PROTOTYPE

Diuretic

Carbonic Anhydrase Inhibitor

Uses: Glaucoma (systemic), Urinary Alkalization, Metabolic Alkalosis, acute mountain sickness, seizure disorder (adjuvant)

Mechanism: Block CA in lumenal membrane in proximal tubule blockin bicarb reabsorption -> reduced H+ availability for Na/H exchange (NHE3) -> Increase Na "loss" to lumen -> Na/K exchanged in Distal Tubule -> K loss

Effects: Bicarb loss , urine alkalization, hyperchloremic metabolic acidosis, decreased CSF and aqueous humor, effectiveness decreases within days

Pharmacokinetics: oral admin., 30 min for effect, renal excretion so decrease dose if renal insufficient

Toxicity: hyperchloremic metabolic acidosis, renal stones, K wasting

Contraindication: cirrhosis, sulfa allergies

Diuretic (not bolded)

Carbonic Anhydrase Inhibitor

Uses: Urinary Alkalization, Metabolic Alkalosis, acute mountain sickness, seizure disorder (adjuvant)

Mechanism: Block CA in lumenal membrane in proximal tubule blockin bicarb reabsorption -> reduced H+ availability for Na/H exchange (NHE3) -> Increase Na "loss" to lumen -> Na/K exchanged in Distal Tubule -> K loss

Effects: Bicarb loss , urine alkalization, hyperchloremic metabolic acidosis, decreased CSF and aqueous humor, effectiveness decreases within days

Pharmacokinetics: oral admin., 30 min for effect, renal excretion so decrease dose if renal insufficient

Toxicity: hyperchloremic metabolic acidosis, renal stones, K wasting

Contraindication: cirrhosis, sulfa allergies

Diuretic (not bolded)

Carbonic Anhydrase Inhibitor

Uses: Urinary Alkalization, Metabolic Alkalosis, acute mountain sickness, seizure disorder (adjuvant)

Mechanism: Block CA in lumenal membrane in proximal tubule blockin bicarb reabsorption -> reduced H+ availability for Na/H exchange (NHE3) -> Increase Na "loss" to lumen -> Na/K exchanged in Distal Tubule -> K loss

Effects: Bicarb loss , urine alkalization, hyperchloremic metabolic acidosis, decreased CSF and aqueous humor, effectiveness decreases within days

Pharmacokinetics: oral admin., 30 min for effect, renal excretion so decrease dose if renal insufficient

Toxicity: hyperchloremic metabolic acidosis, renal stones, K wasting

Contraindication: cirrhosis, sulfa allergies

Diuretic (not bolded)

Carbonic Anhydrase Inhibior

Uses: Glaucoma (topical), Urinary Alkalization, Metabolic Alkalosis, acute mountain sickness, seizure disorder (adjuvant)

Mechanism: Block CA in lumenal membrane in proximal tubule blockin bicarb reabsorption -> reduced H+ availability for Na/H exchange (NHE3) -> Increase Na "loss" to lumen -> Na/K exchanged in Distal Tubule -> K loss

Effects: Bicarb loss , urine alkalization, hyperchloremic metabolic acidosis, decreased CSF and aqueous humor, effectiveness decreases within days

Pharmacokinetics: oral admin., 30 min for effect, renal excretion so decrease dose if renal insufficient

Toxicity: hyperchloremic metabolic acidosis, renal stones, K wasting

Contraindication: cirrhosis, sulfa allergies

Diuretic (not bolded)

Carbonic Anhydrase Inhibitor

Uses: Glaucoma (topical), Urinary Alkalization, Metabolic Alkalosis, acute mountain sickness, seizure disorder (adjuvant)

Mechanism: Block CA in lumenal membrane in proximal tubule blockin bicarb reabsorption -> reduced H+ availability for Na/H exchange (NHE3) -> Increase Na "loss" to lumen -> Na/K exchanged in Distal Tubule -> K loss

Effects: Bicarb loss , urine alkalization, hyperchloremic metabolic acidosis, decreased CSF and aqueous humor, effectiveness decreases within days

Pharmacokinetics: oral admin., 30 min for effect, renal excretion so decrease dose if renal insufficient

Toxicity: hyperchloremic metabolic acidosis, renal stones, K wasting

Contraindication: cirrhosis, sulfa allergies

PROTOTYPE

Loop Diuretic (sulfonamide)

Uses: CHF, Pulmonary Edema, impaired renal function; 

Mechanism: Block NKCC2 in thick ascending limb (medullary) -> decreased Na and Cl reabsorption -> loss of K (Na exchanged), Cl and H20

Effects: Mg and Ca excretion,  hypochloremic hypokalemic alkalosis (K loss, no Na for H+ exchange), diminished lumen positive potential (less H+), induce PG synthesis, relieve pulmonary congestion by increasing systemic venous compliance

Pharmacokinetics: Oral, 30-60 min till onset, renal excretion

Toxicities: hypokalemic metabolic alkalosis, hypocalcemia and hypomagnesemia, hyperuricemia, ototoxicity

Drug interactions: aminoglycosides (enhanced ototoxicity), lithium (loss of Na+ increases Li+ retention, ↑ toxicity), digoxin (loss of potassium ↑ toxicity) 

Loop Diuretic (sulfonamide)(not bolded)

Loop Diuretic (sulfonamide)

Uses: CHF, Pulmonary Edema, impaired renal function; 

Mechanism: Block NKCC2 in thick ascending limb (medullary) -> decreased Na and Cl reabsorption -> loss of K (Na exchanged), Cl and H20

Effects: Mg and Ca excretion,  hypochloremic hypokalemic alkalosis (K loss, no Na for H+ exchange), diminished lumen positive potential (less H+), induce PG synthesis, relieve pulmonary congestion by increasing systemic venous compliance

Pharmacokinetics: Oral, 30-60 min till onset, renal excretion

Toxicities: hypokalemic metabolic alkalosis, hypocalcemia and hypomagnesemia, hyperuricemia, ototoxicity

Drug interactions: aminoglycosides (enhanced ototoxicity), lithium (loss of Na+ increases Li+ retention, ↑ toxicity), digoxin (loss of potassium ↑ toxicity) 

Loop Diuretic (sulfonamide)(not bolded)

Loop Diuretic (sulfonamide)

Uses: CHF, Pulmonary Edema, impaired renal function; 

Mechanism: Block NKCC2 in thick ascending limb (medullary) -> decreased Na and Cl reabsorption -> loss of K (Na exchanged), Cl and H20

Effects: Mg and Ca excretion,  hypochloremic hypokalemic alkalosis (K loss, no Na for H+ exchange), diminished lumen positive potential (less H+), induce PG synthesis, relieve pulmonary congestion by increasing systemic venous compliance

Pharmacokinetics: Oral, 30-60 min till onset, renal excretion

Toxicities: hypokalemic metabolic alkalosis, hypocalcemia and hypomagnesemia, hyperuricemia, ototoxicity

Drug interactions: aminoglycosides (enhanced ototoxicity), lithium (loss of Na+ increases Li+ retention, ↑ toxicity), digoxin (loss of potassium ↑ toxicity) 

Loop diuretic (aryloxyacetic acid derivative)(not bolded)

Loop Diuretic (sulfonamide)

Uses: CHF, Pulmonary Edema, impaired renal function, pts allergic to sulfonamide diuretics

