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Pharmacology > Antihyperlipidemic Drugs > Flashcards

Antihyperlipidemic Drugs Flashcards

1
Q

increased risk of cardiovascular mortality is closely linked to what

A

elevated level of LDL cholesterol
decreased level of HDL cholesterol
hypertriglyceridemia (esp with low HDLs)

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2
Q

other risk factors of cardiovascular diseases

A

smoking
obesity
diabetes
hypertension

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3
Q

primary causes of hyperlipidemia

A

monogenic diseases
genetic polymorphisms
gene environment interactions

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4
Q

how does excessive alcohol intake cause VLDL production

A

alcohol increases the synthesis of FA which are esterified to form triglycerides

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5
Q

how does type II DM cause hyperlipidemia

A
  • insulin suppresses VLDL production by the liver but with insulin resistance in type II DM, there is lack of suppression and increased VLDL production
  • also apoCIII levels are increased with insulin resistance leading to reduced breakdown of chylomicrons and VLDL
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6
Q

common secondary causes of hyperlipidemia

A
  • hypertrigylcerides: DM, renal failure, hypothyroidism, alcohol excess, contraceptives, beta blockers, glucocorticoids
  • hypercholesterolemia: hypothyroidism, nephrotic syndrome, obstructive liver disease, glucocorticoids
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7
Q

what can dyslipidemia cause

A

symptomatic vascular disease such as CAD and peripheral artery disease

high TGs can cause acute pancreatitis

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8
Q

how to diagnose hyperlipidemia

A
  • measure serum lipids after 10 hour fast: gives you tot cholesterol, TGs, and HDL
  • if TGs is less than 400mg/dL and patient has been fasting, LDL = TC - [HDL + (TG/5)]
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9
Q

5 main classes of drugs available for the treatment of hyperlipidemia

A
  • HMG-CoA reductase inhibitors
  • Niacin
  • Bile acid binding resins
  • Cholesterol absorption inhibitors
  • fibrate derivatives
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10
Q

what are the HMG-CoA reductase inhibitors

A

FiRe SLAP

Fluvastatin
Rosuvastatin
Simvastatin
Lovastatin
Atorvastatin
Pravastatin
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11
Q

mechanism of statins

A
  • competitive inhibitor of HMG-CoA reductase the enzyme that catalyzes the first committed step of cholesterol synthesis
  • therefore deplete intracellular cholesterol
  • upregulation of LDL receptors
  • increased clearance of LDL from the blood
  • improve endothelial functions
  • decrease platelet aggregation
  • stabilize atherosclerotic plaque
  • reduce inflammation
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12
Q

statin in order of decreased potency in lowering TGs and LDL

A

Rosuvastatin, Atorvastatin, Simvastatin, Lovastatin = Pravastatin, then last is Fluvastatin

RAS LP F

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13
Q

which statins are prodrugs and how are they activated

A

Lovastatin and Simvastatin which are inactive lactones that are hydrolyzed in the GI to yield the active beta hydroxyl derivatives

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14
Q

clinical uses of statins

A
  • drug of choice for LDL reduction
  • reduce cardiovascular mortality
  • useful also when combined with bile acid binding resins, niacins, or ezetimbe
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15
Q

who does statins not benefit

A

those who are homozygous for familial hypercholesterolemia IIA because they have non functional LDL receptors

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16
Q

what types of people should not take statins

A

women who are pregnant, lactating, or likely to become pregnant

17
Q

four major statin benefit groups

A
  • pts with clinical atherosclerotic cardiovascular disease (ASCVD)
  • pts with LDL 190mg/dL or higher
  • pts 40-75 with diabetes and LDL 70-189mg/dL
  • pts without ASCVD or diabetes with LDL 70-189mg/dL and an estimated 10 year risk of ASCVD or higher
18
Q

adverse effects of statins

A
  • elevation of aminotransferases

- myopathy and rhabdomyolysis

19
Q

most effective drug for increasing HDL and most may reduce lipoprotein a

A

niacin

20
Q

mechanism of niacin

A
  • inhibits adenylyl cyclase in adipocytes (via Gi) –> inhibition of hormone sensitive lipase –> reduces transport of fatty acids to liver and decreases hepatic TG synthesis
  • decreased TG –> decreased VLDL production –> reduced LDL levels
  • increases LPL –> increases clearance of chylomicrons and VLDL TGs
  • catabolic rate of HDL decreased –> increased HDL
21
Q

uses of niacin

A
  • raise HDL levels
  • pts with combined hyperlipidemia with low HDL
  • effective with statins
22
Q

adverse effects of niacin

A
  • red flushed face with first dose or increased dose but can be decreased with NSAIDs prior to intake of drug
  • Hyperglycemia and Hyperuricemia
  • Hepatotoxicity (increased serum transaminases)

4Hs

23
Q

what are the fibrate derivatives

A

Fenofibrate

Gemfibrozil

24
Q

mechanism of fibrates (name them again)

A

fenofibrate and gemfibrozil

  • activate the nuclear receptor PPAR-α (peroxisome proliferator activated receptor)
  • decreased in TGs due to increased expression of lipoprotein lipase, decreased apoCIII (liver), and increased hepatic oxidation of FA
25
Q

uses of fibrates

A

severe hypertrigylceridemia

26
Q

adverse effects of fibrates

A
  • myositis (inflammation and degeneration of muscle tissues)
  • rhabdomyolysis (destruction of striated muscle cell
  • lithiasis (gallstones)
  • mild GI disturbances
27
Q

types of pts that should avoid fibrates

A

those with hepatic or renal dysfuncton

28
Q

drug interaction with gemfibrozil

A
  • inhibits hepatic uptake of statins by OATP1B1 hence increasing plasma conc of statins
  • also competes for same glucuronosyl transferase that metabolizes most statins hence both drugs will be increased in plasma
  • hence higher chance of rhabdomyolysis is more likely
29
Q

what are the bile acid binding resins

A

cholestyramine
colestipol
colesevelam

30
Q

mechanism of action for bile acid binding resins (name them again)

A

cholestyramine, colestipol, colesevelam

polymeric anionic exchange resins that are insoluble in water that bind to anionic bile acids in intestinal lumen and preventing their absorption and excrete them in feces –> leads to more conversion of cholesterol to bile acids hence depleting amount of intracellular cholesterol –> upregulation of LDL receptors –> decreased LDL in plasma

partially offset by increased cholesterol synthesis due to upregulation of HMG-CoA reductase

31
Q

uses of bile acid binding resins

A
  • used with statins and niacins to reduce LDL

- drug of choice for children and women planning to become pregnant

32
Q

type of pts that bile acid binding resins are not effective on

A

those with defective LDL receptors

33
Q

adverse effects of bile acid binding resins (name the drugs again)

A

cholestyramine, colestipol, colesevelam

GI symptoms: bloating, nausea, cramping, constipation

34
Q

contraindications of bile acid binding resins

A

those with hypertriglyceridemia because it increase TGs

35
Q

drug interactions of bile acid binding resins

A

cholestyramine and colestipol impair the absorption of fat soluble vitamins A, D, E, and k

Pharmacology (79 decks)

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