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;
154 Cards in this Set
- Front
- Back
alpha2 adrenoreceptor agonists- clinical uses
|
blood pressure lowering with decreased HR
Sedation |
|
clonidine
class, use |
class: alpha2 adrenoreceptor agnoist
use: blood pressure lowering, patch once per week sfx: sedation, dry mouth, bradycardia, rebound withdrawal effects |
|
alpha methyldopa
class, use |
drug of choice in pregnancy!
class: alpha2 adrenoreceptor agonist use: blood pressure lowering |
|
Dexmedetomidine
class, use |
class: alpha2 adrenoreceptor agonis t
use: sedation |
|
alpha 1 adrenergic receptor stimulation- clincial uses
|
mediate vasoconstriction, contract vascualr smooth muscle,
post-synaptic receptor, contract smooth muscle in bladder and urethra contract iris dilator muscle, which dilates the pupil |
|
selective peripheral alpha 1 adrenoreceptor antagonists- clinical use
|
use: hypertension, prostatic hyperplasia
|
|
Prazosin
class, use |
class- selective peripheral alpha 1 blockade
use- hypertension side effects- hypotension, dizziness, headache |
|
-osins
class! |
-osins are selective peripheral alpha1 blockade
|
|
Terazosin
class, use |
class- alpha 1 selective antagonist
use- hypertension, benign prostatic hyperplasia |
|
Doxasosin
class, use |
class- selective peripheral alpha1 blockade
use- hypertension, benign prostatic hyperplasia |
|
nonselective alpha blockade (alpha1 and alpha2) clinical use
|
pheocrhomocytoma
|
|
phentolamine
class, use |
class- nonselective alpha blockade
use- pheochromocytoma |
|
phenoxybenzamine
class, use |
class- nonselective alpha blockade
use- pheochromocytoma |
|
beta1 adrenergic antagonists- clinical use
|
reduce heart rate,
slow AV nodal conduction reduce blood pressure |
|
beta1 adrenergic agonists- clinical use
|
increased chronotropy and inotropy, increased AV node conduction velocity
increased renin release |
|
beta2 adrenergic blockade- clinical uses
|
1. coronary artery disease
2. tachyarrhythmias 3. congestive heart failure 4. hypertension 5. hypertrophic cardiomyopathy |
|
What kind of beta blockers should be avoided in patients with asthma? Why?
|
nonselective beta blockers!
blocking beta2 means vasoconstriction |
|
propranolol
class, use |
class: nonselective Beta blocker
use: Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
|
atenolol
class use |
class- beta1 selective blocker
use: Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
|
metroprolol
class, use |
class- beta1 selective blocker
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
|
nadolol
class, use |
class- nonselective beta blocker
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
|
esmolol
class, use |
class- beta1 selective beta blocker
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
|
Labetalol
class, use |
class- beta blocker with alpha1 blcokade
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
|
Carvedilol
|
class- beta blocker with alpha1 blockade
use- Angina, arrhythmias, CHF, MI, hypertension, hypertrophic cardiomyopathy |
|
Among antiarrhythmic drugs, only ______, reduce mortality
during long-term therapy |
beta blockers, maybe amiodarone
|
|
antiarrhythmic mechanism of action- beta blockers
|
Decreased phase 4 slope
|
|
antiarrhythmic mechanism of action - Na+ block
|
increased threshold
|
|
antiarrhythmic mechanism of action- adenosine, acetylcholine
|
increased maximum diastolic potential
|
|
antiarrhythmic mechanism of action- K+ block
|
increased action potential duration
|
|
Major risk of K+ blocking drugs
|
Torsades de Pointes
|
|
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 |
|
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 |
|
lidocaine
class, MOA, use |
Class 1b. Na+ channel blocker, local anesthetics
fast time course of recovery, antiarrhythmic Digitalis toxicity! increases threshold for AP |
|
flecainide
class, MOA, use, major ECG change |
Class 1c. Na+ channel blocker, local anesthetic
marked increase in PR, QRS |
|
Sotalol- class, use, MOA, ECG changes
|
class II anti arrhythmic, beta blocker, increases phase 4, decreased HR, increases PR interval
AND Class III antiarrhythmic, K+ channel blocker, increases QT interval |
|
esmolol (as an antiarrhythmic)- class, use, MOA, ECG
|
class II anti arrhythmic, beta blocker, increases phase 4, decreased HR, increases PR interval
|
|
amiodarone- class, use, MOA, ECG
|
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 |
|
Verapamil- class, use, MOA, ECG
|
class IV antiarrhythmic, Ca++ blocker, increases threshold increases PR interval
great potency for AV nodal blocking no good for WPW syndrome |
|
diltiazem- class use, MOA, ECG
|
class IV antiarrhythmic, Ca++ blocker, increases threshold increases PR interval
|
|
Adenosine- class use, MOA ECG
|
class IV antiarrhythmic,purinergic receptor blocker increases threshold increases PR interval
diagnosis or termination of stable, narrow complex tschycardias not for asthmatics! |
|
for any unstable rhythm causing hemodynamic compromise,what is treatment of choice?
