week 1

Question 1

MAFLD and NAFLD require a

Answer 1

5% level or hepatic steatosis

Question 2

obesity, fatty liver and insulin all have

Answer 2

decreased adiponectin (helps remove glucose)

Question 3

hepatocellular pattern (biliari tree not effected)

cholestatic pattern (biliary tree problem)

Answer 3

hepatocellular- increased AST and ALT
normla to mild elevation of ALP or GGT

cholestatic- increase ALP and GGT
normal or mild elevation of AST or ALT

Question 4

ALT vs AST more specific for hepatocyte damage

Answer 4

ALT

Question 5

if hepatocyte is damaged then

Answer 5

conjugated bilirubin increases

if unconjugated increases then RBC problem or enzyme in conjugation deficit

Question 6

what vitamin to clot for PT/iNR

Answer 6

vitamin K

Question 7

acute vs chronic hepatocellular injurgt

Answer 7

acute- ALT> AST (both elevated a lot)

chronic, ALT>AST (modest increase), decrease albumin, increase PT/INR and conjugated/unconjugated bilirubin

Question 8

cholestasis (stal or slow of bile)

Answer 8

AST and ALT are fine
ALP and GGT very elevated

increase conjugated bilirubin

Question 9

satiety and hunger signals

Answer 9

hunger- ghrelin

satiety- Leptin, GLP1, CCK, PYY, vagal afferents

Question 10

insulin resistance and B cells

Answer 10

will compensate and hyper secrete insulin then eventually fail

Question 11

resting metabolic rate vs basal metabolic rate

Answer 11

RMR- energy expenditure in an individual that is at rest and has not recently eaten
–>post-absorptive (i.e. not right after a meal) state at
any time of day, at rest

BMR- ▪ Completely rested subjects in the morning, after 8 hours of sleep, fasting for 12 hours, and at a room temperature of between 22 – 26 Celsius

Question 12

main determinant of resting metabolic rate

Answer 12

free fat mass

Question 13

reduce eating behaviour / satiety

Answer 13

increase MSH , serotonin

inhibit AGRP and NP Y

Question 14

hedonic model of eating

Answer 14

dopamine neruons in VTA

Question 15

orexigenic- cause to eat

Answer 15

ghrelin (in the stomach)

Question 16

adipose derived

Answer 16

Leptin, adiponectin, resistin, retinol- binding protein 4 (RBP-4), FGF-21

Question 17

GI derived

Answer 17

GI-derived:
* Stomach – ghrelin (orexigenic)

• Rest of the GI tract:
  GLP-1, CCK, peptide YY, oxyntomodulin

and

pancreas: insulin

Question 18

brown fat for

Answer 18

thermogenesisi

mitochondria to burn fat

Question 19

leptin

Answer 19

secreted by white fat in presence of insulin and inhibited by catecholamines

anoreixgenic- suppress NPY and AGRP, increase MSH

Question 20

ghrelin

Answer 20

orexigenic, release in gastric fungus when fasting, increase AGPR and NPY and inhibit MSH

Question 21

CCK, GLP1 and PYY in small intestine

Answer 21

for satiety

Question 22

adiponectin, resisting and RBP 4

Answer 22

increases insulin sensitivity

Question 23

excess fat in liver

Answer 23

VLDL –> IDL –> LDL

makes insulin resistance worse

causes palmitic acid (FFA) accumulation in pancreatic beta cells

beta cells die and cant help w insulin

Question 24

in insulin resistance and too much fat in pancreas

Answer 24

beta cells can become alpha cells which secrete glucagon

Question 25

diabetes and alzheimers

Answer 25

hyperglycemia can cause leaky BBB and AGEs get in and cytokines –> glial activation and damage neurons

and more FFAs

Question 26

primary bile acids and secondary bile acids

Answer 26

primary bile acid: cholic acid and chenodeoxycholic acid

released in response to food And CCK

secondary acids: deoxycholic acid and lithocholic acid