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Bugs and Drugs > Cholinergic Drugs > Flashcards

Cholinergic Drugs Flashcards

1
Q

What is the major cholinergic agonist?

A

Ach- the natural transmitter

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2
Q

What are the major muscarinic agonist drugs?

A

bethanechol

pilocarpine

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3
Q

What are the major muscarinic antagonists?

A

atropine
tropicamide
tolterodine
tiotropium

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4
Q

What are the major Achesterase inhibitors?

A

physostigmine
neostigmine
donepezil
sarin

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5
Q

What is a cholinesterase reactivator?

A

pralidoxime

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6
Q

What is a nicotinic ganglionic agonist?

A

nicotine

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7
Q

What is a nicotinic ganglionic antagonist?

A

trimethaphan

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8
Q

What is the main depolarizing neuromuscular blocker?

A

succinylcholine

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9
Q

What are the major non-depolarizing neuromuscular blockers?

A

d-tubocurarine

vecuronium

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10
Q

What is a major Ach Release inhibitor

A

Onabotulinumtoxin A (Botox)

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11
Q

What type of cholinergic drug is succinylcholine?

A

a depolarizing neuromuscular blocker

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12
Q

What type of drug is trimethaphan?

A

a nicotinic ganglionic antagonist

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13
Q

What type of drug is physostigmine or neostigmine?

A

Acetylcholine esterase inhibitor

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14
Q

What type of drug is nerve gas (sarin)?

A

acetylcholine esterase inhibitor

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15
Q

If someone has been exposed to sarin, what drug would you give them? Why?

A

pralidoxime because it reactivates Achesterase

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16
Q

What contributes to the really short clearance time from the synaptic cleft?

A

the easily cleavable ester bond

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17
Q

What two structural features of Ach also have functional properties?

A
  1. easily cleaved ester bond

2. NH4+ quarternary amine which attracts it to its site of action

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18
Q

What receptor is found at all cholinergic AND adrenergic ganglia?

A

Ng (nicotinic)

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19
Q

What receptor is found at the parasympathetic neuroeffector junctions? What tissue specifically are affected?

A

Muscarinic on exocrine glands, smooth muscle and viscera

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20
Q

The somatic neuromuscular junction has what type of receptor?

A

Nm (nicotinic)

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21
Q

The central nervous system has which cholinergic receptors?

A

M and N

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22
Q

Where would one see non-innervated tissue with AchR? what type of receptor is present?

A

Muscarinic receptors are present in endothelial cells of blood vessels that cause vasodilation

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23
Q

How does choline enter the nerve terminal?

What drug can block choline transport into the nerve terminal?

A

It is co-transported with Na+ and is a rate-limiting step.

It can be blocked by hemicholinium

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24
Q

What does hemicholinium do?

A

It blocks choline from entering the nerve terminal. It is not specific or useful therapeutically

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25
Q

What are the three steps for synthesis and storage of Ach?

A
  1. choline enters the nerve terminal (via cotransport with Na+, blocked by hemicholinium)
  2. Acetyl CoA + choline -(CAT)–> Ach
  3. Ach is packaged into vesicles
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26
Q

What blocks the release of Ach from vesicles?

What facilitates excessive release?

A 
Botulinum toxin (onabotulinumtoxin A) stops release of Ach
A-latrotoxin from black widows cause excessive release of Ach by increasing Ca2+ influx
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27
Q

What are the two receptors for Ach?

What is a natural agonist and antagonist for each?

A

N agonist- nicotine
N antagonist- d-tubocurarine
M agonist- muscarine
M antagonist- atropine

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28
Q

What are potential effects of Ach binding to receptors?

A
  1. excitatory- depolarization of postsynaptic membrane and Ca2+ influx
  2. inhibitory- hyperpolarization of postsynaptic membrane
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29
Q

What are the two potential mechanisms by which latrotoxin releases Ach vesicles?

