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Block 2 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Adrenergic Agonists

A
  • “OL” = albuterol, isoproterenol
  • “INE” = epinephrine, norepinephrine, phenylephrine
  • +Clonidine
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2
Q

Phenylephrine

A
  • “Flannel friends” in alpha1 camp. One of them has a red nose.
  • Stimulates alpha1 receptors
  • Causes vasoconstriction in nasal mucosa –> less swelling –> treats nasal congestion
  • Therapeutic use: nasal congestion
  • Therapeutic effects: vasoconstriction
  • Toxic effects: hypertension, cardiac arrhythmias, agitation
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3
Q

Norepinephrine

A
  • “NORth facing compass” in between alpha1 and alpha2 camps with bulging BIceps
  • Stimulates alpha1 and alpha2 receptors with SOME beta1 activity
  • Causes vasoconstriction and increased BP
  • Therapeutic use: acute hypotension (shock)
  • Therapeutic effects: vasoconstriction, increased cardiac output
  • Toxic effects: hypertension, cardiac arrhythmias, agitation
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4
Q

Isoproterenol

A
  • “Iso-pro-tunnel” in Beta1 camp
  • B1 and B2 agonist
  • B1 –> Increased HR
  • B2 –> vasodilation –> increased cardiac output
  • Therapeutic use: bradycardia, heart block (emergency)
  • Therapeutic effects: increased HR and contraction, increased cardiac output
  • Toxic effects: palpitations, tachycardia, headache, flushing
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5
Q

Albuterol

A
  • Beta-tuba player breathing deeply holding a ROL call sheet –> albuteROL
  • B2 stimulation –> bronchodilation
  • Therapeutic use: asthma
  • Therapeutic effects: bronchodilation
  • Toxic effects: palpitations, tachycardia, headache, flushing
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6
Q

Clonidine

A
  • Alpha2 agonist
  • Therapeutic use: hypertension, ADHD
  • Therapeutic effects: reduced sympathetic outflow (CNS effect), vasodilation (presynaptic alpha2 receptors)
  • Toxic effects: sedation, dry mouth

**Alpha2 are in presynaptic neuron and CNS and blood vessels. Blood vessels cause vasoconstriction, but the other 2 locations cause vasodilation. That’s why this is used to treat hypertension.

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7
Q

Adrenergic Antagonists

A
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8
Q

Alpha antagonists

A
  • “Phantom of the alpha” = phentolamine
  • Phantom’s tattoo of a phoenix = phenoxybenzamine
  • Opera SINger = “osin” = prazosin
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9
Q

Phentolamine

A
  • “Phantom of the alpha”
  • Alpha antagonist
  • inhibits alpha1 and alpha2
  • Therapeutic use: To diagnose pheochromocytoma
    • This is short-acting
  • Therapeutic effects: vasodilation
    • Stimulation of alpha1 causes vasoconstriction, so blocking it causes vasodilation
  • Toxic effects: cardiac arrhythmia, postural hypotension, tachycardia
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10
Q

Phenoxybenzamine

A
  • Phantom’s tattoo of a phoenix = phenoxybenzamine
  • Blocks alpha1 and alpha2 receptors
  • Therapeutic use: hypertensive emergency
    • Phentolamine is used to diagnose pheochromocytoma; phenoxybenzamine is used to treat hypertensive emergency from it
  • Therapeutic effect: vasodilation
  • Toxic effects: cardiac arrhythmia, postural hypotension, tachycardia
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11
Q

Prazosin

A
  • Opera SINger = “osin” = prazosin
  • alpha1 antagonist
  • Therapeutic use: hypertension
  • Therapeutic effects: vasodilation
  • Toxic effects: postural hypotension
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12
Q

Common toxic effects of alpha antagonists

A
  • hypotension
    • alpha1 stimulation causes vasoconstriction –> increased BP
    • Block alpha1 –> vasodilation –> decreased BP
  • cardiac arrhythmia
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13
Q

Common toxic effects of adrenergic agonists

A
  • Hyperactivation of sympathetic nervous system
  • Hypertension (due to alpha1 stimulation)
  • Cardiac arrhythmias
  • tachycardia
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14
Q

Beta blockers

A
  • Brahm’s LOLiby = propanoLOL, labetaLOL, metoproLOL
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15
Q

Common toxic effects of beta blockers

A
  • cardiac failure (due to B1), bronchospasm (due to B2), cardiac arrhythmia, hypotension
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16
Q

Metoprolol

A
  • The single A-BEAM spotlight on our lone Beta-1 Bugler
  • M = metoprolol
  • Selective for B1 antagonism (and B2 at high doses)
  • Therapeutic use: hypertension, angina, cardiac failure
  • Therapeutic effects: decreased HR, contractility
  • Toxif effects: bronchospasm, cardiac failure, hypotension, bradycardia
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17
Q

labetalol

A
  • Organ with alpha and beta signs on it –> “alpha-beta-lol” –> labetalol
  • Blocks alpha1, beta1 and beta2
  • Therapeutic use: hypertension
  • Therapeutic effects: decreased HR, decreased contractility, decreased peripheral resistance
  • Toxic effects: cardiac failure, bronchospasm, cardiac arrhythmia, orthostatic hypotension
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18
Q

What causes orthostatic hypotension?

