Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

STEP 1 > 07b: GI 2 > Flashcards

07b: GI 2 Flashcards

1
Q

List the mechanism behind which fatty alcohol liver changes occur

A

High alcohol = high acetaldehyde and low NAD+ so decreased gluconeogenesis, FA oxidation, and lipoprotein assembly and increased FA synthesis/buildup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Alcoholic hepatitis can be distinguished from fatty liver by which histological findings?

A

Swollen, NECROTIC hepatocytes with PMN infiltration and mallory bodies (eosinophilic inclusions of damaged keratin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Viral hepatitis, apoptosis and cell shrinkage, nuclear fragmentation, and intensely eosinophilic remnants called (X).

A

X = councilman (“acidophilic”) bodies

Note: different from mallory bodies, which are intracytoplasmic inclusions seen in alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List some triggers for hepatic encephalopathy that work by increasing (X) substance

A

X = NH3

  1. Dietary intake
  2. GI bleed (Hgb breakdown increases nitrogen products in gut and bac synthesis of NH3)
  3. Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List some triggers for hepatic encephalopathy that work by decreasing (X) substance removal

A

X = NH3

  1. Renal failure, diuretics
  2. Bypassed hepatic blood flow (post-TIPS procedure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Rx of hepatic encephalopathy

A
  1. Lactulose

2. Rifaximin or neomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lactulose mechanism of action

A

Catabolized by gut flora, increased short chain FA, decrease colon pH, and increase NH3 conversion to NH4+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Universal vaccination against (X) would likely cause steep decline in hepatocellular carcinoma.

A

X = HBV (countries with high rates of HBV have over 85% of all HCC cases!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

T/F: Chronic HBV infection can lead to HCC with our without cirrhosis.

A

True (integration of viral genome into host DNA triggers neoplastic change)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aflatoxin ingestion causes (X) change in (Y) gene.

A 
X = G:T to T:A transversion
Y = p53
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Most common benign liver tumor

A

Cavernous hemangioma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

35 yo patient with RUQ fullness/pain and liver mass presents with recent-onset seizures and neuro deficits. Diagnosis?

A

Cavernous hemangioma (frequently involves brain; may cause intracerebral hemorrhage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Malignant liver tumor associated with CD31 positive cells and (X) exposure.

A

Angiosarcoma

X = arsenic, vinyl chloride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Budd-Chiari syndrome:

A

Thrombosis/compression of hepatic veins (centrilobular congestion/necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Alpha1 antitrypsin deficiency: liver histology

A

PAS positive, diastase-resistant globules

Diastase normally breaks down glycogen, but globules in AAT deficiency are resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of unconjugated hyperbilirubinemia

A
  1. Hemolysis
  2. Physiologic (newborn)
  3. Crigler-Najjar
  4. Gilbert syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Abetalipoproteinemia: (AD/AR/X-linked) mutation of (Y). What’s the typical clinical presentation?

A

AR
Y = MTP (microsomal TG transfer protein; necessary for proper apo-B folding and lipid transfer to chilomicrons/VLDL)

Child (under 1 yo) presenting with malabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Abetalipoproteinemia: expected biopsy findings of small intestine

A

Normal villi/mucosal architecture, but enterocytes at tips of villi contain clear/foamy cytoplasm (lipid accumulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

2 month old boy born at term via uncomplicated vaginal delivery presents with jaundice, dark urine, pale stool, and firm hepatomegaly. Diagnosis? Rx?

A

Biliary atresia (obstruction of extrahepatic bile ducts; conjugated hyper-bilirubinemia)

Urgent surgical intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

All hereditary causes of hyper-bilirubinemia are inherited in (X) fashion

A

X = AR

Gilbert, Crigler-Najjar, Dubin-Johnson, Rotor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Relatively common, benign cause of (conjugated/unconjugated) hyperbilirubinemia that comes about during stress, illness, fasting.

A

Gilbert

Unconjugated (mildly decreased UDP-glucuronosyltransferase conjugation and impaired BR uptake)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Crigler-Najjar pathogenesis:

A

Absent UDP-glucuronosyltransferase (type I) or low enzyme levels (type II), leading to high levels of unconjugated BR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Crigler-Najjar Type II Rx:

A

Phenobarbital (increases liver enzyme synthesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Patient with jaundice and grossly black liver

A

Dubin-Johnson (conjugated hyper-BRemia due to defective liver excretion of BRDG into bile)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

(X) is a milder version of Dubin-Johnson

A

X = Rotor (impaired hepatic excretion of BRDG into bile)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Wilson’s disease: (AD/AR/X-linked) mutation in (X) causing (increase/decrease) in (production/excretion) of (Y).