A
  1. Ca-dependent stimulation of neurotransmitter vesicle fusion with plasma membrane
  2. Release of cytoplasmic transmitter into nerve junctions via pores induced in the cell membrane by the toxin
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30
Q

What are the symptoms associated with a-latrotoxin?

A
  1. severe pain and muscle spasms spreading from site of spider bite
  2. sweating, stomach cramps. nausea, vomit
  3. tightness of chest, hard time breathing
  4. increased BP
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31
Q

How exactly does botulinum toxin prevent the release of Ach?

A

It is a protease that cleaves SNAP25, VAMP or syntaxin preventing the fusion of the vesicle with the plasma membrane to allow exocytosis

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32
Q

How is onobotulinumtoxinA administered? How long does it last? What happens to the muscles in the area?

A

It is administered by local injection, lasts weeks, and the muscles atrophy

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33
Q

What are the six things botox are typically used to treat?

A
  1. strabismus
  2. focal dystonia
  3. chronic blinking (blepharospasm)
  4. wrinkles
  5. hyperhidrosis (sweat glands)
  6. migranes
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34
Q

How are botulinum and tetanus similiar? How are they different?

A

Botulinum toxin acts on excitatory nerve endings and blocks release of Ach (thus having an inhibitory effect and causing flaccid paralysis)
C. tentani (tetanus toxin) acts on inhibitory nerve endings by the same mechanism of botulinum (prevents vesicle fusion). This inhibits the inhibitory response thus causing tentanic contraction of muscle

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35
Q

What are the two main types of cholinesterases?

Where is each found?

A
  1. acetylcholinesterase - at the synaptic cleft

2. butyrylcholinesterase- serum/plasma

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36
Q

Butyrylcholinesterase is of specific interest in the metabolism of what drug?

A

succinylcholine

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37
Q

What are the two general categories of Achesterase inhibitors? What is an example of each?

A

Reversible- physostigmine

Irreversible- DFP and organic phosphates (insecticides)

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38
Q

What snake toxin irreversibly inhibits cholinergic receptors?

A

alpha toxin

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39
Q

What is myasthenia gravis?

A

an autoimmune disorder where Ab are made against nicotinic receptors

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40
Q

What cholinergic receptor has an

“ALL or NOTHING” response?

A

Nicotinic receptors have an all or none response. If two Ach bind to the alpha subunits, the channel will allow depolarization and if it is enough depolarization will cause an AP and transmission of a downstream signal

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41
Q

What is “dual response”? What type of receptor is it associated with?

A

It is when continuous stimulation of a nicotinic receptor leads to:

  1. failure to repolarize at the postsynaptic junction
  2. desensitization of the receptors
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42
Q

What preferentially blocks Ng receptors?

A

Hexamethonium at synapses in autonomic ganglia and adrenal medulla

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43
Q

What preferentially blocks Nm receptors?

A

Decamethonium at synapses at the neuromuscular junction of somatic systems

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44
Q

Compared to nicotinic receptors, muscarinic have a __________, more _________ response.

A

Slower more graded response often used to regulate intrinsic activity.

MODULATION NOT CONTROL

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45
Q

M2 and M4 operate through what G protein? What is the result?

A

Gi - increased K, decreased cAMP, decreased Ca

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46
Q

M135 work through what G protein? What is the result?

A

Gq- increased PLC->IP3/DAG–> increased Ca

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47
Q

What natural drug blocks all muscarinic receptors?

A

atropine

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48
Q

What are the two most important things to consider when deciding the utility of a drug?

A
  1. what is the SPECIFICITY for the receptor?

2. will it get to the SITE OF ACTION (availability)?

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49
Q

Cholerginc drugs that are _______ amines are more likely to have effects in the CNS whereas ______ amines are largely excluded.

A

tertiary enter CNS, quarternary are excluded

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50
Q

How does hydrophobicity determine distribution of drugs?

