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Pharmacology Exam 2 > Intro to Cholinergic Pharmacology > Flashcards

Intro to Cholinergic Pharmacology Flashcards

1
Q

What are the 2 methods of ACh metabolism?

A
  1. De novo synthesis (minor)

2. Alternative synthesis (major) - most choline is recycled from ACh

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2
Q

Describe the steps of de novo ACh synthesis

A
  1. ACh synthesis is a 2-step conversion of serine to choline.
    - Step 1 requires enzyme serine decarboxylase.
    - Step 2 requires choline N-methyl transferase and S-adenosyl methionine.
  2. The enzyme choline acetyltransferase (ChAT) is responsible for the acetylation of choline. ChAT resides in the cytoplasm so ACh must be in the cytoplasm. Acetyl-CoA comes from the inner layer of the mitochondria and comes out of the mitochondria as citrate.
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3
Q

What modifications must ACh undergo to have activity in the brain and nervous system?

A

ACh is the major NT in the brain, but choline is charged so there is a BBB to overcome. Once inside the brain, choline remains charged and has to be transported into the neurons into the brain. ChAT converts choline into ACh by adding an acetyl group which allows it to be an active NT in neurons.

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4
Q

How is ACh stored and released?

A

ACh is stored in synaptic vesicles. Cholinergic vesicles contain 2 important transporters which are required to concentrate ACh:
1. proton ATPase
2. ACh-H+ antiport
This has reverse vs. depot pools. ACh-H+ antiport concentrates ACh. The vesicle contains ATP and heparin proteoglycans. Every time ACh is released, heparin sulfate proteoglycans are also released. There are 2 types of pools for release:
1. readily release pool
2. reverse pool - this pool waits for an action potential to be released, then it moves into position for supply.

Release of ACh can be done either by spontaneous or stimulated release.

  1. spontaneous release from terminal has constitutive activity of the NT at the synapse and produces a synaptic potential
  2. stimulated release relies on stimulation by an action potential.
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5
Q

Describe the function and mechanism of SNARE proteins

A

SNARE proteins anchor and release vesicles that contain NTs. There are SNARE proteins on the vesicles (v-SNAREs): synaptotagmin and synaptobrevin as well as SNARE proteins on the terminal membrane: SNAP-25 and Syntaxin.
Synaptotagmin is a Ca2+ receptor and Synaptobrevin binds to syntaxin and SNAP-25 on the membrane to form the ternary complex.
There are 3 steps to vesicle release of NT: 1. docking, 2. priming, and 3. fusion.
n-sec-1 binds syntaxin in the initial state, but it disassociates in order for synaptobrevin to interact with syntaxin and SNAP-25.
This complex tightens and leads to fusion and exocytosis when Ca2+ enters the neuronal terminal and binds to synaptotagmin. This leads to release of NT into the synaptic cleft. Then ATP is required to disassemble the ternary complex by releasing synaptobrevin from syntaxin and SNAP-25 to disassociate from synaptobrevin.

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6
Q

How does the botulinum toxin drug act upon SNARE proteins?

A

Botulinum toxin degrades the SNAP-25 SNARE protein on the terminal membrane and thus prevents vesicle docking on the membrane. This prevents vesicle fusion and exocytosis of ACh, so that it is unable to be released from the vesicle into the synaptic cleft.

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7
Q

What are 3 ways that ACh is degraded and recycled and describe their mechanism of action.

A

Metabolism of ACh:

  1. ACh is made from choline and acetyl CoA
  2. ACh is broken down by AChase in synpatic cleft
  3. Choline is transported back to the axon terminal
  4. Acetylcholinesterase
    - this is found in the vicinity of cholinergic synapses and in RBCs
    - it has a high affinity for ACh and degrades the NT in the synaptic cleft
  5. Pseudocholinesterases (plasma or butyrlcholinesterase_
    - found in plasma
    - T1/2 range from 8-16 hours
    - concentrations may directly affect succinylcholine therapy
  6. Fate of metabolites
    - choline is taken up by special choline transporters into pre-synaptic neurons
    - coenzyme A is released from the mitochondria
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8
Q

How is ACh activity implicated in pts with Alzheimer’s?

A

Acetylcholinesterase will break down ACh and stop it from having effects.
Pseudocholinesterase is used in Tx of Alzheimer’s disease.

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9
Q

What are properties of muscarinic cholinergic receptors?

