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Pharmacology Drugs > Drugs > Flashcards

Drugs Flashcards

1
Q

Hemicholium

A

Prevents the uptake of Choline into presynaptic cell.

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2
Q

Vesicholium

A

Prevents entry of ACh into the synaptic vesicle

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3
Q

Botulism toxin

A

Prevents the release of Vesicles into the synaptic cleft

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4
Q

AChEI

A

prevent the degradatio of ACh in the junction

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5
Q

LEMS

A

Lambert Eaton Myasthenic Syndrome. Prevents opening of Ca channels on presynaptic bulb. prevents release of ACh into junction.

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6
Q

Metyrosine

A

Block Tyrosine Hydroxylase: this revents the formation of dopa from tyrosine.

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7
Q

Reserpine

A

This prevents the entry of Dopamine into the sympathetic synaptic vesicle. Works on VMAT

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8
Q

Cocaine,

A

prevents the reuptake of NE into the presynaptic cell

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9
Q

Bretylim, Guanethidine

A

Prevent the release of NE from the presynaptic cell

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10
Q

TCA

A

tricyclic antidepressants: prevent reuptake of NE

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11
Q

Ang II

A

prevent reuptake of NE

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12
Q

Sympathomimetics

A

These are poor agonists of adrenergic receptors. Get into the presynaptic cell using NET and into the synaptic vesicle. Cause the displacement of NE into the synaptic bulb. Concentrations of NE cause movement of NE out into junction via NET. Increase in NE increase in sympathetic response.

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13
Q

Amphetamines

A

These are poor agonists of adrenergic receptors. Get into the presynaptic cell using NET and into the synaptic vesicle. Cause the displacement of NE into the synaptic bulb. Concentrations of NE cause movement of NE out into junction via NET. Increase in NE increase in sympathetic response.

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14
Q

Formation of Catechols

A

Tyrosine hydroxylase converts Tyr to DOPA. DOPA decarboxylase turns DOPA to DA, enters vesicle. DA-beta hydroxylase turns DA into NE. (DOPA is first catecol, two hydroxyls)

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15
Q

COMT vs. MAO

A

both are Catacholemine breakdown enzymes. COMT is in Liver, GI, Kidney and other targets.

MAO is in neural tissue, mostly.

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16
Q

Modification of Beta carbon Catecholamines

A

Any addition will greatly enhance alpha and beta receptor affinity

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17
Q

Modification of ALpha carbon in Catecholamines

A

Modification here will greatly reduce the half-life by inhibiting MAO. will also allow the drug to work as an idnirect sympathomimetic

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18
Q

Modification of Amine group on Catecholamines.

A

Methyl Here confers high alpha selectivity. The smaller the group the more alpha effect there is.

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19
Q

M1

A

CNS neurons Gq

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20
Q

M2

A

Heart Gi (decrease cAMP)

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21
Q

M3

A

Exocrine Glands, vessels, iris circular muscle (Gq (Ip3, DAG)

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22
Q

Nn

A

autonomic ganglia adrenal medulla (open Na/K channels and depolarize)

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23
Q

Nm

A

NMJ open Na/K channels and depolarize

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24
Q

alpha1

A

Smooth muscles, Iris radial muscles (Gq–>IP3 DAG)

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25
Q

Alpha2

A

smooth muscle, presynaptic cells

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26
Q

Beta1

A

Heart, juxtaglomerular apparatus of renal tube (Gs increase cAMP)

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27
Q

Beta2

A

Smooth muscles, heart, lungs (Gs increase cAMP)

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28
Q

Alpha2 autoreceptor

A

activate when NE in Synaptic cleft exceeds threshold. Inhibits calcium flow into presynaptic cell down regulating its ability to fire.

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29
Q

Phenoxybenzamine

A

POB. indicated for pheochromocytoma. Inhibits alpha1 and alpha 2. negative feedback by alpha2 is blocked. Released Epi and NE can bind B1 in heart and icnrease HR. POB lower BP by inhibiting alpha1 but NE and EPI can act on B2 to raise BP

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30
Q

Autonomic Receptors on the eye

A

M3 (iris circular muscle) alpha1 (iris radial muscle) Beta1: ciliary epithelium. M3: ciliary muscle

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31
Q

Beta1 eye

A

facilitates production of aqueous humor from ciliary body

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32
Q

M3

A

Miosis and accommodation. tenses and opens pores in trabecular mesh work to improve aqueous humor outflow.

