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RCS > L32- Antihyperlipidemic Drugs > Flashcards

L32- Antihyperlipidemic Drugs Flashcards

1
Q

hyperlipidemia, aka (1), is defined as (2) and is associated with an increased risk for (3)

A

1- dyslipidemia
2- high LDL, high TGs and or low HDL
3- CVD

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2
Q

discuss the risk of cardiovascular mortality and hyperlipidemia

A
  • closely linked to elevated LDL and low HDL

- elevated TGs are an independent risk factor

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3
Q

hyperlipidemia and _______ are risk factors for CVD

A
  • HTN
  • cigarette smoking
  • obesity
  • diabetes
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4
Q

list the primary causes for hyperlipidemia

A
  • monogenic diseases
  • genetic polymorphisms
  • gene-environment interactions
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5
Q

Type I Hyperlipidemia disease:

(1) alternate name
(2) lipid profile
(3) etiology

A

1- familial hyperchylomicronemia
2- elevated CMs
3- LPL or apoCII deficiency

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6
Q

Type II-A Hyperlipidemia disease:

(1) alternate name
(2) lipid profile
(3) etiology

A

1- familial hypercholesterolemia
2- elevated LDL
3- dec or non-functional LDL receptor expression

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7
Q

Type II-B Hyperlipidemia disease:

(1) alternate name
(2) lipid profile
(3) etiology

A

1- familial combined hyperlipidemia
2- elevated VLDL, LDL
3- overproduction of VLDL in liver

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8
Q

Type III Hyperlipidemia disease:

(1) alternate name
(2) lipid profile
(3) etiology

A

1- familial dysbetalipoproteinemia
2- elevated IDL
3- abnormal apoE

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9
Q

Type IV Hyperlipidemia disease:

(1) alternate name
(2) lipid profile
(3) etiology

A

1- familial hypertriglyceridemia
2- elevated VLDL
3- overproduction and or impaired catabolism of VLDL

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10
Q

Type V Hyperlipidemia disease:

(1) alternate name
(2) lipid profile
(3) etiology

A

1- familial mixed hypertriglyceridemia
2- elevated CM, VLDL
3- inc production or dec clearance of VLDL, CMs

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11
Q

_____ and _____ are the most common hyperlipidemia disorders

A
  • Type II-B, familial combined hyperlipidemia (high LDL, VLDL)
  • Type IV, familial hypertriglyceridemia (high VLDL)
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12
Q

most hyperlipidemias stem from a (primary/secondary) cause

A

secondary

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13
Q

list some secondary causes of hypertriglyceridemia

A

(obviously: sedentary lifestyle, + excess dietary intake of saturated fat, cholesterol, trans FAs)

  • DM
  • CRF
  • hypothyroidism (also => hypercholesterolemia)
  • excess EtOH
  • contraceptives (oral)
  • β-blockers
  • glucocorticoids (also => hypercholesterolemia)
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14
Q

list some secondary causes of hypercholesterolemia

A

(obviously: sedentary lifestyle, + excess dietary intake of saturated fat, cholesterol, trans FAs)

  • nephrotic syndrome
  • obstructive liver disease
  • hypothyroidism (also => hypertriglyceridemia)
  • glucocorticoids (also => hypertriglyceridemia)
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15
Q

list some secondary causes of hypercholesterolemia

A

(obviously: sedentary lifestyle, + excess dietary intake of saturated fat, cholesterol, trans FAs)

  • nephrotic syndrome
  • obstructive liver disease
  • hypothyroidism (also => hypertriglyceridemia)
  • glucocorticoids (also => hypertriglyceridemia)
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16
Q

list the types of Antihyperlipidemic Drugs

A
  • HMG-CoA reductase inhibitors (statins)
  • Niacin
  • bile acid-binding resins
  • cholesterol absorption inhibitors
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17
Q

list the HMG-CoA reductase inhibitors in order of potency + indicate the most efficacious drugs

A

[note- mainly for LDL reduction]

  • rosuvastatin (also best for TGs)
  • atorvastatin (also best for TGs)
  • simvastatin
  • pravastatin, lovastatin
  • fluvastatin
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18
Q

HMG = (1)

