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154 Cards in this Set
- Front
- Back
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alpha2 adrenoreceptor agonists- clinical uses
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blood pressure lowering with decreased HR
Sedation |
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clonidine
class, use |
class: alpha2 adrenoreceptor agnoist
use: blood pressure lowering, patch once per week sfx: sedation, dry mouth, bradycardia, rebound withdrawal effects |
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alpha methyldopa
class, use |
drug of choice in pregnancy!
class: alpha2 adrenoreceptor agonist use: blood pressure lowering |
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Dexmedetomidine
class, use |
class: alpha2 adrenoreceptor agonis t
use: sedation |
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alpha 1 adrenergic receptor stimulation- clincial uses
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mediate vasoconstriction, contract vascualr smooth muscle,
post-synaptic receptor, contract smooth muscle in bladder and urethra contract iris dilator muscle, which dilates the pupil |
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selective peripheral alpha 1 adrenoreceptor antagonists- clinical use
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use: hypertension, prostatic hyperplasia
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Prazosin
class, use |
class- selective peripheral alpha 1 blockade
use- hypertension side effects- hypotension, dizziness, headache |
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-osins
class! |
-osins are selective peripheral alpha1 blockade
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Terazosin
class, use |
class- alpha 1 selective antagonist
use- hypertension, benign prostatic hyperplasia |
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Doxasosin
class, use |
class- selective peripheral alpha1 blockade
use- hypertension, benign prostatic hyperplasia |
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nonselective alpha blockade (alpha1 and alpha2) clinical use
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pheocrhomocytoma
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phentolamine
class, use |
class- nonselective alpha blockade
use- pheochromocytoma |
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phenoxybenzamine
class, use |
class- nonselective alpha blockade
use- pheochromocytoma |
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beta1 adrenergic antagonists- clinical use
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reduce heart rate,
slow AV nodal conduction reduce blood pressure |
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beta1 adrenergic agonists- clinical use
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increased chronotropy and inotropy, increased AV node conduction velocity
increased renin release |
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beta2 adrenergic blockade- clinical uses
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1. coronary artery disease
2. tachyarrhythmias 3. congestive heart failure 4. hypertension 5. hypertrophic cardiomyopathy |
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What kind of beta blockers should be avoided in patients with asthma? Why?
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nonselective beta blockers!
blocking beta2 means vasoconstriction |
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propranolol
class, use |
class: nonselective Beta blocker
use: Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
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atenolol
class use |
class- beta1 selective blocker
use: Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
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metroprolol
class, use |
class- beta1 selective blocker
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
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nadolol
class, use |
class- nonselective beta blocker
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
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esmolol
class, use |
class- beta1 selective beta blocker
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
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Labetalol
class, use |
class- beta blocker with alpha1 blcokade
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
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Carvedilol
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class- beta blocker with alpha1 blockade
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
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Among antiarrhythmic drugs, only ______, reduce mortality
during long-term therapy |
beta blockers, maybe amiodarone
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antiarrhythmic mechanism of action- beta blockers
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Decreased phase 4 slope
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antiarrhythmic mechanism of action - Na+ block
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increased threshold
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antiarrhythmic mechanism of action- adenosine, acetylcholine
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increased maximum diastolic potential
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antiarrhythmic mechanism of action- K+ block
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increased action potential duration
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Major risk of K+ blocking drugs
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Torsades de Pointes
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quinidine
class, MOA, use, major ECG change |
Class 1a. Na+ channel blocker, local anesthetics
intermediate time course of recovery, antiarrhythmic increases threshold for AP increases QRS, increases QT used for chronic oral therapy of atrial fib/flutter |
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procainamide
class, MOA, use, major ECG change |
Class 1a. Na+ channel blocker, local anesthetics
intermediate time course of recovery, antiarrhythmic intravenously for supraventricular and ventricular arrhtyhmias increases threshold for AP increases QRS, increases QT |
