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Pharm Block 10 > Acetylcholinesterase Inhibitors > Flashcards

Acetylcholinesterase Inhibitors Flashcards

1
Q

It’s therapeutic use is in the treatment of anti cholinergic toxicity (such as in atropine)

A

Physostigmine

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2
Q

If the name has -stigmine in it

A

Acetylcholinesterase inhibitors

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3
Q

What kind of amine is physostigmine

A

Tertiary amine, very lipid soluble, no charge, can go anywhere in the body

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4
Q

What is the downside to physostigmine

A

Can enter CNS and cause convulsions

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5
Q

What do we use for an atropine overdose?

A

Physostigmine

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6
Q

What is the primary use for pyridostigmine and neostigmine

A

For myasthenia gravis treatment

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7
Q

What are the reversible acetylcholinesterase inhibitors

A

Physostigmine, pyridostigmine, neostigmine, edrophonium, donepezil

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8
Q

Antibodies attack nicotinic (Nm) receptors at the NMJ

A

Myasthenia gravis

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9
Q

Acts to reverse no depolarize get blocking agents (rocuronium)

A

Pyridostigmine

Neostigmine

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10
Q

Pyridostigmine and neostigmine and the CNS

A

They are quaternary amines so have less potential to enter CNS and cause convulsions

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11
Q

Why is pyridostigmine or neostigmine a better choice for myasthenia gravis than physostigmine

A

Because physostigmine can reach the CNS and cause convulsions. It can definitely treat MG, but there’s not advantage to it. The other two dont reach CNS to cause convulsions so they are the best choice

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12
Q

It’s therapeutic use is to diagnose myasthenia gravis

A

Edrophonium

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13
Q

Why is edrophonium good for diagnosis MG

A

Has a short duration of action (10-20m) and IV injection leads to a rapid increase in muscle strength in those with MG. Inhibits Achase and increases Ach

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14
Q

Clinical presentation of myasthenia gravis

A
  • ptosis
  • difficulty chewing and swallowing
  • anhydrosis
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15
Q

It’s therapeutic use is to treat mild to moderate Alzheimer’s

A

Donepezil

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16
Q

Oldest and most common drug to treat mild to moderate Alzheimer’s

A

Donepezil

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17
Q

Why do we use an Achase inhibitor to treat Alzheimer’s

A

Patients have a loss of neurons in the cortex and disproportionate loss of cholinergic neurons. Want to increase ACH as the primary therapeutic strategy

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18
Q

Examples of irreversible achase inhibitors

A

Sarin
Parathion
Malathion

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19
Q

What is sarin

A
  • irreversible achase inhibitor
  • nerve gas
  • binds strongly with achase
  • long 1/2 life
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20
Q

These are examples of organophosphate which are used as insecticides

A

Parathion and malathion

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21
Q

What is the danger of using an irreversible Achase inhibitor such as sarin, parathion, or malathion?

A

The binding of drug to achase is not easily reversed since it forms a covalent bond.

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22
Q

How do you get rid of an Achase inhibitor that is irreversibly bound?

A

With a chemical reactivator such as pralidoxime (PAM)

  • this can break the bonds between the irreversible achase and achase inhibitor is given before chemical aging occurs.
  • breaks the covalent bonds
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23
Q

Toxicity of Achase inhibitors

A

DUMBBEELSS

  • diarrhea, urination, miosis, bradycardia, bronchoconstriction, excitation (of CNS and skeletal muscles), emesis, lacrimation, salivation, sweating
  • looks like excess parasympathetic plus sweating plus nicotinic effects
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24
Q

Receptors that are affected in Achase inhibitor toxicity

A

mostly M3s, some M2 and M1, also N activation

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25
Q

Treatment for an achase inhibitor overdoes

A

Atropine +/- pralidoxime

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26
Q

What does atropine do in the case of an Achase inhibitor overdose

A
  • M blocker

- does not stop anything nicotinic!!

27
Q

Why can someone still die from an achase inhibitor overdose even if they are started on atropine

A

Because the diaphragm is muscel which is innervated by Nm receptors. Atropine is an M blocker, and will not block the Nn receptor. If the diaphragm is paralyzed, you will die

28
Q

When do you need to give pralidoxime with atropine in the case of an achase inhibitor overdose

A

Needed in extreme cases to target the Nm receptor on the diaphragm. Atropine will not block the Nm receptor so the pt could die

29
Q

Chemical aging

A
  • nerve gases change chemical structure after some time in the body
  • pralidoxime has a hard time binding the enzyme to remove the nerve gas effectively
  • have to act very quickly to get it taken care of
  • atropine will relieve symptoms but wont get the diaphragm
30
Q

Hyperthermia induced by anti muscarinic drugs; causes mainly by inhibition of sweating

