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Block 2: Pharmacology > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

Acetylcholine is a?

A

Neurotransmitter

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2
Q

Nicotine?

A

Mix of Parasympathetic and Sympathetic (cardiac only)

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3
Q

(Drugs to Know and Love)
Direct-Acting Cholinomimetics?

A

(directly on receptor)
-Acetylcholine (endogenous ligand)
-Bethanechol
-Nicotine (nicotine cessation)
-Pilocarpine

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4
Q

(Drugs to Know and Love)
Indirect-Acting Cholinomimetics?

A

(targets breakdown to increase half-life)
-Edrophonium (diagnosis of MG)
-Physostigmine (treament of MG)
-Echothiophate

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5
Q

(Drugs to Know and Love)
Muscarinic Inhibitors?

A

(sympathetic)
-Atropine (bradycardia)
-Ipratopium (asthma)
-Tiotropium (asthma)

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6
Q

(Cholingeric Juncture)
(Synthesis, Storage and Release)
ACh signal is terminated by?

A

Acetylcholine esterase

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7
Q

(Cholingeric Juncture)
(Synthesis, Storage and Release)
ACh is produced?

A

Outside of vesicle then transported into vesicle

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8
Q

(Cholingeric Juncture)
(Synthesis, Storage and Release)
Excess ACh is mainly?

A

Broken down via ACh Esterase, Choline is transported back into cell to be reused

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9
Q

(Cholingeric Juncture)
(Synthesis, Storage and Release)
Acetylcholine Receptors?

A

-Nicotinic (Ion Channels)
-Muscarinic (GPCR)

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10
Q

(Cholingeric Juncture)
(Synthesis, Storage and Release)
Steps?

A

1) Choline transported into cell, acetyl CoA originates from pyruvate
2) Acetyl CoA + choline –> ACh via choline acetyl transferase
3) ACh stored in vesicle
4) Ca increases and ACh is released
5) Binds to receptor (N or M) (depending on rec/location = effect)

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11
Q

(Direct-Acting Acetylcholine Receptor Agonists)
Acetylcholine?

A

(charged)
-Choline Ester
-++++ (AChE)
-+++ (AChR)
-+++ (AChr)

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12
Q

(Direct-Acting Acetylcholine Receptor Agonists)
Methacholine?

A

(charged)
-Choline Ester
-+ (AChE)
-++++ (AChR)
– (musc only) (AChr)

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13
Q

(Direct-Acting Acetylcholine Receptor Agonists)
Bethanechol?

A

(charged)
-Choline Ester
– (AChE)
-++ (AChR)
– (AChr)

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14
Q

(Direct-Acting Acetylcholine Receptor Agonists)
Carbachol?

A

(charged)
– (AChE)
-++ (AChR)
-+++ (AChr)

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15
Q

(Direct-Acting Acetylcholine Receptor Agonists)
Muscarine?

A

(uncharged)
-Alkaloid
– (AChE)
-++++ (AChR)
– (musc only) (AChr)

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16
Q

(Direct-Acting Acetylcholine Receptor Agonists)
Pilocarpine?

A

(uncharged)
-Alkaloid
– (AChE)
-+++ (AChR)
– (musc only) (AChr)

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17
Q

(Direct-Acting Acetylcholine Receptor Agonists)
Nicotine?

A

(uncharged)
-Alkaloid
– (AChE)
– (AChR)
-++++ (AChr)

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18
Q

Acetylcholine is charged?

A

Hydrophilic/Lipophobic so can be stored in vesicles

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19
Q

Pilocarpine is uncharged?

A

Hydrophobic/Lipophilic so can cross membranes

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20
Q

(Muscarinic Receptors (GPCR))
M1, M3, M5?

A

-Gq-coupled
-PLC activation
-Increased DAP and IP3 production
-Increased Ca2+

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21
Q

(Muscarinic Receptors (GPCR))
M2 and M4?

A

-Gi-coupled
-Decreased cAMP
-Decreased PKA (restricted to CNS)

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22
Q

(Muscarinic Receptors (GPCR))
M2 and M4?

A

-Gi-coupled
-Decreased cAMP
-Decreased PKA (restricted to CNS)

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23
Q

IP3 is?

A

Inositol Triphosphate

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24
Q

(Muscarinic Receptor Location)
Post ganglionic nerve?

A

Effector nerve that innervates tissue

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25
Q

(Muscarinic Receptor Location)
Parasympathetic?

