Drugs for Heart Failure Flashcards

1
Q

Give the 9 drug classes / drugs that are used for heart failure

A
  1. ACE-Is / ARBs
  2. Beta blockers
  3. Loop diuretics
  4. Sacubitril-Valsartan
  5. Mineralocorticoid receptor antagonists
  6. Nitrates
  7. Hydralazine
  8. Ivabradine
  9. Cardiac glycosides (digitalis)
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2
Q

Name 4 beta blockers that can be used to treat heart failure and state their cardioselectivity

A
  1. Carvedilol: Non selective
  2. Bisoprolol: Beta-1 selective
  3. Metoprolol XL: Beta-1 selective
  4. Nebivolol: Mixed selectivity
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3
Q

Give 3 other features of carvedilol use besides its use in hypertension and heart failure

A
  1. Can bind to alpha-1 receptors to reduce peripheral vascular resistance
  2. Antioxidative
  3. Anti-ischaemic
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4
Q

Name the natriuretic peptide that increases with heart failure

A

Brain natriuretic peptide (BNP)

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5
Q

Give 4 effects of BNP

A
  1. Promotes vasodilation
  2. Promotes natriuresis
  3. Promotes diuresis
  4. Antagonises RAAS which has favourable effects on heart failure
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6
Q

Name the enzyme that breaks down NPs

A

Neprilysin

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7
Q

Name 3 molecules that are broken down by neprilysin

A
  1. Natriuretic peptides eg BNP
  2. Angiotensin II
  3. Bradykinin
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8
Q

Intended MOA of sacubitril

A

Inhibits neprilysin leading to prolonged BNP effects which is good for HF

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9
Q

Why must valsartan be given with sacubitril?

A

Since neprilysin also breaks down Ang II, valsartan is given to act as an Ang II blocker which can reduce the side effects of prolonged Ang II, which is bad for HF

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10
Q

Sacubitril-Valsartan is known as an ___ inhibitor

A

ARNi: Angiotensin receptor/neprilysin inhibitor

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11
Q

Clinical use of sacubitril-valsartan

A

Heart failure with reduced ejection fraction (HFrEF)
*Can replace ARB / ACEIs

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12
Q

State 5 ADRs of sacubitril-valsartan use

A
  1. Hypotension
  2. Hyperkalemia
  3. Dry cough (due to increase in bradykinin)
  4. Renal failure
  5. Angioedema
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13
Q

Name 3 loop diuretics

A
  1. Furosemide
  2. Bumetanide
  3. Ethacrynic acid
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14
Q

Describe MOA of loop diuretics

A

Inhibit the luminal Na+/K+/2Cl- ion transporter in the thick ascending limb of the loop of Henle.
This increases the excretion of Mg2+ and Ca2+ (loss of lumen positive electric potential that decreases reabsorption of cations)

Also induces renal PG synthesis and increases renal blood flow (furosemide)

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15
Q

____ interfere with the actions of loop diuretics by ____ PG synthesis

A

NSAIDs (eg aspirin)
Reducing

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16
Q

State 4 clinical uses of loop diuretics

A
  1. Acute pulmonary oedema and other edema
  2. Acute hyperkalemia
  3. Acute renal failure
  4. Anion overdose: toxic ingestions of bromide, fluoride, iodide
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17
Q

State 4 ADRs of loop diuretic use

A
  1. Hypokalemic metabolic alkalosis
  2. Ototoxicity
  3. Hyperuricemia
  4. Hypomagnesemia
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18
Q

Loop diuretics should not be given together with ____ antibiotics (due to increased risk of ototoxicity)

A

Aminoglycosides

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19
Q

Where in the nephron do mineralocorticoids primarily work at

A

Collecting duct cells (specifically principal cells)

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20
Q

Name 4 potassium-sparing diuretics (mineralocorticoid receptor antagonists)

A
  1. Spironolactone
  2. Eplerenone
  3. Triamterene
  4. Amiloride
21
Q

MOA of spironolactone and eplerenone

A

Binds and blocks the aldosterone receptor

22
Q

MOA of triamterene and amiloride

A

Binds and blocks the sodium channel

23
Q

2 clinical uses of potassium-sparing diuretics

A
  1. Diuretic
  2. Hyperaldosteronism
24
Q

Does spironolactone have a slow or fast onset of action?

