Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
98 Cards in this Set
- Front
- Back
|
Mipomersen
|
Anti hyperlipidemia drug; antisense RNA for ApoB100; stops VLDL production, thereby lowering VLDL and LDL; used in patients with familial hyperlipidemia that does not respond to conventional therapy (e.g. statins) because they do not have the LDL receptor in the liver which is necessary for those drugs to work (they lower the cholesterol pool of the liver, increasing LDL receptor expression, drawing more LDL out of the blood)
|
|
|
Glycerol Phenylbutyrate
|
Prodrug that releases chemical that grabs NH3 from glutamine and is renally excreted; great for treating urea cycle deficiencies
|
|
|
Rifampin
|
Anti TB or prophylactic meningitis treatment; blocks prokaryotic RNA pol complex formation (alpha2, beta and beta prime); can cause tears, sweat and especially urine to turn orange
|
|
|
Alpha-amantin
|
AKA the deathcap mushroom, it's not a drug but a poison; inhibits RNA pol II, the eukaryotic RNA pol that is responsible for mRNA transcription
|
|
|
What would you use as a non specific antidote for weak base overdose (e.g. meth and PCP) and weak acid OD (e.g aspirin)?
|
Weak bases: NH4Cl - ammonium chloride makes the urine acidic, ionizing the weak bases; NaHCO3 - sodium bicarb makes the urine basic; these actions ionize the drug, facilitating renal excretion
|
|
|
Noncompetitive antagonists (5 drugs/groups)?
|
Phenoxybenzamine, digoxin, allopurinol, PPIs, ASA
|
|
|
Drugs with low TI? "high yeild examples"
|
Theophylline, digoxin, warfarin and lithium
|
|
|
Slow acetylaters are at risk of drug-induced SLE with which drugs?
|
Hydralazine, procainamide and isoniazid
|
|
|
Hemicholinium
|
Blocks choline uptake by preganglionic neuron, thereby limiting the production of Ach, resulting in decreased muscarinic/nicotinic stimulation. This is not a drug used clinically.
|
|
|
Botulinum toxin mechanism
|
Binds to synaptobrevin, inhibiting Ca++ from causing vesicle release
|
|
|
Bethanechol
|
Direct acting M agonist; Rx paralytic ileus (esp. postop/neurogenic) and urinary retention; not hydrolyzed well by AChE
|
|
|
Methacholine
|
Direct acting M agonist (M>N); not used therapeutically, just to Dx bronchial hyperreactivity to muscarinics (typical in asthma); it is hydrolyzed by AChE but not nearly as quickly as Ach
|
|
|
Pilocarpine
|
Direct acting M agonist; used topically to induce secretions for xerostomia or miosis for glaucoma; not well hydrolyzed by AChE
|
|
|
Edrophonium
|
AChE inhibitor; reversible; extremely short acting; used to Dx myasthenia vs cholinergic crisis (a desensitization of Ach receptors due to AChE overuse)
|
|
|
Physostigmine
|
AChE inhibitor; reversible; tertiary amine so can pass BBB; used in atropine OD and glaucoma
|
|
|
Neostigmine
|
AChE inhibitor; reversible; quaternary amine so cannot pass BBB; used therapeutically for myasthenia gravis, ileus and urinary retention; also useful for reversing NM blockade used during surgery
|
|
|
Pyridostigmine
|
Just like Neostigmine
|
|
|
Donepezil
|
AChE inhibitor; reversible; used solely for Alzeimers to increase Ach in hippocampus and cortex
|
|
|
Tacrine
|
Like Donepezil, but no longer used
|
|
|
Echothiophate
|
Organophosphate (so irreversible AChE inhibitor) used therapeutically for glaucoma
|
|
|
Malathion
|
Organophosphate (so irreversible AChE inhibitor); used as insecticide so only clinical application would be from poisoning; note that chronic exposure results in demyelination (akin to MS) because it is so lipophilic
|
|
|
Parathion
|
Organophosphate (so irreversible AChE inhibitor); used as insecticide so only clinical application would be from poisoning; note that chronic exposure results in demyelination (akin to MS) because it is so lipophilic
|
|
|
Pralidoxime (aka 2-PAM)
|