A

The more hydrophobic a drug, the better it can penetrate, concentrate and provide selective action in the CNS

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51
Q

If 10microg/kg Ach is administered, what happens to:

  1. the autonomic ganglia firing rate
  2. HR
  3. BP
  4. GI contraction
A
  1. nothing because it is not enough to effect Ng receptors
  2. decreased (but potentially a reflex tachycardia)
  3. decreased
  4. increased
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52
Q

What happens if atropine is given with 10mg/kg Ach to:

  1. ganglion firing rate
  2. HR
  3. BP
  4. GI contractility
A

There will be no change in anything because this is not enough to influence nicotinic receptors and all the muscarinic receptors are blocked by atropine

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53
Q

If a large dose of Ach (100mg/kg) is given with atropine, what happens to:

  1. autonomic ganglia firing rate
  2. HR
  3. BP
  4. GI contractility
A

100mg/kg is enough to excite muscarinic, nicotinic sympathetic ganglia neurons so:

  1. firing rate increases
  2. HR increases (bc of sympathetic)
  3. BP increases (bc of sympathetic)
  4. nothing happens to GI
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54
Q

If 100mg/kg Ach is given with atropine and a&b blockers, what happens to:

  1. firing rate
  2. HR
  3. BP
  4. GI contractility
A
  1. increases because nicotinic receptors are still being stimulated to fire at ganglia
  2. normal
  3. normal
  4. normal
    2-4 because BOTH parasympathetic and sympathetic are blocked
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55
Q

What happens if 100 mg/kg Ach is given with atropine, a&b blocker AND hexamonium to the:

  1. firing rate
  2. HR
  3. BP
  4. GI contractility
A

they all are cancelled because:

effector parasympathetics AND sympathetics are blocked as well as Ng by the hexamonium

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56
Q

Where would cholinergic agonists act?

A
  1. M receptors at NEJ
  2. M receptors in non-inervated vasculature
  3. Mg receptors (depending on penetration)
  4. Ng and Nm receptors IF THE CONCENTRATION OF DRUG IS HIGH ENOUGH
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57
Q

Why is Ach typically not given as a cholinergic drug?

A

because it is rapidly degraded

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58
Q

What is bethanechol?
Where is its site of action?
How is it taken?
Why is it better than the prototype drug?

A

A muscarinic agonist
GI and urinary smooth muscles
Taken orally or subcutaneously
Resistant to BchE and AchE

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59
Q

What is the effect of giving Ach with an AchE inhibitor?

A

Synergistic effect because it is prolonging Ach life in the synaptic cleft and providing more Ach to act on the effector muscle

60
Q

How are Ach and bethanechol different in their sites of action?

A

Ach can have nicotinic effects but bethanechol does not

61
Q

What would be the relationship if you use bethanechol with AchE inhibitor?

A

they would have an additive effect because bethanechol is ALREADY resistant to being degraded. You would have extra Ach and bethanechol at receptors then

62
Q

Why do you take bethanechol orally or s.c.?

A

So it has good specificity to the site of action (GI and urinary smooth muscle) and decreases the toxicity (action on the vasculature)

63
Q

What are the four major uses for bethanechol?

A
  1. urinary retention- to help release pee
  2. GI stasis- to get bowels moving post-op
  3. Diagnosis of atropine intoxication
  4. Topically for closed angle glaucoma
64
Q

What are the three major contraindications for using muscarinic agonists?

A
  1. Asthma- Ach can bronchoconstrict
  2. coronary insufficiency- Ach can cause hypotension via vascular dilation
  3. Peptic ulcers- Ach can stimulate secretion of gastric acid
65
Q

I have asthma. Why would I be wary of taking a muscarinic agonist?

A

Muscarinic receptors cause bronchoconstriction

66
Q

I have been known to get peptic ulcers. What type of drug should I avoid?

A

I should avoid muscarinic agonists because parasympathetic response is to increase gastric secretion (rest and DIGEST)

67
Q

I have a history of fainting due to low BP. Why would I not want to take a muscarinic agonist?

