Drugs Flashcards
1
Q
Hemicholium
A
Prevents the uptake of Choline into presynaptic cell.
2
Q
Vesicholium
A
Prevents entry of ACh into the synaptic vesicle
3
Q
Botulism toxin
A
Prevents the release of Vesicles into the synaptic cleft
4
Q
AChEI
A
prevent the degradatio of ACh in the junction
5
Q
LEMS
A
Lambert Eaton Myasthenic Syndrome. Prevents opening of Ca channels on presynaptic bulb. prevents release of ACh into junction.
6
Q
Metyrosine
A
Block Tyrosine Hydroxylase: this revents the formation of dopa from tyrosine.
7
Q
Reserpine
A
This prevents the entry of Dopamine into the sympathetic synaptic vesicle. Works on VMAT
8
Q
Cocaine,
A
prevents the reuptake of NE into the presynaptic cell
9
Q
Bretylim, Guanethidine
A
Prevent the release of NE from the presynaptic cell
10
Q
TCA
A
tricyclic antidepressants: prevent reuptake of NE
11
Q
Ang II
A
prevent reuptake of NE
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.
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.
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)
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.
16
Q
Modification of Beta carbon Catecholamines
A
Any addition will greatly enhance alpha and beta receptor affinity
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
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.
19
Q
M1
A
CNS neurons Gq
20
Q
M2
A
Heart Gi (decrease cAMP)
21
Q
M3
A
Exocrine Glands, vessels, iris circular muscle (Gq (Ip3, DAG)
22
Q
Nn
A
autonomic ganglia adrenal medulla (open Na/K channels and depolarize)
23
Q
Nm
A
NMJ open Na/K channels and depolarize
24
Q
alpha1
A
Smooth muscles, Iris radial muscles (Gq–>IP3 DAG)
25
Alpha2
smooth muscle, presynaptic cells
26
Beta1
Heart, juxtaglomerular apparatus of renal tube (Gs increase cAMP)
27
Beta2
Smooth muscles, heart, lungs (Gs increase cAMP)
28
Alpha2 autoreceptor
activate when NE in Synaptic cleft exceeds threshold. Inhibits calcium flow into presynaptic cell down regulating its ability to fire.
29
Phenoxybenzamine
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
30
Autonomic Receptors on the eye
M3 (iris circular muscle) alpha1 (iris radial muscle) Beta1: ciliary epithelium. M3: ciliary muscle
31
Beta1 eye
facilitates production of aqueous humor from ciliary body
32
M3
Miosis and accommodation. tenses and opens pores in trabecular mesh work to improve aqueous humor outflow.
33
ALpha1 alpha2 eye
A1: mydriasis A2: inhibits aqueous humor production
34
Ways to reduce Glaucoma
betablocker stopping production. stimulate alpha2 stopping production. M3 agonist facilitating the outflow. carbonic anhydrase inhibitors reduce aqueous humor production.
35
Muscarinics
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
36
Muscarinic agonists
either alkaloids or choline esters.
37
Pilocarpine
Muscarinic agonist. Tertiary cholinomimetic. well absorbed PARTIAL AGONIST!!!
38
Choline Esters
modified ACh to make them less suseptible to degradation and increase their affinity for muscarinic receptors (Methy increases selectivity) Carbamol decrease affinity for AChE
39
Methacholine
quaternary Muscarinic Choline ester: methyl makes it more selective for muscarinic receptors
40
Carbachol
quaternary Muscarinic agonist choline ester. amine makes it harder to degrade by AChE
41
Bethanochol
quaternary Muscarinic agonist choline ester. amine and methyl.
42
Choline Ester effects on: SA node
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
43
Choline Ester effects on:Atria
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
44
Choline Ester effects on:AV node
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
45
Choline Ester effects on: ventricle
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
46
M3 on lungs
Bronchoconstriction, increased secretion
47
M3 GI
Increased contraction, increased secretion, relaxati of sphincters
48
M2, M3 urinary bladder
contract detruser, relax the trigone and sphincter
49
M3 glands
increase secretion
50
clinical use: Acetylcholine
induce miosis for eye surgery
51
clinical use: methacholine
Asthma diagnosis; bronchi are hyperreactive to muscarinics. metha choline can trigger bronchoconstriction
52
clinical use carbacol
Miosis inductio for surgery, glaucoma
53
clinical use Bethanechol
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.
54
clinical use Pilocarpine
Sjogrens syndrome, glaucoma
55
Cevimeline
new direct acting agonist for treament of dry mouth from Sjogrens.
56
DUMMBBELS
Diarhea, urination, muscle weakness, miosis, bronchospasm, bradycardia, excitation, lacrimation, seizueres.
