01 Pharm Test 2

Front 1

Activate the 5HT-1b/d receptors found in cerebral vessels and causes vasoconstriction, including AV anastomoses. It is thought to modulate NT release from neuronal terminals which may inhibit pro inflammatory neural peptides.

SE: paraesthesias / asthenia and fatigue/ flsuhing/*feelings of pressure, tightness or pain in chest*/drowsiness/ dizziness / nausea and sweating

CI: CAD and peripheral or cerebral vascular disease / MAO-I's

Back 1

Sumatriptan and all other -triptans.

Naratriptan is metabolized by CYPs and was the longest lasting -triptan (replaced by frovatriptan)

Hint 1

Medications for abortive migraine therapy

Serotonin 5TH agonists

Front 2

More potent than 5-HT-1b/d agonists, but have wider side effects due to activating other 5-HT receptors. As a vasoconstrictor it counteracts the vasodilation of the extracranial and external carotid arteries.

SE: N/V / diarrhea

CI'ed in: CAD and PVD/Cerebral VD / impaired hepatic/renal function/pregnancy.

Back 2

Dihydroergotamine
Ergotamine
Methylergonovine

Dihydroergotamine can be given parenteral in emergneices when given IV or IM

Hint 2

Medications for abortive migraine therapy

Ergot Alkaloids

Front 3

Blocks prostaglandin synthesis. May be used safely in pts with vascular disease. While it still causes GI symptoms, these are typically less than ergot alkaloids.

CI: peptic ulcer disease (inhibits mucus secretion) and severe renal disease (decreases renal blood flow)

Back 3

Meclofenamate sodium
Indomethacin
Naproxen

Hint 3

Medications for abortive migraine therapy

NSAIDS

Front 4

Slow onset of action (8-12 hrs)

Used only when other drugs are not effective in aborting the attack

Back 4

Methylprednisolone
Dexamethasone

Hint 4

Medications for abortive migraine therapy

Corticosteroids

Front 5

Effective in aborting the visual or neurological symptoms and subsequent headaches. prevents the vasoconstriction associated with ischemic pain. Not given as prophylaxis becasue you will make things worse (long term vasodilation)

Back 5

Nitroglycerin
Isoproterenol
Nifedipine

*Nifedipine, while a Ca2+ channel blocker is never used as a prophylaxis

Hint 5

Medications for abortive migraine therapy

Vasodilators

Front 6

First choice should be non-addicting/non-habituating drugs. Narcotics indicated if no other therapy is effective

Back 6

Analgesics

Hint 6

Medications for abortive migraine therapy

Pain medication

Front 7

Potent neuro-inflammaotry mediator that regulates CGRP. Good alternative for patients who cannot tolerate triptans. Reduces substance P levels which reduces pain.

Does not cause vasoconstriction which means it can be used in patients with peripheral artery disease

Back 7

CGRP agonist

Hint 7

Medications for abortive migraine therapy??

Front 8

Given to patients where ergotamine is contraindicated.

Has mild vasoconstrictive effect (less than ergotamine) but is better tolerated

Back 8

Isometheptene Mucate

Hint 8

Medications for abortive migraine therapy

Sympathomimetic Amine

Front 9

First line prophylactic drug for migraines that don't respond to abortive therapy.

Blocks B2 receptors which prevents vasodilation (arterial relaxation). Rebound effect if pulled off too soon

Back 9

Propranolol

Hint 9

Medications for prophylactic migraine therapy

Beta blockers

Front 10

Are as effective as beta blockers in migraine prophylaxis. Decrease cranial vasoconstriction (internal carotids) during the prodrome of the attack.

Back 10

Verapamil
Flunarizine

Flunarizine may protect against brain ischemia and hypoxia and decrease frequency of migraine attacks.
Verapamil has anti-platelet effects

Hint 10

Medications for prophylactic migraine therapy

Calcium channel blockers

Front 11

Alpha 2 agonists that diminishes sympathetic outflow which inhibits the initial vasoconstriction (internal carotids) that occurs during the onset of a migraine attack

Back 11

Clonidine

Hint 11

Medications for Prophylaxis Migraine therapy

A2 receptor agonist

Front 12

Antihistamine with mild to moderate antiserotonin activity. Less effective of the options, but used for pts who can't take any other medication
Useful in children.
SE: sedation / dry mouth / appetite stimulation

Back 12

Cyproheptadine

Hint 12

Medications for Prophylaxis Migraine therapy

Antihistamine

Front 13

Prevents the imbalance between GABA and L-glutamate neurotransmission.