A

They vasodilate which would decrease BP even more causing severe hypotension

68
Q

What is a cholinomimetic?

A

A cholinergic agonist

69
Q

What type of drug is pilocarpine?

A

a tertiary amine that acts as a cholinergic agonist (mostly muscarinic)

70
Q

What are the three main clinical uses of pilocarpine?

A
  1. Topical application to treat acute glaucoma
  2. Orally to treat Sjogren’s (inability to form saliva/tears)
  3. Sweat test for CF
71
Q

What is Sjogren’s syndrome? What might I use to treat the symptoms?

A

It is an autoimmune disease that attacks endocrine glands presenting with chronic dry eyes and mouth that can be treated by:

  1. pilocarpine
  2. M3 selective agonist
72
Q

What is the “Belladonna” alkaloids?

What type of amine are they and what do they block?

A

Atropine and scopolamine which are tertiary amines that competitively block muscarinic receptors

73
Q

What is tropicamide?
What is advantageous about its half life?
When would you NOT want to use it?

A

a muscarinic antagonist that helps dilate the eyes for eye exams.
It has a short half life, so the pupils return to normal quickly after the exam.
You would not want to use tropicamide if the person has narrow angle glaucoma because it will block outflow of aq. humor even more and increase intraocular pressure and pain

74
Q

What is the benefit of using a quarternary amine over a tertiary amine? What would be a drawback?

A

Quarternary amines have more localized effect and cannot get into the CNS, but they frequently increase blockage of nicotinic receptors too.

75
Q

What would be the specific instance when you would use atropine as a drug?

A

If the person had AchE poisoning because atropine would block the receptors from the excess Ach

76
Q

What would the effect of an antimuscarinic drug be on the eyes?

A
  1. mydriasis (pupil dilation)

2. cycopegia (paralysis of ciliary muscles)

77
Q

What would the effect of an antimuscarinic drug be on the heart? What is controversial about this use?

A

It would cause tachycardia which is sometimes used:

  1. in myocardial infarct where bradycardia is prominent
  2. intraoperative to control bradycardia
78
Q

What is the effect of antimuscarinic drugs on vasculature?

A

Not much because dominant tone in the vasculature is sympathetic

79
Q

What is the effect of antimuscarinic drugs on the GI and urinary tract?

A

It will decrease motility, secretions, and reduce voiding

80
Q

What is the major drug used for reducing urge incontinence (uninhibited detrussor contraction)?

A

Tolterodine an M3 specific blocker which will relax the detrusser

81
Q

What is tolterodine?

A

An M3 specific antagonist used for relaxing the detrusser muscle to treat urge incontinence

82
Q

What is the effect on a muscarinic antagonist on salivation and sweating?

A

It will decrease salivation and sweating

83
Q

What is the effect of a muscarinic antagonist on the respiratory tract?

A
  1. Bronchodilation

2. reduces secretions

84
Q

What drug is inhaled to selectively reduce constriction of the bronchioles?

A

Tiotropium is given as a M blocker in the lungs to remove the parasympathetic contraction

85
Q

What is the function of tiotropium?

A

it is a muscarinic antagonist that is inhaled (and Nh4+ so it will stay locally) to relax bronchial constriction

86
Q

What are the two potential types of drug that could treat asthma and COPD?

A
  1. M antagonist (tiotropium)

2. B agonist (albuterol)

87
Q

What is the effect of atropine on the CNS?

A

High doses cause restlessness, delirium and hallucinations

88
Q

What is scopolamine? What does it treat?

A

It is a muscarinic antagonist that treats car sickness (motion)

89
Q

What are three potential causes of muscarinic inhibitor overdose?

A
  1. accidental (systemic spread of topical application)
  2. eating berries with alkaloids
  3. Deliberate (sleeping pills)
90
Q

What are the symptoms of a cholinergic inhibitor overdose?