A

3-OH-3-methylglutarate

Note- statins are HMG analogs

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19
Q

discuss the steps / process of Statin’s MOA

A

1) Statins are HMG analogs and are reversible inhibitors of HMG-CoA reductase
2) depleted intracellular supply of cholesterol (liver)
3) upregulation of LDL receptors and HMG Co-A reductase (liver)
4) improved LDL clearance from blood

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20
Q

what is the main effect of Statins on lipid profile

A

**most effective at lowering LDL

  • moderate dec in plasma TGs
  • small inc HDL
21
Q

what are 2 major contraindications for Statin use

A
  • pregnant Pts

- homozygotes for familial hypercholesterolemia – lack of functional LDL receptors —> dec benefit from Statins

22
Q

what are the main groups prescribed Statins

A
  • LDL >190
  • DM Pts, 40-75 y/o with LDL from 70-189 (pretty much all)
  • ASCVD Pts (atherosclerotic CVD)
  • Pts w/o DM, w/o ASCVD and w/ LDL 70-189 with estimated 10yr risk of ASCVD of >7.5%
23
Q

what are the ‘other effects’ of Statin therapy

A
  • improve endothelial function
  • dec platelet aggregation
  • stabilize atherosclerotic plaques
  • reduces inflammation
24
Q

discuss the adverse effects of Statin therapy and how it is monitored

A

1) elevated aminotransferases
- no other evidence of liver toxicity
- measured baseline, then every 1-2 mos, followed by every 6-12 mos
- a 3x inc of aminotranferases is considered significant

2) myopathy / rhabdomyolysis (rare)
- myoglobinuria => lethal renal injury
- measure CKs at baseline, then after reports of muscle pain / weakness
- discontinue immediately if CKs are elevated

25
Q

Niacin, aka (1), has the main effect of (2). It is the most effective agent for (3). It is the only agent that will (4). It is only limited due to (5).

A 
1- nicotinic acid
2- dec VLDL, dec LDL, dec Lp(a), inc HDL
3- inc HDL
4- dec Lp(a)
5- many adverse effects
26
Q

discuss the steps / process of Niacin’s MOA

A

I:

1) Niacin inhibits adenylyl cyclase in Adipocytes
2) inhibition of hormone-sensitive lipase
3) dec transports of FAs to liver
4) reduction in liver TG synthesis
a) niacin inhibits synthesis and esterification of FAs (+ TGs)
b) dec VLDL –> dec LDL

II: inc LPL activity –> more FA uptake into Adipocytes / Myocytes

III: dec catabolic rate of HDL –> inc HDL

27
Q

Niacin is used in (1) patients, usually with (2). (3) is an important characteristic to consider when prescribing niacin.

A

1- combined hyperlipidemia and low HDL** levels
2- statins also
3- no evidence that it improved morbidity and mortality // many adverse effects

28
Q
  • (1) is a common adverse effect with Niacin, so (2) is usually administered beforehand
  • (3) are minor adverse effects
  • (4) are major adverse effects
  • (5) are rare adverse effects
A

1- intense cutaneous flush
2- ASA (b/c PG mediated)
3- pruritis, rashes, dry skin, acanthosis nigricans, nausea, abdominal discomfort
4- hepatotoxicity, hyperglycemia (via insulin resistance), elevated uric acid / gout
5- atrial arrhythmias, toxic amblyopia, toxic maculopathy

29
Q

The main fibrates are (1) and their main function is to (2).

A

1- gemfibrozil, fenofibrate
2- lower VLDL, inc HDL

Note- used to lower TGs where high TGs may cause underestimations of LDL levels, so LDL may appear to increase

30
Q

discuss the steps / process of Fibrates’ MOA

A

1) activation of PPAR-α (peroxisome proliferator activated receptor-α) in Liver and Brown Adipocytes
2) dec in plasma TG, inc plasma HDL
3) dec plasma TG => inc lipoprotein lipase expression, dec apoC-III expression (liver), inc hepatic oxidation of FAs (liver)

31
Q

Fibrates are the drug of choice for (1) and are strongly considered for (2).

