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BMS 200 > NALFD > Flashcards

NALFD Flashcards

1
Q

What is the 2 hit model of NAFLD?

A

Pathophysiology:
1) hepatic fat accumulation
2) increased oxidative stress

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2
Q

what makes NASH different from NAFLD?

A

NASH is steatohepatitis (involves inflammation of the liver)

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3
Q

How does MAFLD differ from NAFLD in terms of diagnostic criteria?

A

Both require a 5% level of hepatic steatosis

NAFLD: exculsion of other causes

MAFLD: inclusion of any one of T2DM, obesity, metaboblic dysfunction composite score

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4
Q

why do diagnostic differences matter b/t NAFLD and MAFLD?

A

1) identify those with higher risks due to metabolic dysregulation
2) under reporting of alcohol ingestion

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5
Q

why do obesity, insulin resistance and fatty liver tend to cluster together? Note the bi directional relationship b/t obesity and insulin resistance.

A

insulin resistance leads to increased FFA, that are converted to TG’s and stored, increasing fat (obesity) and hepatic TG synthesis (steatosis).

as intra-abdominal fat increases, adiponectin decreases leading to less glucose utilization so blood sugar rises.

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6
Q

what is the hepatocelluar pattern?

A

in situations where hepatocytes suffer damage but the biliary tree does not:
- high ALT and AST
- normal or mild ALP or GGT

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6
Q

what is adiponectin?

A

an adipokine released by viseral fat, it increases glucose utilization and fatty acid oxidation

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7
Q

what is the cholestatic pattern?

A

when the primary problem is obstruction/inflammation of the biliary tree:
- high ALP and GGT
- normal or mild AST and ALT

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8
Q

T/F: is ALT relatively specific for hepatocyte damage?

A

yes because it is found mainly in the cytosol of hepatocytes

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9
Q

T/F: is AST more specific for hepatocyte damage than ALT?

A

NO
AST is found in cytosol and mitochondria of hepatocytes and many other cells

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10
Q

if someone who was pregnant had high levels of ALP, would you be immediately concerned?

A

NO, ALP is expressed by the placenta so increased during pregnancy.
NOTE: also during childhood because its expressed in bone too.

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10
Q

what is the preferred ‘double check’ whether an elevation of ALP means hepatobiliary disease?

A

GGT, it is rather non-specific on its own.

also 5-NT

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11
Q

what does an elevation in conjugated bilirubin (direct) indicate?

A

hepatocyte damage

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12
Q

what about elevation in ONLY unconjugated bilirubin (indirect)?

A

Usually RBC or enzyme problem

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13
Q

what normally causes decreases in serum albumin?

A

chronic liver disease

this is because it has a long half life so liver dysfunction has to be present for awhile before it drops.

NOTE: albumin is good indicator of acute or chronic because it won’t change in acute.

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14
Q

why would a deficiency in Vitamin K cause increase in PT/INR lab?

A

Increased PT/INR means it takes longer to form a blood clot. The liver is the source of almost all coagulation factors and they depend on vitamin K. So less vitamin K means an increase is clotting time and thus an increase in PT/INR.

15
Q

Will ALT or AST be more elevated than the other with ACUTE hepatocellualr injury?

A

Both ALT and AST will be very elevated but ALT > AST

16
Q

ALT and AST in chronic hepatocellular injury?

A

both will be modestly increased, ALT > AST

17
Q

what would a very elevated ALP and GGT with large increase in conjugated bilirubin likely indicate?

A

cholestatsis

18
Q

in states where weight loss is NOT occurring, does an obese person use more or less calories than a lean person?

A

More calories.

obese use less calories than lean during weight loss states

19
Q

why is central obesity more crucial risk factor in insulin resistance?

A

non-esterified fatty acids (NEFA) increase insulin resistance and more are released from central fat.

20
Q

What are the systemic inflammatory effects of obesity?

A

production of IL-6 and TNF-alpha by the adipocyte.
these are pro-inflammatory cytokines lead to insulin resistance.

21
Q

what is the main determinant of RMR?

A

what is the main determinant of RMR?

22
Q

The more fat mass you have, the more calories you burn. WHY?

A

obese individuals have a higher EE than lean individuals

main compartments contributing to this is RMR and NEAT

23
Q

differentiate between the homeostatic pathway and hedonic pathway for hunger/satiety

A

homeostatic: controls energy balance by increasing motivation to eat based on depletion of energy stores.

hedonic pathway: Reward based pathway, less by nutrient availability, can override the homeostatic pathway.

24
Q

in the arcuate nucleus (ACN) of the hypothalamus, there are appetite stimulating and suppressing neurons. What are they?

A

Stimulating: AGRP and NPY

Suppressing: POMC -> MSH

25
Q

What happens when nutrients are present (MSH and AGRP)?

A

MSH is released -> PVN and drives behaviour to stop eating.
AGRP is inhibited (AGRP blocks MSH receptors)

26
Q

What mediates satiety in the homeostatic pathway?

A

increase MSH signalling, directly by MSH release or indirectly by inhibition by AGRP

27
Q

what is the role of serotonin signalling in the homeostatic pathway?

A

increased serotonin signaling -> activation of MSH and inhibition of AGRP/NPY neurons. This would increase satiety and suppress appetite

so when ur happy you dont feel the need to eat so much ice cream

28
Q

what is the reward deficiencyt hypothesis and how does it impact obese people?

A

activation of hedonic pathway anticipating eating something you like.
in obese: impaired dopamine release and greater corticolimbic system activity.

so Increasde reward expectation + decreased reward upon eating = increased eating behaviour

29
Q

where is leptin secreted?

A

white adipocytes in the presence of insulin, inhibited by catecholamines.

30
Q

what is the role of leptin?

A

anorexigenic: suppresses NPY and AGRP, increased MSH

31
Q

T/F: obese people have less leptin levels because the hypothalamus is resistant to leptin

A

false, they have more leptin

the hypothalamus is resistant to it.

32
Q

What is the connection between insulin and dopamine?

A

Insulin is secreted in pancreatic beta-cells in response to elevated blood glucose. Receptors for insulin are present in the ventral striatum and are linked to increased dopamine signalling in the area.

So, increased hedonic pathway signaling can amplify homeostatic satiety signaling in the hypothalamus.

33
Q

what is the only orexgenic hormone?

A

ghrelin, released in gastric fundus in response to fasting.

34
Q

adiponectin can increase insulin sensitivity. What adipokines can increase insulin resistance?

A

resistin
retinol binding protein 4

BMS 200 (7 decks)

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