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DEMS > Lab Review > Flashcards

Lab Review Flashcards

1
Q

Possible causes of an epigastric mass

A

Non-neoplastic: Bezoar, pseudocyst, gastric distension

Neoplastic: Carcinoma, lymphoma, GIST

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2
Q

Types of gastric adenocarcinoma

A

Diffuse

Intestinal

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3
Q

Cutaneous signs of gastric adenocarcinoma

A

Leser trelat sign= acanthosis nigricans

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4
Q

Exposures associated with intestinal gastric adenocarcinoma

A

H pylori, smoked foods, tobacco, achlorydia, chronic gastritis

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5
Q

Appearance of intestinal gastric adenocarcinoma

A

gland-forming, ulcerated with heaped margins, lesser curvature

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6
Q

Exposures associated with diffuse gastric adenocarcinoma

A

none

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7
Q

Appearance of gastric diffuse adenocarcinoma

A

signet ring cells, linitis plastic (leather stomach)

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8
Q

stool gap calculation

A

Stool osmgap=290-2(stoolNa+stoolK

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9
Q

duodenal scalloping

A

celiac disease

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10
Q

Marsh classification used to classify what

A

histologic findings present in celiac disease

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11
Q

abdominal angina with postprandial abdominal pain and sitophobia

A

small bowel ischemia

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12
Q

on KUB, thumbprinting of colonic mucosa

A

ischemic colitis

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13
Q

how to treat pseduomembranous colitis

A

Metronidazole, oral vancomycin

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14
Q

Sequesters iron to limit bacterial growth

A

lactoferrin

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15
Q

Composition of esophagus muscle: upper 1/3

A

skeletal only

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16
Q

Composition of esophagus muscle: middle 1/3

A

both skeletal and smooth

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17
Q

Composition of esophagus muscle: lower 1/3

A

smooth only

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18
Q

Centrilobular coagulative necrosis without significant infiltrate indicates what etiology

A

Acetaminophen toxicity (or other drug induced toxicity)

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19
Q

Mutation of C282Y

A

mutation of HFE gene causing hemochromatosis

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20
Q

Less common mutations causing hemochromatosis

A

H63D (HFE), or hemojevulin, hepcidin, ferroportin)

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21
Q

Gland forming tumor with marked desmoplasia

A

cholangiocarcinoma

pancreatic, colonic and gb adenos also have this appearance

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22
Q

Tumor associated with PSC

A

Cholangiocarcinoma

23
Q

tumor that leads to thickened hepatic plates with unpaired arteries

A

hepatocellular carcinoma

24
Q

tumor that occurs almost exclusively in cirrhotics

A

hepatocellular carcinoma

25
Q

tumor of the liver that predominates in females

A

hepatocellular adenoma

26
Q

tumor that forms a normal thickness hepatic plate with unpaired arteries

A

hepatocellular adenoma

27
Q

tumor of the liver associated with OCPs

A

hepatocellular adenoma

28
Q

most common tumor of the liver

A

hemangioma

29
Q

tumor of the liver that forms a central scar with malformed vessels

A

focal nodular hyperplasia

30
Q

PAS-positive, diastase resistant globules in hepatocytes

A

alpha 1 antitrypsin

31
Q

If patient has high IgM think…

A

PBC, Autoimmune hepatitis

32
Q

plasma cell rich centrilobular hepatitis

A

autoimmune hepatitis

33
Q

Male > Female predominance of disease

A

primary sclerosing cholangiitis

34
Q

Diffuse septation and parenchymal nodularity

A

liver cirrhosis

35
Q

Granulomatous lymphocytic cholangitis / florid duct lesion

A

PSC

36
Q

Aspects that figure into MELD calculation

A

Bilirubin, INR, Creatinine

37
Q

Criteria for dx of IBS

A

recurrent abdominal pain or discomfort for at least 3 days per month in the last 3 months associated with 2 or more of the following – improvement with defecation, onset associated with a change in frequency of stool, and onset associated with a change in form (appearance) of stool.

38
Q

Risk factors for CRC

A
  • Advanced age
  • Obesity
  • FAP/HNPCC
  • Long-standing ulcerative colitis
  • Excessive alcohol
  • Smoking
39
Q

CRC patients are all screened for what mutation to guide therapy

A

KRAS (if constitutively activated, our EGFR inhibitors won’t work)

40
Q

HRS Criteria

A 
Cr >1.5mg/dl or Cr Clearance <40 ml/min
No shock, infection, nephrotox 
No GI/renal source of fluid loss 
No improvement with 1.5 L saline 
Urinary protein <500 mg/dl
41
Q

Causes of extreme AST/ALT elevation

A

Ischemia, Acute viral hepatitis (hepatitis A, B, C, E and herpes), medications leading to hepatic necrosis (e.g. acetaminophen), autoimmune hepatitis, Wilson’s disease, and acute Budd-Chiari syndrome

42
Q

What percentage of alcoholics will develop pancreatitis ?

A

10%

43
Q

Charcot’s triad indicates

A

acute bacterial cholangitis: pain, jaundice, fever

44
Q

Reynaud’s pentad indicates

A

acute bacterial cholangitis: pain, jaundice, fever, hypotension, AMS

45
Q 
Predominant cell -> what type of liver injury? 
Lymphcytes
Eosinophils 
Neutrophil
Plasma cell
A

Viral
Drug induced
Steatohepatitis
Autoimmune hepatitis

46
Q

Councilman bodies are present in

A

acute hepatitis (irreversible injury), eosinophilic body

47
Q

Ground glass in hepatocytes

A

HBV infection

48
Q

lymphoid aggregate near portal tract

A

chronic hepatitis B

49
Q

Non Liver sources of AST

A

cardiac myocytes, skeletal muscle, hemolysis

50
Q

Non liver sources of ALT

A

bone, placenta, intestine

51
Q

Mallory Body associations

A

alcoholic liver disease. Also seen in NASH, biliary disease, and copper toxicity (Wilson’s disease or Indian childhood cirrhosis – due to excessive copper intake), hepatocellular carcinomas.

52
Q

Phases of gastric acid secretion

A

Cepahlic
Gastric
Intestinal

53
Q

Serious side effect of metoclopramide

A

tardive dyskinesia

54
Q

Four differences b/w salivary and pancreatic secretions

A
  1. Salivary have myoepithelial cells
  2. Salivary have KHCO3 while pancreatic have NaHCO3
  3. Salivary are neuronally mediated only (pancreatic both neuronal and hormonal
  4. Salivary secretions change significantly with flow rate, pancreatic do not

DEMS (5 decks)

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