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Pharmacology > PNS Pharmacology > Flashcards

PNS Pharmacology Flashcards

1
Q

ANS Divisions

A

o Parasympathetic
• Preganglionic neurons arise in CNS → send axons out through spinal cord from the cranial and sacral spinal nerves
• Axons synapse in peripheral ganglia (close or within target organ)
• Postganglionic neurons arise within ganglia → send axons to synapse at end organs
• 1st neuron long; 2nd neuron short
• Discrete output
o Sympathetic
• Preganglionic neurons arise in CNS → send axons out through spinal cord from thoracic and lumbar spinal nerves
• Axons synapse in 3 prevertebral ganglia or in 22 pairs of paravertebral ganglia along the spinal cord
• Postganglionic neurons arise within ganglia → send axons to synapse at end organs
• 1st neuron short; 2nd neuron long
• Distributed output (systemic effects)

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2
Q

Basic neuron electrophysiology

A

o Resting electrical potential of about -70 mV (determined by K+ gradient)
o When neuron fires (reaches threshold potential) → wave of potential reversal travels along axon → synapse
o Electrical potential rises, becomes positive
• Caused by Na+ rushing into cell
• At AP peak: Na+ channels become inactivated, K+ channels open
o At synapse: voltage change causes voltage-sensitive Ca2+ channels to open
• Ca2+ flows in and initiates vesicular fusion
• Exocytosis via SNARE complex
• Release of NTs → can bind receptors on post-synaptic cell

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3
Q

Describe Cholinergic neurons

A

release acetylcholine:
o All motor neurons to skeletal muscle
o All preganglionic ANS neurons (first synapse in ANS is always cholinergic)
o All postganglionic parasympathetic neurons
o Some postganglionic sympathetic neurons
• Most sweat glands
• Some skeletal muscle blood vessels

o Acetylcholine metabolism
• Choline transported into neuron terminal with Na+ via CHT
• Choline + acetyl CoA (via ChAT: Choline-acetyl transferase) → acetylcholine
• Packaged into vesicle: exchanged for H+ via VAT
• Ca2+ dependent exocytosis
• In synapse (via AChE: Acetylcholine esterase) → degraded to choline + acetic acid

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4
Q

Describe adrenergic neurons

A

release norepinephrine, epinephrine, or dopamine (all are catecholamines):
o Most postganglionic sympathetic neurons release NE
o Adrenal medulla (a modified sympathetic ganglion) releases E and NE
o Some postganglionic neurons release DA

o Catecholamine metabolism:
• Tyrosine precursor → (via TH: tyrosine hydroxylase) DOPA → (via AAAD: aromatic amino acid decarboxylase) Dopamine
• Dopamine transported into vesicle via VMAT
• Dopamine→ (via DβH: dopamine β-hydroxylase) norepinephrine
• Released in synapse
• Can be recycled → autoreceptor
• Converted (adrenals) → (via PNMT: phenylethanolamine-N-methyltransferase) epinephrine
• Different dopamine metabolism:
• Via MAO: monoamine oxidase & ALDH: aldehyde dehydrogenase
• Via COMT: catechol-O-methyltransferase
• Forms HVA (Homovanillic acid)
o Common metabolite, excreted in urine
o Marker for dopamine
• Different NE and E metabolism:
• Via MAO, ALDH and COMT → vanillylmandelic acid (VMA)
o Common metabolite
o Excreted in urine

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5
Q

parasympathetic vs. sympathetic stimulation in physiology of major organs

A

Parasympathetic

Eye: Constriction
salivatry gland: Stimulates saliva flow
Heart: Slows HR
bronchi: Constricts
GI: Stimulates peristalsis and secretion
Liver:Stimulates bile release

Bladder: Contracts

**Sympathetic **

Dilates pupil
Inhibits flow salivary gland
Accelerates HR
Dilates bronchi
Inhibits GI tract
Conversion of glycogen to glucose in liver
Secretion of adrenaline and noradrenaline in adrenals
Inhibits contraction in bladder

