Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Final > Lecture 19 > Flashcards

Lecture 19 Flashcards

1
Q

What is the protypical muscarinic antagonist drug? Which modern drugs replace it?

A

Atropine

Glycopyrrolate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the primary action of muscarinic antagonists on smooth muscle (5 examples)?

A

Relaxation of smooth muscle: Decreased GI motility, bladder, bronchi, biliary, eye (midriasis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the effects of muscarinic antagonists like atropine in the eye.

A

They cause dilation of the pupils by preventing contraction of the ciliary muscles. They also impair near vision.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do exocrine glands respond to muscarinic antagonists (examples)?

A

Muscarinic antagonists reduce secretions from glands.

Examples: salivary glands, sweat glands, lacrimal glands, and bronchial secretions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cardiovascular effects of atropine are dose dependent. Explain how and why.

A

At low doses, atropine increases vagal tone on the heart causing bradycardia.
At high doses, it blocks muscarinic AChR, causing slight tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the direct effect of atropine on blood pressure (trick question)?

A

It has no direct effect on blood pressure because there is nothing to antagonize (no parasympathetic innervation to vasculature).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain 6 potential clinical uses of muscarinic antagonists (atropine and its derivatives)?

A

Atropine: dilate pupils for eye exam; reduce salivary and bronchial secretions during surgery (pre-anesthetic); decrease GI motility and bladder tone during surgery (anti-spasmodic); reduce vagal tone on the heart (prevent bradycardia); antidote for cholinergic toxicity; bronchodilation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are adverse effects and symptoms of muscarinic antagonist toxicity?

A

Tachycardia, dry mouth, photophobia, constipation, urine retention, elevated temperature, restlessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What kind of drugs may be used as potential antidotes of muscarinic antagonist toxicity?

A

Acetylcholine Esterase Inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are 3 examples of other drug classes with anti muscarinic activities?

A

Antihistamines/anti-emetics (diphenhydramine)

Tricyclic Antidepressants (amitryptyline)

Phenothiazine tranquilizers (acepromazine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name two ganglionic stimulants (what are they)?

A

Nicone and Acetylcholine

nACh stimulants that favor the neuronal AChR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are signs of acute nicotine poisoning and how do symptoms change if toxicity persists?

A

They originally present with stimulatory/excitatory signs such as excitement, hyperpnea, pulse rate irregularities, diarrhea, and then depressive signs come on such as tachycardia, ataxia, dyspnea, coma and death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the two classes of neuromuscular junction blockers?

What are drug examples of each class?

A

Non-depolarizing (competitive antagonists) and depolarizing.

Depolarizing: Succinylchoiline

Non-depolarizing: Atracurium, pancurium, curare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Explain how depolarizing NMJ blockers work.

A

They overstimulate the ACh receptors at the NMJ with ACh until they become desensitized.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the clinical uses of NMJ blockers?

A

Relax smooth muscles for surgery (easier intubation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an important ethical problem with NMJ blockers? What about pain relief?

A

They only paralyze the muscle, they do not provide pain relief. Their effects are enhanced by volatile anesthesia.

17
Q

What is a side effect of atracurium and tubocurarine but not succinylcholine?

A

Histamine release

18
Q

What is the cause of death in NMJ blocker overdose toxicity?

A

Paralysis of the diaphragm causing inability to breath

19
Q

Discuss cholinesterase inhibitors as antidotes for depolarizing versus non-depolarizing NMJ blocker toxicity.

A

AChE inhibitors can work as antidotes for non-depolarizing NMJ blockers because they are competitive antagonists to the ACh receptors in the NMJ. The AChE inhibitors will put more strain on the system for depolarizing blockers since they work by overstimulating the receptors until they desensitize.

20
Q

What 3 factors may enhance a non-depolarizing neuromuscular block?

A

Volatile anesthetics, hypokalemia, hypocalcemia, hypomagnesemia, aminoglycoside antibiotics.

21
Q

Are ACh esterase inhibitors useful for reversing succinylcholine activity?

A

No

22
Q

How can succinylcholine indirectly cause cardiac arrhythmia?

A

It’s muscle depolarization properties causes an increase in plasma K+ levels.

23
Q

What are other side effects of succinylcholine?

A

Malignant hyperthermia.
Intraocular and intracranial pressure.
Painful muscle contraction.
Potential for muscarinic activation resulting in bradycardia and increased bronchial salivary secretion.

24
Q

What is important about the use of depolarizing NMJ blockers in birds?

A

It will KILL them. Their receptors don’t desensitize and the sustain muscle contraction.

25
Q

Explain how depolarizing neuromuscular junction blockers are used as nematocides.

A

They same way they are used in mammals.

26
Q

What are the risks associated with these nematocides? What is the therapeutic window?

A

They work on nematodes the same way they work on mammals so you have to be careful with the dose so that you only have a toxic effect on the worms and not the host. There is a narrow therapeutic window.

27
Q

Name 4 examples of acetylcholinesterase inhibitors?

A

Neostigmine
Edrophonium
Demecarium
Physostigmine

28
Q

What is the main effect of ACh esterase inhibitors at the cellular level?

A

Increase concentration of ACh at the synapse to stimulate muscle contraction or activation of ACh receptor.

29
Q

Which of the ACh esterase inhibitors act more on NMJ or neuronal postganglionic sites?

A

Neostigmine and edrophonium are more active at the NMJ.

Demercarium and physostigmine act more on neuronal postganglionic sites.

30
Q

On which synapses will ACh esterase inhibitors work most effectively?

A

The synapses that are active (have a high tone)

31
Q

What is 2-PAM and how does it work?

A

It’s and antidote to organophosphate poisoning. It works by binding to the AChE inhibitor, causing it to let go of the AChE enzyme.

32
Q

What are three clinical cholinesterase inhibitor effects?

A

Enhance muscarinic effects, enhance ACh at the synapse, CNS effects.

33
Q

What are 5 clinical uses of cholinesterase inhibitors?

A
  1. Improve muscle contraction in myasthenia gravis patients
  2. Improve GI motility
  3. Improve bladder contraction
  4. Reduce intraocular pressure in glaucoma patients
  5. Antidote for organophosphate poisoning.
34
Q

Explain how edrophonium is used to diagnose myasthenia gravis (and what is MG).

A

Myasthenia gravis is an autoimmune disease where autoantibodies are directed against acetyl choline receptors. Edrophonium is and AChE inhibitor that causes a high concentration of ACh to remain at the NMJ, increasing saturation of functioning AChR. If the animal has myasthenia gravis and is administered edrophonium, they will regain muscle tone and functionality for a short period of time (10 minutes).

35
Q

Describe how neostigmine can be used as an antidote and to counteract what poison?

A

Neostigmine can counteract Belldonna (atropine) poisoning. Atropine (and belladonna) are muscarinic antagonists. By flooding synapses with ACh (2* to AChE inhibition), you can out compete atropine binding to mAChR.

36
Q

What are adverse effects of cholinesterase inhibitors (7)?

A
  1. Miosis
  2. Bradycardia
  3. Muscle twitching or weakness
  4. Bronchoconstriction and increased secretions
  5. Diarrhea
  6. Increased secretions
  7. Ureter constriction
37
Q

What conditions require extreme caution when administering cholinesterase inhibitors?

A

Urinary obstruction, GI onbstuction, asthma/bronchoconstriction, pneumonia, cardiac arrhythmias

38
Q

What is an effective antidote to accidental cholinesterase inhibitor overdosing?

A

Atropine

Pharmacology Final (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions