CVS pharmacology Flashcards
what is an ionotrope?
an ionotrope is an agent that alters the force or energy of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions.
Positively inotropic agents increase the strength of muscular contraction.
what is a chronotrope?
chronotropes are agents that change the HR. chronotropic drugs may change the HR by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node.
Positive chronotropes increase heart rate
negative chronotropes decrease heart rate.
what is a dromotrope?
A dromotrope is an agent that affects AV nodal conduction.
A positive dromotrope increases AV nodal conduction.
A negative dromotrope decreases AV nodal conduction.
what is lusitropy?
lusitropy is myocardial relaxation. A lusitrope affects diastolic relaxation.
catecholamines are positive lusitropes, they incr. rate of relaxation
negative lusitropy is due to:
- Ca2+ overload
- reduced rate of Ca2+ removal through Ca2+ ATPas and/or Na+/Ca2+ exchanger
- impaired sarco-endoplasmic reticulum Ca2+ ATPase
What are the 5 classes of antiarrhythmic drugs?
- Class 1- sodium channel blockers
- Class 2- ß-blockers
- Class 3- potassium channel blockers
- Class 4- calcium channel blockers
- Class 5-other
when treating start with class I and ascend as needed
What are the class I antiarrhythmics (sodium channel blockers)?
Procainamide
Quinidine
Disopyramide
Lidocaine
Mexiletine
Phenytoin
Flecainide
Propafenone
Class: Class IA antiarrhythmic
MOA: it blocks Na+ channels slowing the upstroke of the AP, slowing conduction, and prolonging the QRS duration of the ECG. it decreases ventricular conduction (incr. QRS interval on ECG) and prolongs ventricular AP (incr. QRS interval on ECG)
it has ganglion blocking properties that decr. peripheral resistance, but these effects are not very prominent
Use: treats atrial and ventricular arrythmias
Route of admin.: oral, IV, and IM
Toxicity: drug-induced lupus and induction of torsades de pointes arrythmia and syncope (shown). rare side effect is hypotension due to excessively rapid infusion or left ventricular dysfunction.
what is the drug?
Procainamide
Procainamide is a Class IA antiarrythmic.
Procainamide: blocks Na+ channels slowing the upstroke of the AP, slowing conduction, and prolonging the QRS duration of the ECG. it decreases ventricular conduction (incr. QRS interval on ECG) and prolongs ventricular AP (incr. QRS interval on ECG)
Procainamide can be prescribed to pts w/ atrial arrythmia and/or ventricular arrythmia
Procainamide side effects are: drug-induced lupus and torsades de pointes arrythmia and syncope. rare side effect is hypotension due to excessively rapid infusion or left ventricular dysfunction.
torsdaes de poites is polyventricular tachycardia
Class: Class IA antiarrhythmic
MOA: it blocks Na+ channels decreasing ventricular conduction (incr. QRS interval on ECG) slowing upstroke of the AP, prolonging ventricular AP (incr. QRS interval on ECG). it also blocks K+ channels prolonging the ventricular AP (incr. QRS interval on ECG)
Use: treats atrial and ventricular arrythmias
route of admin.: oral, IV
toxicity: cinchonism (a syndrome of headache, dizziness, and tinnitus) and torsades de pointes (pictured)
what is the drug?
Quinidine
Quinidine is a Class IA drug
MOA: Quinidine blocks Na+ channels decreasing ventricular conduction (incr. QRS interval on ECG) slowing upstroke of the AP, prolonging ventricular AP (incr. QRS interval on ECG). it also blocks K+ channels prolonging the ventricular AP (incr. QRS interval on ECG)
Qunidine is rarely used, but can be used to treat atrial and ventricular arrythmias
quinidine can be administered via IV or oral
Quinidine toxicity presents as cinchonism (a syndrome of headache, dizziness, and tinnitus) and torsades de pointes (pictured)
Class: Class IA antiarrhythmic
MOA: it’s more potent than quinidine. it decreases ventricular conduction (incr. QRS interval on ECG) and prolongs ventricular AP (incr. QT interval on ECG)
Use: treats atrial and ventricular arrythmias
Route of admin.: oral, typical dosage is 150 mg 3 times a day (tid)
toxicity: de novo heart failure due to its negative ionotropic effects, urinary retention, dry mouth, blurred vision, constipation, worsening of preexisting glaucoma, and prostatic hyperplasia in males.
what is the drug?
