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Mandies Pharm III > atherosclerosis > Flashcards

atherosclerosis Flashcards

1
Q

cholesterol

A
  • essential component of animal cell membranes, allows fluidity
  • dietary sources: animal fats; cholesterol biosynthetic p/way (25% total cholesterol production occurs in the liver)
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2
Q

HMG CoA Reductase

A

converts HMG CoA to Mevalonic Acid, essential for cholesterol synthesis

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3
Q

triglycerides

A

ester

  • glycerol & fatty acids
  • one of the main components in animal fat and vegetable oils
  • store and circulate fat
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4
Q

lipoproteins

A

complex of lipids and PRO, hydrophobic core w cholesteryl esters and triglycerides

  • unesterified cholesterol, phospholipids, apoproteins at membrane
  • enable transport of lipids, TG, cholesterol
  • PRO components of lipoproteins are called apolipoproteins
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5
Q

exogenous lipid metabolism

A
  1. absorption of dietary cholesterol and FA
  2. in intestinal cell: FFA combine with glycerol to form TG; cholesterol esterified to form cholesterol esters via ACAT; TG and cholesterol are assembed into chylomicrons
  3. enter circulation
  4. lipoprotein lipase removes TG in extrahepatic tissues, remnants taken up by hepatocytes
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6
Q

Apolipoproteins on HDL

A

A1, AII, C, E, D (more dense)

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7
Q

Apolipoproteins for LDL

A

b-100

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8
Q

Apolipoproteins for IDL

A

b100, E, C

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9
Q

VLDL Apolipoproteins

A

C, B100, E (less dense, increased diameter)

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10
Q

chylomicron Apolipoproteins

A

B48, C, E, A1, AII

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11
Q

ENDOgenous pway of cholesterol synthesis

A

Chylomicron remnants taken up by liver, converted to VLDL. VLDL (TG>CE) loses TG via lipoprotein lipase in tissues and becomes IDL (CE>TG). IDL can be converted to LDL by further removal of TG via hepatic lipase. LDL can be internalized in liver and non hepatic tissues. Liver converts to bile acids and secretes, non hepatic used for hormone prod, cell membrane synth, or stored. Enters macrophages and other tissues to form plaques. HDL formed from hepatic and intestinal synthesis of particles containing phospholipids and apolipoproteins, surface components from triglyceride depeleted chylomicron and VLDL remnants, aquisitiion of free chol from tissue sites and other lipoproteins. HDL converts to IDL if too much is produced.

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12
Q

TG can be stored or _____

A

produce nutrients via liver

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13
Q

Total cholesterol: desirable, borderline, high

A

240

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14
Q

LDL: desirable, borderline, high

A

160

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15
Q

HDL: high; desirable

A

> 60; men: > 40; women: >50

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16
Q

triglycerides: desirable, borderline, high

A

200

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17
Q

rx of borderline high hypercholesterolemia

A

dietary and lipoprotein analysis, possible drug therapy if CHD or 2 other risk factors (male, family history of CHD, smoker, HTN, low HDL, diabetes, obesity

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18
Q

rx high hypercholesterolemia

A
  1. dietary if no CHD or less than 2 risk factors

2. dietary & drug if CHD and 2 + risk factors

19
Q

rx very high hypercholesterolemia

A

(LDL > 190) dietary and drug.

20
Q

omega 3 fatty acids

A

activate PPARalpha, decreases triglycerides and may decrease LDL

  • only those in fish oils, not from plant sources, are active
  • avoid in pt with fish/shellfish allergies
  • available OTC or as mixed omega 3 acid ethyl ester (lovaza), purified and chemically altered
21
Q

cholestyramine

A
  • large polymeric cationic exchange resins, insoluble in H20
  • safe and effective, but not appetizing (4-5 g 3-4x day)
  • available as granular resins or tabs
  • resins have to be taken w meals
  • can effect vitamin absorption
  • binds to and interacts with bile acids so they can’t be reabsorbed
  • bind BA through ionic and hydrophobic interactions to prevent reabsorption
  • increase uptke of LDL from upreg of LDL receptors
  • increase hepatic prod of VLDL, increases TG by 15-20%
22
Q

colesevelam

A
  • fewer SE
  • can reduce hyperglycemia
  • large polymeric cationic exchange resins, insoluble in H20
  • safe and effective, but not appetizing (4-5 g 3-4x day)
  • available as granular resins or tabs
  • resins have to be taken w meals
  • can effect vitamin absorption
  • binds to and interacts with bile acids so they can’t be reabsorbed
  • bind BA through ionic and hydrophobic interactions to prevent reabsorption
  • increase uptke of LDL from upreg of LDL receptors
  • increase hepatic prod of VLDL, increases TG by 15-20%
23
Q

CYP7A1

A

rate limiting enzyme to convert cholesterol to BA

24
Q

FGF 15/19

A

hormone that neg fb regulates CYP7A1

25
Q

SE of bile acid sequestrans

A

cholestyramine and colesevelam

  • dyspepsia, constipation, bloating diarrhea (reduced for colesevelam)
  • malabsoprtion of vitamin K (reduced for colesevelam)
  • impaired absoprtion of other drugs: digoxin, thyroxine, coumadin, thiazides, iron salts, pravastatin, fluvastatin, ezetimide, folic acid, aspirin, ascorbic acid. colesevelam does not bind digoxin, warfarin, or reductase inhibitors.
26
Q

niacin

A

water soluble vitamin incorporated into nicotinamide adenine dinucleotide (NAD)

