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Physiology > ANS drugs and receptors and shit > Flashcards

ANS drugs and receptors and shit Flashcards

1
Q

Neostigmine

A
  • Reversible Anticholinesterase
  • Carbamic acid derivative
  • used to treat Myasthenia gravis, reversal of neuromuscular blockers
  • longer half-life
  • parasympathomimetic
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2
Q

Malathion

A
  • Irreversible Anticholinesterase
  • toxic, used in pesticides
  • organophosphate
  • increased Ach stimulates receptors causing muscle paralysis and death
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3
Q

Botulinum Toxin

A
  • Botox
  • Prevent release of Ach by degrading synaptobrevin (SNARE) which inhibits exocytosis
  • Used in cases with increased muscle tone, focal dystonia, diagnose Lambert-Eaton Syndrome
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4
Q

Edrophonium

A
  • Reversible Anticholinesterase
  • short duration
  • useful for diagnosing myasthenia gravis and Lambert-eaton
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5
Q

Pyridostigmine

A
  • Reversible Anticholinesterase

* even longer half-life

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6
Q

Physostigmine

A
  • Reversible Anticholinesterase
  • Carbamic acid derivative
  • used to treat Myasthenia gravis, reversal of neuromuscular blockers
  • longer half-life
  • parasympathomimetic
  • lipophilic, can cross the Blood Brain barrier-used to treat Atropine poisoning
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7
Q

Reversible Anticholinesterases

A

•Neostigmine, Physostigmine, Pyridostigmine, Edrophonium
•Parasympathomimetic (increases parasympathetic tone)
-decrease intraocular pressure (from glaucoma) by increasing outflow of aqueous humor
-increase smooth muscle motility of GI tract
-reversal of anti-cholinergic poisoning (atropine)
•increase central cholinergic neurotransmission in dementia-improves cognitive symptoms in dementia and alzheimer’s; titration phase; delay symptoms by 6 mo
•reverse paralysis from non-depolarizing neuromuscular blockers (overcome competitive antagonists)
•excessive muscarinic stimulation (salivation, lacrimation, miosis, diarrhea, bradycardia)
•excessive nicotinic stimulation (muscle weakness and paralysis; nerve gasses)

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8
Q

Succinylcholine

A
  • Neuromuscular Nicotinic agonist
  • desensitizes receptor leading to muscle paralysis (depolarizing neuromuscular blocker)
  • short t1/2
  • used in intubations (and other short procedures)
  • side effects: bradycardia, K+ release from prolonged depolarisation, prolonged paralysis; malignant hyperthermia
  • Increasing Ach would exacerbate effects (i.e.: an AchE inhibitor)
  • metabolized by pseudocolinesterase
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9
Q

Pancuronium

A
  • Neuromuscular Nicotinic Antagonist
  • Competitive antagonist (non-depolarizing Nm blocker)
  • Long acting
  • Uses: induce flacid paralysis for surgery*, induce anesthesia, intubation, using a ventilator
  • effects overcome with AchE inhibitor (neostigmine)
  • more selective for Nm than Nn
  • Side effects: hypertension, apnea, broncospasm, salivation, flushing, and respiratory failure
  • metabolized by liver)
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10
Q

Acetylcholine

A
  • Muscarinic Agonist (& nicotinic too right?)
  • endogenous agonist
  • not used clinically-very short t1/2
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11
Q

Pilocarpine

A
  • Muscarinic Agonist
  • alkaloid to muscarine
  • until recently only drug in this class
  • treat glaucoma–>constrictor pupillae–>miosis–>drain aquous humor and dec intraocular pressure
  • treat dry mouth in sjogrens syndrome
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12
Q

Methacholine

A
  • Muscarinic Agonist
  • resistant to hydrolysis by AChE
  • little affinity for Nicotinic receptors
  • Used in diagnosis of asthma–>M3 receptors on glands in airway–>asthmatics are more sensitive and respond to lower dose than normal people
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13
Q

Bethanechol

A
  • Muscarinic Agonist
  • almost completely selective for muscarinic receptors
  • agent of choice for promoting GI and UT motility; assists in bladder emptying (M3 receptors)
  • used post-operative, postpartum, and with drug related urine retention
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14
Q

Muscarinic Agonists

A
  • Acetylcholine, Methacholine, Pilocarpine, Bethancechol
  • causes contraction of constrictor pupillae–>miosis–>increases outflow of aqueous humor–>dec intraocular pressure–>benefit glaucoma
  • contraction of GIT, Bladder, adn urinary tract smooth muscle–>inc motility–>restore GI & UT motility after anesthesia/surgery
  • increase salivation–>benefit xerstomia (dry mouth)
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15
Q

