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581 - Pharmacology I > Exam 5 - Cholinergic Antagonists & Adrenergic Receptors > Flashcards

Exam 5 - Cholinergic Antagonists & Adrenergic Receptors Flashcards

1
Q

Cholinergic agonists site of action

A
  • Pre-ganglion of adrenal medulla/sympathetic/parasymp
  • Post-ganglion of parasympathetic
  • skeletal muscle
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2
Q

Cholinergic antagonist site of action

A 
- Same as cholinergic agonists...but in sub-groups
Sub-groups:
- Selective muscarinic blockers
- Ganglionic blockers
- Neuromuscular blockers
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3
Q

Cholinergic antagonist

A
  • bind to cholinoceptors and prevent effects of Ach/cholinergic agonists
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4
Q

Selective muscarinic blockers

A
  • Most clinically useful
  • Block at post-ganglion of parasympathetic
  • anticholinergic/muscarinic agents
  • parasympolytics
  • sympathetic stimulation not interrupted
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5
Q

Ganglionic blockers

A
  • block nicotinic receptors of sympathetic and parasymp preganglia
  • are not selective…block all ANS
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6
Q

Neuromuscular blockers

A
  • block impulses to skeletal muscles
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7
Q

Antimuscarinics

A
  • one of selective muscarinic blockers
  • most can selectively block (except Atropine)
  • block sympathetic cholinergic neurons (sweat/salivary glands)
  • No action at NMJ
  • No action at autonomic ganglia
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8
Q

Atropine

A
  • Belladonna alkaloid
  • Competitive
    Actions:
  • eye dilation (like at eye doctor)
  • GI relax
  • dry mouth/ no sweat/ no tears
  • high dose: increase HR (block SA node)
  • low dose: decrease HR (block autoreceptors)

Uses:

  • Relax GI for IBS
  • treat bradycardia
  • block respiratory secretions for pre-op
  • antidote for organophosphate poisoning or agonist overdose
  • AV block
  • Pulseless electrical activity
  • ENTERS CNS

Dose: 1.0 mg/ml

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9
Q

Scopolamine

A

Like atropine but…

  • longer duration
  • better on CNS

Uses:

  • motion sickness
  • nausea / vomiting
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10
Q

Ipratropium (Atrovent)

A
  • Derivative of atropine
  • Bronchodilator for COPD
  • Inhaled
  • Positive charge…can’t enter systemic circulation
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11
Q

Emphysema

A
  • destruction and enlargement of air spaces
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12
Q

Bronchitis

A
  • increased mucosa and inflammation
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13
Q

COPD

A
  • Emphysema w/ chronic bronchitis
  • Irreversible block of airflow
  • smoking greatest risk factor
  • therapy aimed at symptoms and prevention of progression
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14
Q

Benztropine (Cogentin)

A
  • centrally acting

- treat Parkinson’s tremors

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15
Q

Parkinson’s Disease

A
  • Decrease in dopaminergic activity
  • leads to imbalance with cholinergic activity
  • too much Ach activity in Parkinson’s
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16
Q

Glycopyrrolate (Robinul)

A
  • for peptic ulcers
  • pre-op to reduce secretions in mouth/throat/airway
    • prevent aspiration
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17
Q

Adverse effects of antimuscarinics

A
  • blurred vision
  • confusion
  • mydriasis (eye dilation)
  • tachycardia
  • constipation
  • urinary retention
  • bad for glaucoma (stops drainage of vitreous)
  • blocks parasympathetic outflow
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18
Q

Atropine poisoning

A
  • Hot as a hare
  • Dry as a bone
  • Blind as a bat
  • Red as a beet
  • Mad as a hatter
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19
Q

Ganglionic blockers

A
  • block entire ANS at nicotinic receptors (symp/para preganglion)
  • RARELY used therapeutically…not selective enough
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20
Q

Nicotine

A
  • poison w/ no therapeutic benefit…bad for health
  • no effect at NMJ
  • depolarizes autonomic ganglia
    • low dose: stimulate
    • high dose: block
  • Increases release of neurotransmitters
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21
Q

Neuromuscular blockers

A
  • block Ach at NMJ
  • similar to Ach and can be:
    • antagonist: nondepolarizing/competitive
    • agonist: depolarizing
  • useful for surgery…muscle relaxation
    • intubation
    • lower anesthesia dose needed
    • less post-op respiratory depression
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22
Q