|
DC cardioversion is treatment of choice
|
|
Great drug for digitalis toxicity?
|
lidocaine!
|
|
Verapamil sholud know be used for which individuals?
|
wolff-parkinson white syndrome
|
|
What drug majorly interacts with quinidine, verapamil, and amiodarone?
|
DIGITALIS
|
|
What antiarrhythmic shouldn't be given to people with renal disease?
|
Sotalol
|
|
What are the drug interactions for amiodarone?
|
warfarin
digoxin statins quinidine |
|
Lidocaine should not be given for which people?
|
Liver disease and heart failure
|
|
-pril designates what kind of drugs
|
ACE inhibitors!
|
|
pharmacological effects of ACE inhibitors
|
reduce arterial pressure
Promotes Na+ excretion Reduces adverse ventricular remodeling Promotes brady kinin1 |
|
Clinical indications of ACE inhibitors
|
hypertension
congestive heart failure diabetic nephropathy ischemic heart disease |
|
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 |
|
ACE inhibitors for CHF
*how work |
reduce after load
increase CO without increasing HR increase renal plasma, increase Na+ excretion increase K+ |
|
Ace inhibitors for diabetic nephropathy
*how work |
decrease glomerular capillary pressure, decrease proteinuria
|
|
adverse effects for ACE inhibitors
|
fetal anomalies
cough angioedema hypotension hyperkalemia renal insufficiency |
|
Adverse effects of ARBs
|
hypotension, hyperkalemia, no pregnant ladies
|
|
hydralazine
class, use watch out for ___ |
arterial vasodilator
hypertension, heart failure good in combination with other drugs DRUG INDUCED LUPUS |
|
hydralazine
class, use |
arterial vasodilator
good for severe hypertension rogaine! used in combination with other diuretics |
|
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 |
|
sildenafil
MOA, use |
dectreases pulmonary vascular resistance in primary pulmonary hypertension
phosphodiesterase 5 inhibitor |
|
Carbachol
Use, classification |
Carbon copy of acetylcholine!
cholinomimetic agent used for glaucoma, pupillary contraction, and relief of intracoular pressure |
|
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 |
|
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 |
|
Methacholine
Challenge test for what? |
Challenge test for asthma! Stimulates muscarinic receptors in brain when activated
|
|
Pralidoxime
use? MOA? |
war gas! Sarin! (inTOXicatrion)
counters cholinesterase inhibitor intoxication by reactivating the cholinesterase enzyme. |
|
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, |
|
Physostigmine
MOA, use |
Atrophine overdose. Increases endogenous Ach, anticholinergic toxcity.
Anticholinesterase |
|
Pyridostigmine
MOA, use |
Pyridostigmine gets rid of myastehnia gravis.
Anticholinesterases. Increases ACh |
|
Insecticides and war gases
|
Cholinesterase inhibitor! Cholinesterase is irreversibly inhibited
|
|
Epinephrine:
Which of these does it stimulate: α1, α2, β1, β2, D1 Applications? |
α1, α2, β1, β2
Anaphylaxis, glaucoma, asthma, hypotension |
|
Norepinephrine:
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
α1, α2, β1,
Hypotension! |
|
Isoprotenerol
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
beta1 and beta2 only
tordsade de points, bradyarrythmias |
|
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 |
|
Dobutamine
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
α1, α2, β1, β2,
MOSTLY BETA1 Heart failure, cardiac stress testzz |
|
Phenylephrine
Which of these does it stimulate? α1, α2, β1, β2, D1 Applications? |
α1, α2,
Hypotension! Rhinitis |
|
-olol drugs do what?
