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Pharmacology > Anti-Hypertensive Pharmacology > Flashcards

Anti-Hypertensive Pharmacology Flashcards

1
Q

Hypertensive values

A

>130/80

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2
Q

Blood pressure equations

A

BP is the pressure exerted against the arterial wall

BP=[EDV-ESV] x HR] x SVR

or

BP=CO x SVR

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3
Q

Ways to reduce cardiac output?

A

Reduce blood volume
Reduce heart rate
Reduce stroke volume

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4
Q

Ways to reduce SVR?

A

Dilate systemic vasculature

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5
Q

What are the four anatomic sites of BP control?

A
  1. Resistance arterioles
  2. Capacitance venules
  3. Pump heart output
  4. Volume kidneys (Renin-angiotensin-aldosterone)
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6
Q

Mechanism of action of Diuretics

A
  1. Deplete body of sodium and H2O
  2. Reduce blood volume (decrease stroke volume)
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7
Q

Type of Diuretics?

A
  • *1. Loop diuretics
    2. Thiazide diuretics
    3. Potassium sparing diuretics**
    4. Osmotic diuretics
    5. Carbonic anhydrase inhibitors (renal specialists)
    6. Vasopressin (ADH) antagonists
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8
Q

Where do loop diuretics act?

A

Blocks the Na/K/Cl exchanger in the ascending Loop of Henle, accounts for 25% less Na/K/Cl retention because it inhibits this pump. 25% more Na/K/Cl is excreted in the urine.

Uses:
Treatment/prevention of edamatous conditions (heart failure), hyperkalemia, HTN (2nd line)

Adverse effects (mainly dehydration):
Na/volume depletion leading to hypotension
Hypokalemia (arrhythmias), hypocalcemia (tetany), hypomagnesemia (arrhythmias), metabolic alkalosis
Ototoxicity (tinnitus, vertigo, deafness) in high concentrations
Hyperuricemia (gout) when used chronically

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9
Q

Where to thiazide diuretics act?

A

Act on a Na/Cl pump in the distal convoluted tubule (DCT) where 5% Na/Cl is excreted to the urine. First line of defense against hypertension because it is less potent, can augment the loop effect

Thiazides to remember:
Hydrochlorothiazide
Chlorthalidone
Indapamide
Metalazone (never used alone)

Adverse effects: Hypovolemia, hypokalemia, hyponatremia (common), hypochloremia, hypomagnesemia, hypercalcemia, hyperuricemia (gout), metabolic acidosis

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10
Q

Where do potassium sparing diuretics act?

A

Work in the collecting duct of the nephron by inhibiting aldosterone (antagonist) or blocking a Na/H/K exchanger. Pretty weak diuretics unless used for specific disease states, can cause hyperkalemia

Na Channel Blockers: triamterene and amiloride, inhibitors of renal epithelial Na+ channels

Aldosterone receptor antagonists: Indicated in HF, spironolactone and eplerenone (indirect effect)*
*Do not act on the luminal side of the tubule

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11
Q

What is the root cause of hypertension?

A

Sympathetic overdrive

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12
Q

Sympathetic receptor review

A
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13
Q

Drugs that alter sympathetic nervous system function?

A
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14
Q

Mechanism of action of a2 agonists

A

Stimulate a2 receptors on presynaptic neuron, reduces central sympathetic flow and increased parasympathetic flow

Adverse effects: Dry mouth, drowsiness/sedation, lethargy, constipation, sexual dysfunction, bradycardia, rebound HTN with withdrawal

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15
Q

Clonidine’s central mechanism of action?

A

Activation of a2 receptor initiates more firing of vagus nerve (decreases HR/SV) and decreases firing of sympathetic nerves leading to decrease in BP

Clinical use: Hypertension (not a first line of defense), resistant hypertension
Hypertensive urgency without acute organ damage
ADHD (guanfacine)
Treatment of withdrawal (Narcotics, alcohol)

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16
Q

What are the more a2 agonist specific drugs?

A
17
Q

Alpha 1 adrenergic antagonists mechanism of action?

A

Inhibit binding of NE to postsynaptic alpha1 receptors by relaxing smooth muscles and decreasing peripheral vascular resistance and venous return

Uses: Mostly used for reducing resistance to urinary flow (relaxes smooth muscle), useful in benign prostatic hypertrophy, n__ot recommended for initial monotherapy

Adverse effects: Drowsiness, fluid retention, diarrhea, postural hypotension, syncope, tachycardia, can increase risk of HF with chronic use
First dose phenomenon: faintness or syncope 30-60min after first dose, use low initial dose (bedtime) and titrate slowly

18
Q

Beta-Blocker effects/adverse effects? Clinical uses?

