Alpha 1 Agonists/antagonists Flashcards

1
Q

Selective alpha 1 agonists

A

“-ine”‘

Aim to increase HR/BP

Vascular SM- vasoconstriction
Nasal Mucosa- vasoconstriction
Eye - vasoconstriction

Midodrine - shock / hypotension, orthostatic Hypotn
Phenyephrine, pseudoephedrine, oxymetaozline - nasal decongestant
Naphazoline = red eye drops

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2
Q

Selective alpha 1 antagonist

A

“-sin”

Least selective: Prazosin, Doxazosin, Terzosin
Vascular SM- vasodilation
Nasal mucosa - vasodilation

Most selective: Tamsulosin, alfuzosin, silodosin* (BPH)

Eye-vasodilation
Bladder- relaxation

ADRS: ED, abnormal ejaculation
Less selective: dizziness, syncope, hypotension, reflex tachy, first dose phenomena

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3
Q

Selective alpha 2 agonist

A

“-ines” pronounced eens - clonadine AND methyldopa (HTN in pregnancy)

Tizanidine, guanfacine, dexmedetomidine, bromododine, apraclonidine, clonidine

CNS - decrease stimulation
Sympathetic Autonomic NS - decrease release of NE/E
Eye - decrease aqueous humor (brimonidine, apraclonidine)

Clinical uses: HTN, ADHD, withdrawal, sedation, muscle spasms

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4
Q

Non selective alpha 2 antagonist

A

Ph “-amines”

Vasodilation while increasing CO

CNS- increase stimulation of SNS
Sympathetic autonomic NS - increase release of NE/E
Eye- increase aqueous humor

Clinical uses: male sexual dysfunction, psychosis

ADRS: nasal congestion, orthostatic hypotension

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5
Q

Selective beta 1 agonist

A

Dobutamine - IV - positive inotropic effects

SA node- increase sinus rate - bradycardia
AV node - increase AV nodal conduction - heart block, cardiac arrest
Atria/ventricle - increase FOC and SV - use AHF, cardiogenic shock, sepsis
Kidney- increase renin release (increase BP) - hypotn

ADRS: may lose selectivity at higher doses

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6
Q

Selective Beta 1 antagonist

A

-olol

Metropolol, atenolol, Nebviolol, bispropolol acebutolol, betxaolol, esmolol
* maintain selectivity at higher doses

SA node - decreease sinus rate - tachycardia, angina
AV node- decrease AV node conduction, arrhythmias
Atrial/ventricle- decrease FOC and SV - post MI, chronic HF, angina, arrhythmias
Kidney- decrease renin release (decrease BP) - HTN

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7
Q

Selective Beta 2 agonist

A

“-Erol” and terbutaline relax !!!! Vasodilation

SABA - albuterol and levalbuterol - asthma, COPD
LABA - all other -erols

Bronchial SM - bronchiodilation, relaxation
Uterine SM - relaxation - stop premature labor
Vascular SM - vasodilation
Skeletal muscle - increase glycogenolysis and tremors
Liver - glycolognlyisis and glucagenesis
Eye - increase aqueous humor production

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8
Q

Non selective beta 1 and 2 agonist

A

-enol

Isoproterenol
Beta 1 - stumiulatory, positive ionotropic - treat bradycardia and HTN

Metaproterenol
Beta 2 - dilation and relaxation - treat asthma and COPS

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9
Q

Non selective beta antagonists

A

-olol

Nadolol, propranolol, carteolol, Timolol, levobutanolol,metripranolol, solatolol (antiarrythmic), pinolol

Bronchial SM - constriction
Uterine SM - contraction
Vascular Sm- vasoconstriction - migraine prophylaxis
Skeletal muscle - decrease glycogenolysis and tremors- tremors, stage fright
Liver- decrease glycogenolysis and glucagenesis, decrease portal venous pressure - dec blood flow
Treat: portal HTN, esophageal vacancies, bleeding prophylaxis
Eye - decrease aqueous humor production - glaucoma, ocular HTN,

ADR: fatigue, masked signs of hypoglycemia, bronchoconstriction when pt taking B2 antagonist, servers peripheral vascular disease, heart blocks

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10
Q

Selective Beta 3 agonists

A

Mirabegron

Target: detrusor muscle in bladder
Effect: muscle relaxation - increase bladder capacity

Uses: overactive bladder, incontienance, urgency and frequency

ADRS: HTN, BP elevations, tachycardia

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11
Q

Why Beta 1 > Beta 2?

A

Mortality reduction in ACS, MI/M ischemia

Decrease O2 demand -> slow pulsate rate

Increase exercise tolerance -> decrease cardiac work

Preferred w arrhythmias -> negative ionotropic and chronotropic effects slow AV node conduction and increase AV refractory period
Slow ventricular response in Afib
Decrease ventricular beats

HTN - may be combined with diuretic, CCB, ACEI, ARB
Chronic use decreased BP due to decrease pulse rate, CO and renin release
Less effective for African Americans

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12
Q

Treatment for HFrEF

A

Carvediol (alpha 1, beta 1 + 2 antagonist)

Metropolol succinate - selective beta 1 antagonist
Bisprolol

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13
Q

Clinical concerns for Beta Blockers

A

Abrupt Cessation -> risk of angina/MI

Drug-drug interactions - consider other drugs with negative chrono/ionotropic effects = severe hypotension, bradycardia, CHF, conduction abnormalities, heart block

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14
Q

Adrenergic

A

SANA

Autonomic ganglia -> Nueronal nictonic receptors only -> ACH

Alpha and beta receptors -> NE/E - cardiac and SM cells, gland cells, nerve terminals

Adrenal medulla -> NE/E

Dopaminergic receptors (D) -> DA - renal vasc SM

Muscarinic receptors (M) -> ACH -> sweat glands

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15
Q

Adernergic transmission

A
  1. Tyrosine enters axon and is converted to dopamine (DA) via tyr hyroxylase
  2. DA transported into vessicle via VMAT where DA is converted -> NE via beta-hydroxylase
  3. NE released via exocytosis from influx of Ca2+ (VAMPS/SNAPS fuse)
  4. NE acts on post-synaptic and pre-synaptic receptors
  5. Noradrenergic transmission termination
  6. Metabolized via MAO, COMT inside axon, NET on aurtoreceptors
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