summary lists

Receptor Class Features Mechanism Location Agonists

Chol sk.muscle NMJ

Chol

Chol Gq - IP3, DAG cascade

Chol

Chol Gq - IP3, DAG cascade

Alpha 1 Adren Gq - IP3, DAG cascade

Alpha 2 Adren

Beta 1 Adren car.muscle

Beta 2 Adren

Nic Musc (Nm)

alpha, beta, gamma, delta subunits, pentamer

Na+/K+ depolarizing ion channel

succinylcholine, nicotine, acetylcholine, carbachol, ambenonium, echothiophate, neostigmine

Nic Neuro (Nn)

alpha, beta subunits, pentamer

Na+/K+ depolarizing ion channel

CNS postganglion cell body, dendrites

nicotine, acetylcholine, carbachol, ambenonium, echothiophate, neostigmine

Musc 1 (M1)

7 transmembrane GPCR signaling

nerves, autonomic ganglia

bethanechol, acetylcholine, methacholine, pilocarpine, ambenonium, echothiophate, neostigmine

Musc 2 (M2, cardiac)


Gi/o - inhibit cAMP production, activate K+ channels

heart, nerves, sm.muscle,

bethanechol, acetylcholine, methacholine, pilocarpine, ambenonium, echothiophate, neostigmine

Musc 3 (M3)


glands, sm.muscle, endothelium

bethanechol, acetylcholine, methacholine, pilocarpine, ambenonium. echothiophate, neostigmine


sm.muscle, vascular, prostate

epi, NE, phenylephrine, ephedrine, pseudoephedrine, amphetamine, tyramine


Gi/o - inhibit cAMP production, activate K+ channels

ganglionic presynaptic autoceptors, vascular sm.musc

epi, NE, clonidine, methyldopa, ephedrine, pseudoephedrine, amphetamine, tyramine


Gs - stimulate adenylyl cyclase and cAMP production

epi, NE, dobutamine, isoproterenol, ephedrine, pseudoephedrine, tyramine


Gs - stimulate adenylyl cyclase and cAMP production

sm. + car.muscle (sk.musc vessels and sm.musc bronchioles)

epi, albuterol, isoproterenol, terbutaline, ephedrine, pseudoephedrine, tyramine, labetalol

Effects Antagonists

decrease stomach mobility and tone, decr ACh release from parasymp nerves yohimbine, phentolamine

effects on parasymp (lowered heart rate) and symp (increased heart rate, elevated blood pressure) for succinylcholine, effect on cardiac muscarinic receptors (low heart rate), longer halflife than ACh

tubocurarine, botulinum toxin, vecuronium, pancuronium, pralidoxime

depends on the prevailing tone of the system (in favor of the dominant tone, e.g. ciliary muscle is parasymp and causes near vision, so nic agonist enhances this), incr BP, variable HR, incr gland secretion, incr GI motility, urinary voiding, few clinical uses, var. effect on pupil dilation depending on prevailing tone

tubocurarine, trimethaphan, botulinum toxin, vecuronium, pralidoxime

limited CNS access, pilocarpine has some CNS access (tertiary amine instead of quaternary amine), act on postsynaptic M1 in sympathetic ganglia leading to incr. BP

atropine, scopolamine, dicyclomine, ipratropium, botulinum toxin, pralidoxime

dilate arterioles at sk.muscle, decr NE release from symp nerves, decr automaticity, contractility, conduction velocity by innervating SA node, atria, AV node, incr refractory period (AV), present but unnervated at ventricles

atropine, scopolamine, dicyclomine, ipratropium, botulinum toxin, pralidoxime

dilate arterioles at sk.muscle, contract sphincter musc iris (constrict pupil), contract ciliary musc (near vision), contract bronchial musc, secr from bronchial glands, contract bladder body, relax bladder neck, water secr from salivary glands, incr mobility and tone of stomach, incr intestinal secr, incr sweat secr

atropine, scopolamine, dicyclomine, ipratropium, botulinum toxin, tolterodine, pralidoxme