A
  1. G-protein coupled receptors (Gq/11 or Gi/o)
  2. 5 distinct subtypes exist in humans: M1 - M5
    - M1/3/5 are stimulatory and coupled to Gq and PLC - increase in Ca/IP3/DAG
    - M2/4 are inhibitory and are coupled to adenylyl cyclase and K+ channels, enhancing K+ conductivity (hyperpolarity)
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10
Q

What are properties of nicotinic cholinergic receptors?

A
  • nAChR exhibit direct ligand-gated conductance
  • enhance K+ and Na+ conductance equally
  • there are 2 subtypes of nAChR:
    1. Nm - skeletal muscles and neuromuscular junction
    2. Nn - autonomic ganglia, adrenal medulla, and CNS
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11
Q

For the M1 receptor, describe:

1) typical locations
2) responses
3) mechanisms
4) prototype agonist
5) prototype antagonist

A

1) autonomic ganglia and CNS
2) late excitatory postsynaptic potential (EPSP), complex: at least arousal, attention, analgesia
3) Gq/11 –> PLC –> increase IP3 + DAG –> increase Ca2+ and PKC
4) agonist: oxotremorine
5) antagonist: pirenzepine

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12
Q

For the M2 receptor, describe:

1) typical locations
2) responses
3) mechanisms
4) prototype agonist
5) prototype antagonist

A

1) heart SA node, AV node, atrium and ventricle
2) slowed spontaneous depolarization; hyperpolarization, decreased conduction velocity, decreased refractory period, decreased contractility force, slight decrease in contractility
3) Beta-gamma portions of G protein inhibit AC and increase K+ channel opening
4) agonist: -
5) antagonist: AF-DX 117

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13
Q

For the M3 receptor, describe:

1) typical locations
2) responses
3) mechanisms
4) prototype agonist
5) prototype antagonist

A

1) location: smooth muscle
2) responses: contraction
3) mechanism: same as M1 (Gq/11 –> PLC)
4) agonist: -
5) antagonist: hexahydrosiladifenidol

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14
Q

For the M4 receptor, describe:

1) typical locations
2) responses
3) mechanisms
4) prototype agonist
5) prototype antagonist

A

1) location: CNS
2) responses: -
3) mechanism: same as M2 (Gi)
4) agonist: -
5) antagonist: Himbacine

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15
Q

For the M5 receptor, describe:

1) typical locations
2) responses
3) mechanisms
4) prototype agonist
5) prototype antagonist

A

1) location: CNS
2) responses: -
3) mechanism: same as M1 (Gq/11)
4) agonist: -
5) antagonist: -

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16
Q

For the Nm receptor, describe:

1) typical locations
2) responses
3) mechanisms
4) prototype agonist
5) prototype antagonist

A

1) location: skeletal muscle at NMJ
2) response: end-plate depolarization; skeletal muscle contraction
3) mechanism: opening of Na+/K+ channels
4) agonist: phenyltrimethylammonium
5) antagonist: tubocurare

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17
Q

For Nn receptor, describe:

1) typical locations
2) responses
3) mechanisms
4) prototype agonist
5) prototype antagonist

A

1) locations: autonomic ganglia, adrenal medulla, CNS
2) response: depolarization and firing of postganglionic neuron, secretion of catecholamines, complex: at least arousl, attention, analgesia
3) opening of Na+/K+ channels
4) agonist: dimethylphenylpiperazinium
5) antagonist: trimethylaphan

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18
Q

Where do muscarinic receptors dominate in the CNS?

A

brainstem and spinal cord

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19
Q

Where do nicotinic receptors dominate in the CNS?

A

substantia nigra, locus coeruleus, and septum

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20
Q

What are 6 locations where both muscarinic and nicotinic receptors are found in the CNS?

A
  1. corpus striatum
  2. cerebral cortex
  3. hippocampus
  4. thalamus
  5. hypothalamus
  6. cerebellum
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21
Q

What are 5 major cholinergic projection centers?

A
  1. septum
  2. nucleus basalis
  3. diagonal band
  4. laterodorsal tegmentum
  5. pendiculopontine tegmentum
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22
Q

Because of their location in this region of the brain, what neurologic disease can cholinergic agents be used as Tx for relief?

A

Cholinergic agents can be used for relief of Parkinson’s Sx because the substantia nigra is packed with nicotinic receptors

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23
Q

What are 3 locations of nicotinic receptors in the peripheral nervous system?

A
  1. autonomic ganglia
  2. adrenal medulla
  3. neuromuscular junction
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24
Q

How do the subunits of Nn receptors differ from Nm receptors?

