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Pharmacology Test #2 > 01 Ganglionic > Flashcards

01 Ganglionic Flashcards

1
Q

what is the structure of the autonomic ganglia and nicotine receptors? (sympathetic and parasympathetic

A

they are ion channels,

  • pentamers, two alpha subunits
  • when open, Na flows in, K flows out
  • Ach binds
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2
Q

Nicotine,

what is the fatal dose?

A 
fatal dose is 40 mg
it is metabolized and excreted rapidly
-it is a ganglionic stimulant
-slight increase in heart rate
-some rise in blood pressure
-modest increase in respiratory rate
-not in the body naturally
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3
Q

what are the toxicity effects on ganglionic stimulants?

A
  • CNS stimulation: convulsions, headache
  • NMJ paralysis: depolarizing blcokade
  • hypertension, hypotension, cardiac arrhythmias
  • vomiting, diarrhea, salivation
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4
Q

if insecticides are ingested, what treatment would be rendered?

A

-induce vomiting

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5
Q

treatment of poisoning from ganglionic stimulants (symptom-directed)

A
  • muscarinic excess: anticholinergic (atropine)
  • NMJ blockade: mechanical respiration
  • CNS stimulation: anticonvulsant (diazepam)
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6
Q

ach is what kind of agonist?

A

nicotinic and muscarinic agonist

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7
Q

what are the ganglionic blocking agents?

A
  • Mecamylamine
  • Timethapan
  • both will cause a drop in blood pressure
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8
Q

Mecamylamine

A

ganglionic blocking agent

  • effective orally, CNS effects
  • causes a drop in blood pressure
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9
Q
  • inactive orally
  • used in hypertensive emergency (CNS origin)
  • controlled hypotension during surgery (causes a drop in bp)
  • short duration of action, 5-10 min, no CNS action
A

Trimethapan

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10
Q

what is the enzyme that breaks down ach?

A

cholinesterase

-ach is NOT taken back up into the nerve terminal

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11
Q

myasthenia gravis

A

normal nerve, but a deficient post-junctional site

  • the body produces antibodies to the nicotinic receptors and they get destroyed
  • muscle weakness and fatigue
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12
Q

diagnosis for myasthenia gravis

A

Edrophonium (Tensilon, short acting) is used for diagnosis and determination of maintenance dose

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13
Q

treatment for myasthenia gravis

A

Treatment: Neostigmine has direct (stimulates receptor) and indirect actions (inhibition of AchE). No cns activity.
-it’s a cholinesterase inhibitor so the ach that is released stays longer

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14
Q

Neuromuscular Junction blocking agents

A
  • competitive (non-depolarizing) agents (curare

- noncompetitive (depolarizing) agents (succinylcholine)

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15
Q

what is the only non-competitive NMJ blocking agent that is clinically used?

A

succinylcholine

-curare is a competitive NMJ blocking agent

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16
Q

non-competitive NMJ blocking agents?

A
  • succinylcholine, , it’s long lasting, especially compared to Ach (minutes compared to milli seconds
  • cannot be reversed, just have to wait for drug to wear off
  • it binds to the site like Ach, causes a depolarization (Na in, K out) muscle contracts, but bc the stimulation is persistent, it causes muscle paralysis
17
Q

competitive (non-depolarizing) agents

A
  • compete with Ach for binding to receptor
  • flaccid, relaxed paralysis
  • non-NMJ effects: ganglia, muscarinic blocking, histamine release
18
Q

how can a NMJ block be reversed?

A

for a competitive agent: can be reversed by AchE inhibitors

-for non-competitive: NMJ block not reversed by AchE inhibitors

19
Q

competitive NMJ blocking agents…

A

(nondepolarizing)

  • Curare is the prototype
  • pancuronium, rocuronium, atracurium
  • tubocurarine, dimethyltubocarine (metocarine)
  • no effect on nerve transmission
  • muscle can still be stimulated
  • can cause histamine release (mast cells)
  • can block ganglionic receptros (higher concentrations)
20
Q

source(s) of curare

A

frog (poison-arrow frog)

some plants, the brighter the animal, the more dangerous it is

21
Q

Pancuronium

A
  • More potent than tubocurarine (X5)
  • reduce histamine release than curare
  • lack of ganglionic blockage
22
Q

Rocuronium

A

-fast onset (1-2 min), 30-40 min duration, hypersensitivity

23
Q

atracurium

A

(about 10 isomers

  • hydrolysis by AchE
  • replaced by cisatracurium, Hoffmann degradation, ORGAN INDEPENDENT, so I guess it’s often used during surgery bc it is more predictable
24
Q

what drug could be used to reverse the affects of competitive NMJ blocking agents?

A

Neostigmine (AchE inhibitors)

25
Q

succinylcholine

A

often used during surgery bc of fast onset

  • depolarizing NMJ blocking agents
  • metabolized by pseudocholinesterase (comes from plasma)
  • some ppl has “atypical” pseudo-AchE which isn’t very good at metabolizing succinycholine so it takes 2-3 hrs instead of 5-10 minutes
  • not reversed by AchE inhibitors (neostigmine would make it worse)
26
Q

what are the adverse effects of succinylcholine and the treatment

A
  • toxicity: similar to competitive blockers with less effects at ganglia or histamine release
  • Treatment: artificial respiration
  • Adverse reactions: ‘Atypical” psuedo-AchE=prolonged apnea (2-3) hours
  • hyperkalemia (esp. burn trauma patients, response delayed 2-7 days)
  • malignant hyperthermia (esp. with halothane)
27
Q

when is succinylcholine contraindicated?

A

a burn or trauma victim two or three days after the incident bc of hyperkalemia

28
Q

what is the treatment for malignant hyperthermia?

A

DOC: dantrolene (decreases Ca release)

the hyperthermia comes from increased Ca which causes increased muscle contractility, increased body temp

29
Q
  • inhibits calcium release from SR - significant liver toxicity
  • muscle weakness
  • DOC for malignant hyperthermia
A

dantrolene (dantrium)

30
Q

what are the “problems/concerns” associated with succinylcholine?

A

1-‘atypical’ psuedo-AchE
2-hyperkalemia (esp burn, trauma patients 2-7 days later), this can lead to cardiac arrest
3-malignant hyperthermia (esp with halothane an anesthetic) treated with Dantrolene

Pharmacology Test #2 (7 decks)

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