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Pharmacology > Autonomic Pharmacology > Flashcards

Autonomic Pharmacology Flashcards

1
Q

What type of functions does the autonomic nervous system control?

A
  • Visceral functions that occur without concious control
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2
Q

What is the “only organ” not innervated by the autonomic nervous system?

A
  • Skeletal muscle
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3
Q

From where does the autonomic nervous system originate?

A
  • The CNS/ lower brainstem
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4
Q

What are the 2 divisions of the ANS?

A
  • Sympathetic

- Parasympathetic

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5
Q

What effect does the parasympathetic/ sympathetic nervous system have on the pupils?

A

Sympathetic: Dilates pupil
Parasympathetic: Constricts pupil

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6
Q

What effect does the parasympathetic/ sympathetic nervous system have on salivation?

A

Sympathetic: Inhibits salivation
Parasympathetic: Stimulates salivation

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7
Q

What effect does the parasympathetic/ sympathetic nervous system have on the heart?

A

Sympathetic: Accelerates the heart
Parasympathetic: Inhibits the heart

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8
Q

What effect does the parasympathetic/ sympathetic nervous system have on the bronchi?

A

Sympathetic: Dilates bronchi
Parasympathetic: Constricts bronchi

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9
Q

What effect does the parasympathetic/ sympathetic nervous system have on digestive activity?

A

Sympathetic: Inhibits digestive activity
Parasympathetic: Facilitates digestive activity

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10
Q

What effect does the parasympathetic/ sympathetic nervous system have on the kidneys and gallbladder?

A

Sympathetic: Stimulates glucose release by the liver
Parasympathetic: Stimulates the gall bladder

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11
Q

What effect does the parasympathetic/ sympathetic nervous system have on the bladder?

A

Sympathetic: Relaxes the bladder
Parasympathetic: Contracts the bladder

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12
Q

What effect does the parasympathetic/ sympathetic nervous system have on the rectum?

A

Sympathetic: Contracts the rectum
Parasympathetic: Relaxes the rectum

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13
Q

What effect does the sympathetic nervous system have on the kidneys?

A
  • Secretion of epinephrine and norepinephrine
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14
Q

What is the main nerve to the heart?

A
  • The vagus nerve
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15
Q

From which spinal segments do the sympathetic fibers originate from?

A

T1 - L3

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16
Q

From which part of the nervous system/ spinal segments do the parasympathetic fibers originate from?

A
  • Midbrain
  • Medulla oblongata
  • Sacral portion of spinal cord
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17
Q

What is an autonomic ganglia?

A
  • Specialized complex structure residing outside the spinal cord that contains axodendritic synapses between preganglionic and postganglionic neurons
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18
Q

Is the sympathetic nervous system closer, or farther away from the spinal cord?

A
  • Sympathetic closer

- Parasympathetic farther away

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19
Q

What does an autonomic ganglion connect?

A

Preganglionic and postganglionic nerves

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20
Q

How do reactions propogate through ganglia?

A

Neurotransmitters

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21
Q

Which neurotransmitter is present in the autonomic ganglia of the sympathetic and parasympathetic nervous systems?

A

Acetylcholine

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22
Q

Why do drugs need to either stimulate or block at the level of the end organ?

A

There is no specificity

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23
Q

Where are receptors located typically?

A

Embedded into the target tissue (nerve, end organ, etc…)

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24
Q

What neurotransmitter is located at the neuro-effector junction of the parasympathetic division?

A

Acetylcholine

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25
Q

What two compounds are acetylcholine synthesized from? What enzyme facilitates this synthesis?

A
  • Acetyl CoA and Choline

- Choline Acetyltranseferase

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26
Q

Where is Acetylcholine broken down?

A

Ganglionic junction or neuro-effector junction

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27
Q

Why can’t acetylcholine be used as a drug?

A

It is resorbed/ disposed of too quickly

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28
Q

What happens to ACh after it is synthesized?

A
  • Stored in vesicle at the nerve terminal
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29
Q

What ions are involved in binding the ACh vesicle to the nerve terminal and releasing ACh into the synapse?