A

Nn receptors are composed only of alpha and beta subunits, whereas Nm is comprised of alpha2-beta-epsilon-gamma (major) or alpha2-beta-gamma-delta

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25
Q

What are 3 major locations of muscarinic receptors in the peripheral nervous system?

A
  1. autonomic ganglia
  2. end organs (parasympathetic, sweat glands)
  3. CNS
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26
Q

Describe the mechianism of M1, M3, and M5 receptors.

A

M1 (autonomic ganglia, CNS), M3 (smooth muscles), and M5 (CNS) are coupled to PLC activation and IP3, DAG, Ca2+ and PKC increases

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27
Q

Describe the mechanism of action of M2 and M4 receptors.

A

M2 (SA node, AV node, atrium, and ventricles) and M4 (CNS) are coupled to adenylyl cyclase inhibition and increase K+ conductance

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28
Q

Describe the cholinergic transmission dysfunction associated with dementia.

A

Dementia is characterized by cognitive decline that leads to reduced or complete loss of ability to carry out daily functions.
Alzheimer’s disease is by far the most frequent and economically important form of dementia. Dysfunction in cholinergic transmission within the CNS is the most consistent neurotransmitter deficit in Alzheimer’s disease.
Trouble begins with the accumulation of neurofibrillary tangles in the entorhinal cortex and hippocampus - 2 of the major destination of cholnergic projections in the CNS.

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29
Q

Where are the 2 locations in the brain that neurofibrillary tangles will be found in someone with dementia and why?

A

neurofibrillary tangles will be found in
1. entorhinal cortex
2. hippocampus
because these are the 2 of the major destinations of cholinergic projections in the CNS

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30
Q

What are 3 drugs that are used in Tx of Alzheimer’s disease and how do they work?

A
  1. Donepezil
  2. Rivastigmine
  3. Galantamine

These drugs work by inhibiting acetylcholinesterase which prolongs life of ACh in the synapse

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31
Q

What is the specific group of neurons in the substantia innominata of the basal forebrain which has a rich supply of ACh that undergoes degeneration in Alzheimer’s?

A

Nucleus basalis

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32
Q

What cholinergic dysfunction is characterized by Parkinson’s and what are the resulting symptoms?

A

Parkinson’s is characterized by selective irreversible loss of dopaminergic neurons in the substantia neigra pars compacta which leads to motor degeneration. These symptoms include:

  1. bradykinesia
  2. rigidity
  3. impaired postural balance
  4. rest tremors
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33
Q

What NT imbalance leads to the characteristic movement dysfunctions in Parkinson’s?

A

An imbalance between dopaminergic input and cholinergic transmission in the putamen

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34
Q

What are effective treatments for relieving Parkinson’s Sx and how do they work?

A

Anti-muscarinic agents such as trihexyphenidyl and benztropine treat Parkinson’s by reducing cholinergic tone in the CNS

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35
Q

How can cholinergic transmission be manipulated for a dilated fundus examination in the eyes?

A

anti-muscarinic agents can be used to induce MYDRIASIS (dilation of the pupil) to observe the inner structures of the eye. Muscles are loaded with M1 receptors - increase and dilate the pupil so the physician can see right through to the pupil

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36
Q

What are 3 drugs that can produce mydriasis?

A

anti-muscarinic agents:

  1. atropine
  2. scopolamine
  3. hyoscyamine
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37
Q

What dysfunction leads to glaucoma?

A

acute angle glaucoma is associated with partial or absolute blockade of the canal of Schlemm. Gluacoma is caused by an increase of aquemous humor which leads to increase pressure in the eyeball. This is due to either slow drainage or overproduction of the aqueous humor.

Normally, the chiliary body makes aqueous humar in the canal of Schlemm. In acute angle glaucoma, the canal of Schlemm is blocked in mydriasis

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38
Q

What are 2 drugs can help relieve Sx of glaucoma?

A

muscarinic agonists:

  1. pilocarpine
  2. phsostigmine
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39
Q

What are 3 disorders of the respiratory tract that are affected by disorders of cholinergic transmission?

A
  1. chronic bronchitis
  2. COPD
  3. Asthma
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40
Q

What leads to asthma?

A

M3 stimulation within airway bronchioles which mediate bronchochonstriction

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41
Q

What are effective Tx for asthma?

A

ipratropium and tiotropium - effective alternatives to B2 adrenergic agonists

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42
Q

What is an effective drug for COPD?

A

Tiotropium with a long plasma half life

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43
Q

What are 3 drugs that help treat hyperhidrosis of sweatglands?

