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Systemic Pharmaco > Drugs for Treatment of Heart Failure > Flashcards

Drugs for Treatment of Heart Failure Flashcards

1
Q

What is congestive HF?

A

A condition in which the heart is unable to pump sufficient blood to meet the needs of the body

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2
Q

What are the 2 forms of congestive HF?

A
  1. Systolic dysfunction: impaired ventricular contraction

2. Diastolic dysfunction: impaired ventricular relaxation

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3
Q

What is chronic HF characterised by?

A
  • Progressive cardiac dysfunction
  • Breathlessness
  • Tiredness
  • Neurohormonal disturbances
  • Sudden death
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4
Q

What are the cardiovascular consequences of HF?

A
  1. Decreased cardiac output
    - Sympathetic activity
    - Decreased BP
    - RAAS to increase fluid volume
    - Edema
  2. Increased venous pressure (backpressure)
    - Edema
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5
Q

What are the 3 broad classes of drugs used in the therapy of chronic HF?

A
  1. Positive inotropic drugs
  2. Vasodilators
  3. Misc. drugs
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6
Q

What do inotropic drugs do?

A

Increase heart contraction

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7
Q

Why is it that therapy for chronic heart failure involves positive inotropic drugs (increase heart contraction) and vasodilators (decrease CO)?

A

It’s therapy for different stages of heart failure
Early HF: decreased ventricular EF
- Therapy is to preserve this by decreasing cardiac load (vasodilators)

Late HF: further reduce in heart pumping will threaten life
- Therapy is not to maintain fn but to maximise survival (positive inotropic drugs)

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8
Q

What are the positive inotropic drugs?

A

Glycosides
Beta agonists
PDE inhibitors

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9
Q

What are the vasodilators?

A

PDE inhibitors
Nitroprusside, Nitrates, AT1R antagonist
Diuretics, ACE inhibitors

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10
Q

What are the misc. drugs?

A

Diuretics, ACE inhibitors

Beta blockers, aldosterone antagonists

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11
Q

What are the beta blockers specifically approved to treat HF?

A

‘Coffee Meets Bagel!!!’:
Carvedilol
Metoprolol
Bisoprolol

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12
Q

What is the pathophysiology of chronic HF?

A
  • As the pump becomes less effective, more blood remains in the ventricles at the end of cycle
  • End-diastolic volume (preload) increases
  • Initially, increased preload may promote increased force of contraction, but further increase in preload causes heart to become overstretched and contract less forcefully
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13
Q

What is the MOA of nitrates?

A

Activates guanylyl cyclase

  • Increase conversion of GTP to cGMP
  • Inactivation of myosin-LC
  • Vasorelaxation (venodilation decreases preload, arteriolar dilation decreases afterload)
  • Decrease O2 consumption
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14
Q

What are the therapeutic effects of nitrates?

A

Vasorelaxation:

  1. Venodilation (decreases preload)
  2. Arteriolar dilation (decreases afterload TPR)
  • Decrease cardiac load and BP
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15
Q

What is the specific nitrate used for chronic HF? What does it do?

A

Sodium nitroprusside (SNP)

SNP donates NO to become = NO + cyanide + methemoglobin

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16
Q

How is SNP administered?

A

IV infusion

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17
Q

What is the indication for SNP?

A

Chronic or refractory HF

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18
Q

What are the adverse effects of SNP?

A
  1. Hypotension
  2. Cyanide poisoning from cyanide side group
  3. Methemoglobin leading to cellular hypoxia bc of decreased O2 carrying capacity compared to Hb
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19
Q

What happens in the loop of Henle? What substances are absorbed at which part of the loop? (thin descending, loop, thick ascending)

A

Thin descending loop: Absorption of water only by osmosis

Loop of Henle: (point where urine is most concentrated)

Thick ascending loop: Absorption of NaCl by active transport. Impermeable to water unlike prox. tubule and thin limb

20
Q

Where in the nephron is only water absorbed?

A
  1. Thin descending limb

2. Collecting duct

21
Q

How is NaCl absorbed in the thick ascending limb? What transporter is involved? How does this affect the membrane potential?

A

Na/K/2Cl cotransporter

  • Excess K+ accumulation within the cell bc of synergistic effect w basal N+/K+ ATPase
  • Back diffusion of K+ into the tubular lumen via a K+ channel
  • Development of lumen-positive electrical potential
  • This electrical potential provides the driving force for the reabsorption of cations - including Mg2+ and Ca2+ via the paracellular pathway
22
Q

What are the loop diuretics (sulfonamide derivatives)?

A
  • Furosemide
  • Bumetanide
  • Ethacrynic acid
23
Q

What are the MOAs of loop diuretics?

A
  1. Selectively inhibit the luminal Na+/K+/2Cl- transporter in the thick ascending limb of Henle’s loop
  2. Increase Mg2+ and Ca2+ excretion because of decreased membrane potential
  3. Induce renal PG synthesis
  4. (Furosemide) Increase renal blood flow
24
Q

Which part of the loop does loop diuretics work on?