A

AR
X = hepatocyte copper-transporting ATPase
Decreased excretion
Y = copper (into bile via incorporation into apoceruloplasmin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hemochromatosis: (AD/AR/X-linked) mutation in (X) causing (increase/decrease) in:

A

AR
X = HFE
Increased intestinal Fe absorption (due to impaired iron sensing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Common cause of death in hemochromatosis

A

HCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

T/F: Both hemochromatosis and Wilson’s present before age 40

A

False - hemochromatosis presents after age 40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Classic hemochromatosis triad:

A
  1. Cirrhosis
  2. DM
  3. Skin pigmentation (“bronze diabetes”)
31
Q

Hemochromatosis: aside from liver/skin, what are other organs susceptible to Fe deposition?

A
  1. Pancreas (DM)
  2. Heart (restrictive/dilated cardiomyopathy)
  3. Pituitary (hypogonadism)
  4. Joints (arthropathy)
32
Q

48 yo M presents with pruritis, jaundice, dark urine and “beading” of bile ducts on ERCP. Diagnosis?

A

Primary sclerosing cholangitis

33
Q

Concentric onion skin fibrosis of bile duct occurs in (X) disease and is associated with (Y) patient population.

A

X = Primary sclerosing cholangitis

Y = IBD patients (esp UC)

34
Q

p-ANCA positive biliary tract disease

A

Primary sclerosing cholangitis

35
Q

Primary sclerosing cholangitis: increased risk for which malignancies?

A

Cholangiocarcinoma and gallbladder cancer

36
Q

Biliary tract disease associated with plane xanthomas

A

Primary biliary cholangitis

37
Q

51 yo F with Hx of Hashimoto thyroiditis presents with extreme generalized pruritis (esp at night) and light-colored stools. Running diagnosis? What labs/tests would you order?

A

Primary biliary cholangitis

  1. Serum alk phos and gamma-glutamyl transpeptidase
  2. BR, cholesterol
  3. Anti-mitochondrial Ab
38
Q

What’s the pathogenesis of Primary sclerosing cholangitis?

A

Autoimmune; lymphocytic infiltrate and granuloma formation; destruction of intra-lobular bile ducts

39
Q

Black, spiculated, friable gallstone is (radiopaque/radiolucent), composed of (X), and seen in (Y).

A

Radiopaque
X = Ca-bilirubinate
Y = hemolysis (ex: SCD)

40
Q

Brown gallstone is (radiopaque/radiolucent), composed of (X), and seen in (Y).

A

Radiolucent
X = bacterial infection of obstructed bile?
Y = biliary infection

41
Q

Patient receiving total parenteral nutrition is at risk for which biliary tract complication? Why?

A

Gallstone formation; low CCK release causes biliary stasis and increase risk of stone formation

42
Q

Acute cholecystitis: most specific method of diagnosis

A

Radionuclide biliary scan (obstructed gallbladder won’t take up radiotracer)

43
Q

Patient with Hx of gallstones presents with colicky pain, N/V, abdominal distension, and high-pitched bowel sounds. Diagnosis? Which imaging finding can help confirm?

A

Gallstone ileus (fistula between gallbladder and intestine allows gallstone to pass in and obstruct ileocecal valve)

Air in biliary tree on imaging

44
Q

Burn patient admitted to hospital and stabilized, but develops severe RUQ pain, radiating to back, along with N/V. What’s the likely diagnosis?

A

Acalculous cholecystitis (likely due to hypoperfusion)

45
Q

Patients with chronic cholecystitis can develop (X) gallbladder, usually found incidentally on imaging. What’s the next step in management?

A

X = porcelain (calcified; dystrophic intramural Ca deposition)

Prophylactic cholecystectomy (high rates of gallbladder adenocarcinoma)

46
Q

Charcot triad for ascending cholangitis:

A

Jaundice, Fever, RUQ pain

47
Q

Reynold’s pentad for ascending cholangitis

A 
Charcot triad (Jaundice, fever, RUQ pain) 
Plus altered mental status, shock/hypotension
48
Q

List the causes of acute pancreatitis. Star the two most common.

A

“I GET SMASHED”

  1. Idiopathic
  2. Gallstones* (#1)
  3. EtOH* (#2)
  4. Trauma
  5. Steroids
  6. Mumps
  7. Autoimmune
  8. Scorpion sting
  9. Hypertriglyceridemia, hypercalcemia
  10. ERCP
  11. Drugs (sulfa, NRTIs, PIs)
49
Q

Acute pancreatitis diagnosed by 2/3 of which criteria?

