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1 Pharm Unit > 9 Cholinergics III > Flashcards

9 Cholinergics III Flashcards

1
Q

Nicotine is medically significant because of….

(for review)

A
  • toxicity
  • presence in tobacco products
  • eliciting increased cardiac rate, vasoconstriction, and plasma levels of epinephrine; decreased mucociliary movement in lungs; mildly stimulates CNS
  • addictive properties
  • small cell carcinoma of the lung
  • cardiovascular disease
  • difficult to determine which chemicals are responsible for toxic effects of tobacco consumption (nicotine, aldehydes, nitrosamines, other alkylating agents)
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2
Q

T/F

Chronic nicotine toxicity is characterized as the largest single preventable cause of illness and premature death in the U.S.

A

True

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3
Q

What is a lethal dose for acute nicotine toxicity?

What population is this a concern for?

A

~40mg

Ingestion of nicotine products by small children & dogs.

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4
Q

What dosages are in an average cigarette and cigar?

A

Cigarette: 13-19mg

Cigar: 15-40mg

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5
Q

What are the symptoms of acute nicotine exposure?

(for review)

A

ANS Effects

  • Nausea
  • Excess salivation
  • Abdominal pain
  • Diarrhea
  • Cold sweat
  • Dizziness
  • Headache

CNS Effects

  • Convulsions
  • Coma
  • Respiratory arrest

Muscle endplate depolarization

  • Blockade
  • Respiratory paralysis

Other

  • Hypertension
  • Cardiac arrhythmias
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6
Q

What 4 out of the 5 major causes of death does nicotine contribute to?

A

Cardiovascular disease

Lung and other cancers

Stroke

COPD

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7
Q

T/F

N2 receptor antagonists have limited clinical use due to their lack of selectivity.

A

False

N1 receptor antagonists because N1 receptors are found on all autonomic ganglia (both sympathetic and parasympathetic)

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8
Q

What symptoms does interruption of sympathetic ganglionic transmission result in?

A

Overall: inhibited cardiovascular reflexes and sweating

Specifically:

Vasodilation with increased peripheral blood flow to some vascular beds and decreased BP

  • orthostatic hypotension
  • tachycardia
  • decreased cardiac output
  • decreased total peripheral resistance
  • fainting

Thermoregulatory and nonthermoregulatory sweating reduced

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9
Q

What 6 symptoms does interruption of parasympathetic ganglionic transmission result in?

A

Dry mouth (xerostomia)

Urinary retention and constipation

Mydriasis (dilated pupil)

Cycloplegia (loss of accommodation)

Impaired sexual function due to prevention of erection/ejaculation

Decreased GI tone/motility and secretions

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10
Q

1) What are the 2 ganglionic blocking agents?
2) What receptor are they affecting?
3) What effect do they have on the receptor?(non/depolarizing; non/competitive; ant/agonist)

A

1) mecamylamine & trimethaphan
2) N1
3) nondepolarizing competitive antagonist

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11
Q

What effect does a high concentration of nicotine produce?

A

persistent depolarization of membranes in regions with N1 and N2 receptors

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12
Q

What 4 clinical problems can ganglionic blocking agents treat?

A

Hypertensive emergencies during surgery or following aortic aneurysm

Adjunct therapy for peripheral vascular resistance - relieve vasoconstriction and increase perfusion of tissue

Adjunct therapy for severe hypertension - not 1st choice therapy

Lowering arterial pressure to control bleeding during surgery

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13
Q
A

Take home: generally if an organ receives both parasympathetic and sympathetic innervation, the dominant tone will be parasympathetic. If an organ only receives sympathetic innervation, the dominant tone will be sympathetic.

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14
Q

What is the distribution of N2 receptors and AChE (acetyl cholinesterase) in the NMJ?

A

N2 receptors are localized at the end plate region at the center of the muscle fibers.

AChE is concentrated in the folds of the end plate region.

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15
Q

AChE inhibitors lead to what overall effect?

A

Increased concentration of ACh at NMJs, facilitating the ability to reach threshold level and generate a muscle action potential

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16
Q

What is denervation supersensitivity?

A

Loss of innervation thru trauma or a degenerative process leads to the threshold dose of ACh needed to trigger a response being significantly reduced.

  • N2 receptors redistribute across the muscle surface
  • Increased numbers of receptors are expressed across the muscle surface
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17
Q

What effect does denervation have on smooth muscle? Skeletal muscle?

A

Smooth muscle does not atrophy

Skeletal muscle atrophies

Both show supersensitivity

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18
Q

What are the clinical applications in the use of neuromuscular blocking agents?

A

Muscle relaxant and adjunct for anesthesia

  • muscle relaxation for intracavitary surgery
  • facilitate tracheal intubation
  • control of ventilation in patients with ventilator failure
  • treatment of convulsions
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19
Q

What are the concerns/considerations of administering a NM blocking agent?

A

Considerations:

  • check respiration
  • ensure adequate ventilation
  • no bronchial airway obstruction
  • no CO2 accumulation
  • require proper training to support respiration and cardiovascular system
20
Q

What are the 3 effects of nondepolarizing N2 receptor competitive inhibitors?