Atropine & other related drugs

A
  • Muscarinic Antagonist
  • plant alkaloid from Atropa belladonna (nightshade)
  • Pupil dialation, Tachycardia, decrease secretions (salivary, bronchial, GIT)
  • sympathetic response (parasympatholytic) by antagonizing parasympathetic

Clinical Uses:

  1. produce mydriasis for ophthalmological exam (topical)
  2. reverse sinus bradycardia (from excessive vagal tone)
  3. inhibit excessive salivation and muscus during anaesthesia and surgery
  4. couteract muscarine poisioning and poisioning with anticholinesterases
  5. reduce GIT motility and tone (antispasmodic in diarrhea); bladder motility; sweating

Reduces SLUDGE (salivation, lacrimation, urination, diaphoresis, GIT motility, Emesis)

Other M antagonists used for: nausea and motion sickness, intestinal cramp, depressant and adjunct to narcotics, treat peptic ulcers, reduce bronchial secretions in COPD, asthma when bronchoconstriction caused by inc cholinergic tone

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16
Q

Amphetamine

A

•inhibits Catecholamine storage (displaces endogenous Catecholamine from storage vesicles, main effect)

  • blocks NET
  • weak MAO inhibitor

(not sure if those last two apply to amphetamine or are referring to the whole class of drugs)

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17
Q

Pseudoephedrine & Ephedrine

A
  • Inhibits Catecholamine storage (sudafed)

* increase NE activity at post synaptic α and β receptors (she is rather vague about this)

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18
Q

Catecholamine storage inhibitors

A

Amphetamine, Pseudoephedrine (and ephedrine)

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19
Q

Imipramine

A
  • Inhibits Catecholamine (NE) reuptake
  • inhibits NET
  • (does a lot of other shit too)
  • used to treat mild depression
  • side effects (postural hypotension and tachycardia)
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20
Q

Cocaine

A
  • Inhibits Catecholamine (NE) reuptake

* inhibits NE transporter (NET)

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21
Q

Iproniazid

A

Inibits Catecholamine metabolism

  • irreversable, nonselective MAO inhibitor (MAOI)
  • discontinued in all of the world except France
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22
Q

Epinephrine

A
  • α and β agonist
  • higher affinity for β2, predominant β effect
  • some effect on α1 at high [ ]
  • high doeses effective for treating anaphylaxis; used for vasoconstriction in conjuction with local anaesthetic
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23
Q

Norepinephrine

A
  • α and β agonist
  • high affinity for α1 and β1
  • low affinity for β2
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24
Q

Oxymetazoline

A
  • full α1(vasoconstrict) and partial α2 (limit NE release, some vasoconstriction) agonist
  • topical/nasal decongestant (vicks, sudafed, afrin, dristan)
  • treats ocular hyperemia (eye redness-Visine)
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25
Q

α and β agonists

A

Epinephrine and Norepinephrine
•E and NE almost same affinity at α1 (E slightly more) but overall receptor is much less sensitive than β receptors & NE is high at synapse, but low from adrenal medulla
•Also equipotent at β1 (but is also a more sensitive receptor than α1); NE high at synapse, E higher from adrenal medulla
•β2 more selective for E

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26
Q

Inhibitors of Catecholamine reuptake

A

Cocaine, Imipramine

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27
Q

Phenylephrine

A
  • α1 agonist
  • constriction/SM contraction
  • Nasal decongestant; treatment of shock
  • side effect: Hypertension
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28
Q

Clonidine

A
  • α2 agonist
  • reduces NE release by stimulating α2’s on presynaptic neuron
  • treatment for hypertension and opoid withdrawal
  • side effects: Bradycardia & hypotension
29
Q

Phenoxybenzamine

A
  • α1 and α2 antagonist
  • non-selective
  • non-competitive
  • irreversable
  • manage hypertension d/t pheochromocytoma
30
Q

Phentolamine

A
  • α2 and α1 antagonist
  • reversible/competitive antagonist
  • manage hypertension d/t pheochromocytoma
31
Q

α1 and α2 Antagonists

A
  • Phenoxybenzamine and Phentolamine
  • prevent vasoconstriction; dec BP
  • Both used to manage hypertension d/t pheochromocytoma
32
Q

Prazosin

A
  • α1 antagonist
  • prevents Vasoconstriction
  • treatment for Hypertension and BPH (urinary hesitancy)
  • side effect: postural orthostatic/hypotension related to 1st dose phenomena
33
Q

Tamsulosin

A
  • α1 antagonist
  • treatment for urinary hesitancy in BPH
  • more selective for genitourinary smooth muscle receptor subtype (α1A)
  • Less postural/orthostatic hypotension
34
Q

