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PHARMACOLOGY > PHARMACOLOGY- Autonomic drugs > Flashcards

PHARMACOLOGY- Autonomic drugs Flashcards

1
Q

Which neurotrasmitter manage parasympathetic effect?

A

ACh

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2
Q

Where does parasympathetic has effects?

A

Cardiac and smooth muscle, gland cells, nerve terminalis

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3
Q

This is the way of parasympathetic Transmission impulse

A

Medula (first neuron)- Second Neuron (free, Nicotinic receptors)- Organ (Stimulated by ACh, Muscarinic receptors)

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4
Q

Who controls the sweat glands?

A

Sympathetic

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5
Q

Which is the way of Sweat gland sympathetic stimulation?

A

Medulla (first neuron-ACh) - Ganglia (Second neuron, Nicotinic receptors)- Organ (Stimulated by ACh, Muscarinic receptors)

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6
Q

Which Structures are stimulated by Sympathetic in α β receptors?

A

Cardiac and smooth muscle, gland cells, nerve terminals

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7
Q

This is the way of sympathetic Transmission impulse until reaching α β receptors

A

Medulla (first neuron-ACh) - Ganglia (Second neuron, Nicotinic receptors)- Organ (Stimulated by NE, α β receptors)

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8
Q

Which Structures are stimulated by Sympathetic in D1 receptors?

A

Renal vasculature, smooth muscle

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9
Q

This is the way of sympathetic Transmission impulse until reaching D1 receptors

A

Medulla (first neuron-ACh) - Ganglia (Second neuron, Nicotinic receptors)- Organ (Stimulated by Dopamine, α β receptors)

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10
Q

Who stimulates adenal medulla?

A

ACh

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11
Q

Once stimulated by ACh produced in the Medulla, what does Adrenal Medulla produces?

A

Epinephrine

Norepinephrine

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12
Q

Who stimulates the somatic impulse?

A

Voluntary motor nerve

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13
Q

Who is the target of Somatic impulse?

A

Skeletal muscle

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14
Q

This is the way of Somatic Transmission impulse until reaching Skeletal muscle

A

Medulla (first neuron) ACh and Skleletal muscle (Nicotinic receptors)

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15
Q

What is the difference of Sweat glands invervation and Adrenal medulla from other Sympathetic nervous system?

A

Sweat glands and Adrenal medulla are part of the sympathetic nervous system but are innervated by cholinergic fibers

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16
Q

What prevents release of neurotransmitter at all cholinergic terminals?

A

Botulinum toxin

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17
Q

These are consider cholinergic fibers

A

Parasympathetic
Sweat glands (sympathetic)
Adrenal medula (sympathetic)
Somatic

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18
Q

This is the way of Nervous system impulse reachs Adrenal Medulla

A

Medulla (first neuron-ACh) - Adrenal Medulla (Nicotinic receptors)- Secretion of Epi, Ne

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19
Q

Which are the receptors of ACh?

A

Nicotinic ACh receptors

Muscarinic ACh receptors

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20
Q

These are the subtypes of Nicotinic ACh receptors

A

Nn (found in autonomic ganglia)

Nm (found in neuromuscular junction)

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21
Q

Which kind of channels do Nicotinic ACh receptors have?

A

Are ligand gated Na+/ K+ channels

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22
Q

Which kind of channels do Muscarinic ACh receptors have?

A

G protein coupled receptors that ussually act through 2nd messengers

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23
Q

Which are the subtypes of Muscarinic receptors?

A

M1, M2, M3, M4, M5

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24
Q

Who have Muscarinic receptors?

A 
Parasympathetic
Sweat glands (Sympathetic)
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25
Q

Where do Nicotinic receptors are found?

A

Somatic (Skeletak muscle)

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26
Q

These are sympathetic receptors

A

α1, α2, β1, β2

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27
Q

Sympathetic receptor α1, Which kind of G protein class is?

A

q

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28
Q

These are the major functions of Sympathetic receptor α1

A

↑ vascular smooth muscle concentration,
↑ pupillary muscle contraction (mydriasis)
↑ intestinal and bladder sphincter muscle contraction

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29
Q

Which kind of G protein class are Sympathetic receptor α2?

A

i

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30
Q

This is the effect of Sympathetic receptor α2 stimulation

A

↓ sympathetic outflow
↓ insulin release
↓ lipolysis
↑ platelel aggregation

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31
Q

Which kind of G protein class are Sympathetic receptor β1 and β2?

A

s

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32
Q

Which are the effects of β1 receptors stimulation?

