Pharmacology Drugs VCU SOM2020

A-methyl-dopa
Use: HTN, Opioid Withdrawal. Mechanism: A2 agonist, decreases sympathetic outflow, inhibits NE release, rebound HT. SE: dry mouth, sedation. Note: A-methyl-dopa is metabolized to A-methyl-NE (A2 agonist)

Cocaine
Inhibits neuronal uptake, can cross into CNS.
I: amphetamines, CA
Always take amphetamines before cocaine

Imipramine
Tricyclic antidepressant, blocks neuronal reuptake of NE. At toxic doses can also bock muscarinic, alpha, and histamine receptors
Use: Depression
SE: Dry mouth, blurred vision, decreased urination
T: Severe anticholinergic effect, respiratory depression, PHT (Orthostatic)
Similar to amitriptylline

Norepinephrine
α1 > α2 > ß1
Use: Hypotension, septic shock
Does not cross BBB

Epinephrine
ß > α
Significantly stronger effect at ß2 than NOR
DOC for anaphylaxis (allergic reactions).
Can be used to treat asthma

Dopamine
D > ß > α
Low dose: Activates D receptors (limited clinical importance)
Moderate dose: Activates ß1 receptors
High dose: Activates A1 in addition to ß1 (Vasoconstriction from A)

Isoproterenol
ß1 = ß2
Substrate for COMT
Used to treat Asthma
Increases HR, decreases BP
Does not cross BBB

Albuterol
B2 selective agonist
Use: Asthma COPD
SE: CV increase HR and BP (less upon inhalation)

Salmeterol
B2 selective agonist, Long acting
Use: Asthma COPD
SE: CV increase HR and BP

Terbutaline
B2 selective agonist, Long acting
Use: Relaxes uterine contractions to prevent premature labor, Asthm
SE: CV increase HR and BP

Dobutamine
B1 agonist
Use: cardiac stimulant, increases force of contraction with minimal HR increase, no change in oxygen demand
RX: Acute treatment of congestive heart failure

Phenylephrine
A1 agonist, increases BP
Use: Hypotension, nasal decongestant
SE: CV: Reflex bradycardia

Methoxamine
A1 agonist (pressor Agent)
Use: HTN and shock
SE: CV: increased BP, reflex bradycardia

Clonidine (guanfacine)
A2 agonist, capable of crossing BBB and lowering sympathetic outflow to inhibit NE release (Lowers SNS activity and therefore BP)
Use: HTN and opioid withdrawal
SE: Dry mouth, sedation,
rebound HTN

A-Methyl-Dopa
A2 agonist, capable of crossing BBB and lowering sympathetic outflow to inhibit NE release (Lowers SNS activity and therefore BP)
(Prodrug)
Use: HTN (especially in pregnancy)
SE: Dry mouth, sedation, rebound HTN

Dexmedetomidine
A2 agonist
Sedation without respiratory depression

Tizanidine
α2 agonist, short acting
Use: Muscle spasticity, multiple sclerosis
CI: CYP1A2 inhibitors

Pramiprexole
Dopamine agonist, crosses BBB to increase dopaminergic response
Use: Parkinson’s disease, restless leg syndrome
SE: Drowsiness

Fenoldopam
D1 agonist, no action on A or B receptors
Use: Acute hypertension
SE: Raises HR and ocular pressure

carbidopa
Prevents conversion of L-dopa to dopamine outside of the CNS (carbidopa cant cross BBB)
Given in conjunction with L-dopa to Parkinson’s patients.

MAO-B Inhibitor
prevents degradation of dopamine, used in Parkinson’s patients

Amphetamine
Inhibits reuptake 1 and displaces NE
CNS stimulant
SE: tolerance, tachyphylaxis
Remember to take amphetamines before cocaine

Ephedrine
A / B receptor agonist, and causes indirect release of NE via displacement
Use: Nasal decongestant, red eyes

Methylphenidate
Inhibits reuptake 1 and displaces NE
Use: ADAH
SE: tolerance, tachyphylaxis

Tyramine
Acts like an amphetamine, normally degraded by non-selective MAO (Tranylcypromine, depression).
Less of a problem with MAObi.
MAOi leads to increased amount of transmitter present in the nerve terminal, tyramine acts like an amphetamine and causes the release of NE from vesicles. Since there is more NE present in the vesicles, this causes a very large release of NE leading to increase BP and HR -> Hypertensive crisis.

Amitriptylline
Tricyclic antidepressant, blocks neuronal reuptake of NE. At toxic doses can also bock muscarinic, alpha, and histamine receptors
Use: Depression
SE: Dry mouth, blurred vision, decreased urination
T: Severe anticholinergic effect, respiratory depression PHT
Similar to imipramine

Atomoxetine
Blocks neuronal reuptake of NE, and is considered a non-stimulant
Use: ADHD

Tranylcypromine
Non-selective MAOi causes an increase in NE by making the synthesis process more efficient -> leading to an accumulation of NE in the nerve terminal
Use: Depression
I: Tyramine -> HT Crisis
SE: Agitation, tremor, insamnia

Selegiline
Selective MAOi-B
Use: Parkinson’s disease
Found in nerve terminals, liver, kidney, and CNS

Tolcapone
COMP inhibitor (COMP is found in effectors tissue)
Use: Parkinson’s disease
SE: Liver failure

Labetalol
A/B blocker, some B-agonist action
(Only B blocker used for hypertensive chrisis because it has A activity)
Use: Hypertensive crisis, pheochromocytoma
SE: PHT (Orthostatic) due to A activity

Phenoxybenzamine
A1 blocker, irreversible covalent bond
Use: Pheochromocytoma, acute and chronic HTN
SE: PHT (orthostatic), reflex increase in HR
Also blocks ACH, histamine, and serotonin. Inhibits uptake 1 and 2

Phentolamine
Non-selective A-blocker, not frequently used
Use: Pheochromocytoma, acute HTN
SE: PHT (orthostatic), reflex tachycardia

Prazosine
A1 competitive blocker
Use: Hypertension, benign prostate hypertrophy
No reflex tachycardia because they don’t affect the A2 receptor (not going to be tested)
SE: 1st pass effect, PHT (orthostatic) nausea, drowsiness

Carvedilol
Competitive antagonist B and A (blocker)
Use: chronic hypertensive
SE: PHT (orthostatic)

Nabivolol
Competitive antagonist B1
Induces NO release, causing gAMP, causing vasodilatation
Use: chronic hypertension

Propranolol
Nonselective B blocker
Use: chronic hypertension, angina, arrhythmias, tremor, migraine,
SE: insomnia, cardiac depression, may make Renaud’s worse

Haloperidol
Dopamine antagonist
Use: Schizophrenia
Se: Tachycardia

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