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Block 2: Pharmacology > Lecture 4 > Flashcards

Lecture 4 Flashcards

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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
(Muscarinic Receptor Location) Parasympathetic?
(From Medulla) Cardiac and smooth muscle, gland cells, nerve terminals
26
(Muscarinic Receptor Location) Sympathetic?
(From Spinal Cord) Sweat glands, skeletal muscle arterioles
27
(Muscarinic Receptor Location) Eye?
(repair) -Parasympathetic -Contraction (M3) -Decreased IOP (treatment for Glaucoma) -Gq, increase Ca
28
(Muscarinic Receptor Location) Urinary?
(rest/digest) -Parasympathetic -Contraction (M3) -Increase micturition -Gq, increase Ca
29
(Muscarinic Receptor Location) Gut?
(digest) -Parasympathetic -Contraction (M3) -Increased motility -Gq, increase Ca
30
(Muscarinic Receptor Location) Mucosal Glands?
(digest) -Parasympathetic -Stimulation (M1) -Increased secretion -Gq, increase Ca
31
(Muscarinic Receptor Location) Lung?
(rest) -Parasympathetic -Contraction (M3) -Bronchoconstriction -Gq, increase Ca
32
(Muscarinic Receptor Location) Heart?
(rest) -Parasympathetic -Decreased contraction, decreased conduction (M2) -Decreased BP, bradycardia -Gi
33
(Muscarinic Receptor Location) Vascular Endothelium?
-No Innervation -EDRF/NO release (M3) (VSM dilation) -Decrease BP, reflex tachycardia (if circulating can activate muscarine rec)
34
(Muscarinic Receptor Location) Sweat Glands?
-Sympathetic -Stimulation (M3) -Increase Secretion -Gq
35
(Direct-Acting Cholinomimetic: Mechanisms of Action and Pharmacology) Activate ______ receptors?
Activate muscarinic receptors (affect all muscarinic receptor subtypes)
36
(Direct-Acting Cholinomimetic: Mechanisms of Action and Pharmacology) Mainly evoke?
Parasympahtomimetic effects (sweating is sympathetic)
37
(Direct-Acting Cholinomimetic: Mechanisms of Action and Pharmacology) Has mild or no?
Desensitization
38
(Open-Angle Glaucoma) High IOP causes loss of?
Optic Nerve and permanent blindness (TOO much aq humor)
39
(Open-Angle Glaucoma) Ocular hypertension can be reduced by?
Increasing aqueous humor flow OUT via canal of schlemm
40
(Open-Angle Glaucoma) Contraction of ciliary muscle (via activation of M3 receptor)?
Opens trabecular meshwork and facilitates aqueous humor outflow
41
(Direct-Acting Cholinomimetic: Clinical Use for Glaucoma) Choline Esters?
(uncharged) -Bethanechol -Not used for Glaucoma -Charged, can't get through membrane
42
(Direct-Acting Cholinomimetic: Clinical Use for Glaucoma) Alkaloids?
(uncharged, lipophilic) -Pilocarpine (treatment for glaucoma) -Used for Glaucoma -Uncharged and can get through
43
(Direct-Acting Cholinomimetic: Adverse Effects Adverse Effects, Contraindications, Interactions) Bethanechol and Pilocarpine?
-Parasympathetic effects (bronchospasm, hypotension and reflex tachycardia secretion) -Asthma, COPD, peptic ulcer, hypotension -B-blockers (both decrease HR)
44
(Distribution of Nicotinic Receptors) Parasympathetic?
(ACh N) Cardiac and smooth muscle, gland cells, nerve terminals
45
(Distribution of Nicotinic Receptors) Sympathetic?
-Sweat Glands (ACh M) -Renal Vascular Smooth Muscle (D)
46
(Distribution of Nicotinic Receptors) Somatic?
(ACh N) Skeletal Muscle
47
(Distribution of Nicotinic Receptors) Nicotine?
Ganglia + Skeletal Muscle
48
(Distribution of Nicotinic Receptors) Nicotine?
Ganglia + Skeletal Muscle
49
(Nicotinic Acetylcholine Receptors) All subtypes are pentameric cation channels activated by?
ACh
50
(Nicotinic Acetylcholine Receptors) Subtypes?
-NMJ -Autonomic ganglia -Brain -Brain
51
(Nicotinic Acetylcholine Receptors) Can desensitize with?
Prolonged agonist
52
(Nicotinic Acetylcholine Receptors) Nm?
Muscle Contraction
53
(Nicotinic Acetylcholine Receptors) Nn?
Ganglia, ESPS (Depolarization)
54
(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology) Activate nicotinic receptors?
-Nicotine affects all nicotinic receptor subtypes -Some agonists are subtype-selective (ex. epibatidine)
55
(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology) Stimulate CNS, all peripheral ganglia (and adrenal medulla) and skeletal muscle (NMJ)?
(get both para and symp) -Parasympathetic -Sympathetic -Catecholamine release -Skeletal Muscle (Somatic NS)
56
(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology) Evoke parasympathomimetic effects in?