A

(From Medulla)
Cardiac and smooth muscle, gland cells, nerve terminals

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26
Q

(Muscarinic Receptor Location)
Sympathetic?

A

(From Spinal Cord)
Sweat glands, skeletal muscle arterioles

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27
Q

(Muscarinic Receptor Location)
Eye?

A

(repair)
-Parasympathetic
-Contraction (M3)
-Decreased IOP (treatment for Glaucoma)
-Gq, increase Ca

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28
Q

(Muscarinic Receptor Location)
Urinary?

A

(rest/digest)
-Parasympathetic
-Contraction (M3)
-Increase micturition
-Gq, increase Ca

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29
Q

(Muscarinic Receptor Location)
Gut?

A

(digest)
-Parasympathetic
-Contraction (M3)
-Increased motility
-Gq, increase Ca

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30
Q

(Muscarinic Receptor Location)
Mucosal Glands?

A

(digest)
-Parasympathetic
-Stimulation (M1)
-Increased secretion
-Gq, increase Ca

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31
Q

(Muscarinic Receptor Location)
Lung?

A

(rest)
-Parasympathetic
-Contraction (M3)
-Bronchoconstriction
-Gq, increase Ca

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32
Q

(Muscarinic Receptor Location)
Heart?

A

(rest)
-Parasympathetic
-Decreased contraction, decreased conduction (M2)
-Decreased BP, bradycardia
-Gi

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33
Q

(Muscarinic Receptor Location)
Vascular Endothelium?

A

-No Innervation
-EDRF/NO release (M3) (VSM dilation)
-Decrease BP, reflex tachycardia (if circulating can activate muscarine rec)

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34
Q

(Muscarinic Receptor Location)
Sweat Glands?

A

-Sympathetic
-Stimulation (M3)
-Increase Secretion
-Gq

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35
Q

(Direct-Acting Cholinomimetic: Mechanisms of Action and Pharmacology)
Activate ______ receptors?

A

Activate muscarinic receptors
(affect all muscarinic receptor subtypes)

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36
Q

(Direct-Acting Cholinomimetic: Mechanisms of Action and Pharmacology)
Mainly evoke?

A

Parasympahtomimetic effects (sweating is sympathetic)

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37
Q

(Direct-Acting Cholinomimetic: Mechanisms of Action and Pharmacology)
Has mild or no?

A

Desensitization

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38
Q

(Open-Angle Glaucoma)
High IOP causes loss of?

A

Optic Nerve and permanent blindness (TOO much aq humor)

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39
Q

(Open-Angle Glaucoma)
Ocular hypertension can be reduced by?

A

Increasing aqueous humor flow OUT via canal of schlemm

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40
Q

(Open-Angle Glaucoma)
Contraction of ciliary muscle (via activation of M3 receptor)?

A

Opens trabecular meshwork and facilitates aqueous humor outflow

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41
Q

(Direct-Acting Cholinomimetic: Clinical Use for Glaucoma)
Choline Esters?

A

(uncharged)
-Bethanechol
-Not used for Glaucoma
-Charged, can’t get through membrane

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42
Q

(Direct-Acting Cholinomimetic: Clinical Use for Glaucoma)
Alkaloids?

A

(uncharged, lipophilic)
-Pilocarpine (treatment for glaucoma)
-Used for Glaucoma
-Uncharged and can get through

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43
Q

(Direct-Acting Cholinomimetic: Adverse Effects Adverse Effects, Contraindications, Interactions)
Bethanechol and Pilocarpine?

A

-Parasympathetic effects (bronchospasm, hypotension and reflex tachycardia secretion)
-Asthma, COPD, peptic ulcer, hypotension
-B-blockers (both decrease HR)

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44
Q

(Distribution of Nicotinic Receptors)
Parasympathetic?

A

(ACh N)
Cardiac and smooth muscle, gland cells, nerve terminals

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45
Q

(Distribution of Nicotinic Receptors)
Sympathetic?

A

-Sweat Glands (ACh M)
-Renal Vascular Smooth Muscle (D)

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46
Q

(Distribution of Nicotinic Receptors)
Somatic?

A

(ACh N)
Skeletal Muscle

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47
Q

(Distribution of Nicotinic Receptors)
Nicotine?

A

Ganglia + Skeletal Muscle

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48
Q

(Distribution of Nicotinic Receptors)
Nicotine?

A

Ganglia + Skeletal Muscle

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49
Q

(Nicotinic Acetylcholine Receptors)
All subtypes are pentameric cation channels activated by?