constrict arterioles at skin, mucosa, lung, abdom.viscera, contract sweat glands for secretion, contract radial muscle iris to dilate pupil, contraction of bladder neck, decr stomach mobility and tone

prazosin, phenoxybenzamine, phentolamine, doxazosin, tamsulosin, labetalol, carvedilol

relaxes ciliary muscle for far vision, decrease stomach mobility and tone, incr automaticity, contractility, conduction velocity by innervating SA node, atria, AV node, his-purkinje system, ventricles, decr refratory period (AV)

metoprolol, propranolol, timolol, atenolol, esmolol, labetalol, carvedilol

dilate arterioles at sk.muscle, relaxes ciliary muscle for far vision, relax bronchial muscle, decr bronchial secretion, incr automaticity, contractility, conduction velocity by innervating SA node, atria, AV node, his-purkinje system, ventricles, decr refractory period (AV), inhibit histamine release

propranolol, timolol, labetalol, carvedilol

Effects

fall in blood pressure due to histamine release (at high concentrations for tubocurarine), increased heart rate due to antimuscarinic action (pancuronium)

decr BP, incr HR, pupil dilation, far vision, decr gland secretion, decr GI motility, urinary retention, few clinica uses (autonomic hyperactivity, control BP)

minimal effect at clinical doses, generally excitatory (restlessness, hallucinations)

no effect on P(art), incr. heart rate, rapid admin. of low doses may lead to decr heart rate (block presynaptic musc. receptors that normally restrict ACh release)

dilate pupil, loss of near vision, bronchodilation, lack of lung secretion, no effect on P(art), incr heart rate (block vagal), decr GI motility/secretion, relax bladder body + contract sphincter (prevents emptying), inhibits sweat/lacrimal/salivary gland secretion

IN GENERAL:

for nicotinic agonists: would stimulate action potential at first (phase I, depolarizing phase), but then with more agonist you hit phase II, where the receptor has become desensitized to the receptor

for nicotinic antagonists: block action potential, would require higher agonist concentration to overcome, at higher antagonist concentration, competitive antagonist may behave as noncompetitive antagonist by blocking the pore of the channel instead of just the agonist binding site

Receptor Site EffectM1 cholinergic neuron stimulate ACh releaseM2 cholinergic neuron reduce ACh releaseM2 adrenergic neuron reduce NE releaseNm cholinergic motor neuron stimulate ACh releasealpha 2 adrenergic neuron reduce NE releasealpha 2 cholinergic neuron reduce ACh releasebeta 2 adrenergic neuron stimulate NE releasebeta 2 cholinergic motor neuron stimulate ACh release

Type Cholinergic Structurechol agonist Carbachol (Miostat) choline ester, 4o aminechol agonist Acetylcholine (Miochol-E) choline ester, 4o aminechol agonist Echothiophate (Phospholine) phosphate group, 4o aminechol agonist Edrophonium (Tensilon) 4o aminechol agonist Isoflurophate (Floropryl) organophosphorous compoundchol agonist Physostigmine (Antilirium) from plant, 3o aminechol agonist Neostigmine (Prostigmin) choline ester, synthetic, 4o aminechol agonist Ambenonium (Mytelase) 4o aminechol agonist pyridostigmine 4o aminechol antag Botulinum Toxin (Botox, Myobloc) proteinchol antag Pralidoxime (Protopam) 4o aminemusc agonist Bethanechol (Urecholine) choline ester, 4o aminemusc agonist Methacholine (Provocholine) choline ester, 4o aminemusc agonist Pilocarpine (Salagen, Isopto, Carpine) alkaloid ester, 3o aminemusc agonist muscarine 4o aminemusc antag Ipratropium (Atrovent) ester, 4o aminemusc antag Dicyclomine (Bentyl) ester, 3o aminemusc antag Scopolamine (Transderm Scop) alkaloid ester, 3o amine musc antag Tolterodine (Detrol) 3o aminemusc antag Atropine (Atropen) alkaloid ester, 3o amine musc antag oxybutynin 3o aminemusc antag darifenacin 3o aminenic (M) agonist Succinylcholine (Quelicin, Anectine) choline ester, two ACh attached @ tailsnic (M) antag Vecuronium 4o aminenic (M) antag Pancuronium (Pavolon) choline ester, 4o aminenic (M) antag Tubocurarine alkaloid, 4o aminenic (N) antag Trimethaphan (Arfonad) 3o aminenic antag mecamylamine 2o amine,nic agonist Nicotine (Nicorette, Nicoderm) 3o amine

beta CH3 group specific to muscarinic receptorscovalent AChE inhibitors decr half-life

