ANS drugs

• Direct muscarinic agonist (4'choline ester)
• -does NOT cross BBB
• -resist AchE

• USE- Post-op or neurogenic illeus (no GI motility), Urinary retention.
• SE- all other para-miosis, accomodation, diarrhea, incontinence, bradycardia (prolong PR), sweat, tear, salivate..
• DO NOT USE IN COPD, ASTHA, PEPTIC ULCER

Direct muscarinic agonist M>N (4'choline ester)

USE-Dx of Asthma, Methacholine-challenge (stimulate M3 in bronchial SM in asthmatics when inhaled)

• Direct muscarinic aganist
• -resist AchE

• USE- stimulate secretions! Treat Glaucoma (1st choice!), Xerostomia, Sjogren's syndrome.Topical.
• -contract ciliary muscle->increase outflow of aq humor thru canal of Schlemm

• SE- topical- stinging, local irritation oral- all other para-miosis, accomodation, diarrhea, incontinence, bradycardia (prolong PR), sweat, tear, salivate..
• DO NOT USE IN COPD, ASTHA, PEPTIC ULCER

cholinesterase inhibitor (indirect cholinergic agonist, both M + N)

USE-Diagnosis of Myasthenia Gravis, Differentiate MG vs Cholinergic crisis (too much Ach i.e. Neostigmine overdose). If muscle tone improves after Edro -> MG ; if NOT -> cholinergic crisis, stop neostigmine!

UNIQUE- does NOT cross BBB, very short acting (so only DX use)

• cholinesterase inhibitor (indirect cholinergic agonist, both M + N)
• does NOT cross BBB, longer acting

• USE- treat Mystenia gravis
• -Reverse non-depolarizing NM blockade "curare"
• -Post-op and neurogenic ileus, Urinary retention

SE- cholinergic crisis!

• cholinesterase inhibitor- (indirect cholinergic agonist, both M + N)
• - does NOT cross BBB, longer acting

• USE- treat Mystenia gravis (longer acting than Neostigmine)
• - Reverse non-depolarizing NM-blockade "curare"
• SE- cholinergic crisis!

• cholinesterase inhibitor- (indirect cholinergic agonist, both M+N)
• - 3'amine! go to CNS!

• USE-Glaucoma
• -reverse Atropine overdose! (must use Physo- b/c Atropine can go to CNS, so antidote should go to CNS)

SE- cholinergic crisis, cataracts with longterm use

• cholinesterase inhibitor- (indirect cholinergic agonist, both M+N)
• -Cross BBB, CNS acting

USE- Alzheimer disease (exclusively!)- Meynert's nucleus.

SE- all other para-miosis, accomodation, diarrhea, incontinence, bradycardia (prolong PR), sweat, tear, salivate..

Similar drugs- Galantamine, Rivastigmine

• Organophosphate!
• Irreversible (noncompetitive-suicide inhibitor) cholinesterase inhibitor
• USE-Glaucoma
• -contract ciliary muscle->increase aq humor drainage thru canal of Schlemm.

SE-Organophosphate toxicity

• Organophosphate!
• Irreversible (noncompetitive-suicide inhibitor) cholinesterase inhibitor
• -- metabolized faster into active AChE inhibitors in insects than mammals.aging 6~8hrs

USE-insecticide (think FAMER!)

• SE-Organophosphate toxicity - coma, respiratory depression, seizures, bradycardia, nasuea, vomiting, diarrhea, blurred vision, sweating, salivation, muscle twitchiing, weakess, flaccid paralysis!
• Rx- Atropine + Pralidoxime (before aging)

• Organophosphate!
• Irreversible (noncompetitive-suicide inhibitor) cholinesterase inhibitor

• USE- nerve gas! only 2~3mins to age!!
• SE-Organophosphate toxicity- coma, respiratory depression, seizures, bradycardia, nasuea, vomiting, diarrhea, blurred vision, sweating, salivation, muscle twitchiing, weakess, flaccid paralysis!
• Rx- Atropine + Pralidozime (before aging) but it ages too fast....

