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Pharmacology II > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

which cholinesterase inhibitors are the carbamates

A

neostigmine and physostigmine

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2
Q

which are the carbamates can enter CNS

A
  • Neostigmine: a quaternary amine, is not well absorbed orally and doesn’t cross the blood brain barrier.
  • Physostigmine is a tertiary amine, so is absorbed orally and will get into the brain
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3
Q

effect time of carbamates

A

form a covalent bond with an effect lasting 30 mins- 6 hrs

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4
Q

route of admininistration and effect time of edrophonium

A
  • Injected
  • binds reversibly
  • very short acting (5-10) minutes
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5
Q

use of organophosphates in today’s society

A
  • Organophosphates are used as pesticides and as nerve gases.
  • They are highly lipid soluble
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6
Q

MOA of Organophosphates

A
  • They phosphorylate the cholinesterase enyzyme and form a very long-lasting bond.
  • This bond then undergoes “aging”; breaking one of the phosphorus oxygen bonds increases the strength of the bond until it becomes irreversible.
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7
Q

after organophosphate poisoning, administration of what can prevent death

A
  • Pradlidoxime (2-PAM)
    • if added before aging occurs, it can prevent aging and regenerate the cholinesterase enzyme.
    • If aging is not prevented, organophosphate poisoning may be fatal.
    • must be used within 3-4 hours
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8
Q

Though controversial, what is a method used in emergency departments to differentiate between organophosphate poisoning and carbamate poisoning

A
  • administer 2-PAM
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9
Q

can pralidoxime (2-PAM) enter CNS

A
  • strong nucleophile
  • does not enter CNS
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10
Q

effects of cholinesterase inhibitors have an effect similar to what other receptor agonists you have learned about

A
  • effects of cholinesterase inhibitors will be similar to stimulation of both muscarinic and nicotinic receptors, because the effect of ACh is enhanced.
  • The effect in a particular tissue will reflect the predominant tone in that tissue.
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11
Q

effects of cholinesterase (AChE) inhibitors in the CNS

A
  • alertness, improve memory
  • convulsions and respiratory arrest with poisoning
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12
Q

The Eye, respiratory tract, GI, and genitourinary tract all have what prevailing tone? So cholinesterase inhibitors will behave like what receptor agonist in these tissues?

A
  • parasympathetic tone is dominant in these tissues
  • the effect is very similar to that of muscarinic agonists
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13
Q

effect of cholinesterase inhibitors in the eye

A
  • miosis
  • near vision
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14
Q

effect of cholinesterase inhibitors in GI, and bladder

A
  • stimulation!
  • diarrhea
  • urination
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15
Q

effect of cholinesterase inhibitors in respiratory tract

A
  • salivation
  • secretion
  • bronchoconstriction
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16
Q

effect of cholinesterase inhibitors on cardiovascular system

A
  • in the heart, mainly parasympathetic responses are seen
    • bradycardia
    • decreased force of atrial contraction
    • decreased cardiac output
  • There is little effect on the vasculature (thus BP) since there is no direct cholinergic innervation.
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17
Q

effect of cholinesterase inhibitors on neuromuscular junction

A
  • Low concentrations will increase the strength of contraction of skeletal muscle
  • Higher or toxic concentrations, fibrillation of the muscle may occur, and neuromuscular blockade may result from desensitization of nicotinic receptors.
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18
Q

treatment for myasthenia gravis

A
  • myasthenia gravis: antibodies against nicotinic receptors
  • treatment: low dose of cholinesterase inhibitors
    • Neostigmine
    • Pyridostigmine
    • ambenonium
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19
Q

action of Neostigmine lasts for how long

A

4 hours

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20
Q

Uses of Neostigmine

A
  • increase bladder motility
  • reverse neuromuscular blockage in surgery
  • treat myasthenia gravis
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21
Q

which cholinesterase inhibitor is used for the diagnosis of myasthenia gravis? why?

A
  • Edrophonium
  • short acting (5-10), if myasthenic, muscle strength will improve for about 5 minutes
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22
Q

How is Edrophonium used to decide if a AChE inhibitor treatment dose is right?