A

They will get sympathetic response so:

  1. red as a beet- vascular dilation
  2. Dry as a bone - anhidrosis
  3. Hot as a hare- can’t sweat so overheat
  4. Mad as a hatter- dilirium
  5. Blind as a bat - dilated eyes (mydriasis)
  6. Full as a flask - urinary retention
91
Q

What would be the treatment for OD on cholinergic inhibitors?

A

Physostigmine- an AchE inhibitor which would allow more Ach to act on the few receptors that remain from the anti-muscarinic drugs

92
Q

What are the two main reasons for using AchE inhibitors?

A
  1. therapeutic (myasthenia gravis, Alzheimer’s, opthamology, atony of GI tract)
  2. Insecticides/chemical warfare
93
Q

What drugs are reversible inhibitors of AchE?

A

Donepezil- competitive antagonist
Physostigmine- carbamoylating agent
Neostigmine- carbamoylating agent

94
Q

Which drugs are carbamoylating agents?

How do they operate?

A

Physostigmine and Neostigmine covalently carbamoylate the active site of the esterase and then are reversed slowly by hydrolysis (2-6 hours)

95
Q

What are irreversible inhibitors of AchE? What is their mechanism of action?

A

Insecticides (DFP) and nerve gases (sarin) and they phosphorylate the active site of the esterase

96
Q

What are the potential sites of action of AchE inhibitors?

A
  1. post-ganglionic parasympathetic muscarinic
  2. ganglionic nicotinic
  3. neuromuscular nicotinic
  4. CNS junction (M and N)
97
Q

What AchE is selective for NMJ action only? How is this achieved?

A

Neostigmine because it is a quaternary amine so it can’t penetrate CNS and stays local

98
Q

At muscarinic sites, AchE will be _________. At nicotinic junctions, the potentiation of Ach will __________.

A

At muscarinic sites it will be stimulatory
At nicotinic junctions, Ach originally causes facilitation, but then will result in blockage of signal transduction because the receptors will desensitize and the membrane will not be able to repolarize to propogate an AP

99
Q

What are the effects of AchEI on the eye?

A

Miosis- pupil constriction (classic pinpoint pupil with organophosphate poisoning)

100
Q

What is the main AchEI used on the eye? What does it treat?

A

Physostigmine treats acute angle glaucoma to allow Aq humor to drain by constricting the pupil

101
Q

What is the role of AchEI on the heart and blood pressure?

A

Not much

102
Q

What is the role of AchEI on the GI tract and urinary tract?

A

It increases gastric contractions and secretions and increasing motility of the bowels

103
Q

What AchEI is used for the gut and urinary tract?

A

neostigmine relieves abdominal distension and atony of the bladder

104
Q

Why can’t AchEI work for gastric atony after a vagotomy?

A

The source of Ach is gone. So AchE inhibitor would not be able to prolong Ach that isnt there

105
Q

What would AchEI do for saliva and tears?

A

It would increase production

106
Q

What would AchEI do for respiratory tract?

A

Bronchoconstriction

107
Q

What drug is used for Alzheimer’s? What class of drug is it and what is the function?

A

Donepezil is an AchEI which leaves Ach in the synpapses and assist the neurons that are left

108
Q

What AchEI aids in poisoning by anti-muscarinic drugs?

A

Physostigmine

109
Q

What is the classic test to diagnose myasthenia gravis?

A

Edrophonium test- administration of this AchEI will result in a dramatic (but temporary) improvement in strength bc it leaves Ach to react with the few receptors that haven’t been attacked by autoantibodies

110
Q

Why is neostigmine given for myasthenia gravis?

A
  1. Because it has specificity for NMJ as a quarternary amine

2. it has some direct stimulatory effects on NMJ receptors

111
Q

What is a myasthenic crisis? How can it be differentiated from a cholinergic crisis?