A

anticholinergic drugs:

  1. oxygutynin
  2. glycopyrrolate
  3. benztropine
44
Q

What drug acts on sinus bradycardia in the heart?

A

Atropine (muscarinic antagonist)

45
Q

How do M2 receptors on SA and AV nodes function on the heart?

A

slow down heart rate when stimulated

46
Q

What are the 1A anti-arrhythmic drugs and how do they work?

A

Anti-arrhythmic drugs: quinine, disopyramide, and procainamide. They work by inhibiting cholinergic input to the heart and must be administered with caution.

47
Q

What drug relieves urinary and bladder difficulties?

A

Oxybutynin

48
Q

What is paralytic ileus?

A

Disruption of normal intestinal peristaltic movements due to mechanical causes, leading ot abdominal discomfort, bloating, and constipation. It usually occurs after certain GI surgical procedures.

49
Q

What drug is used for treatment of paralytic ileus?

A

Neostigmine (effective but limited due to side effects)

50
Q

What is associated with Sjogren’s Syndrome?

A

Sjogren’s syndrome is an AI disease that attacks the parotid glands and leads to dry mouth. One of the Sx will be dry everything: hollow organs of the body will be very dry because antibodies attack the perotid gland. Xerostomia is also associated with Sjogren’s syndrome.

51
Q

What treatment is used for Sjogren’s syndrome?

A

Pilocarpine - muscarinic agonist

52
Q

What Tx is used for peptic ulcers?

A

Prenzepine - muscarinic antagonist

53
Q

What is used for ogilvie syndrome?

A

impairment in the ability of the intestine to propel food through the GI tract. It is usually caused by mechanical injury to the intestinal smooth muscles and can lead to abdominal distention, pain, and constipation (depending on the location of lesion along the GI)

54
Q

What is used to treat ogilvie syndrome?

A

Pyridostigmine

55
Q

What chemicals are found in the poisonous mushrooms amanita muscaria and inocybe erubescens?

A

They are loaded with muscimol, ibotenic acid, and muscarine

Muscarine will avidly stimulate muscarinic receptors and lead to asthma-like Sx

56
Q

Why are organophosphates poisonous?

A

They inhibit acetylcholinesterase so you get an overload of ACh in the synaptic cleft which leads to excessive contraction. Sympathetic innervation to the heart will also be affected by organophosphates. Excessive ACh will lead to more parasympathetic activity.

57
Q

Describe the mechanisms and clinical manifestations of tetanus toxin.

A

mechanism: degrades SNARE protein synaptobrevin

Clinical manifestations: trismus (lockjaw), risus sardomicus (facial spasms), opisthotonos (arching of the back)
tetanus toxin attacks synaptobrevin receptor

Contraction is due to not being able to relax the muscles - it will KO GABA which is more important for relaxing the muscle

58
Q

What leads to motion sickness?

A

Motion sickness is caused by motion that is felt but not seen. i.e. sitting in a cruise ship with no windows. You can feel the movement with the semi circular canals in the ears but cannot see the movement. The body thinks that there is a toxin doing this and triggers emesis.
Includes car sickness, sea sickness, air sickness, and dizziness due to spinning

59
Q

What is treatment for motion sickness?

A

Scopolamine

60
Q

Describe Lambert-Eaton Syndrome

A

misguided antibodies against pre-synaptic V-gated Ca2+ channels.
Common Sx are weakness, fatigue, and blurred vision

61
Q

Describe Myasthenia Gravis

A
  • antibodies are directed against nicotinic receptors at the NMJ
  • Sx can be improved with cholinesterase inhibitors but other forms of therapy are available
62
Q

What is a good aid for surgical operations?

A

neuromuscular blockers

63
Q

What are 2 inhibitors of acetylcholine synthesis, storage, and release?

A
  1. hemicholinium-3: blocks choline transport into neuron
  2. Vesamicol blocks ACh uptake into vesicles

*Both are for experimental uses only (no clinical applications to date)

64
Q

What is the mechanism of action for the botulinum toxin?

A

Botulinum toxin may either digest synaptobrevin, syntaxin, or SNAP-25 (depending on the type of botulinum toxin) and interferes with cholinergic tnrasmission at the synapse

65
Q

What are the clinical applications of the botulinum toxin?

A

used for a variety of conditions including focal dystonia, torticolis, achalasia, strabismus, blepharospasm, wroinkles, and hyperhidrosis

66
Q

What are complications caused by botulinum toxin?