Nondepolarizing neuromuscular blockers

A
  • started as Curare….poison darts to paralyze prey
  • block post-synaptic receptors (nicotinic)
  • increase safety for anesthesia…but NO substitute
    Mechanism:
    -low dose: competitively block Ach at receptor / no depol
    overcome w/ ACE inhibitors (neostigmine, edrophonuium)
    -high dose: block ion channels of motor end plate
    Cannot be overcome w/ ACE inhibitors
  • Not effective orally….IV or IM
  • Cannot enter cells or BBB
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23
Q

Muscle recovery of Nondepolarizing blockers

A
  • Face/eye (first to paralyze)
  • Fingers/limbs/neck/trunk
  • Intercostals
  • Diaphragm
  • Recover in reverse order
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24
Q

Nondepolarizing blockers drug interactions

A
  • Cholinesterase inhibitor: antagonize effect if not in ion channel
  • Halogenated hydrocarbon anesthetics: enhance
  • Aminoglycoside antibiotic: enhance effect
  • Ca channel blockers: enhance effect
  • Last two block Ca from entering neuron
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25
Q

Nondepolarizing blocker drugs

A 
- Vecuronium
    45 min
- Cisatracurium (Nimbex)
    90 min
- Pancuronium (Pavulon)
    90 min
- Rocuronium (Zemuron)
    45 min
  • decrease O2 consumption on CPB…Venous sats will tell
26
Q

Nondepolarizing blocker reversal drug

A

Sugammadex (Bridion)

  • reverses Roc / Vecuronium / Pancuronium
  • does not inhibit ACE
  • no cholinergic side effects
  • surrounds blocker and prevents its interaction
27
Q

Depolarizing neuromuscular blocker

A
  • Depolarize muscle fiber like Ach
  • resistant to ACE and remains attached to receptor
  • constant stimulation and persistent depolarization
    • prevents repolarization
  • removed by psuedocholinesterase in plasma (not at NMJ)
  • patient will convulse first….then paralyzed
28
Q

Succinylcholine (Anectine)

A
  • Sux
  • rapid onset (good for intubation)
  • last only minutes
  • IV
  • Respiratory muscles last to be paralyzed
  • May cause muscle soreness (initial convulsions)
    • can deliver nondepolarizer first to help with this

Side effects:

  • Hyperthermia (can induce malignant hyperthermia)
  • Apnea (in Persian Jews / Indian Hindu)
  • Hyperkalemia (increased K)
    • burn patients susceptible
29
Q

Malignant hyperthermia

A
  • extra metabolism in muscles….life threatening
  • inherited disorder
  • triggered by sux and volatile anesthesia
  • increase CO2 / heat production
  • activates SNS
  • DIC: disseminated intravascular coagulation
  • multiple organ dysfunction
  • death
30
Q

Depolarizing vs Nondepolarizing blockers

A
  • Depolarizing cause persistent contraction…NonD stop depolarization altogether
  • Depolarizing paralyze large muscles -> short -> resp
    NonD paralyze short muscles -> large -> resp
  • Depolarizing irreversible…NonD reversible
  • Depolarizing stimulate first, then flaccid…NonD just flaccid
31
Q

Antimuscarinics

A
  • Atropine
  • Glycopyrrolate (Robinul)
  • Benztropine (Cogentin)
  • Scopolamine
  • Ipratropiuim (Atrovent)
32
Q

Ganglionic Blcokers

A
  • Nicotine
33
Q

Nondepolarizing NM Blcokers

A
  • Vecuronium
  • Cisatracurium (Nimbex)
  • Pancuronium (Pavulon)
  • Rocuronium (Zemuron)
34
Q

Nondepolarizing NM Blocker Reversal

A
  • Sugammadex (Bridion)
35
Q

Depolarizing NM Blocker

A
  • Succinylcholine (Anectine)
36
Q

NE

A
  • primary transmitter released by adrenergic neurons

- CNS and sympathetic

37
Q

Epi

A
  • released from adrenal medulla as hormone
38
Q

Sympathomimetics

A
  • drugs that activate adrenergic receptors

- can be direct or indirect acting

39
Q

Sympatholytics

A
  • drugs that block activation of adrenergic receptors
40
Q

Steps of adrenergic neurotransmission

A 
- similar to cholinergic, except NE is neurotransmitter 
Steps:
- synthesis
- storage
- release 
- receptor binding
- removal
- metabolism
41
Q