Mechanism: Block NKCC2 in thick ascending limb (medullary) -> decreased Na and Cl reabsorption -> loss of K (Na exchanged), Cl and H20

Effects: Mg and Ca excretion,  hypochloremic hypokalemic alkalosis (K loss, no Na for H+ exchange), diminished lumen positive potential (less H+), induce PG synthesis, relieve pulmonary congestion by increasing systemic venous compliance

Pharmacokinetics: Oral, 30-60 min till onset, renal excretion

Toxicities: hypokalemic metabolic alkalosis, hypocalcemia and hypomagnesemia, hyperuricemia, ototoxicity (HIGHER RISK)

Drug interactions: aminoglycosides (enhanced ototoxicity), lithium (loss of Na+ increases Li+ retention, ↑ toxicity), digoxin (loss of potassium ↑ toxicity) 

Prototype

Thiazide diuretic

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide-related diuretic

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Pharmacokinetics: slowly absorbed so longer duration, oral, excreted by organic acid secreting system (uric acid competition)

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide-related diuretic

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Pharmacokinetics: oral, excreted by biliary system so good for pts with renal insufficiency, extensive hepatic metabolism

Effects: Does not increase lipid levels, pronounced vasodilation, Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide diuretic (not bolded)

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide diuretic (not bolded)

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide-related diuretic (not bolded)

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Effects: Increases diuresis in pts with decreased GFR Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide diuretic (not bolded)

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide diuretic (not bolded)

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide diuretic (not bolded)

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Thiazide-related diuretic (not bolded)

Uses: HTN, CHF, Nephrolithiasis, nephrogenic diabetes insipidus

Mechanism: Distal convoluted tubule, blocks NCC (Na/Cl cotransporter), inhibits Na and Cl reabsoprtion; effect depends on PG synthesis and can be inhibited by NSAIDS

Effects: Increased ATP dependent K channel opening, hypokalemia, hyperuricemia (decreased uric acid excretion), decreased Ca excretion, Mg loss, iodide and bromide loss, hyperglycemia

Pharmacokinetics: oral, excreted by organic acid secreting system (uric acid competition)

Toxicities/Adverse effects: hypokalemia, hyperglycemia and carb intolerance, hyperuricemia, increased lipid levels, hypercalcemia, allergic rxn, photosensitivity, increased lithium tox, aggravated jaundice in adults 

Prototype

K-sparing diuretic

Uses: Edema from CHF cirrhosis or nephrotic syndrome, hyperaldosteronism, 

Mechanism: @Collecting tubule, aldosterone inhibitor decreases Na reabsorption, increases Na excretion, promotes K reabsorption; binds glucocorticoid and sex hormone receptors at high doses

Toxicities: gynecomastia, occasional hyperkalemia

K-sparing diuretic

Uses: Edema from CHF cirrhosis or nephrotic syndrome, hyperaldosteronism, 

Mechanism:@collecting tubule, selective aldosterone receptor antagonist (SARA) decreases Na reabsorption, increases Na excretion, promotes K reabsorption; LESS ENDOCRINE RELATED SIDE EFFECTS

Toxicity: increased hyperkalemia risk

NOTE: reduced all-cause mortality in for patients with acute myocardial infarction complicated by left ventricular dysfunction and heart failure 

K-sparing diuretic

Uses: main use is in combination with potassium losing diuretics, Edema from CHF cirrhosis or nephrotic syndrome,

Mechanism: @collecting tubule, Direct Na influx inhibitor

Toxicities: Hyperkalemia, inhibits dihydrofolate reductase

Should not be given with spironolactone

K-sparing diuretic

Uses: DOC for lithium induce diabetes insipidus, main use is in combination with potassium losing diuretics, Edema from CHF cirrhosis or nephrotic syndrome,

Mechanism: @collecting tubule, Direct Na influx inhibitor

Pharmacokinetics: weak diuretic effect, oral administration, absorption from G.I. tract is rapid, excreted in the urine, action is not significantly affected by either acidosis or alkalosis 

Toxicities: Hyperkalemia,

PROTOTYPE
Osmotic Diuretic
Mechanism: filtered but not absorbed in kidney, keeps water in tubule causing diuresis

Osmotic Diuretic (not bolded)
Mechanism: filtered but not absorbed in kidney, keeps water in tubule causing diuresis

Osmotic Diuretic (not bolded)
Mechanism: filtered but not absorbed in kidney, keeps water in tubule causing diuresis

Osmotic Diuretic (not bolded)
Mechanism: filtered but not absorbed in kidney, keeps water in tubule causing diuresis

ADH agonist (anti-diuretic)

Uses:  to prevent or control polyuria, polydipsia, and dehydration in patients with central diabetes insipidus 

intravenous vasopressin is included in the Advanced Cardiac Life Support (ACLS)

algorithm as an alternative to epinephrine for the treatment of cardiac arrest associated with asystole or pulseless electrical activity 

ADH agonist (anti-diuretic)

Uses: Hemophilia A and von Willebrand disease and used in the treatment of bleeding esophagus varices 

Pharmacokinetics: more potent and longer lasting than vasopressin; works on V2 and has hemostatic properties

Diuretic, ADH antagonist

Uses: CHF, SIADH

Pharmacokinetics: V1, V2 action (vasopressin receptors)

Effects: Increases urine output, decreases H2O reabsorption

Diuretic, ADH antagonist

Uses: CHF, SIADH

Pharmacokinetics: V1, V2 action (vasopressin receptors)

Effects: Increases urine output, decreases H2O reabsorption

Diuretic, ADH antagonist

tetracyclic abx

produces a nephrogenic diabetes insipidus by uncoupling the V2 receptor from adenylyl cyclase enzyme

Less toxic than lithium 

 Diuretic, ADH antagonist

produces a nephrogenic diabetes insipidus by uncoupling the

V2 receptor from adenylyl cyclase enzyme 

More toxic than demeclocycline

1. Reduce Preload - diuretic and venodilator
2. Reduce Afterload - Arteriodilator
3. Increase Contractility - inotropic drug
4. Decrease HR (energy expenditure) - B-blockers

CHF drug

Cardiac Glycoside

Use: CHF

Mechanism: inhibits Na/K ATPase -> increases free Ca concetration; Increases intracellular Na concenctration whil decreasing Ca expulsion

Effects: Increases contractilty by increasing interaction of actin and myosin

Given oral or IV; narrow margin of safety

Calsium enhances digitals toxicity; Potassium (competititive) and Magnesium decrease toxicity

Toxicities: earliest seen in GI i.e. anorexia, nausea, diarrhea etc;  most dangerous are cardiac toxicities = arrhythmias including sinus brady, ectopic v-beats, AV block, bigeminy, v-fib

Tx for toxicity: discontinue, K (oral or IV), lidocaine, phenytoin, propranolol, digitalis immune Fab

Prototype

CHF drug

Phosphodiesterase Inhibitor (bipyridine); inodilator

Uses: CHF when digitalis, vasodilators and diuretic are ineffective (must monitor closely in hosptial)

Mechanism: inhibit phosphodiesterase, increasing cAMP -> increased Ca influx -> vasodilation + increased contractility

Effect: increases CO, decreases survival

Route: IV

CHF drug (not bolded)

