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Step 1 > GI random facts > Flashcards

GI random facts Flashcards

1
Q

What affects zone 2 of the liver?

A

Yellow fever

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2
Q

What affects zone 3 of the liver?

A

Ischemia, metabolic toxins, alcoholic hepatitis

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3
Q

What are the spermatic cord fascia layers and where do they come from?

A

Extern spermatic fascia from the external oblique, cremaster in muscle and fascia from the internal oblique, and internal spermatic fascia from the transversal is fascia

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4
Q

What increases gastrin secretion?

A

Chronic atrophic gastritis, Z-E syndrome, and chronic PPI use

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5
Q

What are the effects of CCK?

A

⬆️ pancreatic secretion, ⬆️ gallbladder contraction,⬆️ sphincter of Oddi relaxation, decrease gastric emptying

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6
Q

How does CCK have its effects?

A

Acts on neural muscarinic pathways to cause pancreatic secretion

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7
Q

Watery diarrhea, hypokalemia, and achlorhydria

A

VIPoma

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8
Q

Regulators of gastric parietal cell and how they work

A

Ach (M3) and gastrin (CCKa) activate a Gq receptors increasing IP3 and Ca. Histamine (H2) activates a Gs protein increasing cAMP. Prostaglandins/misoprostol and somatostatin activate a GI protein, inhibiting cAMP.

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9
Q

Where is iron absorbed?

A

Duodenum

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10
Q

Where is folate absorbed

A

Small bowel

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11
Q

Where is B12 absorbed?

A

Terminal ileum with bile salts, requires intrinsic factor

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12
Q

What catalyzes the rate limiting step in bile synthesis?

A

Cholesterol-7-alpha-hydroxylase

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13
Q

What is the body’s only mechanism of cholesterol elimination?

A

Bile secretion

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14
Q

How does bile have antimicrobial activity?

A

Via membrane disruption

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15
Q

What catalyzes the conjugation of bilirubin?

A

UDP-glucuronosyl-transferase

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16
Q

What causes achalasia?

A

Loss of myenteric (Auerbach) plexus

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17
Q

What does achalasia predispose you to?

A

Squamous cell carcinomA

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18
Q

Histopathology of esophageal squamous cell carcinoma

A

Solid nests of neoplasticism squamous cells with abundant eosinophilia cytoplasm and distinct borders. Areas of keratinization and the presence of intercellular bridges

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19
Q

Ménétrier disease

A

Gastric hyperplasia of mucosa causes hypertrophied rugae, excess mucus production with resultant protein loss and parietal cell atrophy with decreased acid production. Precancerous

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20
Q

What affects zone 1 of the liver?

A

Viral hepatitis

21
Q

Which types of colonic polyps are non-neoplastic, neoplastic, and premalignant?

A

Hyperplastic and hamartomatous are non-neoplastic, adenomatous is neoplastic, and serrated is premalignant

22
Q

Which type of adenomatous polyp has more malignant potential: villous or tubular?

A

Villous

23
Q

How are serrated polyps premalignant ?

A

Via CpG hypermethylation phenotype pathway with microsatellite instability and mutations in BRAF

24
Q

“Saw tooth” pattern of crypts

A

Serrated polyp

25
Q

FAP

A

AD, mutation of APC on chromosome 5q

26
Q

Gardner syndrome

A

FAP plus osseous and soft tissue tumors, congenital hyper trophy of retinal pigment epithelium, impacted/supernumerary teeth

27
Q

Turcot syndrome

A

FAP plus malignant CNS tumor

28
Q

Peutz-Jeghers syndrome

A

AD, numerous hamartomatous polyps plus hyperpigmentation, increased risk of colorectal, breast, stomach, small bowel, and pancreatic cancer.

29
Q

Pigmented mucocutaneous Macules on the buccal mucosa

A

Peutz-Jeghers syndrome

30
Q

What is fetor hepaticus?

A

Musty smelling breath from liver cell failure/cirrhosis

31
Q

When can you see elevated amylase

A

Acute pancreatitis/mumps

32
Q

Mechanism of Reye syndrome

A

Aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzymes

33
Q

Risk factors for angiosarcoma of the liver

A

Arsenic and vinyl chloride

34
Q

Cirrhosis with PAS positive granules in liver

A

Alpha-1-antitrypsin deficiency

35
Q

Treatment for Crigler-Najjar syndrome

A

Not good, but plasmapheresis and phototherapy. Type II responds to phenobarbital, which increases liver enzyme synthesis

36
Q

How is copper normally excreted?

A

Into bile by hepatocyte copper transporting ATPase (ATP8B gene)

37
Q

Pathology of primary biliary cirrhosis

A

Autoimmune reaction so lymphocytic infiltrate and granulomas causing destruction of intralobular bile ducts

38
Q

Antibody in PBC

A

Anti-mitochondrial antibody, including IgM

39
Q

Pathology of PSC

A

Concentric onion skin bile duct fibrosis, alternating structures and dilation with “beading” of intra and extra hepatic bile ducts on ERCP, MRCP

40
Q

Where does pancreatic adenocarcinoma come from

A

Arises from pancreatic dicta (disorganized glandular structure with cellular infiltration)

41
Q

When do you take H2 blockers

A

Before you dine. Think “table for two”

42
Q

Which h2 blocker is a cyp450 inhibitor

A

Cimetidine, it also has anti-androgens can effects and can cross bbb causing confusion, dizziness, headaches. Can also cross the placenta

43
Q

MOA of misoprostol

A

A PGE1 analog. Increases production and secretion of gastric mucous barrier, decreases acid production. Also used off label for induction of labor (ripens the cervix)

44
Q

Side effects of aluminum hydroxide

A

Constipation and hypophosphotemia, proximal muscle weakness, osteodystrophy, seizures

45
Q

Side effects of calcium carbonate

A

Hypercalcemia, rebound acid increase, can chelate and decrease the effectiveness of other drugs (eg, tetracycline)

46
Q

Side effects of magnesium hydroxide

A

Diarrhea, hyporeflexia, hypotension, cardiac arrest

47
Q

How does lactulose work for hepatic encephalopathy?

A

Gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4

48
Q

MOA of ondansetron

A

5HT3 antagonist

49
Q

MOA of metoclopramide

A

D2 receptor antagonist

Step 1 (18 decks)

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