week 1 Flashcards
MAFLD and NAFLD require a
5% level or hepatic steatosis
obesity, fatty liver and insulin all have
decreased adiponectin (helps remove glucose)
hepatocellular pattern (biliari tree not effected)
cholestatic pattern (biliary tree problem)
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
ALT vs AST more specific for hepatocyte damage
ALT
if hepatocyte is damaged then
conjugated bilirubin increases
if unconjugated increases then RBC problem or enzyme in conjugation deficit
what vitamin to clot for PT/iNR
vitamin K
acute vs chronic hepatocellular injurgt
acute- ALT> AST (both elevated a lot)
chronic, ALT>AST (modest increase), decrease albumin, increase PT/INR and conjugated/unconjugated bilirubin
cholestasis (stal or slow of bile)
AST and ALT are fine
ALP and GGT very elevated
increase conjugated bilirubin
satiety and hunger signals
hunger- ghrelin
satiety- Leptin, GLP1, CCK, PYY, vagal afferents
insulin resistance and B cells
will compensate and hyper secrete insulin then eventually fail
resting metabolic rate vs basal metabolic rate
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
main determinant of resting metabolic rate
free fat mass
reduce eating behaviour / satiety
increase MSH , serotonin
inhibit AGRP and NP Y
hedonic model of eating
dopamine neruons in VTA
orexigenic- cause to eat
ghrelin (in the stomach)
adipose derived
Leptin, adiponectin, resistin, retinol- binding protein 4 (RBP-4), FGF-21
GI derived
GI-derived:
* Stomach – ghrelin (orexigenic)
- Rest of the GI tract:
GLP-1, CCK, peptide YY, oxyntomodulin
and
pancreas: insulin
brown fat for
thermogenesisi
mitochondria to burn fat
leptin
secreted by white fat in presence of insulin and inhibited by catecholamines
anoreixgenic- suppress NPY and AGRP, increase MSH
ghrelin
orexigenic, release in gastric fungus when fasting, increase AGPR and NPY and inhibit MSH
CCK, GLP1 and PYY in small intestine
for satiety
adiponectin, resisting and RBP 4
increases insulin sensitivity
excess fat in liver
VLDL –> IDL –> LDL
makes insulin resistance worse
causes palmitic acid (FFA) accumulation in pancreatic beta cells
beta cells die and cant help w insulin
in insulin resistance and too much fat in pancreas
beta cells can become alpha cells which secrete glucagon
diabetes and alzheimers
hyperglycemia can cause leaky BBB and AGEs get in and cytokines –> glial activation and damage neurons
and more FFAs
primary bile acids and secondary bile acids
primary bile acid: cholic acid and chenodeoxycholic acid
released in response to food And CCK
secondary acids: deoxycholic acid and lithocholic acid