Phosphodiesterase Inhibitor (bipyridine); inodilator

Uses: CHF when digitalis, vasodilators and diuretic are ineffective (must monitor closely in hosptial)

Mechanism: inhibit phosphodiesterase, increasing cAMP -> increased Ca influx -> vasodilation + increased contractility

Effect: increases CO, decreases survival

Route: IV

• Sympathomimetic (not bolded)
• Uses: Acute Heart Failure
• selective beta-1 agonist
• positive inotropic effect, somewhat less tachycardia
• increased oxygen consumption
• IV administration 

Sympathomimetic (Not bolded)

Use: Acute Heart failure

Mechanism: Direct inotropic effect; increases CO and renal bf

Given IV

Effects: lowers peripheral resistance, increases Na excretion

CHF Drug

B type natriuretic peptide (hBNP)

Prototype

ACE inhibitor

Uses: CHF

 decreasing afterload (decreased peripheral resistance) from decreasing angiotensin-vasoconstriction

decreasing preload - decreases aldosterone release 

ACE inhibitor

Uses: CHF

 decreasing afterload (decreased peripheral resistance) from decreasing angiotensin-vasoconstriction

decreasing preload - decreases aldosterone release 

ACE inhibitor (not bolded)

Uses: CHF

 decreasing afterload (decreased peripheral resistance) from decreasing angiotensin-vasoconstriction

decreasing preload - decreases aldosterone release 

ACE inhibitor (not bolded)

Uses: CHF

 decreasing afterload (decreased peripheral resistance) from decreasing angiotensin-vasoconstriction

decreasing preload - decreases aldosterone release 

ACE inhibitor (not bolded)

Uses: CHF

 decreasing afterload (decreased peripheral resistance) from decreasing angiotensin-vasoconstriction

decreasing preload - decreases aldosterone release 

ACE inhibitor (not bolded)

Uses: CHF

 decreasing afterload (decreased peripheral resistance) from decreasing angiotensin-vasoconstriction

decreasing preload - decreases aldosterone release 

Prototype

Beta-blocker

Use: CHF, angina

Effects: reduce renin, decreases catecholamine effect, decrease HR, 

Dangerous due to decrease inotropic effect but decreases mortality

Antiarrhythmic effect; no coronary vasodilatory effect

Beta blocker (not bolded)

Use: CHF, angina

Effects: reduce renin, decreases catecholamine effect, decrease HR, 

Dangerous due to decrease inotropic effect but decreases mortality

Antiarrhythmic effect; no coronary vasodilatory effect

Beta-blocker (not bolded)

Use: CHF, angina

Effects: reduce renin, decreases catecholamine effect, decrease HR, 

Dangerous due to decrease inotropic effect but decreases mortality

Antiarrhythmic effect; no coronary vasodilatory effect

Vasodilator

Uses: CHF

Given IV, dilates veins and arteries, decreases preload and afterload

Vasodilator

Uses: CHF

Effect: arterial vasodilator, decreases peripheral resistance

Vasodilator

Uses: CHF

Given orally

Lowers preload more than afterload; tolerance occurs

Prototype

Class IA Antiarrhythmic

Uses: every arrhythmia, a-fib/flutter, V-tach

Mechanism: binds open and activated Na channels; decreased automaticity, increased diastolic threshold, slows rate of rise of AP, prolonged AP duration prolonging Effective Refractory Period (ERP) -> preventing re-entry circuit; blocking K channels (prolongs depolarization)

Other Effects: muscarinic receptor blockade (increases HR and AV conduction), wide QRS and QT interval, SA and AV block; blocks alpha receptors (hypotension) -> reflex tachy (maybe); cinchonism (tinnitus, headache, vertigo, allergy)

Pharmacokinetics: oral, first pass effect, T1/2 = 6 hr

Toxicity: low therapeutic index, cardiac toxicity, severe hypotension (alpha block); diarrhea

Class IA Antiarrhythmic

Uses: every arrhythmia, a-fib/flutter, V-tach

Mechanism: binds open and activated Na channels; decreased automaticity, increased diastolic threshold, slows rate of rise of AP, prolonged AP duration prolonging Effective Refractory Period (ERP) -> preventing re-entry circuit; blocking K channels (prolongs depolarization)

Other Effects: muscarinic receptor blockade (less than quinidine, increases HR and AV conduction), wide QRS and QT interval, SA and AV block; blocks alpha receptors (hypotension) -> reflex tachy (maybe); cinchonism (tinnitus, headache, vertigo, allergy)

Pharmacokinetics: oral, first pass effect, metabolite has class III effect (K channel block), T1/2 = 3-4 hr

Toxicity: lupus erythematosus, low therapeutic index, cardiac toxicity, severe hypotension (alpha block); diarrhea

Prototype

Class IA Antiarrhythmic

Uses: ONLY V-ARRHYTHMIAS

Mechanism: binds open and activated Na channels; decreased automaticity, increased diastolic threshold, slows rate of rise of AP, prolonged AP duration prolonging Effective Refractory Period (ERP) -> preventing re-entry circuit; blocking K channels (prolongs depolarization)

Other Effects: negative inotropic effect, anticholinergic effect (dry mouth etc.); muscarinic receptor blockade (increases HR and AV conduction), wide QRS and QT interval, SA and AV block; blocks alpha receptors (hypotension) -> reflex tachy (maybe); cinchonism (tinnitus, headache, vertigo, allergy)

Pharmacokinetics: oral, first pass effect, T1/2 = 6 hr

Toxicity: low therapeutic index, cardiac toxicity, severe hypotension (alpha block); diarrhea

Prototype

Class IB Antiarrhythmic

Use: V-arrhythmias

Mechanism: Binds inactivated sodium channels, decreases AP duration, shorten ERP due to block of slow Na "window" currents

Effects: not for supraventricular arrhytmias, no depressant action on contractility, no vagal blocking

Pharmacokinetics: IV (NOT oral)

Toxicity: convulsion, negative inotropic effect (least of all the antiarrhythmics) aka brady

Not bolded

Class IB Antiarrhythmic

Use: V-arrhythmias

Mechanism: Binds inactivated sodium channels, decreases AP duration, shorten ERP due to block of slow Na "window" currents

Effects: not for supraventricular arrhytmias, no depressant action on contractility, no vagal blocking

Pharmacokinetics: IV (NOT oral)

Toxicity: convulsion, negative inotropic effect (least of all the antiarrhythmics) aka brady

Not bolded

Class IB Antiarrhythmic

Use: V-arrhythmias

Mechanism: Binds inactivated sodium channels, decreases AP duration, shorten ERP due to block of slow Na "window" currents

Effects: not for supraventricular arrhytmias, no depressant action on contractility, no vagal blocking

Pharmacokinetics: IV (NOT oral)

Toxicity: convulsion, negative inotropic effect (least of all the antiarrhythmics) aka brady

Not bolded

Class IB Antiarrhythmic

Use: V-arrhythmias

Mechanism: Binds inactivated sodium channels, decreases AP duration, shorten ERP due to block of slow Na "window" currents

Effects: not for supraventricular arrhytmias, no depressant action on contractility, no vagal blocking

Pharmacokinetics: IV (NOT oral)

Toxicity: convulsion, negative inotropic effect (least of all the antiarrhythmics) aka brady

