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CVS Pharm > CVS Pharm > Flashcards

CVS Pharm Flashcards

1
Q

Antihypertensive drug classes

A

First-line:
1. ACE-inhibitors
2. AT1 blockers
3. Beta blockers
4. Ca2+ channel blockers
5. Diuretics
Second-line:
1. Hydralazine
2. Alpha-adrenergic antagonists

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2
Q

Heart failure therapeutic drug classes

A
  1. ACE inhibitors
  2. Angiotensin-2 receptor blockers
  3. Sacubitril-Valsartan
  4. Beta blockers
  5. Ivabradine
  6. Nitrates
  7. Diuretics
  8. Hydralazine
  9. Digitalis
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3
Q

Ischemic heart disease drug classes

A
  1. Nitrates
  2. Ca2+ channel blockers
  3. Beta-blockers
  4. Ivabradine
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4
Q

Lipid-lowering drug classes

A
  1. Statins
  2. PCSK9 inhibitors
  3. Fibrates
  4. Omega-3-acid ethyl esters
  5. Resins
  6. Inhibitors of intestinal sterol absorption
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5
Q

Anti-clotting drug classes

A

Anti-platelet drugs:
1. NSAIDs
2. GpIIb/GpIIIa receptor blockers
3. Other platelet aggregation inhibitors
Anticoagulants:
1. Heparin
2. Wafarin
Thrombolytic agents:
1. Tissue plasminogen activator

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6
Q

Anti-arrhythmics

A
  1. Na+ channel blocker
  2. Beta blocker
  3. K+ channel blocker
  4. Non-DHP Ca2+ channel blocker
  5. Adenosine
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7
Q

ACE-inhibitor MOA

A

Inhibition of Angiotensin converting enzyme, preventing activation of RAAS system → reduced vasoconstriction and reduced secretion of aldosterone → reduced BP

Increase bradykinin levels, resulting in increased NO and PG production → vasodilation → reduced BP

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8
Q

ACE-inhibitor example

A

Lisinopril

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9
Q

ACE-inhibitor ADRs

A

Severe hypotension
Acute renal failure
Hyperkalemia
Angioedema & dry cough (bradykinin)

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10
Q

AT1 blocker MOA & characteristic

A

Blocks Angiotensin II from binding to AT1 receptor, prevention of activation of RAAS system

Less/no dry cough

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11
Q

AT1 blocker example

A

Valsartan

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12
Q

Beta-blocker MOA

A

Blockade of beta-1 receptors in cardiac myocytes leads to decreased contractility → decreased cardiac output and BP

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13
Q

Beta-blocker examples

A

Non-selective: Propanolol, carvedilol
Selective: Bisoprolol, metoprolol XL
Mixed: Nebivolol

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14
Q

Beta-blocker ADRs

A

Hypotension
Bradycardia
AV nodal block
Bronchoconstriction
Beta-blocker blues

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15
Q

Diuretics - Thiazides MOA

A

Block Na+/Cl- transporter to inhibit NaCl reabsorption → reduced water reabsorption → reduced blood volume → decreased BP

Enhance Ca2+ reabsorption in distal convoluted tubule, hence used in nephrolithiasis due to idiopathic hypercalciuria

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16
Q

Diuretics - Thiazides Example

A

Hydrochlorothiazide

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17
Q

Diuretics - Thiazides ADRs

A

Hypokalemic metabolic alkalosis
Hyponatremaia
Hyperuricemia
Hyperglycemia
Hyperlipidemia
Hypercalcemia

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18
Q

Hypokalemia = hyperglycemia, how?

A

Decreased K+ in interstitium of pancreatic B cells means cell is hyperpolarised. Hyperpolarised cell does not allow for opening of voltage-gated Ca2+ channels. Hence no exocytosis of insulin-containing granules, and hyperglycemia.

