Drugs to Know Flashcards
Botulin Toxin
(most potent natural toxin)
Prevents Ca2+ influx; no ACh
release = muscle paralysis
Uses: Botox; paralyzes muscles
of the face for wrinkles
Side Effects: Causes death d/t
paralysis of diaphragm muscle
Nicotine
Binds at 1 or 2 α sites on the
nicotinic receptors, induces a
conformational change to open
the cation channel
Uses: Smoking cessation
Muscarine
Effects the muscarinic receptors
(M1-M3) of the CV system, CNS,
and glands (but poisonous)
Bethanechol
Orally administered, but not
absorbed by GI tract b/c it is
charged.
Activated M3 receptors in GI
Uses: Post-surgical stimulation of
peristalsis in the GI tract
Carbachol
Slows hydrolysis by AChE;
Charged d/t quaternary N–
cannot be absorbed;
Constricts eye muscles to drain
aqueous humor and decr.
intraocular pressure
Uses: Short-term treatment of
glaucoma (eye drops)
Curare
NMJ blocker: 10C between 2N’s;
Paralyzes the muscle by
preventing effect of ACh
Uses: Surgery–temporary muscle
paralysis
Side Effects: Toxic @ high doses
Hexamethonium
Trimethaphan
Ganglionic blocker: 6C between 2N’s; Blocks ANS completely
Uses: Hypertensive crisis (decr. SM contraction)
Side Effects: PNS suppression
(tachycardia, dry mouth, etc.);
orthostatic hypotension
Atropine
Blocks muscarinic receptors resulting in anti-cholinergic activity; M3 receptors are not innervated, so they are not affected; Can cross the BBB and cause hallucinogenic effects
**Uses**: Bradycardia; Sarin gas poisoning treatment (along w/ pralidoxime)
Side Effects: Anti-cholinergic
• Eye dilation (blurred vision) • No secretions (dry mouth) •Bronchodilation • Increased HR • No peristalsis (constipation)
• Urinary retention • No BP effects • Increase temperature (decreased sweating) • No sexual function • Hallucinations
Tolterodine
Blocks muscarinic receptors
Uses: Urinary retention
Side Effects: Anti-cholinergic
Homatropine
Blocks muscarinic receptors
Uses: Pupil dilation
Side Effects: Blurred vision
Physostigmine
Carbamate group (analogous to acetate) is hydrolyzed slower than acetate group; ACh levels increase while AChE is inhibited
Uses: Glaucoma; Anti-cholinergic poisoning (atropine, etc.)
Side Effects: Cholinergic
syndrome
Neostigmine
Carbamate group (analogous to acetate) is hydrolyzed slower than acetate group; ACh levels increase while AChE is inhibited
Uses: Myasthenia gravis; reverse muscle relaxants
Side Effects: Cholinergic syndrome
Edrophonium
Binds to the negative charges in the binding sits of cholinesterases; short-lasting effects (5-10 min.)
Uses: Reverses curare blockade
Donepezil
Rivastigmine
AChE inhibitors. Uncharged, tertiary amines that can cross the blood brain barrier.
Uses: Treatment of neurogenerative disorders like Alzheimer’s
Organophosphates (e.g. Sarin)
Irreversible inhibitors of AChE; phosphate group forms a covalent bond w/ Ser on AChE resulting in exacerbation of cholinergic effects
“Uses”: Chemical Warfare
Side Effects: Death via
overstimulation of ACh receptors
Pralidoxime
Cleaves bond between organophosphate and Ser on AChE; Return AChE to normal activity
Uses: Sarin gas poisoning treatment (along w/ atropine)
Metyrosine
Competes with tyrosine; inhibits catecholamine synthesis
Uses: Anti-hypertensive; pts. w/ pheochromocytomas
L-DOPA
Crosses BBB and is converted into dopamine
Uses: Parkinson’s disease (insufficient dopamine d/t cell death in basal ganglia)
Carbidopa
Inhibits conversion of L-DOPA to dopamine; Cannot cross BBB, but used with L-DOPA to incr. amount of dopamine conversion in brain
Amphetamines
Competes with re-uptake pumps (prolong catechol. in the synapse), inhibits VMAT and MAO (increase NE and Epi in the cytoplasm), so NE and Epi travel down conc. gradient into synapse;
Result: incr. [NE & epi] in
periphery, [NE, 5-HT, DA] in CNS
Uses: ADHD; narcolepsy; general stimulant
Side Effects: High abuse potential; tolerance (d/t receptor desensitization)
Ephedrine (Ephedra)
Enters nerve terminal to displace NE from the cytoplasm; causes bronchi relaxation, stimulates heart, and incr. BP
Uses: Asthma; CNS stimulant; appetite suppressant
Pseudoephedrine
Enters nerve terminal to displace NE from the cytoplasm; causes bronchi relaxation, stimulates heart, and incr. BP
Uses: Nasal decongestant; OTC cold drugs
Side Effects: Rebound hyperemia
Tyramine
Enters SNS nerve terminals via reuptake pump; incr. release of NE; found in high conc. In fermented foods; MAO takes care of it, but not when combined with MAOI
Side Effects: Hypertensive crisis if [tyramine] accumulates in periphery (can occur when MAO inhibitor is given)
Cocaine
Competitively blocks both peripheral and CNS re-uptake of NE, DA, and serotonin (5-HT); the reward centers in the brain from dopamine are responsible for addiction and abuse of cocaine
Uses: Local anesthetic in ENT
Side Effects: CNS excitation, anorexia, euphoria; high abuse potential; incr. BP & HR, vasoconstriction
Note: If given w/ a β-blocker, patient will go into hypertensive crisis
Desipramine
A tricyclic antidepressant that selectively blocks NE re-uptake but not serotonin re-uptake in periphery & CNS
Uses: Anti-depressant
Side Effects: Tolerance, but no risk of abuse (no DA involvement, so no euphoria)
Phenelzine
Inhibits MAO-A/B causing a buildup of NT is the cytoplasm; reverses uptake pumps, and NT flow down their conc. gradient into the synapse.