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lidocaine
class, MOA, use |
Class 1b. Na+ channel blocker, local anesthetics
fast time course of recovery, antiarrhythmic Digitalis toxicity! increases threshold for AP |
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flecainide
class, MOA, use, major ECG change |
Class 1c. Na+ channel blocker, local anesthetic
marked increase in PR, QRS |
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Sotalol- class, use, MOA, ECG changes
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class II anti arrhythmic, beta blocker, increases phase 4, decreased HR, increases PR interval
AND Class III antiarrhythmic, K+ channel blocker, increases QT interval |
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esmolol (as an antiarrhythmic)- class, use, MOA, ECG
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class II anti arrhythmic, beta blocker, increases phase 4, decreased HR, increases PR interval
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amiodarone- class, use, MOA, ECG
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Class III antiarrhythmic, K+ channel blocker, increases QT interval
most powerful drug for refractory VT/VF most effective drug to prevent atrial fibrilaltion/flutter ALL THE CLASSES not first line therapy because of multiple toxicities |
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Verapamil- class, use, MOA, ECG
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class IV antiarrhythmic, Ca++ blocker, increases threshold increases PR interval
great potency for AV nodal blocking no good for WPW syndrome |
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diltiazem- class use, MOA, ECG
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class IV antiarrhythmic, Ca++ blocker, increases threshold increases PR interval
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Adenosine- class use, MOA ECG
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class IV antiarrhythmic,purinergic receptor blocker increases threshold increases PR interval
diagnosis or termination of stable, narrow complex tschycardias not for asthmatics! |
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for any unstable rhythm causing hemodynamic compromise,what is treatment of choice?
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DC cardioversion is treatment of choice
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Great drug for digitalis toxicity?
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lidocaine!
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Verapamil sholud know be used for which individuals?
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wolff-parkinson white syndrome
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What drug majorly interacts with quinidine, verapamil, and amiodarone?
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DIGITALIS
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What antiarrhythmic shouldn't be given to people with renal disease?
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Sotalol
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What are the drug interactions for amiodarone?
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warfarin
digoxin statins quinidine |
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Lidocaine should not be given for which people?
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Liver disease and heart failure
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-pril designates what kind of drugs
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ACE inhibitors!
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pharmacological effects of ACE inhibitors
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reduce arterial pressure
Promotes Na+ excretion Reduces adverse ventricular remodeling Promotes brady kinin1 |
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Clinical indications of ACE inhibitors
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hypertension
congestive heart failure diabetic nephropathy ischemic heart disease |
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ACE inhibitors for hypertension!
*How work *good for which people? |
lowers BP by reducing systemic vascular resistance without increasing heart rate
good for HIGH renin/normal-rto-high renin |
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ACE inhibitors for CHF
*how work |
reduce after load
increase CO without increasing HR increase renal plasma, increase Na+ excretion increase K+ |
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Ace inhibitors for diabetic nephropathy
*how work |
decrease glomerular capillary pressure, decrease proteinuria
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adverse effects for ACE inhibitors
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fetal anomalies
cough angioedema hypotension hyperkalemia renal insufficiency |
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Adverse effects of ARBs
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hypotension, hyperkalemia, no pregnant ladies
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hydralazine
class, use watch out for ___ |
arterial vasodilator
hypertension, heart failure good in combination with other drugs DRUG INDUCED LUPUS |
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hydralazine
class, use |
arterial vasodilator
good for severe hypertension rogaine! used in combination with other diuretics |
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Neseritide
use, |
natruretic peptide
secreted from atrium and ventricles under stress increases vasodilation, Na+/water excretion, decreases activation ofRA used for decompensated congestive heart failure |
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sildenafil
MOA, use |
dectreases pulmonary vascular resistance in primary pulmonary hypertension
phosphodiesterase 5 inhibitor |
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Carbachol
Use, classification |
Carbon copy of acetylcholine!
cholinomimetic agent used for glaucoma, pupillary contraction, and relief of intracoular pressure |
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Bethanechol
use, classification |
Bethany, call me, maybe, if you want to activate your bowels and bladder.