Prototype

Class IC Antiarrhythmic

Mechanism: binds all Na channels

Uses: Supraventricular arrhythmias, life threatening V-arrhythmias

Effect: no ANS effect, STRON PRO-ARRHYTHMIC EFFECT (CHF clinical study)

Pharmacokinetics: oral

Not bolded

Class IC Antiarrhytmic

Mechanism: binds all Na channels

Uses: Supraventricular arrhythmias, life threatening V-arrhythmias; should be reserved for refractory pts with severe, life threatening arrhythmias from the strong pro-arryhtmic effects

Pharmacokinetics: Oral

Not Bolded

Class IC

Use: life threatening V-arrhythmias

Mechanism: blocks all Na channels

Bolded

Beta blocker

Mechanism: blocks all B rececptors -> decreased HR and contraction force

Not bolded

Beta blocker

Mechanism: B1 blocker -> decreased HR and contraction force

Not bolded

Beta blocker

 Mechanism: blocks all Beta receptors -> decreased HR and contraction

Not bolded

Beta blocker

Mechanism: blocks all beta receptors -> decreased HR and contraction

Not bolded

Beta blocker

Not bolded

Beta blocker

Mechanism: blocks beta receptors -> decreased HR and contractility

Not bolded

Beta blocker

Mechanism: blocks beta receptors -> decreased HR and contraction

Prototype

Class III antiarrhytmic

Uses: supraventricular and ventricular arrhytmias

Mechanism: blocks K channels prolonging repolarizaion (class III), block inactive Na channels (Class I), Ca block (Class IV)

Pharmacokinetics: oral, T1/2 13-103 days, 

Toxicity: No torsades; brandy heart block, HF; deposits in tissues i.e. cornea (yellow-brown), skin (grayis-blue), photodermatitis

Bolded

Class IC antiarrhytmic

Uses: V and supraV arrhytmias

Mechanism: blocks K channel, prolonging repolarization; also nonselective Beta blocker

Pharmacokinetics: oral, excreted by kidney

Not bolded

Class III antiarrhythmic

Uses: V-fib and unstable V-tachy

Mechanism: K channel blocker, prolongs repolarization

Effects: initial increase in BP and HR, followed by a rapid adrenergic blockade

Pharmacokinetics: IV or IM, duration of action 6-12 hrs, cleared by kidney and kidney disease decreases clearance

Not bolded

Class III antiarrhythmic

Uses: rapid conversion of A-fib/flutter, no effect on BP, HR, and EKG is normal

Mechanism: promotes Na influx in slow Na channel, prolongs AP duration

Pharmacokinetics: IV

Not bolded

Class III antiarrhythmic

Uses: A-fib/flutter conversion to and maintenance of normal sinus rythm

Mechanism: POTENT K channel block, prolonging repolarization and ventricular refratoriness

Pharmacokinetics: oral

Prototype

Class IV antiarrhythmic

Uses: Angina, Re-entrant supraventricular tachycardia, reduces Ventricular rate in A-fib/flutter

Mechanism: blocks slow Ca channels, slows AV nodal conduction, decreases HR

Pharmacokinetics: IV

Beneficial effects: decreases cardiac workload and contractilty, bradycardia by SA and AV effect (decrease); less likely to cause reflex tachy

Toxicities: GI intolerance, brady, AV block; contraindicated in presence of CHF, avoid w/ beta blockers; inhibition of insulin and platelet aggregation

Not Bolded

Class IV antiarrhythmic

Uses: paroxysmal supraventricular tachy, ventricular rate, a-fib/flutter, (prinzmetal and stable) angina, HTN, prevention of injury following angioplasty

Mechanism: Ca channel blocker, inhibits Ca movement from ECM to ICM in myocardial and vascular smooth muscle

Effects: reduces HR -> increases excercise capacity, myocardial perfusion

Harmful effect = serious cardia depression, inhibition on insulin and platelet aggregation

Pharmacokinetics: Oral, IV available

Not Bolded

Class IV antiarrhythmic

Uses: Angina

Mechanism: Ca block

Prolongs AP

Rarely used

Antiarrhythmic, Naturally occuring

Uses: Paroxysmal supraventricula tachycardia, wolff-parkinson-white syndrom

Mechanism: slows AV conduction, involves enhanced K+ conductance and inhibition of cAMP-induced Ca++ influx. 

Antiarrhythmic

Uses: digitalis induced arrhytmias, torsades, seizures

IV admin

Bolded

Antiarrhythmic

Effects: resting potential depolarization, membrane stamilization (increased K permeability)

Hypokalemia increaes risk of afterdepolarization

hypo and hyperkalemia ar arrhythmogenic

Antiarrhythmic

Uses: prevent and control seizures in preeclampsia and eclampsia, digitalis induced arrhythmias, polymorphic ventricualr tachyt (torsades)

Bolded

Centrally acting sympatholytic

Uses: HTN

Mechanism: stimulate medullary A2 adrenergic receptors to reduce peripheral sympathetic nerve activity; reduces NT release (presynaptic) and inhibits postsynaptic neurons

Effects: lowers BP, decreases renal renin secretion

Pharmacokinetics: oral, also transdermal patch

Common adverse effects: sedation, sudden withdrawal = hypertensive crisis

Effect inhibited by tricyclic antidepressants and yohimbine (A2 inhibitor)

Bolded

Centrally acting sympatholytic (prodrug)

Uses: HTN

Mechanism: stimulate medullary A2 adrenergic receptors to reduce peripheral sympathetic nerve activity; reduces NT release (presynaptic) and inhibits postsynaptic neurons

Effects: lowers BP, decreases renal renin secretion

Pharmacokinetics: oral

Common adverse effects: sedation, sudden withdrawal = hypertensive crisis, hemolytic anemia with positive coombs test

Not bolded
Centrally acting sympatholytic

Uses: HTN
relatively selective alpha2-adrenoceptor agonist with centrally mediated sympatholytic, sedative, and analgesic effects
administered I.V.
used in anesthesiology and postoperative care 

Ganglion blocker

Uses: HTN

capable of entering the CNS shows promise in treating Tourette’s syndrome 

Not bolded (don't spend time on this)
Adrenergic neuron blocker
Uses: HTN
taken up by the nerve ending
replaces NE in the vesicles
inhibits exocytosis

 interaction with TCAs, cocaine, indirect sympathomimetics 

Bolded
Adrenergic Neuron Blocker
Uses: HTN
o inhibits the active transport of NE into the vesicle
o released NE is metabolized by MAO enzyme
o serious interaction with MAOIs
adverse effects: sedation, psychic depression, stuffy nose, dry mouth, and
gastrointestinal disturbances 

Bolded

A1-antagonist

Uses: HTN

Mechanism: A1-adrenergic block reduces norepinephrine vasoconstriction to dilate both arteries and veins 

BP falls from decreases peripheral resistance

First dose postural hypotension

Bolded

A1-antagonist

Uses: HTN

Mechanism: A1-adrenergic block reduces norepinephrine vasoconstriction to dilate both arteries and veins 

BP falls from decreases peripheral resistance

First dose postural hypotension

Bolded

A1-antagonist

Uses: HTN

Mechanism: A1-adrenergic block reduces norepinephrine vasoconstriction to dilate both arteries and veins 

BP falls from decreases peripheral resistance

First dose postural hypotension

Beta blocker

Uses: HTN

Mechanism: modulates NO release causing vasodilation

Most preferred: angina, post MI, migraine

Least preferred: high physical activity, african heritage, asthma, DM, hypercholesterolemia, PVD