α1 Antagonists

A
  • Prazosin and Tamsulosin

* prevent vasoconstriction, promote micturition

35
Q

Dobutamine

A
  • β1 Agonist
  • prominent ionotropic effect–>inc contractility and CO but not HR (minimal Δ)– no Δ in peripheral resistance
  • Short t1/2 (COMT metabolism)
  • acute management of heart failure (there is more than just β1 activity)
36
Q

Albuterol

A
  • β2 Agonist
  • treatment of asthma–>avoids cardiac (β1) and skeletal (β2) effects (d/t route of administration)
  • rapid acting (15 min), short duration (4-6 hr)
  • ‘asthma reliever’
37
Q

Propranolol

A
  • Non-selective β blocker (antagonist)
  • treat hypertension and angina
  • side effects: more severe (than atenolol) sedation, bronchoconstriction and dyspnea
38
Q

Pindolol

A
  • non-selective partial β agonist
  • still a β blocker
  • treatment of Htn in pts with bradycardia or low cardiac reserve
  • Useful for Pts with diabetes (doesn’t affect carbohydrate metabolism as much)
39
Q

Atenolol

A
  • Selective β1 blocker (full antagonist)
  • dec HR and contractility, reduce renin secretion–>reduce blood volume, fluid overload and vasomotor tone
  • treats hypertension and angina, reduce blood volume
  • side effects: sedation and dyspnea
40
Q

SNS innervaton only:

A
  • Vascular smooth muscle
  • Sweat glands
  • Piloerector muscles
  • Liver
  • Adipose (via circulating E and NE from adrenal medulla?)
  • Kidney
41
Q

Myasthenia Gravis

A
  • autoimmune against Nicotinic Ach receptors @ NMJ
  • diagnose with Edrophonium
  • can treat with neostigmine and physostigmine
42
Q

Lambert-Eaton

A
  • autoimmunie agains presynaptic Ca2+ channels
  • Treat with carbamic acid derivative anticolinesterases: Neostigmine and Phyystostigmine
  • Diagnosed with Botox or Edrophonium
43
Q

PSNS innervation only:

A

Gastric/pancreatic secretions

Lacrimal Glands

44
Q

Hexamethonium

A

Nicotinic receptor antagonist, specific for post-ganglion neuron receptor (N2)

45
Q

SNS and PSNS preganglionic NT and receptor? Somatic?

A

ANS and Somatic: Ach, Nicotinic (slight differences between skeletal muscle-N1/m and nerve-N2/n nicotinics)

46
Q

SNS post gang NT and receptors

A
  • most tissues: NE and α and β, 1 and 2
  • vascular smooth muscle within skeletal smooth muscle and sweat glands: Ach, Muscarinic
  • renal vascular SM: Dopamine, D1 receptor
47
Q

PSNS post gang NT and receptors

A

Ach, muscarinic

48
Q

Adrenal medulla details

A
  • Modified postganglionic sympathetic–>chromaffin cells (neuroendocrine)
  • Pregang: Ach and N receptor, secretes 80% epi and 20% NE
  • Epi is more potent at interacting with skeletal muscle than NE
  • affects adipose and RBCs that otherwise don’t have SNS innervation
49
Q

Speed of neurotransmission

A
  • Nicotinic-fast excitatory (EPSP)
  • M2/neuromodulator-Slow inhibitory (IPSP)
  • M1-slow excitatory (EPSP)
  • peptide-late slow excitatory (EPSP)
50
Q

Myelination of ANS?

A

•only preganglionic neurons of SNS and PSNS are lightly myelinated

51
Q

Muscarinic receptors

A
  • M1, M3, M5-mediated by Gq—>increased PLC, [Ca2+], MAP kinases, down M current; excitatory
  • M2, M4-mediated by Gi–>down adenylyl cyclase, up MAP kinases, up GIRK channels, down Voltage-gated Ca2+ channels; inhibitory
52
Q

Nicotinic receptors

A
  • 5 subunit ionotropic receptors (ligand gated channel)
  • 2 Ach to open, bind to α subunits
  • CNS and Ganglionic receptors (N2/Nn)
  • NMJ (N1/Nm)
  • binding and dissociation kinetics are rapid
  • shows desensitization to high levels/porlonged activation of ACh
  • equally permeable to Na+ and K+; more Na+ enters thank K+ leaves
53
Q

effects of α1

A

SNS

  • mediated by Gq (increase IP3/DAG/Ca2+/PKC)
  • vasoconstriction of peripheral vessels, pupil dilation, ejaculation
  • Ca2+ activates myosin light chain kinase (MLCK) (phosphorylatesd myosin) which leads to contraction
  • present on vascular smooth muscle (skin and splanchnic) (increase total peripheral resistance), radial muscle of iris contraction, genitourinary smooth muscle
  • GIT sphincters–>contraction
  • vas deferns–>contract–>ejac
  • trigone of bladder–>contration while filling bladder
54
Q