A

Atropine fever

31
Q

Marked cutaneous vasodilation of the arms and upper torso and head by anti muscarinic drugs; mechanism unknown

A

Atropine flush

32
Q

A chemical antagonist that binds the phosphorus of organophosphates and displaces achase

A

Cholinesterase regenerator

33
Q

Paralysis of accommodation

A

Cycloplegia

34
Q

Flaccid skeletal muscle paralysis causes by persistent depolarization of the neuromuscular end plate

A

Depolarizing blockade

35
Q

A drug that constricts the pupil

A

Miotic

36
Q

Drug that dilates the pupil

A

Mydriatic

37
Q

Flaccid skeletal muscel paralysis caused by blockade of the nicotinic end plate receptor

A

Nondepolarizing blockade

38
Q

A chemical change in the organophosphate molecule that occurs after binding of the organophosphate to cholinesterase for a period of time; renders the enzyme-inhibitor complex less susceptible to regeneration by pralidoxime

A

Organophosphate aging

39
Q

A drug that block the muscarinic receptors of autonomic effector tissue and reduces the effects of parasympathetic nerve stimulation

A

Parasympathetic

40
Q

Selectivity of effect hat is achieved by local administration or special distribution of a drug, not by a receptor sensitivy

A

Pharmacokinetic selectivity

41
Q

Classification for anti muscarinic agents

A

Selectivity for muscarinic receptor subtypes

-non-selective, will bind all M receptor subtypes

42
Q

What is a common name for anti muscarinic agents?

A

Anything with “trop” or “scop” in the name

43
Q

Belladonna alkaloid with high affinity for muscarinic receptors, can block M receptors in both the periphery and PNS

A

Atropine

44
Q

Prototypical antimuscarinic drug

A

Atropine

45
Q

Pharmacokinetics of atropine

A
  • tertiary amine which makes it lipid soluble
  • well distributed into the CNS and other organs
  • short 1/2 life except in the eye
46
Q

Mechanism of action of atropine

A
  • competitive antagonist at muscarinic receptors

- can use physostigmine as antidote for overdose

47
Q

Effects of muscarinic blockers on the blood vessels

A

Nothing will happen at the M3 receptors in the blood vessels since there is no physiologic function of them. There WILL be a response if patient is already taking an M agonist though, since those will be acting on the M3 receptors

48
Q

Effects of muscarinic blockers on skeletal muscles

A

None, nicotinic

49
Q

Clinical uses of atropine

A

Used to dilate pupils and to paralyze accommodation; duration is <72 hours
-not used a whole lot because of how long it lasts

50
Q

What are the top muscarinic blockers for dilated eye exam

A

Atropine
Homatropine
Cyclopentalte
Tropicamide

51
Q

Used for motion sickness and for Parkinson’s

A

Scopolamine

M blocker

52
Q

What kind of drug is scopoloamine

A

M blocker

53
Q

Why do we used scopolamine for Parkinson’s, when that is an issue with dopamine?

A

Parkinson’s is causes by loss of dopaminergic neurons, as a result there is an imbalance in NT where dopamine is too low and ACh is too high
-M blockers balance the two.

54
Q

Motion sickness and M receptors

A

Stimulation of muscarinic receptors causes nausea and vomiting; in motion sickness, the main effect of muscarinic blockers is on the vestibular apparatus

55
Q

Atropine for asthma and COPD

A

M blockers are good for asthma because they bronchodialte

56
Q

Would you want to use an M blocker or an M agonist to treat asthma

A

Blocker

-want to bronchodilate the airway

57
Q

What are some M antagonists that work on the bladder to reduce urgency

A

Tolterodine

Oxybutynin

58
Q

What is urinary incontinence treated with

A

Muscarinic blockers

59
Q

Toxicity of muscarinic antagonists

A 
Dry as a bone
Red as a beet 
Hot as a pistol
Mad as a hatter 
Blind as a bat
60
Q

Muscarinic antagonists and sweating

A
  • Blockade of thermoregulatory mechanisms (sweating) may cause hyperthermia or “atropine fever”, this is potentially fatal in infants
  • dry as a bone because sweating, salivation, and lacrimation are all significantly reduced or stopped
61
Q

What effect do muscarinic antagonists have in the elderly

A

Acute angle-closure glaucoma because it decreases aqueous humor drainage

62
Q

CNS effects of muscarinic blockers

A

Sedation, amnesiac, hallucinations

63
Q

Cardiovascular effects of M blockers

A

Dilation of the cutaneous vessels of the periphery, also known as atropine flush and may be diagnostic of an overdose

64
Q

Is atropine flush due to the effects of the drug?

A

Purely a compensation to increased temp because you are hot and cannot sweat, so blood vessels dilate. Drugs themselves NOT causing vasodilation

Pharm Block 10 (6 decks)

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