A
  • Sodium

- Calcium

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30
Q

Where does norepinephrine function as a neurotrasmitter in the autonomic nervous system?

A
  • Neuro-effector junction of sympathetic nervous system
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31
Q

What group of chemicals does norepinephrine belong to?

A
  • Catecholamines
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32
Q

What 2 other chemicals are catecholamines?

A
  • Dopamine

- Epinephrine

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33
Q

What chemical do the adrenal glands release?

A
  • Epinephrine
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34
Q

What catecholamine is a precursor to norepinephrine?

A
  • Dopamine
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35
Q

What is the main way that NE is removed from the synapse?

A
  • Re-uptake by pre-synaptic fibers
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36
Q

What mediates re-uptake of norepinephrine?

A

Alpha-2 receptors

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37
Q

What are 2 methods of inactivation of NE?

A

Breakdown by:

  • Monoamine oxidase
  • Catechol-o-methyltransferase
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38
Q

What 2 factors of a cell can be affected by NE or ACh?

A
  • Metabolism

- Ion channels

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39
Q

What is the presynaptic receptor in the sympathetic nervous system? What is its function?

A
  • Alpha-2 receptor
  • If activated by an excess of NE in the synapse, it sends a signal to the nerve terminal to decrease norepinephrine synthesis
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40
Q

What two subtypes of receptors mediate ACh’s effects?

A
  • Muscarinic (M)

- Nicotinic (N)

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41
Q

Where are M receptors found?

A
  • Neuro-effector junction in parasympathetic division
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42
Q

Where are N receptors found?

A
  • Autonomic ganglia of both sympathetic and parasympathetic divisions of the ANS, and at the neuro-muscular junction
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43
Q

What is the source of the name of nicotinic receptors?

A

Nicotine

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44
Q

What is the source of the name of muscarinic receptors?

A

Mushrooms

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45
Q

What is meant by neuro-effector junction?

A

At the end organ

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46
Q

What type of reactions are muscarine receptors related to?

A

Parasympathetic

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47
Q

What type of reactions are nictonic receptors related to?

A

Both sympathetic and parasympathetic

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48
Q

What two subtypes of receptors mediate the effects of norepinephrine, and epinephrine?

A

Alpha and beta receptors

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49
Q

What are the 2 types of alpha receptors?

A

Alpha-1

Alpha-2

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50
Q

Where are alpha-1 fibers found, and what is their function?

A
  • Present in arteriolar smooth muscles

- Activation causes vasocontriction

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51
Q

Where are alpha-2 fibers found, and what is their function?

A
  • Found pre-ganglionically, and in the CNS

- Decreases sympathetic flow from the CNS

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52
Q

What neurotransmitter production is inhibited by alpha-2 stimulation?

A
  • Norepinephrine
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53
Q

What are the 2 types of beta receptors?

A

Beta-1

Beta-2

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54
Q

Where are Beta-1 receptors found? What is their function?

A
  • Found in the heart and kidney

- Increases heart rate, force of contration, and secretion of renin from kidney

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55
Q

Where are Beta-2 receptors found? What is their function?

A
  • Found in smooth muscles of blood vessels and bronchi

- Vasodilates, and bronchodilates

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56
Q

What are adrenergic impulses?

A
  • Norepinephrine reactions

- Sympathetic nervous system

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57
Q

What are cholinergic impulses?

A
  • Acetylcholine reactions

- Parasympathetic nervous system

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58
Q

What is the function of adrenergic and cholinergic impulses on the radial muscle of the eye?

A

Adrenergic: Contraction/ Opens eyes
Cholinergic: No effect

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59
Q

What is the function of adrenergic and cholinergic impulses on the spincter muscles of the eye, iris?

A

Cholinergic: Contraction/ closes eyes
Adrenergic: No efefct

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60
Q

What is the function of adrenergic and cholinergic impulses on the ciliary muscles of the eye?

A

Adrenergic: Relaxation for far vision
Cholinergic: Contraction for near vision

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61
Q

What is the function of adrenergic and cholinergic impulses on the lacrimal glands of the eye?

A

Adrenergic: No effect
Cholinergic: Increased secretions/ tearing

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62
Q

What is the function of adrenergic and cholinergic impulses on the SA node of the heart?