Used to recover AChE from organophosphate exposure, only effective if given before "aging" occurs (hydrolysis of organic moeity from the phosphate); organophosphates have a higher affinity for 2-PAM than AChE, so often administered with atropine in organophosphate poisoning
|
|
|
Atropine
|
Antimuscarinic; mainly used as management of organophosphate OD
|
|
|
Tropicamide
|
Antimuscarinic; used in ophthalmology to dilate pupil (is short acting compared to 30+ hour half-life for atropine)
|
|
|
Ipratropium
|
Antimuscarinic; used to treat asthma and COPD, dilates bronchi and decreases secretions without decreasing viscosity (mucous still able to protect); does not enter DNS
|
|
|
Scopolamine
|
Antimuscarinic; used in motion sickness; can cause sedation and anterograde memory loss
|
|
|
Benztropine
|
Antimuscarinic; used in parkinsons
|
|
|
Trihexyphenidyl
|
Antimuscarinic; used in parkinsons
|
|
|
Hexamethonium
|
Ganglion blocker; results in complete blockade of the ANS so each tissue will oppose their dominant disposition (e.g. vessels and sweat glands are predominantly SANS so this would result in vasodilation and anhydrosis; everything else is PANS); MOST IMPORTANTLY: would also block the baroreceptor so drugs that act on vessels will not cause a reflex change in heart rate; note this drug is not used clinically
|
|
|
Mecamylamine
|
Ganglion blocker; results in complete blockade of the ANS so each tissue will oppose their dominant disposition (e.g. vessels and sweat glands are predominantly SANS so this would result in vasodilation and anhydrosis; everything else is PANS); MOST IMPORTANTLY: would also block the baroreceptor so drugs that act on vessels will not cause a reflex change in heart rate; note this drug is not used clinically
|
|
|
alpha 1 affects on liver and kidney
|
Increase glycogenolysis; decreases renin release (think of it as a safety valve, alpha already causes so much vasocontriction, we don't need any more)
|
|
|
alpha 2 affects on platelets and pancreas
|
Increase aggregation (duh, want epi to stop hemorrhage in flight/flight); decrease insulin secretion (duh, want to give glucose to brain and muscle in flight/flight); so these are obviously not good in HTN patients with atherosclerotic plaques (most of them) or DM
|
|
|
beta 1 affects on kidney
|
increase renin release (compliments increased heart rate and contractility - vs alpha which inhibits renin release. Note that beta is more sensitive here but alpha will dominate in high concentrations)
|
|
|
beta 2 affects on liver and kidney
|
Increase gluconeogenesis, glycogenolysis (lipolysis is also increased to provide the energy for this); in the pancreas it slightly increases insulin secretion to help the muscle uptake this new glucose
|
|
|
Fenoldopam
|
D1 agonist; used in sever HTN (I assume to increase RBF to get rid of Na+)
|
|
|
Phenylephrine
|
Direct A1 agonist
|
|
|
Methoxamine
|
Direct A1 agonist; no longer used except to induce a vagal reflex from increased blood pressure to lower the heart rate in patients with paroxysmal atrial tachycardia
|
|
|
Clonidine
|
A2 agonist; used to treat HTN and opiate withdrawl; can cause edema thanks to reflex release of renin
|
|
|
Methyldopa
|
A2 agonist; used to treat HTN; can cause edema thanks to reflex release of renin; highly protein bound so safe for preggers but can cause formation of autoantibodies (positive coombs test)
|
|
|
Isoproterenol
|
B1=B2 agonist
|
|
|
Dobutamine
|
B1>B2 agonist
|
|
|
Albuterol
|
B2 agonist; fast acting bronchodilator
|
|
|
Ritodrine
|
B2 agonist; used to prevent premature labor
|
|
|
Terbutaline
|
B2 agonist; fast acting bronchodilator
|
|
|
Salmeterol
|
B2 agonist; slow acting bronchodilator, used prophylactically
|
|
|
Dopamine
|
D1 at low doses, D1 and B1 at medium doses, D1, B1 and A1 at high doses
|
|
|
Epinephrine
|
A1, A2, B1, B2
|
|
|
Norepinephrine
|
A1, A2, B1
|
|
|
Tyramine
|
Releases catecholamines from mobile pool; usually metabolized by MAOa in the gut and liver (caveat: MAOa inhibitors for depression!)