Disopyramide
Disopyramide is a class IA antiarrythmic
Disopyramid blocks NA+ channels. t’s more potent than quinidine. it decreases ventricular conduction (incr. QRS interval on ECG) and prolongs ventricular AP (incr. QT interval on ECG).
Disopyramide is used to treat atrial and ventricular arrythmias
recommended dosage is 150 mg Disopyramide po 3 times a day
Patient w/ disopyramide toxicity may present w/ heart failure, urinary retention, dry mouth, blurred vision, constipation, worsening glaucoma, and prostatic hyperplasia, if male
Class: Class IB
MOA: it blocks Na+ channels. it slows conduction and increases threshold for firing of abnormal cells. it blocks activated and inactivated Na+ channels w/ rapid kinetics. the inactivated state block ensures greatr effects on cells w/ long AP such as purkinje cells and ventricular cells. it increases the repolarization phase. it does NOT affect the QRS complex.
use: treats acute ventricular arrhythmias and arrhythmias associated w/ acute MI
route of admin. : IV
toxicity: CV depression and CNS depression (paresthesias, tremor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech, and convulsions)
what is the drug?
Lidocaine
Lidocaine is a class Ib antiarrhythmic
Lidocaine is a Na+ channel blocker. it slows conduction and increases threshold for firing of abnormal cells. it blocks activated and inactivated Na+ channels w/ rapid kinetics. the inactivated state block ensures greatr effects on cells w/ long AP such as purkinje cells and ventricular cells. it does NOT affect the QRS complex.
Lidocaine is used to treat acute ventricular arrhythmias and arrhythmias associated w/ acute MI
Lidocaine is only administered by IV. Lidocaine is one of the least cardiotoxic of the Class I antiarrhythmics (Na+ channel blockers). Lidocaine overdose (toxicity) presents as CV depression and CNS depression (paresthesias, tremor, nausea of central origin, lightheadedness, hearing disturbances, slurred speech, and convulsions)
Class: class IB antiarrhythmic
MOA: it blocks Na+ channels. it slows conduction and increases threshold for firing of abnormal cells. it lengthens the repolarization phase. it does NOT affect the QRS complex.
Use: treats ventricular arrhythmias
route of admin.: oral and IV
toxicity: CNS depression (tremor, blurred vision, lethargy, and nausea)
what is the drug?
mexiletine
mexiletine is a class Ib antiarrhythmic.
mexiletine blocks Na+ channels. it slows conduction and increases threshold for firing of abnormal cells. it lengthens the repolarization phase. it does NOT affect the QRS complex.
mexiletine is used to trear ventricular arrhythmias
mexiletine can be given orally or via IV
mexiletine toxicity presents as CNS depression (tremor, blurred vision, lethargy, and nausea)
Class: class Ib antiarrhythmic
MOA: it blocks Na+ channels. it slows conduction and increases threshold for firing of abnormal cells.
use: treats ventricular tachycardia and paroxysmal atrial tachycardia after other antiarrhythmic agents have failed.
route of admin.: oral
toxicity: drug induced lupus, hirsutism, gingival enlargement, and it’s a teratogen.
what is the drug?
Phenytoin
phenytoin is a class Ib antiarrhythmic
phenytoin locks Na+ channels. it slows conduction and increases threshold for firing of abnormal cells.
it’s used to treat ventricular tachycardia and paroxysmal atrial tachycardia after other antiarrhythmic agents have failed.
it’s given po.