Activates bowel and bladder smooth muscle, resistant to Acetylcholinesterase. Use: postoperative ileus, neurogenic ileus, urinary retention |
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Pilocarpine
use, classification |
You cry, drool, and sweat on your pillow.
COntracts ciliary muscle of eye (open-angle glaucoma), potent stimulator of sweat, tears, and salva. Open angle and closed angle claucoma |
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Methacholine
Challenge test for what? |
Challenge test for asthma! Stimulates muscarinic receptors in brain when activated
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Pralidoxime
use? MOA? |
war gas! Sarin! (inTOXicatrion)
counters cholinesterase inhibitor intoxication by reactivating the cholinesterase enzyme. |
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Neostigmine
MOA, use |
Neo CNS= No cns penetration
indirect agonist (anticholinesterase) Anticholinesterases. Increases ACh good for postoperative and neurogenic ileus, urinar y retention, myestenia gravis, |
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Physostigmine
MOA, use |
Atrophine overdose. Increases endogenous Ach, anticholinergic toxcity.
Anticholinesterase |
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Pyridostigmine
MOA, use |
Pyridostigmine gets rid of myastehnia gravis.
Anticholinesterases. Increases ACh |
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Insecticides and war gases
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Cholinesterase inhibitor! Cholinesterase is irreversibly inhibited
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Epinephrine:
Which of these does it stimulate: α1, α2, β1, β2, D1 Applications? |
α1, α2, β1, β2
Anaphylaxis, glaucoma, asthma, hypotension |
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Norepinephrine:
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
α1, α2, β1,
Hypotension! |
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Isoprotenerol
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
beta1 and beta2 only
tordsade de points, bradyarrythmias |
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Dopamine
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
LOW DOSE *renal dose*: D1 only
Med dose: b1 and b2 HIGH DOSE: alpha1, alpha2 shock, heart failure, inotropic, chronotropic |
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Dobutamine
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
α1, α2, β1, β2,
MOSTLY BETA1 Heart failure, cardiac stress testzz |
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Phenylephrine
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
α1, α2,
Hypotension! Rhinitis |
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-olol drugs do what?
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beta agonist!
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-terol drugs do what?
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beta 2 antagonist!
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Digoxin
Use? |
Inotropic agent
cardiac glycoside |
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-pril drugs do what?
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ACE inhibitors!
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Digoxin- cllinical use, mechanism, toxicity
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clinica use -- increase contractility in CHF, decrease AV node conduction (atrial fibrillatino)
direct inhibition of Na+/K+ ATPase, leads to direct inhibition of Na+/Ca++ exchangers toxicity --> increase PR, decrease QT, ST scooping, AV block, arrhythmia nausa, vomiting, diarrhea, blurry yellow vision |
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pharmacologic treatment of essential HT
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diuretics, Ace-I, ARBs, Ca channel blockers
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pharmacologic treatment of CHF
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diuretics, ace i/arb, beta blockers, K+ sparing diuretics
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Nifedipine
class use toxicity |
block Ca++ channels in heart, reduce muscle contractility
use- HT, angina, reynaud's toxicity- cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
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verapamil
class use toxicity |
block Ca++ channels in heart, reduce muscle contractility
use- HT, angina, arrythmias, reynaud's toxicity- cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation toxicity- cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
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diltiazem
class use toxicity |
block Ca++ channels in heart, reduce muscle contractility
use- HT, angina, arrythmias, reynaud's toxicity- cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
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amplodipine
class use toxicity |
block Ca++ channels in heart, reduce muscle contractility
use- HT, angina, arrythmias, reynaud's toxicity- cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
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Nitroprusside
class use toxicity |
malignant hypertension!
