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NURS 3550 > ANS Drugs > Flashcards

ANS Drugs Flashcards

1
Q

What are the 2 main divisions of the nervous system?

A

CNS

PNS

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2
Q

What are the 2 divisions of the PNS?

A

Afferent, and Efferent

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3
Q

What do the afferent neurons do?

A

Carry sensory input to the CNS.

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4
Q

What do the efferent neurons do?

A

Carry motor signals from the CNS to peripheral areas in the body.

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5
Q

What does the autonomic nervous system do?

A

Major involuntary part of the NS.

Responsible for automatic, unconscious bodily functions like BP, HR, GIT and GUT function.

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6
Q

What does the parasympathetic nervous system do?

A
  1. Rest and digest
  2. Save energy
  3. Dialate blood vessels.
  4. Decrease HR
  5. Increase digestion
  6. Constrict smooth muscle of bronchi
  7. Increase sweat gland
  8. Contract smooth muscles of urinary bladder.
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7
Q

What does the sympathetic system do?

A

Dominates during activity, fight or flight.

  1. Direct sympathetic activation of the effector organs
  2. Simulation of the adrenal medulla, to release epinephrine
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8
Q

How are the ANS and Endocrine systems similar?

A
  1. High level integration in the brain
  2. Ability to influence distant regions in the body.
  3. Extensive use of negative feedback
  4. Use chemical transmission.
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9
Q

How are the ANS and Endocrine systems different?

A
  • Rapid response/ Slower response
  • Brief duration/Long duration
  • Transmission of electrical impulses over nerve fibers/Sends signals to target tissue by varying the level of blood-borne hormone
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10
Q

How do cholinergic drugs affect the ANS?

A

They act on receptors activated by acetylcholine.
Acts on pre and post ganglionic in the parasympathetic system.
Acts on all pre ganglionic fibers in the sympathetic system.
Acts on very few post ganglionic fibers in the sympathetic system.

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11
Q

How do adrenergic drugs affect the ANS?

A

Acts on receptors via the simulation of norepinephrine.

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12
Q

What are the parasympathetic receptors?

A

-Cholinergic receptors
-Muscarinic (M1 to M5)
Nicotinic receptors

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13
Q

What are the sympathetic receptors?

A
  • Adrenergic receptors
  • Alpha 1, alpha 2
  • Beta 1 to Beta 3
  • Dopamine (D1 to D5)
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14
Q

Where are the musicarnic receptors located?

A

Heart, smooth muscle, brain, exocrine glands, salivary glands, bladder, GI smooth muscle, eyes

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15
Q

What do agonists that affect M1, M3 and M5 do?

A

Increases IP3 which leads to an increase in Ca+. Ca+ stimulates or inhibits enzymes which cause hyperpolarization, secretion and contraction.
MOSTLY EXITATORY

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16
Q

What do agonists that affect M2 do?

A

Decreases cAMP, decreases Ca+ channels, increases K+.

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17
Q

Where are nicotonic receptors located?

A

– CNS,
– adrenal medulla,
– autonomic ganglia,
– neuromuscular junction.

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18
Q

What are Nn receptors responsible for?

A

-CNS stimulation
-decreased fatigue
- increased alertness.
- Ligand-gated ion channel.
• Binding of two Ach molecules elicits a
conformational change that allows the entry of
Na+ ions, resulting in the depolarization of the
effector cells.
• Nicotine initially stimulates and then blocks the
receptors

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19
Q

What are the 3 types of nicotonic receptors and where are they located?

A

Nn- CNS, Adrenal Medulla
Ng- autonomic ganglia
Nm- Skeletal muscle

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20
Q

What are Ng receptors responsible for?

A

Ganglionic transmission, stimulate both sympathetic and parasympathetic receptors. Produces mixed effects.

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21
Q

What are Nm receptors responsible for?

A

Produce contraction!!! Depolarization causes contraction.

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22
Q

Alpha 1 Receptor

Location and Role

A

Location: Smooth musclesurrounding blood vessels in skin and intestinal tract
Role:Mydriasis, contraction of sphincters, and vasoconstriction leading to increased blood pressure

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23
Q

Alpha 2 Receptor

Location and Role

A

Location:At the end of adrenergic neurons located in the cardiovascular system, GI tract, and genitourinary system, and CNS.
Role:Inhibition of norepinephrine, acetylcholine, and insulin release

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24
Q

Beta 1 Receptor

Location and Role

A

Location:Heart, fat cells, kidney
Role:Increase heart rate and strength of contraction, increased release of renin, increased release of fat

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25
Q

Beta 2 Receptor

A

Location:Smooth muscle surrounding blood vessels of the heart, skeletal muscles, arterioles, and the terminal bronchioles
Role:Vasodilation and bronchodilation, increased release of glucagon

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26
Q

What do musicarnic agonists do?