Not bolded

lowers BP in HTN crisis, by blocking a and b receptors

Adverse effects: orthostatic, bronchospasm, hepatotoxicity

lipid neutral

Bolded

lowers BP in HTN crisis, by blocking a and b receptors

Adverse effects: orthostatic, bronchospasm, hepatotoxicity

lipid neutral

Not bolded

Vasodilator

Uses: Severe HTN

Mechanism: Increase NO like nitrites; dilates arteries but not veins

Pharmacokinetics: Oral

Toxicity: headache, nausea, anorexia, palpitations, sweating, flushing ; angina, ischemic arrhythmias; SLE in slow acetylators 

Not Bolded

Vasodilator

Uses: Baldness, HTN

Mechanism: opens K channel, stabilizing membrane; dilates arteries but not veins; 

Toxicity: hypertrichosis

Given orally

Not bolded

Vasodilator

Uses: HTN

Mechanism: dilates both arteries and pain rapidly lowers blood pressure (in minutes), and effect disappears in minutes after discontinuation 

IV

Not Bolded

Vasodilator

Uses: HTN, pts with insulinoma

Mechanism: activates  ATP-sensitive potassium channels, 

Oral

Adversce effects: hyperglycemis, Na and H2O retention, hyperuricemia, excessive hair growth (children)

Not bolded

D1 receptor agonist

Mechanism: relaxes arterial smooth muscle

IV

Not bolded

Calcium channel blocker

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing arteriole smooth muscle, causing vasodilation and decreased BP

Not bolded

Calcium channel blocker

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing arteriole smooth muscle, causing vasodilation and decreased BP

Not bolded

Calcium channel blocker

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing arteriole smooth muscle, causing vasodilation and decreased BP

Not bolded

Calcium channel blocker

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing arteriole smooth muscle, causing vasodilation and decreased BP

Bolded

Calcium channel blocker (strongest vasodilator of CCBs)

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing arteriole smooth muscle, causing vasodilation and decreased BP

Beneficial effects: coronary vasodilation increases O2 supply and decreases afterload

Adverse effects: most likely to cause reflex tachy, enhances MI development

Not bolded

Calcium channel blocker

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing arteriole smooth muscle, causing vasodilation and decreased BP; cerebral vasodilator

Not bolded

Calcium channel blocker

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing arteriole smooth muscle, causing vasodilation and decreased BP

Bolded

Calcium channel blocker (vasodilator); papaverine related

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing cardiac smooth muscle

Effects: relaxes all smooth muscle especially cardiac sm, arterioles are more sensitive than veins; negative inotropic, slowed AV conduction, reduced impulse generation (SA node)

Not bolded

Benzodiazepine

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing smooth muscle

Not bolded

Ca channel blocker

Uses: HTN, angina

Mechanism: Blocks slow Ca channels, decreasing intracellular Ca, relaxing smooth muscle

Bolded

ACE inhibitor

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

ACE inhibitor (prodrug)

Uses: HTN

Mechanism: Decreases angiotensin II decreasing vasoconstriction, lowering BP

Enhanced with diuretics

Oral

Not bolded

Angiotensin receptor blocker

Uses: HTN

More specific than ACE inhibitors

Oral

Not bolded

Angiotensin receptor blocker

Uses: HTN

More specific than ACE inhibitors

Oral

Not bolded

Angiotensin receptor blocker

Uses: HTN

More specific than ACE inhibitors

Oral

Not bolded

Angiotensin receptor blocker

Uses: HTN

More specific than ACE inhibitors

Oral

Not bolded

Angiotensin receptor blocker

Uses: HTN

More specific than ACE inhibitors

Oral

Not bolded

Angiotensin receptor blocker

Uses: HTN

More specific than ACE inhibitors

Oral

Not bolded

Angiotensin inhibitor

Uses: HTN

blocks formation of angiotensin I in the kidney

Bolded

Nitrate/Nitrite; short acting (10-30 min)

Uses: Angina

Mechanism: nitrates cause vasodilation by releasing nitrite ion -> metabolized to nitric oxide -> activates guanylyl cyclase -> increases cGMP -> relaxes vascular smooth muscles 

Relief by 2 factors: decreases myocardial O2 requirement and redistribution of blood to ischemic areas

Effects primarily large veins, both preload and afterload are decreased

Sublingual

Adverse Effects: reflex tachy -> increased cardiac workload; acute toxicity leading to orthostatic hypotension, tachy and headaches

Not bolded

Nitrate/Nitrite (short acting, 10-60 min)

Uses: Angina

Mechanism: nitrates cause vasodilation by releasing nitrite ion -> metabolized to nitric oxide -> activates guanylyl cyclase -> increases cGMP -> relaxes vascular smooth muscles 

Relief by 2 factors: decreases myocardial O2 requirement and redistribution of blood to ischemic areas

Effects primarily large veins, both preload and afterload are decreased

Sublingual

Adverse Effects: reflex tachy -> increased cardiac workload acute toxicity leading to orthostatic hypotension, tachy and headaches

Not bolded

Nitrate/Nitrite (long acting (6-10 hrs)

Uses: Angina

Mechanism: nitrates cause vasodilation by releasing nitrite ion -> metabolized to nitric oxide -> activates guanylyl cyclase -> increases cGMP -> relaxes vascular smooth muscles 

Relief by 2 factors: decreases myocardial O2 requirement and redistribution of blood to ischemic areas

Effects primarily large veins, both preload and afterload are decreased

Sublingual

Adverse Effects:reflex tachy -> increased cardiac workload  acute toxicity leading to orthostatic hypotension, tachy and headaches

Not bolded

Nitrate/Nitrite (very short acting, 3-5 min)

Uses: Angina

Mechanism: nitrates cause vasodilation by releasing nitrite ion -> metabolized to nitric oxide -> activates guanylyl cyclase -> increases cGMP -> relaxes vascular smooth muscles 

Relief by 2 factors: decreases myocardial O2 requirement and redistribution of blood to ischemic areas

Effects primarily large veins, both preload and afterload are decreased

Sublingual

Adverse Effects: reflex tachy -> increased cardiac workload acute toxicity leading to orthostatic hypotension, tachy and headaches

Bolded

Partial fatty acid oxidase inhibitor (PFox)

Uses: Angina

Mechanism: PFox, inhibits late sodium current, decreases LV wall stiffness

Oral

Metabolized by liver

Bolded

Beta blocker

Use: Angina

Actions and effects: decrease CO, decrease renin secrtion, CNS reduction of sympathetic vasomotor tone

No cardiac vasodialtion

Bolded

Beta blocker

Use: Angina

Actions and effects: decrease CO, decrease renin secrtion, CNS reduction of sympathetic vasomotor tone

No cardiac vasodialtion

Bolded

Beta blocker

Use: Angina

Actions and effects: decrease CO, decrease renin secrtion, CNS reduction of sympathetic vasomotor tone

No cardiac vasodialtion

Bolded

Beta blocker

Use: Angina

Actions and effects: decrease CO, decrease renin secrtion, CNS reduction of sympathetic vasomotor tone

