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module 2a > 10/28 > Flashcards

10/28 Flashcards

1
Q

reverse cholesterol transport

A

acquire cholesterol from tissues and bring it back to the liver
mediated by ApoA-1 and ApoE

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2
Q

ApoB-100

A

LDL receptor ligand - allows internalization of LDL

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3
Q

atherosclerosis

A

excess accumulation of cholesterol in vascular smooth muscle

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4
Q

hypertriglyceridemia

A

pancreatitis, xanthomas, inc risk of CHD

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5
Q

atherosclerosis MOA

A

inflammatory process, occurs when LDL becomes oxidized and they initiate a response in T cells (secrete cytokines), causes accumulation of monocytes in layer between endothelium and smooth muscle

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6
Q

goals of drug therapy

A
  • decrease reabsorption of excreted bile acids
  • decrease secretion of VLDL from liver
  • decrease synthesis of cholesterol
  • increase hydrolysis of lipoprotein triglycerides
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7
Q

each __% reduction in cholesterol is associated with __% reduction in incidence of CHD

A

10%; ~10-30%

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8
Q

drugs for high cholesterol

A

bile acid binding resins
inhibtors of cholesterol absorption
HMG-CoA reductase inhibitors
PCSK9 inhibitors

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9
Q

drugs for high triglycerides

A

fibrates
niacin
omega 3 FAs

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10
Q

bild acid binding resins MOA

A

inhibit reabsorption of bild acids from intestine by binding bile acids to form insoluble complex excreted in feces
-up-regulate LDL receptors in the liver

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11
Q

bild acid binding resins therapeutic use

A
  • treatment of primary hypercholesterolemia (inc LDL)
  • produces ~20% dec in LDL in 2-4 weeks
  • may cause ~5% inc in HDL
  • may inc TG
  • taken before meals
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12
Q

bile acid binding resins SE

A

constipation and bloating

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13
Q

bile acid binding resin drug interactions

A

may bind other drugs and interfere w their absorption: acetaminophen, thiazides, warfarin, digoxin, fibrates, ezetimibe, OC, CS, TZDs`

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14
Q

ezetimibe

A

cholesterol absorption inhibitor

-inhibits intestinal absorption of phytosterols and cholesterol

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15
Q

ezetimibe mechanism

A

inhibits intestinal absorption of cholesterol from diet and reabsorption of cholesterol excreted in bile (inhibits NPC1L1)

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16
Q

indication of ezetimibe

A
  • primary clinical effect is reduction of LDL levels (~17%)

- usually used in combination with statins (may enhance statin action 20%)

17
Q

ezetimibe AE

A
  • (low incidence) liver/skeletal muscle damage

- well tolerated

18
Q

HMG-CoA reductase inhibitor

A

“statin”

lovastatin and simvastatin are prodrugs

19
Q

statin MOA

A
  • completely inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol biosynthesis
  • upregulate LDL receptors enabling more LDL delivered to liver, thus dec plasma cholesterol
20
Q

statin indications

A
  • hypercholesterolemia: elevated LDL, elevated LDL w slightly elevated TGs
  • standard practice to initiate therapy immediately after MI, irrespective of lipid levels
21
Q

statin expected results

A

20-60% reduction in LDL
10-33% reduction in TG
5-10% increase in HDL

22
Q

statin dosing

A

short half-life statins are taken in the evening to inhibit nocturnal cholesterol biosynthesis

  • lovastatin should be taken w evening meal (facilitates absorption)
  • rosuvastatin, atorvastatin, pravastatin, pitavastatin and fluvastatin XL are QD any time of day
23
Q

statin AE

A 
skeletal muscle effects
-rhabdomolysis with renal dysfunction secondary to myoglobinuria
-dose related
-monitor serum creatine phosphokinase
-inc incidence when co-adm with CYP inhibitors; may occur w gemfibrozil
hepatatoxicity
-monitor serum transaminase activity
-~2% incidence
24
Q

Juxtapid

A

ApoB lipoprotein synthesis inhibitor

  • small molecule inhibitor of microsomal TG transfer protein
  • PO
  • indicated as adjunct to other treatments for patients with: homozygous familial hypercholesterolemia - LDLR mutation
  • high risk of liver damage
25
Q

mipomersen

A

ApoB lipoprotein synthesis inhibitor

  • hybridizes ApoB100 mRNA in liver and promotes degradation
  • SQ
  • indicated as adjunct to other treatments for patients with: homozygous familial hypercholesterolemia
  • high risk of liver damage
26
Q

PCSK9 inhibitors

A

increase LDLR# and reduce serum LDL levels

27
Q

fibric acid derivatives

A

reduce serum TGs

-fibrates bind to PPARa and regulated gene transcription along with the retinoic acid receptor (RXR)

28
Q

fibric acid derivatives effectiveness

A

reduce LDL 6-20%
reduce serum TGs 35-53%
elevate HDL 15-30%

29
Q

fibric acid derivatives indications

A

hypertriglyceridemia in which VLDL prodominate

30
Q

fibric acid derivatives SE

A

gallstones, rhabdomyolysis (use cation w statins)

31
Q

omega-3-fatty acid indications

A

severe hypertriglyeridemia >500

32
Q

omega 3 AE

A

can inc LDL-C levels

combined w statins to reduce LDL-C levels

33
Q

niacin

A

vitamin at dietary levels

high doses lowers serum lipids

34
Q

niacin targets

A
  • adipose tissue: inhibits TG lipolysis by hormone-sensitive lipase - dec FA transport to liver
  • liver: inhibits FA synthesis and esterification (reduce TG export via LDL)
  • macrophages: inc expression of CD36 and ABCA1 - dec CE contant via HDL-mediated reverse transport
35
Q

niacin indications

A

mixed hyperlipidemia, hypertriglyceridemia w risk of pancreatitis, raising HDLs (15-35%), used in combo w resin drugs to treat severe cases of hyperlipidemia; also combined w statins

36
Q

niacin AE

A

vasodilation (flushing), itching, tingling of upper body, HA (treat w aspirin or ibuprofen
hepatotoxicity

module 2a (13 decks)

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