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Pharmacology I > 1 - PNS Part I > Flashcards

1 - PNS Part I Flashcards

1
Q

Most neuropharmacological agents act by altering ________

A

synaptic transmission

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2
Q

Drugs that act by altering axonal conduction are _______ selective

A

less

the process of conducting an impulse along an axon is essentially the same in all neurons, so a drug that alters axonal conduction affects all nerves with pretty much no specificity

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3
Q

What is an example of a drug that decreases axonal conduction?

A

Local anesthetics!

they are nonselective inhibitors of axonal conduction

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4
Q

Why are drugs that alter synaptic transmission so much more selective?

A

unlike axons, synapses at different sites vary widely from one another

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5
Q

The effect of a drug on a neuronally regulated process is dependent on:

A

the ability of that drug to directly or indirectly influence receptor activity on target cells

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6
Q

What are the five steps of synaptic transmission?

A
  1. Transmitter Synthesis
  2. Transmitter Storage
  3. Transmitter Release
  4. Receptor Binding
  5. Termination of Transmission
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7
Q

Transmitters can be removed from the synaptic gap by three processes:

A

Reuptake

Degradation

Diffusion

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8
Q

How does a drug that increases transmitter synthesis impact receptor activation?

A

storage vesicles will contain transmitter in abnormally high amounts, causing more transmitter to be released, and more transmitter available to receptors on the postsynaptic cell

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9
Q

Amphetamines are drugs that act by:

A

promoting transmitter release

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10
Q

Botulinum Toxin acts by ______

A

inhibiting transmitter release

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11
Q

Drugs that directly activate receptors are called:

A

agonists

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12
Q

drugs that prevent receptor activation are called

A

antagonists

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13
Q

Drugs can interfere with the termination of transmitter action by two mechanisms:

A
  1. Blockade of transmitter reuptake
  2. Inhibition of transmitter degradation
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14
Q

For every PNS drug you should know three things:

A

The identity of the receptors at which that drug acts

The normal response to activation of those receptors

Whether the drug increases or decreases receptor activation

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15
Q

The PNS has two major subdivisions:

A

Autonomic (parasympathetic and sympathetic)

Somatic (skeletal muscle movement)

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16
Q

What are the three principle functions of the autonomic nervous system?

A
  1. Regulation of Heart
  2. Regulation of Secretory Glands
  3. Regulation of Smooth Muscle
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17
Q

What are the seven main effects of Parasympathetic nervous system stimulation?

A
  1. Slowing HR
  2. Increasing gastric secretion
  3. Emptying the bladder
  4. Emptying the bowels
  5. Focusing the eye for near vision
  6. Constricting the pupil
  7. Contracting bronchial smooth muscle
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18
Q

Therapeutic agents that alter parasympathetic function are used primarily for:

A

effects on the GI tract, bladder, and eyes

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19
Q

The sympathetic nervous system has three main functions:

A
  1. Regulating the CV system
  2. Regulate temperature
  3. Implement the acute stress response
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20
Q

By influencing heart and blood vessels, the sympathetic nervous system can achieve three homeostatic objectives:

A

Maintain blood flow to the brain

Redistribute blood flow during exercise

Compensate for blood loss by constricting vessel

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21
Q

How does the sympathetic nervous system control temperature?

A
  1. Regulating blood flow to the skin
  2. stimulating sweat glands
  3. Inducing piloerection
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22
Q

Generally speaking, stimulation of the sympathetic nervous system causes five things:

A
  1. Increased HR and BP
  2. Shunting blood away from skin and viscera into skeletal muscles
  3. Dilating bronchi to improve oxygenation
  4. Dilating pupils
  5. Mobilizing stored energy to provide glucose to the brain and fatty acids to the muscles
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23
Q

In a reflex arc, the sensor is responsible for _____ and the effector is responsible for ______

A

monitoring the status of a physiologic process

making appropriate adjustments to the process

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24
Q

In most organs, the _______ nervous system provides the predominant tone

A

Parasympathetic

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25
Q

The vascular system is regulated almost exclusively by the _______ nervous system

A

sympathetic

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26
Q

How many neurons are in the pathway leading from the spinal cord to organs innervated by parasympathetic nerves?