direct NO release! NitrOprusside |
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Nitroglycerin
class use |
NO releaser! vasodilate, veins >> arteries. decreases PRELOAD
angina, pulmonary edema |
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Isorbide dinitrate, isorbide mononitrate
class use |
NO releaser! vasodilate, veins >> arteries. decreases PRELOAD
angina, pulmonary edema |
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lovastatin
pravastatin simvastatin atorvastatin rosuvastatin effect on LDL, HDL, triglycerides MOA |
Decreases bad cholesterol and TG
increases good cholesterol inhibits conversion of HMG-CoA to mevalonate, a cholesterol precursor HMG-CoA reductase inhibitors |
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Cholestarymine
effect on LDL, HDL, triglycerides MOA |
decreases LDL,
prevents intestinal absorption of bile acids, liver must use cholesterol to make more |
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Ezetimibe
effect on LDL, HDL, triglycerides MOA |
decreases LDL
prevents cholesterol reabsorption at small intestine brush border. cholesterol absorption blockers |
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fenofibrate
effect on LDL, HDL, triglycerides MOA |
upregulates LPL, increased triglyceride clearance
REALLY decreases TG |
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Niacin (vitamin B3)
effect on LDL, HDL, triglycerides MOA |
decreases bad cholesterol, increases good cholesterol.
inhibits lipolysis in adipose tissue, reduces hepatic VLDL secretion |
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What's the gene target for CML?
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BCR/ABL
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Common mechanism of action of chemotherapy
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anticancer drugs interfere with some mportant step in cellular replication.
This triggers the cell to stop in G1=S phase of cell cycle, where it needs to repair itself or gets stuck in apopotosis All chemo drugs work by initiating programmed cell death |
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General principles of chemotherapy
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use combinations of active trigs
use drugs which are active when used alone use drug combinations with non-overlapping toxicity give several treatments in cycles |
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Differentiate between induction, adjuvant, and neoadjuvant chemotherapy. What are they, and what are the outcome measures?
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induction --> chemotherapy used as the major treatment modality. Measures: response rate, survival, QOL
adjuvant --> given after potentially curative surgery or radiation, designed to kill remaining tumor cells which are not detected by exam, imaging. measure: survival neoadjuvant: given before surgery or radiation to make the surgery easier or less extensive. Measure: survival, QOL |
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Cyclophosphamide
class, use, toxicity |
alkylating agent!
Adds carbon groups to DNA. Interacts with DNA at N7 position of guanine solid tumors, leukemia, lymphoma myelosuppression, hemorrhagic cystitis |
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Cisplatin, carboplatinum
class, use, toxicity |
Platinum drugs. Cross link DNA.
Testicular, bladder, ovary, lung cancer nephrotoxicity, acoustic nerve dmaage |
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Doxorubicin /Anthracyclines
class, use, toxicity |
Topoisomerase II inhibiitor. generates free radicals. Noncovalently breaks in DNA so decreased replication
Solid tumors, leukemias, lymphomas CARDIAC TOXICITY |
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Etoposide/epipodophyllotoxins
class, use, toxicity |
Topoisomerse II inhibitors:
generates free radicals. Noncovalently breaks in DNA so decreased replication Solid tumors, leukemias, lymphomas CARDIAC TOXICITY |
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Irinotecan
class/use/toxicity |
topoisomerase I inhibitor, prevents DNA from unwinding
colon cancer |
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Methotrexate
class/use/toxicity |
Antimetabolite, interferes with basic building blocks of DNA
decreased DNA and protein synthesis folic acid analog that inhibits dihydrofolate reductase decreased |
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5-FU, cytosine arabinoside, capcitabine
class/use/toxicity |
antimetabolite pyrimidine analog, inhibits dna and protein synthesis.
colon cancer, basal cell carcinoma myelosuppression, photosensitivity |
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Vincristine
class/use/toxicity |
Microtubules are vines of your cells
Microtubule binding agents solid tumors, leukemias, lymphoma neurotoxicity |
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Taxanes- Paclitaxel
class/use/toxicity |
microtubule inhibitors --> stick mitotic spindle in M phase, so it can't break down, anaphase can't occur
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Tamoxifem
class/use/toxicity |
receptor antagonist in breast, blocks binding of estrogen to estrogen receptor-positive cells
breast cancer treatment and prevention |
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Aromatase inhibitors
class/use/toxicity |
block formation of estrogen. Can't work on ovary, but block in adrenal and fatty tissue.
