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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
What is a mnemonic for Anticholinergic Poisoning?
Hot as a hare Dry as a bone Red as a beet Blind as a bat Mad as a hatter
26
Adrenergic agonists are often referred to as \_\_\_\_\_ Why?
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
27
Drugs can activate adrenergic receptors in four ways:
1. Direct Receptor Binding 2. Promotion of NE release (indirect) 3. Blockade of NE reuptake (indirect) 4. Inhibition of NE inactivation (indirect)
28
What mechanism do almost all adrenergic agonists use to produce adrenergic stimulation?
Direct binding to receptors
29
What are some examples of drugs that block NE reuptake?
Cocaine, Tricyclic Antidepressants
30
What are some examples of drugs that promote NE release?
Ephedrine, Amphetamines
31
What are some drugs that inhibit NE inactivation?
MAOIs
32
Structurally, how do catecholamines differ from noncatecholamines?
Contain a catechol group and an amine group
33
What is a catechol group?
A benzene ring with hydroxyl groups on two adjacent carbons
34
Because of their chemistry, all catecholamines have three properties in common:
1. cannot be used orally 2. have a brief DOA 3. cannot cross the BBB
35
Why do catecholamines have short half lives?
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.
36
Name three adrenergic agonists that are noncatecholamines
Ephedrine Albuterol Phenylephrine
37
Why aren't noncatecholamines broken down as quickly?
The lack of a catechol group means COMT doesn't break them down, and MAO does so slowly
38
Which is more polar: catecholamines or non?
Catecholamines, which is why they can't cross the BBB BUT Noncatecholamines CAN and do cross the BBB
39
The ability of a drug o selectively activate certain receptors exclusively depends on:
the dose At low doses, selectivity is maximal As the dose increases, selectivity decreases
40
Activation of Alpha 1 receptors elicits two responses that can be therapeutic:
Vasoconstriction Mydriasis
41
Alpha 1 agonists are usually used for (5):
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
What are adverse effects of alpha 1 activation?
HTN Necrosis Bradycardia (Alpha mediated vasoconstriction elevates BP, which triggers a baroreceptor reflex)
43
Alpha 2 activation causes:
inhibition of NE release PRESYNAPTICALLY More important in the CNS than the PNS
44
By activating CNS alpha 2 receptors, what happens?
1. Reduction of sympathetic outflow to the heart and blood vessels 2. Relief of severe pain
45
All of the clinically relevant responses to Beta 1 activation result from activating Beta 1 receptors in which organ?
The heart Action of renal beta 1 receptors is not associated with any effects whatsoever (good or bad)
46
What are therapeutic uses of beta 1 receptor activation?
Inotropy (shock, heart failure) Increased AV conduction (AV heart block) Initiating contraction during cardiac arrest
47
What are adverse effects of Beta 1 activation?
Dysrhythmias Angina (increases myocardial oxygen demand)
48
Applications of Beta 2 activation are limited to which two organs?
The lungs the uterus
49
What are therapeutic applications of Beta 2 activation?
Asthma (usually inhalation) Delay of preterm labor
50
What are adverse effects of Beta 2 activation
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
**EPINEPHRINE** Receptor specificity Chemical Classification Onset Metabolism Half Life Elimination
Receptor: Alpha 1, Alpha 2, Beta 1, Beta 2 Classification: Catecholamine Onset: Immediate Metabolism: MAO and COMT Half Life: \<5 min Elimination: Urine
52
**NOREPINEPHRINE** Receptor specificity Chemical Classification Onset Metabolism Half Life Elimination
Receptors: Alpha 1, Alpha 2, Beta 1 Class: Catecholamine Onset: Immediate Metabolism: MAO and COMT Duration: 1-2 min Elimination; Urine
53
**ISOPROTERENOL** Receptor specificity Chemical Classification Onset Metabolism Half Life Elimination
Receptor: Beta 1 and Beta 2 Class: Catecholamine Onset: Immediate Metabolism: COMT Half life: 2.5-5 min Elimination: Urine
54
**DOPAMINE** Receptor specificity Chemical Classification Onset Metabolism Half Life Elimination
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
**DOBUTAMINE** Receptor specificity Chemical Classification Onset Metabolism Half Life Elimination
Receptor: Beta 1 Class: Catecholamine Onset: 1-2 min Metabolism COMT Half Life 2 min Elimination Urine
56
**PHENYLEPHRINE** Receptor specificity Chemical Classification Onset Metabolism Half Life Elimination
Receptor: Alpha 1 Class: noncatecholamine Onset: Immediate Metabolism: Hepatic (Deamination) Half LIfe 5 min Elimination Urine
57
Adrenergic Agonists interact with what drugs?