A

cardiac arrhythmias, syncope, hepatotoxicity, and anaphylaxis

67
Q

What are 5 acetylcholinesterase inhibitors?

A
  1. edrophonium
  2. neostigmine
  3. pyridostigmine
  4. ambenonium
  5. phsostigmine
68
Q

What are 3 clinical uses of acetylcholinesterase inhibitors?

A
  1. Dx of Lambert-Eaton syndrome and myasthenia gravis (tensilon test)
  2. Management of glaucoma, urinary or GI motility drugs, myasthenia gravis (neostigmine, pyridostigmine, and ambenonium)
  3. antidote to anti-cholinergic toxicity, induced paralysis in surgery (phsostigmine)
69
Q

What are complications of acetylcholinesterase inhibitors?

A

bronchospasm, bradycardia, cardiac arrest, hypotension, salivation, hyperhidrosis

70
Q

What are 3 centrally-acting acetylcholinesterase inhibitors?

A
  1. donepezil
  2. rivastigmine
  3. galantamine
71
Q

What are clinical uses of acetylcholinesterase inhibitors?

A

mild to moderate Alzheimer’s disease (dementia) - produce modest improvements in cognition and behavior
complications: diarrhea, nausesa, vomiting, cramps, anorexia, and vivid dreams

72
Q

Describe the mechanism of action for methacoline

A

Methacoline is used in bronchial challenge est for differential diagnosis of allergic asthma. Its muse may be associated with headache, pruritus, and throat irritation. It is contraindicated in recent heart attack or stroke, aortic aneurysm, or uncontrolled hypertension.
Methacoline makes ACh at muscarinic receptors to check for asthma.
Should not give to a pt with heart attack or stroke because it affects these areas.

73
Q

What muscarinic agonist is used in the treatment of glaucoma?

A

carbachol

74
Q

What muscarinic agonist is used to facilitate urinary tract motility?

A

bethanechol

75
Q

What muscarinic agonist is used in the treatment of xerostomia in Sjogren’s syndrome?

A

cevimeline and pilocarpine

76
Q

What is the nicotinic receptor agonist succinylcholine (suxamethonium) used for?

A

to immobilize patients and facilitate surgical procedures like intubation

77
Q

What are some side effects of suxamethonium?

A

bradycardia, cardiac arrest, malignant hyperthermia, rhabdomyolysis and respiratory depression
other complications include muscle rigidity, myalgia and raised intraocular pressure

78
Q

what patients is succinylcholine contraindicated in?

A

patients with upper motor neuron lesions, skeletal muscle myopathies or malignant hyperthermia

79
Q

What are the clinical uses of atropine?

A

Atropine is a muscarinic antagonist that serves as an antidote for mushroom poisoning and anti-cholinesterase overdose. It may also be used against organophosphate poisoning as well as against nerve gas attacks. It is used as treatment of acute symptomatic bradycardia, excessive salivation and mucus secretions during surgery.

80
Q

What are complications associated with atropine?

A

cardiac arrhythmia, respiratory depression, raised intraocular pressure, xerostomia, constipation, and blurred vision

81
Q

What are contraindications of atropine use?

A

narrow angle glaucoma, its autonomic effects in all organs disappear rapidly except in the eyes (up to 72 hours)

82
Q

What is Scopolamine used for?

A

Muscarinic antagonist used for Tx of motion sickness, nausea, and vomiting

83
Q

What are Sx of Scopolamine?

A

Drug-induced psychosis, somnolence, xerostomia, and blurred vision

84
Q

Who is Scopolamine contraindicated in?

A

narrow-angle glaucoma

85
Q

What are pirenzepine, methscopolamine, and glycopyrrolate used in?

A
  • All muscarinic antagonists

- used against peptic ulcer disease, surgically-induced or vagally induced bradycardia (glycopyrrolate)

86
Q

What are complications of pirenzepine, methscopolamine, and glycopyrrolate?

A

cardiac arrhythmias, malignant hyperthermia, anaphylaxis, constipation, xerostomia, and urinary retention

87
Q

What are ipratropium and tiotropium used for?

A

muscarinic antagonists effective for COPD and asthma. More effective than B-adrenergic agonist in treating COPD than in asthma

88
Q

What are complications of ipratropium and tiotropium?

A

paralytic ileus, anaphylaxis, and oropharangeal edema?

89
Q

What are oxybutynin, propantheline, and terodiline used for?

A

Muscarinic antagonists used for Tx of hyperreflective and overactive bladder and urge incontinence

90
Q

What are complications of oxybutynin, propantheline, and terodiline?