Phenytoin toxicity presents as drug induced lupus, hirsutism, and gingival enlargement. Phenytoin is a teratogen.
Class: class Ic
MOA: it blocks Na+ channels. it decreases ventricular conduction (incr. QRS interval on ECG).
uses: treats ventricular arrhythmias, paroxysmal atrial fibrillation, and paroxysmal supraventricular tachycardia.
route of admin.: oral
toxicity: it can cause arrhythmias, especially in post-MI patients and drug-induced interstitial lung disease
contraindications: it is contraindicated after MI
what is the drug?
Flecainide
Flecainide blocks Na+ channels and decreases ventricular conduction (incr. QRS interval on ECG)
Flecainide treats ventricular arrhythmias, paroxysmal atrial fibrillation, and paroxysmal supraventricular tachycardia.
Flecainide is admitted orally
Flecainide can cause arrythmias, especially in post MI patients, and drug-induced interstitial lung disease.
Flecainide is contraindicated post-MI
Class: Class IC
MOA: it blocks Na+ channels. it decreases ventricular conduction (incr. QRS interval on ECG).
uses: treats ventricular arrhythmias, paroxysmal atrial fibrillation, and paroxysmal supraventricular tachycardia.
route of admin.: oral
toxicity: it can cause drug-induced lupus like syndrome, CNS disturbances (dizziness), and bronchospasm
what is the drug?
propafenone
propafenone is a Class IC antiarrhythmic
propafenone blocks Na+ channels. it decreases ventricular conduction (incr. QRS interval on ECG).
propafenone is used to treat ventricular arrhythmias, paroxysmal atrial fibrillation, and paroxysmal supraventricular tachycardia.
propafenone is given orally under a doctor’s care while being monitored on an ECG.
propafenone can cause drug-induced lupus like syndrome, CNS disturbances (dizziness), and bronchospasm
Class: class II antiarrhythmic
MOA: it’s a ß1 blocker. it decreases AV nodal conduction (incr. PR interval on ECG). it reduces HR and contractility by blocking ß1 effects
use: treats ventricular and supraventricular arrhythmias
route of admin.: IV
toxicity: bradycardia and AV block (pictured)
what is the drug?
Esmolol
Esmolol is a class II antiarrhythmic
Esmolol is a ß1 receptor blocker. it decrease AV nodal conduction (incr. PR interval on ECG). it reduces HR and contractility by blocking ß1 effects
esmolol is used to treat ventricular and supraventricular arrhythmias
esmolol can cause bradycardia and AV block (pictured)
Class: class II
MOA: it’s a selective ß1 blocker. it decreases AV nodal conduction (incr. PR interval on ECG). it reduces HR and contractility by blocking ß1 effects
use: treats supraventricular tachycardia (SVT),ventricular tachycardia, HTN,angina, acute MI, congestive heart failure(CHF), and prevention of migraine headaches.
route of admin.: oral
toxicity: bradycardia, AV block (pictured), dizziness, ataxia, problems sleeping, ED, diarrhea, and vision problems
what is the drug?
Metoprolol
metoprolol is a class II antiarrhythmic
metoprolol is a ß1 blocker. it decreases AV nodal conduction (incr. PR interval on ECG). it reduces HR and contractility by blocking ß1 effects
metoprolol is used to treat supraventricular tachycardia (SVT),ventricular tachycardia, HTN,angina, acute MI, congestive heart failure(CHF), and prevention of migraine headaches.
metoprolol is administered orally
metoprolol can cause bradycardia, AV block (pictured), dizziness, ataxia, problems sleeping, ED, diarrhea, and vision problems
Class: class II antiarrhythmic
MOA: it’s a non-selective ß-blocker. it decreases AV nodal conduction( incr. PR interval on ECG). it reduces HR and contractility by blocking ß1 effects.
use: treats ventricular and supraventricular arrhythmias
route of admin.: oral or parenteral injection
toxicity: bradycardia, AV block (pictured), bronchoconstriction, blunting of hypoglycemic response
what is the drug?