A

Adverse effects:

  1. Smooth muscle spasm (bronchospasm especially with non-selectives)
  2. Exaggeration of cardiac therapeutic actions (too much bradycardia/hypotension)
  3. CNS penetration (insomnia, depression, some more lipid soluble than others)
  4. Worsened quality of life (weight gain, fatigue, ED)
  5. Adverse metabolic side effects (loss of glycemic control, masks hypoglycemia)
  6. Withdrawal phenomenon

Clinical uses: Ischemic heart disease, HF with reduced EF (only metoprolol, carvedilol, bisoprolol), tachyarrhythmias, controlling acute panic symptoms, glucoma, variceal bleeding from portal hypertension/cirrhosis

19
Q

Non-selective/cardioselective/vasodilating B-Blockers

A
20
Q

What are the vasodilating B-Blockers, and what do they do?

A

BP reduction from decrease in HR and SVR

a1 and B1 antagonist

21
Q

What are the two types of Ca channel blockers?

A

T (transient) type: opens at more neg. potentials, involved in initial depolarization of SA/AV nodes

L-type: located on vascular smooth muscle, cardiac myocytes, cardiac nodal tissue
Dominant in AV node, required for CICR from SR, Phase 0 and Phase 2 of action potential
Activity increased by catecholamines

22
Q

Difference between DHPs and Non-DHPs

A

Dihydropyridines (DHP): -pine suffix, act on on arterioles

Non-DHPs: Act directly on the heart decreasing HR and contraction

23
Q

B-blockage effects vs. CCBs

A
24
Q

Clinical uses of verapamil or diltiazem?

A
  • Hypertension
  • Supraventricular tachyarrhythmias
  • Coronary spasm
  • Chronic stable angina
25
Q

With an ischemic heart, how do non-CCB help? What are some contraindications? Adverse effects?

A

Decreasing the demand of the heart (decreased HR/contractility) allows more supply
Vasodilation increases O2 supply to the heart

_Contraindications_: Severe hypotension/cardiogenic shock
LV dysfunction (EF \<40%)
2nd or 3rd degree AV block (except with artificial pacemaker)

Adverse effects: GI distress/constipation (verapamil more so), headache, edema, dizziness, edema, fatigue, bradycardia, HF, AV block

26
Q

Dihydropyridine CCBs

A

Nifedipine was first DHP CCB. Long acting capsules are preferred

Short acting capsules have many routes of administration (nasal, inhalation, rectal), act by rapidly vasodilating to relieve sever HTN and terminate coronary spasm -> rapid reflex adrenergic activation with tachycardia

Clinical uses: Hypertension (first line of defense regardless of race), chronic stable angina, coronary spasm, Raynaud’s phenomenon (ankle edema is side effect), no rebound tachycardia

27
Q

What are the direct vasodilators, and how do they work?

A

Hydralazine (IV) and Minoxidil

MOA: specific for arterial resistance vessels (dilates them), lowers afterload (important in HF)

Adverse effects: headaches, flushing, baroreceptor reflex tachycardia (boxed warning), salt and water retention
Minosidil -> hypertrichosis, pericardial effusion (boxed warning)

Uses: hypertension, midoxidil is last line of defense if no other therapies work, heart failure (hydralazine combined with isosorbide dinitrate)

28
Q

What combination of drugs are recommended for black HF patients who remain symptomatic despite therapy?

A

Isosorbide dinitrate -> venodilation and reduction in preload, increase in NO bioavailability

Hydralazine -> arterial dilation to reduce afterload and increase SV and CO
Increase in NO bioavailability secondary to reduction in oxidative stress

29
Q

Sodium nitroprusside

A

Source of NO, potent and very rapid peripheral vasodilator affecting arteries and venules (decreasing preload/afterload)

Keep dose low/short (<72hours), monitor level and renal function (CI in renal failure), continuous IV required

30
Q

Fenoldopam

A

Selective D1-like dopamine receptor, rapid acting arteriolar vasodilator

Induces natriuresis, preventing ARF

Major toxicities: reflex tachycardia, headache, flushing, hypokalemia, avoid in glaucoma and use with BB -> substancial hypotension because BB inhibit sympathetic reflex response to fenoldopam

31
Q

Nitrate mechanism of action

A

Actions of nitrates on circulation

Indications: Chronic stable/unstable angina and ACS, acute HF and pulmonary edema, CHF (combo with hydralazine), hypertension with pulmonary edema

Pharmacology (17 decks)

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