better than tamoxifem in post-menopausal women in metastatic breast cancer |
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LHRH agonists- Leuprolide
class/use/toxicity |
LHRH is a hormone released to stimulate FSH and LH
pituitary gets exhausted, no longer makes FSH or LH, no more testosterone or estrogen! men with prostate cancer! premenopausal women with breast cancer! |
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Imatinab,
class/use/toxicity |
tyrosine kinase inhibitor, GLEEVEC
imatinib--> BCR/ABL |
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erlotinib
class/use/toxicity |
tyrosine kinase inhibitors
EGFR inhibitor diarrhea, skin rash common within first 2 month, no |
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sorafanib
class/use toxicity |
inhibitor of VEGF tryosine kinase, RAF kinase
oral! renal cell cancers, hand foot syndrome, skin rash |
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Rituximab
class/use/toxicity |
monoclonal antibody against CD20, B-cell neoplasms
non hodgkins lymphoma MYOCLONAL ANTIBODY |
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bevacizumab
class/use |
monoclonal antibody against VEGF, inhibits angiogenesis
solid tumors |
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everolimus
class/use |
MTOR inhibitors
renal cell, neuroendocrine cancer, |
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aspirin- mechanism of action
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COX-1 and COX-2 inhibitor, irreversibly. platelets can't make new enzyme so effect lasts until new platelets are produed.
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heparin
MOA how is it monitored? |
activates antithrombin, which decreases action of IIa and factor Xa
monitored via PTT (intrinsic pathway) anticoagulant |
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warfarin
MOA how is it monitored? |
impairs synthesis of vitamin-K dependent clotting factors II, VII, IX, X
PT/INR (extrinsic pathway) |
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ondasetron
what drug i take sometimes . . . |
zofran!
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flutamide
class/use. |
hormonal therapy, for prostate cancer, competitive testosterone inhibitor
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taxanes- paclitaxel
class |
microtubulin inhibitors-- keeps microtubules stuck in assembly
Taxol!!!! ovarian, breast, all sorts of caners |
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clopidogrel
class/use |
inhibits platelet aggregation, blocks ADP receptors.
stops fibrinogen binding, prevetns glycoprotein 2b/3a from binding to fibrinogen good for acute coronary syndrome, coronary stunting, |
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dabigatran
classs/use |
oral, direct thrombin inhibitor
oran anticoagulant |
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captopril
class/use/side effect |
ACE inhibitor
inhibits conversion of angiotensin 1 to angiotensin 2 --> decreases GFR by preventing constriction of efferent arterioles. prevents inactivation of bradykinin hypertension/CHF, proteinuria, diabetic renal disease cough, angioedema, teratogen, hyperkalemia, |
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lisinopril
class/use/side effect |
ACE inhibitor
inhibits conversion of angiotensin 1 to angiotensin 2 --> decreases GFR by preventing constriction of efferent arterioles. prevents inactivation of bradykinin hypertension/CHF, proteinuria, diabetic renal disease cough, angioedema, teratogen, hyperkalemia, |
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site of action of loop diuretics
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thick ascending limb
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site of action of thiazide diuretics
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distal convoluted tubule
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site of action of potassium-sparing diuretics
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collecting tubule
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furosemide
mechanism/clinical use/toxicity |
inhibits cotransport system (Na+, K+, 2 Cl-)
THICK ASCENDING LIMB of henle messes up the hypertonicity of the medula, which means that urine can't be concentrated. It stimulates PGE release Increases Ca++ excretion. loops lose calcium. used for *CHF, cirrhosis, nephrotic sysndrome, pulmonary edema, hypertension, hypercalcemia Toxicity: Ototoxicity, hypokalemia, dehydration, allergy, nephritis, gout |
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Hydrochlorothiazide
mechanism/clinical use/toxicity |
inhibits NaCl in EARLY DISTAL TUBULE, which makes the nephron not so great at diluting urine. decreases ca++ excretion.
use: hypertension, CHF, idiopathic hypercalciuria, nephrogenic DI toxicity: hypokalemia, hyperglycemia, hyperlipidemia, hypercalcemia |
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Amiloride
mechanism/clinical use/toxicity |
K+ sparing diuretic! Blocks Na+ channels in the cortical collecting tubule.