57
Antimuscarinics
Inverse agonists. Parasympatholytics: atropine scopolomine, ipratropium, tiotropium, tolterodine
58
Naturally occuring Antimuscarinics
alkaloids: atropine scopolamine
59
semisynthetic Antimuscarinics
iprotropiium tiotropium
60
synthetic antimuscarinics
tolteridine
61
CNS effects antimuscarinics
Low dose scopolamine does CNS depression (drowsiness amnesia" atropine vagal excitation. High dose: both scopolamine and atropine cause hallucinations delirium and coma.
62
Antimuscarinics effect on eye
unopposed sympathetics lead to mydriasis, increased IOP. weaken contraction of ciliary muscle lead to cycloplegia.
63
Antimuscarinics Cardiovascular
Low dose decrease HR, due to blockade of M1 which limit ACh release. High dose always get tachycardia.
64
Antimuscarinic effects Lungs
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
Clinical uses Scopolamine
Prophylactic treatment of motion sickness vomiting and nausea
66
Clinical uses Atropine
non-selective M) antidote for parasympathomimetic drugs
67
Clinical uses Ipratropium
Non-selective M COPD nasal discharge
68
Clinical uses Tiotropium
M1, M3 COPD
69
Clinical uses Tolteridine
M3 Overreactive lbladder
70
Clinical uses Dycyclomine M3
irritable bowel syndrome
71
Nicotinic receptors
Found in autonomic ganglia (Adrenal medulla included) and at the NMJ. Iontrophic channels that move Na/K flux depolarizing the cell.
72
Nicotinic Alkaloids
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
Cholinergics readily excreted by acidifying the urine
Pilocarpine, nicotine and Lobeline.( cuz they all be like weak bases for realz)
74
Nicotinic choline esters
high affinity for nicotinic receptors. resistant to AChE. Used to induce muscle paralysis during Sx by depolarizing blockade
75
Succinylcholine
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
High nicotine on CNS
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
side effects nicotine
CNS: convulsions to respiratory arrest. Increased hypertension and cardiac arrythmias. skeletal muscle endplate depolarization blockade and respiratory paralysis.
78
Ganglio-blocking agents
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
Hexamethonium
Nondepolarizing competitive antagonist: binds directly to nicotinic ion channel
80
Trimethaphan
Non depolarizing competitive antagonist (nicotinic receptor)blocks the nicotinic receptor not the pore
81
Mecamylamine
non-depolarizing competitive antagonist crosses BBB and causes sedation tremor, choreiform movements and mental abberations. No longer used
82
Ganglion blocking effects Eye
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
Ganglion-blocking agents effects cardiovascular
In blood vessels sympathetics reign so there will be an increase in vasodilation. In the heart parasympathetics reign so there will be tachycardia.
84
Ganglion blocking agents Effects GI
in gut Parasympathetics reign so decreased GI motillity, decreased secretion
85
ganglion blocking agents effects genitourinary
blockade causes hesitency in urination. may precipitate urinary retintion in men with prostatic hyperplasia.
can't get boner or cum.
86
ChEI
reduce choline metabolism and increase endogenous choline concentration.
3 classes simple alcohols
carbamic acid esters
organiophosphates.
87
Edrophonium
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
Neostigmine
quaternary carbamic acid ChEI: nondepolarizing reversal of neuromuscular blockade, urinary retention (myosthenia gravis)
has an additional direct nicotinic agonist activity
89
Pyridostigmine
quaternary carbamic ChEI. used for long term treatment of Myosthenia gravis. slower than neostigmine but last longer.
prhylactic for organophosphate poisoning
90
physostigmine
Tertiary ChEI carbamic acid.Glaucoma, reversal of anticholinergic toxicity
used to antagonize central anti-cholinergic toxicity.
metabolized by plasma esterases.
91
echothiopate
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
ChEI organ effects CNS
generalized convulsions, coma respiratory arrest
93
ChEI effects eye respirtory tract GI, urinary
similar to direct acting cholinomimetics: miosis, GI motility urination, secretion defication. also secretio from sweat lacrimal salivary and nasopharyngeal glands.
94
ChEI effects ardiovascular
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
ChEI effects at NMJ
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
Side effects ChEI
muscarinic side effects predominate early. Convulsions coma, followed by peripheral nicotinic effects (depolarizing neuromusclar blockade))
97
Pralidoximine
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
Pretreatment with reverisble enzyme inhibitor cholinergic poisoning
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
Beta blocker receptors
carteolol pindolol prpranolol counter productive in asthmatics
100
Propranolol nadolol timolol
used to treat hypertension. TImolol for glaucoma.