GI, GU, Glands, Lungs (constrict)
57
(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology) Evoke sympathomimetic effects in?
CV (increased cardiac output and BP, sweat glands)
58
(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology) Receptor desensitization occurs following?
Long exposure
59
(Direct-Acting Nicotinic Agonists: Mechanisms of Action and Pharmacology) Major clinical use?
Smoking cessation
60
(Muscarinic Antagonists (Antimuscarinics): Mechanisms of Action and Pharmacology) Inhibit muscarinic receptors?
Drugs available clinically generally act on all receptor subtypes (limited selectivity)
61
(Muscarinic Antagonists (Antimuscarinics): Mechanisms of Action and Pharmacology) Evoke ______ effects?
Parasympatholytic effects (sympathetic effects)
62
(Muscarinic Antagonists (Antimuscarinics): Mechanisms of Action and Pharmacology) Antagonists only have an effect if there is?
Also an agonist present (tonic control)
63
(Muscarinic Receptor Location) Eye?
-Parasympathetic -Contraction (M3) -Decreased IOP (ACh) -Dilation increased IOP (mAChR antagonist)
64
(Muscarinic Receptor Location) Urinary?
-Parasympathetic -Contraction (M3) -Increased micturition (ACh) -Dilation decreased micturition (mAChR antagonist)
65
(Muscarinic Receptor Location) Gut?
-Parasympathetic -Contraction (M3) -Increased motility (ACh) -Dilation decreased motility (mAChR antagonist)
66
(Muscarinic Receptor Location) Mucosal glands?
-Parasympathetic -Stimulation (M1) -Increased secretion (ACh) -Decreased secretion (mAChR antagonist)
67
(Muscarinic Receptor Location) Lung?
-Parasympathetic -Contraction (M3) -Bronchoconstriction (ACh) -Bronchodilation (mAChR antagonist)
68
(Muscarinic Receptor Location) Heart?
-Parasympathetic -Decreased conduction, decreased atrial contraction (M2) -Bradycardia, decreased BP (ACh) -Increased conduction tachycardia (mAChR antagonist)
69
(Muscarinic Receptor Location) Vascular Endothelium?
-None -EDRF/NO release (M3): VSM dilation -Decreased BP, reflex tachycardia (ACh) -Increased VSm contraction, increased BP (mAChR antagonist)
70
(Muscarinic Receptor Location) Sweat Glands?
-Sympathetic -Stimulation (M3) -Increased secretion (ACh) -Decreased secretion (mAChR antagonist)
71
(Muscarinic Receptor Location) CNS?
-Multiple -Excitation (ACh) -Decreased excitation, sedation (mAChR antagonist)
72
Naturally occurring muscarinic antagonists?
Belladonna Alkaloids (Tropic acid (binds to receptor) required for activity, amine determines bioavailability)
73
Tropicamide?
(Tertiary Amine) Aid for eye examination (mydriadic)
74
Benztropine?
(Tertiary Amine) Treats Parkinson's
75
Propantheline?
(Quaternary Amine) Treats gut hypermotility
76
Ipratropium?
(Quaternary Amine) Treats asthma
77
Tertiary Amine?
(uncharged) Good Absorption
78
Quaternary Amine?
(charged) Poor Absorption
79
Parasympathetic Lung "Repair" in Asthma/Chronic Obstructive Pulmonary Disease?
Irritant --> Afferent --> CNS --> Parasympathetic Efferent --> Contracts smooth muscle --> produce mucous
80
(Clinical Use of Anitmuscarinics) Atropine?
Bradycardia
81
(Clinical Use of Anitmuscarinics) Ipratropium?
(Quaternary) (Inhaled) Bronchospasm in Chronic obstructive pulmonary disease (COPD), and asthma
82
(Clinical Use of Anitmuscarinics) Tiotropium?
(Quaternary) (Inhaled) (JUST BLOCKS M3) Bronchospasm in Chronic obstructive pulmonary disease (COPD), and asthma
83
Quaternary Amine can't go through?
Surface because it is charged. If inhaled it will stay in Lungs
84
Ipratropium blocks?
ACh-mediated secretion and contraction
85
(Toxic Effects of Muscarinic Antagonists) Eye?
Blurred vision, Photosensitivity (pupil very dilated)
86
(Toxic Effects of Muscarinic Antagonists) CNS?
Agitation, hallucinations, delirium, coma
87
(Toxic Effects of Muscarinic Antagonists) Heart?
Tachycardia, angina
88
(Toxic Effects of Muscarinic Antagonists) Mucosal Glands and Sweat Glands?
Dry mouth, nasal congestion, hot/flush skin, hyperthermia
89
(Toxic Effects of Muscarinic Antagonists) Urinary?
Dysuria, retention
90
(Toxic Effects of Muscarinic Antagonists) Gut?
Nausea, distention, cramps, constipation
90
(Toxic Effects of Muscarinic Antagonists) Gut?
Nausea, distention, cramps, constipation
91
(Muscarinic Antagonists are Contraindicated for Open-Angle Glaucoma) Atropine prevents activation of?
