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Neuroscience and NeuroAnatomy > 5 - Cholinergic Drugs > Flashcards

5 - Cholinergic Drugs Flashcards

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1
Q

Botulinum Toxin is how many more times as deadly when compared to Cyanide?

A

200,000,000

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2
Q

Botulinum Toxin Pathophys

A

Targets Cholinergic System (all Cholinergic synapses, not just NMJ)
Binds to protein found in presynaptic cholinergic terminal plasma membrane
Gets taken up into the cytoplasm
Cleaves an enzyme essential for the exocytosis of ACh
Careful! Don’t let it get to the diaphragm!
Wears off, so if you want extended effect, repeated injections are required

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3
Q

Uses of Botulinum Toxin

A 
Paralyze skeletal muscle
(e.g. blepharospasm, hemifacial spasm, strabismus, focal dystonia, wrinkles)
Stroke paralysis
Migraine headaches
Facial tics
Stuttering
Lower back pain
Incontinence
Writer's Ccramp
Carpal tunnel syndrome
Tennis elbow
Spasmodic dysphonia
Experimental treatments (morbid obesity, ulcer prevention, vaginal spasms, newborns with club feet, excessive sweating, overactive bladder)
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4
Q

Blepharospasm

A

An involuntary closure of the eyelids.

Treat with botulinum toxin

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5
Q

Hemifacial Spasm (HFS)

A

Involuntary twitching of the facial muscles on one side of the face.
Treat with multiple injections of botulinum toxin

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6
Q

Strabismus

A

Lazy eye
Eyes are misaligned
Inject botulinum toxin into one or more of the extraocular muscles to weaken them

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7
Q

Dystonia

A

Disorder of posture

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8
Q

Focal Dystonia

A

A confined disorder of posture. Treat with botulinum toxin and deep tissue massage to ease the spasms.

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9
Q

Anticholinesterases

A

Block Acetyl Cholinesterase, prolongs the effect of ACh, facilitates nerve transmission in both Muscarinic and Nicotinic synapses.

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10
Q

How is ACh’s action in the synaptic cleft normally terminated?

A

Hydrolysis via Acetyl Cholinesterase

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11
Q

How do Anticholinesterases behave differently at nicotinic synapses, when compared to their action at muscarinic synapses?

A

At nicotinic synapses, a sufficiently long-lasting Anticholinesterase has a biphasic effect: Initial facilitation of transmission, followed by receptor desensitization/blockade.

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12
Q

Mechanism of Acetylcholinesterases

A

ACh binds to the Esteratic Site of the Active Center of Acetylcholinesterase, and is cleaved to Acetic Acid, while the rest covalently bonds to the Acetylcholinesterase

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13
Q

Mechanism of the 3 types of Anticholinesterases

A

Anticholinesterase binds competitively to Esteratic Site of Active Center of Acetylcholinesterase

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14
Q

3 Types of Anticholinesterases

A 
Truly Reversible Anticholinesterases (Short-Acting)
Reversible Carbamates (Long-Acting)
Organophosphorous Anticholinesterases (Irreversible)
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15
Q

Truly Reversible Anitcholinesterases

A

Binds weakly, falls off easily, short-acting

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16
Q

Reversible Carbamates

A

Has similar molecular structure to ACh, is hydrolyzed in much the same mechanism, but takes much longer than ACh does. Longer-acting. e.g. Neostigmine

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17
Q

Neostigmine

A

Reversible Carbamate (Anticholinesterase), competitively binds to Acetylcholinesterase

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18
Q

Organophosphorus Anticholinesterases

A

Irreversible. Phosphorus covalently bonds to Esteratic Site, ruining it for any ACh in the future.
Lipid-soluble. Crosses skin, lungs readily. Enters bloodstream readily. Crosses Blood-Brain Barrier readily.

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19
Q

Why does Sarin cause diaphragmatic paralysis?

A

Sarin, an Organophosphorus Anticholinesterase, has a bi-phasic effect on the nicotinic synapses of the phrenic nerve. After spasm, we see blockade.

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20
Q

How do you treat acute Organophosphorus Anticholinesterase poisoning?

A

3 drugs in concert:
Atropine (competitive muscarinic antagonist)
Benzodiazepines (to suppress seizures)
Pralidoxime

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21
Q

Atropine

A

Competitive Muscarinic Antagonist. High doses penetrate CNS

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22
Q

Benzodiazepines

A

Diazepam

Blocks seizures

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23
Q

Pralidoxime

A

Treats Organophosphorous Anticholinesterase poisoning. The phosphorous has a higher affinity for the Pralidoxime’s oxygen, than for the Acetyl Cholinesterase Esteratic Site’s oxygen

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24
Q

What must be kept in mind when administering Pralidoxime?

A

Do it quickly. After about 1 hour, the phosphorylated enzyme “ages” and becomes impervious to Pralidoxime.
Pralidoxime also only works peripherally. It does not penetrate CNS.

