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Pharmacology I > 1 - PNS Part II > Flashcards

1 - PNS Part II Flashcards

1
Q

There are three categories of anticholinergic drugs:

A

Muscarinic antagonists
ganglionic blocking agents
neuromuscular blocking agents

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2
Q

muscarinic antagonists block Ach at:

A

muscarinic receptors

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3
Q

Ganglionic blocking agents block Ach at:

A

NicotinicN receptors (at ganglions)

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4
Q

Neuromuscular blocking agents block Ach at:

A

NicotinicM receptors (NMJ)

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5
Q

Why are Muscarinic agonists referred to as parasympatholytic drugs?

A

Most Muscarinic receptors are located on structures innervated by the ParaSNS

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6
Q

What are alternative names for muscarinic antagonists?

A

Parasympatholytics

Antimuscarinics

Muscarinic blockers

Anticholinergic drugs

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7
Q

When you think “anticholinergic” think ______

A

Muscarinic antagonist

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8
Q

What is the prototype anticholinergic?

A

Atropine

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9
Q

How does atropine produce its effects?

A

prevents receptor activation by binding competitively at muscarinic receptors

At therapeutic doses its selective for muscarinic cholinergic receptors

At high doses, it can effect nicotinic receptors

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10
Q

Muscarinic agonists primarily exert their effects on which organs?

A

Heart (increases heart rate)

Exocrine Glands (decreases salivation/sweat/gastric glad function)

Smooth Mm (relaxation of bronchi, decreased urinary tone, decreased GI tone and motility)

Eyes (mydriasis - pupil dilation, focusing the lens for far vision)

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11
Q

Why is atropine given before procedures?

A

Procedures that stimulate baroreceptors of the carotids can initiate reflex slowing of the heart, so pretreating with atropine prevents the body from being able to mount a response (drop the heartrate)

Prevents excessive secretions

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12
Q

If atropine is a bronchodilator, why isn’t it often used in asthmatics?

A

It causes drying and thickening of bronchial secretions, making them even more tenacious

Plus, better drugs are available that don’t come with all the other antimuscarinic side effects (dry mouth, urinary retention, etc.)

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13
Q

Why would atropine help provide short term relief of biliary colic from a gallstone?

A

It causes decreased GI tone, including the sphincter of Oddi

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14
Q

What drug would you expect to be given to someone admitted with an organophosphate poisoning?

A

Atropine

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15
Q

What are the adverse effects of muscarinic antagonists?

A

Xerostomia
Blurred Vision and Photophobia
Elevation of IntraOcular Pressure (IOP)
Urinary Retention
Constipation
Anhidrosis (inability to sweat)
Tachycardia
Asthma (by worsening tenacity of secretions)

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16
Q

How does scopolamine differ from atropine?

A

It produces sedation rather than excitation/irritability

Suppresses emesis and motion sickness

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17
Q

One of the biggest uses of anticholinergics is:

A

Overactive Bladder (OAB)

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18
Q

Why do anticholinergics help with OAB?

A

OAB is caused by overactivity of the detrusor muscle, which anticholinergics block

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19
Q

How can side effects be limited in an OAB patient placed on anticholinergics?

A
  1. Use long-acting formulations
  2. Use drugs that are selective for muscarinic receptors in the bladder
  3. use drugs that don’t cross the BBB
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20
Q

Which Muscarinic receptor subtype is responsible for bladder innervation?

A

M3

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21
Q

Which anticholinergic is highly selective for M3?

A

Darifenacin (Enablex)

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22
Q

Which anticholinergic is primarily selective for M3?

A

Oxybutynin

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23
Q

What are symptoms of antimuscarinic poisoning?

A

Dry Mouth

Blurred Vision

Photophobia

Hyperthermia

CNS (hallucinations, delirium)

Skin: hot, dry, flushed

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24
Q

What is the treatment for antimuscarinic poisoning?

A
  1. Minimizing intestinal absorption (charcoal)
  2. Giving Physostigmine (allows Ach to congregate, competing more heavily for receptor binding sites)
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25
Q

What is a mnemonic for Anticholinergic Poisoning?

A

Hot as a hare

Dry as a bone

Red as a beet

Blind as a bat

Mad as a hatter

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26
Q

Adrenergic agonists are often referred to as _____

Why?