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19
Q

Alpha-adrenergic antagonists MOA

A

Alpha-adrenergic antagonists oppose alpha-1 mediated vasoconstriction → reduced peripheral vascular resistance → reduce BP

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20
Q

Alpha-adrenergic antagonists ADRs

A

Reflex tachycardia, orthostatic hypotension
Depression, urinary frequency

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21
Q

Sacubitril-Valsartan MOA

A

Brain natriuretic peptide (BNP) promotes vasodilation, natriuresis, diuresis and antagonises RAAS. BNP is broken down by neprilysin, and sacubitril is a neprilysin inhibitor, thus prolonging the effects of BNP

Neprilysin also breaks down angiotensin II, so neprilysin inhibition prolongs angiotensin II effects. To countereffect this, Valsartan, an AT1 blocker, is administered.

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22
Q

Sacubitril-Valsartan ADRs

A

Hypotension, hyperkalemia, renal failure, angioedema and dry cough

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23
Q

Loop Diuretic MOA

A

Selectively inhibit Na+-K+-2Cl- transporter in thick ascending limb of Henle’s loop → reduce fluid reabsorption and increase Mg2+ and Ca2+ excretion

Also induce renal prostaglandin synthesis

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24
Q

Loop Diuretic Example

A

Furosemide

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25
Q

Loop Diuretics ADRs

A

Hypokalemic metabolic alkalosis
Ototoxicity
Hyperuricemia
Hypomagnesemia

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26
Q

Potassium-sparing diuretics MOA

A

Block aldosterone receptor and inhibit aldosterone activation of Na+ channel → decrease Na+ and hence fluid reabsorption, and decrease K+ secretion (spironolactone)

Block Na+ channel → decrease Na+ and hence fluid reabsorption, and decrease K+ secretion (triamterene)

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27
Q

Potassium-sparing diuretics Example

A

Spironolactone
Triamterene

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28
Q

Potassium-sparing diuretics ADRs

A

Hyperkalemia
Metabolic acidosis
Gynecomastia (spironolactone only)
Acute renal failure (triamterene + indomethacin)
Kidney stones (triamterene)

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29
Q

Hydralazine MOA

A

Inhibits IP3-mediated release of calcium from smooth muscle cell sarcoplasmic reticulum → vasodilation → reduce peripheral resistance → compensatory release of epinephrine → increase venous return and cardiac output

30
Q

Hydralazine ADRs

A

Baroreflex associated sympathetic activation: flushing, hypotension, tachycardia
Hydralazine-induced lupus syndrome (arthralgia, myalgia, serositis, fever)
Contraindicated in coronary artery disease because of sympathetic activation - increased CO may cause myocardial ischemia

31
Q

Digitalis

A

Increases contractility of heart
Digoxin & Digitoxin

32
Q

Nitrates MOA

A

Nitrates form nitric oxide, which promotes vasodilation by stimulating guanylyl cyclase → reduce afterload, decrease oxygen consumption of cardiac muscle, therapy of angina

33
Q

Nitrates Examples

A

Nitroglycerin
Isosorbide dinitrate

34
Q

Nitrates ADRs

A

Reflex tachycardia
Hypotension
Headache

35
Q

DHP Calcium Channel Blockers MOA

A

Block entry of calcium into smooth muscle cells by blocking the voltage-gated calcium channels

Decrease myocardial contractility → decrease oxygen requirement → treat angina

Decrease vascular smooth muscle tone → vasodilation → decrease BP

36
Q

Non-DHP Calcium Channel Blockers MOA

A

Same, blocks voltage gated calcium channels and entry of calcium into the cell but acts more on the heart

Suppress SA node and AV node firing → treat supraventricular reentry tachycardia

37
Q

Non-DHP Calcium Channel Blocker ADRs

A

Cardiac depression: bradycardia, AV block, heart failure

38
Q

DHP Calcium Channel Blocker ADRs

A

Hypotension
Heart failure
Myocardial infarction

39
Q

Ivabradine MOA

A

Inhibits cardiac pacemaker cells → reduction in cardiac workload and myocardial oxygen consumption

40
Q

Ivabradine ADRs

A

Luminous phenomena
Bradycardia related symptoms: fatigue, hypotension, dizziness

41
Q

Statins MOA

A

Statins inhibit HMG-CoA reductase, the rate-limiting step in cholesterol synthesis → decrease endogenous cholesterol

42
Q

Statins Example

A

Atorvastatin

43
Q

Statin ADRs

A

Biomedical abnormalities in liver function
Muscle myopathy and rhabdomyolysis
Affects neurodevelopment of fetus and children