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6
Q

Describe dual innervation with respect to the sympathetic and parasympathetic divisions of the autonomic nervous system

A

• Dual innervation
o Eye
o Heart
o Bronchial tree
o GI tract
o Salivary glands
o Urinary bladder
o Sex organs
• Single (sympathetic) innervation
o Blood vessels
o Spleen
o Piloerector muscles
o Sweat glands

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7
Q

Identify the major cholinergic and adrenergic receptors in the autonomic nervous system

A

• Cholinergic receptors responding to Ach
1) Muscarinic receptors
• G-protein coupled
• Respond to plant alkaloid muscarine
• Five subtypes (M1-M2)
2) Nicotinic receptors
• Ligand-gated ion channels
• Respond to plant alkaloid nicotine
• Two subtypes (Nm & NN)
• Adrenergic receptors responding to NE and E
1) α receptors: two subtypes (α1 and α2)
• Each subtype has 3 subtypes (α1A, α1B, α1D and α2A, α2B, α2C)
2) β receptors: three subtypes (β1 – β3)
• One type receptor responds to D: five subtypes (D1 – D5)

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8
Q

Explain the concept of predominant tone.

A
  • Vessels: sympathetic (adrenergic)
  • Sweat glands: sympathetic (cholinergic)
  • Heart, iris, ciliary muscle, GI tract, urinary bladder, salivary glands: parasympathetic (cholinergic)
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9
Q

M1 receptors

A

Tissue: autonomic ganglia

Response: depolarizes post-synaptic neurons (slow EPSP)

Mechanism: increase PLC –> Increase IP3, DAD, Ca2+

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10
Q

M2 receptors

A

Tissue: Heart

Response: decrease HR, decrease conduction velocity, decrease contractility

Mechanism: decrease AC –> decrease cAMP; increase K+ channel efflux, increase Ca2+ channel influx

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11
Q

M3 receptors

A

Tissue: Smooth muscle (eye, bronchioles, GI tract, UG system)

Response: contraction

Mechanism: increase PLCL –> increase IP3, DAG, Ca2+

Tissue: secretory glands

Response: increase secretion

Mechanism: increase PLCL –> increase IP3, DAG, Ca2+

Tissue: vascular endothelium

Response: dilation

Mechanism: Ca2+/CaM activates eNOS –> increases NO –> increases cGMP –> relaxation

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12
Q

N(m) receptors

A

Tissue: NMJ

Response: skeletal muscle contraction

Mechanism: opens Na+/K+ channels –> depolarization

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13
Q

N(N) receptors

A

Tissue: Autonomic ganglia

Response: depolarizes postsynaptic neurons

Tissue: adrenal medulla

Response: depolarizes medullary cells –> secretion of catecholamines

Mechanism (both): opens Na+/K+ channels –> depolarization

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14
Q

a1 receptor

A

Tissue: smooth muscle (eye, vascular, UG, hair follicles)

Response: contracts smooth muscle

Tissue: liver

Response: increase GNG and glycogenolysis

Mechanism (both): increase PLC –> increase IP3, DAG, Ca2+

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15
Q

a2 receptor

A

Tissue: axon terminals (autoreceptors)

Response: decrease NE release

Tissue: pancreatic B cells

Response: decrease insulin release

Tissue: vascular smooth muscle

Response: contract smooth muscle

Tissue: platelets

Response: aggregation

Mechanism (all): decrease AC –> decrease cAMP, increase K+ channel efflux, decrease L-and N-type Ca2+ channel influx, increase PLC –> increase IP3, DAG, Ca2+

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16
Q

B1 receptors

A

Tissue: heart

Response: increase HR, conduction velocity, contractility

Tissue: kidney (juxtaglomerular cells)