A

1) Block opening of Na channel
2) Unbound ACh is hydrolyzed by AChE at NMJ
3) Motor weakness -> total flaccid paralysis -small rapidly moving muscle function lost first -limb, neck, and trunk muscle function lost next -intercostal muscles and diaphragm function lost last

21
Q

What are the 2 factors in selecting a nondepolarizing inhibitor?

A
  • duration of drug action
  • minimizing cardiovascular and other side effects (cross-reactivity with N1/M and histamine release)
22
Q

What is the actual nicotine delivery through cigarette? Where does the rest go?

A

Actual drug delivery ~1-2.5mg with most nicotine lost thru burning or as 2nd hand smoke

23
Q

What is another way of exposure to nicotine besides cigarettes & cigars?

A

Exposure to insecticides with nicotine as the active ingredient

24
Q

What happens with re-innervation after denervation supersensitivity?

A

With re-innervation, denervation supersensitivity will disappear and cholinergic receptors will reestablish an organized end plate region.

25
Q

Do the NM blocking agents posses tertiary or quaternary nitrogen(s)? What does this mean for solubility?

A

All NM blocking agents possess 1-2 quaternary nitrogen groups, resulting in poor lipid solubility and inability to cross BBB.

26
Q

What would happen if neostigmine is used alongside a nondepolarizing N2 receptor competitive inhibitor?

A

Neostigmine is an AChE inhibitor and will elevate effective concentration of ACh at NMJ and allow ACh to compete off nondepolarizing agent.

27
Q

What is the duration of drug action of d-tubocurarine (aka. curare) & pancuronium?

A

Long-acting

28
Q

What is the duration of drug action of cisatracurium & vecuronium?

A

Intermediate-acting

29
Q

What chemical group are d-tubocurarine (aka. curare), vecuronium, and mivacurium in?

A

benzylisoquinolines

30
Q

What are the effects of benzylisoquinolines (d-tubocurarine (aka. curare), vecuronium, and mivacurium)?

A

No vagolytic (M receptor cross-reactivity) or ganglionic blocking activity (N1 receptor cross-reactivity)

Elicit some histamine release

31
Q

What chemical group are pancuronium, vecuronium, and rocuronium in?

A

ammonio steriods

32
Q

What are the effects of ammonio steroids (pancuronium, vecuronium, and rocuronium)?

A

Virtually no histamine release

Some muscarinic block

Elicit vagal blockade and tachycardia (newer agents eliminate tachycardia)

33
Q

What is a phase I NM block?

A

Depolarizing

Membrane remains depolarized and unresponsive to later impulses; flaccid paralysis results due to lack of repolarization; ChE inhibitors augment block

34
Q

What is a phase II NM block?

A

Desensitizing

With prolonged exposure, membrane repolarizes but is resistant to further depolarization

35
Q

Succinylcholine has what effect on what receptor?(non/depolarizing; non/competitive; ant/agonist)

A

Noncompetitive N2 receptor agonist, opening Na+ channels (ACh mimic)

36
Q

What enzyme breaks succinylcholine down?

What does this mean for its half-life?

A

Plasma ChE rapidly hydrolyzes -> short half-life

*Not a substrate for AChE

37
Q

What class are mecamylamine & trimethaphan in?

A

ganglionic blocking agents

38
Q

Which describes succinylcholine’s action? Phase I block or phase II block?

A

Phase I block (it is the only depolarizing NM blocker)

39
Q

What are possible contraindications of nondepolarizing blockers?

(for review)

A
  • patients with liver &/or renal dysfunction will have an impaired ability to metabolize and excrete metabolic products
  • some may induce hypotension by blocking ganglionic receptors or by releasing histamine from mast cells
  • several antibiotics may potentiate neuromuscular blocking activity
  • patients with myasthenia gravis already have decreased functional cholinergic interactions at skeletal muscle
40
Q

What are the 4 possible contraindications for succinylcholine? Patients with…

A

1) Plasma ChE gene mutations - patients may exhibit prolonged neuromuscular blockade
2) Organophosphate intoxication - Plasma ChE in patients will be inhibited and thus succinylcholine activity will be potentiated if administered
3) Congestive heart failure, burns, trauma, or neuromuscular disease - excess K+ release into the blood during depolarization of skeletal muscle may result in cardiac arrest
4) Open anterior eye chamber due to injury - Depolarization of extraocular muscles can elicit rapid contraction resulting in increased intraocular pressure

41
Q

What class of drugs are edrophonium and neostigmine in?

A

AChE inhibitor

42
Q

1) AChE inhibitors will readily reverse (antagonize) what effect?
2) What side effects are of concern?
3) What drug can be used in addition to limit these side effects?

A

1) Neuromuscular blockade produced by competitive blocking agents
2) Muscarinic and N1 receptors also affected -> hyperactivity of PS NS
3) Atropine

43
Q

What drugs can antagonize neuromuscular inhibition by succinylcholine?

A

None

44
Q

What is the duration of action of edrophonium?

A

10 minutes

45
Q

What is the duration of action of neostigmine?

A

60 minutes

46
Q

1) What class are mecamylamine & trimethaphan in?
2) What effect do they have on the N1 receptor?(non/depolarizing; non/competitive; ant/agonist)

A

1) ganglionic blocking agents
2) nondepolarizing competitive antagonist

1 Pharm Unit (14 decks)

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