A

sympathomimetics

Adrenergic agonists activate adrenergic receptors, through which the sympathetic nervous system acts

Responses to adrenergic agonists are very similar to stimulation of the SNS

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27
Q

Drugs can activate adrenergic receptors in four ways:

A
  1. Direct Receptor Binding
  2. Promotion of NE release (indirect)
  3. Blockade of NE reuptake (indirect)
  4. Inhibition of NE inactivation (indirect)
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28
Q

What mechanism do almost all adrenergic agonists use to produce adrenergic stimulation?

A

Direct binding to receptors

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29
Q

What are some examples of drugs that block NE reuptake?

A

Cocaine, Tricyclic Antidepressants

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30
Q

What are some examples of drugs that promote NE release?

A

Ephedrine, Amphetamines

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31
Q

What are some drugs that inhibit NE inactivation?

A

MAOIs

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32
Q

Structurally, how do catecholamines differ from noncatecholamines?

A

Contain a catechol group and an amine group

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33
Q

What is a catechol group?

A

A benzene ring with hydroxyl groups on two adjacent carbons

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34
Q

Because of their chemistry, all catecholamines have three properties in common:

A
  1. cannot be used orally
  2. have a brief DOA
  3. cannot cross the BBB
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35
Q

Why do catecholamines have short half lives?

A

MAO and COMT

Both are located in the liver and intestinal walls and account for almost 100% clearance of first pass effect

Even IM and SubQ injections are broken down too rapidly by these bad boys to be useful

It has to be circulating in the plasma (IV) to be useful. Once it hits the liver it’s over.

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36
Q

Name three adrenergic agonists that are noncatecholamines

A

Ephedrine

Albuterol

Phenylephrine

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37
Q

Why aren’t noncatecholamines broken down as quickly?

A

The lack of a catechol group means COMT doesn’t break them down, and MAO does so slowly

38
Q

Which is more polar: catecholamines or non?

A

Catecholamines, which is why they can’t cross the BBB

BUT

Noncatecholamines CAN and do cross the BBB

39
Q

The ability of a drug o selectively activate certain receptors exclusively depends on:

A

the dose

At low doses, selectivity is maximal

As the dose increases, selectivity decreases

40
Q

Activation of Alpha 1 receptors elicits two responses that can be therapeutic:

A

Vasoconstriction

Mydriasis

41
Q

Alpha 1 agonists are usually used for (5):

A
  1. Hemostasis through vasoconstriction
  2. Nasal Decongestion
  3. Adjunct to local anesthesia (keeps blood away from area, prolonging action)
  4. Elevating BP
  5. Mydriasis (dilating pupils)
42
Q

What are adverse effects of alpha 1 activation?

A

HTN

Necrosis

Bradycardia (Alpha mediated vasoconstriction elevates BP, which triggers a baroreceptor reflex)

43
Q

Alpha 2 activation causes:

A

inhibition of NE release PRESYNAPTICALLY

More important in the CNS than the PNS

44
Q

By activating CNS alpha 2 receptors, what happens?

A
  1. Reduction of sympathetic outflow to the heart and blood vessels
  2. Relief of severe pain
45
Q

All of the clinically relevant responses to Beta 1 activation result from activating Beta 1 receptors in which organ?

A

The heart

Action of renal beta 1 receptors is not associated with any effects whatsoever (good or bad)

46
Q

What are therapeutic uses of beta 1 receptor activation?

A

Inotropy (shock, heart failure)

Increased AV conduction (AV heart block)

Initiating contraction during cardiac arrest

47
Q

What are adverse effects of Beta 1 activation?

A

Dysrhythmias

Angina (increases myocardial oxygen demand)

48
Q

Applications of Beta 2 activation are limited to which two organs?

A

The lungs

the uterus

49
Q

What are therapeutic applications of Beta 2 activation?