Mechanismbind directly to nicotinic and muscarinic receptor, used for glaucoma, AChE insensitivebind directly to receptor, used clinically to cause miosisinhibits AChE covalently (phosphorylated), irreversible, used mostly for glaucoma, used topicallyinhibits AChE non-covalently, reversible, competitive, used to diagnose myasthenia gravisinhibits AChE covalently (phosphorylated), irreversible, treat glaucoma, used topically, used as insecticide, highly lipid solubleinhibits AChE covalently (carbamoylated), reversible, treat glaucoma, indirectly stimulates nic and musc receptors, CNS effectsinhibits AChE covalently (carbamoylated), reversible, treat myasthenia gravis, stimulate GI/urinary tract, reverse tubocurarineinhibits AChE non-covalently, competitive, treat myasthenia gravisAChE inhibitor (carbamoylated), reversible, treat myasthenia gravis, reverse muscle relaxant, longer halflife than neostigmineinhibits docking process, used to treat cervical dystoniareactivates AChE, treats poisons that have AChE inhibiting activity, must be used immediately in order to avoid "aging" of AchEbind directly to muscarinic receptor (mostly M3), incr gastric motility and bladder voiding, most AChE insensitivebind directly to muscarinic receptor, bronchoconstrictor used for asthma challenge testbind directly to musc receptor, incr parasymp tone, tachy (M1), not susceptible to AChE, treat glaucoma, M1 receptorexcessive secretion, ab pain, nausea/diarrhea, blurred vision, labored breathing, respiratory/cardiac failure, antidote: atropinebind directly to muscarinic receptor, bronchodilatorbind directly to muscarinic receptor, prevent muscle spasm in GI tractbind directly to muscarinic receptor, reversible, treat motion sickness, colicky abdominal pain, acts on CNS, AChE insensitivebind directly to muscarinic receptor, used to treat overactive bladderhighly selective for musc over nic receptors, significant access to CNS, used to treat bradycardia, AChE insensitivetreat overactive bladderblocks receptor, treat overactive bladderbind directly to nic musc, musc relaxant (constant depolar), decr HR, incr HR (symp ganglia), hyperkal, hist release, hypertherm bind directly to nic mus receptor, competitive, prevents ACh binding, prevent muscle contractionbind directly to nic mus receptor, competitive, prevents ACh binding, used to relax muscle, incr HR due to antimusc actionbind directly to nic mus receptor, competitive, AChE insensitive, decr BP due to gangl block, release histamine, non-depolbind directly to nic neur recep, release hist, cause hypotension, comp inh of ACh, promote opp of dominant tone, non-depolcompetitive inhibitor of ACh, ganglionic blocker, treat hypertensionbind directly to nicotinic receptor, treat smoking cess, 1st stimul parasymp and symp neurosystems, then ganglion blockade

Type Adrenergic Structureagonist Dopamine (Intropin) catecholagonist Epinephrine (Adrenalin) catecholagonist Ephedrineagonist Pseudoephedrine (Sudafed)agonist Amphetamine (Adderall)agonist dextroamphetamine lipophilagonist hydroxyamphetamine monoamine alkaloidagonist methamphetamineagonist methylphenidateagonist Tyramineagonist Cocainealpha, beta 1 agonist Norepinephrine (Levophed) catecholantag, noncomp Reserpinealpha agonist oxymetazolinealpha antag Phentolamine (Regitine)alpha1 agonist Phenylephrine (Neosynephrine) 1 OH groupalpha1 antag Tamsulosin (Flomax)alpha1 antag Doxazosin (Cardura)alpha1 antag Prazosin (Minipress, Vasoflex)alpha1 antag terazosinalpha1 antag Phenoxybenzamine (Dibenzyline)alpha1, beta antag Labetalol (Normodyne, Trandate) 3rd gen