A

Myasthenic crisis is muscle weakness due to lack of nicotinic receptors on muscle and brevity of Ach to activate the receptors that are left.
Cholinergic crisis occurs when there is too much AchEI and the Ach remains in the cleft too long overstimulating the receptors so they don’t repolarize and AP can’t propogate

You do the Edrophonium test. If Myasthenia crisis, things will improve. If Cholinergic crisis, things will get worse

112
Q

When doing the edrophonium test, what should you have on hand in case it is cholinergic crisis and not myasthenic crisis?

A

atropine (to block muscarinic receptors) and a ventilator (bc bronchoconstriction due to Ach)

113
Q

AchEI toxicity can occur via accidental exposure to pesticides or suicidal attempts. The effects will be local if the exposure was ________ and will be systemic if the exposure was ________.

A

Local-dermal

Systemic- respiratory

114
Q

How would an OD on AchEI appear?

A

SLUDGE (salivation, lacrimation, urination, defecation, GI effects, emetic)
They will also have muscle weakness and twitching, pinpoint eyes, tightness in the chest

115
Q

What is the cause of death in a nerve gas poisoning? How long does it take?
How do you recover?

A

It is respiratory failure bc the excess Ach causes bronchoconstriction
Death can occur between 5min and 24 hrs if pulmonary ingested
You recover by resynthesizing AchE which takes about a day

116
Q

What treatment is given for an AchE inhibitor poisoning?

A
  1. Atropine to reduce muscarinic effects (lungs)
  2. artificial respiration
  3. Cholinesterase reactivators (pralidoxime)
117
Q

What is pralidoxime?

A

a cholinesterase reactivator that is only effective against phosphorylated AchE

118
Q

Will pralidoxime help in a physostigmine, neostigmine or doneprezil overdose?

A

No because it only reactivated phosphorylated AchE. Neo and physo are carbamoylated

119
Q

What would the physiological effects of nicotine be?

A

It would stimulate Ng receptors thus triggering parasympathetic, sympathetic and CNS responses because nicotinic receptors are on the post-synaptic neuron at every ganglion

120
Q

Low doses of nicotine effect stimulation of many organs and excitation of ___________ is especially pronounced. With repeated doses, minor effects dissipate but _________________ effects persist.

A 
Respiration is pronounced
Cardiovascular responses (increased rate/BP) persist
121
Q

Why is nicotine assumed to be addictive?

A

It affects a4b2 receptor in the nucleus accumbens and prefrontal cortex and is considered to be a “reward” by stimulated release of dopamine

122
Q

What are the three strategies for quitting smoking?

A
  1. give low doses of nicotine (patch, gum, etc) so withdrawal is avoided but harmful tobacco agents are gone
  2. Partial a4b2R agonist so reward is partially stimulated and withdrawal symptoms are not there. Additionally, bc the receptor will be occupied, continued smoking will not provide the reward it usually does
  3. Antidepressant enhances noradrenergic and dopaminergic activity by inhibiting reuptake and can antagonize nicotinic receptors
123
Q

What would cause a toxic overdose of nicotine? What would be the physiological results?
How would you treat toxicity?

A

Children ingesting cigarettes or insecticide poisoning
First stimulation, but then depression of nerves because of inability to depolarize –>AP leading to respiratory paralysis
Therapy is to do a stomach lavage using charcoal

124
Q

What drugs inhibit Ng receptors?

What is the physiological effect?

A

Hexamethonium
Trimethaphan- quarternary sulfonium and preferred method

The drugs are used locally and withdrawal the autonomic tone (so whichever was more prominent)

125
Q

What is the dominant tone of arterioles? What happens with a Ng inhibitor?

A

sympathetic is natural tone so with Ng inhibitor you would see a parasympathetic effect–> vasodilation

126
Q

What is the dominant tone of veins? What would happen with a Ng inhibitor?

A

Sympathetic so with a Ng inhibitor the veins would dilate and blood would pool

127
Q

What is the dominant tone of the heart? What would happen with a Ng inhibitor?

A

Parasympathetic so with Ng inhibitor it would increase HR and contractility

128
Q

What is the dominant tone of the iris? What would happen with an Ng inhibitor?

