Cholinergic Agonist

Muscarinic and Nicotinic Receptors

BP DECREASES with IV infusion

Very rapidly hydroplyzed by AChE

No clinical use

Cholinergic Agonist (Quaternary)

Muscarinic Receptors

Primarily GI and Bladder; Increases urination and peristalsis, Post Op Ildus

NO CNS EFFECT

Cholinergic Agonist (Tertiary)

Muscarinic Receptors only

Glaucoma (decreases IO pressure); Xerostomia (increases salivation)

CNS effects

Cholinergic Agonist

M3 agonist

Xerostomia (increases salivation W/ LESS SWEATING)

Direct acting Cholingergic Agonist

Muscarinic and Nicotinic Receptors

Decrease intraocular pressure and pupil constriction

Direct-Acting Cholinergic Agonist

Nicotinic Receptors (All autonomic Ganglia, NMJ)

Binds Na Channel

DESENSITIZES RAPIDLY!

SNS - HTN, tachy, arrythmia

PNS - Brady, Nausea, vomit, diarrhea

NMJ - Twitch progressing to paralysis

Brain - Increased alertness in low doses, convulsions, coma respiratory arrest in high doses

TREATED WITH ATROPTINE, ANTICONVULSANTS (diazepam) AND RESPIRATORY ASSIST 

Direct Acting Cholinergic Agonist

Nicotinic Receptors

Partial agonist

decreases cravings and competes w/ nicotine for receptor

Side effects: nausea, vomit, constipation, flatulence, sleep problems, psychosis, vivid nightmares

Cholinesterase Inhibitor

Reversible, very short acting (5-20 min)

NO CNS, must be injected

Used Post Sx reverse of NMJ block and to diagnose myasthenia gravies and ACE inhibitor dose

Cholinesterase Inhibitor

Quaternary, NO CNS EFFECT

Used in myasthenis gravis and post surgery revers of NMJ block

30 min-6 hr duration

Hydrolyzed by AChE

Cholinesterase Inhibitor (Carbamate)

Tertiary, CNS EFFECTS

Used for glaucoma (decreased IO pressure) and to treat Atropine OD

30 min-6 hr duration

Hydrolyzed by AChE

Cholinesterase Inhibitor

Chronic Therapy of Myasthenia Gravis

Fast acting, given several times a day

Cholinesterase Inhibitor

Chronic Therapy of Myasthenia Gravis

Short acting, givin several times a day

Cholinesterase Inhibitor

IRREVERSIBLE

Long-term organophosphate

can be used to treat Glaucoma (decrease IO pressure) long term

Cholinesterase Inhibitor

Long lasting, irreversible w/ "aging"

Pralidoxime (2-PAM) prevents aging if it hasn't occured yet

Cholinesterase Inhibitor

Competes w/ Organophosphates (treatment)

Treats pesticide poisoning and atropine OD

Cholinesterase Inhibitor

Lipid soluble, enter CNS

Long action

Used to treat alzheimers'

Cholinesterase Inhibitor

Lipid soluble, CNS effects

Long action

Treat Alzheimers

Cholinesterase Inhibitor

Lipid soluble, CNS effects

Long action

Treat Alzheimers

Direct Acting Cholinergic Agonist

Stimulate Muscarinic and Nicotinic Receptors

PROTOTYPE

Alpha 1 Agonist!

BP up/Baroreceptor mediated decreased HR

Vasoconstrict Peripheral BVs (increased peripheral resistance) and mucosa

Mydriasis, Contract and promote urinary continence (prostate, bladder base, urethral sphincter) RELAX intestinal smooth muscle Stimulate pilomotor smooth muscle

Can be used in hypotensive emergency, decongestant

PROTOTYPE

Alpha 2 agonist

Inhibit NT release (presynaptic)

Decrease NE release and SNS activity

Overall Decrease in BP/ may decrease HR

Uses: HTN, addiction, alcoholism (decreased cravings) and withdrawal, hot flashed in menopause, pre-anesthetic medication.