|
|
|
Amphetamines
|
Releases catecholamines from mobile pool and blocks uptake; treats narcolepsy and ADHD, also a drug of abuse
|
|
|
Ephedrine
|
Rleases catecholamines; used to be used as cold medication
|
|
|
Cocaine
|
Blocks catacholamine reuptake
|
|
|
Doxazosin
|
A1 antagonist; used in HTN or to treat urinary frequency in BPH, can cause first dose sycope and orthostatic HTN
|
|
|
Prazosin
|
A1 antagonist; used in HTN or to treat urinary frequency in BPH, can cause first dose sycope and orthostatic HTN
|
|
|
Terazosin
|
A1 antagonist; used in HTN or to treat urinary frequency in BPH, can cause first dose sycope and orthostatic HTN
|
|
|
Tamsulosin
|
A1 antagonist; I believe this is used in glaucoma
|
|
|
Yohimbine
|
A2 antagonist; very old drug, used in postural hypotension and impotence
|
|
|
Mirtazapine
|
A2 antagonist; antidepressant that also causes weight gain, perfect for a depressed anorexic
|
|
|
Phenoxybenzamine
|
A1 and A2 noncompetitive, irreversible antagonist; DOC for pheochromocytoma;
|
|
|
Phentolamine
|
A1 and A2 competitive antagonist; reversible, only useful in acute HTN episodes
|
|
|
Acebutolol
|
B1 partial agonist; used as class II antiarrhythmic
|
|
|
Atenolol
|
B1 antagonist; least sedative of the beta blockers because it is water soluable
|
|
|
Metoprolol
|
B1 antagonist
|
|
|
Esmolol
|
B1 antagonist; used IV in acute SVTs
|
|
|
Pindolol
|
B1, B2 partial agonist
|
|
|
Propranolol
|
B1, B2 antagonist; very sedative; also inhibits deiodinases making it useful for thyrotoxicosis; used post MI and for SVTs
|
|
|
Timolol
|
B1, B2 antagonist; used to Tx glaucoma
|
|
|
Betaxolol
|
B1, B2 antagonist; used to Tx glaucoma
|
|
|
Labetalol
|
A1, B1, B2 antagonist; used in CHF
|
|
|
Carvedilol
|
A1, B1, B2 antagonist; used in CHF
|
|
|
Quinidine
|
Class 1A Na+ channel blocker (open channels); also has anti muscarinic (can cause torsades) and alpha blocker (reflex tachy also bad) activity; digoxin is normally given with it to decrease risk of arrhythmias
|
|
|
Procainamide
|
Class 1A Na+ channel blocker (open channels); also has anti muscarinic (can cause torsades); it is metabolized by acetyl transferases (caveat: slow acetylators) and is a good hapten (caveat: SLE)
|
|
|
Disopyramide
|
Class 1A Na+ channel blocker (open channels)
|
|
|
Lidocaine (heart)
|
Class 1B Na+ channel blocker (inactivated channels); used post MI to block activity of hypoxic (and therefore depolarized) tissue; also good for dixogin toxicity for the same reason
|
|
|
Mexiletine
|
Oral formulation of lidocain for prescription use, as lidocain has high first pass metabolism
|
|
|
Tocainide
|
Oral formulation of lidocain for prescription use, as lidocain has high first pass metabolism
|
|
|
Flecainide
|
Class 1C Na+ channel blocker (all channels); only used as hail mary if other antiarrythmics don't work
|
|
|
Amiodarone
|
Class III K+ channel blocker; it also mimics all the other classes (Na+ blocker, B blocker and Ca++ blocker); has a ridiculous half life (80 days), is a great hapten (caveat: SLE) and a host of side effects ranging from pulmonary fibrosis, to blue skin and thryoid dysfunction due to the ability to iodinate (amIODarone) sugars.