Response: increase renin release

Mechanism (both): increase AC –> increase cAMP –> increase PKA –> increase Ca2+ channel influx

17
Q

B2 receptors

A

Tissue: smooth muscle (eye, bronchioles, GI, UG, vascular)

Response: relax smooth muscle

Tissue: heart

Response: increase HR, contractility

Tissue: liver and skeletal muscle

Response: increase glycogenolysis, GNG in liver

Mechanism (all): increase AC –> increase cAMP; inhibits smooth muscle MLCK –> decrease myosin-PO4 –> relaxation

18
Q

B3 receptors

A

Tissue: lipocytes

Response: activates lipolysis

Mechanism: increase AC –> increase cAMP

19
Q

D1 receptors

A

Tissue: vascular smooth muscle, especially renal vasculature

Response: dilates blood vessels

Mechanism: increase AC –> increase cAMP

20
Q

D2 receptors

A

Tissue: axon terminals (autoreceptors); cholinergic neurons in gut

Response: decrease DA release; decrease GI motilit

Mechanism: decrease AC –> decrease cAMP; increase K+ efflux, decrease Ca2+ influx

21
Q

list the major cholinergic agonists

A

o Acetylcholine
o Bethanechol
o Carbachol
o Methacholine
o Nicotine
o Pilocarpine

22
Q

list the major Cholinesterase inhibitors

A

o Edrophonium
o Neostigmine
o Physostigmine
o Ecothiophate
o Pralidoxime

23
Q

Describe the mechanism of hydrolysis of acetylcholine by acetylcholinesterase

A

• Enzyme contains esteratic site and anionic site
o Anionic site: binds positively charges quaternary amine of acetylcholine
o Esteratic site: contains catalytic triad (serine, histidine, glutamate)
• Site where hydrolysis of ACh → choline and acetic acid:
• Serine oxygen attacks carbonyl; H stabilizes ester oxygen
• H2O attack frees acetic acid from enzyme

24
Q

List the major cholinesterase inhibitors

A
  • Edrophonium
  • Neostigmine
  • Physostigmine
  • Ecothiophate
  • Pralidoxime
25
Q

List the major muscarinic antagonists

A
  • Atropine
  • Ipratropium
  • Oxybutynin
  • Varenicline (partial agonist)
26
Q

List the ganglionic nicotinic antagonists.

A

• Mecamylamine

27
Q

List the major neuromuscular blockers

A
  • Atracurium
  • Cisatracurium
  • Mivacurium
  • Pancuronium
  • Rocuronium
  • Succinylcholine
  • D-Tubocurarine
  • Vecuronium
28
Q

ANS in the eye

A

pupil diameter

  • iris circular motion
    • M3 activation –> muscle contraction –> miosis
    • B2 activation –>muscle relaxation –> mydriasis
  • iris radial muscle
    • a1 activation –> muscle contraction –> mydriasis

Lens shape

  • ciliary smooth muscle
    • M3 activation –> muscle contraction –> relaxes ligament –> accomodation for near vision
    • B2 activation –> muscle relaxation –> stretches ligament (slight effect)

Secretion

  • Lacrimal glands
    • M3 activation –> lacrimation
29
Q

ANS in lungs

A

Bronchial smooth muscle

  • M3 activation –> muscle contraction –> bronchoconstriction
  • B2 activation –> muscle relaxation –> bronchodilation

Bronchial glands

  • M3 activation –> mucous secretion
  • B2 actiavation –> watery secretion via CFTR activation
30
Q

ANS in heart

A
  • M2 activation –> bradycardia (SA node), decrease AV node conductivity, decrease atrial contractility
  • B1 and B2 activation –> tachycardia (SA node), increase AV node automaticity and conductivity, increase His-Purkinje automaticity and conductivity, increase ventricular automaticity and contractility
31
Q