A
  1. Acute epigastric pain (radiates to back)
  2. Serum amylase/lipase 3x normal
  3. Imaging findings
50
Q

(Amylase/lipase) more specific for pancreatic pathology

A

Lipase

51
Q

Pancreatic pseudocyst is lined by which type of tissue?

A

Fibrous, granulation tissue (not epithelium)

52
Q

(Hyper/hypo)-calcemia is a cause of acute pancreatitis and (hyper/hypo)-calcemia is a complication of aute pancretitis.

A

Hypercalcemia; hypocalcemia (Ca soaps precipitate)

53
Q

T/F: Amylase/lipase are always elevated in acute and chronic pancreatitis.

A

False - may not be elevated in chronic disease, but always in acute

54
Q

Hereditary pancreatitis: (X) gene is mutated, leading to abnormal (Y)

A 
X = SPINK1 or trypsinogen
Y = trypsin (not susceptible to inactivation/cleavage)
55
Q

Pancreatic adenocarcinoma arise from (X) pancreatic structure and are associated with which tumor marker?

A

X = ducts (disorganized glandular structures)

CA 19-9 (and CEA, but less specific)

56
Q

Risk factors for pancreatic adenocarcinoma

A
  1. Smoking (2x)
  2. Chronic pancreatitis
  3. Diabetes
  4. Age over 50
  5. Jewish/AA males
57
Q

Courvoisier sign:

A

Obstructive jaundice (dark urine, pale stools) with palpable, non-tender gallbladder

Seen in pancreatic adenocarcinoma

58
Q

Nodular regeneration of hepatocytes is typically found in which patients?

A

Those with cirrhosis (due to chronic HBV/HCV infection)

59
Q

Confirming fat malabsorption can be done using (X) stain for stool.

A

X = Sudan III (most sensitive screen for malabsorptive disorders)

60
Q

Stool microscopy in watery diarrhea (ex: vibrio cholerae) will show (leukocytes/erythrocytes/mucus)

A

Mucus (and some sloughed off epithelial cell) = “rice water stool”

61
Q

(X) and (Y) bind directly on parietal cell and decrease acid production via which common pathway?

A 
X = somatostatin
Y = prostaglandins

Gi (decrease cAMP)

62
Q

(X) and (Y) bind directly on parietal cell and increase acid production via which common pathway?

A 
X = ACh
Y = Gastrin

Gq (increase IP3/Ca)

63
Q

“Alkaline tide” occurs as a result of (X). Describe this phenomenon.

A

X = meal/vomiting (high gastric acid secretion)

H+ secretion from parietal cell into lumen means increased HCO3- excretion from cell into blood (since carbonic anhydrase generates H+ and HCO3- from H2O and CO2); this leads to high blood pH

64
Q

T/F: The actions of both Cimetidine and Lansoprazole are irreversible.

A

False - H2 blockers (cimetidine) are reversible, PPIs inhibit irreversibly

65
Q

All antacids can cause which electrolyte abnormality?

A

Hypokalemia

66
Q

(X) antacid can cause constipation and (Y) antacid can cause diarrhea.

A 
X = aluminum hydroxide (aluMINIMUM amount of feces)
Y = Mg hydroxide (Mg2 = Must Go2 bathroom)
67
Q

(X) drug inhibits gastric and pancreatic lipase, thus decreasing fat breakdown/absorption. Clinically used for (Y).

A 
X = orlistat
Y = weight loss
68
Q

Psyllum and methylcellulose are in (X) class of drugs

A

X = bulk-forming laxatives

Draw water into gut lumen

69
Q

List examples of osmotic laxatives

A
  1. PEG (Polyethylene glycol)
  2. Lactulose
  3. Mg hydroxide, Mg citrate (questionable efficacy)
70
Q

Senna belongs in (X) class of drugs and works by:

A

X = Stimulant laxatives

Stimulates enteric nerve and colonic contraction

71
Q

Docusate belongs in (X) class of drugs and works by:

A

X = emollient laxatives

Promoting water and fat incorporation into stool

72
Q

Aprepitant belongs in (X) class of drugs and works by:

A

X = anti-emetic (substance P antagonist)

blocks NK1 (neurokinin 1) receptors in brain

73
Q

Patient with Roux-en-Y gastric bypass experiences diarrhea, nausea, sweating, palpitations and flushing after meals. What’s the diagnosis/mechanism and treatment?

A

Dumping syndrome (eating high levels of simple CHO causes hyperosmotic fluid shift since food enters jejunum directly; diarrhea and volume contraction increases release of vasoactive substances like bradykinin/VIP)

Eat small, more frequent meals that are low in simple CHO and high in protein

STEP 1 (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions