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BMS200 > week 1, lecture 1 > Flashcards

week 1, lecture 1 Flashcards

1
Q

NAFLD pathologic findings

A

hepatocyte ballooning, lobular inflammation, steatosis

progress to fibrosis and cirrhosis

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2
Q

2 hit model of NAFLD

A
  1. hepatic fat accumulation
  2. increased oxidative stress
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3
Q

cirrhosis

A

liver scarring remodels into nodules

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4
Q

pathogenesis of cirrhosis

A

activate stellate cells and differentiate into fibrogenic myofibroblasts
–>activated by cytokines, ROS, toxins,
–>TGF beta, IL17 signalling

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5
Q

what % of hepatic steatosis to diagnose NAFLD

A

5%

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6
Q

MAFLD criteria (1 of 3)

A

T2D
overweight/obese
metabolic risk abnormalities (i.e. BP, HDL, CRP)

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7
Q

MAFLD increases risk of… (over NAFLD)

A

diabetes, chronic kidney disease, worsened lung function

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8
Q

why do insulin resistance and fatty liver cluster together?

A

Insulin resistance –> increased FFA liberation from adipocytes –> conversion into triglycerides and storage in hepatocytes

Elevated glucose and insulin levels –> hepatic triglyceride synthesis

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9
Q

what happens to adiponectin levels when abdominal fat increases

A

decreases

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10
Q

what is adiponectin

A

adipokine released by visceral fat

it increases glucose utilization and fatty acid oxidation

(helps remove glucose)

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11
Q

what vitamin reduces oxidative stress in hepatocytes and can educe inflmmation in steatohepatits

A

vitamin E

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12
Q

3 tests to measure function of liver

A
  1. serum albumin (oncotic pressure)
  2. bilirubin (breakdown product of heme)
  3. PT/INR (coagulation/ time to clot)
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13
Q

what happens to serum albumin in liver damage?

A

decreases

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14
Q

what happens to bilirubin in liver damage?

A

increases

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15
Q

what happens to PT/INR in liver damage?

A

increases

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16
Q

what are the 2 types of patterns of damage

A
  1. hepatocellular pattern
  2. cholestatic pattern
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16
Q

what is the hepatocellular pattern?

A

hepatocytes damaged, but biliary tree fine

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17
Q

what is cholestatic pattern?

A

obstructer or inflamed biliary tree (intra or extra hepatic bile ducts or wall of gallbladder)

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18
Q

what happens to AST, ALT, ALP and GGT in the hepatocellular pattern?

A

major increase in AST and ALT
normal or mild elevation in ALP and GGT

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19
Q

what happens to AST, ALT, ALP and GGT in the cholestatic pattern?

A

major increase in ALP and GGT
normal or mild elevation in AST and ALT

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20
Q

what does ALT stand for and where is it found?

A

alanine aminotransferase
found in cytosol of hepatocytes mainly

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21
Q

what pattern is ALT relatively specific for

A

hepatocellular pattern

bc mainly found in hepatocytes and for hepatocyte damage

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22
Q

what are the liver enzymes tests looking at

A

serum levels of enzymes increase with damage

damage to hepatocytes or biliary tree cause enzymes to leak into bloodstream

23
Q

what does AST stand for and where is it found

A

aspartate aminotransferase

found in cytosol and mitochondria of hepatocytes
and many other cells… skeletal myocyte, cardiomyocsyte, renal, pancreatic

24
Q

what is more specific for hepatocyte damage, AST or ALT?

A

ALT

-ALT only found in cytosol of hepatocytes
-AST found in cytosol and mitochondria and many other cells (skeletal myocyte, cardiomyocsyte, renal, pancreatic)

25
Q

what does ALP stand for and where is it found? when does it increase?

A

alkaline phosphatase

found at canalicular membrane of hepatocytes

and bone and by placenta

damage to biliary apparatus - i.e. cholestasis, cholecystitis

26
Q

what does GGT stand for and where is it found

A

gamma-glutamyl transpeptidase

found in cell membranes of wide variety of cells (hepatocytes & cholangiocytes, kidney, pancreas, spleen, heart…)

27
Q

what is 5’ nucleotidase (5-NT) found and increase in what disease

A

many cells types

increases in hepatobiliary disease

28
Q

what is the purpose of testing GGT and 5-NT

A

to double check if elevated ALP means hepatobiliary disease

29
Q

what is bilirubin

A

heme portion when hemoglobin is broken down

30
Q

how does bilirubin get broken down

A

in macrophage : heme –> biliverdin (unconjugated bilirubin) –> goes through serum –> into hepatocyte its conjugated into bilirubin glucuorinde

31
Q

what are the 2 forms of bilirubin

A
  1. unconjugated bilirubin (indirect)
  2. conjugated bilirubin (direct)
32
Q

unconjugated bilirubin (indirect) is found where?

A

in serum, not yet complexed to bilirubin glucuronide

33
Q

unconjugated bilirubin (indirect) is due to what?

A

hematomas (RBC damage) and disorders affecting bilirubin conjugation

34
Q

conjugated bilirubin (direct) is found where

A

it was in hepatocyte but leaked back into blood stream

35
Q

conjugated bilirubin (direct) is due to what?

A

blocked biliary system

inability to transport conjugated bilirubin into canaliculi

damage to hepatocytes

36
Q

main preseason for elevation in serum bilirubin

A

hepatocyte damage or impaired bile flow

… could be deficit in liver function though

37
Q

when a hepatocyte is damaged what happens to bilirubin and which form is affected

A

when a hepatocyte is damaged, conjugated bilirubin increases in the serum more than unconjugated bilirubin

38
Q

what does an elevation in unconjugated bilirubin indicate?

A

Elevations in only unconjugated bilirubin is almost always an RBC problem or an enzyme deficit in conjugation

39
Q

what is albumin?

A

protein synthesized by the liver

carry hydrophobic molecules (i.e. bilirubin) and established oncotic pressure in capillary

40
Q

what causes a decrease in serum albumin

A

deficiency in production from chronic liver disease (or serious protein malnutrition)

41
Q

PT/ INR (prothrombin time/ international normalized ratio); what happens in liver damage?

A

increased (ratio >1) ; take longer to form blood clot

42
Q

what vitamin is needed for coagulation in the liver

A

vitamin K

43
Q

acute vs chronic for assessing liver function;;; PT/INR vs albumin

A

acute= PT/INR
chronic= albumin

44
Q

in acute haptocyte injury what happens to ALT, AST and GGT and ALP, albumin and bilirubin

A

ALT and AST very elevated (ALT more than AST)

GGT and ALP maybe elevated or normal

not enough time for albumin to change

direct and indirect bilirubin increase

45
Q

in chronic haptocyte injury what happens to ALT, AST and GGT and ALP, albumin and bilirubin , PT/INR

A

ALT and AST slight increase (ALT > AST)
ALP and GGT normal or slight increase

albumin decreased
PT/INR increase
unconjugated and conjugated bilirubin increase

46
Q

liver function tests (albumin, bilirubin, PT/INR) in chronic vs short term

A

Decreased liver function is often a result of late-stage disease – early disease often exhibits normal bilirubin, PT/ INR, and albumin

47
Q

in hepatocellular injury what happens to ALT and AST and which one is more impacts

A

ALT and AST increase (ALT>AST)

48
Q

cholestasis (bile duct slow)- what happens to AST, ALT, ALP, GGT, bilirubin, PT/INR, albumin

A

ALP and GGT very elevated
AST and ALT normal or moderate elevation

Usually large increase in serum bilirubin, especially conjugated, but PT/INR and albumin are normal

49
Q

when is ALP and GGT very elevated

A

cholestasis

50
Q

SEE SLIDE 32 for diagram of liver lab patterns

A

xx

51
Q

eating disorder psychological factors

A

OCD traits, cognitive rigidity, emotion sensitivity and impulsivity as well as history of developmental stressors/ trauma and challenging interpersonal relationships, body dissatisfaction, sports

52
Q

eating disorder biological factors

A

50% due to multiple genetic effects

Dysfunction in serotonin, dopamine, norepinephrine, opioid and cholecystokinin systems

Hypothalamic regulation (amenorrhea can precede weight loss!)

Some research suggests changes within peripheral satiety network

Vicious cycle as malnourishment can exacerbate the comorbid psychiatric conditions and further the behaviours

53
Q

sociocultural factors of eating disorders

A

idealization of thinness

54
Q

eating disorder complications

A

death, vitamin deficiencies, stunted growth, reduced gastric motility, osteopenia, myopathies, metabolic alkalosis, bradycardia, hypotension, hypothermia,

purging: hematemesis, metabolic acidosis, hypokalemia, cardiomyopathies

BMS200 (43 decks)

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