propanolol
propanolol is a class II antiarrhythmic
propanolol is a non-selective ß-blocker. it decreases AV nodal conduction( incr. PR interval on ECG). it reduces HR and contractility by blocking ß1 effects.
propanolol is used to treat ventricular and supraventricular arrhythmias
propanolol is administered orally or parenterally
propanolol can cause bradycardia, AV block (pictured), bronchoconstriction, blunting of hypoglycemic response
Class: class III
MOA: it’s a K+ channel blocker. it prolongs phase 3 of the ventricular AP (incr. QT interval on ECG). it also shows beta blocker-like and potassium channel blocker-like actions on the SA and AV nodes, increases the refractory period via sodium- and potassium-channel effects, and slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects. it is chemically similar to thyroxine(T4) and it binds to the thyroxine (T4) receptor. it also causes peripheral vasodilation
uses: treats and prevents ventricular arrhythmias
route of admin.: oral and IV
toxicity: pulmonary fibrosis, hepatotoxicity, thyroid disease, bradycardia, and AV block (pictured)
what is the drug?
Amiodarone
amiodarone is a class III antiarrhythmic
amiodarone is a K+ channel blocker. it prolongs phase 3 of the ventricular AP (incr. QT interval on ECG). it also shows beta blocker-like and potassium channel blocker-like actions on the SA and AV nodes, increases the refractory period via sodium- and potassium-channel effects, and slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects. it is chemically similar to thyroxine(T4) and it binds to the thyroxine (T4) receptor. it also causes peripheral vasodilation
amiodarone is used to treat and prevent ventricular arrhythmias
amiodarone can be administered orally or by IV
amiodarone can cause pulmonary fibrosis, hepatotoxicity, thyroid disease, bradycardia, and AV block (pictured).
Class: class III
MOA: it’s a K+ channel blocker. it prolongs ventricular AP (incr. QT interval on ECG). it acts on potassium channels and causes a delay in relaxation of the ventricles. By blocking these potassium channels, it inhibits efflux of K+ ions, which results in an increase in the time before another electrical signal can be generated in ventricular myocytes. This increase in the period before a new signal for contraction is generated, helps to correct arrhythmias by reducing the potential for premature or abnormal contraction of the ventricles but also prolongs the frequency of ventricular contraction to help treat tachycardia.
use: treatement and prevention of ventricular arrhythmias
route of admin.: oral
toxicity: torsades de pointes (due to incr. QT interval) (pictured)
what is the drug?
sotalol
sotalol is a class III antiarrhythmic
sotalol is a a K+ channel blocker. it prolongs ventricular AP (incr. QT interval on ECG). it acts on potassium channels and causes a delay in relaxation of the ventricles. By blocking these potassium channels, it inhibits efflux of K+ ions, which results in an increase in the time before another electrical signal can be generated in ventricular myocytes. This increase in the period before a new signal for contraction is generated, helps to correct arrhythmias by reducing the potential for premature or abnormal contraction of the ventricles but also prolongs the frequency of ventricular contraction to help treat tachycardia.
sotalol is used to treat and prevent ventricular arrhythmias
sotalol is administered orally
sotalol may cause torsades de pointes (due to incr. QT interval) (pictured)
Class: class III antiarrhythmic
MOA: it’s a K+ channel blocker.
Class: class IV antiarrhythmic
MOA: it’s a Ca2+channel blocker. it decreases AV nodal conduction. it blocks activated and inactivated L-type Ca2+ channels. it usually slows SA nodal conduction. it decreases O2 demand, HR, and contractility.
use: supraventricular arrhythmias
route of admin.: oral
toxicity: constipation, bradycardia, galactorrhea, gingival hyperplasia, and AV block (pictured)
what is the drug?
verapamil
verapamil is a class IV antiarrhythmic.