Vasoconstriction in coronary, skin, mucosal and renal BV

Decreased ACh release (decreases intestinal tone, secretion, small effect, dry mouth)

Decrease insulin secretion - minor effect

Platelet Aggregation

Side effects: dry mouth, sedation, sexual dysfunction, HTN with rapid withdrawl of drug

PROTOTYPE

Beta 1 agonist (short acting, 2 min)

HEART EFFECTS: increased HR, force of contration, conduction in SA node, automaticity/conduction AV node, ventricular contractility, conduction, automaticity, pacemaker rate

Kidney effect: Increased release of renin (indirect increase in BP)

PROTOTYPE

Beta 2 Agonist

HEART EFFECTS (same but less than B1): increased HR, force of contration, conduction in SA node, automaticity/conduction AV node, ventricular contractility, conduction, automaticity, pacemaker rate

Relax bronchial smooth muscle, uterus, bladder, GI muscle

Relax Skeletal Muscle BVs

K+ uptake into skeletal muscle

Glycogenolysis/gluconeogenesis (liver)

Lipolysis in fat cells (B3)

Catecholamine

Beta 1 and Beta 2 Agonist

Increased HR(B1,B2+Baro Reflex)/Decreased BP(B2)

Heart Effects: Increased HR, force of contraction, CO increased

Vascular effects: Vasodilation, decreased BP

Uses: Emergent cardiac arrest, complete heart block, emergent asthma

Side effects: large doses may cause tachycardia, palpitations and arrhythmias

Catecholamine

Beta 1 (NO B2) and Alpha agonist

Increased BP/Increased HR then decreased HR (Baro reflex)

Pulse pressure unchanged (systolic-diastolic = PP)

W/ Atropine, vagal response is blocked and HR will remain elevated

Side effect: vasoconstriction at infusion site leading to necrosis

PROTOTYPE

Cholinergic (Muscarinic) Antagonist

DECREASED PNS ALL AROUND

Decreased salivation and sweat at low doses; bronchoconstriction

Eye: mydriasis, decreased accomodation, 

Heart: Bradycardia at low dose, Tachy at high

 TOXICITY: blind as a bat, dry as a bone, mad as a hatter and red as a beet

Cholinergic Antagonist

Enter CNS easily

Used for motion sickness; other CNS effects include drowsiness, memory loss, decreased secretions

Toxic = hallucinations, agitation, coma

Cholinergic Antagonist

Used to restore balance between DA/ACh when DA is low or receptors blocked in CNS

Treatment for Parkinson's disease; decrease symptoms from antipsychotic drugs

Cholinergic Antagonist

Used to treat the eye

MydriasisBlocks iris sphincter muscle

Decreased accomodation = Inhibits ciliary muscle

Can cause/exacerbate Glaucoma

Cholinergic Antagonist

Used during surgery to prevent vagal responses

Cholinergic Antagonist

GI antisposmodic

Cholinergic Antagonist

Used to treat COPD and asthma

Cholinergic Antagonist

M3 antagonist

Increases bladder continence in the elderly

Cholinergic antagonist

M3 antagonist

Used for overactive bladder, little effect on salivation

Cholinergic Antagonist

Used to prevent bladder spasm post prostate Sx

Catecholamine: Adrenergic stimulant

A, B1 and B2 stimulation

EFFECTS DEPENDENT ON DOSE:

LD: Increased HR/Increased pulse pressure, little overall pressure change

HD: Increased HR/Increased PP/Increased Overal pressure

Low dose: Heart (B1)-positive inotropic and chronotropic effect; Alpha - vasoconstriction in skin, mucosa and kidney increasing systolic and diastolic pressure; Skeletal muscle (B2) - vasodilation, decreasing diastolic pressure

High Dose: Alpha effects impart a PRESSOR EFFECT

Uses: anaphylactic shock, cardiac arrest and complete heart block, vasoconstrictor property is used to decrease diffusion of injected drugs, glaucoma (increased removal/decreased production of aquesous humor)