A
  • Anything that blocks alpha1 receptors
  • Because blocking alpha1 blocks the reflex response
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19
Q

Propanolol

A
  • It’s the only one that inhibits both Beta1 and Beta2
  • Therapeutic use: Angina, atrial fibrillation, hypertension, cardiac failure
  • Therapeutic effects: decreased HR, decreased contractility
  • Toxic effects: cardiac failure, bronchospasm, cardiac arrhythmia
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20
Q

Indirect-Acting drugs on adrenergic receptors

A
  • Amphetamine
  • Cocaine
  • Reserpine
  • Tyramine
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21
Q

Amphetamine

A
  • Causes NE to be released from vesicles in presynaptic neuron, which then leaks out into synapse
  • Also blocks NE reuptake
  • Therapeutic use: ADHD, narcolepsy
  • Therapeutic effects: CNS stimulation
  • Toxic effects: hypertension, tachycardia, dependence, dysphoria
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22
Q

Cocaine

A
  • Blocks reuptake of norepinephrine
  • Therapeutic use: local anesthetic
    • Remember cocaine was first originally used in eye surgeries
  • Therapeutic effect: sodium channel disruption
  • Toxic effects: hypertension, tachycardia, dependence, dysphoria, local tissue necrosis
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23
Q

Where are alpha1 receptors located?

A
  • Smooth muscle vasculature
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24
Q

What is the mechanism of alpha1 stimulation?

A
  • Increased calcium –> smooth muscle contraction
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25
Q

What are the physiologic responses to alpha1 stimulation?

A
  • Vasoconstriction –> increased peripheral resistance
  • Vasoconstriction –> sphincter constriction –> urinary retention
  • Radial muscle constriction –> pupillary dilation
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26
Q

Where are alpha2 receptors located?

A
  • Presynaptic neuron
  • CNS
  • Directly on blood vessels
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27
Q

physiologic responses of alpha2 stimulation

A
  • CNS sympathetic signal decrease
  • NE release inhibition at presynaptic terminal
  • Smooth muscle relaxation in GI
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28
Q

Where is Beta1 receptor located?

A
  • In the heart
    • Myocardial cells
    • Pacemaker node
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29
Q

What are the physiologic responses of beta1 stimulation?

A
  • Increased HR due to pacemaker stimulation
  • Increased cardiac output due to myocardial stimulation
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30
Q

Where are Beta2 receptors located?

A
  • Lungs
  • Vascular (skeletal and conorary artery)
  • Eye: ciliary muscle (NOT circular muscle)
    • ciliary muscle adjust curvature of the lens
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31
Q

What is the mechanism of beta2 stimulation?

A
  • increased cAMP –> relaxation of smooth muscle
32
Q

What are the physiologic responses of Beta2 stimulation?

A
  • Beta2 –> increased cAMP –> smooth muscle relaxation
  • Remember Beta2 Bugler taking a deep breath
  • Bronchodilation
  • vasodilation in coronary and skeletal muscle arteries –> decreased peripheral resistance and increased blood flow
  • Detrusor relaxation in bladder
33
Q

How is norepinephrine/epinephrine synthesized?

A
  • Tyrosine –> L-DOPA –> Dopamine –> norepinephrine
  • Norepinephrine –> epinephrine in adrenal medulla
    • Recall that stimulation of the adrenal medulla results in epinephrine release
34
Q

How is norepinephrine inactivated after release into the synapse?

A
  • Can be degraded by monoamine oxidase (MAO)
35
Q

What is the reflex response?

