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101 Cards in this Set

  • Front
  • Back
Uninnervated receptors
muscarinic on vascular endothelium
A receptor that binds one of the catecholamine neurotransmitters (norepi, epi, dopamine)
Homeostatic reflex
A compensatory mechanism for maintaining a body function at a predetermined level. eg. baroreceptor reflex
Primary PBT nerve receptor for dopamine
Located in the kidney, sympathetic D1 receptor
Rate-limiting step in ACH synthesis
Transport of choline into the nerve terminal
Choline transport inhibitor
Name of transporter responsible for packing ACH into small dense vesicles? Inhibition?
The VAT H+ antiporter, inhibited by the research drug vesamicol.
Cholinergic VAT inhibitor
Vesicle-associated proteins that respond to influx of Ca at nerve terminal?
Synaptobrevin, synaptotagmin
Nerve-ending membrane associated proteins that release vesicular contents?
SNAP25, syntaxin, etc.
Effect of botulinum toxin
Prevent neurotransmitter release via altering synaptobrevin and other docking/fusion proteins in cholinergic neurons
Effect of dopamine on renal smooth muscle
Vasodilation. Important treatment in shock that results in oliguria.
Rate limiting step in catecholamine synthesis
Conversion of Tyrosine to L-DOPA via tyrosine hydroxylase
Inhibitor of tyrosine hydroxylase
Role of MAO in adrenergic nerve endings
Inactivates a small portion of newly synthesized catecholamine neurotransmitters, resulting in less stored.
Inhibition of adrenergic vesicular transport?
Inhibition of adrenergic docking/fusion proteins?
Inhibition of catecholamine reuptake?
Cocaine and tricyclic antidepressants
Does metabolism stop the effect of adrenergic neurotransmitters?
No, only reuptake does.
Metabolism of catecholamines outside the synaptic cleft?
How many subtypes of muscarinic receptors are there?
5, only 3 are truly important in peripheral autonomic transmission
How many subtypes of nicotinic receptors are there?
2, M and N referring to muscular and neuronic, respectively.
M1 receptors: location/mechanism/function
Nerve endings/Gq/IP3 and DAG cascade
M2 receptors: location/mechanism/function
Heart/Gi/decrease cAMP and open potassium channels
M3 receptors: location/mechanism/function
Smooth, glands, endo/Gq/IP3 and DAG cascade
Major function of nicotinic receptors
depolarization and activation of the action potential
Which system dominates the pupil and the SA node? Therefore, what will happen if you remove all autonomic input?
Mydriasis and tachycardia
alpha-1 receptors: location/mechanism/function
Smooth, glands/Gq/contraction and secretion
alpha-2 receptors: location/mechanism/function
Nerve endings, smooth/Gi/contraction, decrease of neurotransmitter release
Beta-1 receptors: location/mechanism/function
Cardiac muscle, juxtaglomerular/Gs/increase heart rate, increase contractile force, increase renin release
Beta-2 receptors: location/mechanism/function
Smooth, liver, heart/Gs/relax smooth muscle, increase glycogenolysis, increase heart rate, force
Beta-3 receptors: location/mechanism/function
Adipose tissue/Gs/increase lipolysis
Effect of dopamine on renal smooth muscle?
Relaxation via Gs receptor
Feedback of norepi on itself? How?
Negative, prohibitory. Alpha-2 receptors on the pre-synaptic nerve membrane (I said pre-synaptic, not pre-ganglionic)
Sym effects on eye
Contraction of radial muscle: distance accomodation/mydriasis, alpha-1 receptor. Relaxation via non-select B receptor.
Parasym effects on eye
Contraction of circular muscle: miosis, near accomodation, M3 receptor. Contraction of ciliary muscle, M3 receptor.
Sym effects on heart
SA: Increase, B1B2
Ectopic pacemaker: Increase, B1B2
Contractility: Increase. B1B2
Parasym effects on heart
SA: Decrease, M2
Contractility: Atrial decrease, M2
Is there parasympathetic innervation to the blood vessels?
Sym effects on vasculature
Skin: contract, A
Skeletal: ?? relax, B2
contract, A
Sym effects on bronchiolar smooth?
Relax via B2
Parasym effects on bronchiolar smooth?
Contract via M3
Sym effects on GI?
Inhibition of secretion via A2. Sphincter contraction via A1. Relaxation of walls via parasym override on A2 and B2
Parasym effects on GI? (digest)
Wall contraction, sphincter relaxation, increased secretion via M3. M1 receptors in Meissner's plexuses are activated.
Sym effects on GU?
Bladder relax via B2. Sphincter contraction via A1. Pregnant uterus relaxes via B2 or contracts via A. Ejaculation via A.
Parasym effects on GU?
Bladder contracts, Sphincter opens, uterine contractions all via M3. Erection via M.
Is there parasympathetic innervation to the skin?
Sym effects on skin
Pilomotor contraction via A. Thermoregulatory sweat via M. Stress sweat via A.
Sym effects on metabolism
Gluconeogenesis/glycolysis via B2, A. Lipolysis via B3. Renin release via B1.
Local anaesthetic effects on nerves
Bind to axons, block Na and conduction
Effect of amphetamine family on adrenergic nerve terminals?
Promote transmitter release
Effect of black widow spider bite on transmitter release? (YIKES)
Explosive release
Effect of 6-hydroxydopamine on transmitter uptake?