|
beta agonist!
|
|
-terol drugs do what?
|
beta 2 antagonist!
|
|
Digoxin
Use? |
Inotropic agent
cardiac glycoside |
|
-pril drugs do what?
|
ACE inhibitors!
|
|
Digoxin- cllinical use, mechanism, toxicity
|
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 |
|
pharmacologic treatment of essential HT
|
diuretics, Ace-I, ARBs, Ca channel blockers
|
|
pharmacologic treatment of CHF
|
diuretics, ace i/arb, beta blockers, K+ sparing diuretics
|
|
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 |
|
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 |
|
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 |
|
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 |
|
Nitroprusside
class use toxicity |
malignant hypertension!
direct NO release! NitrOprusside |
|
Nitroglycerin
class use |
NO releaser! vasodilate, veins >> arteries. decreases PRELOAD
angina, pulmonary edema |
|
Isorbide dinitrate, isorbide mononitrate
class use |
NO releaser! vasodilate, veins >> arteries. decreases PRELOAD
angina, pulmonary edema |
|
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 |
|
Cholestarymine
effect on LDL, HDL, triglycerides MOA |
decreases LDL,
prevents intestinal absorption of bile acids, liver must use cholesterol to make more |
|
Ezetimibe
effect on LDL, HDL, triglycerides MOA |
decreases LDL
prevents cholesterol reabsorption at small intestine brush border. cholesterol absorption blockers |
|
fenofibrate
effect on LDL, HDL, triglycerides MOA |
upregulates LPL, increased triglyceride clearance
REALLY decreases TG |
|
Niacin (vitamin B3)
effect on LDL, HDL, triglycerides MOA |
decreases bad cholesterol, increases good cholesterol.
inhibits lipolysis in adipose tissue, reduces hepatic VLDL secretion |
|
What's the gene target for CML?
|
BCR/ABL
|
|
Common mechanism of action of chemotherapy
|
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 |
|
General principles of chemotherapy
|
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 |
|
Differentiate between induction, adjuvant, and neoadjuvant chemotherapy. What are they, and what are the outcome measures?
|
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 |
|
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 |
|
Cisplatin, carboplatinum
class, use, toxicity |
Platinum drugs. Cross link DNA.
Testicular, bladder, ovary, lung cancer nephrotoxicity, acoustic nerve dmaage |
|
Doxorubicin /Anthracyclines
class, use, toxicity |
Topoisomerase II inhibiitor. generates free radicals. Noncovalently breaks in DNA so decreased replication
Solid tumors, leukemias, lymphomas CARDIAC TOXICITY |
|
Etoposide/epipodophyllotoxins
class, use, toxicity |
Topoisomerse II inhibitors:
generates free radicals. Noncovalently breaks in DNA so decreased replication Solid tumors, leukemias, lymphomas CARDIAC TOXICITY |
|
Irinotecan
class/use/toxicity |
topoisomerase I inhibitor, prevents DNA from unwinding
colon cancer |
|
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 |
|
5-FU, cytosine arabinoside, capcitabine
class/use/toxicity |
antimetabolite pyrimidine analog, inhibits dna and protein synthesis.
colon cancer, basal cell carcinoma myelosuppression, photosensitivity |
|
Vincristine
class/use/toxicity |
Microtubules are vines of your cells
Microtubule binding agents solid tumors, leukemias, lymphoma neurotoxicity |
|
Taxanes- Paclitaxel
class/use/toxicity |
microtubule inhibitors --> stick mitotic spindle in M phase, so it can't break down, anaphase can't occur
|
|
Tamoxifem
class/use/toxicity |
receptor antagonist in breast, blocks binding of estrogen to estrogen receptor-positive cells
breast cancer treatment and prevention |
|
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 |
|
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! |
|
Imatinab,
class/use/toxicity |
tyrosine kinase inhibitor, GLEEVEC
imatinib--> BCR/ABL |
|
erlotinib
class/use/toxicity |
tyrosine kinase inhibitors
EGFR inhibitor diarrhea, skin rash common within first 2 month, no |
|
sorafanib
class/use toxicity |
inhibitor of VEGF tryosine kinase, RAF kinase
oral! renal cell cancers, hand foot syndrome, skin rash |
|
Rituximab
class/use/toxicity |
monoclonal antibody against CD20, B-cell neoplasms
non hodgkins lymphoma MYOCLONAL ANTIBODY |
|
bevacizumab
class/use |
monoclonal antibody against VEGF, inhibits angiogenesis
solid tumors |
|
everolimus
class/use |
MTOR inhibitors
renal cell, neuroendocrine cancer, |
|
aspirin- mechanism of action
|
COX-1 and COX-2 inhibitor, irreversibly. platelets can't make new enzyme so effect lasts until new platelets are produed.
