quick pharm adrenergics chat cards

Rate-limiting step of catecholamine synthesis

Tyrosine → DOPA via tyrosine hydroxylase

Enzyme converting DOPA to dopamine

DOPA decarboxylase

Enzyme converting dopamine to norepinephrine

Dopamine β-hydroxylase

Enzyme converting norepinephrine to epinephrine

PNMT (phenylethanolamine N-methyltransferase)

Primary storage location of catecholamines

Synaptic vesicles via VMAT transporter

Trigger for catecholamine release

Ca2+ influx leading to vesicle fusion

Most important mechanism of NE removal from synapse

Reuptake via NET (norepinephrine transporter)

Enzyme that metabolizes catecholamines intracellularly

Monoamine oxidase (MAO)

Enzyme that metabolizes catecholamines extracellularly

Catechol-O-methyltransferase (COMT)

α1 receptor signaling pathway

Gq → ↑IP3/DAG → ↑Ca2+

α1 receptor main effect

Vasoconstriction → ↑BP

α2 receptor signaling pathway

Gi → ↓cAMP

α2 receptor main effect

↓ NE release (negative feedback)

β1 receptor signaling pathway

Gs → ↑cAMP

β1 receptor effects

↑ HR, ↑ contractility, ↑ renin release

β2 receptor signaling pathway

Gs → ↑cAMP → inhibits MLCK

β2 receptor effects

Bronchodilation, vasodilation, ↑ glucose

Which receptor subtype causes smooth muscle contraction

α1

Which receptor subtype causes smooth muscle relaxation

β2

Which receptor subtype primarily affects the heart

β1

Epinephrine receptor selectivity (low dose)

β > α

Epinephrine receptor selectivity (high dose)

α1 > β2

Low-dose epinephrine effect

↓ TPR, ↑ HR

High-dose epinephrine effect

↑ BP via vasoconstriction

Norepinephrine receptor activity

α1, β1 (minimal β2)

Norepinephrine effect on BP

Strong ↑ BP → reflex bradycardia

Dopamine low dose receptor

D1 → renal vasodilation

Dopamine moderate dose receptor

β1 → ↑ cardiac output

Dopamine high dose receptor

α1 → vasoconstriction

Epinephrine clinical use

Anaphylaxis, cardiac arrest

Epinephrine adverse effects

Arrhythmias, hypertension

Norepinephrine clinical use

Septic shock (first-line)

Norepinephrine adverse effect

Tissue necrosis with extravasation

Drug used to treat NE extravasation

Phentolamine

Phenylephrine receptor selectivity

α1 agonist

Phenylephrine effect

↑ TPR, ↑ MAP, reflex bradycardia

Phenylephrine clinical use

Shock, mydriasis

Clonidine mechanism

α2 agonist → ↓ sympathetic outflow

Clonidine clinical use

Hypertension, withdrawal

Clonidine adverse effects

Sedation, rebound hypertension

Methyldopa mechanism

Prodrug → α2 agonist

Methyldopa clinical use

Hypertension in pregnancy

Methyldopa adverse effects

Sedation, drug-induced lupus

Isoproterenol receptor activity

β1 = β2 agonist

Isoproterenol clinical use

Bradycardia, heart block

Isoproterenol adverse effects

Tachycardia, arrhythmias

Dobutamine receptor selectivity

β1 agonist

Dobutamine clinical use

Acute heart failure, cardiac stress testing

Dobutamine adverse effects

↑ HR, ↑ BP

Albuterol receptor selectivity

β2 agonist

Albuterol clinical use

Acute asthma (rescue inhaler)

Salmeterol clinical use

Long-term asthma control

Terbutaline clinical use

Tocolysis (preterm labor)

β2 agonist adverse effect

Tremor, mild hyperglycemia

Tyramine mechanism

False transmitter → ↑ NE release

Cocaine mechanism

Blocks NET, DAT, Na+ channels

Cocaine clinical danger

Intense vasoconstriction → MI risk

Why β-blockers are avoided in cocaine use

Unopposed α1 vasoconstriction

Amphetamine mechanisms

↑ release, ↓ reuptake, ↓ MAO of catecholamines

Amphetamine clinical use

ADHD, narcolepsy

Ephedrine mechanism

Mixed acting (direct + ↑ NE release)

Pseudoephedrine clinical use

Nasal decongestant

Mixed agonist adverse effects

HTN, tachycardia, restlessness

Nonselective α-blockers

Phenoxybenzamine, phentolamine

Nonselective α-blocker use

Pheochromocytoma

Nonselective α-blocker adverse effects

Orthostatic hypotension, reflex tachycardia

α1-selective blockers

Prazosin, terazosin, doxazosin, tamsulosin

α1-blocker clinical use

BPH, hypertension

Tamsulosin advantage

Selective for prostate → less hypotension

α1-blocker adverse effect

First-dose syncope

Best use of α1 blockers in clinic

BPH with hypertension

α2 agonist withdrawal effect

Rebound hypertension

Baroreceptor reflex response to ↑ BP

↓ HR via ↓ sympathetic output

Drug causing reflex bradycardia

Norepinephrine, phenylephrine

β-blocker generations

1st: nonselective, 2nd: β1 selective, 3rd: α+β

Nonselective β-blocker example

Propranolol

β1-selective blocker examples

Metoprolol, atenolol

Mixed α and β blocker example

Labetalol

Propranolol properties

Lipophilic, crosses BBB, short acting

Propranolol clinical uses

Anxiety, migraine, angina

Metoprolol use

Hypertension, heart disease

Atenolol property

Less CNS penetration

Labetalol clinical use

Hypertensive emergency, pregnancy HTN

β-blocker adverse effects

Bradycardia, AV block, hypotension

β-blockers contraindicated in

Asthma (nonselective), AV block

β-blocker effect on glucose

Masks hypoglycemia symptoms

β-blocker CNS effects

Depression, nightmares, sedation

Nonselective β-blocker risk

Bronchospasm

Raynaud phenomenon cause with β-blockers

Peripheral vasoconstriction

Most important adrenergic termination mechanism

Reuptake via NET