Destroys synaptic terminals
Alpha receptor agonist
Alpha receptor antagonist
Beta receptor agonist
Beta receptor antagonist
Nicotinic receptor agonist
Nm receptor antagonist
Muscarinic receptor agonist
Muscarinic receptor antagonist
Effect of neostigmine on acetylcholinesterase
Inhibition, prolongs ACH action and intensity.
Effect of tranylcypromine on MAO
Inhibition, increases stored catecholamine neurotransmitters
What is metanephrine?
A metabolite of epinephrine created by COMT. A high presence in plasma indicates a pheochromocytoma, or adrenal tumor.
Do sympathetic neurotransmitters block the release of parasym neurotransmitters? Vice versa?
Yes. Yes. This is heteroreceptor mediated feedback.
Vasodilator. Used in the treatment of hypertension.
Homeostatic effect of baroreceptors
Modulation of heart rate (brady/tachycardia)
Homeostatic effect of renin-angiotensin system?
Regulation of salt-water retention/release. And that's probably the worst oversimplification I've ever been guilty of.
Outline of cholinomimetic drugs (drugs that either mimic cholinergic ligands or stop the destruction of cholinergic ligands)
1. Direct
a. Muscarinic
i. Choline esters
ii. Alkaloids
b. Nicotinic
2. Indirect
a. Edrophonium (short)
b. Carbamates (medium)
c. Organophosphates (long)
Prototype for a direct-acting cholinomimetic? Indirect?
ACH. Neostigmine.
Characteristic choline esters
ACh, Methacholine, Carbachol, Bethanechol.
Characteristic alkaloids
Muscarine, pilocarpine, nicotine, lobeline
Why is an indirect-cholinomimetic called that?
Because it inhibits acetylcholinesterase, thus potentiating ACh effects indirectly.
Organophosphate aging
After organophosphate binding to (and inhibition of) cholinesterase, the compond will age, becoming more covalent and harder to displace
Where are botulinum receptors for endocytosis located?
On the membrane of cholinergic neurons, but not adrenergic
Which muscarinic receptors use Gq?
M1 and M3
Which muscarinic receptor uses Gi?
M2, downregulating cAMP via the alpha subunit, while opening K channels via the beta-gamma subunit
Pharmacokinetics of bethanechol and carbachol
Muscarinic agonist, acts for 30min-2hr. Carbachol is identical but it also works on nicotinic receptors.
Can edrophonium or neostigmine cross the BBB?
No, they have quaternary ammonium groups, rendering them totally lipid insoluble
What is the problem with using physostigmine as a treatment for myasthenia gravis (block ACHesterase)
It is lipid soluble, able to cross the BBB, and causes unpleasant, frequent CNS side effects.
The most dangerous organophosphate
What happens when you inject someone with muscarinic cholinomimetics?
Relaxation of blood vessels, BUT, resultant drop in blood pressure activates sympathetic discharge to heart via baroreceptors, results in tachycardia (not expected response) If there was a true parasym discharge to the heart, the result would be bradycardia. Additionally, the thermoregulatory sweat glands (muscarinic receptors!) will activate.
Effect of nicotinic drugs on vasculature (Blood vessels are dominated by sympathetic control)
Vasoconstriction due to stimulation of nicotinic receptors at ganglionic synapse (remember both parasym and sym have nicotinic receptors at ganglion)
Effect of nicotinic drugs on gut (GI is dominated by parasym control)
Motility and secretion increase due to parasym nerve endings firing. (remember both parasym and sym have nicotinic receptors at ganglion)
Effects of cholinomimetics on the bronchi?
Do we use nicotinic agonists clinically?
No, they are way too non-specific
Use of bethanechol
Postop/neurogen intestinal or urinary retention to activate bowel movement and voiding
Use of pilocarpine
Topical treatment of glaucoma and stimulation of salivation
Use of neostigmine (indirect-acting cholinomimetics in general)
Treatment of myasthenia gravis, antidote to neuromuscular blocks
Use of topical physostigmine
Treatment of glaucoma
Use of malathion (organophosphate)
Kill scabies, lice, etc.
Use of metrifonate (organophosphate)
Kill helminths
Use of edrophonium
Rapid treatment of depolarizing neuromuscular blockade, differential of myasthenia verses cholinergic crisis--it will strengthen myasthenia patients and weaken those suffering from cholinergic crisis
Use of succinylcholine
Paralysis via nondepolarizing neuromuscular block, because it cannot be degraded by acetylcholinesterase
Outline of Anticholinergic Drugs
1. Antimuscarinic
a. M1-selective
b. non-selective
2. Antinicotinic
a. ganglion blockers
b. Neuromuscular blockers
Requirement for eye/CNS muscarinic blockers
Lipid solubility
Prototype of nonselective muscarinic blocker. Characteristics?
Atropine. Alkaloid, tertiary amine, good lipid solubility, 2hr half life
Atropine fever/flush
Sweating caused by muscarinic inhibition, cutaneous vasodilation
Paralysis of accomodation
Depolarizing blockage vs. nondepolarizing blockade
Skeletal paralysis caused by persistent depolarization of end plate vs. blockade of the nicotinic endplate receptor
Are muscarinic blocking agents competitive or irreversible antagonists?