Brainscape's Knowledge GenomeTM

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


See full index

GI Exam > Liver Function Tests > Flashcards

Liver Function Tests Flashcards

1
Q

liver - major metabolic functions

A

*nutrient processing (amino acid synthesis, glycogen synthesis and storage, etc)
*lipid metabolism
*vitamin & mineral storage
*plasma protein synthesis (albumin, clotting factors [INR])
*bile secretion
*detoxification

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

important hepatic enzymes that we measure using liver function tests

A

*AST
*ALT
*alkaline phosphatase
*GGT

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

alanine-amino transferase (ALT)

A

*transaminase that regulates amino acid homeostasis by catalyzing the transfer of an amino group between alanine and pyruvate
*location: mainly hepatocytes
*important role in gluconeogenesis
*requires pyridoxal-PO4 (vitamin B6) as cofactor

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

aspartate-amino transferase (AST)

A

*transaminase that regulates amino acid homeostasis by catalyzing the transfer of an amino group between aspartate and glutamate
*location: hepatocytes (also muscle, heart, intestine)

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

normal ratio of AST:ALT

A

AST:ALT < 1 (except in alcoholic hepatitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

impact of hepatocyte injury on AST and ALT levels

A

*hepatocyte injury (by viruses, toxins, or hypoxia) releases AST and ALT into plasma
*finding elevated levels of AST and ALT indicates that the hepatocytes are “sick”

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

alkaline phosphatase (ALP)

A

*location: canalicular membrane, bile duct epithelium
*assists with phosphate reabsorption and detoxification of lipopolysaccharides
*also present in BONE, intestine, and kidney
*plays role in BILE FORMATION AND SECRETION

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

gamma-glutamyl transpeptidase (GGT)

A

*location: canalicular membrane, bile duct epithelium
*not present in other tissues (but harder to assay than alkaline phosphatase)

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

impact of bile duct obstruction on alkaline phosphatase levels

A

*bile duct obstruction increases ALP synthesis and release into plasma

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

important plasma proteins measured in liver function tests

A

*albumin
*clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

albumin

A

*hepatic synthesis (most abundant plasma protein)
*slow turnover: half-life = 20 days (level affected by nutrition, hydration, acute inflammation, renal disease)
*limited utility in assessing acute liver injury

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

clotting factors

A

*hepatic synthesis (except factor VIII and vonW factor)
*note - synthesis of II, VII, X, require vitamin K
*rapid turnover: half-life = 6-60 hours
*INR measures collective function of I, II, V, VII, X
*useful to assess acute liver injury, MELD score

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

what does INR measure

A

*collective function of clotting factors: I, II, V, VII, and X
*useful to assess acute liver injury

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

bilirubin synthesis

A
  1. macrophages: RBC destruction, heme degradation, & bilirubin synthesis
  2. liver: bilirubin uptake, bilirubin conjugation (UDP-glucuronyl transferase), secretion into bile
  3. intestine: bacterial degradation, urobilinogen absorption, stercobilin excretion
  4. kidney: urobilinogen uptake; urobilin excretion (pigments the urine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

causes of elevated unconjugated (indirect) bilirubin

A

*hemolytic anemia (increased red cell destruction)
*decreased UDP glucuronyl transferase activity (Crigler-Najjar & Gilbert’s syndromes; neonatal jaundice)

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

causes of elevated conjugated (direct) bilirubin

A

*hepatocyte bilirubin transporter dysfunction (Dubin-Johnson and Rotor syndromes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

causes of elevated conjugated + unconjugated bilirubin (total bili)

A

*hepatocyte injury or dysfunction
*bile duct obstruction

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

causes of elevated ALT & AST

A

*hepatocyte cell injury or necrosis

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

causes of elevated alkaline phosphatase

A

*bile duct obstruction
*cholestasis (pathophysiological cessation of bile flow)

20
Q

hemolytic anemias - pathophysiology

A

*decreased RBC lifespan; increased RBC destruction -> overwhelms the transport capacity of OATP
*extra-vascular and/or intra-vascular
*causes: autoimmune, mechanical, vasculitis, infections, toxins, drugs, hemoglobinopathies, leukemias

21
Q

hemolytic anemias - clinical findings

A

*schistocytes
*nucleated RBCs
*RBC agglutination

22
Q

hemolytic anemias - lab findings

A

*total bilirubin: mildly elevated
*direct bilirubin: NORMAL
*urine: bilirubin (-); INCREASED UROBILINOGEN
*plasma: increased LDH; decreased haptoglobin
*CBC: increased reticulocytes; increased RDW

