HEART MEDS Flashcards

1
Q

Antagonizes both B1 and B2 receptors thus inhibiting the effects of catecholamines on these receptors

A

adrenergic modulating meds

non selective beta blockers

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2
Q

Antagonizes B1 receptors to a greater extent than B2 receptors in typical doses

A

adrenergic modulating meds selective beta blockers

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3
Q
  1. These agents are considered third-generation beta-blockers
  2. They posses non-selective beta blocking activity like propranolol and alpha blocking activity like prazosin.
  3. Effects seen:
    a) Decrease heart rate
    b) Decrease contractility
    c) Vasodilation
A

alpha/beta adrenergic receptor antagonists

  • labetalol
  • carvedilol
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4
Q
  1. Block peripheral A1 - receptors thus causing vasodilation secondary to inhibiting catecholamine mediated vasoconstriction. These agents block both arterial and venous A1 - receptors.
  2. decrease afterload of the heart
  3. decrease peripheral vascular resistance
A

selective alpha1 adrenergic blockers

  • doxazosin
  • prazosin
  • terazosin
  • tamsulosin
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5
Q
  1. Alpha2 – receptors are located in the central nervous system. They are pre-synaptic receptors thus stimulation will result in a decrease in sympathetic out flow.
  2. The resulting effect is a lowering of blood pressure and to a lesser degree heart rate.
A

Central Acting A2 – Adrenergic Receptor Agonist

  • clonidine
  • guanabenz
  • guanfacine
  • methyldopa
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6
Q

located throughout the body

needed for cardiac contraction, smooth muscle contraction, and is required for pacemaker activity in the heart (sino-atrial (SA) node depolarization) and atrio-ventricular (AV) node conductance.

L-type channels
T-type channels

A

Calcium Channel Blockers

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7
Q

freely filtered into the lumen of the nephron and not reabsorbed. This causes an increase in solutes in the nephron and thus water will follow this high solute concentration

A

Osmotic Diuretics: Mannitol

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8
Q

bind to the Na+/K+/2Cl- transport system blocking the reabsorption of Cl- thus sodium and water will follow

A

Loop diuretics

Bumetanide (Bumex)
Ethacrynic acid (Edecrin)
Furosemide (Lasix)
Torsemide (Demadex)

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9
Q

Inhibits aldosterone effects in the cortical collecting tubule and late distal tubule

A

Potassium Sparing diuretics

Spironolactone/Eplerenone

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10
Q

Inhibits sodium transport through ion channels in the cortical collecting tubule and late distal tubule

A

Potassium Sparing diuretics

Amiloride and Triamterene

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11
Q

a) are found in the brush border cells in the lumen of the nephron
b) Inhibition of this enzyme decreases sodium bicarbonate reabsorption in the proximal tubule thus water follows.
c) This may cause a metabolic acidosis which decrease the effectiveness for diuresis.

A

Carbonic Anhydrase Inhibitors

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12
Q

Inhibit ADH antagonists in the collecting ducts of the nephron to promote free water excretion

A

Antidiuretic Hormone (ADH) Antagonists (vasopressin antagonists)

Conivaptan - Vaprisol®
Tolvaptan - Samsca®

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13
Q

inhibit conversion of angiotensin I to angiotensin II

A

Angiotensin Inhibitors

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14
Q

– Blocks angiotensin II (ATII) from binding to angiotensin type 1 receptors (AT1), therefore blocking the vasoconstrictor and aldosterone secreting effects of angiotensin II
– Blocks the effect of ATII regardless of whether ATII is generated by ACE, or some other enzymatic route (non-ACE pathway)
– Does not interfere with metabolism of kinins or
neuropeptides

A

Angiotensin II Receptor

Blockers (ARBs)

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15
Q

Blocks conversion of angiotensinogen to angiotensin I, therefore decreasing formation of angiotensin II

A

Direct Renin Inhibitor

-Aliskiren (Tekturna®)

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16
Q

– Organic nitrates are “prodrugs”
– Metabolically converted to nitric oxide (NO) in
vascular smooth muscle
– NO has vasodilating effects & reduces platelet
adhesion and aggregation
• NO also called EDRF-endothelium-derived relaxing
factor
– Nitrates preferentially affect venous dilation
– Larger doses can affect arterial dilation

A

Nitrates

17
Q

Arteriolar vasodilator
– Exact MOA unknown
– Vasodilation causes SNS stimulation with increase HR, increase contractility, increase plasma renin activity, and increase fluid retention
– Tachyphylaxis to BP lowering lowering effects
when used as monotherapy. Combination with NTG improves BP lowering effects

A

Miscellaneous Vasodilators

-Hydralazine

18
Q

Venous and Arteriolar vasodilator
– Metabolized by smooth muscle cells to active metabolite nitric oxide (NO). NO activates guanylate cylase to form cGMP and vasodilation
– Metabolic activations is catalyzed by different NO generating system than for NTG
– Unlike minoxidil, hydralazine, and other arteriolar vasodilators, SNP usually produces only a modest increase in HR and an overall decrease in myocardial O2 demand

A

Miscellaneous Vasodilators

-Sodium Nitroprusside (SNP)

19
Q

Arteriolar vasodilator
• Relaxation of smooth muscle with little effect on veins
• decrease Systemic Vascular Resistance (SVR) with decrease Blood Pressure (BP) produced by minoxidil triggers sympathetic, vagal inhibitory, and renal homeostatic mechanism leads to increase in heart rate (HR), increase Cardiac Output (CO) and increase in sodium and fluid retention

A

Miscellaneous Vasodilators

-Minoxidil

20
Q

Inhibits late phase of inward sodium channel (late INa) in

ischemic cardiac myocytes during cardiac repolarization

A

Miscellaneous Vasodilators

-Ranolazine (Ranexa™)

21
Q

neutral endopeptidase***

enzyme that metabolizes natriuretic peptides

natriuretic peptides produce vasodilation and natriuresis

A

ARNi (Sacubitril/Valsartan)

-Neprilysin

22
Q

combination of an ARB Valsartan and a neprilysin inhibitor sacubitril***

  • vasodilation
  • decreases aldosterone release
  • decreases catecholamine release
  • decreases ADH or vasopressin release
A

ARNi (Sacubitril/Valsartan)

-entresto