Termination of NE signalling

A
  • uptake into presynaptic neuron-uses NET (active transport), recycled or deaminated by MAO
  • uptake into postsynaptic cell-broken down by MAO and COMT
55
Q

VMAT

A

vesicular mono amine transporter–>dopamine/H+ antiporter that transports dopamine into vesicles containing Dopamine β-hydroxylatse

(H+ gradient established by H-ATPase in vesicle)

56
Q

effects of α2

A

SNS

  • mediated by Gi (inhibits adenlyl cyclase, inhibitory)
  • presynaptic–> -ve feedback, close neuronal Ca2+ channels, decrease NE release
  • GI tract–>wall relaxation
  • β cells of pancreas–>decrease insulin relase
57
Q

effects β1 receptors

A

SNS

  • mediated by Gs (inc adenylate cyclase, cAMP, PKs, phosphorylation of cellular proteins including ion channels e.g. L-type Ca channels in heart)
  • SA node–>inc excitable, inc heart rate (+ chronotropic)
  • AV node, myocardium–>inc contractablity (+ inotropic)
  • Juxtaglomerular cells–>inc renin release (up angiotensin–>up aldosterone and vasoconstriction–>up blood volume)
  • Adipose–>inc lipolysis
  • salivary glands–>inc secretion
58
Q

ANS in micturition

A

Filling: SNS mediated (NE)–>destrusor has β2 receptors (relaxed); Trigone has α1 receptors–>contracted

Releasing: PSNS mediated (Ach)–>destrusor has M3 receptors (contraction); trigone receptors unclear (M2or4 maybe or neuropeptide mediated) (relaxes)

59
Q

M2 receptor

A

PSNS

  • mediated by Gi–>dec cAMP–>open K+ channels
  • SA node-dec excitablity
  • AV node-dec conduction velocity
  • myocardial muscle-decrease force (atria only)
  • overall dec Hr
60
Q

Effects of β3 receptors

A

is on adipose, mediated by Gs, ups PKA,and probs lipolysis

61
Q

Effects of β2 receptors

A

SNS

  • mediated by Gs (inc adenylate cyclase, cAMP, PKA–|MLCK–>SM relaxation, inc glycogenolysis, gluconeogenesis
  • Destrusor–>SM relaxation for bladder filling
  • GI tract–>relaxation of SM walls
  • Ciliary muscle–>relaxation–>pupil dialation
  • Uterus–>relaxation
  • Bronchial smooth muscle–>relax–>bronchodialation
  • adipose–>lipolysis, minor
  • intramuscular vascular smooth muscle–>dialation
62
Q

M1 receptor

A
  • Gq mediated (excitatory)
  • CNS autonomic ganglia
  • exocrine glands
  • parietal cells
  • intramuscular vascular smooth muscle–>constriction
63
Q

M3 receptor

A
  • mediated by Gq (exitatory)
  • mostly nonvascular smooth muscle contraction
  • GI gland secr
  • Bronchial Secr
  • Salivation
  • Sweat (SNS)
  • Circular muscle of eye->contraction->pupil constriction/miosis
  • ciliary muscle->contraction->accommodation
  • Nasal glands
  • Lacrimal gland
  • Bronchial smooth muscle–>bronchoconstriction
  • destrusor->contraction->micturition
  • vasodialation in male erection (M3 turns on NO synthase, NO diffuses to neighboring cell, turning on guanyl cyclase that leads to smooth muscle relaxation, NO also opens Ca2+ dependent K channel that hyperpolarizes cell, sildenafil inhibits cGMP phosphodiesterase)
  • GIT wall–>increase motility and tone
64
Q

M4

A
  • mediated by Gi

- in CNS

65
Q

M5

A
  • mediated by Gq

- in CNS

66
Q

PSNS to trigone and GIT sphincters

A

may be mediated by neuropeptieds, maybe some M receptor, lecture is unclear (and perhaps science)

67
Q

Predominant effect of NE and E on vascular smooth muscle

A
  • vasoconstricing–>inc BP

- α1 mostly causes constriction in arteries and veins, β2 can cause some dialation during excersise

68
Q

Nonselective β agonists

A
  • β1-inc HR, force of Contraction, and output
  • β2-relaxion/vasodilation
  • isoproternol used for emergency arrhythmia and bronchospasm (side effects: htn, palpitations, tremor); don’t have to know
69
Q

Nonselective β and α1 antagonist

A
  • used in chronic heart failure
  • β1–>reduce HR, reduce renin and then blood volume
  • α1–>vasodialation

(Carvediol)

Physiology (1 decks)

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