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33
Q

ALpha1 alpha2 eye

A

A1: mydriasis A2: inhibits aqueous humor production

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34
Q

Ways to reduce Glaucoma

A

betablocker stopping production. stimulate alpha2 stopping production. M3 agonist facilitating the outflow. carbonic anhydrase inhibitors reduce aqueous humor production.

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35
Q

Muscarinics

A

direct acting agonist that activate post-ganglionic muscarinic receptor and increase response. 2 exceptions (ACh vasodilate BV but no parasympathetic innervation to blood vessels. ACh released from sweat glands by sympathetics

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36
Q

Muscarinic agonists

A

either alkaloids or choline esters.

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37
Q

Pilocarpine

A

Muscarinic agonist. Tertiary cholinomimetic. well absorbed PARTIAL AGONIST!!!

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38
Q

Choline Esters

A

modified ACh to make them less suseptible to degradation and increase their affinity for muscarinic receptors (Methy increases selectivity) Carbamol decrease affinity for AChE

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39
Q

Methacholine

A

quaternary Muscarinic Choline ester: methyl makes it more selective for muscarinic receptors

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40
Q

Carbachol

A

quaternary Muscarinic agonist choline ester. amine makes it harder to degrade by AChE

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41
Q

Bethanochol

A

quaternary Muscarinic agonist choline ester. amine and methyl.

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42
Q

Choline Ester effects on: SA node

A

Decrease in HR M2 mediates an increase in K+ current in cardiac cells to cause hyperpolarization, reduce action potential duration, and decrease the contractility of the heart

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43
Q

Choline Ester effects on:Atria

A

decrease in contractile strength M2 mediates an increase in K+ current in cardiac cells to cause hyperpolarization, reduce action potential duration, and decrease the contractility of the heart

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44
Q

Choline Ester effects on:AV node

A

decrease in conduction velocity M2 mediates an increase in K+ current in cardiac cells to cause hyperpolarization, reduce action potential duration, and decrease the contractility of the heart

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45
Q

Choline Ester effects on: ventricle

A

small decrease in contractile strencth M2 mediates an increase in K+ current in cardiac cells to cause hyperpolarization, reduce action potential duration, and decrease the contractility of the heart

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46
Q

M3 on lungs

A

Bronchoconstriction, increased secretion

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47
Q

M3 GI

A

Increased contraction, increased secretion, relaxati of sphincters

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48
Q

M2, M3 urinary bladder

A

contract detruser, relax the trigone and sphincter

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49
Q

M3 glands

A

increase secretion

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50
Q

clinical use: Acetylcholine

A

induce miosis for eye surgery

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51
Q

clinical use: methacholine

A

Asthma diagnosis; bronchi are hyperreactive to muscarinics. metha choline can trigger bronchoconstriction

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52
Q

clinical use carbacol

A

Miosis inductio for surgery, glaucoma

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53
Q

clinical use Bethanechol

A

urinary retention. is agent of choice for PO PP drug related Urinary retention. Incresase the tone of lower esophogeal sphincter in patients with reflux esophogitis.

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54
Q

clinical use Pilocarpine

A

Sjogrens syndrome, glaucoma

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55
Q

Cevimeline

A

new direct acting agonist for treament of dry mouth from Sjogrens.

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56
Q

DUMMBBELS

A

Diarhea, urination, muscle weakness, miosis, bronchospasm, bradycardia, excitation, lacrimation, seizueres.

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57
Q

Antimuscarinics

A

Inverse agonists. Parasympatholytics: atropine scopolomine, ipratropium, tiotropium, tolterodine

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58
Q

Naturally occuring Antimuscarinics

A

alkaloids: atropine scopolamine

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59
Q

semisynthetic Antimuscarinics

A

iprotropiium tiotropium

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60
Q

synthetic antimuscarinics

A

tolteridine

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61
Q

CNS effects antimuscarinics

A

Low dose scopolamine does CNS depression (drowsiness amnesia” atropine vagal excitation. High dose: both scopolamine and atropine cause hallucinations delirium and coma.

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62
Q

Antimuscarinics effect on eye

A

unopposed sympathetics lead to mydriasis, increased IOP. weaken contraction of ciliary muscle lead to cycloplegia.