Causes an increase in glutamate in the synaptic cleft

Back 13

Topiramate
Valproic acid

Hint 13

Medications for Prophylaxis Migraine therapy

Anti-epileptics

Front 14

Non-electrolyte agents that undergo free glomerular filtration, limited tubular reabsorption, are
pharmacologically inert and resistant to metabolic alteration. These agents remain in the tubular
lumen and “hold” water by means of their osmotic effects. This effect is seen over all regions of the
tubule, but most pronounced in the proximal tubule where water/sodium reabsorption is the highest.
Mannitol is used for (1) prophylaxis of acute renal failure and (2) reduction of CSF volume and
pressure.

Back 14

Urea
Mannitol

Hint 14

Diuretics

Osmotic Diuretics

Front 15

Inhibit brush boarder and intracellular carbonic anhydrase in the proximal tubule. The major effect is
HCO3 (bicarb) excretion and a loss of Na+ due to failure of the Na/H transporter. Body bicarb levels
drop resulting in metabolic acidosis. Rarely used as diuretics. Commonly used in the tx of glaucoma
(inhibition of bicarbonate formation reduces production of aqueous humor and lowers intraocular
pressure) and urinary alklinization (to enhance renal excretion of weak acids i.e. uric acid, aspirin, etc).
Also used to treat metabolic alkalosis (usually caused by other diuretics) when volume repletion is
contraindicated (heart failure). Acetazolamide is used for altitude sickness by decreasing pH of CSF
and stimulating respiration.
In general, CAI’s are contraindicated in hepatic encephalopathy and hyperammonemia syndromes
because the elevated pH converts NH4+ to rapidly reabsorbed NH3.

Back 15

Acetazolamide
Methazolamide

Hint 15

Diuretics

Carbonic anhydrase inhibitors

Front 16

Antagonists block the A1 adenosine receptor which leads to an increase in cAMP levels (the receptor is normally Gi). The increased cAMP will then inhibit the Na/HCO3 cotransporter, which causes more Na+ and HCO3- to be excreted, taking water with it.

Back 16

Caffeine (non-selective) / Methylxanthines

No specific drug yet

Hint 16

Diuretics

Adenosine A1 receptor antagonist

Front 17

Inhibit the Na/Cl/K cotransporter of the ascending limb by binding to the Cl portion of the cotransporter
and stopping the cycle. Used in the tx of edema (cardiac, hepatic, renal). Also prevents Ca and Mg
reabsorption (used in tx of hypercalcemia). Used in the tx of moderate, severe and malignant HTN by lowering blood volume. Relatively short acting (4 hrs). NSAIDS decrease effectiveness. Ethacrynic
acid is a phenoxyacetic acid derivative (loop 1). The remainder are sulfonamide derivatives.
Furosemide toxicities: ototoxic when combined with aminoglycosides, metabolic hypokalemic alkalosis, hypomagnesemia/hypocalcemia, hyperuricemia.

Back 17

Ethacrynic acid
Furosemide
Bumetanide
Torsemide

Hint 17

Diuretics

Loop diuretics

Front 18

Inhibit NaCl transport in the early distal tubule by binding the Cl portion of the cotransporter. Drug of
choice in the tx of edema (cardiac, hepatic or renal). First line drug for patients with mild HTN or in
diabetic pts with HTN due to lowering blood volume. Antihypertensive effect is achieved with doses below the required max diuretic effect. Causes an increase in calcium reabsorption (used for kidney stones).

Back 18

Hydrochlorothiazide
Indapamide
Chlorthalidone*

Hint 18

Diuretics

Thiazides

Front 19

Aldosterone antagonist by blocking aldosterone receptors in the late distal tubule/collecting system.
Decreases Na+ reabsorption which reduces potassium excretion. Weak diuretics and used with
thiazides or loop diuretics to prevent hypokalemia.

Back 19

Spironolactone
Eplerenone

Spironolactone also affects androgen receptors

Hint 19

Diuretics

Potassium sparing diuretic

Front 20

Blocks the Na channel found on the luminal surface of the late distal tubule/collecting system.
Decreases Na+ reabsorption which reduces potassium excetion. Mostly used with thiazides to
maintain K+ levels.