CORTICAL COLLECTING TUBULE Used for: hyperaldosteronism, CHF, hypokalemia |
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triamterene
mechanism/clinical use/toxicity |
K+ sparing diuretic
Works on CORTICAL COLLECTING TUBULE blocks Na+ channels used for CHF, hyperaldosteronism, K+ depletion watch out for hyperkalemia |
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Spironolactone
mechanism/clinical use/toxicity |
K+ sparing diuretic!!!!!!
Works on CORTICAL COLLECTING TUBULE! competitive inhibitor of aldosterone! used for CHF, hyperaldosteronism, K+ depletion watch out for hyperkalemia |
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Effect of diuretics on
urine NaCl urine K+ blood pH urine Ca++ |
urine NaCl= UP
urine K+= UP for everything except for K+ sparing blood pH= UP for loops and thiazide, DOWN for K+ sparing urine Ca++= UP with loops, DOWN with thiazide |
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Kayexalate
mechanism/clinical use/toxicity |
used for hyperkalemia
acute and chronic kidney disease, can suffer from irregular heartbeat |
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Acetazolamide
mechanism/use/toxicity |
carbonic anhydrase inhibitor.
messes with bicarb reabsorption in kidneys, alkalyzes urine good for diuresis in CHF |
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CD19 cells are expressing what?
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B cells
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are + for what?
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Chronic MY
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reserpine
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sympathetic nerve antagonist
inhibits norepinephrine uptake lowers BP |
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effects of Na+ channel blocking drugs
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slowed conduction in fast response tissue --> increased QRS duration on ECG
increased refractoriness, terminates reentry, allows less room for premature beats increased threshold increase automaticity, increase PR interval |
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effects of beta-adrenergic blocking drugs on arrhythmias
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decreases phase 4 slope.
decreases SA nodal automaticity and sinus rate increases PR interval, slows AV nodala conduction |
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effects of K+ channel block on arrhythmias
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increased QT interval and refractoriness
decreases normal automaticity watch out for torsades de pointes! |
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Ca++ channel block effect on arrhythmias
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slows conduction, sinus rate, increases PR interval
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clinical indications for ACE inhibitors
|
HT
CHF diabetic nephropathy primary and secondary MI prevention |
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adverse effects of ace inhibitors
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no pregnant!
cough angioedema hyperkalemia renal perfusion |
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Clinical use of hydralazine
what s |
arterial vasodilator, used for severe HT and heart failure.
Bidil! combo with beta blockers, diuretics, nitrates watch out for lupus! |
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minoxidil clinical use, watch out!
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minoxile is an arterial vasodilator!
great for hypertension that's mad severe |
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Adenosine clinical use!
What shouldn't it be used for? |
Purine nucleoside, vasodilator, short half life, diagnosis or termination of stable, narrow, complex tachycardias
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Are CCB's better for low or high renin HT?
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low renin! (AA's)
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Best drug for supraventricular tachycardia?
|
Calcium channel blocker!
diltiazem, verapamil |
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best drug for subarachnoid hemorrhage
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Nimodipine
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What is streptokinase?
How does it work? fibrin specific? elimination time? immunogenic? Adverse effects? |
natural bacterial protein
indirectly activates plasminogen non-fibrin specific immunogenic long elimination adverse effects! |
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t-PA
how does it work? fibrin specific? elimination time? immunogenic? Adverse effects? |
recombinant human protein
directly activates plasminogen fibrin specific non-immunogenic shorter elimination time well-tolerated, bleeding |
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What are the typical uses for thrombolytics?
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Acute MI
Acute ischemic stroke Acute arterial thrombo-occlusion Manstem pulmonary embolism Thrombosed prosthetic valves Thrombosed AV shunts |