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63
Q

Antimuscarinics Cardiovascular

A

Low dose decrease HR, due to blockade of M1 which limit ACh release. High dose always get tachycardia.

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64
Q

Antimuscarinic effects Lungs

A

Bronchodilation (not as good as betablockers for asthma). not effective for treatment of COPD because of blockade of parasympathetic postganglionic presynaptic M2 autoreceptors.) administered before inhalent anesthetics to decrease secretion.

65
Q

Clinical uses Scopolamine

A

Prophylactic treatment of motion sickness vomiting and nausea

66
Q

Clinical uses Atropine

A

non-selective M) antidote for parasympathomimetic drugs

67
Q

Clinical uses Ipratropium

A

Non-selective M COPD nasal discharge

68
Q

Clinical uses Tiotropium

A

M1, M3 COPD

69
Q

Clinical uses Tolteridine

A

M3 Overreactive lbladder

70
Q

Clinical uses Dycyclomine M3

A

irritable bowel syndrome

71
Q

Nicotinic receptors

A

Found in autonomic ganglia (Adrenal medulla included) and at the NMJ. Iontrophic channels that move Na/K flux depolarizing the cell.

72
Q

Nicotinic Alkaloids

A

Nicotine and lobeline are nicotinic alkaloids.Both are tertiary so get into CNS and absorb well. No clinical use of lobeline. Nicotine only for smoking cessation

73
Q

Cholinergics readily excreted by acidifying the urine

A

Pilocarpine, nicotine and Lobeline.( cuz they all be like weak bases for realz)

74
Q

Nicotinic choline esters

A

high affinity for nicotinic receptors. resistant to AChE. Used to induce muscle paralysis during Sx by depolarizing blockade

75
Q

Succinylcholine

A

Choline ester: can cause depolarizing blockade. because its resistant to degradation it continuously activates the nicotinic receptors. The receptor will become resistant to stimulation and deactivate. Neuromuscular blockade for surgery, rapid intubation

76
Q

High nicotine on CNS

A

Presynaptic nicotinic receptor regulate release of neurotransmitters. High concentrations of nicotine causes tremors emesis and respiratory stimulation. at extremely high concentration convulsions and coma.

77
Q

side effects nicotine

A

CNS: convulsions to respiratory arrest. Increased hypertension and cardiac arrythmias. skeletal muscle endplate depolarization blockade and respiratory paralysis.

78
Q

Ganglio-blocking agents

A

competively block Nicotinic receptors in both parasympathetic and sympathetic ganglia. Important for research but no clinical use.

Tetraethylammonium (TEA)
Heamethonium protypicall
decamethonium
mecamylamine
trimethaphan
79
Q

Hexamethonium

A

Nondepolarizing competitive antagonist: binds directly to nicotinic ion channel

80
Q

Trimethaphan

A

Non depolarizing competitive antagonist (nicotinic receptor)blocks the nicotinic receptor not the pore

81
Q

Mecamylamine

A

non-depolarizing competitive antagonist crosses BBB and causes sedation tremor, choreiform movements and mental abberations. No longer used

82
Q

Ganglion blocking effects Eye

A

cycloplegia with loss of accomodation. due to the ciliary muscle being primarily parasympathetic innervated. parasympathetics also predominate pupil and blockade will dilate the eye moderately.

83
Q

Ganglion-blocking agents effects cardiovascular

A

In blood vessels sympathetics reign so there will be an increase in vasodilation. In the heart parasympathetics reign so there will be tachycardia.

84
Q

Ganglion blocking agents Effects GI

A

in gut Parasympathetics reign so decreased GI motillity, decreased secretion

85
Q

ganglion blocking agents effects genitourinary

A

blockade causes hesitency in urination. may precipitate urinary retintion in men with prostatic hyperplasia.

can’t get boner or cum.

86
Q

ChEI

A

reduce choline metabolism and increase endogenous choline concentration.

3 classes simple alcohols
carbamic acid esters
organiophosphates.

87
Q

Edrophonium

A

Simple alcohol with a quaternary amine group. short acting reversible ChEI that hydrogen bonds to serine.

Used to diagnose Myasthenia Gravis. if Myosthenia gravis then person will get better for 5 min. if its because of ChEI then muscle weakness worsens.