A

↑ heart rate
↑ Contractility
↑ renin release
↑ lipolysis

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33
Q

These are the effects of β2 receptors stimulation

A 
Vasodilation, bronchodilation
↑ heart rate
↑ Contractility
↑ lipolysis
↑ insulin release
↓ uterine tone (tocolysis)
Ciliary muscle relaxation
↑ aqueous humor production
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34
Q

Name the parasympathetic receptors

A

M1, M2, M3

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35
Q

What kind of G protein class does each Muscarinic receptor has?

A 
M1= q
M2= i
M3= q
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36
Q

Where are M1 receptors found?

A

CNS, enteric nervous system

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37
Q

This is the effect of M2 receptors stimulation by parasympathetic

A

↓ Heart rate and contractility of atria

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38
Q

Which is the effect of M3 receptors?

A

↑ exocrine gland secretions (eg lacrimal, salivary, gastric acid)
↑ gut peristalsis
↑ Bladder contraction
bronchoconstriction
↑ pupillary sphincter muscle contraction (miosis)
Ciliary muscle contraction (accomodation)

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39
Q

Which is the effect of Dopamine in D1 receptors?

A

Relaxes renal vascular smooth muscle

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40
Q

This is the effetc of Dopamine in D2 receptors

A

Modulates Transmitter release, especially in brain

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41
Q

Which kind of G protein class are Dopamine receptors?

A 
D1= s
D2= i
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42
Q

Name the Histamine receptors

A

H1

H2

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43
Q

These are histamine receptor G protein class

A 
H1= q
H2= s
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44
Q

Vasopresin receptors

A

V1

V2

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45
Q

This is the effect of V1 receptor stimulation

A

↑ vascular smooth muscle contraction

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46
Q

What is the effect of V2 receptor stimulation?

A

↑ H2O permeability and reabsorption in the collecting tubules of the kidney

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47
Q

Which receptors are Gq?

A

H1, α1, V1, M1, M3

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48
Q

This is the process of how receptor that have G protein class produce Smooth muscle relaxation

A

Receptor → Phospholipase C→ Acts in PIP2 → IP3 → ↑ Ca2+ in → Smooth Muscle relaxation

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49
Q

This is the menominc for Gq receptors

A

HAVe 1 M&M

H1, α1, V1, M1, M3

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50
Q

Which are the two pathways for PIP2?

A

DAG→ Protein kinase C

IP3 → ↑ Ca2+ in → Smooth Muscle relaxation

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51
Q

These are the receptors associated to Gs

A

β1, β2, D1, H2, V2

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52
Q

Who are the receptors associated to Gi?

A

M2, α2, D2

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53
Q

What is the process after Gs and Gi are stimulated?

A

Adenylyl cyclase → ATP → cAMP → Proteinkinase A

Which leads to ↑ Ca2+ in (heart) and Myosin light chain kinase (smooth muscle)

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54
Q

How is the process of cholinergic impulse?

A

Choline is incorporated to the axon → Choline+ Acetyl-CoA→ ACh→ACh incorporated to vesicles→ Liberation of ACh vesicles→ ACh reach the receptor in Post synaptic membrane

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55
Q

Who inhibits Choline incorporation to DNA?

A

Hemicholinium

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56
Q

Who can inhibite ACh incorporation to Vesicles?

A

Vesamicol

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57
Q

This cofactor positivively interacts in ACh vesicles liberation

A

Ca2+

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58
Q

Who inhibits ACh liberation in pre synaptic membrane?

A

Botulinun

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59
Q

Which is the process of Noradrenergic impulse until reachinng the receptor?

A

Tyrosine incorporated to Axon→ Tyrosine → DOPA → Dopamine → NE in vesicles→ liberation of NE in presynaptic membrane→ Adrenoreceptors α or β in post synaptic membrane

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60
Q

These are the other outcomes of Noradrenergic secretion

A

Negative feedback

Diffusion, metabolism

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61
Q

Who modulates release of norepinephrine from a sympathetic nerve ending?

A

Norepinephrine itself

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62
Q

Where does Norepinephrine acts?

A

On presynaptic α2 autoreceptors, angitensin II and other substances

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63
Q

How are cholinomimetic agents classified?

A

Direct agonist

Indirect agonists

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64
Q

Which drugs are Cholinomimetic Direct agonist?

A

Bethanechol
Carbachol
Pilocarpine
Methacholine

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65
Q

Which is the clinical application for Bethanechol?

A

Postoperative ileus, neurogenic ileus, and urinary retention

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66
Q

Which is the mechanism of Action of Bethanecol?