alpha1, beta antag Carvedilol (Coreg) 3rd genalpha2 agonist Methyldopa (Aldomet, Apo-methyldopa, Novomedopa) catechol, CH3alpha2 agonist Clonidine (Catapres, Dixarit)alpha2 antag Yohimbine (Yocon)beta agonist Isoproterenol (Isuprel) catechol, large alkyl groupbeta antag Timolol (Blocadren, Timoptic) 1st gen beta antag Propranolol (Inderal) 1st gen, hydrophobebeta antag nadolol 1st genbeta1 agonist Dobutamine (Dobutrex) catechol, chiral Cbeta1 antag Esmolol (Brevibloc) 2nd genbeta1 antag Atenolol (Tenormin) 2nd gen, hydrophilbeta1 antag (inv agon) Metoprolol (Toprol, Lopressor) 2nd genbeta2 agonist Albuterol (Ventolin, Proventil)beta2 agonist Terbutaline (Brethrin, Brethaire) catechol

beta1 has equal affinity for both indirect drugs act on NE, so doesn't affect beta2 receptorsbeta2 have more affinity for epi than for NE large alkyl group = bind better to beta2 receptorsalpha: epi > or = NE >> isoproterenol OH groups make catechol more hydrophilicbeta: isoproterenol > epi > or = NE substitution at alpha carbon blocks oxidation by MAO (incr t1/2)

para OH required for COMT degradation (as a catechol)amphetamines can treat narcolepsy and suppress appetitebeta blockers have local anesthetic effect via blockade of Na channels, except timolol1st gen beta blockers: equal affinity for both beta1 and beta22nd gen beta blockers, beta1 selective, safer for pts with asthma3rd gen beta blockers: more complex effects