88
Q

Neostigmine

A

quaternary carbamic acid ChEI: nondepolarizing reversal of neuromuscular blockade, urinary retention (myosthenia gravis)

has an additional direct nicotinic agonist activity

89
Q

Pyridostigmine

A

quaternary carbamic ChEI. used for long term treatment of Myosthenia gravis. slower than neostigmine but last longer.

prhylactic for organophosphate poisoning

90
Q

physostigmine

A

Tertiary ChEI carbamic acid.Glaucoma, reversal of anticholinergic toxicity

used to antagonize central anti-cholinergic toxicity.

metabolized by plasma esterases.

91
Q

echothiopate

A

organic group released upon binding leaving phosphorous covalently bound to AChE

Glaucoma, esotropia with accomodative compensation. can lead to acquired cholinesterase deficiency and prolonged block form neuromuscular blocking drugs.

92
Q

ChEI organ effects CNS

A

generalized convulsions, coma respiratory arrest

93
Q

ChEI effects eye respirtory tract GI, urinary

A

similar to direct acting cholinomimetics: miosis, GI motility urination, secretion defication. also secretio from sweat lacrimal salivary and nasopharyngeal glands.

94
Q

ChEI effects ardiovascular

A

increase both sympathetic and parasympathetic, but parasympathetic predmonate so decrease in heart rate. Increase in vascular tone from sympathetics (quaternary agents at autonomic ganglia and lipid soluble at central sympathetic centers).

Net: moderate dose modest bradycardia and increased vascular tone=increased BP. High dose: bradycardia and hypotension.

95
Q

ChEI effects at NMJ

A

Low dose=therapeutic. intensifies actions of ACh increases muscle weakness from curare or myosthenia gravis

high: antidromic firing back into the axon causing fasiculations. Depolarizing muscular blockade followed by nondepolarizing.

96
Q

Side effects ChEI

A

muscarinic side effects predominate early. Convulsions coma, followed by peripheral nicotinic effects (depolarizing neuromusclar blockade))

97
Q

Pralidoximine

A

regenerates ChE. Not effective at doing CNS, b/c it is quaternary. Nor recommended for reversal of inhibition form carbamate inhibitors.

pretty much any oximine will work as long as the phosphorous hasn’t aged.

98
Q

Pretreatment with reverisble enzyme inhibitor cholinergic poisoning

A

Pyridostigmine. prevents binding of irreverisble organophosphate inhibitor. Reserved for situations in which possible lethal poisoning is anticipated. Simulatanous use of atropine is required to control muscarinic excess.

mushroom poisoning=pyridostigmine treatment.

99
Q

Beta blocker receptors

A

carteolol pindolol prpranolol counter productive in asthmatics

100
Q

Propranolol nadolol timolol

A

used to treat hypertension. TImolol for glaucoma.

101
Q

Beta-1 specific beta-blockers

A

Metropolol, atenolol, nevibinol

102
Q

Nevibinol

A

Beta1 specific antagonist. decreases heart rate and vasodilates. its a twofer

103
Q

uses of alpha-1 antagonists

A

used todecrease blood pressure. can also reduce urethral tone and alleviates bladder outlet obstruction in BPH

104
Q

Prazosin

A

Highly selective alpha-1 antagonist. decreases blood pressure. dilates arteries and veins, relative absence of tachycardia. decreases after load.

105
Q

Phenoxybenzamine

A

irreversible blockade of alpha receptors, slightly selective for alpha1 over alpha2.

may increase cardiac output (peripheral alpha2 blockade, reflex tachycardia) orthostat HTN tachy, inhbit ejaculation

reflex tachcardia

106
Q

Alpha2 agonists

A

autoreceptor activation decreasing sympathetic output.

107
Q

Clonidine

A

alpha2 adrenergic agonist used for hypertension. act by inhibiting sympathetic outflow from CNS decreasing heartrate contractility and vasomotor tone

108
Q

Guanabenz

A

alpha-2 adrenergic agonist. act by inhibiting sympathetic outflow from CNS and decreasing heart rate.

109
Q

Carvedilol

A

Carvedilol: more potent at Beta receptors than at alpha1. especially effective for treatment of chronic heart failure with decreased systolic function.