Uses: 3rd-line treatment for depression d/t food & drug interactions
Side Effects: Serotonin syndrome can occur when taken with opiates, anti-depressants, decongestants
Selegiline
Selectively inhibits MAO-B; MAO-A is still functional in the periphery
Uses: Parkinson’s disease treatment
Aminophylline (aka theophylline)
Potentiates effect of cAMP by increasing [cAMP] causing bronchiole SM relaxation (β2), cardiac stimulation (β1 & β2)
Uses: Asthma; COPD; heart failure
Side Effects: arrhythmias, anxiety, convulsions
Sildenafil
Increase [cGMP] to relax SM of corpora cavernosa of penis; decr. pulmonary vascular resistance; incr. cerebral blood flow
Uses: ED; pulmonary HTN; acute RDS; altitude sickness
Side Effects: Dangerous drop in BP
Epinephrine
Gs-PCR causes incr. [cAMP]; β2: SM relaxation (bronchi, vasculature); β1: incr. cardiac contractility, HR, ~incr. BP (from kidney renin) (incr. vasodilation at low dose OR incr. vasoconstriction at high dose)
Uses (Low Dose): Cardiac arrest, asthma
Uses (High Dose): Anaphylactic shock; w/ anesthetic to prolong vasoconstriction
Side Effects: Arrhythmias
Norepinephrine
Incr. diastolic BP via α1 stimulation, leads to incr. TPR; baroreceptor reflex causes decr. sympathetic tone and incr. vagal output to decr. HR
Result: incr. BP and cardiac force; HR and CO do not change
Uses: Septic shock; hypotensive states (anesthesia); incr. perfusion pressure w/o incr. HR decreases arrhythmia risk
Isoproterenol
- *β1**: incr. HR, SV, and CO
- *β2**: decr. diastolic BP via vasodilation
- *Result**: MAP decr. slightly, TPR decr.
Uses: Heart failure (but there are better drugs for this, e.g. dobutamine, β-blockers)
Side Effects: Arrhythmias
Dopamine
D1: Gs-PCR (just like β2) incr. [cAMP] causes dilation of renal, mesenteric, coronary vessels; incr. renal blood flow
β1: cardiac stimulation
α1: maintain vascular tone; may
override renal vasodilation
- *D1 Use**: Maintain kidney perfusion
- *D1 & β1 Use**: incr. HR, CO, and flow to kidneys & mesentery
- *Over-administration (α1)**: vasoconstriction
Dobutamine
Less β2 vasodilation & modest α1 activation leads to less reflex tachycardia via baroreceptors;
Result: increased contractility compared to rate increase
- *Uses**: Acute heart failure (incr. CO w/o incr. in TPR = heart beating more efficiently)
- *Side Effects**: Tachyphylaxis if used chronically
Albuterol
Gs-PCR causes incr. [cAMP]; β2: SM relaxation (bronchi, vasculature); No β1 activity means fewer heart side effects
Uses: Asthma; bronchospasm
Side Effects: Cardiac stimulation at high/repetitive doses
Phenylephrine
Gq-protein receptors coupled to phospholipase C; when activated increases IP3 and DAG from PIP2, and IP3 stimulates the release of Ca2+ causing contraction of vascular muscle;
Result: Incr. BP & reflex bradycardia
Uses: OTC nasal decongestant
Side Effects: rebound hyperemia (incr. redness of eye) & ischemia
Clonidine
High doses via IV cause vasoconstriction; Low oral dose causes activation of α2A receptors at CNS vasomotor center and decreases SNS outflow and lowers BP
Uses: Anti-hypertensive
Side Effects: Hypertensive episode during withdrawal
Brimonidine
Decreases aqueous humor production so decreases intraocular pressure (unknown mechanism)
Uses: Glaucoma treatment
Propranolol
Decreases CO (by decr. HR & contractility, and decr. BP from no renin release from kidney); Prevents Epi-mediated bronchodilation (β2); Partially blocks Epi-mediated glycogenolysis in liver (β2)
- *Uses**: (see clinical uses), also decr. performance anxiety and essential tremors
- *Side Effects**: Bronchoconstriction in pts. w/ asthma; masks hypoglycemic symptoms in pts. w/ insulin-dependent diabetes
Metoprolol
Decreases CO (by decr. HR & contractility); no β2 effects, so incr. exercise capacity
Uses: Incr. exercise tolerance for pts. w/ peripheral vascular disease
Pindolol
“Partial agonist” meaning intrinsic sympathomimetic activity on β receptors.