Toxicities: tremor, headache, increased BP, tachycardia, angina, cerebral hemorrhage, V-arrhythmias; severe HTN in pts on beta-blockers

Adrenergic stimulant

a and B receptor

enhances NE release; increases HR and BP; bronchodilation

Long duration

Adrenergic Stimulant

treats postural hypotension and autonomic insufficiency; can cause HTN upon lying down so given during the day

Adrenergic Stimulant

Alpha agonist

Used as decongestant, may increase BP in HTN pts

Precursor to methamphetamine

Adrenergic Stimulant

Alpha agonist

Applied to nasal mucosa and eye for vasoconstriction (decongestion); rebound effect can ocur

contraindicated in glaucoma

Adrenergic Stimulants

Alpha 2 agonist

Applied to nasal mucosa and eye for vasoconstriction (decongestion); rebound effect can ocur

can cause hypotension in large quantitiy (systemic)

contraindicated in glaucoma

Adrenergic Stimulant

Used on eye for vasoconstriction (decreases redness)

contraindicated in glaucoma

Adrenergic Stimulant

Alpha 2 agonist

Clonidine effects

Inhibit NT release (presynaptic)

Decrease NE release and SNS activity

Overall Decrease in BP/ may decrease HR

Uses: HTN, addiction, alcoholism (decreased cravings) and withdrawal, hot flashed in menopause, pre-anesthetic medication.

Adrenergic Stimulant

Alpha 2 receptor

used in eye to decrease IO pressure through vasoconstriction and reduced aqueous humor

Adrenergic Stimulant

Alpha 2 receptor

used in eye to decrease IO pressure through vasoconstriction and reduced aqueous humor

Adrenergic Stimulant

Beta 2 agonist

Used to relax the uterus and suppress premature labor; given orally or IV

Side effects: tachycardia, tremor of skeletal muscle

Adrenergic Stimulant

Beta 2 agonist

bronchodilation; used for asthma treatment

Side effects: tachycardia, tremor of skeletal muscle

Adrenergic Stimulant

Beta 2 agonist

bronchodilation; used for asthma treatment

Side effects: tachycardia, tremor of skeletal muscle

Adrenergic Stimulant

Beta 2 agonist

Rarely used; Oral administration; bronchodilation; used for asthma treatment

Side effects: tachycardia, tremor of skeletal muscle

Adrenergic Stimulant

D1 receptor agonist/ B1 at high doses

Increases renal blood flow (vasodilation), increased GFR and Na excretion

given IV for cardiac shock, but not very effective, 

High dose: increases inotropic and chronotropic effect

Side effects: nausea, vomiting

Adrenergic Stimulant

D1 receptor agonist

Cuases dilation of vascular beds, decreasing BP

used short term to produce rapid decrease of BO in severe HTN

Adrenergic Stimulant

indirect acting-displaces NE (and DA), increasing their release from neurons, especially in CNS

Effects: alertness, decreased sleep need, decreased appetit, euphoria; has been used in enuresis, causes strong contraction of urinary bladder sphincter

Side effects: tachycardia, HTN, psychosis, dizziness, restlessness, tremor, irritability, fever, aggression

Adrenergic Stimulant; drug of abuse

indirect acting-displaces NE (and DA), increasing their release from neurons, especially in CNS

Effects: alertness, decreased sleep need, decreased appetit, euphoria

Adrenergic Stimulant

indirect acting-displaces NE (and DA), increasing their release from neurons, especially in CNS

Used for ADHD

Effects: alertness, decreased sleep need, decreased appetit, euphoria

Adrenergic Stimulant; drug of abuse, highly addictive

Inhibits re-uptake of DA and NE into nerve terminals

Effects: alertness, decreased sleep need, decreased appetit, euphoria

Side effects: HTN, stroke, arrhythmias, MI, psychosis

May be used for nasopharyngeal surgery to decrease blood flow and produce local anesthesia