MAOIs Tricyclics (can intensify and prolong epinephrine's effects) General anesthetics (render the myocardium hypersensitive to B1 activation)
58
Adrenergic antagonists cause:
direct blockade of adrenergic receptors
59
Adrenergic Antagonists can be divided into two groups:
Alpha blockers Beta Blockers
60
What are some therapeutic applications for alpha blockade (5)?
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
What are adverse effects of alpha 1 blockade?
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
Adverse effects of alpha 2 blockade include:
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
**PRAZOSIN** Actions and Uses Adverse Effects
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
**TERAZOSIN** Actions and Uses Adverse Effects
ALPHA 1 ANTAGONIST HTN and BPH Same AE as usual, but high incidence of headaches
65
When you se “-osin” think:
Alpha antagonist
66
There is only one non-competitive Alpha Antagonist:
Phenoxybenzamine Blocks alpha 1 and alpha 2 irreversibly. A single dose persists for several days. Only approved for use for patients with pheochromocytoma
67
Beta 1 blockade results in:
1. Reduced Heart Rate 2. Reduced Inotropy 3. Reduced velocity through AV node
68
Beta blockers are especially helpful in treating dysrhythmias that:
involve excessive electrical activity in the SA node and atria Prevents the ventricles from being driven by the excess atrial activity
69
What are the parameters for giving Beta blockers to high-risk patients having noncardiac surgery?
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
Only three beta blockers have been show effective in heart failure:
Carvedilol Bisoprolol Metoprolol
71
Why are beta blockers prescribed for hyperthyroidism?
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
Why are beta blockers prescribed for migraines?
They work as prophylaxis only, won't stop an active headache. No one is totally sure why.
73
What are adverse effects of Beta 1 blockade?
1. Bradycardia 2. Reduced Cardiac Output 3. Heart Failure 4. AV Block 5. ***Rebound cardiac excitation***
74
Adverse effects of beta 2 blockade
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
There are three groups of beta blockers:
* 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
**PROPANOLOL** Generation Receptors
First Generation Beta 1 and Beta 2
77
Which kind of beta blocker do you not want to give a patient with asthma?
Beta 2 You want a selective Beta 1 blockade, like metoprolol
78
Why are beta blockers doubly dangerous for diabetics?
Not only do they predispose to hypoglycemia, they mask the effects of hypoglycemia until it's severe
79
Which two beta blockers also have alpha blocking capabilities?
Carvedilol and labetalol
80
Abrupt discontinuation of any beta blocker can cause:
Rebound cardiac excitation
81
How does a centrally acting alpha 2 agonist effect peripheral sympathetic neurons?
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
The prototypical central alpha 2 agonist is:
Clonidine
83
What is the action of Clonidine?
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
Why doesn't clonidine cause orthostatic hypotension?
It's effects are not posture dependent
85
What are adverse effects of clonidine?
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
Two side effects of methyldopa can be severe:
hemolytic anemia and hepatic necrosis
87
What is the prime difference between clonidine and methyldopa?
It's a prodrug It has to be converted in the brainstem to methylnorepinephrine
88
The only indication for methyldopa is"
Hypertension (particularly during pregnancy)
89
Approximately 10-20% of patients who take methyldopa chronically will have:
a positive coombs test (detects the presence of antibodies directed against the patient's own red cells)
90
Can a patient with a positive Coombs test keep taking methyldopa?
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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