A

Slow

25
Q

Triamterene is metabolised in the ___

A

Liver

26
Q

Compared to amiloride, triamterene has a shorter or longer half-life?

A

Shorter

27
Q

State 5 ADRs of potassium-sparing diuretic use

A
  1. Hyperkalemia
  2. Metabolic acidosis
  3. Gynacomastia (spironolactone use)
  4. Acute renal failure (triamterene with indomethacin)
  5. Kidney stones (triamterene)
28
Q

Name a potassium-sparing diuretic associated with gynaecomastia

A

Spironolactone

29
Q

Name a potassium sparing diuretic associated with acute renal failure and kidney stones

A

Triamterene

30
Q

Name an NSAID when used with triamterene that increases the risk of acute renal failure

A

Indomethacin

31
Q

MOA of hydralazine

A

Direct arteriole vasodilator.
Inhibits the inositol triphosphate (IP3) induced release of calcium from the smooth muscle sarcoplasmic reticulum.
This reduces peripheral resistance causing compensatory release of NE and E leading to increased venous return and cardiac output

32
Q

2 clinical uses for hydralazine

A
  1. HFrEF
  2. Acute onset severe peripartum and postpartum hypertension
33
Q

Route of administration of hydralazine for HFrEF

A

Oral

34
Q

Route of administration of hydralazine for acute onset severe peri and postpartum HTN

A

IV

35
Q

In treating HFrEF with hydralazine, combination therapy with ____ should be used.

A

Isosorbide dinitrate (ISDN)

36
Q

Hydralazine is a good second line medication for what condition?

A

Hypertension

37
Q

2 ADRs of hydralazine use

A
  1. Baroreflex associated sympathetic activation symptoms: Flushing, hypotension, tachycardia
  2. Hydralazine-induced lupus syndrome (HILS)
38
Q

State 4 clinical presentations of hydralazine induced lupus syndrome (HILS)

A
  1. Arthralgia
  2. Myalgia
  3. Serositis
  4. Fever
39
Q

Treatment for HILS

A

Discontinue hydralazine therapy

40
Q

Hydralazine is contraindicated in patients with

A

Coronary artery disease
(because hydralazine stimulates sympathetic nervous system causing increased CO / O2 demand, thus causing myocardial ischaemia)

41
Q

Name 2 forms of digitalis (which are cardiac glycosides)

A
  1. Digoxin
  2. Digitoxin
42
Q

Route of administration of digitoxin and digoxin

A

Oral

43
Q

Digitoxin is extensively metabolised in the ___ and excreted in the ___

A

Liver
Feces

44
Q

Is digoxin extensively metabolised?

A

No

45
Q

Primary excretion route for digoxin

A

Unchanged by the kidney

46
Q

MOA of digitalis

A

Directly inhibits the Na+/K+ ATPase pump in the cardiac myocytes, thus increasing intracellular sodium concentration
This leads to less Ca2+ efflux by the Ca2+/Na+ exchanger, leading to higher intracellular calcium concentration, causing stronger systolic contractions

47
Q

2 clinical uses of digitalis

A
  1. Systolic dysfunction
  2. Atrial fibrillation
48
Q

3 ADRs of digitalis use

A
  1. Progressively more severe dysrhythmia: AV block, AF, VF
  2. GI effects: nausea, anorexia, vomitting
  3. CNS effects: fatigue, confusion, headache, blurred vision
49
Q

4 treatment for digitalis toxicity

A
  1. Discontinue cardiac glycoside therapy
  2. Correction of potassium or magnesium deficiency
  3. Antiarrythmic drugs (if automaticity predominant, use lidocaine or propranolol)
  4. Digoxin antibody (eg FAB fragments, digibind)