M3 (causes dilation of ciliary muscle) (decreases humor outflow --> increased IOP)
92
(Indirect-Acting Cholinomimetics: AChE Inhibitors) Inhibits breakdown of?
ACh therefore increase in ACh
93
Key Sites on AChE?
-Choline Subsite -Acyl Pocket -Anionic Site
94
(Key Sites on AChE) Choline Subsite?
Electrostatic attraction of choline group
95
(Key Sites on AChE) Anionic Site?
Allosteric modulation of AChE activity (inhibition by tricyclic antidepressants, Fasciculin snake venom)
96
Acetate needs to leave for?
Acetyl choline esterase to be active again. Drugs block this
97
Once Choline leaves, Edrophonium will?
Bind to that subsite, blocking acetate from leaving
98
(General Classes of Cholinesterase Inhibitors) Reversible?
-Quaternary Alcohol -Carbamates
99
(General Classes of Cholinesterase Inhibitors) Irreversible?
Organophosphates
100
(General Classes of Cholinesterase Inhibitors) (Reversible) Quaternary Alcohol?
-Edrophonium -Bind to choline subsite and H+ bond to acyl pocket
101
(General Classes of Cholinesterase Inhibitors) (Reversible) Carbamates?
-Physostigmine (tertiary) and Neostigmine (quaternary) -Bind like ACh with covalent bond, decarbamoylation rate slower than deacetylation rate (affects acetyl pocket)
102
(General Classes of Cholinesterase Inhibitors) (Irreversible) Organophosphates?
-Echothiophate -Some bind like ACh some only to acyl pocket with covalent bond, dephospho rylation rate slower than decarbamoylaiton and deacetylation rate
103
(Physiological Effects of Cholinesterase Inhibition) Nicotinic?
Brain and NMJ and all ganglia (catecholamine release)
104
(Physiological Effects of Cholinesterase Inhibition) Lymphatic System?
Low dose: indirect decreases BP, High dose: increases sympathetic drive
105
(Physiological Effects of Cholinesterase Inhibition) Heart?
Parasympathetic, Bradycardia
106
(Therapeutic Use of Reversible) Cholinesterase Inhibitors - Myasthenia Gravis?
-"Looking up" eye test shows muscle fatigue -AChE inhibitor boosts NMJ function
107
(Therapeutic Use of Reversible) (Cholinesterase Inhibitors - Myasthenia Gravis) Edrophonium?
Eye test for MG (rapid short acting, prevents fatigue of eyelid muscle)
108
(Therapeutic Use of Reversible) (Cholinesterase Inhibitors - Myasthenia Gravis) Physostigmine?
Treatment (addition of AChE inhibitor)
109
(Therapeutic Use of Reversible) (Cholinesterase Inhibitors - Myasthenia Gravis) Physostigmine?
Treatment (addition of AChE inhibitor)
110
(NMJ Architecture in MG) Less nicotinic receptors and not as dense. Less ACh release so no?
ESPS for muscle contraction, loss of muscle contractions
111
(AChE Inhibition in MG) If we block AChE we increase?
Half-life of ACh so we can have bigger activation of receptors leading to ESPS and better muscle contractions
112
(Pharmacokinetics of Reversible Cholinesterase Inhibitors) Alcohols?
-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
(Pharmacokinetics of Reversible Cholinesterase Inhibitors) Carbamates?
-Physostigmine -Neostigmine -Pyridostigmine
114
(Pharmacokinetics of Reversible Cholinesterase Inhibitors) (Carbamates) Physostigmine?
-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
(Pharmacokinetics of Reversible Cholinesterase Inhibitors) (Carbamates) Neostigmine?
-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
(Pharmacokinetics of Reversible Cholinesterase Inhibitors) (Carbamates) Pyridostigmine?
-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
(Open-Angle Glaucoma) Ocular hypertension can be reduced by increasing?
Aqueous humor flow OUT via canal of schlemm
118
(Open-Angle Glaucoma) Contraction of ciliary muscle (via activation of M3 receptor) opens?
Trabecular meshwork and facilitates aqueous humor outflow
119
(Open-Angle Glaucoma) AChE Inhibitors (physostigmine/echothiophate, in eye drops) increase?
Half-life of endogenous ACh --> increases ciliary contraction --> decreased IOP
120
(Toxic Effects of Cholinesterase Inhibition) Excess acetylcholine causes?
Desensitization for nicotinic receptors, not muscarinic
121
(Toxic Effects of Cholinesterase Inhibition) CNS?
Increased EEG and Increased Alertness (convulsions --> coma (desensitization))
122
(Toxic Effects of Cholinesterase Inhibition) Heart?
Parasympathomimetic
123
(Toxic Effects of Cholinesterase Inhibition) NMJ?
Increased Strength --> blockage (desensitization)
124
AChE Inhibitors used to treat Muscarinic Inhibitor Poisoning?
-Atropine toxicity (dry as a bond, blind as a bat...) -Need to increase endogenous ACh -Physostigmine (tertiary)
125
Muscarinic Inhibitors used to treat AChE Inhibitor Poisoning?
-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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