Pharmacology 1 Flashcards

(32 cards)

1
Q

What is spasticity?

A

Abnormally high muscle tone, often from motor neuron lesions.

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2
Q

What is hypotonia?

A

Decreased muscle tone.

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3
Q

What is flaccidity?

A

Loss of muscle tone (paralysis), usually due to lower motor neuron lesions.

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4
Q

Which muscles do muscle relaxants target?

A

Only skeletal muscles—not cardiac or smooth muscles.

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5
Q

What happens when an action potential reaches the nerve terminal?

A

Calcium channels open and calcium enters the cell.

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6
Q

How is acetylcholine (ACh) released?

A

Calcium influx triggers fusion of vesicles → ACh released into synaptic cleft.

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7
Q

What happens when ACh binds to its receptors?

A

Na+/K+ channels open → depolarization → muscle contraction.

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8
Q

How is synaptic transmission terminated?

A

Acetylcholinesterase degrades ACh.

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9
Q

What are the two main types of neuromuscular blockers?

A

Non-depolarizing (antagonists) and depolarizing (agonists like succinylcholine).

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10
Q

What is the role of non-depolarizing agents?

A

They compete with ACh for nicotinic receptors and block muscle contraction.

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11
Q

What reverses non-depolarizing blockers?

A

Cholinesterase inhibitors like neostigmine (with atropine to block side effects).

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12
Q

Why aren’t non-depolarizing blockers taken orally?

A

They are highly polar and not absorbed in the gut—given IV.

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13
Q

What is the prototype of non-depolarizing NM blockers?

A

Tubocurarine (no longer used due to histamine release).

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14
Q

What is the sequence of muscle paralysis?

A

Face & eyes → fingers → limbs → trunk → diaphragm (recovery is reversed).

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15
Q

What is the fastest-acting non-depolarizing agent?

A

Rocuronium.

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16
Q

What is Mivacurium used for?

A

Short procedures like esophagoscopy—short duration, fast recovery.

17
Q

Why was cisatracurium developed?

A

To avoid side effects of atracurium (histamine release, seizures).

18
Q

What is pancuronium’s special effect?

A

It has sympathomimetic and vagolytic effects—no need for atropine.

19
Q

What is the main depolarizing agent?

A

Succinylcholine.

20
Q

What are the phases of succinylcholine action?

A

Phase I: depolarizing block
Phase II: desensitization (resembles non-depolarizing block)

21
Q

What are side effects of succinylcholine?

A

Fasciculations, hyperkalemia, malignant hyperthermia, muscle pain, apnea.

22
Q

What treats malignant hyperthermia?

A

Dantrolene (blocks Ca²⁺ release from sarcoplasmic reticulum).

23
Q

Who should NOT get succinylcholine?

A

Patients with eye injuries, muscle trauma, malignant hyperthermia, or allergy.

24
Q

What is the MOA of dantrolene?

A

Binds RyR1 receptor → blocks Ca²⁺ release from sarcoplasmic reticulum.

25
What are the side effects of dantrolene?
Hepatotoxicity—requires liver monitoring.
26
What is baclofen’s MOA?
GABA-B receptor agonist—used for ALS spasticity.
27
What is diazepam’s MOA in spasticity?
Facilitates GABA-A transmission—reduces motor neuron output.
28
What are spasmolytics used for?
Reducing spasticity in central conditions (MS, stroke, fibromyalgia, etc.)
29
What does botulinum toxin treat?
Wrinkles, cerebral palsy, bladder overactivity, chronic migraines.
30
What drugs potentiate non-depolarizing NM blockers?
Aminoglycosides, halothane, calcium channel blockers.
31
What drugs potentiate depolarizing NM blockers?
Inhaled anesthetics (isoflurane), aminoglycosides.
32
What interaction causes malignant hyperthermia?
Succinylcholine + volatile anesthetics.