Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
66 Cards in this Set
- Front
- Back
Monobactam
|
beta-lactam cell wall synthesis inhibitor
-narrow spectrum (-) -bactericidal, time dependent -some resistance to beta-lactamase |
|
Carbapenem
|
-beta-lactam cell wall synthesis inhibitor
-broad spectrum -bactericidal, time dependent -may induce beta lactamases |
|
Vancomycin
|
-Binds to peptidoglycan polymers
-PO for C. dificile -IV for gram + that dont respond to beta-lactams -Van A prevents binding, combine with methicillin if that's the case |
|
Macrolides
|
Erythomycin
Clarithomycin Telithromycin -prevent tRNA translocation |
|
minoxidil
|
* - direct vasodilator
* - oral drug: used for outpatient treatment of hypertension * - highly effective with lots of side effects (fyi: hypertrichosis); reserved for severe hypertension that does not respond to other drugs * - inc hair growth = rogaine |
|
Statins
|
* HMG-CoA Reductase Inhibitors
* – HMG-CoA reductase is a key liver enzyme for the synthesis of cholesterol * – By inhibiting cholesterol synthesis in the liver, cellular concentrations are reduced andLDL receptors are up-regulated resulting in increased removal of LDL from the blood. * - Also produce modest increases in HDL (less than niacin) and decreases in VLDL (lessthan niacin/fibric acid drugs) |
|
prazosin
|
* SYMPATHOLYTIC DRUGS
* Block sympathetic n.s. induced contraction of arterial smooth muscle a1 adrenergic receptor antagonists * -OSIN |
|
valsartan
|
# Angiotensin Receptor Blockers (ARBs) inhibit binding of angiotensin IIto the AT1 receptor
# - ARTAN |
|
sodium nitroprusside
|
* - PARENTERAL DRUGS: used for emergency situations (hypertension crises)Too efficacious for outpatient use: too many side effects for outpatient use
* - nitrate drug * - dinitrated to NO = vasodilator |
|
T-PA
|
* - tissue plasminogen activator drugs
* - destroy blood clots after they have formed * - digests fibrin and breaks down fibrin-rich clots (red-thrombi) |
|
fluvastatin
|
- statin drug
|
|
Ezetimibe
|
* Binds to protein on GI epithelial cells that promotes cholesterol absorption in the small intestine.
* • Inhibits of intestinal absorption of dietary cholesterol * • Reduces LDL levels (tx. hypercholestolemia) * • GI side effects |
|
Aspirin
|
* - acetylates and inhibits COX-1 to reduce TXA2 sythesis
* - anti-thrombotic * -75-81 mg (one baby aspirin/day) is sufficient to protect against acute MI in moderate tohigh risk individuals * -At time of heart attack: four baby aspirin (325 mg; chewed) to protect against re-occlusion and subsequent heart attack * -Maintain on higher-dose (325 mg) aspirin after acute MI to protect against another heartattac |
|
nifedipine
|
- Short-acting dihydropyridines CCBs = increased risk ofmyocardial infarction relative to patient taking diuretics or beta blockers
|
|
Abciximab
|
* PLATELET RECEPTOR ANTAGONISTS
* • Antagonize receptors on platelet cell membranes to prevent physicalinteraction of platelets with fibinogen and therefore platelet aggregation * • Administered parenterally for Percutaneous Coronary Interventions (PCIs;new term for angioplasty) to prevent reocclusion of coronary vessel * - anti-GPIIb/IIIa antibody * - given during PCI surgery |
|
Niacin
|
* - TREATMENT OF HYPERTRIGLYCERIDEMIA INVOLVES DECREASINGCIRCULATING VLDL LEVELS
* - increases HDL levels * - does have net dec in LDL due to mainly acting on dec vldl syn in liver |
|
enalapril
|
* - ACE Inhibitors: inhibit conversion of angiotensin to angiotensin II byangiotensin converting enzyme (ACE)
* - PRIL * - pro-drug |
|
Gemfibrozil
|
