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pharm > Block 1 Parasympathetic > Flashcards

Block 1 Parasympathetic Flashcards

1
Q

Preganglionic neurons originate within

A

CNS

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2
Q

Postganglionic neurons originate where and terminate where

A

Originate at the ganglion and terminate via the effector organs

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3
Q

Parasympathetic preganglionic nerves are ______ and postganglionic nerves are ______

A

Parasympathetic
Preganglionic = long
Postganglionic = short

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4
Q

Sympathetic preganglionic nerves are _____ and postganglionic nerves are _____

A

Sympathetic
Preganglionic = short
Postganglionic = long

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5
Q

6 most common neurotransmitters

A
  • Norepi / Epi
  • Acetylcholine
  • Dopamine
  • Serotonin
  • Histamine
  • GABA (y-aminobutyric acid)
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6
Q

Acetylcholinesterase (AChE)

A

hydrolyzes or breaks down acetylcholine

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7
Q

Acetylcholinesterase Inhibitor (AChEI)

A
  • prevents acetylcholine from being hydrolyzed (broken down)
  • prolongs action of acetylcholine at muscarinic receptor site
  • indirect agonist
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8
Q

3 ways cholinergic agents modulate Ach effects

A
  • Mimic (agonist)
  • Antagonize (antagonist)
  • Prolong Actions (indirect agonist)
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9
Q

Drugs that mimic or prolong actions of Ach are called…

A
  • Parasympathomimetics

- Cholinomimetics

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10
Q

Drugs that antagonize or block Ach are called…

A
  • Anticholinergics
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11
Q

Cholinergic agonists =

A
  • Cholinomimetics
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12
Q

Cholinergic Agonist has 2 main acronyms…

A
  • DUMBBELLS

- SLUDE

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13
Q

DUMBBELLS

A
  • Defecation
  • Urination
  • Miosis
  • Bradycardia
  • Bronchospasms
  • Emesis
  • Lacrimation
  • Lethargy
  • Salivation
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14
Q

SLUDE

A
  • Salivation
  • Lacrimation
  • Urination
  • Diarrhea
  • Excessive emesis / excretion
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15
Q

Major therapeutic uses of Cholinomimetics (cholinergic agonist)

A
  • Anti-cholinergic overdose
  • Glaucoma (caused by increased IOP)
  • Xerostomia (dry mouth due to lack of saliva
  • Reduced GI / GU motility
  • Alzheimer’s
  • At neuromuscular junction (Myasthenia Gravis)
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16
Q

Contraindications to Cholinomimetics (cholinergic agonists)

A
  • Night time driving
  • Bradycardia / hypotension
  • Asthma
  • Peptic Ulcer Disease
  • GI / GU obstructions
  • Parkinson’s Disease
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17
Q

Cholinergic effects on the eye (Muscarinic Receptors M3)

A
  • Contract ciliary muscle and iris to produce accommodation

- Outflow of aqueous humor which reduces intraocular pressure

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18
Q

Does Acetylcholine have clinical utility?

A
  • Low clinical utility
  • Poor bioavailability
  • Rapidly hydrolyzed in GI tract
  • Quickly inactivated by AcHE
  • Non-specific for nicotinic or muscarinic receptors
  • One use is for ophthalmic use, used to produce miosis for various eye procedures (cataract surgery, iridectomy)
19
Q

Pilocarpine

MOA

Indication

Adverse events

A

Cholinergic agonist

MOA:

  • Eye: increase aqueous humor outflow by contraction of ciliary muscle
  • Oral: stimulates secretions

Indication:

  • Eye: reduce IOP in patients with glaucoma, ocular hypertension, or prevention of of post-op elevated IOP with laser surgery
  • Oral: xerostomia (dry mouth) after radiation therapy and for Sjogren’s Syndrome

Adverse events:

  • Eye: miosis, decrease far vision
  • Oral: excessive cholinergic stimulation (DUMBBELLS)
20
Q

Angle-closure glaucoma

  • How does it happen?
  • Treatment?
A
  • Increased IOP pushes iris against trabecular meshwork closing the ocular angle and preventing drainage of aqueous humor
  • Pilocarpine: constricts the iris’ circular and ciliary muscles, which opens ocular angle and stretches open the trabecular network
21
Q

Bethanechol

MOA

Indication

Adverse events

Contraindication

A

Cholinergic agonist

MOA:

  • Increases bladder muscle tone
  • Detrusor muscle contractions
  • Trigone sphincter relaxion
  • All lead to urination
  • Increases peristalsis -> defecation

Indication:

  • Treat acute post-op and postpartum non-obstructive urinary retention
  • Neurogenic atony of the urinary bladder with retention or ileus

Adverse effects:
- Excessive cholinergic stimulation (DUMBBELLS)

Contraindications:

  • Physical obstruction of GI or GU tract or when bladder wall integrity is in question
  • Asthma
  • Peptic Ulcer Disease
  • Bradycardia
22
Q

Direct-Acting cholinergic agents

A
  • Increase resistance to degradation by cholinesterases

- Increase selectivity for muscarinic receptors relative to nicotinic receptors

23
Q

Indirect-acting cholinergic agent

A
  • Inhibit AchE from metabolizing Ach, thereby prolonging the effects of Ach
24
Q

Edrophonium

MOA

Indication

Adverse effects

Contraindication

A

Indirect-acting cholinergic agonist

MOA:

  • Plant-derived competitive AchE inhibitor that potentiates Ach activity by inhibiting its destruction
  • Short acting (effects manifest within 30-60 seconds, last average of 10 minutes)

Indication:

  • DDx of myasthenia gravis
  • Adjunct in evaluation of treatment requirement of myasthenia
  • Used to evaluate emergency treatment of myasthenia crisis
  • Reverse the effects of non-depolarizing neuromuscular blocking agents

Adverse effects:
- Excessive cholinergic stimulation (DUMBBELLS)

Contraindication:

  • Physical obstruction of GI or GU
  • Integrity of bladder wall in question
25
Q

Physostigmine Salicylate

MOA

Indication

Monitoring

Adverse effects

Contraindication

A

Indirect-acting cholinergic agonist

MOA:

  • Plant-derived competitive AchE inhibitor that potentiates Ach activity by inhibiting its destruction
  • Medium acting (3-8 hr.)

Indication:

  • Reverses Ach overdose (toxic doses of Ach)
  • Reserve use for severe or life-threatening symptoms (NOT for routine use)

Monitoring:
- ECG , vitals , seizures

Adverse effects:
- excessive cholinergic stimulation (DUMBBELLS)

Contraindications:

  • Physical obstruction of GI or GU
  • Integrity of bladder wall in question
  • Respiratory distress & seizures
26
Q

Neostigmine

MOA

Indication

Formulation

Adverse effects

Caution

Contraindication

A

Indirect-acting cholinergic agonist

MOA:

  • Synthetic competitive AchE inhibitor that potentiates Ach activity by inhibiting its destruction
  • Medium acting (3-8 hr.)

Indication:

  • Symptomatic treatment of myasthenia gravis
  • Reverse effects of nondepolarizing neuromuscular blocking agents

Formulation:

  • Oral or IV
  • Neostigmine more polar than physostigmine, does not cross CNS and seizures not observed

Adverse effects:
- excessive cholinergic stimulation

Caution:
- Asthma , PUD , bradycardia

Contraindication:

  • physical obstruction of GU or GI
  • Integrity of bladder wall in question
27
Q

Pyridostigmine

MOA

Indication

Adverse effects

Caution

Contraindication

A

Indirect-acting cholinergic agonist

MOA:

  • Synthetic competitive AchE inhibitor that potentiates Ach activity by inhibiting its destruction
  • Medium acting (3-8 hr.)
  • Generally has longer duration and fewer GI side effects than neostigmine
  • Permits freer transmission of nerve impulses across neuromuscular junction