A

Thick ascending limb

25
Q

Do loop diuretics have a fast or slow onset? What is the duration of effect of furosemide?

A
  • Rapidly absorbed
  • Extremely rapid onset after IV injection
  • Furosemide duration of effect: 2-3h
26
Q

How are loop diuretics excreted?

A

Eliminated by tubular secretion & glomerular filtration

27
Q

What are the clinical uses of loop diuretics?

A
  1. Acute pulmonary edema and other edema
  2. Acute hyperkalemia
  3. Acute renal failure
  4. Anion overdose: toxic ingestions of bromide, fluoride, and iodide
28
Q

What are the adverse effects of loop diuretics?

A
  1. Hypokalemic metabolic alkalosis
  2. Ototoxicity leading to deafness
  3. Hyperuricemia (ion imbalance)
  4. Hypomagnesemia
29
Q

What is the contraindication for loop diuretics?

A

Avoid using together w aminoglycosides if possible

30
Q

What happens in the distal convoluted tubule? What substances are absorbed and by what transporters? How is it different from in the thick ascending limb?

A
  • Relatively impermeable to water
  • NaCl reabsorption by electrically neutral Na+ and Cl- cotransporter (vs. Na/K/Cl cotransporter in the thick ascending limb), further dilutes the tubular fluid
  • Active reabsorption of Ca2+ by apical Ca2+ channel and basolateral Na+/Ca2+ exchanger
31
Q

What are the thiazide diuretics?

A
  • Hydrochlorothiazide
  • Indapamide
  • Chlorthalidone
32
Q

What are the MOAs of thiazide diuretics?

A
  1. Inhibit Na+/Cl- transporter in the distal convoluted tubule
    - Inhibit NaCl reabsorption
    - Decrease H2O reabsorption, more excreted
  2. Enhance Ca2+ reabsorption
  3. Action is dependent on renal PG synthesis
    !!! NSAIDs interfere w this by reducing PG synthesis
33
Q

What are the clinical uses of thiazide diuretics?

A
  1. Hypertension
  2. Congestive heart failure
  3. Nephrolithiasis due to idiopathic hypercalciuria
  4. Nephrogenic diabetes insipidus
34
Q

What are the adverse effects of thiazide diuretics?

A
  1. Hypokalemic metabolic alkalosis
  2. Hyperuricemia (ion imbalance)
  3. Hyperglycemia
  4. Hyperlipidemia
  5. Hyponatremia
35
Q

In what group of individuals are thiazide diuretics less unsuitable for?

A

Diabetics (bc an adverse effect is hyperglycemia)

36
Q

What are the functions of the collecting tubule?

A
  1. Final site of NaCl reabsorption
  2. Responsible for volume regulation and for determining final Na+ conc. of the urine
  3. Site at which mineralocorticoids (eg. aldosterone) exert a significant influence
  4. Site of potassium secretion
37
Q

What cells are in the collecting tubule? What are their significance?

A

Principal cells: Major sites of Na+, K+, H2O transport

Intercalated cells: Primary sites of proton (H+) secretion

38
Q

What happens in the collecting tubule? What substances are absorbed and what hormones have effects in this area?

A
  • Na+, K+, H2O transport (principal cells) and H+ proton secretion (intercalated cells)
  • Na+ reabsorption via epithelial Na+ channel is coupled w K+ secretion - regulated by aldosterone
  • Membrane water permeability regulated by ADH-induced fusion of vesicles containing performed water channels w the apical membranes
39
Q

What are the potassium sparing diuretics? What are they also known as?

A
  • Spironolactone
  • Triamterene
  • Amiloride
  • Eplerenone

Mineralocorticoids antagonists

40
Q

What is the MOA of spironolactone and triamterene?

A

Downregulate the aldosterone receptor

  • Decrease Na+ reabsorption, H2O reabsorption, more H2O excretion
  • Decrease K+ secretion “potassium sparing”
41
Q

What is the MOA of amiloride and eplerenone?

A

Downregulate the Na+ channel expression

  • Decrease Na+ reabsorption, H2O reabsorption, more H2O excretion
  • Decrease K+ secretion “potassium sparing”
42
Q

Do potassium-sparing diuretics have a fast or slow onset?

A

Spironolactone has a slow onset (vs. loop diuretics), requires several days before full therapeutic effect is achieved

43
Q

How are triamterene and amiloride metabolised? How are they different in terms of duration of onset?

A

Triamterene: Liver
- Shorter half life, must be given more frequently

Amiloride: Not metabolised at all, excreted unchanged

44
Q

What are the clinical uses of potassium-sparing diuretics?

A
  1. Diuretic

2. Hyperaldosteronism

45
Q

What are the adverse effects of potassium-sparing diuretics? How is it different from loop diuretics & thiazides?

A
  1. Hyperkalemia
    * **DOES NOT CAUSE hypokalemia unlike loop diuretics & thiazides
  2. Metabolic acidosis
  3. Gynecomastia (except eplerenone)
  4. Acute renal failure (triamterene + indomethacin)
  5. Kidney stones (triamterene)

Systemic Pharmaco (6 decks)

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