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Pharmacology 3001 > ANS > Flashcards

ANS Flashcards

1
Q

Somatic NS

A
  • voluntary
  • conscious body functions
    ex: posture, locomotion
  • no pre/post ganglionic fibres
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2
Q

Autonomic NS

A
  • involuntary
  • unconscious body functions
  • pre + post ganglion fibres

divided into parasymp and sympathetic NS

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3
Q

Parasympathetic NS

A
  • cranio-sacral
  • rest and digest

Cholinergic –> (Nicotinic receptors) –> Cholinergic –> (M receptors)

increases SLUDGE response

  • salivation
  • lacrimation
  • urination
  • diaphoresis/sweating
  • GI motility
  • emesis/vomitting
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4
Q

Sympathetic NS

A
  • thoraco-lumbar
  • fight or flight

Cholinergic –> (Nicotinic receptors) –> Adrenergic fibres –> A and B adrenergic receptors

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5
Q

Adrenergic neurotransmission is terminated by:

A

1) Re-uptake via U1 receptor (pre-synaptic cell)
2) Removal via U2 receptor (target cell)
3) COMT in target cell degrades it
4) a2 adrenergic receptors in presynaptic cell inhibits further release of NT
5) degradation via MOA in mitochondria

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6
Q

Cholinergic receptors

A

Muscarinic receptors

  • GPCRs
  • M1, M2, M3, M4, M5 (1,3,5 coupled to IP3 and DAG, excitatory, 2 and 4 are inhibitory)
  • subtype selective drugs UNCOMMON

Nicotinic receptor

  • ligand gated ion channels (Na+/K+)
  • Nn (peripheral ganglia)
  • Nm (neuromuscular junction)
  • both coupled to Na+/K+ depolarizing channels
  • subtype selective drugs are COMMON
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7
Q

Drugs stimulating PNS

A
  • synthetic choline esters and plant alkaloids
  • ACT ONLY ON THE M RECEPTORS
  • less sensitive to metabolism, have a longer half life than ACh

Direct acting cholinergic agonists
-bind directly to the M receptors

Indirect acting cholinergic agonists

  • inhibit acetylcholinerase
  • Group A: reversible, ionic site
  • Group B: reversible, both sites
  • Group C: irreversible, covalent site

*NOT ALL CAN CROSS BBB

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8
Q

Use of muscarinic agonists

A
  • Xerostomia, dry mouth
  • activates parasympathetic NS

Stimulates vasodilation

  • acetylcholine binds to the endothelial cell –> Nitric oxide to be produced by nitric oxide synthase –> causes relaxation of your smooth muscle, vasodilation bitch
  • indirect acetylcholinesterase inhibitors are not effective at vasodilation (do a good job at inhibiting break down, don’t do anything to receptor
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9
Q

Cevimeline

A
  • selective M1 and M3 agonist
  • causes salivation in treatment of xerostomia
  • should NOT BE USED IN ASTHMA (cholinergic stimulation causes bronchoconstriction)
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10
Q

Uses of acetylcholinesterase inhibitors

A

MYASTHENIA GRAVIS

  • autoimmune loss of N receptors
  • muscle gets paralyzed because ACh not being used
  • AChE inhibitors keep ACh in synapse longer –> increases muscle contraction

GLAUCOMA

  • intra-ocular pressure build up
  • AChE inhibitors cause MIOSIS (constriction of pupil)

DEMENTIA OF ALZHEIMERS DISEASE

  • patients lose cholinergic neurons
  • AChE inhibitors prolongs ACh, not a permanent cure, will not improve the number of neutron viability
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11
Q

Neostigmine

A

increases ACh at end plate

-group B acetylcholinesterase inhibitor

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12
Q

Symptoms of overdose of AChE inhibitors

A

MUSCARINIC EFFECTS

  • increased sludge response
  • blurred vision
  • miosis

NICOTINIC EFFECTS

  • muscle weakness
  • tachycardia

CNS EFFECTS
-anxiety, tremors, decreased respiratory

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13
Q

nicotinic antagonists

A

block the PNS

Nn receptor blockers

  • ganglion blockers
  • block the Nn receptors, bad consequences, not used

Nm receptor blockers

  • block the Nm receptors at the neuromuscular junction
  • loss of skeletal muscle control
  • muscle relaxation (helps intubation, i.v drips)
  • two types, non depolarizing NMJ and depolarizing NMJ blockers
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14
Q

Succinyl choline

A
  • depolarizing NMJ blocker
  • short acting, weakly acts like ACh
  • intrinsic activity: stimulates depolarization like ACh

PHASE 1: PROLONGED DEPOLARIZATION

  • fasciculations= tiny disorganized twitches
  • muscle cell contracting, using up all energy stores, use up all the ATP
  • leads to DEPOLARIZATION BLOCK: muscle becomes flaccid

PHASE 2: DESENSITIZATION/CHANNEL BLOCK

  • locks channel closed, no more depolarization
  • muscle relaxation
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15
Q

Non depolarizing NMJ blockers

A
  • no intrinsic activity (no ability to produce functional response)
  • competitive inhibitors, bind to the Nm receptor, lock gate so it doesn’t open
  • muscle can’t contract

