Pharmacology Flashcards

1
Q

What are the compensatory mechanisms in heart failure ?

A

1- Renin-angiotensin-aldosterone system
2-sympathetic nervous system
3- neuro-humoral mechanisms such as secretion of bradykinin

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2
Q

Vasodilators - ACE inhibitors

A

ACEI lower the preload and afterload by blocking the synthesis of A2
such as Enalapril, ramipril ad lisinopril.
no parenteral formulations
used in chronic left or biventricular heart failure

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3
Q

adverse effects of ace inhibitors:

A

Renal failure
due to increased bradykinin levels: -chronic cough and angioedema
hypotension

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4
Q

Is ACEI used in patients with chronic heart failure ( diastolic )?

A

No, they’re only used in patients with systolic heart failure where the ejection fraction is reduced, it helps in reducing mortality and prolonging the life

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5
Q

ACEI contractions?

A

Renal artery stenosis
Aortic stenosis “ increases resistance across the aortic valve “
Angioedemas
pregnancy

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6
Q

A2 receptor antagonists

A

Competitive antagonists of A2 can also be called angiotensin receptor blockers

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7
Q

A2 receptor antagonists/ARB’S

A

Does not produce cough, mostly used for hypertension
examples are; losartan, candesartan ( for hf also), and irbesartan.
decreases afterload

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8
Q

Nitrates

A

symptom relief:
Glyceryl trinitrate (short-acting) - sublingual
also treats angina
Isosorbide (longer action)
all-cause the release of nitric oxide that would induce smooth ms. relaxation = reduced venous return

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9
Q

Nitrates side effects

A
if its IV:
dose-related hypotension
if its tablets:
Headache
can be used in combination with hydralazine when intolerant to ACEI
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10
Q

Loop Diuretics

A

A symptom relief

  • Inhibits the Na 2cl K+ pump in the thick ascending loop of Henle.
  • decreases blood volume and preload, additional time for the heart to relax.
    example: furosemide> at high concentrations can act as a vasodilator
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11
Q

Loop diuretics side effects :

A
Dehydration can develop into shock.
Hypokalemia
Hyperuricemia and gout
ototoxicity
reduced glucose tolerance
**they're actually effective in renal function so avoid adding impaired renal function as a side effect :)
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12
Q

Diuretics ( Thiazides) are used for what mainly?

A

Hypertension

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13
Q

Diuretics ( Thiazides) mechanism of action ?

A

Acts on the distal tubule prevent the reabsorption of 3 to 5% of filtered Na+
examples: Bendroflumethiazide & Metolazone.

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14
Q

Side effects of the Thiazides are:

A
Hypokalemia
Hyperurecimia and gout
Reduced glucose tolerance
Impotence
Renal failure
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15
Q

Aldosterone antagonists

A

Reduces mortality in patients with reduced ejection fraction.

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16
Q

Aldosterone antagonists

A

these agents antagonize the activity of aldosterone. Therefore, they will result in retention of K+ and excretion of NA+
in combination with the loop or thiazide classes for additive diuretic effect and to prevent hypokalaemia.

17
Q

Aldosterone antagonists

A

Spironolactone is an aldosterone antagonist that has a similar structure to Progesterone. Hence, other than the fact that they block androgen receptors preventing the formation of androgens, they also bind to the progesterone receptors causing Gynaecomastia in men and menstrual irregularities in women.
Eplerenone has lesser side effects

18
Q

When used with ACEI , hyperkalemia occurs as a side effect?

A

Aldosterone antagonists

19
Q

Beta-Blockers

A

Negative inotropes, decrease the force of contractility of the heart and worsens the heart failure
reduces mortality with diuretics and ACEI

20
Q

Examples of Beta-blockers

A

Carvedilol, Bisoprolol, Metoprolol and Nevivolol

21
Q

When are Beta-blockers given?

A

If a patient is newly diagnosed, we wait until he is decongested and treated with symptom relief and then we can start the beta-blockers.
**Notice that once the beta-blockers are given you never never never withdraw them from the patient even if he has acute heart failure symptoms!

22
Q

Ionotropic drugs

A

used to increase the force of ventricular contraction when myocardial systolic function is impaired. They enhance cardiac contraction by increasing the intracellular calcium concentration, thus augmenting actin and myosin interactions.
stroke volume and cardiac output are increased.

23
Q

Ionotropic drugs example

A

Dobutamine

24
Q

ionotropic drugs

A

These drugs are commonly used after large MI with a Cardiogenic Shock.
These drugs are also associated with high mortality rates.
These drugs are administered only when the net clinical benefit is positive.
- Low BP, poor renal/splanchnic perfusion, acute renal failure.

25
Q

Dobutamine

A

• Dobutamine is given I.V. with a very short half-life. Therefore, infusion rate
determines plasma concentration.
• With lower infusion rates, increased contractility and CO will be noticed.
• With higher infusion rates, arterial constriction and tendency to reduce
splanchnic perfusion

26
Q

Oral inotropes

A

Digoxin

27
Q

Digoxin is

A

symptom relief, oral inotrope