110
Q

4 types of receptors

A

VG-ion channels
Ligand gated ion channels
Membrane delimited metabotrophic
second messanger delimited metabotrophic

111
Q

Toxin blocking Na channels

A

Tetrodotoxin

112
Q

Toxin blocking Nicotinic

A

Alphabungarotoxin

113
Q

Toxin blocking GABAa

A

Picrotoxin

114
Q

Toxin blocking glycine

A

Strychnine.

115
Q

Nuclei producing NE in the brain

A

Locus Coerulus and a bunch of nuclei called A something.

116
Q

Projection sites of NE in the brain

A

Hypothalamus
Subiculum
Cortex

some other shit too olfactory bulb, thalmus amydala, midcentral central gray

117
Q

Selective norepinephrine re-uptake inhibitors

A

Used to treat depression, prevent the reuptake into the presynaptic bulb

118
Q

deipramine

A

SNRI

119
Q

maprotyline

A

SNRI

120
Q

Protryptiline

A

SNRI

121
Q

Cocaine

A

NE reuptake transporter blocker

122
Q

Rauwolfia alkaloids

A

release NE by disrupting synaptic vesicle tranporters.

123
Q

Guanathedine

A

Inhibits the release of NE from Nerve endings. taken up by NET.

124
Q

Dopamine pathways

A

Nigrostriatal, mesolimbic tuberoinfundbular

125
Q

Nuclei making dopamine

A

Ventral tegmental
substantia nigra
tuberoinfundibular

126
Q

Tuberoinfudibular system target

A

neurohypophysis, median eminence

127
Q

substancia nigra dopamine target

A

Caudate/putamen

128
Q

Mesolimbic pathway

A

VTA and substantia nigra to nucleus accumbens

129
Q

L-dopa Carbedopa

A

used to treat Parkinson’s (death of substantia nigra)

130
Q

Spiroperidol

A

DA2 receptor antagonist, Anti-psychotic (mesolimbic system)

131
Q

Haldoperidol

A

DA2 receptor antagonist Antipsychotic

132
Q

Pimozide

A

DA2 receptor antagonist Antipsychotic

133
Q

Amphetamines Meth

A

release DA, also are weak agonist of NE which displace it.

134
Q

Nuclei producing serotonin

A

Raphe Magnus

135
Q

Projection sites for Serotonin

A

hypothalamus
cortex
seubiculum

136
Q

Flouoxitine

A

5-HT Reuptake inhibitor

137
Q

Trazadone

A

5-HT Reuptake inhibitor

138
Q

Imiprimine

A

5-HT Reuptake inhibitor

139
Q

Fluvoxamine

A

5-HT Reuptake inhibitor

140
Q

paroxetine

A

5-HT Reuptake inhibitor

141
Q

methysergide

A

antagonist of serotonin receptors

142
Q

LSD

A

is an agonist of serotonin receptors

143
Q

Excitalopram

A

5-HT reuptake inhibitor

144
Q

Receptor and agonist for: Acetycholine

A

Muscarinic (M1) muscarine

145
Q

Receptor and agonist for:Dopamine

A

D1, D2 bromocriptine

146
Q

Receptor and agonist for: GABA

A

GABAa; muscimol barbituates

147
Q

Receptor and agonist for: GLycine

A

Taurine, Beta alanine

148
Q

Receptor and agonist for: 5-HT

A

LSD 5-HT1A

149
Q

Receptor and agonist for: Glutamate

A

NMDA

150
Q

Valium

A

Benzodiazapine makes GABA more likely to open

151
Q

Librium

A

Benzodiazapine makes GABA more likely to open

152
Q

Barbituates

A

opens GABA channels

153
Q

Zolpidem

A

same as benzodiazepine

154
Q

Flumazenil

A

blocks benzodiazepine

155
Q

Epinephrine

A

adrenergic withhigher affinity for beta over alpha. specifically Beta2. increase blood flow to muscles, dilate airways

156
Q

NE

A

higher affinity for alpha than beta. increase total peripheral vascular resistance.exhibit positive ionotopiceffecton theheart.

157
Q

2 indications for terazosin

A

Alpha-1 selective antagonist used for the treatment of HTN and urinary complications associated with BPH

158
Q

2 specific indications for Labetalol

A

has both alpha and beta antagonist effects (slightly selective for alpha1).

treatment of hypertensive emergencies

pregnancy-induced HTN

may induce hepatitis.

Pharmacology Drugs (2 decks)

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