Cardio: Lipid Lowering Agents Flashcards Preview

Pharmacology > Cardio: Lipid Lowering Agents > Flashcards

Flashcards in Cardio: Lipid Lowering Agents Deck (23)
Loading flashcards...
1

HMG-CoA reductase inhibitor drugs:

  • Lovastatin
  • Pravastatin
  • Simvastatin
  • Atorvastatin
  • Rosuvastatin

2

Effect of HMG-CoA reductase inhibitors

  • ↓↓↓ - LDL
  • ↑ - HDL
  • ↓ - TG

3

Mechanism of Action for HMG-CoA reductase inhibitors:

Inhibit conversion of HMG-CoA to
mevalonate (a cholesterol precursor)

4

Side Effects of HMG-CoA reductase:

  • Hepatotoxicity (↑ LFTs) - minor elevations in serum aminotransferase levels during the 1st month of use: use reduced dosage for patients with hepatic parenchymal disease)
  • Rhabdomyolysis (esp. when used with Fibrates and Niacin)
  • Pregnant women should use Bile acid resins and should never use 'Statins'

5

Effect of Niacin (Vitamin B3):

  • ↓↓ LDL
  • ↑↑ HDL
  • ↓ TG
  • ↓ Lp(a)

6

Mechanism of Action of Niacin (Vitamin B3)

  • Decreases the production and secretion of VLDL in the Liver
  • Inhibits Lipolysis in Adipose tissue
  • which leads to reduction of Hepatic VLDL synthesis

7

Side Effects of Niacin (Vitamin B3)

  • Red, flushed face (due to PGD2), which is ↓ by aspirin or longterm use
  • Hyperglycemia (Acanthosis Nigricans)
  • Hyperuricemia (exacerbates gout)

 

8

Bile acid resin (sequestraints) drugs:

  • Cholestyramine
  • Colestipol
  • Colesevelam

9

Effect of Bile acid resins:

  • ↓↓ LDL
  • Slightly ↑ HDL
  • Slightly ↑ TG

10

Mechanism of Bile acid resins:

  • Prevent intestinal reabsorption of bile acids
  • Therefore the Liver must use Cholesterol to make more

11

Side Effects of Bile acid resins:

  • Patients HATE IT - it tastes bad and causes GI discomfort
  • ↓ Absorption of Fat-soluble vitamins
  • Cholesterol gallstones

12

Cholesterol absorption blocking drugs:

  • Ezetimibe

13

Effects of Cholesterol Absoprtion blockers (Ezetimibe)

  • ↓↓ LDL
  • No effect HDL
  • No effect TG

14

Mechanism of Action of Cholesterol absorption blockers

  • Prevent cholesterol absorption at small intestine brush border

15

Side Effects of Cholesterol absorption blockers

  • Rare ↑ LFTs
  • Fatigue, Abdominal pain, and Diarrhea

16

Fibrate drugs:

  • Gemfibrozil
  • Clofibrate
  • Bezafibrate
  • Fenofibrate

17

Effect of Fibrates:

  • ↓ LDL
  • ↑ HDL
  • ↓↓↓ TG
  • They ↓ the incidence of MI and CHD

18

Mechanism of Fibrates:

  • Acts as a ligand at Peroxisome Proliferating Activating Receptors - PPAR-α receptors 
  • Upregulate LPL → ↑ TG clearance → ↑ VLDL and Chylomicron catabolism → ↓ VLDL secretion and by Liver
  • Reduces Hepatic synthesis of Cholesterol
  • Activates PPAR-α to induce HDL synthesis → ↑ ApoA-1 synthesis

19

Side Effects of Fibrates:

  • Myositis (↑ risk with concurrent statins)
  • Hepatoxicity (↑ LFTs)
  • Cholesterol gallstones (esp. w/ concurrent Bile acid resins)

20

Cardiac Glycosides drugs:

  • Digoxin (Lanoxin)
  • Digitoxin (discontinued in the United States)
  • Ouabain - glycoside plant not used clinically

21

Mechanism of Cardiac glycosides:

  • Are carbdenolides that contain a lactone rein and a steroid moiety attached to sugar molecules.
  • Direct inhibition of Na+ / K+ ATPase leads to indirect inhibition of Na+ / Ca2+ exchanger / antiport
  • ↑ [Ca2+] → each action potential produces a greater release of Ca2+ → net result is a positive inotropic effect
  • Increase stroke volume and enhance cardiac output
  • Stimulates Vagus nerve → inhibition of SA node and delayed conduction of AV node → ↓ HR

22

Clinical use of Cardiac glycosides:

  • CHF (↑ contractility)
  • Atrial Fibrillation (↓ conduction at AV node and depression of SA node)
  • Administer Potassium-sparing diuretics to avoid Potassium depletion

23

Toxicity of Cardiac glycosides:

  • Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think of Van Gogh's Starry Night)
  • ECG - ↑ PR, ↓ QT, ST scooping, T-wave inversion, arrhythmia, AV block
  • Can lead to Hyperkalemia, which indicates poor prognosis
  • Predisposing factors: Renal failure (↓ excretion), Hypokalemia (permissive for digoxin binding at K+ -binding site on Na+ / K+ ATPase) Verapamil, Amiodarone, Quinidine (↓ digoxin clearance; displaces digoxin from tissue-binding sites)