Similar drugs- Soman, Tabun

DUMBBELSS

• too much Ach at M and N everywhere!! including CNS
• Muscarinic:
• Diarrhea
• Urination
• Miosis
• Bradycardia (AV blockade)
• Bronchospasm
• Lacrimation
• Salivation
• Sweating
• CNS stimulation--> seizures!
• Nicotinic:
• Paralysis
• CNS stimulation

• CURE- Atropine- Muscarinic antagonist
• - Pralidoxime- regenerate AchE (MUST use BEFORE againg of the organophosphate bond occurs!) Only for organophosphates (P-bonds), useless for carbamylated AchEs like Neostigmine.

• Peripheral neuropathy->muscle weakness, sensory loss
• Demyelination--> Multiple sclerosis like presentation

• HAS NOTHING TO DO WITH ACUTE SYMPTOPMS!
• NO signs of cholinergic crisis!!!!

• antimuscarinic (prototype!)
• 3'amine- cross BBB
• Effects-- mydriasis, cycloplesia
• decrease secretions, acid secretion, GI motility
• tachycardia (wide QRS, QT--> torsades de pointes)
• hyperthermia (bc no sweat)
• urinary retention, constipation
• delirium, excitation, hallucination
• sedation (how?)

• USE- Rx bradycardia (AV block), Diarrhea,
• Organophosphate/anti-AchE toxicity, Optho-mydriasis+cycloplesia (but long acting, just use Tropicamide), Decongestant, Antispasmodic (how?), COPD, Peptic ulcer disease

• SE-HOT as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter.
• Can cause acute angle-closure glaucoma in elderly, urinary retention in BPH, hyperthermia in infants
• Anterograde amnesia

DO NOT USE IN NARROW ANGLE GLAUCOMA! DRY PPL, LIKE SJOGRENS!

• Antimuscarinic
• similar to Atropine

• USE-optho for pupil dilation
• SE- cycloplesia

• Antimuscarinic
• similar to Atropine

USE- optho for pupil dilation (topical)

SE- cycloplesia (unlike alpha-agonists)

• Cardiotoxicity (vent tachycardia-->torsades de pointes)
• Coma
• Convulsion

• Antihistamines
• TCAs
• Antipsychotics
• Quinidine (anti-arrhythmic)
• Amantidine (anti-microbial)
• Meperidine

Physostigmine!

• Anti-muscarinic (lipid soluable! cross BBB!)
• Block cholinergic neruons in corpus striatum
• USE- Parkinson's disease

SE- hyperthermia, glaucoma, urinary retention, dry mouth, constipation, blurry vision, sedation, amnesia. delirium, hallucinations (just like any other antimuscarinic)

DO NOT USE IN NARROW ANGLE GLAUCOMA AND DRY PATIENTS

• Anti-muscarinic (lipid soluable! cross BBB!)
• Block cholinergic neruons in corpus striatum

USE- Parkinson's disease

• SE- hyperthermia, glaucoma, urinary retention, dry mouth, constipation, blurry vision, sedation, amnesia. delirium, hallucinations (just like any other antimuscarinic)
• DO NOT USE IN NARROW ANGLE GLAUCOMA AND DRY PATIENTS

• Antimuscarinic
• 3' amine alkaloid (like atropine)

USE- motion sickness

• SE- sedation, shorterm anterograde amnesia
• +atropine-toxicity at high dose

• Antimuscarinic
• 4'amine, does NOT cross BBB!

• USE- inhaled
• COPD (first line!), Asthma (2nd line)
• decrease bronchoconstriction, broncial secretions, lower volume of mucus, but does NOT change viscosity of mucus!

• SE- minimal! b/c poorly absorbed systemically
• sedation, dry mouth

Similar Drug- Tiotropium

• Antimuscarinic
• 4'amine, does NOT cross BBB (like ipratropium)

• USE- Urinary incontinence (reduce urgency in mild cystitis, reduce bladder spasms)
• relax bladder SM, increase sphincter tone

SE- parasympathetic blockade

DO NOT USE IN PYLORIC OBSTRUCTION, URINARY RETENTION, NARROW ANGLE GLAUCOMA

Similar Drugs: Tolterodine

Antimuscarinic

• USE- preop- decongestant.
• reduce salivary, tacheobronchial, pharyngeal secretions!

