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Pharm > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

leading cause of death in US

A

atherosclerosis

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2
Q

types of deposits in arteries

A

plaque formation, occlusion, CAD

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3
Q

MAjor lipids

A

PGDs, glycolipids, triglycerides, cholesterol, phospholipids, free fatty acids

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4
Q

structure of triglycerides

A

glycerol esters and free fatty acids

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5
Q

triglycerides form ___ and are the main ___ form of fats

A

adipose tissue, storage

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6
Q

stored triglycerides can be catabolized into free ____ and used for ___ during fasting or between meals

A

fatty acids, energy

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7
Q

important precursors for sterols include

A

steroid hormone, cell membranes, vitamin D, bile salts

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8
Q

what are the structural elements in the amphipathic shell of lipoprotein particles?

A

apoliproteins

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9
Q

___ are complexed with lipids to form lipoproteins, which are then soluble

A

apoliproteins

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10
Q

apoliproteins are the ___ moiety of lipoproteins

A

protein

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11
Q

chylomicrons are formed where?

A

intestine

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12
Q

what do chylomicrons carry?

A

triglycerides and cholesterol

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13
Q

what are chylomicrons degraded by?

A

cells in liver

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14
Q

what secretes VLDL

A

liver then travel to peripheral tissues

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15
Q

what is converted to IDL, LDL

A

VLDL

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16
Q

LDL excess is deposited where?

A

arteries

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17
Q

HDL is the ____ of cholesterol from cells, other lipoproteins

A

scavenger

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18
Q

do we see decrease or increased levels of HDL with atherosclerosis

A

decreased HDL

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19
Q

what type of relationship exists b/W HDL chonesterol and coronary risk?

A

inverse

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20
Q

what do we calculate first?

A

LDL

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21
Q

VLDL equation

A

triglycerides/5

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21
Q

LDL equation

A

total chol - VLDL-HDL

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22
Q

are macrophages pro inflammatory?

A

yes

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23
Q

average LDL/HDL chonesterol risk ratio for men and women

A

3.55: 3.22

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24
Q

most typical drug treatment for all hyperlipoproteinemias?

A

niacin

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25
Q

oxidized LDL can go back to where?

A

the bloodstream

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25
Q

can macrophages break down cholesterol alone?

A

no

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26
Q

when macrophages swallow cholesterol it becomeas what?

A

a foam cell

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27
Q

when a foam cell ruptures it causes more what?

A

inflammatory response

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28
Q

ruptured foam cells bring in what?

A

more WBCs

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29
Q

is flow of blood inhibited with plaque formation?

A

yes

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30
Q

increased cholesterol increases what?

A

LDL

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31
Q

fat, alcohol, excess calories increase what?

A

triglycerides

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32
Q

sucrose and fructose increase what

A

VLDL

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33
Q

hyperlipidemia drug classes include

A

statins, niacin, fibrates, binding resins, absorption inhibitors, mAbs

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34
Q

MOA of statins

A

HMG-CoA reductase inhibitors

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35
Q

de novo synthesis means what

A

liver makes cholesterol

36
Q

MOA of niacin

A

blocck transport to VLDL

37
Q

MOA of fibrates

A

PPAR mediated lipolysis

38
Q

MOA of binding resins

A

cationic bile acid binding

39
Q

MOA of absoprtion inhibitors

A

inhibit cholesterol absorption

40
Q

MOA of Mabs

A

PCSK9 inhibitor

41
Q

primary site of action of anticholesterol

A

hepatocyte

42
Q

statins reduce ___

A

LDL

43
Q

what is prescribed with coronary syndrome regardless of lipidemia

A

statins

44
Q

Lipitor, crestor, mevacor are

A

statins

45
Q

what other effects of statins besides lowering LDL

A

decrease triglycerides and increase HDL

46
Q

what groups do we avoid giving statins to

A

pregnant women and children

47
Q

toxicity of statins

A

elevated liver enzymes, CK elevation

48
Q

Niacin decreases __ and __. Niacin increases ___

A

VLDL and LDL, increases HDL

49
Q

LDL is around __ and HDL is around ___ in healthy pts

A

120 and 40

50
Q

toxicity of niacin

A

cutaneous vasodilation, rash, dry skin, Nausea, elevation of liver enzymes

51
Q

fibrate drugs

A

lopid (gemfibrozil)

52
Q

Fibrates decrease __ and modest decrease in ___

A

VLDL and LDL

53
Q

toxicity of fibrates but rare

A

GI upset

54
Q

estrogen therapy, anorexia and DM increase what

A

cholesterol

55
Q

what else do fibrates do in the liver?

A

increase lipolysis

56
Q

bile acid binding resin drugs

A

colestipol and cholestryamine

57
Q

bile acid binding resins will have isolated increases in ___ and may increase ___

A

LDL and VLDL

58
Q

granular preparations must be with ___

A

meals

59
Q

when do we give bile acid binding resins

A

primary hypercholesterolemia

60
Q

toxicity with bile acid binding resins

A

constipation, bloating, steatorrhea

61
Q

when can we not take BABR

A

oral drug absorption impairment

62
Q

drug associated with sterol inhibitors

A

ezetimibe

63
Q

toxicity with sterol inhibitors

A

possible hepatic (pending), arterial wall thickening

64
Q

PCSK9 are what drug class

A

mabs

65
Q

mab drug

A

repatha

66
Q

repatha lowered LDL by what %

A

65

67
Q

side effects of repatha

A

nasopharyngitis, allergies, can drop LDL very llow <25

68
Q

hypocholesterolemia is associated with what diseases

A

cancer, hemorrhagic stroke, depression, anxiety, preterm birth and low birth weight

69
Q

statins reduce ____ the most when combined with ___

A

LDL, mAbs

70
Q

niacin increases___ the most by 25%

A

HDL

71
Q

Binding resins are typically given with what other drugs

A

statins

72
Q

Mabs lower cholesterol how?

A

binds to receptor before PCSK9 can and allows cholesterol to enter the cell and be used

73
Q

statin therapy upregulates what

A

PCSK9

74
Q

most effective on LDLs

A

statins

75
Q

too much LDLD gets deposited where

A

in the intima of the arteries

76
Q

WBC come into the area and become ___

A

macrophages

77
Q

what receptors on macrophages detect cholesterol

A

CDX and SR-A

78
Q

what do the macrophages do to cholesterol

A

phagocytose the cholesterol molecules

79
Q

after the macrophages swallow the cholesterol molecules, what do they release?

A

reactive oxygen species and myeloperoxidase

80
Q

ROS and MPO lead to what

A

oxidation of the LDL molecule

81
Q

whats wrong with the LDL molecule becoming oxideized

A

it can be rereleased into the bloodstream and its very antigenic

82
Q

because the oxidized LDL is very antigenic, what happens with the immune response

A

it becomes elevated

83
Q

can the macrophage break down cholesterol?

A

no

84
Q

when the foam cell is overfilled with crystallized cholesterol and therefore bursts open, what is released?

A

cytokines, inflammatory response, IL-1, more WBC

85
Q

when the foam cells get destroyed over and over what forms

A

a calcified plaque

86
Q

can the foam cells become necrotic?

A

yes

87
Q

Typical cholesterol pathway without PCSK9 inhbition

A

cholesterol binds to LDL-R, enters cell via clathirin coated pit, lysosome degrades, uses cholesterol and recycles the receptor

88
Q

how do PCSK9 work in the cell

A

binds to LDL-R, brings the receptor into the cell and degrades the receptor. less LDL-R and less cholesterol in the blood

Pharm (22 decks)

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