Back 20

Triamterene
Amiloride

Hint 20

Diuretics

Potassium sparing diuretic

Front 21

Alpha2-adrenoceptor agonists that diminishes sympathetic (NE) outflow and decreases total peripheral resistance of choice for tx of HTN during pregnancy. SE: sedation, postural hypotension, dizziness,
dry mouth, headache, water retention. Sudden withdrawal may cause rebound hypertension.

Back 21

Alpha-methyldopa

Hint 21

Sympatholytic Antihypertensives

Alpha 2 agonists

Front 22

Activates alpha2 and imidazoline receptors which decrease CNS outflow and NE release. Faster
onset than alpha-methyldopa. Tx for hypertension, heart failure, alcohol withdrawal and to diagnose
pheochromocytoma. SE same as alpha-methyldopa except less water retention. May cause rebound
hypertension due to upregulation of NE receptors; stopping the drug returns NE levels to normal (but
now you have added NE receptors which causes a pronounced level of response).

Back 22

Clonidine

Hint 22

Sympatholytic Antihypertensives

Alpha 2 agonists

Front 23

Alpha2 agonists which also exhibit natriuretic activity (which eliminates water retention associated with
a2-agonists).

Back 23

Guanabenz
Guanfacine

Hint 23

Sympatholytic Antihypertensives

Alpha 2 agonists

Front 24

Selective agonist at the imidazoline receptor subtype 1 (I1) which causes a decrease in sympathetic
nervous system activity and, therefore, a decrease in blood pressure. The receptor subtype is found in both the rostral ventro-lateral pressor and ventromedial depressor areas of the medulla oblongata.

Back 24

Rilmenidine
Moxonidine

Moxonidine binds with much greater affinity to the imidazoline I1-receptor than to the α2-receptor
(clonidine binds to both receptors with equal affinity).

Hint 24

Sympatholytic Antihypertensives

Imidazoline-1 agonists

Front 25

Competitive antagonists of Ach binding at the Nn receptor.
Must be given IV. Carry severe side effects (blurred vision, constipation, urination hesitancy and, perhaps the worst of all, sexual dysfunction).

Back 25

Hexamethonium
Mecamylamine
Trimethaphan

Hint 25

Sympatholytic Antihypertensives

Ganglionic blockers

Front 26

Displaces NE from storage vesicles (early) and prevents catecholamines from leaving the nerve terminal and depletes the levels of NE in the synaptic cleft (later). NE is still produced by the nerve,
but it remains trapped inside. Drug does not enter the CNS, thus they effect only peripheral receptors.
SE: orthostatic hypotension (prevents the reflex response that normally prevents this), diarrhea
(knocking out the SANS causes the PANS to have complete control of the GI system).

Back 26

Guanethidine

Hint 26

Sympatholytic Antihypertensives

Adrenergic neuron blocker

Front 27

Blocks the vesicular transporter and prevents vesicle storage. This eventually depletes the stores of
catecholamines and 5-HT. Crosses the BBB, so has a CNS action. SE: drowsiness/sedation,
depression, migraines, water retention. May cause GI ulcers and hemorrhage. Used in low doses
(due to toxic side effects).

Back 27

Reserpine

Hint 27

Sympatholytic Antihypertensives

Adrenergic neuron blocker

Front 28

Blocks both alpha1 and alpha2 receptors. Alpha1 effects decreases the availability of NE to bind to the receptor and decreases the vasoconstrictive response (causing decreased BP). Blocking alpha2 receptors blocks inhibition of NE (causing an increased amount of NE released from the nerve terminal). Nonselective adrenergic antagonists are more likely to cause reflexive tachycardia (due to their alpha2 blocking effects; increased NE availability for the beta1 receptors of the heart). Giving a beta-blocker would minimize this effect.

Back 28

Phentolamine
Phenoxybenzamine (permanent)

Hint 28

Adrenoreceptor blockers

Non-selective alpha antagonists

Front 29

Alpha1-receptor antagonist that causes vasodilation due to blocking NE from alpha1 receptors. Leaving alpha2 receptors open, it allows for a decrease in NE levels due to negative feedback response (NE binding to alpha2 receptors inhibits further release of NE). May cause first dose-effect phenomenon (sudden decrease in BP resulting in syncope).

Back 29

Prazosin
Terazosin

Hint 29

Adrenoreceptor blockers

Selective alpha1 antagonists