verapamil is a Ca2+ channel blocker. it decreases AV nodal conduction. it blocks activated and inactivated L-type Ca2+ channels. it usually slows SA nodal conduction. it decreases O2 demand, HR, and contractility.
verapamil is used to treat supraventricular arrhythmias
verapamil is administered orally
verapamil may cause constipation, bradycardia, galactorrhea, gingival hyperplasia, and AV block (pictured)
Class: class IV
MOA: it’s a Ca2+ channel blocker. it decreases AV nodal conduction. it blocks L-type Ca2+ channels. it decreases O2 demand, HR, and contractility. it has negative ionotropic effect which decreases HR, negative chronotropic effect which decreases HR and SA nodal conduction, and negative dromotropic effects which decrease AV nodal conduction.
uses: treats supraventricular arrhythmias
route of admin.: oral
toxicity: constipation, bradycardia, dizziness, hypotension, and AV block (pictured)
what is the drug?
diltiazem
diltiazem is a class IV antiarrhythmic.
diltiazem is a Ca2+ channel blocker. it decreases AV nodal conduction. it blocks L-type Ca2+ channels. it decreases O2 demand, HR, and contractility. it has negative ionotropic effect which decreases HR, negative chronotropic effect which decreases HR and SA nodal conduction, and negative dromotropic effects which decrease AV nodal conduction.
diltiazem is used to treat supraventricular arrhythmias.
diltiazem is administered orally.
diltiazem may cause constipation, bradycardia, dizziness, hypotension, and AV block (pictured)
Class: class V antiarrhythmic
MOA: it is a nucleoside, it decreases AV nodal conduction. it is a negative dromotrope (negative dromotropes decr. AV nodal conduction).
uses: treats supraventricular arrhythmias
route of admin.: IV
toxicity: flushing, hypotension, diaphoresis (profuse sweating), and chest pain
what is the drug?
Adenosine
Adenosine is a class V antarrhythmic
adenosine is a nucleoside and a negative dromotrope, it decr. AV nodal conduction.
adenosine is used to treat supraventricular arrhythmias/ supraventricular tachycardia (SVT)
adenosine is administered via IV
adenosine may cause flushing, hypotension, diaphoresis (profuse sweating), and chest pain
Class: class V antiarrhythmic
MOA: it ‘s a cardiac glycoside. it blocks the Na+-K+ ATPase resulting in incr. intracellular Na+. the high levels of intracellular Na+ reduce the activity of the Na+-Ca2+ exchanger and more Ca2+ remains intracellular. the high levels of intracellular Ca2+ improve cardiac contractility. it also decrease AV nodal conduction. it is a positive inotrope (it incr. contractility), a negative dromotrope (it decr. AV nodal conduction), it is a negative lusitrope (it decr. activity of the Na+-Ca2+ exchanger, incr. intracellular Ca2+ levels). it also has some parasymp. activity
uses: chronic heart failure, atrial fibrillation (A-fib), and atrial flutter
route of admin.: oral
toxicity: arrhythmias and blurry yellow vision
what is the drug?
digoxin
digoxin is a class V antiarrhythmic
digoxin is a cardiac glycoside, it blocks the Na+-K+ ATPase resulting in incr. intracellular Na+. the high levels of intracellular Na+ reduce the activity of the Na+-Ca2+ exchanger and more Ca2+ remains intracellular. the high levels of intracellular Ca2+ improve cardiac contractility. it also decrease AV nodal conduction. it is a positive inotrope (it incr. contractility), a negative dromotrope (it decr. AV nodal conduction), it is a negative lusitrope (it decr. activity of the Na+-Ca2+ exchanger, incr. intracellular Ca2+ levels). it also has some parasymp. activity.
digoxin is used to treat chronic heart failure, atrial fibrillation (A-fib), and atrial flutter.
