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CVS Pharm Flashcards

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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
Loop Diuretics ADRs
Hypokalemic metabolic alkalosis Ototoxicity Hyperuricemia Hypomagnesemia
26
Potassium-sparing diuretics MOA
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)
27
Potassium-sparing diuretics Example
Spironolactone Triamterene
28
Potassium-sparing diuretics ADRs
Hyperkalemia Metabolic acidosis Gynecomastia (spironolactone only) Acute renal failure (triamterene + indomethacin) Kidney stones (triamterene)
29
Hydralazine MOA
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
Hydralazine ADRs
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
Digitalis
Increases contractility of heart Digoxin & Digitoxin
32
Nitrates MOA
Nitrates form nitric oxide, which promotes vasodilation by stimulating guanylyl cyclase → reduce afterload, decrease oxygen consumption of cardiac muscle, therapy of angina
33
Nitrates Examples
Nitroglycerin Isosorbide dinitrate
34
Nitrates ADRs
Reflex tachycardia Hypotension Headache
35
DHP Calcium Channel Blockers MOA
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
Non-DHP Calcium Channel Blockers MOA
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
Non-DHP Calcium Channel Blocker ADRs
Cardiac depression: bradycardia, AV block, heart failure
38
DHP Calcium Channel Blocker ADRs
Hypotension Heart failure Myocardial infarction
39
Ivabradine MOA
Inhibits cardiac pacemaker cells → reduction in cardiac workload and myocardial oxygen consumption
40
Ivabradine ADRs
Luminous phenomena Bradycardia related symptoms: fatigue, hypotension, dizziness
41
Statins MOA
Statins inhibit HMG-CoA reductase, the rate-limiting step in cholesterol synthesis → decrease endogenous cholesterol
42
Statins Example
Atorvastatin
43
Statin ADRs
Biomedical abnormalities in liver function Muscle myopathy and rhabdomyolysis Affects neurodevelopment of fetus and children
44
PCSK9 Inhibitor MOA
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
PCSK9 inhibitor Example
Evolocumab
46
PCSK9 inhibitor ADRs
Contraindicated in patients who develop hypersensitivity reactions Injection site inflammatory reactions Nasopharyngitis and sinusitis
47
Fibrates MOA
Activation of PPAR-alpha pathway → stimulate lipoprotein lipase activity → decreased plasma triglyceride, decreased VLDL
48
Fibrates Example
Fenofibrate
49
Fibrates ADRs
GI effects: Nausea Skin rashes Gallstones Myositis
50
Omega-3-acid ethyl esters MOA
Functional inhibition of enzyme responsible for TG biosynthesis
51
Omega-3-acid ethyl esters Example
Omacor: EPA + DHA ethyl esters
52
Omega-3-acid ethyl esters ADRs
Contraindicated in fish allergies GI symptoms Reduce production of thromboxane A2, leading to increased bleeding time
53
Bile acid-binding resins MOA
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
Bile acid-binding resins Example
Cholestyramine
55
Resins ADRs
GI effects: constipation, nausea, flatulence, steatorrhea Impaired absorption: Vit. ADEK
56
Inhibitors of intestinal sterol absorption MOA
Reduce cholesterol absorption at small intestine by inhibiting sterol transporter
57
Inhibitors of intestinal sterol absorption Example
Ezetimibe
58
Inhibitors of intestinal sterol absorption ADRs
Diarrhea, flatulence Rhabdomyolysis (more common when combined with statins) Low incidence of reversible hepatotoxicity
59
NSAIDs MOA
Inhibit cyclooxygenase synthesis of prostaglandins using arachidonic acid → decreased production of TXA2, PGI2, PGE2 → TXA2 required for platelet aggregation, platelets unable to aggregate
60
NSAIDs ADRs
Bleeding Gastric upset and ulcers
61
GpIIb/IIIa receptor blocker MOA
Prevent binding of fibrinogen to IIb/IIIa complex → prevent platelet aggregation
62
GpIIb/IIIa receptor blocker Example
Abciximab (humanised monocloonal antibody) Epitifibatide (analog of fibrinogen) Tirofiban (small molecule blocker)
63
Clopidogrel MOA
Block ADP from binding to ADP receptor → prevent platelet aggregation
64
Dipyridamole MOA
Inhibit PDE and prevent cAMP activation to 5'-AMP → prevent platelet aggregation
65
Heparin MOA
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
Heparin ADRs
Hemorrhage Thrombocytopenia
67
Warfarin MOA
Inhibits vitamin K reductase → less vitamin K available for coagulation factor synthesis (II, VII, IX, X) → inhibition of coagulation cascade
68
Warfarin ADRs
Bleeding Pregnancy - can cross placenta easily
69
Thrombolytic Agents Example
tPA Streptokinase Urokinase
70
Fibrinolytic MOAs
Stimulate activation of plasminogen to plasmin → Increased degradation of fibrin to form fibrin degradation product → thrombolysis
71
Thrombolytics ADRs
Bleeding Healing wound, pregnancy

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