Antimuscarinic

USE- Peptic ulcer treatment

SE-parasympathetic blockade

• Antimuscarinic blockade
• USE- Peptic ulcer treatment

SE-parasympathetic blockade

Antimuscarinic blockade

USE- Peptic ulcer treatment, urinary incontinence

SE-parasympathetic blockade

• Nicotinic antagonist
• Ganglionic blocker!
• -Ganglionic blockers do NOT prevent changes in HR elicited directly by a drug.

• USE-no clinical use, experimental!
• WIPE OUT ENTIRE ANS, REDUCE DOMINANT TONE
• WIPE OUT BARORECEPTOR REFLEX!

• Nicotinic antagonist
• Ganglionic blocker!

• USE-no clinical use, experimental!
• WIPE OUT ENTIRE ANS, REDUCE DOMINANT TONEWIPE OUT BARORECEPTOR REFLEX!

Ganglionic blockers do NOT prevent changes in HR elicited directly by a drug.

• Indirect anticholinergic
• -Block Na+/Choline transporter in cholinergic nerver terminal.
• -Block recycling of Choline (precursor to Ach)

USE- no clinical use, just decrease Ach in synapse.

• Indirect anticholinergic
• Block choline acetyltransferase (ChAT) in Ach storage vesicle membrane

USE-no clinical use? decrease Ach in synapse

• Indirect antiadrenergic
• -Block Tyr-hydroxylase ( RLS in NE synthesis)
• -Tyrosine analog

USE- no clinical use, but decrease NE in synapse

• Indirect antiadrenergic
• Block Vesicular DA-beta hydroxylase (in NE storage vesicle, marker enzyme of NE-neurons)

USE- used to be anti-hypertensive, but removed because it causes SEVERE DEPRESSION!

• Indirect antiadrenergic
• Block excocytosis of NE vesicles

USE-?

• Direct sympathomimetic
• -does NOT cross BBB

USE-decompensated heart failure, shock!

• -at low dose, D1--> vasodilate renal, coronary BV, increase blood flow to kidney, heart
• -at higher dose, B1--> increase CO!
• -at even higher dose, Alpha1--> increase SVR! maintain BP.

SE- arrhythmias

• D1-agonist
• Dopamine analog
• vasodilate renal, coronary vessels.
• -only D1, unlike Dopamine (activate beta1, alpha1 receptors at higher doses)

USE-(IV) severe hypertension, hypertensive crisis!!

SE- hypotension, arrhythmias, hypokalemia, increase intraocular pressure

• alpha-1 agonist
• vasoconstrict
• Systemic- increase BP (systolic+diastolic), no change in PP, may elicit reflex bradycardia!
• (increase afterload and preload!)
• - NOT inactivated by COMP (b/c not a catecholamine), so it's long-acting!

USE-Nasal decongestant in cold meds (vasoconstrict mucoal cap), Optho-mydriasis w/out cycloplesia.

SE- HTN, vasoconstrict-->ischemia.

• Alpha-1 agonist
• -vasoconstrict, Systemic- increase BP (systolic+diastolic), no change in PP, may elicit reflex bradycardia!(increase afterload and preload!)

USE- old med! used to be for paroxysmal atrial tachycardia through vagal reflex.

• Alpha-2 agonist
• (presynaptic NE synapse--> neg feedback)
• Indirect antiadrenergic
• Decrease NE release
• - b/c it's indirect, NO immediate effect! it takes time to work.

• USE-mild to moderate HTN (esp w/renal disease)
• Opioid withdrawl
• Antidiarrheal in patients with autonomic neuropathy

SE- immediate stopping-->rebound HTN, so taper off gradually!! Dry mouth, sedation, sexual dysfunction.

• alpha-2 agonist
• Analog of L-dopa (converted to methyl-NE in brain)
• decrease NE release in vasomotor center, decrease BP.

USE-mild to moderate HTN, esp in Pregnancy (safe)! also with renal disease (b/c does NOT decrease blood flow to kidney)

SE- Hemolytic anemia, hepatotoxic, edema, impotence, sedation, lactation (prolactin incr)

• direct beta-agonist (B1>>B2)
• -increase contractility, HR (a lil), decrease SVR (afterload), actually decrease O2-demand.

USE- decompensated CHF

• SE-arrhythmia, hypotention.
• DO NOT USE IN HYPOTENTION, HYPERTROPHIC CARDIOMYOPATHY !!