Mechanismdirect, bind dopamine receptor (vasodilate), primary act on beta (stimulate myocard), alpha receptors (vasoconstriction), incr HR, cardiac contractilitydirect, bind receptor, treat anaphylaxis, sepsis, rapid IV incr BPindirect, some direct, cause NE to leak out of vesicles, bind alpha and beta receptors, access to CNS, mild stimulant, nasal decongestant, weight lossindirect, cause NE to leak out, enantiomer of ephedrine, less potent at inducing tachy/hypertension/CNS stimulation, contraindicated with MAO inhibitorsindirect, CH3 at alpha carbon, block reuptake of catech, makes NT vesicles leaky, higher BP (periph effect of NE release), stimulant, narcolepsy, ADDstereoisomer of amphetamine, used to treat ADHD, more potent for CNS, less potent for peripheralrelated to ephedrine, used to decrease appetite, amphetaminetreat ADHD, exogenous obesity, triggers release of NE, more potent than amphetamineamphetamine-like, treat ADD, narcolepsy, block dopamine uptake in central adrenergic neurons, fewer peripheral effects than amphetamineindirect, displacement and release of NE, contraindicated with MAO inhibitors (metabolized by MAO), in foodsindirect, prevents uptake-1 by prejunc neuron, nasopharyng surgery, stop blood flow, local anesthesia, blocks Na+ channels, block dopamine reuptakedirect, bind receptor, decr access to CNS, treat vasodilatory shock, treat hypotensionindirect, prevent storage of NTs in presynap vesicles, prevents dopamine from moving into vesicles and turning into NE, treat hypertensiontreat nasal congestion, constricts arterioles in nasal passagesdirect, bind receptor and block signal, used in pheochromocytoma and cocaine-induced hypertension, not very specific, reduce peripheral resistancedirect, bind receptor, no access to CNS, dilates pupils, nasal decongestant (sprays), binds alpha1 receptors, incr periph resistance, incr BP, reflex bradydirect, bind receptor and block signal, blocks alpha1 activity preferentially at prostate, good treatment for BPHdirect, bind receptor and block signal, similar to prazosin, longer half life (22hrs), treat hypertension, BPHdirect, bind receptor and block signal, treat hypertension, relax vascular smooth muscle, selective for alpha1, induce smaller incr in HR (alpha2 role)treat BPH, hypertensiondirect, bind receptor covalently, irreversible, somewhat selective for alpha1, treats pheochromocytoma, postural hypotensiondirect, bind receptor and block signal, partial agonist for b2, 3rd gen, a1 selective, reversible antag, vasodilation, bronchodilation, treat hypertensionlower BP w/o big effect on HR, block uptake of NEdirect, block receptor, 3rd generation, used for hypertension, post-heart attack patients, low side effects, lower chance of 2nd heart attackindirect?, resistant to MAO, decr BP, preferred for hypertension during pregnancy, less disruptive of blood flow from mom to fetus, works through CNS?direct, bind receptor, treat hypertens, decr hyperactiv (ADHD), decr HR and BP, dry mouth, sedation, sex dysfun, bradymech unknown, selective, acts in CNS to incr arterial pressure and HR, opposite of clonidine, renal failure, seizures, death, body building, treat impotencedirect, bind receptor, treat brady, anaphylaxis (inhaled), bronchodilatordirect, bind receptor and block signal, relieve pressure in eye topically, treat glaucoma, treat hypertension, prevent heart attack, prevent migrainedirect, bind receptor and block signal, used to prevent migraines, keep steady HR, lowers blood pressure, half life ~3hrs, decr COtreat arrhythmia, hypertension, migraine, tremor, angina pectoris, long half-life, competitive antagdirect, bind receptor, low dose: incr CO (reflex to slow HR), little effect on HR and PR, high dose: both HR and cardiac output incr, heart failure, stress testdirect, bind beta1 receptor and block signal, used for urgent need to decr BP, IV, used to bring symp stimulation down (i.e. during surgery), short half-lifedirect, bind receptor and block signal, prevent migraines, no CNS access, safer for patients with bronchoconstriction than propranolol, treat hypertensiondirect, bind to receptor, block signal, inverse agon, decr mortality for pts with severe heart failure, decr constitutive activity of recep, treat hypertensiondirect, bind receptor, relieve bronchospasmdirect, bind receptor, relieve long-term or acute bronchospasms, arrest early labor

indirect drugs act on NE, so doesn't affect beta2 receptorslarge alkyl group = bind better to beta2 receptorsOH groups make catechol more hydrophilicsubstitution at alpha carbon blocks oxidation by MAO (incr t1/2)para OH required for COMT degradation (as a catechol)amphetamines can treat narcolepsy and suppress appetitebeta blockers have local anesthetic effect via blockade of Na channels, except timolol1st gen beta blockers: equal affinity for both beta1 and beta22nd gen beta blockers, beta1 selective, safer for pts with asthma3rd gen beta blockers: more complex effects

PoisonCarbon Monoxide

Aspirin

Acetaminophen

Cyanide

Alcohols

Pesticides

Lead poisoning

Merury poisoningArsenic

CadmiumTrichloroethylene (TCE)

Benzene

TCDD (Dioxin)

Polychlorinated Biphenyl

Total: 14

Noteshigher affinity for Hb than O2, decr delivery of O2 to peripheral tissues, binds to cytochrome oxidasesymptoms: headache, vasodilation, dizziness, unconsciousness, incr HR, RR, seizures, hypotension, vent depression , deathuncouples oxidative phosphoryl, 1st resp alka w/comp metab acido, later combined resp and metab acido, hyperventilationlethal dose: 10-30g (less than one bottle)metabolism: 60% glucuronide, 35% sulfate, 5% mercapturic acid, covalent binding to hepatocytestherapeutic window for NAC after ingestion is ~36 hrsHCN gas as pestide, binds tightly to Fe+3, major target is cytochrome oxidase, lactic acidosislethal dose: KCN ~ 200mg, HCN ~ 50mgthiosulfate helps neutralize the cyanideformic acid from methanol is toxic to retinamethanol: severe metab acido, 15mL to cause blindness, 100mL fatal, isopropanol (forms ketone instead of aldehyde) is less toxicincr muscarinic (nausea/vomiting, incr pulm secretion, brady) and nicotinic (hypertension, muscle weakness, twitching)effects, CNS effects (anxiety, restlessness, seizures, coma)