A

Adrenergic: Increased heart rate
Cholinergic: Decreased heart rate/ vagal arrest

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63
Q

What is the function of adrenergic and cholinergic impulses on the atria of the heart?

A

Adrenergic: Increased contractility and conduction velocity
Cholinergic: Decreased contractility

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64
Q

What is the function of adrenergic and cholinergic impulses on the AV node of the heart?

A

Adrenergic: Increased conduction velocity and automaticity
Cholinergic: Decreased conduction velocity

65
Q

What is the function of adrenergic and cholinergic impulses on the ventricles of the heart?

A

Adrenergic: Increased contractility
Cholinergic: Slight decrease in contractility

66
Q

What is the function of adrenergic and cholinergic impulses on the coronary arterioles?

A

Adrenergic: Contriction with Alpha-1; Dilation with Beta-2
Cholinergic: (Contriction with endothelial damage)

67
Q

What is the function of adrenergic and cholinergic impulses on the pulmonary arterioles?

A

Adrenergic: Constriction with Alpha-1; Dilation with Beta-2
Cholinergic: Dilation

68
Q

What is the function of adrenergic and cholinergic impulses on renal arterioles?

A

Adrenergic: Constriction with Alpha-1; Dilation with Beta-2
Cholinergic: No effect

69
Q

What is the function of adrenergic and cholinergic impulses on system veins?

A

Adrenergic: Constriction with alpha-1; Dilation with beta-2

70
Q

What is the function of adrenergic and cholinergic impulses on the tracheal and bronchial muscles of the lungs?

A

Adrenergic: Relaxation with beta-2
Cholinergic: Contraction

71
Q

What is the function of adrenergic and cholinergic impulses on the bronchial glands of the lungs?

A

Adrenergic: Decreased secretion by alpha-1; Increased secretion with beta-2
Cholinergic: Increased secretion

72
Q

What is the function of adrenergic and cholinergic impulses on the motility and tone of the stomach?

A

Adrenergic: Decreased with alpha-1
Cholinergic: Increased

73
Q

What is the function of adrenergic and cholinergic impulses on the sphincters of the stomach?

A

Adrenergic: Contraction with alpha-1
Cholinergic: Relaxation

74
Q

What is the function of adrenergic and cholinergic impulses on the secretions of the stomach?

A

Adrenergic: Inhibition
Cholinergic: Stimulation

75
Q

What is the function of adrenergic and cholinergic impulses on the motility and tone of the intestine?

A

Adrenergic: Decreased with alph-1
Cholinergic: Increased

76
Q

What is the function of adrenergic and cholinergic impulses on the sphincters of the intestines?

A

Adrenergic: Contraction
Cholinergic: Relaxed

77
Q

What is the function of adrenergic and cholinergic impulses on the secretions of the intestines?

A

Adrenergic: Inhibition
Cholinergic: Stimulation

78
Q

What is the function of adrenergic and cholinergic impulses of the gallbladder and ducts of the intestine?

A

Adrenergic: Relaxation with beta-2
Cholinergic: Contraction

79
Q

What is the function of adrenergic and cholinergic impulses on renin secretion in the kidney?

A

Adrenergic: increase with beta-1
Cholinergic: No effect

80
Q

What is the function of adrenergic and cholinergic impulses on the sphincter of the urinary bladder?

A

Adrenergic: Contraction by alpha-1
Cholinergic: Relaxation

81
Q

What is the function of adrenergic and cholinergic impulses of the water and potassium secretions of salivary glands?

A

Adrenergic: No effect
Cholinergic: Increased

82
Q

What is the function of adrenergic and cholinergic impulses of amylase secretion of salivary glands?

A

Adrenergic: No effect
Cholinergic: Increased

83
Q

What is the function of adrenergic and cholinergic impulses of nasopharyngeal glands of the salivary glands?

A

Aderenergic: No effect
Cholinergic: Increased secretion

84
Q

What are parasympathomimetics?

A
  • Drugs that mimic the effects of parasympathetic nerve stimulation
85
Q

What is another name for parasympathomimetics?