A

1- severe hypertriglyceridemia

2- moderate hypertriglyceridemia

32
Q

list in order of most to least effective the drugs that lower TG levels

A
  • fibrates
  • niacin
  • ω-3 FAs
  • statins
  • ezetimibe
33
Q

list the adverse effects of Fibrates

A
  • mild GI disturbances
  • Myositis: pts with renal insufficiency at risk for rhabdomyolysis (although rare- less of a risk with Fenofibrate than gemfibrozil)
  • Lithiasis: inc in biliary cholesterol excretion => inc risk of gallstones
34
Q

discuss the important drug interactions of fibrates

A
  • Gemfibrozil:
  • inhibits hepatic uptake of statins –> inc plasma [statins]
  • also competes for glucuronosyl transferase which metabolizes statins
  • inc plasma levels of both => inc risk of rhabdomyolysis

Fenofibrate, no such interaction with statins, therefore no inc risk

35
Q

(1) are the bile acid-binding resins that are used for (2)

A

1- cholestyramine, colestipol, colesevelam

2- hyperlipidemias with isolated increases in LDL

36
Q

discuss the properties and MOA of bile acid-binding resins

A

-insoluable in water, large MWs (no absorption / metabilism) => totally excreted in feces

1) bind to anionic bile acids –> prevents reabsorption –> inc excretion in feces
2) liver inc conversion of cholesterol –> bile acids (due to depletion)
3) dec intracellular cholesterol –> LDL receptor + HMG CoA reductase regulation
4) net dec LDL, and inc HDL

37
Q

Bile acid-binding resins are the drug of choice for (1). They are also useful in (2) patients. They are limited in (3) individuals.

A

1- pregnant women and children
2- in adjunct with statins or niacin to improve LDL reduction
3- little effect in people lacking functional LDL receptors (+ inc TG, contraindicated for hypertriglyceridemia)

38
Q

list the adverse effects and drug interactions of bile acid-binding resins

A
  • GI: bloating, nausea, cramping, constipation
  • colesevelam has least GI adverse effects
  • TGs may increase, contraindicated in hypertriglyceridemia
  • cholestyramine, colestipol reduce absorption of several drugs and ADEK vitamins
39
Q

(1) is the main cholesterol absorption inhibitor, primarily used to (2)

A

1- ezetimibe

2- lower LDL (dec cholesterol and phytosterol absorption)

40
Q

discuss the steps / process of Ezetimibe’s MOA

A

1) inhibits transport protein NPC1L1 that takes up cholesterol from the GI lumen
2) reduces cholesterol absorption 54%
3) compensatory inc in cholesterol synthesis (then use statin for inhibition here)
4) upregulation of LDL receptors (liver) to enhance LDL clearance

Note- max efficacy in 15-20% LDL reduction

41
Q

Ezetimibe is mainly used as (1). It is a first line drug for (2) patients.

A

1- 1st adjunct drug to statin therapy for patients not reaching LDL goal on monotherapy

2- monotherapy in statin-intolerant patients

42
Q

list the adverse effects and drug interactions of Ezetimibe

A
  • low incidence of impaired hepatic function –> small inc in incidence when used with statin (often the case)
  • rarely Myositis (rhabdomyolysis)

-bile acid-binding resins inhibits Ezetimibe absorption, NOT given together

43
Q

The main ω-3 FAs are (1), they are used for (2) in (3) fashion

A

1- EPA, DHA
2- reduce TG synthesis and inc FA oxidation in the liver + inc HDL
3- adjunct to TG diet restrictions in patients with very high TGs

44
Q

rank the Antihyperlipidemics in terms of decreasing effectiveness for:

(1) lowering LDL
(2) raising HDL
(3) lowering TGs

A

1- statins > resins > niacin > ezetimibe

2- fibrates > niacin

3- fibrates > niacin > ω-3 FAs > statins

45
Q

the suggested drug for lipid profile with elevated LDL is (1)- additions are as follows: (2)

A

1- statins

2- niacin, resin, ezetimibe

46
Q

the suggested drug for lipid profile with elevated LDL and TG is (1)- additions are as follows: (2)

A

1- statins

2- niacin, fibrate, ω-3 FAs

47
Q

the suggested drug for lipid profile with isolated low HDL is (1)- additions are as follows: (2)

A

1- statin

2- niacin

48
Q

the suggested drug for lipid profile with isolated severe hypertriglyceridemia is (1)- additions are as follows: (2)

A

1- fibrate (or niacin, ω-3 FAs)

2- statin

RCS (29 decks)

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