A
  • Edrophonium would decrease muscle strength if dose is too high
  • would increase muscle strength if dose is too low
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23
Q

what is Echothiophate

A
  • organophosphate with a very long duration of action
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24
Q

use of Echothiophate

A
  • It is applied in the eye when long-term control of intraocular pressure is required, often in glaucoma emergency situations
  • Not lipid soluble, so does not get absorbed systemically
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25
Q

What are Soman, Sarin, and Tabun

A
  • organophosphates
  • Nerve gases
26
Q

What are Parathion and Malathion

A
  • organophosphates
  • used as pesticides
  • lipid soluble
  • inactivated fairly rapidly by birds and mammals.
27
Q

Treatment of open-angle glaucoma

A
  • Both physostigmine (cholinesterase inhibitors) and echothiophate (cholinesterase inhibitors) may be used to treat open-angle glaucoma, although pilocarpine (Direct-Acting Cholinergic Agonist) is used more often.
28
Q

Acute closed-angle (aka narrow angle) glaucoma is treated with

A
  • combination of pilocarpine and a cholinesterase inhibitor until the pressure is controlled and surgery can correct the problem.
29
Q

What is used in the reversal of neuromuscular blockade in surgery

A
  • The effects of the non-depolarizing neuromuscular blocking agents can be reversed by administration of cholinesterase inhibitors.
    • Neostigmine
    • edrophonium
30
Q

what is Myasthenia Gravis

A
  • autoimmune disease: antibodies to nicotinic ACh receptors
  • not enough ACh can be released to produce the same number of open ion channels
  • weakness and fatigue worsen with exercise
31
Q

List the AChE inhibitor toxicity symptoms

A

SLUDGE

  • Salivation
  • Lacrimation
  • Urination
  • Defecation
  • Gastric distress
  • Emesis

+ neuromuscular stimulation followed by blockade, causing paralysis

32
Q

Treatment of organophophate AChE inhibitor poisoning

A
  1. administer atropine until pupils dilate
  2. administer 2-PAM is less than 3-4 hours since exposure
  3. maintain respiration
  4. Diazepam for convulsions
33
Q

What are Carbaryl, Propoxur, and Aldicarb

A

Carbamates (AChE inhibitors) insecticides

34
Q

MOA of Antimuscarinic (Anticholinergic) drugs

A
  • bind to muscarinic receptor
  • do not activate receptor
  • will displace acetylcholine or agonist from receptor
  • Their effect will be to antagonize the actions of parasympathetic stimulation.
35
Q

prototype Antimuscarinic (Anticholinergic) drug

A

Atropine

36
Q

List the Muscarinic Antagonists

A
  • Atropine
  • Scopolamine
  • Tropicamide
  • Homatropine
  • Ipratropium (Atrovent)
  • Tiotropium (Spiriva)
  • Dicyclomine (Bentyl)
  • Tolterodine (Detrol)
  • Oxybutynin
  • Glycopyrrolate
37
Q

route of administration of muscarinic antagonists.

A
  • Atropine and Scopolamine are well absorbed orally
  • Scopolamine can be absorbed through skin
38
Q

Effect of Scopolamine on CNS function

A
  • Euphoria
  • Sedation
  • Amnesia
39
Q

Scopolamine can be given by transdermal patch to treat what?

A

motion sickness

40
Q

which muscarinic antagonist can enter CNS

A
  • Atropine enters CNS only at high doses
  • Scopolamine enters CNS very easily
41
Q

Why does Atropine effect certain tissues only at certain doses

A
  • The effect of blocking muscarinic receptors will depend to a great deal on the amount of prevailing parasympathetic tone in different tissues
  • Because of this, there is a dose-related sequence of effects of cholinergic blockade
42
Q

Which tissues are affected by Atropine at low doses, medium doses, high doses?