A
  • Muscarinic receptor agonists
86
Q

What is the mechanism of action of direct-acting parasympathetics?

A
  • Stimulation of M receptors at the neuro-effector junction with no or little N receptor stimulation
87
Q

What are 4 therapeutic uses of muscarinic receptor agonists?

A
  • GI disorders
  • Urinary bladder disorders
  • Xerostomia (dry mouth)
  • Opthalamological (reduce acute narrow angle glaucoma attack)
88
Q

What is the use of bethanchol in the GI tract?

A
  • Stimulates gi tract following abdominal distension and gastric atony
89
Q

How do indirect-acting parasympathomimetics work?

A
  • Prolong duration of action of ACh by inhibiting ACh esterase
90
Q

What are the therapeutic uses of indirect-acting parasympathetics?

A
  • Similar to direct acting muscarinics
91
Q

How are indirect-acting parasympathetics used to treat dementia?

A
  • Donepezil manage the dementia associated with alzheimer disease
92
Q

What are some examples of irreversible ACh esterase inhibitors?

A
  • Paraxon
  • Malaoxon
  • Nerve gas sarin
  • Insecticides
93
Q

How is exposure to irreversible ACh inhibitors treated?

A
  • Atropine (an M receptor blocker) and pralidoxime (2-PAM) given before binding of organophosorous compounds becomes permanent
94
Q

What can used to treat serious toxic reactions to muscarinic agonists?

A
  • Atropine sulfate administered by IV or subcanteously

- Epinephrine for cardiovascular or bronchoconstrictor responses

95
Q

What are parasympatholytics?

A

Muscarinic Receptor Antagonists

96
Q

What is the mechanism of action of muscarinic receptor antagonists?

A
  • Competitive blocking of muscarinic receptors at neuro-effector sites on smooth muscle, cardiac muscle, gland cells, and in the CNS with little blockage of the effects of ACh at nicotinic receptor sites
97
Q

Do muscarinic receptor blockers show selectivity towrads the muscarinic receptor subtypes?

A
  • No, except for pirenzepine that are selective towards M1 receptors
98
Q

How are muscarinic receptor anatogonists used in relation to the heart?

A
  • Increases heart rate by blocking vagal nerve effects on M2 receptors on the SA nodal pacemaker
99
Q

Do muscarinic receptor antagonists have an effect on blood vessels when administered in isolation? Why?

A

No, because, there is no parasympathetic control of the vascular system

100
Q

What effect can muscarinic receptor antagonists have on choline esters?

A
  • Block vasodilation induced by choline esters effects on endothelial M3 receptors
101
Q

What roles does the parasympathetic nervous system play in the respiratory tract?

A
  • Regulate bronchomotor tone/ constrict broncioles

- Facilitate secretions in the nose, pharynx and bronchi

102
Q

What effect do muscarinic receptor antagonists have on the respiratory tract?

A
  • Bronchodilation by means of blocking the M3 receptor

- Block secretions of the nose, pharynx, and bronchi

103
Q

What is a danger of muscarinic receptor antagonists to the respiratory tract?

A
  • May dry the lungs out to the point of irritation
104
Q

What effect do muscarinic receptor antagonists have on the gastrointenstinal tract?

A
  • Inhibit motility and secretions

- Inhibit gastric acid secretion

105
Q

What effect do muscarinic receptor antagonists have on the urinary tract?

A
  • Decrease the tone and amplitude of contractions of the bladder
106
Q

What effect do muscarinic receptor antagonists have on sweat glands?

A
  • Inhibition of sweating

- Skin can become hot and dry, raising body temperature

107
Q

What determines a muscarinic receptor antagonists effect on the CNS?

A
  • Its ability to cross the blood brain barrier
108
Q

What effects can muscarinic receptor antagonists have on the CNS if they can cross the blood brain barrier?

A
  • Depression of the CNS

- May be preceded by central excitation if atropine is used

109
Q

What are the effects of muscarinic receptor antagonists on the eyes?

A
  • Pupil dilation/ mydriasis

- Cycloplegia (lack of accomodation of the eye due to a paralysed ciliary muscles

110
Q

What effect does atropine have at a 0.5 mg dose?