digoxin is administered orally
digoxin may cause arrhythmias and blurry yellow vision
Class: class V antiarrhythmic
MOA: it ‘s a cardiac glycoside. it’s more potent than digoxin. it blocks the Na+-K+ ATPase resulting in incr. intracellular Na+. the high levels of intracellular Na+ reduce the activity of the Na+-Ca2+ exchanger and more Ca2+ remains intracellular. the high levels of intracellular Ca2+ improve cardiac contractility. it also decrease AV nodal conduction. it is a positive inotrope (it incr. contractility), a negative dromotrope (it decr. AV nodal conduction), it is a negative lusitrope (it decr. activity of the Na+-Ca2+ exchanger, incr. intracellular Ca2+ levels). it also has some parasymp. activity.
uses: chronic heart failure, atrial fibrillation (A-fib), and atrial flutter
route of admin.: oral
toxicity: arrhythmias and blurry yellow vision
what is the drug?
Digitoxin.
Digitoxin is a class V antiarrhythmic and a cardiac glycoside. digitoxin is more potent than digoxin.
digitoxin blocks the Na+-K+ ATPase resulting in incr. intracellular Na+. the high levels of intracellular Na+ reduce the activity of the Na+-Ca2+ exchanger and more Ca2+ remains intracellular. the high levels of intracellular Ca2+ improve cardiac contractility. it also decrease AV nodal conduction. it is a positive inotrope (it incr. contractility), a negative dromotrope (it decr. AV nodal conduction), it is a negative lusitrope (it decr. activity of the Na+-Ca2+ exchanger, incr. intracellular Ca2+ levels). it also has some parasymp. activity.
digitoxin is used to treat chronic heart failure, atrial fibrillation (A-fib), and atrial flutter
digitoxin is administered orally.
digitoxin may cause arrhythmias and blurry vision
Class: class V antiarrhythymic
MOA: unkown
use: treats Torsades de pointes (pictured)
route of admin.: IV
toxicity: respiratory depression
what is the drug?
Mg2+.
Mg2+ is a class V antiarrhythmic.
it’s MOA is unknown.
Mg2+ is used to treat Torsades de pointes (pictured)
Mg2+ is administered via IV
Mg2+ may cause respiratory depression
MOA: it inhibits topoisomerases I or II, preventing DNA replication and inducing DNA double-strand breaks. it’s often used in combination with other drugs. it’s part of ABVD treatment regimen and Stanford V treatment regimen. it’s combined w/ ifosamide and mesna to treat angiosarcoma.
Cell cycle specific: No it’s cell cycle non-specific.
Use: angiosarcoma, breast carcinoma, thyroid carcinoma, testicular carcinoma, and lymphoma
toxicity: cardiotoxicity. it causes dilated cardiomyopathy
what is the drug?
Doxorubicin (AKA adriamycin)
doxorubicin is a non-cell cycle specific chemotherapy drug. doxorubicin inhibits topoisomerases I or II preventing DNA replication and inducing DNA double-strand breaks. it’s often used in combination with other drugs. it’s part of ABVD treatment regimen and Stanford V treatment regimen.
doxorubicin is used to treat angiosarcoma, breast carcinoma, thyroid carcinoma, testicular carcinoma, and lymphoma
doxorubicin has cardiac toxicity, it causes dilated cardiomyopathy
MOA: it’s an alkylating agent. it covalently cross-links DNA at guanine N7. it requres activation by the CYP-450 enyme system in the liver. it’s combined w/ mesna and doxorubicin to treat angiosarcoma.
Cell cycle specific: No, it’s not cell cycle specific
use: treats angiosarcoma, non-hodgkins lymphoma (NHL), breast, and ovarian cancer.
toxicity: hemorrhagic cystitis. it has toxic metabolite acrolein that causes hemorrhagic cystitis. co-admin. of mesna w/ this drug via IV prevents hemorrhagic cyctitis. Another mjr side effect is encephalopathy. other side effects include myelosuppression and extreme nausea.
what is the drug?
ifosfamide
ifosfamide is an alkylating agent, similar to cyclophosphamide.