A

Activates bowel and bladder smooth muscle; resistant to AChE

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67
Q

When is recommended the clinical use for Carbachol?

A

Glaucoma, pupillary constriction, and relief of intraocular pressure

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68
Q

This is the clinical application for Pilocarpine

A

Potent stimulator of sweat, tears and saliva

Open angle and closed angle glaucoma

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69
Q

This is the mechanism of action of pilocarpine

A

Contracts ciliary muscle of eye (open angle glaucoma), pupillary sphincter (closed angle glaucoma)

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70
Q

Direct Agonist used as Challenge test for diagnosis of astha

A

Methacholine

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71
Q

What is the action of Methacoline?

A

Stimulates muscarinic receptors in airway when inhaled

72
Q

Alternative name for Indirect agonist

A

Anticholinesterases

73
Q

Name anticholinesterase drugs

A 
Neostigmine
Pyridostigmine
Physostigmine
Donepezil
Rivastigmine
Galantamine
Edrophonium
74
Q

These are the clinical use for Neostigmine

A

Postoperative and neurogenic ileus and urinary retention
Myasthenia gravis
Reversal of neuromuscular junction blockade (postoperative)

75
Q

Which is the effect of Neostigmine?

A

↑ Endogenous ACh

76
Q

How much penetreation does Neostigmine has to CNS?

A

No CNS penetration

77
Q

When is recommended to use Pyridostigmine?

A 
Myastenia gravis (long acting)
Does not penetrate CNS
78
Q

This is the effect of Pyridostigmine

A

↑ Endogenous ACh

79
Q

Which is the effect of all Cholinomimetic indirect antagonists?

A

↑ Endogenous ACh

80
Q

What is different in Physostigmine compared to other Anticholinesterases drugs?

A

Anticholinergic toxicity (crosses blood brain barrier → CNS)

81
Q

Which clinical use does Physostigmine has?

A

For atropine overdose

82
Q

Which anticholinesterase drugs are used for Alzheimer disease?

A

Donepezil
Rivastigmine
Galantamine

83
Q

Historically, diagnosis of myasthenia gravis (extremely short acting)

A

Edrophonium

84
Q

How is Myastenia gravis nowdays diagnose?

A

By antiAChR Ab (anti-acetylcholine receptor antibody) test

85
Q

Before administering Cholinomimetic agents we need to be careful for…

A

Watch exacerbation of COPD, asthma, and peptic ulcers when giving to susceptible patients

86
Q

When is often to see Cholinesterase inhibitor poisoning?

A

Often due to organophosphates, such as parathion, that irreversibly inhibit AChE

87
Q

These are the clinical manifestations of Cholinesterase inhibitor poisoning

A 
DUMBBELSS
Diarrhea
Urination
Miosis
Bronchospasm
Bradycardia
Excitation of skeletal muscle and CNS
Lacrimation
Sweating
Salivation
88
Q

Where can we find organophosphates?

A

Insecticides

89
Q

Who usually suffer organophospate poisoning?

A

Farmers

90
Q

This is the antidote for Cholinesterase inhibitor poisoning

A

Atropine (competitive inhibitor)+ pralidoxime (regenerates AChE, if given early)

91
Q

Drugs Consider Muscarinic antagonists

A 
Atropine, homatropine, tropicamide
Benztropine
Scopolamine
Ipratropium, tiotropium
Oxybutynin, darifenacin and solfenacin
Glycopyrrolate
92
Q

Clinical application for Atropine

A

To treat Bradycardia

Produce mydriases and cyclopegia

93
Q

This is the clinical use for Benztropine

A

Parkinson disease

94
Q

Muscarinic antagonist for motion sickness

A

Scopolamine

95
Q

Which family are Ipratroium, tiotropium?

A

Muscarinic antagonist

96
Q

Clinical use for Ipratrpium, tiotropium

A

COPD, asthma

97
Q

These muscarinic antagonists reduce the urgency in mild cystitis and reduce bladder spasms

A

Oxybutynin, Darifenacin and Solifenacin

Other agents are Tolterodine, fesoterodine, trospium

98
Q

How can Glycopyrrolate be administered?

A

Parenteral

Oral

99
Q

Which is the benefit of using Glycopyrrolate parenteral?

A

Preoperative use to reduce airway secretions

100
Q

Clinical use of Glycopyrrolate oraly

A

Drooling, peptic ulcer

101
Q

Which group of drugs is Atropine?