Step 1 of NE transmission

A
  • Tyrosine is co-transported into neuron
  • Tyrosine converted to DOPA (via tyrosine hydroxylase)
    • RATE LIMITING
  • DOPA converted to dopamine inside neuron
42
Q

Step 2 of NE transmission

A
  • Dopamine moved into vessicle
  • Dopamine into NE (via dopamine B-hydroxylase)
  • step inhibited by Reserpine
43
Q

Step 3 of NE transmission

A
  • Action potential causes influx of Ca
  • Vessicle fuses w/ membrane
  • Exocytosis release NE and cofactors into synapse
  • Release blocked by Guanethidine
44
Q

Step 4 of NE transmission

A
  • NE binds to receptors on effective organ and auto-receptors
  • NE is metabotropic….2nd messenger system
45
Q

Step 5 of NE transmission

A

NE removed from synapse via:

  • diffuses out
  • taken back into neuron
  • metabolized by COMT into inactive metabolites into urine
46
Q

Step 6 of NE transmission

A
  • COMT metabolizes in cleft
  • MAO metabolizes once taken back into neuron
  • Both convert to inactive metabolites into urine
47
Q

Adrenergic receptor location

A
  • post-synaptic ganglia of sympathetic and adrenal medulla
48
Q

Alpha adrenoreceptors affinity

A

Epi
NE
Isoproterenol

  • High down to low…EPI/NE much higher than Iso
  • divided into a1 and a2
49
Q

Beta adrenoreceptor affinity

A

Isoproterenol
Epi
NE

High down to low…Iso much higher than Epi/NE
Divided into B1/B2/B3

50
Q

Alpha 1 adrenoreceptor

A
  • high affinity for phenylephrine
  • mostly affects vasculature
  • postsynaptic membrane of effector organ
  • Smooth muscle constriction (adrenergic effects)
  • activates G-protein 2nd messenger systems
    • DAG: turns on other proteins
    • IP3: release of Ca into cytosol
  • further divided into A/B/C/D
51
Q

Alpha 1 effects

A
  • increase vascular tone -> increase BP
  • increase PVR
  • mydriasis
  • increase bladder tone
  • increase tension in prostate
  • Think fight or flight
52
Q

Alpha 2 adrenoreceptors

A
  • high affinity for clonidine
  • affects CNS feedback loops for HTN and sedation
  • sympathetic PREsynaptic nerve ending (also PRE para)
  • control release of NE (inhibitory autoreceptors)
  • effect mediated by inhibition of adenylyl Cyclades / drop in cAMP
  • divided into A/B/C
53
Q

Alpha 2 effects

A
  • blocks NE release / sympathetic tone
  • blocks Ach release
  • blocks insulin release
  • used as sedative in CV surgery
54
Q

B1 adrenoreceptor

A
  • Equal affinity for NE/Epi (both much less than iso)

- major role on heart

55
Q

B1 effects

A
  • tachycardia
  • increase contractility
  • increase in renin from kidneys (increase BP…hold water)
  • increase in lipolysis (for energy)
56
Q

B2 adrenoreceptors

A
  • higher affinity for EPI over NE

- mostly in lungs

57
Q

B2 effects

A
  • relaxation of pulmonary smooth muscle (airway open)
  • vasodilation of skeletal muscles (more flow)
  • decrease PVR
  • increase glucagon release (for energy)
  • uterine muscle relaxation
58
Q

B3 adrenoreceptors

A
  • involved in lipolysis
  • effects muscles of bladder
  • not big player
59
Q

Dopaminergic Receptors

A

5 subtypes:

  • D1/D2: peripheral mesenteric and renal beds
  • D2: presynaptic adrenergic neurons
  • Dopamine can bind to all other adrenergic receptors (a/B)
  • interfere with release of NE

Dopamine sites of action:

  • brain
  • renal/visceral arterioles (dilation/natriuresis…Na in urine)
  • CV system (activate B receptors…HR/contractility up)
  • Vascular PVR (up or down depending on dose)
60
Q

Receptor desensitization

A 
- prolonged exposure to catecholamines reduces responsiveness (NE/Epi/Dopa)
Via:
- sequestration of receptors
- down-regulation
- deactivation of G protein

581 - Pharmacology I (6 decks)

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