- receptor downregulation decrease efficacy after 1 week. Broken down by MAO and COMP.

• Beta agonist (B1=B2)
• B1- increase HR, SV, CO->incr sys BP-> increase PP
• B2- vasodilate, decrease SVR-> decrease dias BP
• NET: increase HR, decrease MAP, Incerase PP!

USE-Bronchodilate (B2), Heart block (B2), Bradyarrhythmia(B2)- but DA or EPi preferred.

• SE- flushing, angia, arrhythmias
• DON'T USE IN ISCHEMIC HEART DISEASE, TACHYARRYTHMIAS!

B2-agonist

• USE-bronchodilate in Asthma, COPD, Bronchitis
• -bronchodilate, decrease airway inflammation, secretion, histamine, leukotriens

• SE- tremor, restlessness, apprehension, tachycardia.
• AVOID USE OF MAO INHIBITORS OR TCA!

B2-agonist (slow-acting)

• USE-bronchodilate in Asthma, COPD, Bronchitis
• -bronchodilate, decrease airway inflammation, secretion, histamine, leukotriens
• -very slow acing, and longer acting, so only prophylaxis.inhaled corticosteroids are better long term control.

• SE- tremor, restlessness, apprehension, tachycardia.
• AVOID USE OF MAO INHIBITORS OR TCA!

• B2-agonist
• USE- IV, bronchodilate in Asthma, COPD, Bronchitis-bronchodilate.
• -supress premature labor (B2-relax uterine SM)

• SE- tremor, restlessness, apprehension, tachycardia.
• AVOID USE OF MAO INHIBITORS OR TCA!

B2-agonist

USE- supress premature labor (B2-relax uterine SM)

SE- tremor, restlessness, apprehension, tachycardia.AVOID USE OF MAO INHIBITORS OR TCA!

• direct sympathomimetic
• alpha-1, alpha-2, beta-1, beta-2 agonist

LOW DOSE- b1,b2 !- increaes HR, increase SV,CO, increase PP, decrease MAP! like ISOPROTERENOL

MEDIUM DOSE- a1,b1,b2- increase HR, opposite BP changes from a1 and b2 cancle, so SAME MAP! like DOBUTAMINE

HIGH DOSE- a1 >b1,b2- increase HR, increase BP, reflex bradycardia. Like NE!!!

• EPI-specific effects:
• bronchodilate, uterus relax, vasodilate
• increase glycogenolysis, gluconeogenesis, imobilize fat, increase insulin

USE- cardiac arrest, adjuct to local anesthetic, hypotension, anaphylaxis (epi only), asthma (epi only).

SE- myocardial ischemia, arrhthmias, hyperglycemia, tremor, narrow angle glaucoma

• DO NOT USE IN PERIPHERAL IV OR INJECT INTO FINGERS, TOES, EARS, NOSE!!!
• DO NOT USE IN PREGNANCY!

• direct sympathomimetic
• a1, a2 > b1. NO b2!!

• increase HR, MAP, PP, reflex bradycardia.
• NE NEVER DECREASE BP!!!

• USE-Cardiac arrest, shock, septic shock, hypotention (but decrease renal perfusion!)
• CANNOT USE FOR ASTHMA, ANAPHYLAXIS!

SE- myocardial ischemia, arrhythmia

DO NOT USE IN PREGNANCY!!!

• Indirect adrenergic agonist
• mobile pool NE releaser!!
• -in WINE and CHEESE
• -metabolized by MAOa in gut, normally, don't cause NE surge. BUT, if on MAOa-inhibitors (antidepressant), can get into systemic--> HYPERTENSIVE CRISIS!!

DO NOT TAKE MAO-INHIBITORS WITH TYRAMINE!!

• Indirect adrenergic agonist
• mobile pool NE releaser! also release DA, 5-HT

USE- ADHD, narcolepsy, appetite-suppressant for obesity

• SE- hypertension, tachycardia
• DO NOT TAKE WITH MAOa-INHIBITORS--> HYPERTENSIVE CRISIS!