A

Muscarinic antagonist

102
Q

These are effects in systems with the use of Atropine

A 
↑ pupil dilation, cycloplegia 
↓ secretions of airway
↓ Acid secretion of Stomach
↓ Gut motility
↓ Urgency in cystitis
103
Q

Which receptors mediate Atropine in Skeletal muscle and CNS?

A

Nicotinic receptors

104
Q

Which are possible toxic effects of Atropine?

A

↑ body temperature (due to ↓ sweating); rapid pulse; dry mouth; dry, flushed skin; cyclopegia; constipation; disorientation

105
Q

What can Atropine cause in eldery?

A

Acute angle closure glaucoma (due to mydriasis)

106
Q

In which patients can atropine cause Urinary retention?

A

Men with prostatic hyperplasia

107
Q

This is a possible side effect of Atropine in infants

A

Hypertermia

108
Q

What is Jimson weed (Datura)?

A

Gardeners pupil (mydriasis due to plant alkaloids)

109
Q

Classification of Sympathomimetics

A

Direct Sympathomimetics

Indirect Sympathomimetics

110
Q

Name Direct Sympathomimetics drugs

A 
Epinephrine
Norepinephrine
Isoproterenol
Dopamine
Dobutamine
Phenylephrine
Albuterol, Salmeterol, Terbutaline
111
Q

Which effect does Epinephrine has?

A

β > α

112
Q

These are applications for Epinephrine

A

Anaphylaxis
Opne angle glaucome
Asthma
Hypotension

113
Q

When does α effect predominates in epinephrine?

A

At high doses

114
Q

These are the receptors where norepinephrine acts

A

α1 > α2 > β1

115
Q

Application for Norepinephrine

A

Hypotension (but ↓ renal perfussion)

116
Q

In these receptors Isoproterenol has its effects

A

β1 = β2

117
Q

In this situation Isoproterenol is used

A

Electrophysiologic evaluation of tachyarrytmhias. Can worsen ischemia

118
Q

These are the receptors for Dopamine

A

D1= D2 > β > α

119
Q

When is recommended the clinical use of Dopamine?

A

Unstable bradycaria, heart failurem shock

120
Q

Which effects predominate at high doses of Dopamine?

A

Inotropic and chronotropic α effects predominate at high doses

121
Q

These are the receptors of Dobutamine

A

β1 > β2, α

122
Q

Clinical uses for Dobutamine

A 
Heart failure (inotropic > chronotropic)
Cardiac stress testing
123
Q

Which are the Phenylephrine receptors?

A

α1 > α2

124
Q

These are the results if Phenylephrine use

A

Hypotension (Vasoconstrictor), Ocular procedures (mydriatic), rhinitis (decongestant)

125
Q

Direct sympathomimetics that work at β2 > β1

A

Albuterol, Salmeterol, Terbutaline

126
Q

When is indicated Albuterol?

A

For Acute asthma

127
Q

Clinical use for Salmeterol

A

Long term asthma or COPD control

128
Q

When is recommended Terbutaline?

A

To reduce premature uterine contraction

129
Q

Indirect sympathomimetics

A

Amphetamine
Ephedrine
Cocaine

130
Q

Effect of Amphetamines

A

Indirect general agonist, reuptake inhibitor, also releases stored catecholamines

131
Q

Clinical use for Amphetamines

A

Narcolepsy, Obesity, Attention defficit disorder

132
Q

Which is the effect of Ephedrine?

A

Indirect general agonist, release stored catecholamines

133
Q

This is the clinical use for Ephedrine

A

Nasal decongestion, urinary incontinence, hypotension

134
Q

What is Cocaine effect?

A

Indirect general agonist, reuptake inhibitor

135
Q

Clinical use for Cocaine?

A

Causes vasoconstriction and local anesthesia

136
Q

If cocaine intoxication is suspected what is contraindicated?

A

Never give β blockers if cocaine intoxication is suspected

137
Q

What hapens if you give β blockers and the patient has Cocaine intoxication?

A

Can lead to unopposed α1 activation and extreme hypertension

138
Q

How does Norepinephrine causes bradycardia at the end?

A

Norepinephrine causes ↑ in systolic and diastolic pressures as a result of α1 mediated vasocontriction → ↑ mean arterial pressure → Bradycardia

139
Q

Which is the mediaction that has oposite effects as Norepinephrine, no longer commonly used?

A

Isoproterenol

140
Q

How does Isoproterenol produces Increased Heart rate?

A

Has a little α effect but causes β2 mediated vasodilation, resulting in ↓ mean arterial pressure and ↑ heart rate through β1 and reflexes activity

141
Q

Which receptors are Sympatholytics?

