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Neuroscience and NeuroAnatomy > 5 - Cholinergic Drugs > Flashcards

5 - Cholinergic Drugs Flashcards

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
Q

Myasthenia Gravis

A

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

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26
Q

How do the Reversible Carbamates (e.g. Neostigmine, Pyridostigmine) treat Myasthenia Gravis?

A

ACh’s effect is prolonged, getting more efficient use of the the muscarinic receptors you have left at the NMJ.

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27
Q

Why must we titrate Reversible Carbamates very carefully when using them to treat Myasthenia Gravis?

A

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
Q

Alzheimer’s Disease

A

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
Q

Donepezil

A

Truly Reversible Anticholinesterase, though at the longer-lasting end of that classfication
Used for Alzheimer’s treatment

30
Q

2 Classes of Nicotinic Blocking Drugs

A

Competitive/Stabilizing Blockers

Depolarizing Blockers

31
Q

Competitive/Stabilizing Nicotinic Blockers

A

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
Q

What sort or receptors predominate autonomic ganglia?

A

Nicotinic receptors

33
Q

D-Tubocurarine

Metocurine

A

Competitive Nictonic Blockers that act at both NMJ and Autonomic Ganglia

34
Q

Arterioles - Dominant Input at Rest

A

Sympathetic (adrenergic)

35
Q

Veins - Dominant Input at Rest

A

Sympathetic (adrenergic)

36
Q

Heart - Dominant Input at Rest

A

Parasympathetic (cholinergic)

37
Q

Iris - Dominant Input at Rest

A

Parasympathetic (cholinergic)

38
Q

Ciliary Muscle - Dominant Input at Rest

A

Parasympathetic (cholinergic)

39
Q

GI Tract - Dominant Input at Rest

A

Parasympathetic (cholinergic)

40
Q

Urinary Bladder - Dominant Input at Rest

A

Parasympathetic (cholinergic)

41
Q

Salivary Glands - Dominant Input at Rest

A

Parasympathetic (cholinergic)

42
Q

Sweat Glands - Dominant Input at Rest

A

Sympathetic (cholinergic)

43
Q

Arterioles - Effect of Ganglionic Blockade

A

Vasodilatation
Increased peripheral flow
Hypotension

44
Q

Veins - Effect of Ganglionic Blockade

A

Dilatation
Pooling of blood
Decreased venous return
Decreased cardiac output

45
Q

Heart - Effect of Ganglionic Blockade

A

Tachycardia

46
Q

Iris - Effect of Ganglionic Blockade

A

Mydriasis

47
Q

Ciliary Muscle - Effect of Ganglionic Blockade

A

Cycloplegia

48
Q

GI Tract - Effect of Ganglionic Blockade

A

Reduced tone and motility, constipation

49
Q

Urinary Bladder - Effect of Ganglionic Blockade

A

Urinary retention

50
Q

Salivary Glands - Effect of Ganglionic Blockade

A

Xerostemia

51
Q

Sweat Glands - Effect of Ganglionic Blockade

A

Anhidrosis

52
Q

Depolarizing Nicotinic Blockers

A

Weak nicotinic agonists that induce a low level of depolarization
Succinylcholine

53
Q

Succinylcholine

A

Bi-phasic effect: Binds like ACh, causes initial increase in transmission, then desensitization/blockade.

54
Q

What do you see differently when you administer a Depolarizing Nicotinic Blocker, when compared to a Competitive/Stabilizing Nicotinic Blocker

A

Competitive (Antagonist): Paralysis

Depolarizing (Agonist): Twitch, then paralysis

55
Q

Pancuronium

A

Competitive Nicotinic Blocker
Steroid derivative
Similar structure to D-Tubocurarine
Acts in the same mechanism

56
Q

What Nicotinic Blocker would you use for a tracheal intubation?

A

Succinylcholine
Fast Onset
Short Duration

57
Q

Atracurium - Origins, Onset, Duration, Side Effects

A

Derivative of Tubocurarine

Onset: 2 - 4 min
Duration: 30 - 60 min
Side Effects: Milder Histamine Release

58
Q

Vecuronium - Origins, Onset, Duration, Side Effects

A

Derivative of Pancuronium

Onset: 2 - 4 min
Duration: 60 - 90 min
Side Effects: No Vagal Side Effects (yay!)

59
Q

Mivacurium - Origins, Onset, Duration, Side Effects

A

Derivative of Atracurium

Onset: 2 - 4 min
Duration: 12 - 18 min
Side Effects: Milder Histamine Release

60
Q

Rocuronium - Origins, Onset, Duration, Side Effects

A

Derivative of Vecuronium

Onset: 1 - 2 min
Duration: 30 - 60 min
Side Effects: No Vagal Side Effects (yay!)

61
Q

Genealogy of Tubocurarine derivatives

A

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
Q

Genealogy of Pancuronium derivatives

A

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
Q

Succinylcholine - Onset, Duration, Side Effects

A

Onset: 1 - 2 min
Duration: 5 - 8 min
Side Effects: Fasciculation

64
Q

Tubocurarine - Onset, Duration, Side Effects

A

Onset: 4 - 6 min
Duration: 80 - 120 min
Side Effects: Histamine Release

65
Q

Pancuronium - Onset, Duration, Side Effects

A

Onset: 4 - 6 min
Duration: 120 - 180 min
Side Effects: Inhibits Vagus input to Heart

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