SIMILAR DRUS- methylphenidate, dextroamphetamine, phentermine

• Indirect adrenergic agonist
• mobile pool NE releaser! also release DA, 5-HT

USE- ADHD, narcolepsy

• SE- hypertension, tachycardia
• DO NOT TAKE WITH MAOa-INHIBITORS--> HYPERTENSIVE CRISIS!

SIMILAR DRUS- dextroamphetamine, phentermine

• indirect adrenergic agonist
• release mobile pool of NE (also direct agonist)
• increase BP, decrease secretions, STIMULATE CNS!

• USE- nasal decongestant in cold meds!
• urinary incontinence, hypotention

• SE-hypertension, hyperthyroidism, CV disease
• DO NOT GIVE WITH MAOa-INHIBITORS --> HYPERTENSIVE CRISIS!

• Indirect adrenergic agonist
• NE-reuptake inhibitor (NE>>Epi)

• USE- local anesthetic (block Na+ channel),
• vasoconstriction

• SE- MI, arrhythmias, CV-damage, tachycardia,
• DO NOT USE WITH MAOa-INHIBITIORS!

• decrease MAP
• -may cause relex bradycardia, salt, water retention (b/c renin increase)

USE- hypertension, pheochromocytoma (nonselective blocker), BPH (selective a1)

SE- miosis, hypotension, incontinence, sexual dysfunction..

• alpha-blocker (nonselective, competative)
• reversible!

• USE- hypertension
• Phenoxybenzamine better for pheochromocytoma b/c phentolamine (competative) will just get competed out by EPI.

• SE-orthostatic hypotension, reflex tachycardia
• DO NOT GIVE TO CAD !!

• alpha-blocker (nonselective, noncompetative)
• irreversible!

• USE- drug of choice for pheochromocytoma!!
• good b/c irreversible, not competed out by high EPI and long lasting.
• - when using b1-blocker in pheo, give b-blocker AFTER phenoxybenzamine to prevent worsening of hypertensive crisis!!!

SE-orthostatic hypotension, reflex tachycardia

USE- BPH (urinary retention) + HTN

SE- orthostatic hypotension

alpha-1 blocker

• USE-BPH (prototype!), HTN
• -Raynaud's phenomenon

SE-orthostatic hypertension, dry mouth, sexual dysfunction, nightmares

alpha-1 blocker

USE-BPH, HTN, Raynaud's phenomenon

SE-orthostatic hypertension, dry mouth, sexual dysfunction, nightmares

alpha-1 blocker

USE-BPH, HTN, Raynaud's phenomenon

SE-orthostatic hypertension, dry mouth, sexual dysfunction, nightmares

alpha-1 blocker

USE-BPH (not much effect on HTN b/c less affinity for BVs)

SE-orthostatic hypertension, dry mouth, sexual dysfunction, nightmares

• alpha-2 blocker
• old drug!

USE- hypotension, impotence! (increase NE b/c take away neg feedback)

alpha-2 blocker

• USE- antidepressant, cause increase appetite.
• great for depressed person who won't eat.

SE- sedation, increase cholesterol, weight gain

5alpha-reductase inhibitor

USE- BPH, actually decrease dihydroxytestosterone, decrease size of hyperplasia in BPH.

NH4Cl

• HEART- decrease HR, SV,CO, O2 demand
• KIDNEY- decrease Renin
• EYE- decrease aqueous humor production

USE- antiarrythmics, angina, MI, HTN, CHF, edema

• NO CLINICAL USE!
• -may ppt bronchospasm, vasospasm, hypoglycemia, hyperlipidemias

-no effect by blockade alone, but worsen symptoms of asthmatics, COPD, DM, vascular disease (prinzmetal, raynauds).

• -receptor upregulation w/ chronic use
• -taper off dose to avoid exaggerated CV-response & arrhythmia.

RX- Glucagon! -thru increase cAMP, reverse effects of beta-blockade (decr. cAMP). Also increase glucose!

• ASTHMA
• COPD
• DM
• VASCULAR DISEASE (raynauds, prinztmetal)
• SEDATED (antidepressants, alcohol, BDZ)

exception!- Partial agonists Pindolol, Acebutolol and B1 selective blockers are safer in COPD, ASTHMA, VASCULAR, DM.

Atenolol safer in sedated patients!!