|
|
heparin
MOA how is it monitored? |
activates antithrombin, which decreases action of IIa and factor Xa
monitored via PTT (intrinsic pathway) anticoagulant |
|
warfarin
MOA how is it monitored? |
impairs synthesis of vitamin-K dependent clotting factors II, VII, IX, X
PT/INR (extrinsic pathway) |
|
ondasetron
what drug i take sometimes . . . |
zofran!
|
|
flutamide
class/use. |
hormonal therapy, for prostate cancer, competitive testosterone inhibitor
|
|
taxanes- paclitaxel
class |
microtubulin inhibitors-- keeps microtubules stuck in assembly
Taxol!!!! ovarian, breast, all sorts of caners |
|
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, |
|
dabigatran
classs/use |
oral, direct thrombin inhibitor
oran anticoagulant |
|
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, |
|
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, |
|
site of action of loop diuretics
|
thick ascending limb
|
|
site of action of thiazide diuretics
|
distal convoluted tubule
|
|
site of action of potassium-sparing diuretics
|
collecting tubule
|
|
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 |
|
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 |
|
Amiloride
mechanism/clinical use/toxicity |
K+ sparing diuretic! Blocks Na+ channels in the cortical collecting tubule.
CORTICAL COLLECTING TUBULE Used for: hyperaldosteronism, CHF, hypokalemia |
|
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 |
|
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 |
|
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 |
|
Kayexalate
mechanism/clinical use/toxicity |
used for hyperkalemia
acute and chronic kidney disease, can suffer from irregular heartbeat |
|
Acetazolamide
mechanism/use/toxicity |
carbonic anhydrase inhibitor.
messes with bicarb reabsorption in kidneys, alkalyzes urine good for diuresis in CHF |
|
CD19 cells are expressing what?
|
B cells
|
|
are + for what?
|
Chronic MY
|
|
reserpine
|
sympathetic nerve antagonist
inhibits norepinephrine uptake lowers BP |
|
effects of Na+ channel blocking drugs
|
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 |
|
effects of beta-adrenergic blocking drugs on arrhythmias
|
decreases phase 4 slope.
decreases SA nodal automaticity and sinus rate increases PR interval, slows AV nodala conduction |
|
effects of K+ channel block on arrhythmias
|
increased QT interval and refractoriness
decreases normal automaticity watch out for torsades de pointes! |
|
Ca++ channel block effect on arrhythmias
|
slows conduction, sinus rate, increases PR interval
|
|
clinical indications for ACE inhibitors
|
HT
CHF diabetic nephropathy primary and secondary MI prevention |
|
adverse effects of ace inhibitors
|
no pregnant!
cough angioedema hyperkalemia renal perfusion |
|
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! |
|
minoxidil clinical use, watch out!
|
minoxile is an arterial vasodilator!
great for hypertension that's mad severe |
|
Adenosine clinical use!
What shouldn't it be used for? |
Purine nucleoside, vasodilator, short half life, diagnosis or termination of stable, narrow, complex tachycardias
|
|
Are CCB's better for low or high renin HT?
|
low renin! (AA's)
|
|
Best drug for supraventricular tachycardia?
|
Calcium channel blocker!
diltiazem, verapamil |
|
best drug for subarachnoid hemorrhage
|
Nimodipine
|
|
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! |
|
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 |
|
What are the typical uses for thrombolytics?
|
Acute MI
Acute ischemic stroke Acute arterial thrombo-occlusion Manstem pulmonary embolism Thrombosed prosthetic valves Thrombosed AV shunts |