Adrenergic Stimulant

increases catecholamine release from nerve terminals; forms octopamine (instead of NE)

usually hydrolyzed by monoamine oxidase (MAO) but if injected acts like NE

In pts with depression and on MAOIs may cause SEVERE HYPERTENSIVE CRISIS

Effects: alertness, decreased sleep need, decreased appetit, euphoria

PROTOTYPE, ALL ALPHA'S

Adrenergic Blocker

Competitive a1 and a2 antagonist

Decreased peripheral resistance, BP/Increased HR (Baro and increased NE from a2 block)

Uses: short term HTN crises (pheochromocytoma), HTN crisis on MAOI and ingested tyramine, HTN crisis from abrupt withdrawal of clonidine, local administration to prevent necrosis after alpha agonist injection (NE)

Other effects: Gastric stimulation, increased gastric acid, peptic ulcer exacerbation

Side effects: Tachyccardia, arrhythmias, MI, Hypotension

Adrenergic Blocker

ONLY NON-COMPETITIVE; Irreversible alpha (1 and 2) blockade

Increased NE (less uptake)

Uses: Pheocromocytoma to decrease SNS (3-6 weeks till tumor removal)

Adrenergic Blocker

Alpha 1 blocker

Decreased Peripheral Resistance and BP; No A2 block, no NE increase, less tachy.

Uses: HTN, BPH

Relaxes arterial AND venous smooth muscle (No HR increase), decreased SNS output

Decreases LDL and TAG, and increased HDL

Oral, half life of 3 hrs, INCREASES IN CHF, must decreased dose

SPECIAL NOTE: FIRST DOSE PHENOMENON, syncompe 30-90 min after 1st dose, keep them lying down first time.

Adrenergic Blocker

Alpha 1 selective

Decreased peripheral resistance and BP w/o Increased HR (no a2 block)

Uses: BPH

t1/2 12 hrs

Can decrease size of prostate by apoptosis

Side effect: first dose phenomenon

Adrenergic Blocker

Alpha 1 selective

Decreased peripheral resistance and BP w/o Increased HR (no a2 block)

Uses: BPH

t1/2 20 hrs

Can decrease size of prostate by apoptosis

Side effect: first dose phenomenon

Adrenergic Blocker

Alpha 1(1a and 1d>1b) specific

Increase urine flow with little effect on BP

Uses: BPH

T1/2 5-10 hrs

Alpha 1a is most prominent in prostate

Side effects: difficulty ejaculating.

Adrenergic Blocker

alpha 2 specific

Increases NE, increases BP, increase HR

Antagonises CLONIDINE!

Side effects: muscle tremor

Adrenergic Blocker

Alpha 1(1a and 1d>1b) specific

Increase urine flow with little effect on BP

Uses: BPH

T1/2 5-10 hrs

Alpha 1a is most prominent in prostate

Side effects: difficulty ejaculating.

Adrenergic Blocker

Alpha 1(1a and 1d>1b) specific

Increase urine flow with little effect on BP

Uses: BPH

T1/2 5-10 hrs

Alpha 1a is most prominent in prostate

Side effects: difficulty ejaculating.

Adrenergic Blocker

Non-selective Beta Blocker (B1 and B2)

Slows HR, AV conduction, Decreases force of contraction, renin release, lipolysis and glycogenolysis

Uses: HTN, post MI, angina, arrhythmias, CHF, prevent migrain, portal vein HTN, "stage fright"

Side Effects: BROCHOCONSTRICTION IN ASTHMATICS

Adrenergic Blocker

Non-specific Beta blocker

Used for Glaucoma (block of B2 decreases aqueous humor and pressure)

Adrenergic Blocker

Non-specific Beta blocker

has long half life and very long duration of action

PROTOTYPE

Adrenergic Blocker

Beta 1-selective

Mostly Heart Effect; decreases rate and force of contraction

Uses: HTN, MI, migraine prophylaxis

Adrenergic Blocker

Beta 1-selective

Mostly Heart Effect; decreases rate and force of contraction

Uses: HTN, MI, migraine prophylaxis

Adrenergic Blocker

Beta 1-selective

Mostly Heart Effect; decreases rate and force of contraction

Uses: HTN, MI, migraine prophylaxis

Adrenergic Blocker

B1-selective

Used for Glaucoma (for some reason)

