Autonomic Drugs

Question 1

Depolarizing NMJ blocker. Strong ACh rc agonist; produces sustained depolarization and prevents muscle contraction.

Reversal of blockade?

Complications include?

Answer 1

Succinylcholine

Reversal of blockade:
PI (prolonged depolarization) - no antidote. Block potentiated by AChE inhibitors
PII (repolarized but blocked; ACh rcs available, but desensitized) - antidote is AChE inhibitors

Complications: hypercalcemia, hyperkalemia, and malignant hyperthermia

Question 2

NMJ blockers. Competitive antagonists at ACh rc

Reversal of blockade?

Answer 2

Nondepolarizing blockers. Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

Reversal of blockade via AChE inhibitors (ex neostigmine, edrophonium)

Question 3

Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle. Used in the treatment of malignant hyperthermia, a rare but life-threatening side effect of inhalation anesthetics (except N2O) and succinylcholine. Also used to treat neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)

Answer 3

Dantrolene

Question 4

AChE inhibitor used in postop and neurogenic ileum and urinary retention, MG, and postop reversal of NMJ blockade.
No CNS penetration

Answer 4

Neostigmine

Question 5

Long-acting AChE inhibitor used in the treatment of MG.

No CNS penetration.

Answer 5

Pyridostigmine

Question 6

Extremely short-acting AChE inhibitor used in the dx of MG.

Answer 6

Edrophonium

Question 7

AChE inhibitor used to treat anticholinergic toxicity (e.g., atropine OD) because it crosses the BBB (i.e., has CNS penetration)

Answer 7

Physostigmine

Question 8

AChE inhibitor used in the treatment of Alzheimer’s Dz.

Answer 8

Donepezil

Question 9

Side effects of all cholinomimetic agents

Answer 9

Exacerbations of COPD, asthma, and peptic ulcers

Question 10

Alpha agonists used in the treatment of glaucoma
Mechanism?
SE?
CI?

Answer 10

Epinephrine, Brimonidine

MOA: decreases aqueous humor synthesis via vasoconstriction

SE: blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus

CI: closed-angle glaucoma (mydriasis further closes the angle)

Question 11

Beta blockers used in the treatment of glaucoma

Mechanism?

Answer 11

Timolol, betaxolol, carteolol

MOA: decrease aqueous humor synthesis

NB: No pupillary or vision changes

Question 12

Diuretic used in the treatment of glaucoma

Mechanism?

Answer 12

Acetazolamide
MOA: decreases aqueous humor synthesis via inhibition of CA
NB: No pupillary or vision changes

Question 13

Direct cholinomimetics (muscarinic agonists) used in the treatment of glaucoma
MOA?
SE?

Answer 13

Pilocarpine, carbachol

MOA: increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

SE: Miosis and cyclospasm/spasms of accommodation (contraction of ciliary m.–>lens is rounded for near vision and can’t see far)
- transient effect (~2 hrs)

Question 14

Cholinomimetic used in closed-angle glaucoma emergencies

Answer 14

Pilocarpine

Question 15

AChE inhibitors used in the treatment of glaucoma
MOA?
SE?

Answer 15

Physostigmine, echothiophate (irreversible)
NB: remember that physostigmine penetrates the CNS and is therefore also used in the treatment of anticholinergic toxicity (ex, atropine OD)

MOA: increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork

SE: Miosis and cyclospasm/spasm of accommodation (contraction of ciliary m.–> lens is rounded for near vision and can’t see far)
- transient effect (~2 hrs)