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CLIN PATH > GIT Block Exam > Flashcards

GIT Block Exam Flashcards

1
Q

The highest concentration of this enzyme is seen in the central veins of the liver.

  • All of the above
  • Aldolase
  • Lactate Dehydrogenase
  • Phosphohexose isomerase
  • Isocitrate Dehydrogenase
A

Isocitrate Dehydrogenase

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2
Q

NEGATIVE result for HBsAg may occur in the following:

  • vaccination
  • core window period
  • All of the above
  • no infection
A

ALL

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3
Q

Cholestasis is characterized by the following:

  • Elevated alanine transaminase (ALT)
  • Elevated alkaline phosphatase (ALP)
  • All of the above
  • Hyperbilirubinemia with bilirubinuria
  • High serum bile salts
  • Hypercholesterolemia
A

ALL

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4
Q

De Ritis ratio of > 1.0 but <2.0 may be seen in the following:

  • All of the above
  • alcoholic liver disease
  • myocardial infarction
  • cirrhosis & non viral hepatitis
  • acute viral hepatitis
A

acute viral hepatitis

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5
Q

The following enzyme helps distinguish between elevated liver and bone isoenzymes of alkaline phosphatase.

  • Glucose-6-Phosphate Dehydrogenase
  • Cholinesterase
  • 5-nucleotidase
  • All of the above
  • Aldolase
A

5-nucleotidase

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6
Q

A 19 y.o. female was referred to your clinic by the police station, either for the confirmation or denial of an alleged rape. Microscopically, the vaginal discharge was negative for sperm cells. Which of the following could assist in your diagnosis?

  • Acid phosphatase
  • Leucine aminopeptidase
  • Gamma-glutamyl transpeptidase
  • All of the above
  • Alkaline phosphatase
A

Acid phosphatase

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7
Q

Infection with this virus increases risk for the development of hepatocellular carcinomas:

A

HBV & HCV

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8
Q

Which of the following is involved in protecting red cells from undergoing hemolysis on exposure to oxidants?

  • NADPH, Glutathione, G6PD
  • G6PD
  • Glutathione
  • None of the above
A

NADPH, Glutathione, G6PD

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9
Q

Trace the fate of heme degradation after the release of hemoglobin from a senescent Red cell.

1) conjugation of bilirubin
2) conversion into stercobilin & urobilin
3) production of urobilinogen
4) heme iron is stored with ferritin
5) production of free bilirubin
6) remnants of heme converted to Biliverdin.

  • 4-6-2-5-1-3
  • 4-6-5-1-3-2
  • 3-4-6-2-5-1
  • 1-3-2-4-6-5
  • 1-2-3-4-5-6
A

4-6-5-1-3-2

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10
Q

The synthetic function of the liver can be monitored by measuring the levels of the following EXCEPT:

  • Platelet Count
  • All of the above
  • Albumin
  • Activated partial thromboplastin time (APTT)
  • Prothrombin time (PT)
A

Platelet Count

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11
Q

Normal Values: gamma-glutamyl transpeptidase in female

A

0 - 45 U/L

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12
Q

Normal Values: acid phosphatase

A

0 to 0.8 U/L

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13
Q

Normal Values: G6PD

A

UI/RBC=220 – 550

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14
Q

Normal Values: ALT

A

6-37 U/L

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15
Q

Normal Values: cholinesterase

A

4.7-11.8 U/L

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16
Q

Characteristic Gross Features of Condition: Focal Nodular Hyperplasia

  • none of the above
  • Infarct of Zahn
  • granuloma with caseating necrosis
  • ”Nutmeg Liver”
  • hyperplastic area with central, stellate fibrous scar
A

hyperplastic area with central, stellate fibrous scar

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17
Q

Characteristic Gross Features of Condition: passive congestion of the liver

A

”Nutmeg Liver”

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18
Q

Portal Hypertension Effects on Lungs: Portopulmonary Hypertension

A

dyspnea on exertion with clubbing of fingers

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19
Q

Characteristic Gross Features of Condition: Intrahepatic thrombosis of portal vein radicle

A

Infarct of Zahn

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20
Q

Portal Hypertension Effects on Lungs: Hepatopulmonary Syndrome

A

Platypnea & orthodeoxia

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21
Q

Describe the characteristic liver disease induced by these toxins: Isoniazid

  • Steatosis
  • Reye syndrome
  • induces an autoimmune-like hepatitis
  • mimics chronic viral hepatitis
  • None of the above
A

mimics chronic viral hepatitis

22
Q

Describe the characteristic liver disease induced by these toxins: minocyclin

  • None of the above
  • Steatosis
  • Reye syndrome
  • mimics chronic viral hepatitis
  • induces an autoimmune-like hepatitis
A

induces an autoimmune-like hepatitis

23
Q

Describe the characteristic liver disease induced by these toxins: aspirin

A

Reye syndrome

24
Q

State how the following Alcohols are metabolized by the liver alcohol dehydrogenase: Isopropyl alcohol

A

acetone

25
Q

State how the following Alcohols are metabolized by the liver alcohol dehydrogenase: Ethylene glycol

A

gycol-aldehyde, glycolic acid, glyoxylic acid

26
Q

State how the following Alcohols are metabolized by the liver alcohol dehydrogenase: Methanol