A

Stimulate parasympathetic nerves.

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27
Q

What is an example of a musicarnic agonist?

A

Bethanecol

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28
Q

What do musicarnic antagonists do?

A

Block acetylcholine at musicarnic receptors.

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29
Q

What are some uses for musicarnic antagonists?

A 
Antispasmodics
Mydriatics
Bronchodilators
Bladder Relaxants
Antiemetic
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30
Q

What is an example of a musicarnic antagonist?

A

Atropine

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31
Q

What are the uses of musicarnic agonists?

A

-bradycardia
-increased secretion from sweat, salivary, bronchial,
gastric glands;
-contraction of intestinal and bronchial smooth muscle; -contraction of the bladder detrusor and relaxation of the bladder trigone and sphincter; and,
-in the eye, miosis and accommodation for near vision.

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32
Q

What does atropine do?

A

blocks the actions of acetylcholine (and all other muscarinic agonists) at muscarinic cholinergic receptors, and thereby

(1) increases heart rate;
(2) reduces secretion from sweat, salivary, bronchial, and gastric glands;
(3) relaxes intestinal and bronchial smooth muscle;
(4) causes urinary retention (by relaxing the bladder detrusor and contracting the trigone and sphincter);
(5) acts in the eye to cause mydriasis and cycloplegia;
(6) acts in the CNS to produce excitation (at low doses) and delirium and hallucinations (at toxic doses).

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33
Q

What are adverse effects of anticholinergic drugs?

A 
dry mouth, 
blurred vision, 
photophobia, 
tachycardia, 
urinary retention, 
constipation, 
 anhidrosis (suppression of sweating).
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34
Q

What is musicarnic agonist poisoning characterized by?

A 
profuse salivation, 
tearing, 
visual disturbances, 
bronchospasm,
 diarrhea, 
bradycardia, 
hypotension
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35
Q

What is musicarnic antagonist poisoning characterized by?

A 
dry mouth,
 blurred vision, 
photophobia, 
hyperthermia,
 hallucinations,
delirium, 
 skin that is hot, dry, and flushed.
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36
Q

How do you reverse musicarnic agonist poising?

A

Atropine

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37
Q

How do you reverse musicarnic antagonist poising?

A

Phycsostigmine, a cholinesterase inhibitor.

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38
Q

What are adrenergic agonists?

A

Produce their effects by activating adrenergic receptors.

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39
Q

What are the 3 properties of catecholamines?

A
  1. They cannot be used orally
  2. They have a brief duration
  3. They cannot cross the blood-brain barrier (polar molecules)
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40
Q

What are the 3 properties of noncatecholamines?

A
  1. Slow metabolism = greater half life
  2. Can be given orally
  3. Can cross the blood brain barrier
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41
Q

What are alpha 1 stimulants given for?

A

To stop bleeding and nasal decongestion.

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42
Q

What do alpha 1 stimulants do?

A

Cause vasoconstriction.

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43
Q

What adverse effects do alpha 1 agonists cause?

A

Bradycardia, hypertension and necrosis at the IV site.

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44
Q

What do alpha 2 stimulants cause?

A
  • Decrease BP

- Decrease pain

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45
Q

What do Beta 1 stimulants do?

A
  • ↑HR, ↑contractility
  • ↑conductivity
  • ↑renin release
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46
Q

What do Beta 2 stimulants do?

A
  • bronchodilation
  • hyperglycemia
  • uterine relaxation
  • skeletal muscle stimulation
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47
Q

What is the mechanism of action for bethanechol?

A

Direct acting muscarinic agonist. Binds reversibly to muscarnic cholinergic receptors to cause activation.

48
Q

What are the therapeutic uses for bethanechol?

A

Approved for urinary retention. Used off label to treat GERD.

49
Q

What are the 4 mechanisms of adrenergic receptors?

A

1) Direct receptor binding
2) Promotion of NE release
3) Blockade of NE reuptake
4) Inhibition of NE inactivation

50
Q

What are the therapeutic applications of B1 activators?

A

HF, Shock, Atrioventricular Heart Block, Cardiac Arrest.

51
Q

What are the adverse effects of B1 activation?

A

Altered heart rhythm/rate, angina pectoris.

52
Q

What are the therapeutic uses of B2 activators?

A

Asthma- promotes bronchiodilation.

Pre-Term Labour- promotes relaxation of uterine muscles.

53
Q

What are the adverse effects of B2 activators?

A

Hyperglycemia- b2 receptors in the liver and skeletal muscles get activated, promoting the breakdown of glycogen to glucose.
Tremor- skeletal muscles enhance contraction.