A
  • Inhibition of sweating, some dryness of the mouth
111
Q

What effect does atropine have at a 1 mg dose?

A
  • Definite dryness of mouth
  • Heart acceleration
  • Mild pupil dilation
112
Q

What effect does atropine have at a 2 mg dose?

A
  • Rapid heart rate
  • Palpitations
  • Marked dilation of pupils
113
Q

What effect does atropine have at a 5 mg dose?

A
  • Inhibition of parasympathetic control of the GI, urinary bladder
  • Inhibited gastric secretions and motility
  • Increased dryness of mouth
  • Heart acceleration
  • Pupil dilation
  • Palpitations
114
Q

What effect does atropine have at a 10 mg dose?

A

Previously listed symptoms, and CNS symptoms:

  • restlessness
  • Excitement
  • Hallucinations
  • Delirium
  • Coma
115
Q

What is ipratropium bromide/ artrovent?

A

A muscarinic receptor antagonist that doesn’t influence the CNS. Its mostly used as a bronchodilator in COPD, but also in asthma

116
Q

What is the effect scopolamine?

A
  • Controls motion sickness
117
Q

What are the therapeutic uses of atropine?

A
  • Reduce salivary/ mucus hypersecretions
  • Protect against reflex bradycardia
  • Antidote for mushroom poisoning
118
Q

What is tolterodine tartrate/ detrol used for?

A

Inhibit an overactive bladder

119
Q

What is Fesoterodine fumarate/ Toviaz used for?

A
  • Treats overactive bladder
120
Q

What are 6 side-effects of muscarinic receptor antagonists?

A
  • Mouth
  • Urinary retention
  • Anhydrosis
  • Tachycardia
  • Palpitations
  • Constipation
121
Q

What are sympathomimetic agents?

A
  • Direct stimulators of the adrenergic receptors
122
Q

What are the 3 endogenous sympathomimetic drugs?

A
  • Epinephrine
  • Norepinephrine
  • Dopamine
123
Q

What are the cardiac effects of epinephrine?

A
  • B-1 receptors are stimulated, causing chronotropic, and postitive iontropic effects (stimulates heart)
124
Q

What are the respiratory effects of epinephrie?

A
  • B-2 receptor stimulation leads to potent bronchodilation (bronchial smooth muscles are relaxed)
125
Q

Why does epinephrine have a short duration of action?

A
  • It is rapidly metabolized by enzymes (MAO and COMT)
126
Q

What may results from rapid intravenous injection of epinephrine? Why?

A 
- Cerebral hemorrhage may occur due to the sharp rise in blood pressure
May also undergo:
- Tremors
- Palpitations
- Anxiety
- Reslessness
127
Q

What are the 2 therapeutic uses of epinephrine?

A
  • Provide rapid relief to hypersensitivity reactions including anaphylaxis to drugs and allergens
  • Restore cardiac rhythm in patients with cardiac arrest
128
Q

What receptors does norepinephrine act most powerfully on? What is the effect of this?

A
  • NE activates alpha-1 receptors powerfully, and weakly activates beta-2
129
Q

What is the therapeutic use of norepinephrine?

A
  • Can be titrated to desired pressor effect in treatment of hypotension (raises blood pressure due to vasocontriction)
130
Q

By what route of administration is NE and epinerphrine not active?

A

The oral route

131
Q

What is the effect of dopamine at lower doses?

A
  • Increases renal, coronary, and mesenteric vasodilation due stimulation of dopamine receptors (D1)
132
Q

What is the effect of dopamine at higher doses?

A
  • Stimulates cardiac beta-1 receptors causing positive iontropic and chronotropic effects. (stimulating the heart)
133
Q

In what pathway is dopamine involved?

A

The synthetic pathway to NE and epinephrine

134
Q

What is the therapeutic use of dopamine?

A
  • Treats severe congestive heart failure in patients with oligurea (low urine output) and low or normal peripheral vascular resistance
135
Q

What is the effect of non-selective beta-agonists? What are their therapeutic effects?