A

ACh

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50
Q

(Nicotinic Acetylcholine Receptors)
Subtypes?

A

-NMJ
-Autonomic ganglia
-Brain
-Brain

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51
Q

(Nicotinic Acetylcholine Receptors)
Can desensitize with?

A

Prolonged agonist

52
Q

(Nicotinic Acetylcholine Receptors)
Nm?

A

Muscle Contraction

53
Q

(Nicotinic Acetylcholine Receptors)
Nn?

A

Ganglia, ESPS (Depolarization)

54
Q

(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology)
Activate nicotinic receptors?

A

-Nicotine affects all nicotinic receptor subtypes
-Some agonists are subtype-selective (ex. epibatidine)

55
Q

(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology)
Stimulate CNS, all peripheral ganglia (and adrenal medulla) and skeletal muscle (NMJ)?

A

(get both para and symp)
-Parasympathetic
-Sympathetic
-Catecholamine release
-Skeletal Muscle (Somatic NS)

56
Q

(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology)
Evoke parasympathomimetic effects in?

A

GI, GU, Glands, Lungs (constrict)

57
Q

(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology)
Evoke sympathomimetic effects in?

A

CV (increased cardiac output and BP, sweat glands)

58
Q

(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology)
Receptor desensitization occurs following?

A

Long exposure

59
Q

(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology)
Major clinical use?

A

Smoking cessation

60
Q

(Muscarinic Antagonists (Antimuscarinics): Mechanisms of Action and Pharmacology)
Inhibit muscarinic receptors?

A

Drugs available clinically generally act on all receptor subtypes (limited selectivity)

61
Q

(Muscarinic Antagonists (Antimuscarinics): Mechanisms of Action and Pharmacology)
Evoke ______ effects?

A

Parasympatholytic effects (sympathetic effects)

62
Q

(Muscarinic Antagonists (Antimuscarinics): Mechanisms of Action and Pharmacology)
Antagonists only have an effect if there is?

A

Also an agonist present (tonic control)

63
Q

(Muscarinic Receptor Location)
Eye?

A

-Parasympathetic
-Contraction (M3)
-Decreased IOP (ACh)
-Dilation increased IOP (mAChR antagonist)

64
Q

(Muscarinic Receptor Location)
Urinary?

A

-Parasympathetic
-Contraction (M3)
-Increased micturition (ACh)
-Dilation decreased micturition (mAChR antagonist)

65
Q

(Muscarinic Receptor Location)
Gut?

A

-Parasympathetic
-Contraction (M3)
-Increased motility (ACh)
-Dilation decreased motility (mAChR antagonist)

66
Q

(Muscarinic Receptor Location)
Mucosal glands?

A

-Parasympathetic
-Stimulation (M1)
-Increased secretion (ACh)
-Decreased secretion (mAChR antagonist)

67
Q

(Muscarinic Receptor Location)
Lung?

A

-Parasympathetic
-Contraction (M3)
-Bronchoconstriction (ACh)
-Bronchodilation (mAChR antagonist)

68
Q

(Muscarinic Receptor Location)
Heart?

A

-Parasympathetic
-Decreased conduction, decreased atrial contraction (M2)
-Bradycardia, decreased BP (ACh)
-Increased conduction tachycardia (mAChR antagonist)

69
Q

(Muscarinic Receptor Location)
Vascular Endothelium?

A

-None
-EDRF/NO release (M3): VSM dilation
-Decreased BP, reflex tachycardia (ACh)
-Increased VSm contraction, increased BP (mAChR antagonist)

70
Q

(Muscarinic Receptor Location)
Sweat Glands?

A

-Sympathetic
-Stimulation (M3)
-Increased secretion (ACh)
-Decreased secretion (mAChR antagonist)

71
Q

(Muscarinic Receptor Location)
CNS?

A

-Multiple
-Excitation (ACh)
-Decreased excitation, sedation (mAChR antagonist)

72
Q

Naturally occurring muscarinic antagonists?

A

Belladonna Alkaloids
(Tropic acid (binds to receptor) required for activity, amine determines bioavailability)

73
Q

Tropicamide?

A

(Tertiary Amine)
Aid for eye examination (mydriadic)

74
Q

Benztropine?

A

(Tertiary Amine)
Treats Parkinson’s

75
Q

Propantheline?

A

(Quaternary Amine)
Treats gut hypermotility

76
Q

Ipratropium?