GI absorption, circulates bound to Hb, long half-life in bone, vague GI effects, hematuria, proteinuria, microcytic/hypochromicanemia, peripheral neuropathy, hypertensionodorless, colorless, tasteless, vapor at room temp, concentration rises in food chain, visual/hearing loss, ataxia, may not be reversibleAs+3 (inhibits sulhydryl enzymes esp Krebs cycle) and AsH3- (denatures Hb) are toxic, causes cirrhosis, muscle weakness, achingmostly ingested through drinking waterNiCd batteries, tobacco smoke, inhalation (acute: pneumonitis, chornic: emphysema, fibrosis), ingestion: renal damage, carcinogenmetabolized into carcinogen, MCLG = 0, MCL = 5ppb, can remove from water via aeration or charcoal filterPEL: TWA (8hrs) = 100ppm, ceiling = 200ppm, maximum peak = 300ppm, 5minacute: anesthetic effect, drowsiness, dizziness, ataxia, chronic: carcinogenic, kidney, liver, esophagus, leukemiabone marrow suppression, carcinogen, CYP converts to epoxide which can bind nucleic acidsMCLG = 0, MCL = 5ppb, remove benzene from water via aeration or charcoal filterPEL: TWA (8hrs) = 10ppm, ceiling = 25ppm, maximum peak = 50ppm, 10minmade from burning organic matter, no odor, low volatility, high lipid solubility (concentration rises in food chain), persists in environmentbinds to AhR (arohydrocarbon receptor) and induces CYP1A1 which metabolizes polycyclic aromatic hydrocarbons to form carcinogensTCDD itself is not metabolized, acute: chloracne, chronic: diabetes mellitus, CNS/PNS damage, hypothyroidism, immunosuppression(PCB), many isomers, low volatility, high lipid solubility, almost inert, acute: chloracne, chronic: cancer (melanoma, non-Hodgins lymphoma,brain, liver, gall bladder, bile duct, Parkinson's, ALS

organophosphates (malathion, parathion, diazinon) and carbamates (carbaryl, baygon)

Management100% O2, mech ventilation, paralysishyperbaric therapy, barbiturate comavomiting, charcoal, alkalinize urine, mech vent, dialysis, acid-base imbalancevomiting, charcoal, N-acetylcystein (actslike glutathione, scavenges for molecule)convert Hb+2 to +3 (IV amyl nitrate, inhaledsodium nitrite), sodium thiosulfate, 100% O2, consider gastric lavagefomezipol (inhibits EtOH dehydrogenase)ethanol for methanol poisoning

skin- bathing, GI- gastric lavage, charcoalatropine (decr secretions), pralidoxime (o-phos)

chelation therapy: EDTA, dimercaprolsuccimer, penicillaminedimercaprol, penicillamine, succimer (not approv.)dimercaprol initially, chronic: pencillamine succimer (not approv.)chelation therapy, drug choice unknownEPA: for public water supplies, private wells, airOSHA: workplace managementwater: MCLG = maximum containment level goalMCL = maximum containment levelMCLG < or = MCLPEL = permissible exposure limitTWA = time weighted averagePELs not established for most organicsCIH = certified industrial hygienist

AgentEDTA

DimercaprolPenicillamineSuccimer

MethodsVomitingGastric LavageActivated CharcoalBowel CleansingIncrease Rate of Clearing

Antidotes

NotesNa2EDTA decreases Ca+2 levels, so often use CaNa2EDTA, heavy metal displaces Ca, must be given IV or IM, causes proximal tubule damage (therapy has to be given in courses with breaks in between, also chelates essential heavy metals (Cu, Zn, Fe)solution in peanut oil, used in combo with EDTA, IM delivery, incr HR and BP (stimulates ANS), requires alkaline urineeffective orally, metabolite of penicillin, long-term outpatient management of Pb poisoning, also used in Wilsons disease (too much Cu), toxicity: autoimmune phenomena, possible allergyeffective orally, less toxic than penicillamine and dimercaprol, does not chelate essential heavy metals, only approved in Pb poisoning, toxicity: chemical hepatitishave to have liver transaminases checked, may require liver transplant