  • inhibits VLDL secretion therefore ultimately decreases prod of LDL
  • decreases triglycerides more than cholesterol
  • no effect on bile production
27
Q

niacin SE

A

1) prostaglanding mediated cutaneous vasodilation: blunted w aspirin/ NSAID (flushed)
2. liver: reversible elevations in LFT, severe dysfunction reported with the use of OTC SR preps. not reported with ER prep.
3. long term niacin rx may increase insuline resistance
4. hyperuricemia: competes w uric acid for excretion by kidneys

28
Q

lovastatin

A

HMG CoA reductase inhibitors

  1. competitively inhibit HMG CoA reductase
  2. prodrug
  3. decrease chol synthesis and upregulate LDL receptors and decrease LDL (really how decreases LDL)
  4. marked first pass metabolism bc liver is the target organ, efficient 1st pass uptake may be more important than high bioavailability to achieve effect.
  5. substrates of CYP3A4
  6. taken in evening
  7. absorption enhanced by food
29
Q

simvastatin

A

HMG CoA reductase inhibitors
1. competitively inhibit HMG CoA reductase
2. prodrug
3. decrease chol synthesis and upregulate LDL receptors and decrease LDL (really how decreases LDL)
4. marked first pass metabolism bc liver is the target organ, efficient 1st pass uptake may be more important than high bioavailability to achieve effect.
5. substrates of CYP3A4
6. taken in evening
7. absorption enhanced by food
more effective

30
Q

pravastatin

A

HMG CoA reductase inhibitors

  1. competitively inhibit HMG CoA reductase
  2. active drug
  3. decrease chol synthesis and upregulate LDL receptors and decrease LDL (really how decreases LDL)
  4. marked first pass metabolism bc liver is the target organ, efficient 1st pass uptake may be more important than high bioavailability to achieve effect.
  5. substrates of CYP
  6. taken in evening
  7. absorption enhanced by food
31
Q

fluvastatin

A

HMG CoA reductase inhibitors
1. competitively inhibit HMG CoA reductase
2. active drug
3. decrease chol synthesis and upregulate LDL receptors and decrease LDL (really how decreases LDL)
4. marked first pass metabolism bc liver is the target organ, efficient 1st pass uptake may be more important than high bioavailability to achieve effect.
5. substrates of CYP2C9
6. taken in evening
7. absorption enhanced by food
less effective

32
Q

HMG CoA reductase inhibitors SE

A

lovastatin, simvastatin, pravastatin, fluvastatin

  • increases in LFT
  • increases in CK, myopathy, rarely rhabdomyolysis
  • worse w concurrent cyclosporin, clofibrate, niacin, erythromycin
33
Q

CYP3A4 interactions (lovastatin, simvastatin)

A

increased drug levels in presence of inhibitors: macrolides, cyclosprine, ketoconazole, fibrates, tacro, paroxetine; 1 L or more of grapefruit juice/day
decreased in inducerts: phenytoin, barbs, rifampin

34
Q

CYP2C( interactions (fluvastatin)

A

increased in presense of inhibitors: ketoconazole, metronidazole, amiodarone

35
Q

all statins are metabolized by _____, interact with _______

A

glycosylation, gemfibrozil

36
Q

gemfibrozil

A
  • serve as ligands for PPARalpha, which upregulates lipoprotein lipase, apo A1, apo A II (apo pros are major components of HDL and promote cholesterol efflux)
  • clears chylomicrons and VLDL quickly
  • lowers triglycerides (VLDL), raises HDL, modest decrease in LDL
  • primarily rx hyperglyceridemia (VLDL)
37
Q

clofibrate

A
  • serve as ligands for PPARalpha, which upregulates lipoprotein lipase, apo A1, apo A II (apo pros are major components of HDL and promote cholesterol efflux
  • clears chylomicrons and VLDL quickly
  • lowers triglycerides (VLDL), raises HDL, modest decrease in LDL
  • primarily rx hyperglyceridemia (VLDL)
38
Q

fenofibrate

A
  • serve as ligands for PPARalpha, which upregulates lipoprotein lipase, apo A1, apo A II (apo pros are major components of HDL and promote cholesterol efflux
  • clears chylomicrons and VLDL quickly
  • lowers triglycerides (VLDL), raises HDL, modest decrease in LDL
  • primarily rx hyperglyceridemia (VLDL)
39
Q

SE of fibric acids

A

fenofibrate, clofibrate, gemfibrozil
-rashes, GI symp, arrythmias, low K, elevation in LFT
-risk of myopathy increased when used in combo w statins
(gemfibrozil increases concentration of most statins by inhibiting mech or glucuronidation of statin acid byproduct. fenofibrate does not use this p’way and has minimal effect on PK of statins)
-increased risk of cholesterol gall stones

40
Q

ezetimibe

A

inhibitor of intestinal sterol absorption

  • impairs intestinal absorption of cholesterol by inhib NPC1L1
  • absorbed and glucuronidated
  • excreted into bile and feces
  • not a CYP450 substrate
41
Q

drug therapy order for high LDL

A
  1. bile acid sequestrans
  2. nicotinic acid or HMG coA reductase inhibitor
  3. combination
42
Q

drug therapy order for high LDL and TG

A
  1. weight loss, alcohol restriction
  2. nicotinic acid or gemfibrozil
  3. bile acid sequestrants or HMG CoA reductatase inhibitors in combo with 2 above
  4. combo of 2 of following: niacin, gemfibrozil, HMG coA reductase inhibitors. increased risk of toxicity
43
Q

drug therapy order for high TG

A
  1. weight loss, ETOH restriction

2. fibrate or nicotinic acid

44
Q

drug therapy order for low HDL

A
  1. diet exercise, smoking cessation

2. nicotinic acid or gemfibrozil

Mandies Pharm III (10 decks)

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