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Block 2 > Pharmacology > Flashcards

Pharmacology Flashcards

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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
What are the physiologic responses to alpha1 stimulation?
* Vasoconstriction --\> increased peripheral resistance * Vasoconstriction --\> sphincter constriction --\> urinary retention * Radial muscle constriction --\> pupillary dilation
26
Where are alpha2 receptors located?
* Presynaptic neuron * CNS * Directly on blood vessels
27
physiologic responses of alpha2 stimulation
* CNS sympathetic signal decrease * NE release inhibition at presynaptic terminal * Smooth muscle relaxation in GI
28
Where is Beta1 receptor located?
* In the heart * Myocardial cells * Pacemaker node
29
What are the physiologic responses of beta1 stimulation?
* Increased HR due to pacemaker stimulation * Increased cardiac output due to myocardial stimulation
30
Where are Beta2 receptors located?
* Lungs * Vascular (skeletal and conorary artery) * Eye: ciliary muscle (NOT circular muscle) * ciliary muscle adjust curvature of the lens
31
What is the mechanism of beta2 stimulation?
* increased cAMP --\> relaxation of smooth muscle
32
What are the physiologic responses of Beta2 stimulation?
* 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
How is norepinephrine/epinephrine synthesized?
* Tyrosine --\> L-DOPA --\> Dopamine --\> norepinephrine * Norepinephrine --\> epinephrine in adrenal medulla * Recall that stimulation of the adrenal medulla results in epinephrine release
34
How is norepinephrine inactivated after release into the synapse?
* Can be **degraded** by monoamine oxidase (MAO)
35
What is the reflex response?
* 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
Muscarinic agonists
* Methacholine * Bethanechol * Pilocarpine * Muscarine
37
Bethanechol
* 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
Pilocarpine
* 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
Methacholine
* 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
Muscarine
* muscarinic agonist * No therapeutic use * No CNS penetration * Toxicity: DUMBBELS
41
Which muscarinic receptors generate an excitatory response?
* M1, M3, M5
42
Which muscarinic receptor generates an inhibitory response?
* M2 (heart)
43
Myasthenia Gravis
* 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
What causes increased secretions?
* Muscarinic acetylcholine stimulation due to increased calcium release
45
Toxic effects of acetylcholinesterase inhibitors
* 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
Reversible acetylcholinesterase inhibitors
* Edrophonium * Pyridostigmine * physostigmine * Donezapil
47
Irreversible acetylcholinesterase inhibitors
* Diisopropyl flourophosphate * Parathion * Sarin
48
acetylcholinesterase regenerator
* Pralidoxime
49
Pyridostigmine
* 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
Edrophonium
* 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
Physostigmine
* 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
Parathion
* THIOL spray = paraTHION * Irreversible acetylcholinesterase inhibitor * Pesticide that is extremely toxic * Causes DUMBBELS
53
Pralidoxime
* 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
Donezapil
* 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
Botulinum Toxin
* Prevents release of acetylcholine at presynaptic vesicle
56
Acetylcholine
* Binds nicotinic and muscarinic receptors * Cannot cross blood-brain barrier * Therapeutic use: Used locally to prep for eye surgery * Causes pupillary constriction
57
How does Ach cause vasodilation in vasculature?
* 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
Nicotinic Agonists
* Acetylcholine * Nicotine * Pancuronium * Succinylcholine
59
Pancuronium
* 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
Succinylcholine
* 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
Muscarinic Antagonists
* Atropine * Scopalamine * Oxybutinin * Ipratropium
62
Atropine
* "Atropine Alice" = the star of the show * Muscarinic antagonist * Blocks muscarinic receptors = mimics sympathetic responses * Decreased secretions * Reverses DUMBBELS * Pupillary dilation --\> "belladonna"
63
Scopalamine
* 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
Oxybutinin
* 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
Ipratroprium
* 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
Reserpine
* 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
Tyramine
* 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
Where are serotonin receptors located?
* GI tract * Platelets * CNS
69
What does serotonin do to platelets?
* Causes platelet aggregation
70
How is serotonin synthesized?
* Tryptophan
71
What enzyme degrades serotonin?
MAO
72
What is most responsible for serotonin inactivation?
serotonin reuptake
73
Sumatriptan
* 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
Fluoxetine
* SSRI * Therapeutic use: Depression, OCD, Panic disorder, social phobia, PTSD * Toxic effects: insomnia, headache, drowsiness, anxiety, decreased libido
75
Ondansetron
* **prototypical 5HT3 (serotonin) ANTAGONIST** * **Therapeutic use: Chemotherapy-induced emesis** * Therapeutic effect: reduced nausea/vomiting

Block 2 (5 decks)

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