Notescannot do if person is unconscious, if substance is volatile or if poison is rapidly absorbedmay cause esophageal perforation, aspirationadsorbs organic lipid-soluble compoundsrapid-acting laxative to clean out the bowels, decrease intestinal absorptionalkalinize urine (NaHCO3, acetazolamide) for barbiturates, salicylates to increase excretion of acidic compounds, acidify urine (NH4Cl) for amphetamines, increase excretion of basic compounds,dialysis (hemodialysis, peritoneal dialysis) for water-soluble, low molecular weight, not protein-boundpharmacologic antagonist, physiological antagonist, chemical antidote

L - lethal NL - nonlethalClass MechanismNerve Agents (L) irreversibly inhibit AChE

severity scale:Tabun (L) LCT: 400, LC: 1000Sarin (L) LCT: 100, LC: 1700Soman (L) LCT: 50, LC: 100VX (L) LCT: 10, LC: 10

Treatment

Blister Agents (NL) alkylating agentex. Sulfur Mustard (NL)Treatment

Blood Agents (L) ex. Cyanide (L)Treatment

Choking Agents (NL) ex. Phosgene (NL)Treatment

Riot Control (NL) ex. Tear Gas (NL)Treatment

Incapacitating Agents (NL) impair cognitive functionex. Quinuclidinyl BenzilateTreatmentex. CarfentanilTreatmentex. Ricin (L)

TreatmentTotal: 11

Additional Noteshigh bioavailability through inhalation or topical absorption, potency measured by LCT50 (mg-min/m3) and LC50 (mg), all organophosphates

low potency, colorless, tasteless, fruity odorvapor heavier than air, degraded by water, lasts longer at high temps, narrow range btwn perceptible and lethal dose, more potent than tabun (inhaled)higher potency than sarin (esp topically, potency increases with incr lipid solubility), narrow range btwn perceptible and lethal dosemost potent, clear, odorless, tasteless oil, sticky, low volatility, more potent after hydrolysis, inactivated by chlorine bleach, branched carbon chainatropine, pralidoxime, diazepam, atropine: may require large doses, can cause brachycardiapralidoxime: reverses AChE inhibition, must be started within minutesdiazepam: decrease airway reflux, important to dry secretions with atropine, must be started within minutes, results in extreme lethargy, apnea unlikely** can give pyridostigmine (reversible AChE inhibitor) to preempt NA poisoning (may cause nausea/vomiting/diarrhea, dyspnea, dizziness, hallucination)effects delayed for hours, cutaneous blisters, eye and pulm irritation, rarely lethal (unless given a high dose, may compromise respiration)

no antidotelow potency, high volatility, rapidly lethal in high concentrations, diffuses away easilyintentional conversion from Hb+2 to Hb+3 to sequester CN- from binding to Fe+3, sodium thiosulfate to neutralize CN-, 100% O2, gastric lavageirritation to resp tract, heavier than air, smells like newly mown grass, narrow range btwn perceptible and toxic, pulm edema can be fatal if untreatedjust get away from it? Treat pulmonary edemaaromatic ring causes profuse tearing and coughing, law enforcement permitted to use thisget away, breathe fresh airmany classes: anticholinergics, opiods, hallucinogens, stimulantsatropine-like drug, aromatic ring makes it lipophilic (affects CNS), scopolamine-like effect, causes confusion, amnesia and delirium, tachycardiaspecific treatment with physostigmine, AChE inhibitortwo aromatic rings, opiod, 10,000 more potent than morphine, small amount can knock out a t-rex (or a YY), used mostly for sedationnaloxene or naltrexone (opiod competitive antagonists)two chain peptide from castor oil beans, one chain attaches to cell memb causing phagocytosis, other chain destroys ribosomes, re-release after cell death toinfect another cell, causes cell death and prolonged time to death of victim (days)no antidote! :(

increased secretions, bronchoconstriction, miosis, increased GI tone, muscle twitching/jerking, confusion and drowsiness, coma, convulsions, apnea