Result: Reduce HR and CO caused by SNS activity (less likely to cause bradycardia); but not as much as a pure antagonist
- *Uses**: Incr. exercise tolerance for pts. w/ low HR (e.g. endurance
athletes) . Note: β-blockers are banned by the NCAA and the IOC
Carvedilol
Decr. in CO (via β effects– decr. HR, conduction, contractility) and decr. TPR (via α effects); Decr. SNS tone from baroreceptor because β receptors are blocked at the heart; Anti-proliferative & antioxidant properties.
Uses: HTN; decr. mortality & morbidity in pts. w/ moderate heart failure
Labetalol
Decr. in CO (via β effects– decr. HR, conduction, contractility) and decr. TPR (via α effects); Decr. SNS tone from baroreceptor because β receptors are blocked at the heart
Uses: pts. who are pregnant; hypertensive emergencies
Phentolamine
Dramatic decr. in BP (α1) with reflex tachycardia from baroreceptor reflex; increase NE release from no neg. feedback on α2 presynaptic receptors.
Uses: Diagnosis & treatment of pre-op. pheochromocytoma surgery (catecholamine-secreting tumor)
Side Effects: Angina from incr. HR (and incr. O2 consumption)
Phenoxybenzamine
Dramatic decr. in BP (α1) with reflex tachycardia from baroreceptor reflex; increase NE release from no neg. feedback on α2 presynaptic receptors. Same as phentolamine, but longer-lasting. Alkylates a-, serotonin, and histamine receptors), making them irreversibly bound.
Uses: pheochromocytoma long-term management
Prazosin
No vasoconstriction so decr. in TPR and BP; less reflex tachycardia because α2 neg. feedback receptors aren’t blocked
Uses: pts. w/ HTN
Side Effects: Orthostatic hypotension
Tamsulosin
Blocks Gq receptors so decr. in Ca2+ causing smooth muscle relaxation of muscles in the prostate
Uses: treatment for BPH (benign prostate hyperplasia)
What are the nicotinic and muscarinic agonists?
Nicotinic: Nicotine
Muscarinic: Muscarine, methachol, bethanechol, carbachol
What are the nicotinic and muscarinic antagonists?
Nicotinic: Trimethaphan, Hexamethonium, Curare
Muscarinic: Homatropine, Atropine, Tolterodine
What are the ACh potentiators (AChE inhibitors)?
Physostigmine, Neostigmine, Rivastigmine, Donepezil, Edrophonium, and organophosphates (VX, Sarin gas, etc.)
What reverses the AChE inhibitors?
Combination of Atropine and Pralidoxime
What drugs affect catecholamine synthesis?
Metyrosine (Tyrosine hydroxylase), L-DOPA (DOPA decarboxylase), Carbidopa (DOPA decarboxylase)
What drugs affect catecholamine release?
Amphetamines (MAO, VMAT, and NE, EPI, 5-HT reuptake transporters) Ephedrine, Pseudoephedrine, Tyramine (pre-synaptic vesicles)
What are the NMJ reuptake blockers?
Cocaine (reuptake transporters)
Desipramine (NET)
What are the MAOIs?
Phenelzine (MAO-A/B), Selegiline (MAO-B), Amphetamines (MAOI general)
What are the PDE inhibitors?
Aminophylline/theophylline (non-selective), Sildenafil (PDE-5)
What are the catecholamines?
Epinephrine (B2>B1), NE (a1/2, B1), Isoproterenol (B1/2), Dopamine (D1, moderate dose D1 + B1, high dose D1 + B1 + a1)
What are the beta agonists?
Dobutamine (B1>B2), Albuterol (B2)
What are the alpha agonists?
Phenylephrine (a1), Clonidine (a2), Brimonidine (a2)
What are the beta blockers?
A-M are B1, N-Z are non-selective (carve+lab block a1 as well)
Carvedilol (B1/2 + a1)
Labetalol (B1/2 + a1)
Metoprolol (B1)
Pindolol (B1/2 partial)
Propranalol (nonselective)
What are the alpha blockers?
Phentolamine (nonselective, competitive and reversible)
Phenoxybenzamine (nonselective, noncompetitive and irreversible)
Prazosin (a1 effect >>> a2, competitive antagonist)
Tamsulosin (a1a, mostly prostate SM)