54
Q

Why is epinephrine used to treat anaphylactic shock?

A

Because epi is not selective and activates a1, b1 and b2 receptors. Activation of these 3 receptors reverse life threatening symptoms of anaphylaxis.

55
Q

Describe Epinephrine

A

A1, A2, B1, B2 receptors
Catecholamine
Broad spectrum adrenergic agonist.

56
Q

What are the therapeutic uses of epinephrine?

A

1) Delay local anesthetic absorption
2) Control superficial bleeding
3) Elevate BP
4) Overcome AV heart block
5) Restore cardiac function
6) Bronchodilation

57
Q

How is epi administered?

A

IM injection or topically

58
Q

What are the adverse effects of epi?

A
  • Hypertensive crisis- alpha 1 activation causes vasoconstrition
  • Dysrythmias- can cause heart to overwork (b1 activation)
  • Angina Pectoris- increase cardiac work, and O2 demand.
  • Necrosis at IV site
  • Hyperglycemia in diabetes pts.
59
Q

Describe Albuterol

A

Activates B2. Noncatecholamine. Used for bronchodilation and smooth muscle relaxation.

60
Q

What are the therapeutic indications for albuterol?

A

Asthma. Highly selective for Beta 2.

61
Q

What are the adverse effects of albuterol?

A

Tremor and tachycardia is most common in high doses.

62
Q

What are the therapeutic uses of alpha 1 blockers?

A

Hypertension, alpha 1 stimulant overdose, treatment of a pheochromocytoma, and treatment of Raynaud’s disease., treatment of bengin prostate hyperplasia.

63
Q

What are the adverse effects of alpha 1 blockers?

A

Orthostatic hypotension, reflex tachycardia (caused by triggered baroreceptor reflex), nasal congestion, inhibition of ejaculation, sodium retention and increased blood volume.

64
Q

What are the adverse effects of an alpha 2 blocker?

A

Potentiation of reflex tachycardia. Could make reflex tachycardia worse.

65
Q

What is prazosin?

A

Competative antagonist that produces selective blockade of A1 receptors. Results in dialation of blood vessels, relaxation of smooth muscles in bladder neck. Only approved for hypertension.

66
Q

What azosin medications are used for hypertension?

A

Prazosin, Terazosin, Doxazosin, Tamsulosin, and more.

67
Q

What are the major consequences to blocking beta 1 receptors in the heart?

A
  • Reduced heart rate
  • reduced force of contraction
  • reduced velocity of impulse conduction through the AV node.
68
Q

Why does angina pectoris occur?

A

The heart itself is not receiving enough oxygen from the coronary system, causing pain.

69
Q

How do beta 1 antagonists help angina pectoris?

A

They block beta 1, causing a decrease cardiac workload.

70
Q

How do beta 1 antagonists help cardiac dysrythmias?

A
  • Decrease rate of sinus nodal discharge

- Suppress conduction of atrial impulses through AV node. This prevents ventricles from pumping too much.

71
Q

How does a beta 1 antagonist help myocardial infractions?

A

Reduces pain, infract size, mortality, and risk of reinfraction.

72
Q

How do beta 1 blockers help hyperthyroidism?

A

Prevent tachydysrythmias and angina (happens in hyperthyroidism due to an increase in catecholamines and noncatecolamines).

73
Q

What are the therapeutic indications for beta 1 blockers?

A
  • Angina
  • Myocardial Infraction
  • Hypertension
  • Cardiac Dysrythmias
  • Reduction of Perioperative Mortality
  • Heart Failure
  • Hyperthyroidism
  • Migraine Prophylaxis
  • Stage Fright
  • Pheochromocytoma
  • Glaucoma
74
Q

What are the adverse effects of a beta 1 blockade?

A
  • Bradycardia
  • Reduced Cardiac Output
  • Worsening HF
  • AV heart block
  • Rebound Cardiac Excitation (if used for long time and discontinued abruptly)
75
Q

What are the adverse effects of a beta 2 blockade?

A
  • Bronchoconstriction

- Hypoglycemia from inhibition of gylcogenolysis from beta 2 receptors in the liver.

76
Q

What are first generation beta blockers?

A

Block B1 and B2 receptors.

77
Q

What are second generation beta blockers?

A

Block only B1 receptors at usual doses.

78
Q

What is propanalol?

A

Widely used first gen non selective beta blocker.

79
Q

What are the pharmacological effects of propanalol?

A
  • Reduce HR
  • Decrease force of ventricular contraction
  • suppress impulse conduction through AV node
  • Suppress renin secretion
  • Bronchoconstriction
  • Vasoconstriction
  • Reduced glycogenolysis
80
Q

What are the main indications for propanolol?