44
Q

PCSK9 Inhibitor MOA

A

Inhibit PCSK9, which targets LDL receptors for degradation in lysosomes → increased density of LDL receptors on cell surface, increased internalisation of circulation LDLs → decreased blood cholesterol

45
Q

PCSK9 inhibitor Example

A

Evolocumab

46
Q

PCSK9 inhibitor ADRs

A

Contraindicated in patients who develop hypersensitivity reactions
Injection site inflammatory reactions
Nasopharyngitis and sinusitis

47
Q

Fibrates MOA

A

Activation of PPAR-alpha pathway → stimulate lipoprotein lipase activity → decreased plasma triglyceride, decreased VLDL

48
Q

Fibrates Example

A

Fenofibrate

49
Q

Fibrates ADRs

A

GI effects: Nausea
Skin rashes
Gallstones
Myositis

50
Q

Omega-3-acid ethyl esters MOA

A

Functional inhibition of enzyme responsible for TG biosynthesis

51
Q

Omega-3-acid ethyl esters Example

A

Omacor: EPA + DHA ethyl esters

52
Q

Omega-3-acid ethyl esters ADRs

A

Contraindicated in fish allergies
GI symptoms
Reduce production of thromboxane A2, leading to increased bleeding time

53
Q

Bile acid-binding resins MOA

A

Bind to bile acids and bile salts in small intestine → cause hepatocytes to increase conversion of cholesterol to bile acids → deplete intracellular cholesterol → increased hepatic uptake of cholesterol-containing LDL → fall in plasma LDL

54
Q

Bile acid-binding resins Example

A

Cholestyramine

55
Q

Resins ADRs

A

GI effects: constipation, nausea, flatulence, steatorrhea
Impaired absorption: Vit. ADEK

56
Q

Inhibitors of intestinal sterol absorption MOA

A

Reduce cholesterol absorption at small intestine by inhibiting sterol transporter

57
Q

Inhibitors of intestinal sterol absorption Example

A

Ezetimibe

58
Q

Inhibitors of intestinal sterol absorption ADRs

A

Diarrhea, flatulence
Rhabdomyolysis (more common when combined with statins)
Low incidence of reversible hepatotoxicity

59
Q

NSAIDs MOA

A

Inhibit cyclooxygenase synthesis of prostaglandins using arachidonic acid → decreased production of TXA2, PGI2, PGE2 → TXA2 required for platelet aggregation, platelets unable to aggregate

60
Q

NSAIDs ADRs

A

Bleeding
Gastric upset and ulcers

61
Q

GpIIb/IIIa receptor blocker MOA

A

Prevent binding of fibrinogen to IIb/IIIa complex → prevent platelet aggregation

62
Q

GpIIb/IIIa receptor blocker Example

A

Abciximab (humanised monocloonal antibody)
Epitifibatide (analog of fibrinogen)
Tirofiban (small molecule blocker)

63
Q

Clopidogrel MOA

A

Block ADP from binding to ADP receptor → prevent platelet aggregation

64
Q

Dipyridamole MOA

A

Inhibit PDE and prevent cAMP activation to 5’-AMP → prevent platelet aggregation

65
Q

Heparin MOA

A

Bind to ATIII and cause a conformational change that exposes its active site to stimulate its breakdown of factors IIa and Xa → inhibition of coagulation cascade

66
Q

Heparin ADRs

A

Hemorrhage
Thrombocytopenia

67
Q

Warfarin MOA

A

Inhibits vitamin K reductase → less vitamin K available for coagulation factor synthesis (II, VII, IX, X) → inhibition of coagulation cascade

68
Q

Warfarin ADRs

A

Bleeding
Pregnancy - can cross placenta easily

69
Q

Thrombolytic Agents Example

A

tPA
Streptokinase
Urokinase

70
Q

Fibrinolytic MOAs

A

Stimulate activation of plasminogen to plasmin → Increased degradation of fibrin to form fibrin degradation product → thrombolysis

71
Q

Thrombolytics ADRs

A

Bleeding
Healing wound, pregnancy

CVS Pharm (1 decks)

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