A

formaldehyde and formic acid

27
Q

Give the Pathogenesis of the Electrolyte Depletion in Alcoholism: hyponatremia

  • increased cellular uptake
  • none of the above
  • phosphorus deficiency
  • leaky membranes; from extracellular to intracellular
  • massive intake of solute-free fluid
A

massive intake of solute-free fluid

28
Q

Give the Pathogenesis of the Electrolyte Depletion in Alcoholism: hypokalemia

A

leaky membranes; from extracellular to intracellular

29
Q

Give the Pathogenesis of the Electrolyte Depletion in Alcoholism: hypomagnesemia

A

phosphorus deficiency

30
Q

Distinguish the different cholestatic liver diseases as to their Morphology: Primary Sclerosing Cholangitis

A

chronic inflammation of largest ducts; onion skinning of smaller ducts

31
Q

Distinguish the different cholestatic liver diseases as to their Morphology: Neonatal Cholestasis

A

extrahepatic biliary atresia with idiopathic Hepatitis

32
Q

Distinguish the different cholestatic liver diseases as to their Morphology: Cholestasis of Sepsis

A

prominent Kupffer cells; canals of Hering with prominent bile plugs

33
Q

Classify the CIRCULATORY DISORDERS of the Liver according to their causes: Cirrhosis

  • Hepatic Vein Outflow Obstruction
  • All of the above
  • Impaired Blood Flow into the Liver
  • Impaired Blood Flow Through the Liver
A

Impaired Blood Flow Through the Liver

34
Q

Classify the CIRCULATORY DISORDERS of the Liver according to their causes: Hepatic Vein Thrombosis
(Budd-Chiari Syndrome)

A

Hepatic Vein Outflow Obstruction

35
Q

Classify the CIRCULATORY DISORDERS of the Liver according to their causes: Subclinical thrombosis of the portal vein (Banti syndrome)

A

Impaired Blood Flow into the Liver

36
Q

Classify the CIRCULATORY DISORDERS of the Liver according to their causes: sickle cell disease

A

Impaired Blood Flow Through the Liver

37
Q

Describe the Biliary Tumors according to their Clinical Manifestation: cause symptoms only when much of the
liver is replaced by tumor.

A

Intrahepatic biliary tumors

38
Q

Describe the Biliary Tumors according to their Clinical Manifestation: jaundice, acholic stools, nausea and vomiting, and weight loss.

A

• Extrahepatic biliary tumor

39
Q

Describe the morphologic appearance of the different stages of Cholecystitis: Acute Cholecystitis

A

gallbladder enlarged, tense, bright red or blotchy, covered by fibrinous exudate.

40
Q

Describe the morphologic appearance of the different stages of Cholecystitis: Chronic Cholecystitis

A

contracted or enlarged; thickened from fibrosis

41
Q

Describe the morphologic appearance of the different stages of Cholecystitis: Gangrenous Cholecystitis

A

edematous, and hyperemic to green-black necrotic organ

42
Q

This is a characteristic of Chronic Hepatitis:

  • widespread scarring
  • muddy-red, mushy appearance
  • wrinkled, baggy capsule
  • slightly mottled
  • None of the above
A

widespread scarring

43
Q

Salient features of Autoimmune Hepatitis EXCEPT:

  • Female predominance (70%)
  • presence of other autoimmune diseases
  • No serologic evidence of viral infection
  • Elevated serum IgM
  • All of the above
A

Elevated serum IgM

44
Q

Excessive iron is directly toxic to tissues by the following mechanisms EXCEPT:

None of the above
• Acts as xenobiotics and triggers for the immune response
• all the above
• Stimulation of collagen formation
• Direct irreversible oxidative damage of iron to DNA
• Lipid peroxidation by iron-catalyzed free radical reactions

A

Acts as xenobiotics and triggers for the immune response

45
Q

Copper cause toxic injury to different organs by these mechanisms EXCEPT:

  • binding to sulfhydryl groups of cellular proteins,
  • displacing other metals in hepatic metalloenzymes.
  • promoting the formation of free radicals,
  • apoceruloplasmin conversion to ceruloplasmin is inhibited
  • All of the above
A

apoceruloplasmin conversion to ceruloplasmin is inhibited

46
Q

Differentiate pre-hepatic & post-hepatic jaundice: Pre-hepatic Jaundice (Elevated serum Bilirubin)

  • Indirect & Total Bilirubin
  • Direct Bilirubin only
  • All Bilirubins
  • Indirect Bilirubin only
  • none of the above
  • Direct & Total Bilirubin
A

Indirect Bilirubin only

47
Q

Differentiate pre-hepatic & post-hepatic jaundice: Post-hepatic Jaundice (Elevated serum Bilirubin)

A

Direct Bilirubin only

48
Q

Differentiate pre-hepatic & post-hepatic jaundice: Urine Bilirubin (Pre-hepatic Jaundice)

A

negative

49
Q

Differentiate pre-hepatic & post-hepatic jaundice: Stool (Pre-hepatic Jaundice)

A

darkly colored

50
Q

Differentiate pre-hepatic & post-hepatic jaundice: Risk of Kernicterus: (Pre-hepatic Jaundice)

A

increased risk

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