A

Hypertension, angina pectoris, cardiac dysrhythmias, myocardial infraction

81
Q

What are the adverse effects of propanolol?

A
  • Bradycardia
  • AV Heart Block
  • HF
  • Rebound Cardiac Excitation
  • Bronchoconstriction
  • Inhibition of glycogenolysis
  • CNS effects
  • Can cross placental barrier.
82
Q

What are important drug interactions for propanolol?

A
  • Ca+ channel blockers- causes excessive cardiosupression

- insulin - can block glycogenolysis.

83
Q

What is metoprolol?

A

Second gen beta 1 blocker, selective at therapeutic doses.

84
Q

What are the therapeutic effects of metoprolol?

A
  • Reduced HR
  • Force contraction
  • Conduction through AV node
85
Q

What are the therapeutic indications of metoprolol?

A

Hypertension
Angina
HF
Myocardial Infraction

86
Q

What are the major adverse effects of metoprolol?

A
  • Bradycardia
  • Reduced CO
  • AV heart block
  • Rebound Cardiac excitation
87
Q

What is tramadol?

A

Moderately strong analgesic, that relieves pain through opioid and nonopioid ways.

88
Q

What is the mechanism of action for tramadol?

A

Analog of codeine, blocks uptake of norepinephrine and serotonin, which activates the monoaminergic spinal inhibition of pain.

89
Q

What are the therapeutic indications for tramadol?

A

Moderate to severe pain.

90
Q

What are the adverse effects of tramadol?

A 
Sedation
Dizziness
Headache
Dry mouth
Constipation
91
Q

What are some important drug interactions for tramadol?

A

Intensifies CNS depressants, SSRIs/ psychotic drugs.

92
Q

What is clonidine?

A

Alpha 2 agonist. Used for hypertension and pain relief.

93
Q

what is the MA for clonidine?

A

Pain: blocks alpha 2 receptors at the spinal cord, blocking pain peripherally from the brain.

94
Q

What are the adverse effects of clonidine?

A

Hypotension, bradycardia, rebound hypertension, catheter-related infection (b/c given through epidural catheter), dry mouth, dizziness, sedation, anxiety, depression.

95
Q

What do beta 2 agonists do?

A

Activate beta receptors. Can be long acting or short acting.

96
Q

How are beta 2 agonists administered?

A

Orally or through inhalation.

97
Q

What are SABAs and what are they used for?

A

Short Acting Beta Agonists, used for asthma and COPD attacks, usually prescribed PRN.

98
Q

What are LABAs and what are they used for?

A

Long Acting Beta Agonists. Used for long term control of asthma/ COPD attacks.

99
Q

What are the adverse effects of SABAs?

A

Tachycardia, angina, tremor.

100
Q

What are the adverse effects of LABAs?

A

Increase risk for severe asthma and asthma related death when used alone for long term control. Not first line therapy.

101
Q

What are the adverse effects of oral beta agonists?

A

Tremor, if dose is wrong, has possibility to activate beta 1 receptors.

102
Q

What is an example of a SABA?

A

Albuterol.

103
Q

What is an example of a LABA?

A

Formoterol

104
Q

What adrenergic agonists act directly on the receptors?

A

Dopamine, epinephrine, isoproterenol.

105
Q

What adrenergic agonists use indirect mechanisms?

A

Amphetamine, cocaine, tricyclic antidepressants, MAOIs.

106
Q

Where are M1 receptors located?

A

Salivary glands and CNS.

107
Q

Where are M2 receptors located?

A

Heart

108
Q

Where are M3 receptors located?

A

Salivary glands, detrusor muscle, GI smooth muscle, iris sphincter, cilary muscle, lacrimal gland.

109
Q

What happens when an M1 receptor is activated?

A

Salivation and enhanced cognition.

110
Q

What happens when an M2 receptor is activated?

A

Bradycardia

111
Q

What happens when an M3 receptor is activated?

A

salivation, muscle contraction and tearing.

112
Q

What happens when an M1 receptor is inactivated?

A

Dry mouth, confusion, hallucinations.

113
Q

What happens when an M2 receptor is inactivated?

A

tachycardia

114
Q

What happens when an M3 receptor is inactivated?

A

Dry mouth, muscle relaxation, decreased tone and motility, pupil dilation, dry eyes.

115
Q

What is BALD FISH (beta blocker side effects)?

A

Bronchoconstriction, bradycardia
Arrhythmias
Lethargy
Disturbance in glucose metabolism

Fatigue
Insomnia
Sexual Dysfunction
Hypotension

NURS 3550 (11 decks)

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