A
  • Increased cardiac output
  • Dilation of muscle and mesenteric arteries
  • Stimulates heart rate in patients with bradycardia or heart block in emergency situations
136
Q

What would be the ideal selective beta-agonist for asthma? Why?

A
  • Higher preferential affinity towards B2 receptor, and no affinity towards B1.
  • Bronchodilation and vasodilation without cardiac effects
137
Q

What types of drugs are used to treat asthma?

A

Beta-2-selective agonists

138
Q

What are some short and long actin beta-2-agonists?

A 
Short:
- Albuterol/ Ventolin
- Terbutaline/ Brethine
Long:
Salmetrol/ Serevent
139
Q

How fast does a short acting beta-2-selective agonist onset? How do the effects last?

A
  • Onsets in 15 minutes

- Lasts 4 - 6 hours

140
Q

How long does a long-acting beta-2-selective agonist last?

A
  • Up to 12 hours
141
Q

How do alpha-adrenergic receptor agonists work?

A
  • Stimulate either alpha-1 or alpha-2 receptors
142
Q

What is a common use of alpha-1-selective agonists? How does it work?

A
  • Nasal decongestant in allergic rhinitis

- Contricts blood vessels in the nasal tissue leading to decreased fluid accumulation

143
Q

What can happen in chronic use of nasal decongestants?

A
  • Loss of efficacy, and worsening of symptoms due to receptor desensitization
144
Q

What drug is a common alpha-2-selective agonist? What is its effect?

A
  • Clonidine/ Catapres selectively stimulates alpha-2 receptors to decrease central sympathetic outflow to lessen vasoconstrictive drive
145
Q

What are some non-direct adrenergic agonists? What is their effect?

A
  • Amphetamine, dextroamphetamine, and methylpehnidate shoot norepinephrine into CNS synapses stimulating CNS to treat ADHD
146
Q

How do adrenergic receptor antagonists work?

A
  • Competitive blockage of alpha and/or beta-adrenergic receptors
147
Q

For what 3 issues are adrenergic receptor antagonists used for?

A
  • Arrythmias
  • Heart failure
  • Hypertension
148
Q

What are alpha-1-selective blockers used for?

A
  • Block receptors in vscular smooth muscles of arterioles and veins, decreasing peripheral resistance and blood pressure over time
149
Q

What is less observed with alpha-1-selective blockers as opposed to non-selective alpha-blockers?

A
  • Tachycardia
150
Q

What are 2 adverse effects of alpha-1-selective blockers?

A
  • First-dose phenomenon: Marked postural hypotension and syncope observe 60 - 90 minutes after the first dose
  • Water retention due to vasodilating effect
151
Q

What is the effect of beta-adrenergic receptor blockers on the heart?

A
  • Blocking of beta-1 receptors slows heart rate and reduces myocardial contratility
152
Q

What is the effect of beta-adrenergic receptor blockers on the pulmonary system?

A
  • No effect on normal individuals, but the blocking of beta-2 receptors in patients with asthma or COPD can lead to life threatening bronchoconstriction
153
Q

What is the effect of beta-adrenergic receptor blockers on peripheral vascular resistance?

A
  • Blockage of B-2 receptors in arteriolar smooth muscle decrease vasular resistance; beta-1 blockers can also reduce peripheral vascular resistance in hypertension patients over time
154
Q

How do non-selective beta-blockers work?

A

Reversibly block beta-1 and beta-2 receptors with no selectivity towards either type

155
Q

What are the therapeutic uses of beta-1-selective blockers?

A
  • Hypertension
  • CHF
  • Angina and MI
156
Q

What may occur in patients with AV conduction defects given beta-1-selective blockers?

A
  • Life-threatening bradyarrhythmias
157
Q

Why should long-term beta-1-selective blockers not be discontinued abruptly?

A
  • Exacerabtes angina, and can bring on sudden heart attack
158
Q

What effect can B2-selective blockers have on asthmatics?

A
  • Worsen brochoconstriction
159
Q

What type beta-selective-blockers produce lss broncho-constriction?

A
  • B1 selective blockers or non-selective b-blockers with partial b2-agonism

Pharmacology (9 decks)

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