101
Beta-1 specific beta-blockers
Metropolol, atenolol, nevibinol
102
Nevibinol
Beta1 specific antagonist. decreases heart rate and vasodilates. its a twofer
103
uses of alpha-1 antagonists
used todecrease blood pressure. can also reduce urethral tone and alleviates bladder outlet obstruction in BPH
104
Prazosin
Highly selective alpha-1 antagonist. decreases blood pressure. dilates arteries and veins, relative absence of tachycardia. decreases after load.
105
Phenoxybenzamine
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
Alpha2 agonists
autoreceptor activation decreasing sympathetic output.
107
Clonidine
alpha2 adrenergic agonist used for hypertension. act by inhibiting sympathetic outflow from CNS decreasing heartrate contractility and vasomotor tone
108
Guanabenz
alpha-2 adrenergic agonist. act by inhibiting sympathetic outflow from CNS and decreasing heart rate.
109
Carvedilol
Carvedilol: more potent at Beta receptors than at alpha1. especially effective for treatment of chronic heart failure with decreased systolic function.
110
4 types of receptors
VG-ion channels
Ligand gated ion channels
Membrane delimited metabotrophic
second messanger delimited metabotrophic
111
Toxin blocking Na channels
Tetrodotoxin
112
Toxin blocking Nicotinic
Alphabungarotoxin
113
Toxin blocking GABAa
Picrotoxin
114
Toxin blocking glycine
Strychnine.
115
Nuclei producing NE in the brain
Locus Coerulus and a bunch of nuclei called A something.
116
Projection sites of NE in the brain
Hypothalamus
Subiculum
Cortex
some other shit too olfactory bulb, thalmus amydala, midcentral central gray
117
Selective norepinephrine re-uptake inhibitors
Used to treat depression, prevent the reuptake into the presynaptic bulb
118
deipramine
SNRI
119
maprotyline
SNRI
120
Protryptiline
SNRI
121
Cocaine
NE reuptake transporter blocker
122
Rauwolfia alkaloids
release NE by disrupting synaptic vesicle tranporters.
123
Guanathedine
Inhibits the release of NE from Nerve endings. taken up by NET.
124
Dopamine pathways
Nigrostriatal, mesolimbic tuberoinfundbular
125
Nuclei making dopamine
Ventral tegmental
substantia nigra
tuberoinfundibular
126
Tuberoinfudibular system target
neurohypophysis, median eminence
127
substancia nigra dopamine target
Caudate/putamen
128
Mesolimbic pathway
VTA and substantia nigra to nucleus accumbens
129
L-dopa Carbedopa
used to treat Parkinson's (death of substantia nigra)
130
Spiroperidol
DA2 receptor antagonist, Anti-psychotic (mesolimbic system)
131
Haldoperidol
DA2 receptor antagonist Antipsychotic
132
Pimozide
DA2 receptor antagonist Antipsychotic
133
Amphetamines Meth
release DA, also are weak agonist of NE which displace it.
134
Nuclei producing serotonin
Raphe Magnus
135
Projection sites for Serotonin
hypothalamus
cortex
seubiculum
136
Flouoxitine
5-HT Reuptake inhibitor
137
Trazadone
5-HT Reuptake inhibitor
138
Imiprimine
5-HT Reuptake inhibitor
139
Fluvoxamine
5-HT Reuptake inhibitor
140
paroxetine
5-HT Reuptake inhibitor
141
methysergide
antagonist of serotonin receptors
142
LSD
is an agonist of serotonin receptors
143
Excitalopram
5-HT reuptake inhibitor
144
Receptor and agonist for: Acetycholine
Muscarinic (M1) muscarine
145
Receptor and agonist for:Dopamine
D1, D2 bromocriptine
146
Receptor and agonist for: GABA
GABAa; muscimol barbituates
147
Receptor and agonist for: GLycine
Taurine, Beta alanine
148
Receptor and agonist for: 5-HT
LSD 5-HT1A
149
Receptor and agonist for: Glutamate
NMDA
150
Valium
Benzodiazapine makes GABA more likely to open
151
Librium
Benzodiazapine makes GABA more likely to open
152
Barbituates
opens GABA channels
153
Zolpidem
same as benzodiazepine
154
Flumazenil
blocks benzodiazepine
155
Epinephrine
adrenergic withhigher affinity for beta over alpha. specifically Beta2. increase blood flow to muscles, dilate airways
156
NE
higher affinity for alpha than beta. increase total peripheral vascular resistance.exhibit positive ionotopiceffecton theheart.
157
2 indications for terazosin
Alpha-1 selective antagonist used for the treatment of HTN and urinary complications associated with BPH
158
2 specific indications for Labetalol
has both alpha and beta antagonist effects (slightly selective for alpha1).
treatment of hypertensive emergencies
pregnancy-induced HTN
may induce hepatitis.
