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SS- Cardio > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

VLDL

A

liver

delivers hepatic TGs to peripheral tissue

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2
Q

LDL

A

formed from IDL

delivers hepatic cholesterol to peripheral tissues

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3
Q

chylomicrons

A

intestine

delivers dietary TGs to peripheral tissue and cholesterol to the liver

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4
Q

Lp(a)

A

LDL + protein (a) that resembles plasminogen

found in atherosclerosis and CAD (inhibits thrombolysis)

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5
Q

desired LDL level

A

160

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6
Q

desired HDL level

A

men: > 40
women: >50
high: >60

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7
Q

desired TG level

A

200

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8
Q

LDL receptor

A

in liver and peripheral tissues

bind ApoB

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9
Q

apolipoproteins

A

hydrophobic core with cholesteryl esters and TGs surrounded by unesterfied cholesterol, phospholipids and apoproteins

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10
Q

CETP

A

found on vascular surface

transfers cholesterol esters to other lipoprotein particles

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11
Q

LPL

A

degrades TGs circulating in chylomicrons and VLDLs

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12
Q

ApoC-II

A

cofactor for LPL

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13
Q

ApoC-III

A

inhibits lipoportein binding to receptors

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14
Q

PPAR-a

A

nuclear transcription factor

upregulates LPL and HDL

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15
Q

ApoB-48

A

intestine

found in chylomicrons

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16
Q

ApoB-100

A

liver
found in VLDL, IDL, LDL
ligand for LDL receptors

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17
Q

primary chylomicronemia

A

apoC-II or LPL defect
elevated chylomicrons, VLDL
pancreatitis

18
Q

familial hypertriglyceridemia

A

LPL defect (defective VLDL metabolism)
elevated VLDL, TG
pancreatitis

19
Q

familial dysbetalipoproteinemia

A

defective metabolism of VLDL, chylomicrons, ApoE defect
elevated IDL, VLDL, cholesterol, TG
atherosclerosis

20
Q

familal combined hyperlipidemia

A

increased ApoB
elevated VLDL, LDL
premature atherosclerosis

21
Q

familial hypercholesterolemia

A

LDL receptor, ApoB defet
elevated LDL
premature atherosclerosis

22
Q

desirable total cholesterol

A

240

23
Q

secondary hyperlipidemia causes: hypertriglyceridemia

A

DM, alcohol, severe nephrosis, estrogen, uremia, corticosteroids, myxedema, hypopituitarism, acromegaly, immunoglobulin-lipoprotein complex disorders, lipodystrophy, protease inhibitors

24
Q

secondary hyperlipidemia causes: hypercholesterolemia

A

hypothyroidism, early nephrosis, resolving lipemia, immunoglobulin-lipoprotein complex disorders, anorexia, cholestasis, hypopituitarism, corticosteroids

25
Q

dietary management of hyperlipidemia

A

limit calories from fat and cholesterol
eat complex carbs and fiber
weight reduction, calorie restriction and alcohol restriction

26
Q

dietary factors that influence hyperlipidemia

A

increased TGs: excess calories, alcohol, total fat
increased LDL: cholesterol, saturated, and trans fat
increased VLDL: sucrose and fructose

27
Q

statins

A

competitive and reversible HMG-CoA reductase inhibitors and upregulate LDL receptors (promote ER to Golgi transport and cleavage of SREBP)
strongest effect on LDL
UGT1A1 responsible for biotransformation of all statins
reduce CHD risk
AE: rhabdomyolysis (creatinine and kidney failure), teratogen, hepatic, GI distress, sleep disturbance/memory loss

28
Q

bile acid resins

A

bind bile acids and prevent reabsorption

AE: GI, bad taste, hypertriglyceridemia, prevents absorption of other drugs and fat soluble vitamins

29
Q

ezetimibe

A

prevents absorption of dietary cholesterol

30
Q

niacin

A

inhibits release of FFA from adipocytes, decrease TG syn., decrease VLDL, increase transfer of cholesterol from macrophage to HDL, and enhances LPL to convert VLDL to LDL
decrease LDL and TG
reduces Lp (a) and increases HDL
reduces VLDL synthesis
AE: flushing (less for ER), hepatic, GI, hyperucemia, insulin resistance, myositis, eyes (conjunctivitis, cystoid macular edema, retinal detachment), and skin (dry, pruritus, ichthyosis, acanthuses nigricans)

31
Q

lovastatin

A

metabolized by CYP3A4

intermediate potency and efficacy

32
Q

simvastatin

A

metabolized by CYP3A4 intermediate potency and efficacy

33
Q

pravastatin

A

metabolized by sulfating, oxidation and glucoronidation

low potency, low efficacy

34
Q

atorvastatin

A

metabolized by CYP3A4 (and beta oxidation and glucoronidation)
long T1/2
high potency, high efficacy

35
Q

rosuvastatin

A

metabolized by CYP2C9 (and glucoronidation)
long T1/2
high potency, high efficacy

36
Q

fluvastatin

A

metabolized by CYP2C9

37
Q

fibrates

A

bind PPARalpha nuclear receptor: upregulates LPL and HDL

AE: gallstones, myopathy, increased liver enzymes, reflux, diarrhea, possible teratogen

38
Q

gemfibrozil

A

metabolized by glucoronidation (UGT1A1)

reduces statin metabolism UGT1A1 responsible for biotransformation of all statins

39
Q

fenofibrate

A

active metabolite: fenofibiric acid

CI: renal disease

40
Q

N-3 fatty acids

A

decrease TG, BP, platelet
anti-arrhythmic
reduce CHD
sources: fatty fish, fish oils, walnuts, flaxseed, rapeseed, soybean, canola oil

SS- Cardio (16 decks)

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