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med > foundations hyperlipidemia/cholesterolemia > Flashcards

foundations hyperlipidemia/cholesterolemia Flashcards

1
Q

morbidity vs mortality

A

morbidity = bad things that come out of a disease that dont actually kill you (vs mortality, which do)

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2
Q

artery layers (3)

A

tunica intima
tunica media
tunica adventitia/externa

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3
Q

atheroma

A

accumulation of degenerative material in tunica intima

debris = macros, lipids, chol, FAs, Ca2+, fibrous CT

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4
Q

hemodynamic pressure: laminar vs turbulent flow

A

laminar = normal flow

turbulent flow = causes damage to endothelium. caused by HTN, atherosclerosis

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5
Q

hypercholesterolemia

A

incr LDL & abnormal lipids; decr HDL
due to 1) LDL Rs on liver decreased
or 2) defective ApoB100 (can’t take up VLDLs, give more cholesterol)

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6
Q

foamy cells

A

macrophages ‘eat’ excess cholesterol and become foamy cells, the lipids not ‘eaten’ can get deposited in intima > intimal thickening

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7
Q

familial hypercholesterolemia

A

defective/absent LDL Rs (cant remove LDL chol from circulation) or defective ApoB100 (cant uptake VLDL)
high LDL and overall cholesterol

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8
Q

xanthelasma palpebrarum

A

yellow patches of cholesterol above eyelids, iris margin, achilles
s/s of hypercholesterolemia
commonly leads to CAD

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9
Q

stenosis definition

A

occlusion of bv
can rupture, ulcerate, or erode b/c of weakened bv walls
if chronic damage: can hemmorhage (new vessels formed attempting to restore flow)

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10
Q

embolism vs thrombosis

A 
thrombosis = block that forms locally
embolism = piece of material breaks away and blocks a vessel elsewhere
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11
Q

dissecting aneurysm (definition, causes)

A

splitting of wall (tear in tunica intima)
always due to structural weakness/damage
most commonly caused by HTN, atherosclerosis

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12
Q

aneurysm definition

false aneurysm vs true aneurysms (saccular, fusiform)

A

aneurysm - abnormal wall dilation
false - hematoma (blood extravasation into extravascular CT)
true: saccular - one side, outpouching
true: fusiform - diffuse dilation

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13
Q

debakey classification of aortic aneurysms

type I, II, III

A

type I - asc, desc, and arch (all)
type II - asc
type III - desc

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14
Q

vessel compliancy (definition, what happens when lost)

A

compliancy - elasticity, ability to modify BP

if lost: can’t modify BP > HTN

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15
Q

NASH (non alcoholic steatohepatitis) def & cause

A

NASH - inflammation, danger of cirrhosis

due to fatty liver (liver has no storage limit for lipids/glycogen)

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16
Q

HSL (H sensitive lipase) action & control

A

HSL: hydolyses TAGs (triacylglycerols) > release FAs to bloodstream (some bind albumin, others = FFAs)
HSL activated by epi, glucagon
HSL inhibited by insulin

17
Q

obesity and FFA uptake

A

normally: need high [FA transporters]=ACAT and high [FFAs] to get best uptake
with obesity: increased FFA uptake! much higher than normal levels

18
Q

FA transporters in cellular uptake:
pm
outer mito
inner mito

A

pm: ACAT (acylcholesterol acyl transferase)
outer mito: CPT I (carnitine palmitoyltransferase)
inner mito: CPT II

19
Q

systemic primary carnitine deficiency

A

impaired transport of FAs > mito > toxic accumulation

weakness, hypoketoic hypoglycemia

20
Q

hypertriglyceridemia

A

high VLDL, TG
can be genetic: auto dominant (hyperproduction of VLDL)
can cause pancreatitis (TG > 1000mg/dl)

21
Q

familial lipoprotein lipase deficiency

A

pancreatitis, hepatosplenomegaly, eruptive/pruritic xanthomas
severe hypertriglyceridemia
chylomicron clearance impaired > milky blood

22
Q

MCAD (medium chain acyl coa dehydrogenase) deficiency

A

accumulation of 8-10C chain FAs in blood

hypoketotic hypoglycemia, liver dysfxn

23
Q

LCAD (long chain acyl coa dehydrogenase) deficiency

A

presents earlier than MCAD deficiency, worse s/s

mother can get fatty liver of pregnancy

24
Q

diabetic ketoacidosis mech

A

glucose uptake decr > fat metab incr > ketone body prod incr > diabetic ketoacidosis

primarily type I diabetes

25
Q

zellweger syndrome (relation to lipids)

A

deficiency/absense of peroxisomes
very long chain/branched FAs normally broken down/modified here > impaired, multiple organ systems affected
usually only live 6 mo> 1 yr old

26
Q

regulation of HMG-CoA Reductase
inhibition (2)
activation (2)

A

inhibition: (1) high glucagon, (2)statins
activation: (1) high insulin, (2) SREBPs (sterol regulatory element binding prots) -monitor low cholesterol, upreg HMG CoA reductase synthesis

27
Q

Niemann-Pick Disease

A

deficiency of Niemann-pick c1 like 1 transporter (normally transports dietary cholesterol > body)

diease: hypocholesterolemia

ezetimide drug acts here!

28
Q

tangier’s disease (ABC1 transporter protein deficiency)

A

ABC1: moves excess cholesterol to outer leaflet for easy access for HDL
tangiers: ABC1 defect > HDL can’t reverse transport > ‘defective’ HDL removed from circulation (HDL levels in these pts: 1-5% of normal)
s/s: orange tonsils, hepatosplenomegaly, lipid deposits in schwann cells (peripheral neuropathy)

29
Q

ApoA1 Milano mutation

A

ApoA1 pt mutation better at reverse chol transport than normal, decreased atherosclerosis
ApoA1 stimulates LCAT: better at ‘trapping’ chol in HDL
low HDL levels, hypertriglyceridemia, but NO atherosclerosis (incr longevity, low CV disease)

30
Q

gallstones (assoc w bile acids)

primary vs secondary bile acids

A

high [lithocholic acid] = incr likelihood of gallstones (lith = stone)
lithocholic = secondary bile acid (has modifications by gut bac)
primary acids = synth by liver

31
Q

lipemia retinalis

A

s/s of high lipids:

bv of eye look milky

32
Q 
normal serum levels:
cholesterol
LDL
HDL
TG
A

chol: 180-200mg/dl

LDL:

33
Q

cholesterol as a biosynthetic mol:

A

used for:
bile acids synth
steroid H synth
vitamin D synth

34
Q

statin mech of action, main effect

A

moa: inhibits HMG-CoA reductase, incr in LDL Rs

large decr LDL, modest decr TG/incr HDL

35
Q

fibrates mech of action, main effect

A

moa: incr LPL activity (incr VLDL catabolism), incr ApoA1 (incr HDL)
large decr TGs, modest incr HDL/decr LDL/chol

36
Q

niacin mech of action, effect, side effect

A

niacin = vit b3
decr hepatic synth of TGs
large decr TG, slight incr HDL/decr chol/LDL

flushing side effect! can give aspirin

37
Q

ezetimibe: moa, effect

A

niemann-pick c1 like 1 transporter inhibitor (inhibits dietary cholesterol abs)
decr total chol/LDL

38
Q

bile acid resins/sequestrants
cholestyramine
moa, effect, side effect

A

inhibs bile acid reuptake > liver uses more chol to synth new bile acids
decr chol/LDL, slight incr HDL/TG

contraindicated in hypertg

gi side effects

med (3 decks)

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