A

(Quaternary Amine)
Treats asthma

77
Q

Tertiary Amine?

A

(uncharged)
Good Absorption

78
Q

Quaternary Amine?

A

(charged)
Poor Absorption

79
Q

Parasympathetic Lung “Repair” in Asthma/Chronic Obstructive Pulmonary Disease?

A

Irritant –> Afferent –> CNS –> Parasympathetic Efferent –> Contracts smooth muscle –> produce mucous

80
Q

(Clinical Use of Anitmuscarinics)
Atropine?

A

Bradycardia

81
Q

(Clinical Use of Anitmuscarinics)
Ipratropium?

A

(Quaternary)
(Inhaled)
Bronchospasm in Chronic obstructive pulmonary disease (COPD), and asthma

82
Q

(Clinical Use of Anitmuscarinics)
Tiotropium?

A

(Quaternary)
(Inhaled)
(JUST BLOCKS M3)
Bronchospasm in Chronic obstructive pulmonary disease (COPD), and asthma

83
Q

Quaternary Amine can’t go through?

A

Surface because it is charged. If inhaled it will stay in Lungs

84
Q

Ipratropium blocks?

A

ACh-mediated secretion and contraction

85
Q

(Toxic Effects of Muscarinic Antagonists)
Eye?

A

Blurred vision, Photosensitivity
(pupil very dilated)

86
Q

(Toxic Effects of Muscarinic Antagonists)
CNS?

A

Agitation, hallucinations, delirium, coma

87
Q

(Toxic Effects of Muscarinic Antagonists)
Heart?

A

Tachycardia, angina

88
Q

(Toxic Effects of Muscarinic Antagonists)
Mucosal Glands and Sweat Glands?

A

Dry mouth, nasal congestion, hot/flush skin, hyperthermia

89
Q

(Toxic Effects of Muscarinic Antagonists)
Urinary?

A

Dysuria, retention

90
Q

(Toxic Effects of Muscarinic Antagonists)
Gut?

A

Nausea, distention, cramps, constipation

90
Q

(Toxic Effects of Muscarinic Antagonists)
Gut?

A

Nausea, distention, cramps, constipation

91
Q

(Muscarinic Antagonists are Contraindicated for Open-Angle Glaucoma)
Atropine prevents activation of?

A

M3
(causes dilation of ciliary muscle)
(decreases humor outflow –> increased IOP)

92
Q

(Indirect-Acting Cholinomimetics: AChE Inhibitors)
Inhibits breakdown of?

A

ACh therefore increase in ACh

93
Q

Key Sites on AChE?

A

-Choline Subsite
-Acyl Pocket
-Anionic Site

94
Q

(Key Sites on AChE)
Choline Subsite?

A

Electrostatic attraction of choline group

95
Q

(Key Sites on AChE)
Anionic Site?

A

Allosteric modulation of AChE activity (inhibition by tricyclic antidepressants, Fasciculin snake venom)

96
Q

Acetate needs to leave for?

A

Acetyl choline esterase to be active again. Drugs block this

97
Q

Once Choline leaves, Edrophonium will?

A

Bind to that subsite, blocking acetate from leaving

98
Q

(General Classes of Cholinesterase Inhibitors)
Reversible?

A

-Quaternary Alcohol
-Carbamates

99
Q

(General Classes of Cholinesterase Inhibitors)
Irreversible?

A

Organophosphates

100
Q

(General Classes of Cholinesterase Inhibitors)
(Reversible)
Quaternary Alcohol?

A

-Edrophonium
-Bind to choline subsite and H+ bond to acyl pocket

101
Q

(General Classes of Cholinesterase Inhibitors)
(Reversible)
Carbamates?

A

-Physostigmine (tertiary) and Neostigmine (quaternary)
-Bind like ACh with covalent bond, decarbamoylation rate slower than deacetylation rate (affects acetyl pocket)

102
Q

(General Classes of Cholinesterase Inhibitors)
(Irreversible)
Organophosphates?

A

-Echothiophate
-Some bind like ACh some only to acyl pocket with covalent bond, dephospho rylation rate slower than decarbamoylaiton and deacetylation rate

103
Q

(Physiological Effects of Cholinesterase Inhibition)
Nicotinic?

A

Brain and NMJ and all ganglia (catecholamine release)

104
Q

(Physiological Effects of Cholinesterase Inhibition)
Lymphatic System?

A

Low dose: indirect decreases BP, High dose: increases sympathetic drive

105
Q

(Physiological Effects of Cholinesterase Inhibition)
Heart?