No cardiac vasodialtion

Bolded

Phosphodiesterase type 5 (PDE5) inhibitor

Uses: ED, pulmonary HTN

Mechanism: selective cGMP inhibitor

Oral

Adverse effects: nasal congestion, visual impairment, headache, flushing, dyspepsia, UTI

Contraindications: pt on nitrate/nitrite, a-blockers

Not bolded

Phosphodiesterase type 5 (PDE5) inhibitor

Uses: ED, pulmonary HTN

Mechanism: selective cGMP inhibitor

Oral

Adverse effects: nasal congestion, visual impairment, headache, flushing, dyspepsia, UTI

Contraindications: pt on nitrate/nitrite, a-blockers

Not bolded

Phosphodiesterase type 5 (PDE5) inhibitor

Uses: ED, pulmonary HTN

Mechanism: selective cGMP inhibitor

Oral

Adverse effects: nasal congestion, visual impairment, headache, flushing, dyspepsia, UTI

Contraindications: pt on nitrate/nitrite, a-blockers

 Bolded

Phosphodiesterase  type 3 (PDE3) inhibitor

Uses: Angina, intermittent claudication

Mechanism: PDE3 inhibiton -> antiplatelet and vasodilation

Endothelin receptor antagonist

Uses: Severe pulmonary HTN

Mechanism: endothelin receptor antagonist of both type A and B endothelin-1 receptors; cause contraction of vascular smooth muscle

Adverse effects: elevated hepatic enzymes, potential teratogenic effects, and multiple drug interactions 

Bolded

Anti-hyperlipidemia Dx

Dx that impairs lipoprotein synthesis

Uses: Heterozygous familial hypercholesterol-emia; combined hyperlipoproteinemia, Hyperlipidemia

Effect: Lowers VLDL and LDL by inhibiting VLDL secretion; inhibits liver cholesterolgenesis, increased LPL pathway clearance, increased HDL

Oral, kidney excretion

Adverse effects: cutaneous vasodilation, nausea, abd discomfort, elevate aminotransferases or alkaline phosphatase, impairs glucose tolerance, may cause severe hepatotoxicity

Bolded

Anti-hyperlipidemia Dx

Fibric acid derivative

Uses: familia dybetalipoproteinemia, hypertriglyceridemia (NOT effective in primary chylomicronemia or familial hypercholesterolemia) 

Mechanism: ligand for peroxisom proliferator-activated receptor-alpha (PPAR-a) which causes effects

Effects: increase LPL activity (VLDL catabolism), decrease TAG (via lower VLDL concentration), decrease cholesterol (inhibit liver cholesterolgenesis)

Oral

Adverse effects: increased incidenc of cholelithiasis or gallstones, may increase LDL

Not bolded

Anti-hyperlipidemia Dx

Fibric acid derivative

Uses: familia dybetalipoproteinemia, hypertriglyceridemia (NOT effective in primary chylomicronemia or familial hypercholesterolemia) 

Mechanism: ligand for peroxisom proliferator-activated receptor-alpha (PPAR-a) which causes effects

Effects: increase LPL activity (VLDL catabolism), decrease TAG (via lower VLDL concentration), decrease cholesterol (inhibit liver cholesterolgenesis)

Oral

Adverse effects: increased incidenc of cholelithiasis or gallstones, may increase LDL

Not bolded

Anti-hyperlipidemia Dx

Fibric acid derivative

Uses: familia dybetalipoproteinemia, hypertriglyceridemia (NOT effective in primary chylomicronemia or familial hypercholesterolemia) 

Mechanism: ligand for peroxisom proliferator-activated receptor-alpha (PPAR-a) which causes effects

Effects: increase LPL activity (VLDL catabolism), decrease TAG (via lower VLDL concentration), decrease cholesterol (inhibit liver cholesterolgenesis)

Oral

Adverse effects: increased incidenc of cholelithiasis or gallstones, may increase LDL

Bolded

Anti-hyperlipidemia Dx

Bile acid binding resin

Uses: Elevated LDL as in hyterozygous familial hypercholesterolemia and combined hyperlipoproteinemia (no effect in homozygous familial hypercholesterolemia)

Mechanism: prevents intestinal reabsorption of bile acids, increases expression of liver LDL receptors, increasing LDL uptake -> lowers plasma cholesterol

Adverse effects: constipation and bloating, gallstone formation, steatorrhea, vitamin K malabsorption; may impair absorption of digitalis, thiazides, tetracycline, thyroxine or aspirin

Not bolded

Anti-hyperlipidemia Dx

Bile acid binding resin

Uses: Elevated LDL as in hyterozygous familial hypercholesterolemia and combined hyperlipoproteinemia (no effect in homozygous familial hypercholesterolemia)

Mechanism: prevents intestinal reabsorption of bile acids, increases expression of liver LDL receptors, increasing LDL uptake -> lowers plasma cholesterol

Adverse effects: constipation and bloating, gallstone formation, steatorrhea, vitamin K malabsorption; may impair absorption of digitalis, thiazides, tetracycline, thyroxine or aspirin

Not bolded

Anti-hyperlipidemia Dx

Bile acid binding resin

Uses: Elevated LDL as in hyterozygous familial hypercholesterolemia and combined hyperlipoproteinemia (no effect in homozygous familial hypercholesterolemia)

Mechanism: prevents intestinal reabsorption of bile acids, increases expression of liver LDL receptors, increasing LDL uptake -> lowers plasma cholesterol

Adverse effects: constipation and bloating, gallstone formation, steatorrhea, vitamin K malabsorption; may impair absorption of digitalis, thiazides, tetracycline, thyroxine or aspirin

Bolded

Anti-hyperlipidemia Dx

Competitive HMG-CoA reductase inhibitor

Uses: Elevated LDL as in heterozygous familial hypercholesterolemia and combined hyperlipoproteinemia

Mechanism: inactive, must be hydrolyzed; reduce plasma LDL by inhibiting HMG-CoA which increased high affinity LDL receptors
Effects: Lowers LDL, decrease TAG, increased HDL; decrease C-reactive protein, increase NO, increase plaque stability, reduce lipoprotein oxidation, decrease platelet aggregation.

Pharmacokinetics: high first pass, given in evening (highest cholesterol synth time)

Adverse effects: liver damage (alcoholics), increase creatine kinase activity, rhabdomyolysis (mannitol to counter)

Drug interactions: grapefruit juice (enhances bioavailability), gemfibrozil (inhibits metabolism)

ALL STATINS ARE CONTRAINDICATED FOR PREGNANCY (CATEGORY X) FOR MEMBRANE DEVELOPMENT

Not Bolded

Anti-hyperlipidemia Dx

Competitive HMG-CoA reductase inhibitor

Uses: Elevated LDL as in heterozygous familial hypercholesterolemia and combined hyperlipoproteinemia

Mechanism: inactive, must be hydrolyzed; reduce plasma LDL by inhibiting HMG-CoA which increased high affinity LDL receptors
Effects: Lowers LDL, decrease TAG, increased HDL; decrease C-reactive protein, increase NO, increase plaque stability, reduce lipoprotein oxidation, decrease platelet aggregation.

