occresponding allele frequencies

48
Q

What describes the presence of different organellar genomes (mutated and wild type) wihtin a single cell, i.e. severity of mitochondrial diseases related to proportion of abnormal:normal mitochondria in pt’s cells

A

heteroplasmy

49
Q

What is the proportion of people with a given genotype who express its associated phenotype?

A

penetrance

50
Q

What is the occurrence of multiple phenotypic manifestations from a single gene?

A

pleitropy

51
Q

What is one of the most common locations affected in Crohn?

A

terminal ileum

52
Q

What is the pathogenesis of Crohn?

A

increased activity of Th1 cells mediated delayed HS reaction and granuloma formation and also produce IL-2 and IFN-g and activate macrophages to synthesize TNF

53
Q

What is the pathogenesis of ulcerative colitis?

A

Th2 cells that activate IL-4, IL-5, IL-6, IL-10

54
Q

What are non-caseating granulomas and cobblestone appearance characteristic of?

A

Crohn disease

55
Q

What do abdominal pain and distention, along with fever, diarrhea, and signs of shock in a pt with ulcerative colitis suggest?

A

toxic megacolon

56
Q

What should be used to Dx toxic megacolon and what diagnostics are contraindicated?

A

plain abdominal xray should be used for Dx

-barium contrast and colonoscopy are contraindicated

57
Q

Describe the involvement of the bowel in CD vs. UC

A

CD: anywhere from mouth to anus; perianal disease is common (fistula, structures)

UC: colorectal intestine, rectum is always involved

58
Q

How do you distinguish CD from UC on light microscopy?

A

CD: transmural infalmmation, noncaseating granulomas, skip lesions, and linear ulceration of the mucosa

UC: mucosal and submucosal inflammation with continuous involvement

59
Q

What are the clinical manifestations in CD v. UC?

A

CD: abdominal pain, diarrhea

UC: bloody diarrhea, abdominal discomfort

60
Q

What are the intestinal complications of CD and UC?

A

CD: fistulas and structures (lead to intestinal obstruction)

UC: toxic megacolon

61
Q

A 32yo Caucasian male with vague abdominal pain, low-grade fever, and diarrhea is treated with antibiotics without significant improvement. Several weeks after Sx onset, he develops a skin lesion in his RLQ that turns out to be an enterocutaneous fistula. What is the most likely Dx?

A

Crohn disease - fistula can form between the intestine itself or intestine and another organ, like bladder, vagina, or skin

62
Q

What are the most common complications of Crohn?

A

fistulas and structures

63
Q

What are anal fissures?

A

a tear in the lining of the anal canal d/t constipation and low-fiber diets
-pts complain of a severe tearing pain associated with the passage of bowel movements and there may be a skin tag on PE

64
Q

Where are most anal fissures located and why?

A

most are located at the posterior midline of the anal verge because the posterior anal canal is relatively poorly perfused, making its mucosa sensitive to trauma by hard fecal masses

65
Q

Where do most duodenal ulcers occur?

A

duodenal bulb (first portion of the duodenum)

66
Q

What does an ulcer found in the distal duodenum suggest?

A

Zollinger-Ellison syndrome

67
Q

Why does diarrhea occur in 50% of pts with ZE syndrome?

A

because pancreatic and intestinal enzymes are inactivated by gastric acid, so the body cannot properly digest nutrients

68
Q

What is seen in chronic gastritis with antral sparing?

A

autoimmune gastritis

69
Q

Why do cholesterol gallstones form in Crohn?

A

When the mucosa of the terminal ileum is inflamed, bile acids are not reabsorbed and they are lost with feces. As a result, a lesser amount of bile acid is present in bile, and the ratio of cholesterol/bile acids increases. Cholesterol precipitates in bile of the gallbladder and forms gallstones

70
Q

Which organ is supplied by a foregut blood supply but is not a foregut derivative? What does it form from?

A

spleen - mesodermal dorsal mesentary

71
Q

What are classic histologic findings for Whipple disease?

A

small intestine mucosa containing enlarged, foamy macrophages, packed with both rod-shaped bacilli and PAS+, diastase-resistant granules (which consist of lysosomes and partially digested bacteria)

72
Q

How does Whipple disease present clinically?

A

It is most commonly seen in middle-aged Caucaian males presenting with darrhea and weight loss along with arthropathy, polyarthritis, psych and cardiac abnormalities

73
Q

What is a necessary cofactor in the synthesis in delta-aminolevulinic acid (which is elevated in cases of lead poisoning?

A

pyridoxal phosphate (B6)

74
Q

What is a transcription factor responsible for cytokine production in the immune response to infectious pathogens and is associated with Crohn disease?

A

NF-kB

75
Q

What is the most common obstructing agent that causes acute appendicitis?

A

fecaliths

76
Q

What is the first event in pathogenesis of acute appendicitis?

A

obstruction of the lumen of the appendix

77
Q

When can carcinoid syndrome occur without liver metastasis?

A

if the primary tumor is outside of the intestine, such as the lung

78
Q

What does VACTERL syndrome stand for?

A 
Vertebral defects
Anal atresia
Cardiac anomalies
Tracheoesophageal fistula
Esophageal atresia
Renal anomalies
Limb anomalies
79
Q

What are the two mechanisms that regulate the lac operon?

A
  1. negatively regulated by repressor protein binding to the operator locus
  2. positively regulated by cAMP-CAP binding upstream from the promoter locus
80
Q

Increased activity of what enzyme can be linked to some forms of colon adenocarcinoma?

A

COX-2

81
Q

What is the first event in pathogenesis of acute appendicitis?

A

obstruction of the lumen by fecaliths, hyperplastic lymphoid follicles, foreign bodies, or tumors

82
Q

What is achalasia?

A

an esophageal motility disorder caused by the loss of ganglion cells in the LES

83
Q

What are the major risk factors for squamous carcinoma of the esophagus?

A

cigarette smoking, alcohol use,achalasia, plummer-vinson syndrome, nitrosamines

84
Q

When is carcinoid syndrome benign and why?

A

when it is confined to the intestine bc its secretory products are metabolized by teh liver

85
Q

When can carcinoid syndrome occur without liver metastasis?

A

when the primary tumor is outside the intestine, such as the lung

86
Q

What is the product of RNAP I?

A

rRNA

87
Q

What is the product of RNAP II?

A

mRNA

88
Q

What is the product of RNAP III?

A

tRNA

89
Q

What do amatoxins from the poisonous mushroom Amanita phalloides inhibit and prevent synthesis of?

A

RNAP II –> prevent mRNA synthesis

mushrooms - mRNA

90
Q

What is a cause of loss of tunnel vision, night blindness, generalized pruritis, and dry skin? What GI cause could leaad to this?

A

Vitamin A deficiency - prolonged biliary obstruction

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