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tv4001 > clinical path - liver > Flashcards

clinical path - liver Flashcards

1
Q

functions of the liver

A 
metabolism of body fuels 
storage functions 
detoxification 
synthesis of most coagulation proteins 
excretory function
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2
Q

what does the liver metabolize

A
  • protein metabolism: albumin, globulin (not immunoglobulin)
  • carbohydrate metabolism: remove glucose from portal blood
  • lipid metabolism: make fatty acids, triglycerides, cholesterol, and apolipoproteins
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3
Q

when does serum enzyme activity increase

A

when the rate an enzyme enters plasma exceeds the rate of enzyme inactivation or removal from plasma

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4
Q

when do you see an increase in enzymes

A

when there are damaged cells,
induction of enzyme synthesis
cell proliferation (neoplasia)
decreased enzyme clearance (decreased renal blood flow)
or ingestion and absorption (GGT from cholesterol, ALP from bones)

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5
Q

what enzymes are released from damaged hepatocytes

A

ALT
AST
SDH
GLDH

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6
Q

What enzymes are associated with cholestasis

A

ALP

GGT

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7
Q

what are the four liver products

A

urea, glucose, albumin, cholesterol

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8
Q

what are some hepatobiliary causes of increased liver enzymes

A

hypoxia, metabolic disease, toxicoses, inflammation, neoplasia, trauma, or intrahepatic/extrahepatic bile duct obstruction

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9
Q

what are some extrahepatic causes of increased liver enzymes

A

endocrine disease, Gi disorders, systemic infections, or drug indication

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10
Q

ALT

A

sensitive indicator of hepatocellular injury, but not specific (found in small amounts of muscle too)

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11
Q

what species can you use ALT

A

Useful in cats and dogs

not useful in ruminants and horses

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12
Q

AST

A

an unspecific enzyme produced by the liver, muscle, and erythrocytes during hemolysis

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13
Q

SDH

A

primary liver enzyme for horses. can also use in ruminants. unstable in vitro, need to run sample immediately

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14
Q

GLDH

A

liver-specific enzymes helpful in detecting hepatocellular injury/necrosis of large animals/ dogs

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15
Q

explain cholestasis

A

interruption or obstruction of the bile flow or excretion. can be intrahepatic (bile caniliculi and bile ducts) or extrahepatic (gall bladder and common bile duct)
may result in release of ALP and GGT

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16
Q

what are the three types of ALP

A
  • B-ALP: bone ALP
  • L-ALP: liver ALP
  • C- ALP: corticosteroid induced ALP (only in dogs)
17
Q

what can increase B-ALP

A
  • bone growth (young healthy dogs)
  • bone fractures (10 days after fracture starts to heal)
  • bone lesions that increase osteoblastic activity (osteosarcoma)
  • hyperthyroid in cats
18
Q

L-ALP

A

sensitive indicator of cholestasis in dogs
increased intrabiliary pressure cause increase ALP production by hepatocytes
often seen in conjunction with GGT and bilirubin

19
Q

what enzyme do you use to detect cholestasis in horses and cattle

A

GGT

20
Q

why is GGT liver sensitive

A

it is predominately associated with the brush border or microvilli of hepatocytes, biliary epithelial cells, renal tubular epithelial cells or mammary cells

21
Q

GGT detection in different species

A
  • horses: GGT is more sensitive for detecting cholestasis than ALP
  • cattle: GGT is more sensitive than ALP for detecting cholestasis
    dogs: ALP is more sensitive than GGT
    cats: GGT may be normal with hepatic lipidosis, but ALP increased
22
Q

explain hepatic insufficiency

A

pathophysiologic state in which the number of functioning hepatocytes is markedly reduced

23
Q

what are the two disorders causing hepatic failure

A
  1. disorders that destroy hepatocytes

2. PSS causing hyperplasia or atrophy of liver due to decreased nutrients

24
Q

what are the three liver function tests

A
  • bile acids
  • ammonia
  • bilirubin
25
Q

explain the general physiology of bile acids

A

bile is synthesized in the liver from cholesterol, conjugated, and secreted into the gall bladder. After a meal, the gall bladder contracts, releasing bile into the intestines. it solubilizes lipids and aids in fat digestion in the intestine
when bile acids reach the ileum, it is transported back into the portal circulation and extracted by hepatocytes

26
Q

where are bile acids found?

A

95% in enterohepatic circulation
5% in the systemic circulation
–> increase in systemic concentration indicates a problem somewhere in enterohepatic circulation

27
Q

causes for increased serum bile acids

A

1) decreased clearance from portal blood
- -> decreased heaptic uptake
- -> PSS
2) decreased bile acid excretion
- -> obstructive choleostasis
- -> functional choleostasis

28
Q

bile acid concentrations suggesting liver dysfunction

A

cats: >20um/l
dogs: >25um/l
horses: >18um/l
cattle: ineffective test

29
Q

ammonia physiology

A

produced in the GIT by the breakdown of AA and urea by GI microflora, where it’s then transported by the portal circulation to the liver and converted into urea. urea is then excreted into the GIT and into the urine

30
Q

where is ammonia found

A

80-90% is shunted into the urea cycle

10-20% metabolized by peripheral tissues (kidneys, brain, heart)

31
Q

explain the physiology of bilirubin

A

bilirubin is a pigment that is produced by the degradation of the heme portion of hemoglobin, mainly by macrophages.
it is then transported to the liver where it is conjugated before being excreted into the bile

32
Q

two types of bilirubin

A

1) unconjugated: not water-soluble, transported in the blood bound to albumin
2) conjugated: water soluble, conjugated to glucuronide

33
Q

what are the three types of hyperbilirubinemia

A

1) pre hepatic
2) hepatic
3) post hepatic

34
Q

explain pre hepatic hyperbilirubinemia

A

due to RBC breakdown (haemolysis), resulting in an increase in unconjugated bilirubin that exceeds the hepatic uptake capacity
this can cause secondary cholestasis as the liver becomes overwhelmed

35
Q

explain hepatic hyperbilirubinemia

A

caused by a decreased hepatic uptake or conjugation within the liver
can be of a hypoxic, anomalous, metabolic, neoplastic, inflammatory, or inheritated nature

36
Q

explain post hepatic hyperbilirubinemia

A

extrahepatic disruption of bile causing a partial or complete blockage
can be due to neoplasia, cholelithiasis, cholangitis, or inflammation of an adjacent organ, i.e pancreas

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