A

PArasympathetic so if that is blocked the pupil will dilate

129
Q

What is the dominant tone of the GI tract? What would happen with a Ng inhibitor?

A

Parasympathetic so if it is blocked, the bowels will slow

130
Q

What are the only situations where an Ng inhibitor is even considered?

A
  1. Hypertensive crisis with acute dissecting aortic aneurysm
  2. To have controlled hypotension in surgery
  3. To control hyperreflexia with upper spinal cord injuries
131
Q

What is the desired effect when using a NMJ inhibitor?

A

flaccid paralysis

132
Q

What are the two types of NMJ inhibitors that act on the nicotinic receptors?

A
  1. Competitive non-depolarizing inhibitors (d-tubocurarine and vecuronium)
  2. Depolarizing agents (decamethonium and succinylcholine)
133
Q

What is different molecularly between tubocurarine/vecuronium and succinylcholine/decameconium?

A

tubo/vecur are bulky, non-flexible

succinylcholine is long and slender

134
Q

What is the mechanism of action for tubocurarine and vecuronium?
What happens when you use AchEI with these drugs?

A

They compete with Ach for the receptor binding site and are antagonized by Ach

AchE inhibitors will antagonize these drugs

135
Q

What is the mechanism of action for succinylcholine and decamethonium?
What happens when you use AchEI with these drugs?

A

They are agonists for the AchR.

  1. stimulate the receptors
  2. Persistent depolarization leads to the inability to have AP transmission
  3. Receptor desensitization (receptors are endocytosed so they cant be bound)

AchEI will potentiate these drugs because Ach will speed the process of depolarization and desensitization

136
Q

What is the sequence of paralysis for tubocuranine and vecuronium?

A

small rapid muscles>limbs/neck> intercostal>diaphragm

137
Q

What is the sequence of paralysis for succinylcholine?

A

limbs/neck>small rapid muscles> diaphragm

138
Q

What NMJ inhibitors can release histamine causing bronchospasm and hypotension?

A

d-tubocuranine and vecuronium

139
Q

How does the recovery of phase I and phase II from succinylcholine inhibition of the NMJ compare?

A

Phase 1 recovery is quick because the membrane will repolarize
Phase 2 is slower because the receptors have to be resensitized

140
Q

Succinylcholine has a short duration of action (2-5 minutes). Why?

A

It is rapidly hydrolyzed by butyrylcholinesterase

141
Q

What are the four major clinical uses of succinylcholine?

A
  1. surgical anesthesia- muscular relaxation and reduces risk of respiratory and cardiac depression
  2. Orthopedic procedures to loosen muscles
  3. Intubation
  4. electroshock
142
Q

What is the drug interaction between succinylcholine and cholinesterase inhibitors?

A

succinylcholine will be prolonged

tubocurarine and vecuronium will be antagonized because they will have to compete for receptors

143
Q

What is the drug interaction between NMJ inhibitors and inhalation anesthetics?

A

The effects of tubocurarine and vecuronium are increased

144
Q

What antibiotics can increase the blockade of NMJ inhibitors?

A

Tetracycline, aminoglycoside, peptide antibiotics

145
Q

What do Ca channel blockers do to the effects of NMJ inhibitors?

A

enhance the blockade

146
Q

What are the four disease conditions that can effect NMJ inhibitor actions?

A
  1. genetic reduced plasma cholinesterase - will enhance succinylcholine and can lead to prolonged apnea
  2. genetic mutation to ryanodine receptor leads to widespread rigidity and hyperthermia with succinylcholine
  3. Tissue damage- succinylcholine can increase hyperkalemia
  4. myasthenia gravis- less receptors to block so reduce amount of succinylcholine given
147
Q

What three things are characteristic of a succinylcholine overdose?

A
  1. prolonged apnea- treat with artificial respiration and O2
  2. Cardiovascular collapse
  3. histamine release

Bugs and Drugs (21 decks)

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