Ifosfamide covalently cross-links DNA at guanine N7. it requres activation by the CYP-450 enyme system in the liver. it’s combined w/ mesna and doxorubicin to treat angiosarcoma.
ifosfamide is not cell-cyclespecific.
ifosfamide is used to treat angiosarcoma, non-hodgkins lymphoma (NHL), breast, and ovarian cancer.
ifosfamide causes hemorrhagic cystitis and encephalopathy. ifosfamide has a toxic metabolite, acrolein, that causes hemorrhagic cystitis. co-admin. of mesna via IV w/ ifosfamide prevents hemorrhagic cyctitis. other side effects include myelosuppression and extreme nausea.
it’s used as an adjuvant in cancer chemotherapy.
it is an antioxidant.
route of admin.: IV (w/ ifosfamide) oral (w/ cyclophosphamide)
it’s co-administered w/ ifosfamide to prevent hemorrhagic cystitis.
it can cause an allergic reaction and pink/red colored urine.
what is the drug?
Mesna.
Mesna stands for 2-MercaptoEthane Sulfonate Na+
Mesna is an anti-oxidant and an adjuvant in cancer chemotherapy.
Mesna is administered via IV
Mesna is co-administered via IV with ifosfamide to prevent hemorrhagic cystitis.
Mesna can cause an allergic reaction and pink/red colored urine
MOA: it’s a vinca (plant) alkaloid. it prevents microtubule formation by interfering w/ tubulin binding. the mitotic spindle can’t form and the M phase does not proceed. it’s used in combination w/ dactinomycin (actinomycin-D) and cyclophosphamide to treat rhabdomyosarcoma.
cell cycle specific: yes, it acts at M phase.
use: it’s used to treat rhabdomyosarcoma, lymphomas, testicular carcinoma, and small-cell lung carcinoma.
toxicity: neurotoxicity (peripheral neuropathy)
what’s the drug?
Vincristine
microtubules are the VINes of the cells (vincristine and vinblasine bind tubulin (microtubules))
Vincristine is a vinca (plant) alkaloid. vincristine prevents microtubule formation by interfering w/ tubulin binding. the mitotic spindle can’t form and the M phase does not proceed. it’s used in combination w/ dactinomycin (actinomycin-D) and cyclophosphamide to treat rhabdomyosarcoma.
vincristine acts at M phase
vincristine is used to treat rhabdomyosarcoma, lymphomas, testicular cancer, and small-cell lung cancer.
toxicity: neurotoxicity (peripheral neuropathy)
MOA: it’s an alkylating agent. it covalently cross-links DNA at guanine N7. it requres activation by the CYP-450 enyme system in the liver. it’s combined w/ vincristine and dactinomycin (actinomycin-D) to treat rhabdomyosarcoma.
Cell cycle specific: No, it’s not cell cycle specific
use: treats rhabdomyosarcoma, non-hodgkins lymphoma (NHL), breast, and ovarian cancer.
toxicity: hemorrhagic cystitis. it has toxic metabolite acrolein that causes hemorrhagic cystitis. co-admin. of mesna w/ this drug orally prevents hemorrhagic cyctitis. other side effects include myelosuppression and extreme nausea.
what is the drug?
cyclophosphamide.
cyclophosphamide is an alkylating agent. it covalently cross-links DNA at guanine N7. it requres activation by the CYP-450 enyme system in the liver. it’s combined w/ vincristine and dactinomycin (actinomycin-D) to treat rhabdomyosarcoma.
cyclophosphamide is used to treat rhabdomyosarcoma, non-hodgkins lymphoma (NHL), breast, and ovarian cancer.
cyclophosphamide is non-cell cycle specific
cyclophosphamide causes hemorrhagic cystitis. it has toxic metabolite acrolein that causes hemorrhagic cystitis. co-admin. of mesna (orally) w/ cyclophosphamide prevents hemorrhagic cyctitis. other side effects include myelosuppression and extreme nausea.
