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Pharmacy Stage 2 > Pharmacology of Heart Failure Drugs > Flashcards

Pharmacology of Heart Failure Drugs Flashcards

1
Q

which four classes of drugs can be used to treat heart failure?

A
  1. vasodilator drugs
  2. positive inotropes
  3. ACE inhibitors
  4. Diuretics
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2
Q

what is the role of positive inotropes?

A

it prevents the reduction of cardiac output caused by heart failure (i.e. increases stroke volume hence reducing left ventricular end diastolic pressure)

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3
Q

what is the role of ACE inhibitors?

A

prevents the formation of angiotensin 2 hence preventing water and sodium ions retention and other factors

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4
Q

what is the role of diuretics?

A

prevents water and sodium ions retention

-reduces pulmonary congestion but doesn’t increase stroke volume

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5
Q

what is the role of vasodilator drugs?

A
  1. prevents rise in preload on the heart
  2. prevents rise in central venous pressure
  3. prevents rise in afterload
  4. stimulates tissue perfusion (passage of blood and fluids through a vessel/channel)
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6
Q

what two things would work best when combined to improve heart failure?

A

combining vasodilators and inotropic therapy

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7
Q

What is the effect of inotropic drugs?

A

improves the cardiac performance so the stroke volume (cardiac output) increases

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8
Q

how do inotropic drugs work?

A

by putting calcium back into the heart muscles causing a more forceful contraction

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9
Q

What is the role of calcium in muscle contraction?

A
  1. calcium enters via voltage-gated calcium channels and stimulates the release of calcium from the sarcoplasmic reticulum into the cytosol
  2. this switches on the contractile machinery (myosin and actin contraction causing heart muscle contraction)
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10
Q

where must calcium be for it to be used for muscle contraction?

A

in the cytosol

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11
Q

where does calcium come from?

A
  1. from outside the cell and enters via the voltage-gated calcium channels - this triggers a calcium induced calcium release
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12
Q

where is calcium stored?

A

from the sarcoplasmic reticulum

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13
Q

what is the mechanism of action of adrenergic agonists on muscle contraction?

A
  • b1-agonists bind to b1-adrenergic receptors in the cardiac myocyte
  • this receptor is coupled to a G-protein.
  • this causes a mechanism associated with adenylyl cyclase
  • ATP is therefore converted to cAMP
  • cAMP activates PKA to phosphorylate calcium channels forcing them open.
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14
Q

give an example of an inotrope?

A

adrenergic agonists

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15
Q

when would you use adrenergic agonists?

A

in an emergency e.g. cardiogenic shock

-because they’re short term and have a short half life and are rapid working

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16
Q

what are risks with adrenergic agonists?

A
  • can cause arrhythmia

- can cause myocardial oxygen demand

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17
Q

what is the mechanism of action of cardiac glycosides on muscle contraction?

A
  • useful for atrial fibrillation and heart failure and antiarrythmia
  • don’t have a direct action on calcium channels unlike b1-agonists
  • slows down conduction from AV node
  • works to block Na+/K+ ATPase pump
  • this slows down Na+ pumping out of the cell causing a build up on Na+ inside the cell
  • The Na+/Ca2+ exchanger usually pumps Ca2+ out of the cell and Na+ in but it won’t be able to do so as there will be no Na+ conc gradient when
  • Therefore no pumping of Ca2+ out of the cell will stop more Ca2+ coming in
  • calcium is also then stored into the sarcoplasmic reticulum. This causes rise for more Ca2+ to be able to be released from the sarcoplasmic reticulum, hence a more forceful contraction.
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18
Q

how does Na+/K+ ATPase work?

A

pumps 3Na+ out of the cell in exchange for 2K+ into the cell

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19
Q

what are the adverse effects of cardiac glycosides?

A
  1. heart block
  2. supraventricular and ventricular arrhytmias
  3. nausea
  4. vomitting
  5. constipation
  6. confusion
  7. visual disturbances
20
Q

what is an ectopic beat?

A

an early depolarisation of the ventricles

21
Q

what do diuretics do?