A

Asthma (usually inhalation)

Delay of preterm labor

50
Q

What are adverse effects of Beta 2 activation

A

Hyperglycemia (activate B2 receptors in the liver and skeletal muscles, which promotes breakdown of glycogen into glucose)

Tremor (activation of B2 receptors in muscles enhances contraction)

51
Q

EPINEPHRINE

Receptor specificity
Chemical Classification
Onset
Metabolism
Half Life
Elimination

A

Receptor: Alpha 1, Alpha 2, Beta 1, Beta 2

Classification: Catecholamine

Onset: Immediate

Metabolism: MAO and COMT

Half Life: <5 min

Elimination: Urine

52
Q

NOREPINEPHRINE

Receptor specificity
Chemical Classification
Onset
Metabolism
Half Life
Elimination

A

Receptors: Alpha 1, Alpha 2, Beta 1

Class: Catecholamine

Onset: Immediate

Metabolism: MAO and COMT

Duration: 1-2 min

Elimination; Urine

53
Q

ISOPROTERENOL

Receptor specificity
Chemical Classification
Onset
Metabolism
Half Life
Elimination

A

Receptor: Beta 1 and Beta 2

Class: Catecholamine

Onset: Immediate

Metabolism: COMT

Half life: 2.5-5 min

Elimination: Urine

54
Q

DOPAMINE

Receptor specificity
Chemical Classification
Onset
Metabolism
Half Life
Elimination

A

Receptors: DOSE DEPENDENT
Dopamine, beta 1, alpha 1 (at high doses)

Class: Catecholamine

Onset <5 min

Metabolism MAO and COMT

Half Life 2 min

Elim Urine

55
Q

DOBUTAMINE

Receptor specificity
Chemical Classification
Onset
Metabolism
Half Life
Elimination

A

Receptor: Beta 1

Class: Catecholamine

Onset: 1-2 min

Metabolism COMT

Half Life 2 min

Elimination Urine

56
Q

PHENYLEPHRINE

Receptor specificity
Chemical Classification
Onset
Metabolism
Half Life
Elimination

A

Receptor: Alpha 1

Class: noncatecholamine

Onset: Immediate

Metabolism: Hepatic (Deamination)

Half LIfe 5 min

Elimination Urine

57
Q

Adrenergic Agonists interact with what drugs?

A

MAOIs

Tricyclics (can intensify and prolong epinephrine’s effects)

General anesthetics (render the myocardium hypersensitive to B1 activation)

58
Q

Adrenergic antagonists cause:

A

direct blockade of adrenergic receptors

59
Q

Adrenergic Antagonists can be divided into two groups:

A

Alpha blockers

Beta Blockers

60
Q

What are some therapeutic applications for alpha blockade (5)?

A

Primarily alpha 1. There are no recognized therapeutic applications for alpha 2 blockade

  1. Essential HTN
  2. Alpha 1 agonist overdose (using phentolamine injections around an area where epi has extravasated)
  3. BPH (reduced contraction of the trigone and sphincter)
  4. Pheochromocytoma (suppressing HTN effect of exogenous catecholamines)
  5. Raynaud’s Disease (suppress alpha mediated vasoconstriction in response to cold)
61
Q

What are adverse effects of alpha 1 blockade?

A
  1. Orthostatic Hypotension
  2. Reflex Tachycardia (from widespread vasodilation and baroreceptor activation)
  3. Nasal congestion
  4. Inhibition of ejaculation
  5. Sodium retention and fluid overload (because they decrease BP, the kidneys retain sodium and water. This is why alpha agents are often used with diuretics.)
62
Q

Adverse effects of alpha 2 blockade include:

A

potentiation of the reflex tachycardia that can occur in response to the blockade of alpha 1 receptors

Alpha 2 receptors naturally inhibit the release of NE presynaptically. If they are no longer inhibited, more NE is released, which makes the reflex tachycardia even worse

63
Q

PRAZOSIN

Actions and Uses

Adverse Effects

A

Selective blockade of ALPHA 1

Dilation of arterioles and veins

Relaxation of smooth mm in the bladder neck and prostate capsule

Orthostatic HypoTN, reflex tachy, nasal congestion

First dose effect: about 1% of people pass out after the first dose, and they should be told not to drive etc for 24 hours after taking for the first time (take right before bed)

64
Q

TERAZOSIN

Actions and Uses

Adverse Effects

A

ALPHA 1 ANTAGONIST

HTN and BPH

Same AE as usual, but high incidence of headaches

65
Q

When you se “-osin” think:

A

Alpha antagonist

66
Q

There is only one non-competitive Alpha Antagonist:

A

Phenoxybenzamine

Blocks alpha 1 and alpha 2 irreversibly. A single dose persists for several days.

Only approved for use for patients with pheochromocytoma

67
Q

Beta 1 blockade results in:

A
  1. Reduced Heart Rate
  2. Reduced Inotropy
  3. Reduced velocity through AV node
68
Q

Beta blockers are especially helpful in treating dysrhythmias that:

A

involve excessive electrical activity in the SA node and atria

Prevents the ventricles from being driven by the excess atrial activity

69
Q

What are the parameters for giving Beta blockers to high-risk patients having noncardiac surgery?