A

Parasympathetic, Bradycardia

106
Q

(Therapeutic Use of Reversible)
Cholinesterase Inhibitors - Myasthenia Gravis?

A

-“Looking up” eye test shows muscle fatigue
-AChE inhibitor boosts NMJ function

107
Q

(Therapeutic Use of Reversible)
(Cholinesterase Inhibitors - Myasthenia Gravis)
Edrophonium?

A

Eye test for MG
(rapid short acting, prevents fatigue of eyelid muscle)

108
Q

(Therapeutic Use of Reversible)
(Cholinesterase Inhibitors - Myasthenia Gravis)
Physostigmine?

A

Treatment
(addition of AChE inhibitor)

109
Q

(Therapeutic Use of Reversible)
(Cholinesterase Inhibitors - Myasthenia Gravis)
Physostigmine?

A

Treatment
(addition of AChE inhibitor)

110
Q

(NMJ Architecture in MG)
Less nicotinic receptors and not as dense. Less ACh release so no?

A

ESPS for muscle contraction, loss of muscle contractions

111
Q

(AChE Inhibition in MG)
If we block AChE we increase?

A

Half-life of ACh so we can have bigger activation of receptors leading to ESPS and better muscle contractions

112
Q

(Pharmacokinetics of Reversible Cholinesterase Inhibitors)
Alcohols?

A

-Edrophonium (diagnose MG)
-Absorbed poorly, destroyed by plasma esterase
-Binds to choline subsite of active center and H+ bond to acyl pocket
-5-15 min

113
Q

(Pharmacokinetics of Reversible Cholinesterase Inhibitors)
Carbamates?

A

-Physostigmine
-Neostigmine
-Pyridostigmine

114
Q

(Pharmacokinetics of Reversible Cholinesterase Inhibitors)
(Carbamates)
Physostigmine?

A

-Absorbed readily, destroyed by plasma esterase, enters CNS
-Binds to acyl pocket of active center via covalent bond and hydrolyzed by enzyme
-1-2 hours

115
Q

(Pharmacokinetics of Reversible Cholinesterase Inhibitors)
(Carbamates)
Neostigmine?

A

-Absorbed poorly, destroyed by plasma esterase, excreted in urine, does not enter CNS
-Binds to acyl pocket of active center via covalent bond and hydrolyzed by enzyme
-1-2 hours

116
Q

(Pharmacokinetics of Reversible Cholinesterase Inhibitors)
(Carbamates)
Pyridostigmine?

A

-Absorbed poorly, destroyed by plasma esterase, excreted in urine, does not enter CNS
-Binds to acyl pocket of active center via covalent bond and hydrolyzed by enzyme
-3-6 hours

117
Q

(Open-Angle Glaucoma)
Ocular hypertension can be reduced by increasing?

A

Aqueous humor flow OUT via canal of schlemm

118
Q

(Open-Angle Glaucoma)
Contraction of ciliary muscle (via activation of M3 receptor) opens?

A

Trabecular meshwork and facilitates aqueous humor outflow

119
Q

(Open-Angle Glaucoma)
AChE Inhibitors (physostigmine/echothiophate, in eye drops) increase?

A

Half-life of endogenous ACh –> increases ciliary contraction –> decreased IOP

120
Q

(Toxic Effects of Cholinesterase Inhibition)
Excess acetylcholine causes?

A

Desensitization for nicotinic receptors, not muscarinic

121
Q

(Toxic Effects of Cholinesterase Inhibition)
CNS?

A

Increased EEG and Increased Alertness
(convulsions –> coma (desensitization))

122
Q

(Toxic Effects of Cholinesterase Inhibition)
Heart?

A

Parasympathomimetic

123
Q

(Toxic Effects of Cholinesterase Inhibition)
NMJ?

A

Increased Strength –> blockage (desensitization)

124
Q

AChE Inhibitors used to treat Muscarinic Inhibitor Poisoning?

A

-Atropine toxicity (dry as a bond, blind as a bat…)
-Need to increase endogenous ACh
-Physostigmine (tertiary)

125
Q

Muscarinic Inhibitors used to treat AChE Inhibitor Poisoning?

A

-Organophosphate toxicity (irreversible AChE inhibitor (paralysis, bronchospasm, diarrhea, hypotension)
-Need to block actions of endogenous ACh at muscarinic receptors
-Atropine (tertiary)

Block 2: Pharmacology (5 decks)

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