A

α2 agonists

142
Q

These drugs are Sympatholytics

A

Clonidine

α methyldopa

143
Q

Which are the applications of Clonidine?

A 
Hypertensive urgency (limited situations); does not decreases renal blood flow
ADHD, severe pain and a variety of offlabel indications (eg ethanol and opiod withdrawal)
144
Q

These cases are consider with Clonidine toxicity

A

CNS depression, bradycardia, hypotension, respiratory depression, and a smell pupil size

145
Q

Sympatholytics used in Hypertension in pregnancy because is safe

A

α methyldopa

146
Q

When is consider that α methyldopa causes toxicity?

A

Direct coombs positive, hemolytic anemia. SLE like syndrome

147
Q

This is the classification of α blockers

A

Non selective
α1 selective
α2 selective

148
Q

α Blockers nonselective

A

Phenoxybenzamine (irreversible)

Phentolamine (reversible)

149
Q

When is recommended Phenoxybenzamine? Why?

A

Pheochromocytoma (used preoperatively) to prevent catecholamine (hypertensive) crisis

150
Q

These are Phenoxybenzamine toxicity manifestations

A

Orthistatic hypotension, Reflex tachycardia

151
Q

In this situations you can administer Phentolamine

A

On MAO inhibitors who eat tyramine- containing foods

152
Q

Which drugs are α1 selective?

A

Prazosin
Terazosin
Doxazosin
Tamsulosin

153
Q

Clinical use for α1 selective blockers

A

Urinary symptos of BPH

Hypertension

154
Q

This is the only α1 selective blockers that is not recommended for hypertension

A

Tamsulosin

155
Q

In this case Prazosin is recommended

A

PTSD (Post-traumatic stress disorder)

156
Q

α2 selective blocker used for depression

A

Mirtazapine

157
Q

Side effects of Mirtazapine

A

Sedation, ↑ Serum cholesterol, ↑ Apetite

158
Q

Name β blockers

A

Metoprolol, Acebutol, btaxolol, carvedilol, esmolol, nadolol, timolol, pindolol, labetalol

159
Q

Applications of β blockers

A 
Angina Pectoris
MI
SVT
Hypertension
CHF
Glaucoma
160
Q

How do β blockers act in Angina pectoris?

A

↓ Heart rate and contractility, resulting in ↓ O2 consumption

161
Q

Which β blockers are used for MI?

A

Metoprolol
Carvedilol
Bisoprolol
Decrease mortality

162
Q

Which β blockers are used for SVT?

A

Metoprolol

Esmolol

163
Q

How are β blockers classified for SVT (Supraventricular Tachycardia) treatment

A

Class II antiarrhythmic

164
Q

Which is the mechanism of antiarrythimc for β blockers?

A

↓ AV conduction velocity

165
Q

How do β blockers work in Hypertension?

A

↓ Cardiac output, ↓ renin secretion

166
Q

Which receptors are blockade by β blockers in order to decrease Renin secretion?

A

β1 receptor blockade on JGA cells

167
Q

What is the purpose to give β blockers in CHF?

A

Slows progression of chronic failure

168
Q

Which β blocker is recommended for Glaucoma?

A

Timolol

169
Q

This is the effect of Timolol in the treatment of Glaucoma

A

↓ Secretion of aqueous humor

170
Q

These are possible secondary effects of β blockers

A

Incompetence
Cardiovascular adverse effects (bradycardia, AV block, CHF)
CNS adverse effects (seizures, sedation, sleep alterations)
Asthmatics/ COPDers (may cause exacerbation)

171
Q

Which β blocker can cause Dyslipidemia?

A

Metoprolol

172
Q

When is recommended to avoid β blockers?

A

Avoid cocaine users due to risk of unopposed α adrenergic receptor agonist activity

173
Q

Which is the relationship of β blockers and Diabetes?

A

Despite theoretical concern of masking hypoglecemia in diabetics, benefits likely outweigh risks; not contraindicated

174
Q

Which drugs are β1 selective antagonist (β1>β2)?

A 
Acetabutolol (partial agonist)
Atenolol 
Betaxolol
Esmolol
Metoprolol
175
Q

β blockers Nonselective antagonist (β1= β2)

A

Nadolol
Pindolol (partial agonist)
Propanolol
Timolol

176
Q

Nonselective α and β antagonist

A

Carvedilol

Labetalol

177
Q

Which is the effect of Nebivolol?

A

Combines Cardiac β1 adrenergic blockade with stimulation of β3 receptors, which activate nitric oxide synthase in the vasculature

PHARMACOLOGY (4 decks)

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