OLD: tubocurarine
-1 to 2 hrs

NEW: cisatracurium

  • 30-45min
  • dont release histamine from mast cells
  • dont block ganglia
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16
Q

Muscarinic antagonists

A

-competes with ACh for M receptors

ALKALOIDS (naturally occurring)
-atropine

SYNTHETIC

  • charged
  • not absorbed through gut
  • less CNS effects
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17
Q

Atropine

A
  • anti-muscarinic drug, naturally occurring
  • antidote for nerve gase poisoning
  • decreases SLUDGE response

TREATS ASTHMA
-cause bronchodilation

CAUSES MYDRIASIS
-dilation of pupil via radial muscle

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18
Q

parasympathetic system causes

A
  • bronchoconstriction
  • vasodilation
  • miosis
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19
Q

sympathetic system causes

A
  • bronchodilation
  • vasoconstriction
  • mydriasis
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20
Q

ANS pathway of adrenal gland

A

preganglionic cholinergic –> releases ACh to adrenal gland, causes adrenal medulla to release catecholamines (NE and E)

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21
Q

Biosynthesis of catecholamines

A

Tyr –> DOPA –> DOPAMINE –> Norepinephrine —> Epinephrine (in the adrenal gland)

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22
Q

catecholamines

A

-catechol derivatives of phenylethylamine

23
Q

alpha 1 adrenergic receptors

A
  • GPCRS
  • in the smooth muscle of BV

Activation causes

  • vasoconstriction (skin, viscera, veins)
  • pupil dilation
  • salivary secretion
  • *via IP3**
24
Q

Phenylephrine

A
  • alpha 1 selective agonist
  • causes vasoconstriction, nasal decongestion
  • smooth muscle contraction, causes mydriasis (pupil dilation)
25
Q

alpha 2 adrenergic receptor

A
  • suppresses NE and E release
  • autoreceptor, in presynaptic cell
  • treats hypertension
26
Q

Clonidine

A
  • alpha 2 adrenergic receptor agonist

- treats hypertension

27
Q

beta 1 adrenergic receptor

A

increases HR and contractility

28
Q

beta 2 adrenergic receptor

A
  • relaxation of smooth muscle in bronchial, GI, uterus,
  • vasodilation of skeletal and heart muscle
  • protein rich salivary secretion
29
Q

isoprenaline/ isoproterenol

A
  • b selective agonist
  • bind b1 and b2
  • bronchodilation and vasodilation
  • cardiac effects
30
Q

alpha adrenergic agonists

A
  • epinephrine
  • norepinephrine
  • phenylephrine
  • ephedrine
  • clonidine
31
Q

beta adrenergic agonists

A
  • epinephrine
  • norepinephrine
  • dobutamine
  • isoproterenol
  • ephedrine
  • salbutamol
32
Q

Direct acting adrenergic agonists

A

-bind to receptor directly and activates it
2 OH groups on catechol ring structure and beta OH
ex: NE and E

33
Q

Indirectly acting adrenergic agonists

A
  • cause release of norepinephrine
  • none or 1 OH on catechol ring + no beta OH

ex: tyramine

34
Q

Mixed acting agonist

A

activates receptor and release of norepinephrine

  • one OH on catechol ring + one beta OH
    ex: ephedrine
35
Q

Non selective alpha adrenergic antagonists

A

non selective antagonists

  • cause VASODILATION
  • block a1 and a2
  • treat hypertension and tachycardia
36
Q

Phentolamine

A

competitive blocker of a1 and a2 receptors

37
Q

Phenoxybenzamine

A

non competitive blocker of a1 and a2 receptors

38
Q

a1 selective antagonists

A

-block only a1, causes VASODILATION

doesn’t block a2, NE release can be suppressed, doesn’t cause increased HR

39
Q

Prazosin

A

short half life: 3 hrs
-treats frostbite and hypertension
blocks a1 receptors

40
Q

Terazosin

A

long half life: 10 hrs
relaxes bladder
-blocks a1 receptors

41
Q

Beta blockers

A 
decreased
chronotropy
dromotropy
inotropy
lusitropy
42
Q

Propanolol

A

-non selective B blocker
-blocks b1 and b2
decreases HR and contractility
-increases vasoconstriction

43
Q

Metoprolol

A

blocks only B1

decreases HR and contractility

44
Q

Chronotropic agents

A

affect heart rate

45
Q

dromotropic

A

affect cardiac conduction

-spreading of heart signals

46
Q

inotropic

A

cardiac contraction, how strong it beats

47
Q

lusitropic

A

cardiac relaxation

48
Q

PNS –> ACH

A

decreases chronotropy, dormitory, inotropy, lusitropy

49
Q

SNS –> NE –> b1/. b2

A

increases

50
Q

carvedilol

A

block both alpha and beta receptors

  • cause vasodilation due to a1 blockage
  • treats hypertension and heart failure
51
Q

guanethidine

A
  • blocks adrenergic neutron itself, not receptors

- inhibits NE release

52
Q

reserpine

A
  • blocks ability for vesicle to hold NT

- adrenergic neuron blocker

53
Q

botulinum toxin

A

-prevents acetylcholine release by degrading the SNAP proteins, vesicles can’t fuse

Pharmacology 3001 (4 decks)

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