Pharmacokinetics: high first pass, given in evening (highest cholesterol synth time)

Adverse effects: liver damage (alcoholics), increase creatine kinase activity, rhabdomyolysis (mannitol to counter)

Drug interactions: grapefruit juice (enhances bioavailability), gemfibrozil (inhibits metabolism)

ALL STATINS ARE CONTRAINDICATED FOR PREGNANCY (CATEGORY X) FOR MEMBRANE DEVELOPMENT

Not Bolded

Anti-hyperlipidemia Dx

Competitive HMG-CoA reductase inhibitor

Uses: Elevated LDL as in heterozygous familial hypercholesterolemia and combined hyperlipoproteinemia

Mechanism: inactive, must be hydrolyzed; reduce plasma LDL by inhibiting HMG-CoA which increased high affinity LDL receptors
Effects: Lowers LDL, decrease TAG, increased HDL; decrease C-reactive protein, increase NO, increase plaque stability, reduce lipoprotein oxidation, decrease platelet aggregation.

Pharmacokinetics: high first pass, given in evening (highest cholesterol synth time)

Adverse effects: liver damage (alcoholics), increase creatine kinase activity, rhabdomyolysis (mannitol to counter)

Drug interactions: grapefruit juice (enhances bioavailability), gemfibrozil (inhibits metabolism)

ALL STATINS ARE CONTRAINDICATED FOR PREGNANCY (CATEGORY X) FOR MEMBRANE DEVELOPMENT

Not Bolded

Anti-hyperlipidemia Dx

Competitive HMG-CoA reductase inhibitor

Uses: Elevated LDL as in heterozygous familial hypercholesterolemia and combined hyperlipoproteinemia

Mechanism: inactive, must be hydrolyzed; reduce plasma LDL by inhibiting HMG-CoA which increased high affinity LDL receptors
Effects: Lowers LDL, decrease TAG, increased HDL; decrease C-reactive protein, increase NO, increase plaque stability, reduce lipoprotein oxidation, decrease platelet aggregation.

Pharmacokinetics: high first pass, given in evening (highest cholesterol synth time)

Adverse effects: liver damage (alcoholics), increase creatine kinase activity, rhabdomyolysis (mannitol to counter)

Drug interactions: grapefruit juice (enhances bioavailability), gemfibrozil (inhibits metabolism)

ALL STATINS ARE CONTRAINDICATED FOR PREGNANCY (CATEGORY X) FOR MEMBRANE DEVELOPMENT

Not Bolded

Anti-hyperlipidemia Dx

Competitive HMG-CoA reductase inhibitor

Uses: Elevated LDL as in heterozygous familial hypercholesterolemia and combined hyperlipoproteinemia

Mechanism: inactive, must be hydrolyzed; reduce plasma LDL by inhibiting HMG-CoA which increased high affinity LDL receptors
Effects: Lowers LDL, decrease TAG, increased HDL; decrease C-reactive protein, increase NO, increase plaque stability, reduce lipoprotein oxidation, decrease platelet aggregation.

Pharmacokinetics: high first pass, given in evening (highest cholesterol synth time)

Adverse effects: liver damage (alcoholics), increase creatine kinase activity, rhabdomyolysis (mannitol to counter)

Drug interactions: grapefruit juice (enhances bioavailability), gemfibrozil (inhibits metabolism)

ALL STATINS ARE CONTRAINDICATED FOR PREGNANCY (CATEGORY X) FOR MEMBRANE DEVELOPMENT

Not Bolded

Anti-hyperlipidemia Dx

Competitive HMG-CoA reductase inhibitor

Uses: Elevated LDL as in heterozygous familial hypercholesterolemia and combined hyperlipoproteinemia

Mechanism: inactive, must be hydrolyzed; reduce plasma LDL by inhibiting HMG-CoA which increased high affinity LDL receptors
Effects: Lowers LDL, decrease TAG, increased HDL; decrease C-reactive protein, increase NO, increase plaque stability, reduce lipoprotein oxidation, decrease platelet aggregation.

Pharmacokinetics: high first pass, given in evening (highest cholesterol synth time)

Adverse effects: liver damage (alcoholics), increase creatine kinase activity, rhabdomyolysis (mannitol to counter)

Drug interactions: grapefruit juice (enhances bioavailability), gemfibrozil (inhibits metabolism)

ALL STATINS ARE CONTRAINDICATED FOR PREGNANCY (CATEGORY X) FOR MEMBRANE DEVELOPMENT

Bolded

Anti-hyperlipidemia Dx

Inhibitor of cholesterol absorption

Mechanism: blocks intestinal absorption; best if combined with a statin

Effects: reduces LDL cholesterol

Discontinued

Bolded

Anti-hyperlipidemia Dx

Inhibits pancreatic lipase

Uses: weight loss

Mechanism: decreases TAG breakdown in intestine

Adverse effects: steatorrhea

Bolded

HMW heparin; anticoagulant

Uses: anticoagulant for operations, IV catheters, prophylaxis against thrombosis (DVT and PE)

Mechanism: contain a unique pentasaccharide that binds to and acts as a catalyst for antithrombin III (AT III); mainly affects Xa and thrombin (inhibits them)

INJECTED IV EXCLUSIVELY; onset is immediate

Adverse effects: hemorrhage, heparin-induced thrombocytopenia (HIT) due to immune response to heparin

Contraindications: Renal/hepatic dysfunction, if pt is actively bleeding, hypersensitive, hemophiliac or for brain, spinal cord or eye Sx

Not Bolded

HMW heparin; anticoagulant

Uses: anticoagulant for operations, IV catheters, prophylaxis against thrombosis (DVT and PE)

Mechanism: contain a unique pentasaccharide that binds to and acts as a catalyst for antithrombin III (AT III); mainly affects Xa and thrombin (inhibits them)

INJECTED IV EXCLUSIVELY; onset is immediate

Adverse effects: hemorrhage, heparin-induced thrombocytopenia (HIT) due to immune response to heparin

Contraindications: Renal/hepatic dysfunction, if pt is actively bleeding, hypersensitive, hemophiliac or for brain, spinal cord or eye Sx

Bolded

LMW heparin; anticoagulant

Mechanism: inhibits factor Xa (inhibiting prothrombin conversion to thrombin)

Can be injected subcutaneously/used in pregnancy, lower incidence of HIT (heparin induced thrombocytopenia)

Adverse effects: hemorrhage, heparin-induced thrombocytopenia (HIT) due to immune response to heparin

Contraindications: Renal/hepatic dysfunction, if pt is actively bleeding, hypersensitive, hemophiliac or for brain, spinal cord or eye Sx

Not Bolded

LMW heparin; anticoagulant

Mechanism: inhibits factor Xa (inhibiting prothrombin conversion to thrombin)

Can be injected subcutaneously/used in pregnancy, lower incidence of HIT (heparin induced thrombocytopenia)

Adverse effects: hemorrhage, heparin-induced thrombocytopenia (HIT) due to immune response to heparin

Contraindications: Renal/hepatic dysfunction, if pt is actively bleeding, hypersensitive, hemophiliac or for brain, spinal cord or eye Sx

Not Bolded

LMW heparin; anticoagulant

Mechanism: inhibits factor Xa (inhibiting prothrombin conversion to thrombin)

Can be injected subcutaneously/used in pregnancy, lower incidence of HIT (heparin induced thrombocytopenia)

Adverse effects: hemorrhage, heparin-induced thrombocytopenia (HIT) due to immune response to heparin

Contraindications: Renal/hepatic dysfunction, if pt is actively bleeding, hypersensitive, hemophiliac or for brain, spinal cord or eye Sx