Adrenergic Blocker

B1-selective (MOST SELECTIVE)

Heart Effect; decreases rate and force of contraction

ALSO CAUSES VASODILATION (NO mediated), lowers arterial pressure and aortic pressure

Adrenergic Blocker

B1-selective

Used in urgen situations where rapid effect is needed i.e. HF, bradycardia, hypotension

Very short duration (t1/2 = 8 min), must be IV, may infuse for as long as needed

Adrenergic Blocker

B-blocker with ISA (intrinsic sympathetic activity)

Non-specific Partial B-antagonist

Used for HTN and angina

Possibly less risk of bradycardia

Adrenergic Blocker

B0blocker with ISA (intrinsic sympathetic activity)

B1-selective

Used for HTN and angina

Possibly less risk of bradycardia

Adrenergic Blocker

B-blocker with ISA (intrinsic sympathetic activity)

Non-specific Partial B-antagonist

Used for HTN and angina

Possibly less risk of bradycardia

Adrenergic blocker

Alpha and Beta blocker combo

B1, B2 and a1 specific

Uses: HTN, CHF, post MI

Causes vasodilation, decreased BP (no tachy!)

Adrenergic Blocker

B1, B2 and A1 specific

decreased BP (a1), no baro reflex (B1 block), 

Used for HTN

Adrenergic Blocker

Inhibits NE release

Previously used for HTN, not used now as it causes complete loss of SNS i.e. postural hypotension, decreased blood flow to brain and heart, ejaculation problems and diarrhea

Adrenergic blocker

Interferes with uptake and storage of biogenic, causes depletion of NE, DA, SA in peripheral nerve and the brain

Low dose: decrease BP

side effect: diarrhea, depression, sedation Parkinson's like symptoms

Adrenergic Blocker

Blocks tyrosine hydroxylase which is the rate limiting step in DA synthesis; this leads to decreased NE and EPI

Used in presurgical treatment of pheochromocytoma w/ phenoxybenzamine; also in pts with inoperable phepchromocytoma

PROTOTYPE

NMJ and Ganglion Blocker

Non-depolarizing, Competitive antagonist

Reduces end plate potential so AP can't be generated, results in paralysis of the muscle

NMJ and ganglion blocker

Competitive antagonist of ACh

Can lower seizure threshold

Uses: surgery, ventilation, orthopedics (bone manipulation), intubation, convulsions

NMJ and ganglion blocker

Competitive antagonist of ACh

Can lower seizure threshold (Laudanosine biproduct of Hofmann elimination)

Uses: surgery, ventilation, orthopedics (bone manipulation), intubation, convulsions

NMJ and ganglion blocker

Used for intubation

Intermediate duration of action (20-35 min) and rapid onset (1-2 min)

NMJ and Ganglion blocker

Causes vagal blockade and tachycardia (ganglionic receptor blocks)

Uses: surgery, ventilation, orthopedics (bone manipulation), intubation, convulsions

NMJ and Ganglion blocker

Metabolized in the liver

intermediate duration (20-40 min) with onset of 2-4 min

Uses: surgery, ventilation, orthopedics (bone manipulation), intubation, convulsions

NMJ and Ganglion blocker 

ONLY DEPOLARIZING BLOCKER

Causes initial stimulation and contraction of muscle followed by NMJ block

Used for tracheotomy or intubation

Pts with extensive soft tissue damage, burns, nontraumatic rhabdomyolysis, spinal cord injures with paraplegia or quadriplegia, or muscular dystrophy should NOT receiv succinylcholine; contraindicated in children under 8

Ganglion Blocker

Nicotinic specific

Tertiary compound, enters brain and blocks nicotinic receptors

Causes mydriasis, orthostatic hypertension, tachycardia, urinary retention

BLOCK AUTONOMIC REFLEXES

Ganglion blocker

only approved for HTN emergency

being studied for tourette's, nicotine and cocaine addiction (desensitisation)