A

Two

Where these neurons synapse is a structure called a ganglion

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27
Q

The anatomy of the Parasympathetic Nervous System offers two general sites at which drugs can act:

A
  1. The synapses between preganglionic neurons and postganglionic neurons
  2. the junctions between postganglionic neurons and their effector organs
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28
Q

The autonomic nervous system always contains ____ neurons in any pathway.

The Somatic nervous system always contains _____ neurons in any pathway

A

Two (pre and post ganglionic)

One (Motor Neuron)

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29
Q

The Peripheral Nervous System employs three neurotransmitters:

A

Acetylcholine, Norepinephrine, Epinephrine

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30
Q

In the peripheral nervous system, acetylcholine is released at which junctions?

A
  1. All preganglionic neurons of the ParaSNS and SNS
  2. All postganglionic neurons of the ParaSNS
  3. All motor neurons to skeletal muscles
  4. Most postganglionic neurons of the SNS that go to sweat glands
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31
Q

In the peripheral nervous system, Norepinephrine is the transmitter released by:

A
  1. Practically all post-ganglionic neurons of the sympathetic nervous systems
  2. The only exception is sweat glands
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32
Q

Epinephrine is the major transmitter released from:

A

the adrenal medulla

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33
Q

There are two primary receptor types in the Peripheral Nervous System:

A

Cholinergic Receptors

Adrenergic Receptors

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34
Q

Cholinergic receptors mediate responses to _____

Adrenergic receptors mediate responses to _____

A

Acetylcholine (mediate response at all junctions where ACh is the transmitter)

Epinephrine and norepinephrine (mediate responses at all junctions where norepinephrine or epinephrine is the transmitter)

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35
Q

There are three major subtypes of cholinergic receptors:

A

NicotinicN

NicotinicM

Muscarinic

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36
Q

There are four major subtypes of adrenergic receptors:

A

Alpha 1

Alpha 2

Beta 1

Beta 2

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37
Q

Where are NicotinicN receptors located?

A

the cell bodies of ALL postganglionic neurons

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38
Q

Where are NicotinicM receptors located?

A

skeletal muscles

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39
Q

Where are muscarinic receptors located?

A

On ALL organs regulated by the ParaSNS AND sweat glands

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40
Q

Where are Adrenergic receptors located?

A

On ALL organs (except sweat glands) regulated by the SNS

AND

all organs regulated by epinephrine release from the adrenal medulla

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41
Q

Activation of NicotinicN receptors promotes:

A

ganglionic transmission at all ganglia of the SNS and ParaSNS

AND

release of epinephrine from the adrenal medulla

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42
Q

Activation of NicotinicM receptors causes:

A

Contraction of skeletal muscle

M is for muscle

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43
Q

Activation of Muscarinic Receptors causes:

A

an appropriate PNS response from the organ involved

  • Eyes: pupil constriction, ciliary contraction (close vision)
  • Heart: Decreased HR
  • Lung: Bronchoconstriction, increased secretions
  • Bladder: promotes voiding
  • GI: Salivation, increase secretions, increased motility
  • Sweat: Sweating
  • Sex: Ejaculation
  • Blood Vessels: Dilation
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44
Q

Most importantly, activation of muscarinic receptors causes:

A
  1. increased glandular secretions (pulmonary, gastric, intestinal, and sweat)
  2. Contraction of smooth muscle (bronchi and GI tract)
  3. Slowing of the Heart Rate
  4. Pupil constriction
  5. ciliary contraction (focuses eye for near vision)
  6. Dilation of blood vessels
  7. Voiding of the bladder
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45
Q

The ParaSNS has pretty much no physiologic effect on human vasculature. So why do muscarinic drugs cause vasodilation?