* - TREATMENT OF HYPERTRIGLYCERIDEMIA INVOLVES DECREASINGCIRCULATING VLDL LEVELS
* - no change in LDL |
|
Heparins
|
* - parenteral anticoagulants
* - Binds to and stimulates ANTITHROMBIN III, an endogenousinhibitor of clotting factors. * • Given as mixture of different sizemolecules purified from animal sources biological units) * • Molecular weight determines activity * - Polysaccharide = very hydrophilic & susceptible to digestion so must be given IV or SC * - reversed by PROTAMINE |
|
Cholestyramine
|
* - tx hypercholestolemia hyperlipidemia
* - bile acid-binding resin * - less bile available for reabsorption * - dec liver bile, lower live cholesterol, increase in ldl receptors, inc ldl uptake into liver |
|
Angiotensin related Agents
|
* Block effects of the renin-angiotensin system, thereby reducing blood pressure primarily by inhibiting angiotensin II induced…
* • Vasoconstriction * • Increases in aldosterone production * • Increases in vasopressin release * • No reflex sympathetic activation (resetting of baroreceptors?) |
|
Colestipol
|
* - tx hypercholestolemia hyperlipidemia
* - bile acid-binding resin * - less bile available for reabsorption * - dec liver bile, lower live cholesterol, increase in ldl receptors, inc ldl uptake into liver |
|
amlodipine
|
- long-acting dihydropuridine
-CCB non-cardiogenic |
|
Ticlopidine
|
* - ADP receptor blocker
* - anti-thrombotic * - More side effects than clopidogrel : GI effects, greater bleeding risk * - Higher-risk individuals for MI; post-MI; post PCI surgery |
|
prazosin
|
* SYMPATHOLYTIC DRUGS
* Block sympathetic n.s. induced contraction of arterial smooth muscle a1 adrenergic receptor antagonists * -OSIN |
|
simvastatin
|
* - Zocor
* - medium efficacy * - available generically |
|
atorvastatin
|
* - Lipitor; most prescribed statin drug
* - High efficacy * - no available generically |
|
Unfractionated Heparin
|
- combination of low and high molecular weights = more activity = more bleeding
|
|
reserpine
|
* - VMAT inhibitor
catecholamine release inhibitor * - indirect acting sympatholytic |
|
Lepirudin
|
- Direct Thrombin Inhibitors (DTI’s) Analogs of Hirudin – purifiedfrom medicinal leeches (Hirudo medicinalis); directly inhibit thrombin
|
|
sodium nitroprusside
|
* - PARENTERAL DRUGS: used for emergency situations (hypertension crises)Too efficacious for outpatient use: too many side effects for outpatient use
* - nitrate drug * - dinitrated to NO = vasodilator |
|
Alteplase
|
- recombinant T-PA
|
|
Triamterine
|
* - Potassium sparing diuretic; 5% Na+
* - Blocker of Na channel * – Reduced Na+/K+ exchange in distal tubule and collecting duct results inreduced Na+ re-absorption and K+ retention * – Commonly too weak to be used alone but counteract hypokalemia associated with other diuretics in high-risk patients * - All diuretics have dehydration as a potential side effect |
|
losartan
|
* - Angiotensin Receptor Blockers (ARBs) inhibit binding of angiotensin IIto the AT1 receptor
* - ARTAN |
|
Nebivolol
|
* - beta blocker that promotes nitric oxide (NO) production
* - dec both CO and TPR * - B blocker/vasodilator |
|
valsartan
|
* - Angiotensin Receptor Blockers (ARBs) inhibit binding of angiotensin IIto the AT1 receptor
* - ARTAN |
|
Vasodilator Side Effects
|
* Postural hypotension
* flushing, sweating * headache * reflex tachycardia: prevented w/ coadmin B Blocker * reflex fluid ret: coadmin w/ diuretic * - Vasodilators are almost always coadmin w/ either to prevent reflexes |
|
lovastatin
|
- statin drug
low-efficacy |
|
propranolol
|
* - Non-selective B Blocker
* - decrease CO * - B2 Activation...lungs, liver, skeletal vasculature |