A
  • Mediated by baroreceptors in the aortic arch and carotid arteries
  • Controlled by the vagus nerve
  • If BP increased –> baroreceptors tell CNS the pressure is too high –> vagus nerve secretes acetylcholine to counteract
36
Q

Muscarinic agonists

A
  • Methacholine
  • Bethanechol
  • Pilocarpine
  • Muscarine
37
Q

Bethanechol

A
  • Muscarinic agonist
  • Acetyl-colA sketch
  • Beth the construction worker drinking a cool bottle of acetyl-colA
  • Muscarinic agonists increase secretion and motor activity of the gut –> colon-looking pipe pouring out cement and Beth holding a hose
  • Bethanechol used to make people pee
  • Therapeutic use: urinary retention
  • Therapeutic effect: urination
  • Atropine reversal: yes
  • CNS penetration: poor
  • Toxicity: DUMBBELS
38
Q

Pilocarpine

A
  • Acetyl-ColA sketch
  • Muscarinic agonist
  • “Pile o’ carp” = pilocarpine
  • The carp have water dripping from their mouths –> pilocarpine increases salivary secretion –> used to treat dry mouth
  • Causes contraction of ciliary body in the eye –> image of the crane with ciliary body
  • Used to treat glaucoma b/c contraction of ciliary body dranes aqueous humor
39
Q

Methacholine

A
  • AcetylColA sketch
  • Muscarinic agonist
  • “Para-city marathon challenge” = methacholine challenge
  • Muscarinic agonists cause bronchoconstriction –> seen by guy wheezing at the finish line
  • Used to diagnose asthma
  • Poor CNS penetration
  • Toxicity: DUMBBELS
40
Q

Muscarine

A
  • muscarinic agonist
  • No therapeutic use
  • No CNS penetration
  • Toxicity: DUMBBELS
41
Q

Which muscarinic receptors generate an excitatory response?

A
  • M1, M3, M5
42
Q

Which muscarinic receptor generates an inhibitory response?

A
  • M2 (heart)
43
Q

Myasthenia Gravis

A
  • Antibodies develop against nicotinic cholinergic receptor
  • Causes problems with stimulation of cholinergic receptor at neuromuscular junction –> muscle weakness
  • Acetylcholinesterase inhibitors used for treatment
    • Remember the “Gravis” sign on the wall in the sketchy video for acetylcholinesterase inhibitors
44
Q

What causes increased secretions?

A
  • Muscarinic acetylcholine stimulation due to increased calcium release
45
Q

Toxic effects of acetylcholinesterase inhibitors

A
  • DUMBBELS
  • diarrhea
  • urination
  • miosis
  • bradychardia
  • bronchospasm
  • emesis (vomiting)
  • lacrimation (crying)
  • salivation

Also sweating b/c sweat glands are activated by Ach muscarinic receptors, even though it’s a sympathetic response

46
Q

Reversible acetylcholinesterase inhibitors

A
  • Edrophonium
  • Pyridostigmine
  • physostigmine
  • Donezapil
47
Q

Irreversible acetylcholinesterase inhibitors

A
  • Diisopropyl flourophosphate
  • Parathion
  • Sarin
48
Q

acetylcholinesterase regenerator

A
  • Pralidoxime
49
Q

Pyridostigmine

A
  • Lady wearing vest “Community PRIDE” cleaning up graffiti that says “GRAVIS”
  • PRIDE = PYRIDostigmine
  • Reversible acetylcholinesterase inhibitor
  • Used to TREAT myasthenia gravis
  • This is a quaternary imine - imagery of quarters in the edrophonium phone booth - so it has poor CNS penetration
50
Q

Edrophonium

A
  • Public PHONE booth on the roof = edroPHONium
  • “Quarters only” = quaternary imine = cannot penetrate blood brain barrier
    • This is also true of pyridistigmine
  • Used in DIAGNOSIS of myasthenia gravis
  • Reversible acetylcholinesterase inhibitor
51
Q

Physostigmine

A
  • PHYS Ed center on the roof = PHYSostigmine
  • “Your brain on drugs” poster in the Phys Ed center = CNS penetration of physostigmine
  • Reversible cholinesterase inhibitor
  • The Phys Ed teacher dragging atropine graffiti punk away = physostigmine reverses atropine overdose
52
Q

Parathion

A
  • THIOL spray = paraTHION
  • Irreversible acetylcholinesterase inhibitor
  • Pesticide that is extremely toxic
  • Causes DUMBBELS
53
Q

Pralidoxime

A
  • Puts a LID on the toxic insecticide = praLIDoxime
  • Reverses toxicity of pesticides and other irreversible acetylcholinesterase inhibitors
  • But this can’t cross blood-brain barrier, so atropine is administered first to reverse CNS effects of irreversible esterase inhibitors
54
Q

Donezapil

A
  • The Alzheimer’s Gala happening on the roof
  • two old folks are DONE with a PUZZLE = DONePEZIL
  • Acetylcholinesterase inhibitor
  • Used to treat Alzheimer’s = extensive CNS penetration
55
Q

Botulinum Toxin

A
  • Prevents release of acetylcholine at presynaptic vesicle
56
Q

Acetylcholine

A
  • Binds nicotinic and muscarinic receptors
  • Cannot cross blood-brain barrier
  • Therapeutic use: Used locally to prep for eye surgery
    • Causes pupillary constriction
57
Q

How does Ach cause vasodilation in vasculature?