A

Blood vessels do have muscarinic cholinergic receptors

No nerves terminate at these receptors, so they aren’t related to the nervous system at all

But they’re still there

So when we give drugs that activate muscarinic receptors, they do become activated, causing vasodilation and a drop in BP

46
Q

Activation of Alpha 1 receptors causes:

A

Vasoconstriction

Ejaculation

Pupil Dilation

47
Q

Alpha 2 receptors of the PNS are located where?

A

On nerve terminals of the ANS, NOT the organs they effect

This is why they’re called presynaptic

48
Q

What is the function of Alpha 2 receptors?

A

To regulate transmitter release

Stimulation of Alpha 2 receptors causes an inhibition of transmitter release

49
Q

Where are alpha 2 receptors clinically relevant?

A

Really only in the CNS, not really at all in the PNS

50
Q

Where are Beta 1 receptors located?

A

The heart

The Kidney

51
Q

Activation of Beta 1 receptors causes:

A

increased rate, force of contraction, and AV conduction velocity

Release of Renin

52
Q

Activation of Beta 2 receptors causes:

A

Bronchial Dilation

Uterine relaxation

VasoDILATION

Glycogenolysis in the liver and skeletal mm

Enhances skeletal muscle contractions

53
Q

In the periphery, the only dopamine receptor of clinical significance is located in the _____

A

Kidney

Dilates renal blood vessels, increasing perfusion

54
Q

Which cholinergic receptors can ACh activate?

How does this differ from adrenergic receptors?

A

All of them

On the other hand, adrenergic receptors are much more picky. Norepinephrine, for example, can’t activate all adrenergic receptors

55
Q

Which receptors can the following transmitters activate?

Epinephrine

Norepinephrine

Dopamine

A

E: All alpha and Beta Receptors, but not dopamine receptors

N: Alpha 1, Alpha 2, Beta 1

D: Alpha 1, Beta 1, dopamine receptors

56
Q

Which transmitters are capable of activating dopamine receptors?

A

Only dopamine

57
Q

There is only one transmitter that can activate Beta 2 receptors:

A

Epinephrine

58
Q

When you think fight or flight, think:

A

Beta 2

The adrenal medulla is responsible for releasing epinephrine in fight or flight situations. As such, Beta 2 response is due solely to adrenal medulla action

59
Q

Describe the life cycle of ACh

A
60
Q

Norepinephrine transmission is terminated by:

A

Reuptake

Once inside the cell, it’s either put back into a vesicle or broken down by MAO

61
Q

Epinephrine is synthesized by ____ in the ______

A

Chromaffin cells

Adrenal Medulla

62
Q

Termination of Epinephrine action is accomplished by:

A

hepatic metabolism

NOT reuptake

63
Q

What are cholinergic drugs?

A

Drugs that influence the activity of cholinergic receptors

THEY MAY ENHANCE OR BLOCK CHOLINERGIC ACTION

64
Q

Cholinergic drugs have more uses as _____ than ____

A

toxins

medication

65
Q

What is the action of muscarinic agonists?

A

selectively mimic the effects of Ach at the muscarinic receptors

66
Q

What do ganglionic stimulating agents do?

A

Selectively mimic the effects of acetylcholine at NicotinicN receptors of autonomic ganglia

67
Q

The only therapeutic value of Ganglionic stimulating agents is:

A

Tobacco cessation drugs

68
Q

What do ganglionic blocking agents do?

A

Selectively block ganglionic nicotinicN receptors

69
Q

What do Neuromuscular Blocking Agents do (chemically)?

A

Block the effects of ACh at NicotinicM receptors at the neuromuscular junction

70
Q

What do cholinesterase inhibitors do?