A
  • Low: salivary, sweat glands, bronchioles
    • dry mouth, decreased sweating
  • Medium: GI, urinary tract, Heart, eye
    • urinary retention
  • High: CNS
43
Q

atropine effect on CNS

A
  • little effect, except at toxic doses
  • CNS stimulation followed by depression
  • can cause confusion and coma
44
Q

scopolamine effect on CNS

A
  • drowsiness, memory loss
  • relieves motion sickness
  • toxic: hallucinations, agitation, coma
45
Q

muscarinic antagonist effect in eye

A
  • tone reduced
  • pupil dilates: mydriasis
    • photophobia
  • lens flattens
    • cycloplegia (loss of accommodation for near vision)
46
Q

contraindication to the use of anticholinergics

A
  • Narrow angle glaucoma
  • Because anticholinergic drugs inhibit the ciliary muscle and close the trabecular system, they may obstruct the outflow of aqueous humor, and increase intraocular pressure, especially in narrow angle (closed-angle) glaucoma
  • Benign prostatic hyperplasia (BPH)
47
Q

Which cholinergic antagonists are short-acting drugs that are useful for producing mydriasis used for ophthalmology

A
  • Tropicamide (6 hr)
  • homatropine
48
Q

Muscarinic Antagonists effect on cardiovascular system

A
  • The atria and sinoatrial node are innervated by the parasympathetic nervous system (vagus nerve), and are thus sensitive to antimuscarinic drugs.
    • Antimuscarinic drugs will block M2 receptors in the heart.
  • With moderate doses of atropine, postsynaptic M2 receptors in the SA node will be blocked, and vagal tone will be decreased, resulting in tachycardia.
    • Also, blockade of presynaptic M2 receptors will remove inhibition of norepinephrine release.
49
Q

Muscarinic Antagonists will have the greatest effect on cardiovascular system of what patient population

A
  • Tachycardia would be most noticeable in a healthy young adult with high vagal tone (increase of 25- 35 bpm).
  • Babies and elderly people have far less vagal tone, so the cardiac effects of muscarinic blockade will be small.
50
Q

does muscarinic antagonists have effect on the cardiac ventricles?

A

Cholinergic antagonists have little or no effect on the ventricles, which don’t receive parasympathetic innervation.

51
Q

what effect do muscarinic antagonists have on blood vessels

A
  • Because blood vessels do not receive parasympathetic inputs, antimuscarinic drugs have little effect on peripheral resistance or blood pressure.
  • However, vasodilation may result from release of nitric oxide from endothelial cells in response to circulating muscarinic agonists.
    • Atropine will completely block the decrease in blood pressure seen with muscarinic agonists.
    • Atropine in toxic doses may cause vasodilation in the face, to get rid of excess heat.
52
Q

what effect do muscarinic antagonists have on respiratory system

A
  • The bronchioles receive parasympathetic inputs and the airway smooth muscles have M3 receptors
  • Blockade of muscarinic receptors may produce bronchodilation
53
Q

the effects of muscarinic antagonists are most helpful in what respiratory condition

A
  • COPD
  • acute asthma attacks
54
Q

which muscarinic antagonists are used for bonchodilation due to their local effect in the lung

A
  • Ipratropium (Atrovent)
  • Tiotropium (Spiriva).
55
Q

What effect do muscarinic antagonists have in GI system

A
  • Muscarinic antagonists generally inhibit motility and secretions in the GI tract, and have been used as antispasmodics.
56
Q

which muscarinic antagonist is used as an antispasmodic

A

Dicyclomine (Bentyl)

57
Q

Atropine is combined with an opioid (Diphenoxylate) to treat diarrhea. Why are these two combined?

A
  • The powerful effect of the opioid to decrease gastrointestinal motility is potentiated by addition of atropine.
  • The unpleasant effect of atropine at high doses lowers the abuse potential of the opioid.
58
Q

muscarinic antagonist effect on bladder

A
  • Smooth muscle of the ureters and bladder wall are relaxed by anticholinergics, and voiding is reduced.
59
Q

which muscarinic antagonists are used to treat overactive bladder and urinary frequency.

A
  • Tolterodine (Detrol), a selective M3 receptor antagonist, no CNS side effects. Because of this, it is the preferred drug in the elderly.
60
Q

which muscarinic antagonist is used to treat or prevent bladder spasms

A

Oxybutynin : prevents bladder spasm after prostate surgery

61
Q

problem with given muscarinic antagonist to men with benign prostatic hyperplasia

A

can cause urinary retention

  • thus, contraindicated
62
Q

muscarinic antagonist effect on Sweat, lacrimal, and Salivary Glands

A
  • inhibition of sweat glands
    • body temp increases with toxic doses
  • inhibition of lacrimal glands
    • dry eyes
  • decreased salivation
    • dry mouth

Pharmacology II (9 decks)

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