|
|
|
Sotalol
|
Class III K+ channel blocker; it is also a pretty selective B1 blocker; used in life threatening ventricular arrhythmia
|
|
|
Verapamil
|
Class IV Ca++ channel blocker; used in SVTs; can cause AV block, especially when combined with other nodal drugs like B blockers and digoxin
|
|
|
Diltiazem
|
Class IV Ca++ channel blocker; used in SVTs; can cause AV block, especially when combined with other nodal drugs like B blockers and digoxin
|
|
|
Adenosine
|
Antiarrhythmic; DOC for paroxysmal SVTs; due to its Gi and Gq activity in heart and lung respectively (mimics M) it can cause profound dyspnea; antagonized by theophylline and methylxanthines like caffiene
|
|
|
Mg++
|
Used for torsades, interferes with Ca++ function because it is so similar physically
|
|
|
Reserpine
|
Neuron SANS blocker; used to be used for HTN, destroys NE, DA and 5HT vesicles; caused severe depression so no longer used (was how they found out the mechanism of depression)
|
|
|
Guanethidine
|
Neuron SANS blocker; prevents NE vesicle release; gains entry to axon button through the NE reuptake channel, so is ineffective when TCAs are used concomitantly
|
|
|
Mechanisms by which beta blockers lower BP
|
I'm sure you know decrease heart rate, but a big factor is decreased renin release; remember alpha inhibits renin release while beta stimulates it, by masking beta, alpha predominates
|
|
|
Hydralazine
|
NO mediated vasodilator; only metabolized (it's a prodrug, so activated) in the arterioles; used in severe HTN; highly protein bound so good for preggers but can cause SLE
|
|
|
Nitroprusside
|
NO mediated vasodilator; dilates arterioles and venules; used short term for HTN emergencies due to toxic metabolite CN-; nitrites and thiosulfate help to remove CN by creating methemoglobin and chelating it respectively
|
|
|
Diazoxide
|
Opens ATP mediated K+ channels; hyperpolarizes smooth muscle and beta cells, causing vasodilation and decreased insulin secretion respectively; used in HTN emergencies
|
|
|
Minoxidil
|
Opens ATP mediated K+ channels; depolarizes smooth muscle and beta cells, causing vasodilation and decreased insulin secretion respectively; used in severe HTN; also used topically (it's Rogain) for alopecia
|
|
|
-dipine
|
(e.g. nifedipine) (aka dihydropyridines) Ca++ channel blocker that acts mainly on vessels instead of the heart; used in vasospastic angina; can cause gingival hyperplasia
|
|
|
-pril
|
(e.g. captopril) ACE inhibitors; ACE converts angiotensin 1 to 2 but also inactivates bradykinin so ACEi may lead to inflammation; can cause dry cough and angioedema; protective against diabetic nephropathy (due to increase glomerular pressure) and cardiac remodeling
|
|
|
-sartan
|
(e.g losartan) Angiotensin receptor blockers (ARBs); otherwise similar to ACEi excepting that they do not effect bradykinin inactivation
|
|
|
Aliskiren
|
Renin inhibitor; decreases angiotensinogen conversion to angiotensin
|
|
|
Bosentan
|
Endothelin (more potent version of angiotensin that especially affects pulmonary vasculature) receptor antagonist; oral; used for pulmonary HTN; CI in preggers
|
|
|
Epoprostenol
|
PGI2 analog; IV; used for pulmonary HTN
|
|
|
Sildenafil
|
(aka viagra) Inhibits type V phosphodiesterases, increasing cGMP; causes pulmonary and penis vasodilation; used for pulmonary HTN and ED
|