23
Q

hemolytic anemias - clinical course

A

*can be indolent or fulminant
*severe cases: hemoglobinuria, CHF, ARDS, shock, renal failure

24
Q

Gilbert’s syndrome - pathophysiology

A

*decreased activity of UDP-glucuronyl transferase (activity ~25% of normal)
*dominant or recessive inheritance of UGT1A1 gene SNPs
*very common

25
Q

Gilbert’s syndrome - clinical findings

A

faint “lemon yellow” scleral icterus

26
Q

Gilbert’s syndrome - lab findings

A

*total bilirubin: mildly elevated
*direct bilirubin: NORMAL
*urine bilirubin: NEGATIVE
*plasma: ALT, AST, AP normal

27
Q

Gilbert’s syndrome - clinical course

A

*first noticed in teens/young adults
*increased bilirubin found on routine labs
*transient mild jaundice with fasting, stress, exercise, illnesses
*without established Dx, patients may be rejected for insurance

28
Q

Crigler-Najjar Syndrome - pathophysiology

A

*serious impairment of UDP-glucuronyl transferase activity
*type I: absent UDP-GT activity
*type II: ~10% UDP-GT activity
*recessive UGT1A1 gene SNPs
*very rare

29
Q

Crigler-Najjar Syndrome - lab findings

A

*type I: total bilirubin = extremely elevated
*type II: total bilirubin = elevated
*direct bilirubin & LFTs NORMAL

note - the elevated total bili is due to elevated unconjugated (indirect) bilirubin (because it is not getting conjugated effectively)

30
Q

Crigler-Najjar Syndrome - clinical course

A

*type I: jaundiced at birth; pale stool; severe risk of kernicterus with acute and chronic neurological damage
*type II: jaundice may appear later after birth; lower risk of kernicterus

31
Q

Crigler-Najjar Syndrome - treatment

A

*type I: phototherapy, exchange transfusions; liver transplantation
*type II: phototherapy, phenobarbital (induces P450 enzymes, including UDP-GT

32
Q

physiologic jaundice of newborn - pathophysiology

A

delayed onset of UDP-glucuronyl transferase activity

33
Q

physiologic jaundice of newborn - lab findings

A

*total bilirubin = elevated
*direct bilirubin & LFTs normal

34
Q

physiologic jaundice of newborn - clinical course

A

*benign if bili < 20
*if > 20, kernicterus

35
Q

physiologic jaundice of newborn - treatment

A

phototherapy

36
Q

how does phototherapy affect neonatal jaundice

A

*makes unconjugated bilirubin water-soluble (without the need to be conjugated)

37
Q

Dubin-Johnson syndrome - pathophysiology

A

*defective canalicular MRP2
*recessive inheritance
*bilirubin is conjugated but not excreted

38
Q

Dubin-Johnson syndrome - lab findings

A

*total bilirubin: mildly elevated
*most bilirubin is conjugated (direct)
*urine bilirubin: positive
*plasma: ALT, AST, AP normal
*normal urine coproporphyrin
*abnormal copro-I/III ratio = 4:1

39
Q

Dubin-Johnson syndrome - clinical course

A

*liver has BLACK PIGMENTATION
*hyperechoic appearance on ultrasound
*gallbladder not visualized on HIDA or OCG

40
Q

Dubin-Johnson syndrome - treatment

A

*benign condition (no treatment)

41
Q

Rotor syndrome - pathophysiology

A

*defective sinusoidal OATP
*bilirubin is conjugated but not excreted

42
Q

Rotor syndrome - lab findings

A

*total bilirubin: mildly elevated
*most bilirubin is conjugated (direct)
*urine bilirubin: positive
*plasma: ALT, AST, AP normal
*increased urine coproporphyrin
*copro-I/III ratio = 1:4

43
Q

Rotor syndrome - clinical course

A

*normal liver appearance
*normal radiological gallbladder visualization

note - contrast these to the findings in Dubin-Johnson (where the liver is black)

44
Q

Rotor syndrome - treatment

A

benign condition (no treatment)

45
Q

what are the “LFTs”

A

*liver function tests:
-total bilirubin
-ALT
-AST
-alkaline phosphatase
-INR

46
Q

physical exam findings indicative of liver disease

A

*scleral icterus
*hepatomegaly
*spider hemangioma
*palmar erythema
*gynecomastia
*abdominal distension, shifting dullness, fluid wave
*peripheral edema
*signs of CHF
*ecchymoses
*asterixis
*caput medusa
*corneal rings

47
Q

imaging for evaluation of liver disease

A

*start with RUQ ultrasound!

GI Exam (54 decks)

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