MOA: it’s an antibiotic. it inhibits transcription. it binds DNA at the transcription initiation complex and preventing elongation of RNA chain by RNAP. it’s used in combination w/ vincristine and cyclophosphamide to treat rhabdomyosarcoma.
use: it’s used to treat rhabdomyosarcoma, gestational trophoblastic neoplasia, Wilm’s tumor, Ewing’s sarcoma, and malignant hydatidiform mole.
toxicity: BM suppression, fatigue, hair loss, diarrhea, mouth ulcer, and loss of appetite.
what is the drug?
dactinomycin
dactinomycin is an antibiotic. it inhibits transcription. it binds DNA at the transcription initiation complex and preventing elongation of RNA chain by RNAP. it’s used in combination w/ vincristine and cyclophosphamide to treat rhabdomyosarcoma.
dactinomycin is used to treat rhabdomyosarcoma, gestational trophoblastic neoplasia, Wilm’s tumor, Ewing’s sarcoma, and malignant hydatidiform mole.
dactinomycin causes BM suppression, fatigue, hair loss, diarrhea, mouth ulcer, and loss of appetite.
MOA: it’s a nitrate. it vasodilates via release of nitirc oxide. the major effect is preload reduction (veins dilate, blood pools in veins, and venous return (VR) to the heart decreases), resulting in decreased O2 demand. may cause some afterload reduction also.
uses: treats stable angina, unstable angina, and prinzmetal angina
route of admin.: sublingual
toxicity: tachycardia, orthostatic hypotension, and headache
what is the drug?
nitroglycerine
nitroglycerine is a nitrate
nitroglycerine vasodilates via release of nitirc oxide. the major effect is preload reduction (veins dilate, blood pools in veins, and venous return (VR) to the heart decreases), resulting in decreased O2 demand. may cause some afterload reduction also.
nitroglycerine is administered sublingually and is used to treat stable angina, unstable angina, and prinzmetal angina
nitroglycerine causes tachycardia, orthostatic hypotension, and headache
MOA: it’s a nitrate. it vasodiates via release of nitirc oxide. the major effect is preload reduction (veins dilate, blood pools in veins, and venous return (VR) to the heart decreases), resulting in decreased O2 demand. may cause some afterload reduction also.
uses: treats stable angina, unstable angina, and prinzmetal angina
route of admin.: oral
toxicity: tachycardia, orthostatic hypotension, and headache
what is the drug?
isosorbide dinitrate
isosorbide dinitrate vasodiates via release of nitirc oxide. the major effect is preload reduction (veins dilate, blood pools in veins, and venous return (VR) to the heart decreases), resulting in decreased O2 demand. may cause some afterload reduction also.
isosorbide dinitrate is used to treat stable angina, unstable angina, and prinzmetal angina.
isosorbide dinitrate is administered orally.
isosorbide dinitrate causes tachycardia, orthostatic hypotension, and headache.
MOA: it’s a nonselective ß-blocker. it blocks ß1 and ß2 receptors. it reduces O2 demand by reducing HR and cardiac contractility by blocking ß1 effects. it’s a negative chronotrope (it decr. HR) it’s a negative inotrope (it decr. cardiac contractility). it also inhibits renin production by blocking ß1 effects. it acts on ß1 receptors on the heart and kidney and ß2 receptors on arterioles.
use: it’s used to treat stable angina and unstable angina, but NOT prinzmetal’s angina.
toxicity: bradycardia and AV block
what is the drug?
propanolol
propanolol is a nonselective ß-blocker. it blocks ß1 and ß2 receptors. it reduces O2 demand by reducing HR and cardiac contractility by blocking ß1 effects. it’s a negative chronotrope (it decr. HR) it’s a negative inotrope (it decr. cardiac contractility). it also inhibits renin production by blocking ß1 effects. it acts on ß1 receptors on the heart and kidney and ß2 receptors on arterioles.
propanolol is used to treat stable angina and unstable angina, but NOT prinzmetal’s angina.
propanolol causes bradycardia and AV block