A

dry mouth, constipation, and urinary retention

91
Q

Name 5 nicotinic receptor antagonsists involved in the induction of neuromuscular blockade in surgery and intubation.

A

pancuroniu, tubocurarine, vecuronium, rocuronium, and mivacurium

pancuronium, tubcurarine = long acting
vecuronium and rocuronium = intermediate acting
mivacurium = short acting

92
Q

What are complications with nicotinic receptor antagonists involved in surgical neuromuscular blockade and intubation?

A

hypertension, tachyarrhythmia, apnea, bronchospasm, and respiratory failure

93
Q

What are 2 Sx involved with mivacurium

A

salivation and flushing

94
Q

What are 2 nicotinic antagonists used in treating hypertension in pts with acute aortic dissection?

A

trimethaphan and mecamylamine

95
Q

What are complications with trimethaphan and mecamylamine?

A

paralytic ileus, urinary retention, respiratory arrest, syncope
orthostatic hypertension, dyspesia, diplopia, sedation

96
Q

Name 5 muscarinic receptor agonists

A
  1. methacholine - bronchial challenge test
  2. carbachol - glaucoma
  3. bethanechol - urinary tract motility
  4. cevimeline - xerostomia
  5. pilocarpine - xerostomia
97
Q

Name 1 nicotinic receptor agonists

A

Succinylcholine - imobilize pts during surgical procedures

98
Q

Name 5 uses of muscarinic receptor antagonists

A
  1. Mushroom poisoning, anticholinesterase overdose, organophosphate poisoning, and nerve gas attack
  2. Tx of motion sickness and nausea - scopolamine
  3. peptic ulcer disease and bradycardia - pirenzepine/methscopolamine/glycopyrrolate
  4. COPD and asthma - ipratropium and tiotropium
  5. Tx of hyperreflexic and overactive bladder - propantheline, terdiline
99
Q

Name 2 uses of nicotinic receptor antagonists

A
  1. induciton of neuromuscular blockade in surgery and intubation - pancuronium, tubocurarine, vecuronium, rocouronium, and mivacurium
  2. hypertension in pts with acute aortic dissection - trimethaphan and mecamylamine
100
Q

Name 5 muscarinic receptor agonists

A
  1. methacholine - bronchial challenge test
  2. carbachol - glaucoma
  3. bethanechol - urinary tract motility
  4. cevimeline - xerostomia
  5. pilocarpine - xerostomia
101
Q

Name 1 nicotinic receptor agonists

A

Succinylcholine - imobilize pts during surgical procedures

102
Q

Name 5 uses of muscarinic receptor antagonists

A
  1. Mushroom poisoning, anticholinesterase overdose, organophosphate poisoning, and nerve gas attack
  2. Tx of motion sickness and nausea - scopolamine
  3. peptic ulcer disease and bradycardia - pirenzepine/methscopolamine/glycopyrrolate
  4. COPD and asthma - ipratropium and tiotropium
  5. Tx of hyperreflexic and overactive bladder - propantheline, terdiline
103
Q

Name 2 uses of nicotinic receptor antagonists

A
  1. induciton of neuromuscular blockade in surgery and intubation - pancuronium, tubocurarine, vecuronium, rocouronium, and mivacurium
  2. hypertension in pts with acute aortic dissection - trimethaphan and mecamylamine
104
Q

Name 5 muscarinic receptor agonists

A
  1. methacholine - bronchial challenge test
  2. carbachol - glaucoma
  3. bethanechol - urinary tract motility
  4. cevimeline - xerostomia
  5. pilocarpine - xerostomia
105
Q

Name 1 nicotinic receptor agonists

A

Succinylcholine - imobilize pts during surgical procedures

106
Q

Name 5 uses of muscarinic receptor antagonists

A
  1. Mushroom poisoning, anticholinesterase overdose, organophosphate poisoning, and nerve gas attack
  2. Tx of motion sickness and nausea - scopolamine
  3. peptic ulcer disease and bradycardia - pirenzepine/methscopolamine/glycopyrrolate
  4. COPD and asthma - ipratropium and tiotropium
  5. Tx of hyperreflexic and overactive bladder - propantheline, terdiline
107
Q

Name 2 uses of nicotinic receptor antagonists

A
  1. induciton of neuromuscular blockade in surgery and intubation - pancuronium, tubocurarine, vecuronium, rocouronium, and mivacurium
  2. hypertension in pts with acute aortic dissection - trimethaphan and mecamylamine

Pharmacology Exam 2 (5 decks)

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