ANS in vascular system

A
  • M3 activation (endothelial cells) –> relaxation –> decrease BP
  • a1 and a2 activation –> constriction –> increase BP
  • B2 activation (liver and skeletal muscles) –> relaxation –> decrease TPR –> increase blood flow to these tissues
  • D1 activation –> dilation of renal arteries and arterioles –> increase renal blood flow
32
Q

ANS in GI tract

A

intestine

  • M3 activation –> contraction of circular and longitudinal muscles in intestinal walls –> increase motility
  • a1 and B1 activation –> relaxation –> decrease motility
  • in Gi smooth muscle, hyperpolarization and relaxation is from activation of Ca2+-dependent K+ efflux channels

GI sphincters

  • M3 activation –> relaxation
  • a1 activation –> contraction

GI secretions

  • M3 activation –> increase acid secretion from parietal cells, increase secretions from gastric and intestinal glands, contraction of gall bladder
  • B2 activation–> decrease gastric acid secretion, relax gall bladder, increase amylase secretion
33
Q

ANS on kidney and bladder

A
  • D1 activation –> vasodilation –> increase blood flow, GFR
  • B1 activation –> stimulates renin release from kidney
  • M3 activation –> contraction of bladder detrusor, relaxation of trigone and sphincter –> promotes urination
  • B2 activation –> relaxes detrusor –> urinary retention
  • a1 activation –> constricts trigone and sphinctor –> urinary retention
34
Q

ANS on penis

A
  • M3 activation –> relaxation of vessels –> erection
  • a1 activation –> contraction of seminal vesicles, prostatic capsule, vas deferens –> ejaculation
35
Q

ANS in uterus

A
  • Nonpregnant: B2 activation –> relaxes uterus
  • Pregnant:
    • M3 activation –> contracts uterus
    • a1 activation –> contracts uterus
    • B2 activation –> relaxes uterus
36
Q

ANS influences on secretions

A
  • M3 activation –> stimulates secretions form salivary, nasopharyngeal, pulmonary, GI, and eccrine sweat glands
  • a1 activation –> stimulates secretions from apocrine sweat glands in axillary and pubic regions; produces viscous salivary secretions
37
Q

ANS influences on Metabolism

A
  • a2 activation –> decrease insulin release from pancreatic B cells
  • B2 activation –> promotes glycogenolysis and GNG in liver, glycogenolysis and K+ uptake in skeletal muscle, increase insulin release from pancreatic B cells (slight)
  • 3 activation –> stimulates lipolysis in adipocytes
38
Q

Describe the difference between depolarizing and nondepolarizing neuromuscular blockers

A

• Nondepolarizing NMBs:
o Competitive antagonists of NMJ nAChR
o Two structurally different classes:
1) Benzylisoquinolines (Tubocurarine)
2) Steroids (Pancuronium, Rocuronium, Vercuronium)
o All are rigid and bulky structures
o Have a permanently positive quaternary N atom
• Depolarizing NMB
o Agonists of the NMJ nAChR
o Depolarize skeletal muscle membrane
o Initially trigger muscle contraction, but disorganized (fasciculations)
o Depolarization is prolonged
• Not hydrolyzed by AChE
o Prolonged depolarization inactivates voltage-gated Na+ channels in muscle

39
Q

Reversal of NM blockade

A

• Competitive antagonism: overcome with excess agonist (ACh)
• Inhibiting AChE at NMJ increases concentration of Ach in synaptic cleft
• Commonly used (add anti-cholinergic to prevent side-effects):
o Neostigmine + glycopyrrolate
o Edrophonium + atropine
• Think about:
–> How complete is the NM blockade?
• Spontaneous recovery vs. reversal
• Muscle strength may appear adequate even when up to 75% nAChR still occupied by NMB
• Too much NMB will not be reversible → important to titrate NMB to effect, plan for reversal
–> Will your reversal outlast the NMB?
• Neostigmine: covalent bond, longer duration
• Edrophonium: competitive, shorter duration

Pharmacology (6 decks)

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