Indication:

  • Treatment of myasthenia gravis
  • Reverses effect of nondepolarizing neuromuscular blocking agents
  • Nerve Agent Pyridostigmine Pretreatment (NAPP)

Adverse effects:
- excessive cholinergic stimulation

Caution:
- Asthma , PUD , bradycardia

Contraindication:

  • physical obstruction of GU or GI
  • Integrity of bladder wall is in question
28
Q

Most irreversible AchE inhibitors find their use as …

A

Poisons or toxins (insecticides or nerve agents)

29
Q

Irreversible AchE inhibitors permanently inactivate AchE

T/F

A

True

  • Restoration of AchE activity requires synthesis of new enzyme
30
Q

Examples of irreversible AchE inhibitors

A
  • Ecothiophate
  • Sarin
  • Parathion
31
Q

Ecothiophate

MOA

Indication

Adverse effects

A

Noncompetitive (IRREVERSIBLE) AchE inhibitor

MOA:

  • Only irreversible AchE inhibitor used on a regular basis
  • Eye: contracts ciliary muscle leading to increase aqueous humor outflow

Indication:
- Glaucoma

Adverse effects:

  • Miosis
  • Decrease far vision (accommodation)
32
Q

Pralidoxime

MOA

Indication

Adverse effects

A

Cholinergic

MOA:

  • Reactivate cholinesterase that has been inactivated by phosphorylation due to organophosphate pesticide or compound
  • Slows the “aging” process of phosphorylated cholinesterase to a non-reactivatable form
  • Detoxifies certain organophosphates by direct chemical reaction
  • Displaces AchE inhibitors from receptor sites (ultimately reverses the paralysis of respiratory muscles)
  • Relieves muscarinic S/S of salivation, bronchospasm

Indication:

  • Antidote in treatment of poisoning due to pesticides which have AchE activity
  • Overdoses of AchE drugs

Adverse effects:
- Anticholinergic effects (blurred vision, dizziness, headache, nausea, hyperventilation, weakness)

33
Q

Major neurotransmitter in the PNS

A

Acetylcholine

34
Q

Acetylcholine is a major neurotransmitter in PNS and also in these other sites…

A
  • CNS
  • Ganglia (para and sympathetic)
  • Somatic nervous system
35
Q

Alzheimer’s disease can be SLOWED by drugs that do what?

A
  • Increase the concentrations of Ach in the CNS
36
Q

4 AchE Inhibitor drugs used for treatment of Alzheimer’s Disease?

MOA

A

MOA:
- Inhibit central AchE, increasing acetylcholinergic levels in CNS

1) Tacrine:
- 4x daily dose (not preferred)

2) Donepezil:
- Once daily dose (preferred)

3) Galantamine

4) Rivastigmine:
- Patch (may be better tolerated)

37
Q

Nicotine

Low Dose

High Dose

A

Ganglionic Stimulant

Low Dose:
- Depolarizes autonomic ganglia resulting in euphoria and arousal

High Dose:
- Blocks autonomic ganglia resulting in decreased BP and possibly respiratory paralysis

38
Q

Anticholinergic agents do what?

A

Block Ach interaction with either muscarinic or nicotinic receptor

39
Q

M receptor antagonist

A

Antimuscarinic

40
Q

Nn receptor antagonist

A

Ganglionic blocker

  • very low therapeutic utility
41
Q

Nm receptor antagonist

A

Neuromuscular (or skeletal) muscle blocking agent

42
Q

Effects of Anticholinergic Agents?

A

Opposite of cholinergic (DUMBBELLS)

43
Q

Major Therapeutic uses of anti-muscarinic agents

A
  • Reduce secretions before anesthesia
  • Induce sedation
  • Alleviate motion sickness
  • Reduce vagal stimulation
  • Produce ophthalmic mydriasis and cycloplegia
  • Reduce GI smooth muscle spasms
  • Treat bronchospasm
  • Control intoxication by cholinergic agonists
  • Parkinson’s Disease

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