A

They increase cholinergic receptor activity indirectly by increasing the amount of ACh in the synaptic space

71
Q

Muscarinic agonists are also known as:

A

parasympathomimetic agents

72
Q

The principle structures affected by muscarinic activation are:

A

Heart

Exocrine glands

smooth mm

eyes

73
Q

Bethanecol

Action

Effect

Therapeutic Use

Adverse Effects

A

Direct-acting Muscarinic Agonist

Effect: Bradycardia, sweating, salivation, bronchial secretions, gastric acid secretion, bronchial constriction, increased GI motility and tone, bladder emptying

Use: Treats urinary retention, GERD, gastric atony/distention

AE: HypoTN, bradycardia, excess salivation, excess gastric acid, abdominal cramps, diarrhea, increased urinary tract pressure, asthma exacerbation

Causes dysrhythmia in patients with hyperthyroidism

74
Q

Why do patients with hyperthyroidism gets dysrhythmias from bethanechol, a drug that usually causes bradycardia?

A

when the take bethanechol, they get bradycardia and HypoTN, which releases NE from the SNS

In a normal patient this would be fine, but in a patient with Hyperthyroidism in can induce dysrhythmias BECAUSE they heart is exquisitely sensitive to NE

75
Q

What is the prototype of a muscarinic agonist?

A

Bethanechol

76
Q

What is the prototype of a cholinesterase Inhibitor?

A

Pyridostigmine

77
Q

What is the prototype of a muscarinic antagonist?

A

Atropine

78
Q

Muscarinic Poisoning results from an overdose of one of two drugs:

A

Direct-acting muscarinic agonists (bethanechol)

Indirect-Acting Cholinomimetics (pyridostigmine)

79
Q

What are the manifestations of muscarinic poisoning?

A

SLUDGE and the Killer Bs:

  • *S**alivation
  • *L**acrimation
  • *U**rination
  • *D**iaphoresis/Diarrhea
  • *G**I Cramping
  • *E**mesis
  • *B**radycardia
  • *B**ronchospasm
  • *B**ronchorrhea
80
Q

For a patient who is taking bethanechol, when should it be taken?

A

1 hour before or 2 hours after meals to decreased N/V

81
Q

Cholinesterase Inhibitors increase transmission in which receptors?

A

ALL cholinergic junctions (muscarinic, ganglionic, and neuromuscular)

They lack selectivity and elicit a broad spectrum of responses

82
Q

Cholinesterase Inhibitors are used to treat which diseases?

A

Myasthenia Gravis
Alzheimer Disease
Parkinson
Poisoning by muscarinic antagonists

Reversing Non-Depolarizing NMBAs

83
Q

There are two basic categories of cholinesterase inhibitors:

A

Reversible

Irreversible

84
Q

Reversible Cholinesterase Inhibitors Include:

A

Pyridostigmine
Neostigmine
Physostigmine
Edrophonium

Several drugs for Alzheimer’s

85
Q

Pyridostigmine is the drug of choice for:

A

Myasthenia Gravis

86
Q

How do reversible cholinesterase inhibitors work?

A

acts as a substrate for cholinesterase

It’s broken down by cholinesterase, but it takes a long time, so it’s basically tying up cholinesterase so it can’t break down Ach

87
Q

When used therapeutically, cholinesterase inhibitors usually only affect:

A

muscarinic receptors on organs

Nicotinic receptors at the NMJ

88
Q

What are the muscarinic effects of Pyridostigmine?

A

Same as muscarinic agonists:

Bradycardia, Bronchial constriction, urinary urgency, increased glandular secretions, increased tone and motility of GI smoth mm, miosis, focusing of the lens for near vision

89
Q

What are the neuromuscular effects of anticholinergics?

A

Therapeutic doses: increase the force of contraction

Toxic doses: reduce the force of contraction (excessive amounts of Ach at the NMJ keep the motor end plate in a state of constant depolarization, causing complete blockade)

90
Q

Why is neostigmine an ideal choice for reversal of a patient with alzheimer’s disease?