A

they reduce pulmonary congestion but don’t increase stroke volume

22
Q

what are the classes of diuretics?

A
  1. Thiazides
  2. Loop
  3. Combination diuretic therapy
  4. Potassium-sparing
  5. Aldosterone antagonists
23
Q

what are thiazides useful for?

A
  • relieving oedema due to chronic heart failure

- reduce blood pressure

24
Q

what are loop diuretics useful for?

A
  • pulmonary oedema due to left ventricular failure
  • for chronic heart failure
  • for antihypertensive treatment in resistant hypertension
  • for vasodilation
25
Q

what is combination therapy useful for?

A
  • patients with oedema resistant to treatment with one diuretic
  • loop diuretics may induce acute hypotension
26
Q

how do thiazides work?

A
  • inhibit Na+/Cl+ co-transport mechanism preventing Na+ reabsorption at the distal convoluted tubule
  • this increases urinary excretion of Na+, K+ and H2O
  • therefore less Na+ buildup in the cytosol meaning Cas+ can leave the cytosol for new ones to enter and cause muscle contraction.
  • also causes vasodilation (making thiazides useful in hypertension also)
27
Q

where do Loop diuretics work?

A

just after the loop of henle and inhibits the Na+/Ca2+/K+ triple symporter from pumping sodium, potassium and chlorine out hence no reabsorption of the ions.

28
Q

why won’t you use thiazides on their own?

A

as they aren’t potent enough

29
Q

give an example of a thiazide used to treat hypertension?

A

indapamide

30
Q

give an example of a thiazide used to treat heart failure?

A

bendroflumethiazide

31
Q

give an example of a cardiac glycoside?

A

digoxin

32
Q

how do thiazides stimulate vasodilation?

A

by stimulating renin secretion, hence angiotensin formation, hence aldosterone release, hence vasodilation

33
Q

what are thiazides most commonly used in conjunction with?

A

Loop diuretics

34
Q

How do loop diuretics works?

A
  • reduce electrolyte reabsorption in the ascending limb of the loop of Henle by inhibiting the Na+/Ca2+/K+ triple symporter from pumping sodium, potassium and chlorine out hence no reabsorption of the ions.
  • this promotes urinary excretion of Na+, Cl-, H20, K+
35
Q

which are more potent, loop or thiazide diuretics?

A

Loop diuretics as more reabsorption takes place in the the loop of henle than in the distal convoluted tubule

36
Q

what are risks of using Loop diuretics?

A
  1. may exacerbate diabetes and gout
  2. increased risk of urinary retention if you have an enlarged prostate
  3. increased risk of hypovolaemia, hypotension and hypokalaemia
37
Q

how can we reduce the hypokalaemia risks in patients taking Loop diuretics?

A

combing with a K+ sparing diuretic

38
Q

how do K+ sparing diuretics and aldosterone antagonists work?

A
  • on their own they’re weak diuretics so usually used in conjunction with others (thiazides or loop)
  • can cause retention of potassium and hyperkalaemia
39
Q

give 2 examples of K+ sparing diuretics?

A
  • amiloride

- triamterene

40
Q

give an example of an aldosterone antagonist?

A

spironolactone

41
Q

what are aldosterone antagonists?

A

potassium-sparing diuretics that potentiate thiazide or loop diuretics

42
Q

what does spironolactone do?

A

blocks the effects of aldosterone to prevent Na+/Cl- transporters binding to the collecting duct membrane hence preventing Na+ and Cl- reabsorption

43
Q

what does aldosterone do?

A

causes Na+/Cl- channels to be added to the collecting duct for reabsorption of Na+ and Cl-

44
Q

how do ACE inhibitors and ARBs promote a diuretic effect?

A
  • block renin-angiotensin-aldosterone pathway.

- no aldosterone = no Na+ and Cl- reabsorption

45
Q

give an example of an ACE inhibitor?

A

Enalapril

46
Q

Give an example of an ARB?

A

Losartan

Pharmacy Stage 2 (85 decks)

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