4.05-4.06 LFT Flashcards

1
Q

The five liver enzymes?

A

AST
ALT
LDH (least liver specific)
ALP
GGT

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2
Q

What enzyme is implicated in liver gluconeogensis (Cori Cycle) ?

A

LDH

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3
Q

What liver enzyme is involved in drug and xenobiotic elimination at the liver?

A

GGT (Gamma-glutamyltransferase)

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4
Q

High serum AST/ALT > 2 with Oral AST below 300 U/L

A

Excessive alcohol

Perivenous hepatocytes damaged (zone 3) by alcohol metabolism production of ROS especially at mitochondria (AST) while peiportal ALT spared

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5
Q

AST/ALT ~1 (but variable), but absolute amount of enzymes are higher

A

Drug induced hepatitis

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6
Q

AST/ALT often slightly < 1 with some variability, very high both enzymes >500 U/L in more extreme cases

A

Acute viral hepatitis

High sensitivity, immune system causing the damage

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7
Q

What LDH isoform is specific to hepatocytes ?

A

LDH-5

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8
Q

What’s the problem with blood panels of LDH?

A

Do not distinguish RBC (1) from liver isoforms (5) of LDH & LDH-5 has short half life = underrepresent liver damage
LOW SENSITIVITY

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9
Q

What happens to GGT and ALP with heptocellular damage?

A

Increase moderately

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10
Q

What damage is “induced” by alcohol and drugs and present at high levels in bile duct cells ?

A

GGT

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11
Q

What tends to result in a massive increase in both GGT and ALP?

A

Cholestasis (bile duct obstruction)

Note
Secreted so can increase without hepatocell lysis

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12
Q

Where does heme catabolism take place?

A

Macrophages in liver or spleen

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13
Q

Heme is broken down into what during catabolism at the macrophage>

A

Unconjugated bilirubin (UCB)
Must hitch ride on albumin to reach over *

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14
Q

How does bilirubin become conjugated?

A

1-2 glucoronic acid molecules via UGT enzyme to make conjugated bilirubin more soluble

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15
Q

Molecule that can’t measure becomes of its extreme hydrophobic and often underestimates truel levels?

A

IBL (indirect bilirubin)

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16
Q

A mature of CB xD often resuls in overestimation

A

Direct bilirubin

17
Q

Total bilirubin (TBIL) ?

A

= UCB + CB

18
Q

What can lead to massive UCB release that often exceed what even the healthiest over can tackle?

A

Massive RBC hemolysis/premature destruction

19
Q

What conditions can cause in prehepatic jaundice or massive RBC damage?

A

G6PD or PK deficiencies

20
Q

What kind of jaundice results in increased UCB, highly elevated IBIL, TBIL, CB BUT normal DBIL?

A

Prehepatic jaundice
(G6PG/PK deficiency)

21
Q

Increased conjugate bilirubin production will lead to what?

A

Elevated urobilinogen in urine
Stools appear darker b/c stercobilin

22
Q

Sky high LDH but little to no increases in other liver enzymes (jaundice)?

A

Prehepatic jaundice

23
Q

What is the major effect of hepatic jaundice?

A

Impaired ability to produce conjugated bilirubin = elevated IBL** + elevated DBIL (hepatocell lysis) + elevated TBIL

24
Q

Higher proportion of the urobilinogen from hepatic jaundice also goes where because of impaired enterohepatic circulation In hepatic jaundice?

A

Kidneys

25
Q

Generally leads to moderate to significant increases in 5 hepatic enzymes?

A

Hepatic jaundice

26
Q

Post hepatic jaundice caused most commonly by?

A

Bile duct obstruction (stones/tumors)

27
Q

Increased DBIL, Normal IBIL, lil to no increase in urobilinogen, sometimes very dark urine from CB, with normal AST, ALT, LDH but very high ALP and GGT (jaundice kind)?

A

Post hepatic jaundice

28
Q

Chronic obstruction of teh bile duct leads to what?

A

Post hepatic jaundice OR proliferation of GGT and ALP secreting cells

29
Q

What molecules implies status of CB in the body/cell?

A

DBIL

30
Q

What molecule implies the status of Unconjugated bilirubin in the body?

A

IBIL