Drug TypeBrimonidine a2 agonistApraclonidine a2 agonistDipivefrin nonselective a, b agonist

Dorzolamide c.a. inhibitorAcetazolamide c.a. inhibitorLatanoprost prostaglandin analogPhysostigmine chol agonistCarbachol chol agonistEchothiophate chol agonistTimolol beta antagCyclopentolate musc antagTropicamide musc antagPhenylephrine alpha agonist

Pilocarpine musc agonistDapiprazole alpha antagHydroxyamphetamine release of NE

Mechanismdecr synthesis of aqueous humor, local eye irritation, possible sedation and dry mouthdecr synthesis of aqueous humor and incr uveoscleral outflow, treat glaucoma, local eye irritation and possible sedation and dry mouthprodrug of epinephrine, causes decr aqueous humor formation (a2), incr uveoscieral outflow (a2), incr outflow through canal of Schlemm (b2), treat glaucoma, less local irritationthan epi, systemic concentrations may cause tachy and hypertension, cause dark pigmentation in the eye decr synthesis of aqueous humor, primary inhibitor of CA, causes local irritation, no systemic effectsdecr synthesis of aqueous humor, rarely used to treat glaucoma, systemic adverse effects, increases pH of urine (kidney stones), metabolic acidosis, allergies to sulfonamidesprostaglandin analog, incr uveoscleral outflow, lowers intraocular pressure, treat glaucomainhibits AChE covalently, reversible, used to treat glaucoma, indirectly stimulates nic and musc receptors, CNS effectsbinding directly to nicotinic and muscarinic receptor, used for glaucomainhibits AChE covalently, irreversible, treat glaucoma, not used commonly, given once per day, topicaldirect, bind receptor and block signal, relieve pressure in eye topically, glaucoma treatmentcycloplegic drug (prevents ciliary musc contraction, can't accommodate, only have far vision), long lasting mydriatic drugshortest acting mydriatic drug, blocks parasympathetic tonecauses mydriasis w/o cycloplegia b/c ciliary muscle not under alpha control, less effective in people with dark irises b/c of nonspecific binding to pigment, hypertensionvia systemic absorptionreverse mydriasis, selective for muscarinic receptor, increase parasymp toneblock agon effect of phenylephrine, reversal of phenylephrine-induced mydriasis, easier than w/tropicamide or cyclopentolatemech same as amphetamine, NE released from presynap side of adren synapses, used to determine location of lesion in pt with horner's syndromedilation = preganglionic, no effect = postganglionic

carbachol brimonidine a2 agon dopamineacetylcholine apraclonidine a2 agon epinephrineedrophonium dipivefrin nonselec a, b agon ephrineechothiophate dorzolamide ca inhibitor pseudoephrineisoflurophate acetazolamide ca inhibitor amphetaminephysostigmine latanoprost PG analog hydroxyamphetamineneostigmine physostigmine chol agon methamphetaminepyridostigmine carbachol chol agon dextroamphetamineambenonium echothiophate chol agon methylphenidatebotulinum toxin timolol beta antag tyraminepralidoxime cyclopentolate musc antag cocainebethanechol tropicamide musc antag norepinephrinemethacholine phenylephrine alpha agon reserpinepilocarpine pilocarpine musc agon oxymetazolinemuscarine dapiprazole alpha antag phentolamineipratropium hydroxyamphetamine adrenergic agon phenylephrinedicyclomine prazosinscopolamine terazosintolterodine doxazosinatropine tamsulosinoxybutynin phenoxybenzaminedarifenacin methyldopasuccinylcholine clonidinevecuronium yohimbinepancuronium labetaloltubocurarine carvediloltrimethaphan isoproterenolmecamylamine timololnicotine propranolol

nadololdobutamineatenololmetoprololesmololalbuterolterbutaline

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