A

pretreatment with small doses that begin several days to weeks before surgery

Low dose initially then titrated up

Treatment should continue for 1 month after surgery

70
Q

Only three beta blockers have been show effective in heart failure:

A

Carvedilol

Bisoprolol

Metoprolol

71
Q

Why are beta blockers prescribed for hyperthyroidism?

A

Hyperthyroidism makes the heart exquisitely sensitive to catecholamines. Even normal SNS activation can result in tachydysrhythmias and angina.

Blockade of Beta 1 receptors suppresses these response

72
Q

Why are beta blockers prescribed for migraines?

A

They work as prophylaxis only, won’t stop an active headache. No one is totally sure why.

73
Q

What are adverse effects of Beta 1 blockade?

A
  1. Bradycardia
  2. Reduced Cardiac Output
  3. Heart Failure
  4. AV Block
  5. Rebound cardiac excitation
74
Q

Adverse effects of beta 2 blockade

A
  1. Bronchoconstriction (usually insignificant, but in patients with asthma any increase in airway resistance can be life threatening)
  2. Hypoglycemia from inhibition of glycogenolysis (this is really only a concern in diabetic patients, who are dependent on beta 2 mediated glycogenolysis as a way of overcoming insulin-induced hypoglycemia. Diabetic patients should get Beta 1 blockers if possible)
75
Q

There are three groups of beta blockers:

A
  • First Generation (nonselective) - block Beta 1 and Beta 2
  • Second Generation (cardioselective) - block Beta 1 receptors
  • Third Generation (vasodilating) - act on blood vessels to cause dilation, but may produce nonselective or cardioselective Beta blockade
76
Q

PROPANOLOL

Generation

Receptors

A

First Generation

Beta 1 and Beta 2

77
Q

Which kind of beta blocker do you not want to give a patient with asthma?

A

Beta 2

You want a selective Beta 1 blockade, like metoprolol

78
Q

Why are beta blockers doubly dangerous for diabetics?

A

Not only do they predispose to hypoglycemia, they mask the effects of hypoglycemia until it’s severe

79
Q

Which two beta blockers also have alpha blocking capabilities?

A

Carvedilol and labetalol

80
Q

Abrupt discontinuation of any beta blocker can cause:

A

Rebound cardiac excitation

81
Q

How does a centrally acting alpha 2 agonist effect peripheral sympathetic neurons?

A

In the CNS, Alpha 2 receptors are located on presynaptic nerve terminals.

As NE accumulates in the synapse, it activates Alpha 2 receptors to stop the synthesis of NE.

A central alpha 2 agonist will decreased production of NE at sympathetic nerve fibers, which will result in decreased sympathetic activation

This results in decreased BP, pain, and ADHD

82
Q

The prototypical central alpha 2 agonist is:

A

Clonidine

83
Q

What is the action of Clonidine?

A

Alpha 2 agonist that causes selective activation of alpha 2 receptors in the CNS (esp. areas in the brainstem associated with autonomic regulation of the CV system)

Reduces sympathetic outflow to blood vessels and the heart

84
Q

Why doesn’t clonidine cause orthostatic hypotension?

A

It’s effects are not posture dependent

85
Q

What are adverse effects of clonidine?

A

Drowsiness

Xerostomia

Rebound Hypertension (from stopping abruptly)

CANNOT BE USED IN PREGNANCY

Lots of people abuse it (as an adjunct to other drugs or by itself)

86
Q

Two side effects of methyldopa can be severe:

A

hemolytic anemia and hepatic necrosis

87
Q

What is the prime difference between clonidine and methyldopa?

A

It’s a prodrug

It has to be converted in the brainstem to methylnorepinephrine

88
Q

The only indication for methyldopa is”

A

Hypertension (particularly during pregnancy)

89
Q

Approximately 10-20% of patients who take methyldopa chronically will have:

A

a positive coombs test (detects the presence of antibodies directed against the patient’s own red cells)

90
Q

Can a patient with a positive Coombs test keep taking methyldopa?

A

Yes, unless/until hemolytic anemia develops If it does develop, it usually resolves after cessation of drug

Pharmacology I (29 decks)

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