A
  • Blood vessels have no parasympathetic control, BUT they do have M3 receptors
  • Stimulation of M3 receptors in vasculature –> nitric oxide synthesis –> smooth muscle relaxation –> vasodilation
58
Q

Nicotinic Agonists

A
  • Acetylcholine
  • Nicotine
  • Pancuronium
  • Succinylcholine
59
Q

Pancuronium

A
  • This is a CURare-like drug = panCURonium
  • Visualize as curare crayons stuck in neuromuscular end plate
  • Nondepolarizing blocking agent = competitive inhibitor of nicotinic Ach receptors
  • Used during surgery for muscle relaxation b/c prevents depolarization at NMJ
  • Temporary muscle paralysis but does not cross blood brain barrier so causes no sedation
60
Q

Succinylcholine

A
  • A clean-up crew gets a shock while trying to clean up graffiti covering the end plate. The graffiti says “SUCKS”
  • SUCKS = succinylcholine
  • This is a depolarizing blocker
  • Does not get metabolized as well as acetylcholine, so it just sits in the nicotinic receptor at NMJ –> muscles stay depolarized and thus unresponsive to further stimulation
  • Used for rapid muscle relaxation for intubation
  • See temporary muscle contractions (fasciculations) followed by paralysis
  • Toxic effects: hyperthermia, hyperkalemia
61
Q

Muscarinic Antagonists

A
  • Atropine
  • Scopalamine
  • Oxybutinin
  • Ipratropium
62
Q

Atropine

A
  • “Atropine Alice” = the star of the show
  • Muscarinic antagonist
  • Blocks muscarinic receptors = mimics sympathetic responses
  • Decreased secretions
  • Reverses DUMBBELS
  • Pupillary dilation –> “belladonna”
63
Q

Scopalamine

A
  • Walrus holding a SCOPE to his dilated eye = SCOPalamine
  • He’s wearing a seasick sailor outfit –> scopalamine used to treat nausea from seasickness
  • Muscarinic antagonist
64
Q

Oxybutinin

A
  • Two servers preparing the tea party for alice in wonderland
  • One of them is an ox = OXybutinin
  • He is plugging the water spigot = used to treat urinary incontinence
  • Muscarinic antagonist
65
Q

Ipratroprium

A
  • Cat-ipa-tio-tropillar
  • Visualized by blue caterpillar smoking hukah
  • The caterpillar puffs on his inhaler
  • He is blue and bloated = signifies COPD
  • Used to treat asthma and COPD by increasing bronchodilation and decreasing bronchial secretions
  • Muscarinic antagonist
66
Q

Reserpine

A
  • Indirect acting drug
  • Depletes synaptic vesicles of norepinephrine
  • The epinephrine gets DEGRADED IN PRESYNAPTIC NEURON, not released
  • Reserpine results in LESS norepinephrine in the synapse
67
Q

Tyramine

A
  • A naturally occurring amine found in many foods
  • Normally it is degraded by MAO
  • People who take MAO inhibitors for depression do not break down tyramine
  • At high doses, tyramine causes norepinephrine to get dumped from presynaptic vesicles
  • Unlike reserpine, after the NE gets dumped from presynaptic vesicles it DOES go into synapse (similar to amphtamine)
  • Results in high levels of NE in synapse –> hypertensive crisis
68
Q

Where are serotonin receptors located?

A
  • GI tract
  • Platelets
  • CNS
69
Q

What does serotonin do to platelets?

A
  • Causes platelet aggregation
70
Q

How is serotonin synthesized?

A
  • Tryptophan
71
Q

What enzyme degrades serotonin?

A

MAO

72
Q

What is most responsible for serotonin inactivation?

A

serotonin reuptake

73
Q

Sumatriptan

A
  • Stimulates 5HT1 receptor
  • Used for acute migraine
  • May improve blood flow to the brain by constricting key intracranial blood vessels
  • side effects are minor but can cause fatigue, flushing nausea and sweating
74
Q

Fluoxetine

A
  • SSRI
  • Therapeutic use: Depression, OCD, Panic disorder, social phobia, PTSD
  • Toxic effects: insomnia, headache, drowsiness, anxiety, decreased libido
75
Q

Ondansetron

A
  • prototypical 5HT3 (serotonin) ANTAGONIST
  • Therapeutic use: Chemotherapy-induced emesis
  • Therapeutic effect: reduced nausea/vomiting

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