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25
Myasthenia Gravis
Autoimmune disease. Body makes Ab against NMJ nicotinic receptor, leads to muscle weakness and fatigue. Treat with immunotherapy OR use Neostigmine, Pyridostigmine, or other Reversible Carbamate
26
How do the Reversible Carbamates (e.g. Neostigmine, Pyridostigmine) treat Myasthenia Gravis?
ACh's effect is prolonged, getting more efficient use of the the muscarinic receptors you have left at the NMJ.
27
Why must we titrate Reversible Carbamates very carefully when using them to treat Myasthenia Gravis?
We want to avoid the bi-phasic effect of Anticholinesterases. We titrate until we see blockade (also known as cholinergic crisis), then dial it back a little.
28
Alzheimer's Disease
Widespread loss of synapses and neurons throughout the brain. Causes dementia. Early stages - Nucleus Basalis of Meynert. One of the only treatments is Anticholinesterases, getting the most efficient use of the cholinergic synapses you have left. Specifically Truly Reversible (but the longer-lasting end of that spectrum). Donepezil
29
Donepezil
Truly Reversible Anticholinesterase, though at the longer-lasting end of that classfication Used for Alzheimer's treatment
30
2 Classes of Nicotinic Blocking Drugs
Competitive/Stabilizing Blockers | Depolarizing Blockers
31
Competitive/Stabilizing Nicotinic Blockers
D-Tubocurarine Large, multi-ringed, inflexible, has positively-charged Ns at opposite ends of the molecule Competitive antagonist. Metocurine is methylated version that is more potent
32
What sort or receptors predominate autonomic ganglia?
Nicotinic receptors
33
D-Tubocurarine | Metocurine
Competitive Nictonic Blockers that act at both NMJ and Autonomic Ganglia
34
Arterioles - Dominant Input at Rest
Sympathetic (adrenergic)
35
Veins - Dominant Input at Rest
Sympathetic (adrenergic)
36
Heart - Dominant Input at Rest
Parasympathetic (cholinergic)
37
Iris - Dominant Input at Rest
Parasympathetic (cholinergic)
38
Ciliary Muscle - Dominant Input at Rest
Parasympathetic (cholinergic)
39
GI Tract - Dominant Input at Rest
Parasympathetic (cholinergic)
40
Urinary Bladder - Dominant Input at Rest
Parasympathetic (cholinergic)
41
Salivary Glands - Dominant Input at Rest
Parasympathetic (cholinergic)
42
Sweat Glands - Dominant Input at Rest
Sympathetic (cholinergic)
43
Arterioles - Effect of Ganglionic Blockade
Vasodilatation Increased peripheral flow Hypotension
44
Veins - Effect of Ganglionic Blockade
Dilatation Pooling of blood Decreased venous return Decreased cardiac output
45
Heart - Effect of Ganglionic Blockade
Tachycardia
46
Iris - Effect of Ganglionic Blockade
Mydriasis
47
Ciliary Muscle - Effect of Ganglionic Blockade
Cycloplegia
48
GI Tract - Effect of Ganglionic Blockade
Reduced tone and motility, constipation
49
Urinary Bladder - Effect of Ganglionic Blockade
Urinary retention
50
Salivary Glands - Effect of Ganglionic Blockade
Xerostemia
51
Sweat Glands - Effect of Ganglionic Blockade
Anhidrosis
52
Depolarizing Nicotinic Blockers
Weak nicotinic agonists that induce a low level of depolarization Succinylcholine
53
Succinylcholine
Bi-phasic effect: Binds like ACh, causes initial increase in transmission, then desensitization/blockade.
54
What do you see differently when you administer a Depolarizing Nicotinic Blocker, when compared to a Competitive/Stabilizing Nicotinic Blocker
Competitive (Antagonist): Paralysis | Depolarizing (Agonist): Twitch, then paralysis
55
Pancuronium
Competitive Nicotinic Blocker Steroid derivative Similar structure to D-Tubocurarine Acts in the same mechanism
56
What Nicotinic Blocker would you use for a tracheal intubation?
Succinylcholine Fast Onset Short Duration
57
Atracurium - Origins, Onset, Duration, Side Effects
Derivative of Tubocurarine Onset: 2 - 4 min Duration: 30 - 60 min Side Effects: Milder Histamine Release
58
Vecuronium - Origins, Onset, Duration, Side Effects
Derivative of Pancuronium Onset: 2 - 4 min Duration: 60 - 90 min Side Effects: No Vagal Side Effects (yay!)
59
Mivacurium - Origins, Onset, Duration, Side Effects
Derivative of Atracurium Onset: 2 - 4 min Duration: 12 - 18 min Side Effects: Milder Histamine Release
60
Rocuronium - Origins, Onset, Duration, Side Effects
Derivative of Vecuronium Onset: 1 - 2 min Duration: 30 - 60 min Side Effects: No Vagal Side Effects (yay!)
61
Genealogy of Tubocurarine derivatives
Tubocurarine Onset: 4 - 6 Duration: 80 - 120 Side Effects: Histamine Release Atracurium Onset: 2 - 4 Duration: 30 - 60 Side Effects: Milder Histamine Release Mivacurium Onset: 2 - 4 Duration: 12 - 18 Side Effects: Milder Histamine Release
62
Genealogy of Pancuronium derivatives
Pancuronium Onset: 4 - 6 Duration: 120 - 180 Side Effects: Inhibits Vagal effect on the heart Vecuronium Onset: 2 - 4 Duration: 60 - 90 Side Effects: No Vagal Side Effects (yay!) Rocuronium Onset: 1 - 2 Duration: 30 - 60 Side Effects: No Vagal Side Effects (yay!)
63
Succinylcholine - Onset, Duration, Side Effects
Onset: 1 - 2 min Duration: 5 - 8 min Side Effects: Fasciculation
64
Tubocurarine - Onset, Duration, Side Effects
Onset: 4 - 6 min Duration: 80 - 120 min Side Effects: Histamine Release
65
Pancuronium - Onset, Duration, Side Effects
Onset: 4 - 6 min Duration: 120 - 180 min Side Effects: Inhibits Vagus input to Heart

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