Not Bolded

LMW heparin; anticoagulant

Mechanism: inhibits factor Xa (inhibiting prothrombin conversion to thrombin)

Can be injected subcutaneously/used in pregnancy, lower incidence of HIT (heparin induced thrombocytopenia)

Adverse effects: hemorrhage, heparin-induced thrombocytopenia (HIT) due to immune response to heparin

Contraindications: Renal/hepatic dysfunction, if pt is actively bleeding, hypersensitive, hemophiliac or for brain, spinal cord or eye Sx

Anticoagulant

natural from leeches

Uses: alternative for HIT (heparin induced thrombocytopenia) pts

Mechanism: direct inhibitor of thrombin

IV only, cleared by kidney

Adverse effects: hypersensitivity, NO ANTIDOTE

Not bolded

Anticoagulant

natural from leeches

Uses: alternative for HIT (heparin induced thrombocytopenia) pts

Mechanism: direct inhibitor of thrombin

IV only, cleared by liver

Adverse effects: hypersensitivity, NO ANTIDOTE

Bolded

SMW heparin: anticoagulant

Uses: alternative in HIT (heparin induce thrombocytopenia)

Mechanism: small molecule

Cleared by liver

continuous IV infusion

Use great caution in pts with poor liver function

bolded

SMW heparin: anticoagulant

Uses: prevent stroke in pts with non-valvular a-fib

Mechanism: ORAL direct inhibitor of thrombin

Cleared by kidney

DO NOT use it pts with mechanical heart valve

AVOID ABRUPT DISONTINUATION, increased risk of thrombotic events

Bolded

Anticoagulant

Direct factor Xa inhibitor

Uses: treat DVT, PE and future clots

Mechanism: ORAL inhibitor of factor Xa

Black box: discontinue 24 hrs prior to lumbar puncture or epidural = increased risk for hematomas (epidural/spinal)

Huge deal, will take over warfarin as DOC!

Not bolded

Anticoagulant

ORAL Direct Factor Xa inhibitor

Uses: stroke and embolisms with non-valvular a-fib

Avoid abrubt discontinuation

PROTOTYPE

Anticoagulant

Uses: prevent embolid -> DVT, thromboembolism (no effect on already formed thrombi)

Mechanism: inhibits reduction of vitamin K -> interferes with synthesis of II, VII, IX and X, protein C and S

Effects: take time to happen, lasts 4-5 days

Oral

Complicated: many conditions affect it, many drug interactions, monitored by INR (2-3)

Adverse effects: hemorrhage, reversed w/ vitamin K (takes time) and FFP (immediate), quickly reduces levels of protein C increasing chance of cutaneous necrosis and infarction

Contraindicated in pregnancy

Drug interactions: Abx, hormones, NSAIDS, albumin displacing Dx, inhibit or induce liver enzymes

Bolded

Heparin antagonist

Uses: reverse anticoagulant effects of heparin

Mechanism: highly +, binds heparin which is highly -

Adverse effects: hypotension, pulmonary HTN, allergies

Contraindications: In the abscence of heparin has anticoagulant effect

Bolded

Uses: Reverse anticoagulant effect of warfarin

Mechanism: Reverses anticoagulant effect; Confers biologic activity on prothrombin and factors VII, IX and X by post-ribosomal modification

IV

Infusion must be slow to avoid chest pain, back pain, dyspnea or death

Bolded

Fibrinolytic agent

Uses: stroke, lyse clots, severe PE, DVT, arterial thrombosis

Endogenously made by endothelial cells

IV

Side effects: serious bleeding

Bolded

Fibrinolytic agent

Uses: not clot-fibrin specific so causes generalised fibrinolytic activity; combined with aspirin it's as good as other fibrinolytics

Mechanism: forms a complex with plasminogen, enhancing fibrinolytic activity

Can cause allergies, pyrexia, and anaphylaxis

Not bolded

Fibrinolytic agent

Not bolded

Fibrinolytic

Bolded

Antifibrinolytic

Uses: bleeding disorders, hemophilia, reversal of fibrinolytic therapy, prophylaxis against re-bleeding in intracranial aneurysms

Mechanism: completely inhibits plasminogen activation, prevents formation of plasmin; inhibits streptokinase/urokinase activity

Oral or IV

cleared by kidney

Adverse effects: can cause IV thrombosis, don't use in pts with DIC or GI bleeding

Not bolded

Antifibrinolytic

Uses: bleeding disorders, hemophilia, reversal of fibrinolytic therapy, prophylaxis against re-bleeding in intracranial aneurysms

Mechanism: completely inhibits plasminogen activation, prevents formation of plasmin; inhibits streptokinase/urokinase activity

Oral or IV

cleared by kidney

Adverse effects: can cause IV thrombosis, don't use in pts with DIC or GI bleeding

Bolded

Antiplatelet drug

Uses: pts at risk of remoblism, primary intervention for MI

Mechanism: irreversible COX inhibiter -> decreases TXA2, lasts the life of the platelet

Don't take before dental procedures or Sx

Bolded

Antiplatelet drug

Uses: DOC prevent thrombosis in coronary stent placement sx; inhibit platelet aggregation in pts who are allergic to aspirin

Mechanism: Irreversibly blocks ADP receptor on platelets

Oral

Adverse effects: bleeding, nausea, diarrhea

Not Bolded

Antiplatelet drug

Uses: DOC prevent thrombosis in coronary stent placement sx; inhibit platelet aggregation in pts who are allergic to aspirin

Mechanism: Irreversibly blocks ADP receptor on platelets

Oral

Adverse effects: bleeding, nausea, diarrhea

Not Bolded

Antiplatelet drug

Uses: DOC prevent thrombosis in coronary stent placement sx; inhibit platelet aggregation in pts who are allergic to aspirin

Mechanism: Irreversibly blocks ADP receptor on platelets

Oral

Adverse effects: bleeding, nausea, diarrhea

Not Bolded

Antiplatelet drug

Uses: DOC prevent thrombosis in coronary stent placement sx; inhibit platelet aggregation in pts who are allergic to aspirin

Mechanism: Irreversibly blocks ADP receptor on platelets

Oral

Adverse effects: bleeding, nausea, diarrhea

Bolded

Antiplatelet drug; monoclonal Ab

Indications: combine with heparin, angioplasty, atherectomy, stent

Mechanism: Inhibits platelet aggregation by inhibiting GPIIb/IIIa receptor from binding fibrinogen

IV

Adverse effects: bleeing, thrombocytopenia

Not bolded

Antiplatelet drug; monoclonal Ab

Indications: combine with heparin, angioplasty, atherectomy, stent

Mechanism: Inhibits platelet aggregation by inhibiting GPIIb/IIIa receptor from binding fibrinogen

IV

Adverse effects: bleeing, thrombocytopenia

Not bolded

Antiplatelet drug; monoclonal Ab

Indications: combine with heparin, angioplasty, atherectomy, stent

Mechanism: Inhibits platelet aggregation by inhibiting GPIIb/IIIa receptor from binding fibrinogen

IV

Adverse effects: bleeing, thrombocytopenia

Bolded

Antiplatelet drug

Indication: promotes vasodilation and inhibits platelet aggregation, intermittent claudication

Mechanism: Phosphodiesterase 3 inhibitor -> increases cAMP level

Oral

Contraindicated with CHF