A

It carries a positive charge and cannot cross the blood brain barrier

91
Q

Which cholinesterase inhibitor crosses the Blood Brain Barrier?

A

Physostigmine

Does not carry a charge

This makes it the drug of choice for treating atropine poisoning/antimuscarinic toxicity

92
Q

Edrophonium is unique in its use:

A

used to diagnose, but not treat, MG (not used that much any more now that better testing is available)

Very short duration of action

93
Q

Which three cholinesterase inhibitors are approved for management of Alzheimer Disease?

A

Donepezil (Aricept)

Galantamine (Razadyne)

Rivastigmine (Exelon)

94
Q

Irreversible Cholinesterase Inhibitors only have one indication:

A

Treatment of Glaucoma

Echothiophate is the only drug used

95
Q

All irreversible cholinesterase inhibitors contain:

A

an atom of phosphorus

This is why they are known as organophosphates

96
Q

Almost all irreversible cholinesterase inhibitors are highly _____ soluble.

How does this impact their absorption?

A

lipid soluble

Can be absorbed readily from all routes of administration, including directly through the skin

97
Q

What can be given to break the bond between an organophosphate inhibitor and cholinesterase?

A

Pralidoxime

A cholinesterase reactivator

98
Q

Organophosphates are employed primarily as:

A

Insecticides

99
Q

Toxic doses of organophosphates produces what condition?

A

Cholinergic Crisis: excessive muscarinic stimulation and depolarizing neuromuscular blockade

100
Q

What is the treatment for cholinergic crisis?

A

giving atropine to reduce muscarinic stimulation

giving parlidoxime to reverse inhibition of cholinesterase at the NMJ

Benzo for seizures

101
Q

Pralidoxime is only effective against:

A

Organophosphates

NOT reversible inhibitors

102
Q

Pralidoxime is a quaternary ammonium compound. What are the implications of this?

A

It cannot cross the BBB

103
Q

Anticholinesterases work in two places. Which one makes it useful in MG?

A

at the NMJ, but they also get accumulation at muscarinic sites (even though they don’t need it there, the disease only attacks at the NMJ)

104
Q

What drug would you give to someone in myasthenic crisis?

A

Neostigmine

105
Q

When a patient has myasthenia gravis and is being treated with anticholinesterases, it can be difficult to tell if they also develop:

A

Cholinergic crisis from toxic levels of cholinesterase inhibitors

106
Q

How can you distinguish myasthenia gravis from cholinergic crisis?

A

Look for muscarinic symptoms (bradycardia, bronchial constriction, urinary urgency, glandular secretions, increased tone and motility of GI smooth mm)

OR

administer a challenge dose of edrophonium, an ultra-short acting cholinesterase inhibitor. If edrophonium helps, it’s MG. If the symptoms get worse, it’s cholinergic crisis

107
Q

Anytime you’re using edrophonium to test for Myasthenia Gravis vs. Cholinergic Crisis, what should you have in the room on hand?

A

Atropine and oxygen

108
Q

A patient with myasthenia gravis knows he is going to take a long walk. When should he time his cholinesterase inhibitor?

A

Right before the walk. The medication will make exertion easier.

109
Q

If an MG patient misses a dose of their anticholinesterase, what should they do?

A

Don’t take it until the next scheduled dose (don’t try to “make up” the dose)

110
Q

What symptoms should you tell your patient to look out for when beginning a cholinesterase inhibitor?

A

difficulty breathing

drooling

N/V/D

Excessive sweating

111
Q

Where are alpha 1 receptors located?

A

Eye (constriction)

Arterioles (constriction)

Veins (constriction)

Penis (ejaculation)

Prostate (contraction)

Bladder (contraction of trigone and sphincter)

112
Q

Where are Beta 2 receptors located?

A

Arterioles (dilation)

Bronchi (dilation)

Uterus (relaxation)

Liver (glycogenolysis)

Muscles (enhanced contraction)

Pharmacology I (29 decks)

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