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Pharm 1 > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

Anticholinergics may also be called: (4)

A

Cholinergic antagonists
Cholinergic-blocking agents
Parasympatholytics
Vagolytics

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2
Q

3 categories of Anticholinergics

A

Antimuscarinics
Ganglionic Blockers
Neuromuscular Blockers

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3
Q

5 Antimuscarinics

A 
Atropine
Glycopyrrolate (Robinul)
Benzotropine (Cogentin)
Propantheline
Scopolamine
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4
Q

Example of Ganglionic Blocker

A

Trimethophan (Arfonad)

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5
Q

2 Types of Neuromuscular Blockers

A

Non-depolarizing

Depolarizing

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6
Q

4 Non-depolarizing neuromuscular blockers

A

Vecuronium
Cisatracurium (Nimbex)
Pancuronium (Pavulon)
Rocuronium (Zemuron)

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7
Q

Example of Depolarizing Neuromuscular Blocker

A

Succinylcholine (Anectine)

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8
Q

2 functions of antimuscarinics

A

Block muscarinic function

Block sympathetic cholinergic receptors

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9
Q

Atropine is a _____

A

Antimuscarinic

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10
Q

Atropine adult dose

A

0.4 to 1.0 mg

May repeat every 3-5 minutes up to 3x for bradycardia

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11
Q

Robinul adult dose

A

0.2 to 0.6 mg

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12
Q

Patients with advanced heart disease often have _____.

A

increased parasympathetic tone

lower heart rate, lower contractility

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13
Q

What are 3 disease processes antimuscarincs are most commonly used?

A

Symptomatic bradycardia
PEA/electromechanical dissociation
AV block

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14
Q

What else might antimuscarins be used for?

A 
Adjunct Parkinson's Disease therapy
Motion sickness (dramamine)
Opthalmic examinations (dilate eyes)
Excessive GI hypermotility (lomotil)
Urinary urge incontinence
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15
Q

Robinul is a _____.

A

antimuscarinic

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16
Q

Common side effects of antimuscarinics:

A

Blind as a bat (dilated pupils)
Red as a beet (vasodilation)
Hot as a hare (hyperthermia)
Dry as a bone (dry skin)
Mad as a hatter (hallucinations/agitation)
Bloated as a Toad (ileus, urinary retention)
And the heart runs alone (tachycardia)

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17
Q

Why do antimuscarinics cause tachycardia?

A

They knock out vagus nerve parasympathetic tone to the heart.

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18
Q

Ganglionic blockers are rarely used for: (3)

A

HTN Crises
Dissecting aortic aneurysms
Reduce bleeding during neurosurgery

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19
Q

Dramine is a _____.

A

antimuscarinic

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20
Q

What are the effects of ganglionic blockers?

A

Profound hypotension
Profound constipation
Negative chronotrope and inotrope (no reflex tachycardia)

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21
Q

How do ganglionic blockers cause profound hypotension?

A

Due to loss of sympathetic tone on vessels and histamine release

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22
Q

Lomotil is an _____.

A

Antimuscarinic

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23
Q

Trimethophan (Arfonad)

  • Route
  • Duration
  • Adult Dose
A

IV
5-15 minutes
Bolus = 1 to 3 mg
Infusion = 0.5 to 6.0 mg/min

24
Q

When are neuromuscular blocking agents mostly used?

A

During surgery to prevent patient movement.

25
Q

What is the most important thing to remember when administering a neuromuscular blocker?

A

They do not sedate, tranquilize, or anesthetize the patient

26
Q

All neuromuscular blockers have some structural resemblance to _____.

A

ACh

27
Q

What started the development of neuromuscular blockers?

A

Curare then tubocurare was developed clinically

28
Q

The nondepolarizing neuromuscular blockers acts as ____ to ACh.

A

Antagonists

29
Q

All nondepolarizing neuromuscular blocking agents are given ___.

A

IV

30
Q

What factors cause variation in non-depolarizing neuromuscular blockers?

A

Half-life length
Metabolism
Propensity to cause histamine release

31
Q

Non-depolarizing neuromuscular blockers are antagonized by _____.

A

Acetylcholinesterase inhibitors

32
Q

What types of drugs are synergistic with non-depolarizing neuromuscular blockers?

A 
Calcium-channel blockers
Halogenated hydrocarbon gas anesthetics 
Aminoglycoside antibiotics (b/c they inhibit ACh release)
33
Q

The depolarizing neuromuscular blockers acts as ____ to ACh.

A

Agonists

34
Q

Depolarizing neuromuscular blockers act as a _______.

A

Non-competitive antagonist

35
Q

Explain the 2 phases of depolarizing neuromuscular blockers.

A

Phase 1 = membrane depolarizes, causing an initial discharge that produces transient small twitches (fasciculations) followed by flaccid paralysis

Phase 2 = membrane repolarizes, but receptor is desensitized to the effect of ACh.

36
Q

Duration of SUX?

A

Less than 8 minutes

Shorter than any of the non-depolarizing blockers

37
Q

SUX is broken down by _____ when circulating in the plasma.

A

Pseudocholinesterase

38
Q

The _____ neuromuscular blockers acts as antagonists to ACh.

A

Nondepolarizing

39
Q

SUX is terminated by when it diffuses away from the neuromuscular junction to be metabolized and allow ___ back to its receptors.

A

ACh

40
Q

There is little pseudocholinesterase at the _____.

A

Neuromuscular junction

41
Q

SUX is historically linked to _____ when used with gas anesthetic Halothane (Fluothane).

A

malignant hyperthermia

42
Q

Prolonged apnea is seen when SUX is given to patients with ______.

A

Genetic pseudocholinesterase deficiency

43
Q

Genetic pseudocholinesterase deficiency is most commonly found in:

A

Persian Jewish

Indian Hindu

44
Q

The _____ neuromuscular blockers acts as agonists to ACh.

A

Depolarizing

45
Q

SUX is historically linked to malignant hyperthermia when used with ______.

A

Gas anesthetic Halothane (Fluothane)

46
Q

1 side effect of SUX

A

Hyperkalemia

47
Q

Why may SUX cause hyperkalemia?

A

Potassium cellular pumps are locked “open”

48
Q

What patients would you be especially considerate of giving them SUX?

A

Patients with electrolyte problems

Burn patients

49
Q

_____ neuromuscular blockers reach the neuromuscular junction, block receptors and cause persistent depolarization.

A

Depolarizing

50
Q

_____ neuromuscular blockers = AKA stabilizers

A

Non-depolarizing

51
Q

_____ neuromuscular blockers effect can be antagonized by reversible inhibitors

A

Non-depolarizing

52
Q

_____ neuromuscular blockers stimulat action potential initially for a short while then flaccid paralysis is followed.

A

Non-depolarizing

53
Q

_____ neuromuscular blockers effect cannot be antagonized.

A

Depolarizing

54
Q

_____ neuromuscular blockers compete with receptors to cause them not to depolarize and the action potential is stopped.

A

Non-depolarizing

55
Q

What is the paralyzation process with Depolarizing Neuromuscular Blockers?

A

First large muscles (abdominal and limb)
Next short muscles (face, ear, nose)
Last respiratory muscles

56
Q

_____ neuromuscular blockers directly lead to flaccid paralysis.

A

Non-depolarizing

57
Q

What is the paralyzation process with Non-Depolarizing Neuromuscular Blockers?

A

First short muscles
Next large muscles
Last respiratory muscles

Pharm 1 (6 decks)

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