• Angina, HTN, post-MI
• CHF
• Antiarrhythmics (class II- propranolol, acebutolol, esmolol)
• Open angle glaucoma (timolol)
• Migraine
• Thyrotoxicosis (Propranolol only- can inhibit deiodinase!)
• Essential tremor (propranolol)

Labetolol, Carvedilol

USE- CHF!

B-blocker AND K-channel blocker

USE- Antiarrhythmic (class III)

beta-1 blocker + partial agonist (ISA)

• USE- angina, MI, HTN, tachyarrhythmias
• - NO hyperlipidemia! Partial agonist activity, less likely to cause bradycardia, bronchospasm, vasospasm.

SE-hypotension, fatigue, sedation (cross BBB)

DO NOT USE IN BRADYCARDIA, HEART BLOCK, SEVERE ASHMA, COPD, PRINZMETAL, COCAINE-INDUCED ANGINA! DECOMPENSATED CHF!

• beta-1 blocker
• (longer acting)

• USE- Angina, MI, HTN, Tachyarrhythmias
• DOES NOT CAUSE SEDATION! (safe to use in sedated patients taking anti-depressants, BDZ, alcohol)

SE-hypotension, bradycardia, bronchospasm, vasospasm, hyperlipidemia

DO NOT USE IN BRADYCARDIA, HEART BLOCK, SEVERE ASHMA, COPD, PRINZMETAL, COCAINE-INDUCED ANGINA! DECOMPENSATED CHF!

beta-1 blocker

USE- Angina, MI, HTN, Tachyarrhythmias

SE-hypotension, bradycardia, sedation, bronchospasm, vasospasm, hyperlipidemia

DO NOT USE IN BRADYCARDIA, HEART BLOCK, SEVERE ASHMA, COPD, PRINZMETAL, COCAINE-INDUCED ANGINA! DECOMPENSATED CHF!

nonselective beta blocker + partial agonist (ISA)

• USE- angina, MI, HTN, tachyarrhythmias
• - NO hyperlipidemia!
• Partial agonist activity, less likely to cause bradycardia, bronchospasm, vasospasm.

SE-hypotension, fatigue, sedation (cross BBB)DO NOT USE IN BRADYCARDIA, HEART BLOCK, SEVERE ASHMA, COPD, PRINZMETAL, COCAINE-INDUCED ANGINA! DECOMPENSATED CHF!

nonselective beta blocker

• USE- angina, MI, HTN, tachyarrhthmias
• Migraine, Thyrotoxicosis, performance anxiety, essential tremor! (block deiodinase)

• SE- cause severe SEDATION!
• hypotension, bradycardia, sedation, bronchospasm, vasospasm, hyperlipidemia

DO NOT USE IN BRADYCARDIA, HEART BLOCK, SEVERE ASHMA, COPD, PRINZMETAL, COCAINE-INDUCED ANGINA! DECOMPENSATED CHF!

• nonselective betal blocker
• Same CV effects as Propranolol

• USE- Open angle Glaucoma! (eye drops)
• -decrease aqeous humor formation, release intraocular pressure.
• -mostly beta-2 receptors in ciliary body epithelium.

SE-hypotension, bradycardia, sedation, bronchospasm, vasospasm, hyperlipidemia

beta-1 blocker

• USE- Open angle Glaucoma!
• mostly beta-2 in ciliary body epithelium, so less effective than Timolol, but better tolerated than timolol for Asthma, COPD, DM, Vascular disease.

• beta blocker + alpha-1 blocker!!
• Vasodilatory beta blocker!

• USE- CHF!!
• - block beta--> decrease O2 demand, decrease renin
• - block alpha--> decrease SVR, decrease afterload, preload.

SE- Hypotension, Bradycardia, Bronchospasm.

DO NOT USE IN DECOMPENSATED HEART FAILURE!

• alpha agonists (ex) phenylephrine (deplete NE stores)
• Nitroglycerin

• beta blocker + alpha-1 blocker + partial beta2-agonist!!
• Vasodilatory beta blocker!

• USE- CHF!!
• - block beta--> decrease O2 demand, decrease renin
• - block alpha--> decrease SVR, decrease afterload, preload.

• SE- Hypotension, Bradycardia, Bronchospasm.
• DO NOT USE IN DECOMPENSATED HEART FAILURE!