|
ACE Inhibitor Side Effects
|
* SIDE EFFECTS:
* • Dry cough (bradykinin effect due to ACE inhibition) * • Angioedema (rapid non-allergic swelling of skin and mucosa; also dueto bradykinin) * • Hyperkalemia (reduced sodium potassium exchange in kidney) * • Reduced kidney function (use with caution if kidney function is alreadyimpaired) * • TERATOGENIC: DO NOT USE DURING PREGNANCY |
|
captopril
|
* - ACE Inhibitors: inhibit conversion of angiotensin to angiotensin II by angiotensin converting enzyme (ACE)
* - PRIL * - no metabolism necessary |
|
Hydrochlorothiazide
|
* – Inhibit sodium reabsorption from distal tubule; 10% Na+
* – Usually used for the long-term outpatient management of hypertension * - deplete potassium = HYPOKALEMIA * - inhibit uric acid elimination = promote gout * - increase LDL levels |
|
aliskiren
|
- Renin Inhibitors: inhibit conversion of angiotensinogen to angiotensin I by the enzyme renin
|
|
pravastatin
|
- low efficacy statin
|
|
terazosin
|
* SYMPATHOLYTIC DRUGS
* Block sympathetic n.s. induced contraction of arterial smooth muscle a1 adrenergic receptor antagonists * -OSIN |
|
Ethacrynic acid
|
* – Loop Diuretic; 35% Na+
* -Usually used for short-term management of more severe hypertension (morepowerful, high efficacy, shorter acting) * – Inhibit sodium, reabsorption from the loop of Henle * - deplete potassium = HYPOKALEMIA * - inhibit uric acid elimination = promote gout |
|
rosuvastatin
|
* - high efficacy statin
* - Crestor * - not available generically |
|
Streptokinase
|
T-PA
most effective w/in 4.5 hours of stroke |
|
dihydropyridines
|
* - DIPINE
* - NON-CARDIOACTIVE CCBs: relax vascular smooth muscle but have little effect on cardiac output * - long-acting orsustained releaseformulations |
|
Carvedilol
|
* - mixed beta-1 and alpha-1antagonist
* - B Blocker/Vasodilator * - dec both CO and TPR |
|
diltiazem
|
* -CCB
* - cardioactive: Block channels in vascular smooth muscle AND in the heart * – Vasodilators AND cardiac inhibitors |
|
nadolol
|
* - Non-selective B Blocker
* - decrease CO * - B2 Activation...lungs, liver, skeletal vasculature |
|
clonidine
|
* - sympatholytic indirect acting
* - a2 receptor agonist * - cns acting to reduce symp n.s. activity * - act at N. Tractus Solitarius |
|
Furosemide
|
* – Loop Diuretic: 35% filtered Na+
* -`Usually used for short-term management of more severe hypertension (morepowerful, high efficacy, shorter acting) * – Inhibit sodium, reabsorption from the loop of Henle * - deplete potassium = HYPOKALEMIA * - inhibit uric acid elimination = promote gout |
|
atenolol
|
* - B1 Selective blocker
* - dec CO |
|
Nitroglycerin
|
* - inactivated through first pass metabolism and therefore are usually given sublingually as a tablet or spray or transdermally
* - organic nitrate * - classic and variant angina |
|
Enoxaparin
|
* - Low molecular weight HEPARIN = less activity
* - anticoagulant * - less risk for bleeding |
|
Vytorin
|
* Ezetimibe (Zetia) + simvastatin
* •ENHANCE study (fyi: Merck and Schering-Plough): although Vytorin produced greaterreductions in LDL than simvastatin alone,coronary atherosclerotic plaque formationwas no different * Implications: * 1. Vytorin is no more protective against coronary heart disease than statinmonotherapy; potentially questions the effectiveness of ezetimibe * 2. Suggests that effectiveness of statins versus coronary heart diseasemay not only involve reductions in LDL; potential anti-inflammatoryeffects |
|
isosorbide di-/mono-nitrate
|
* - organic nitrate
* - admin orally * - classic and variant angina |
|
Warfarin
|
* ORAL ANTICOAGULANT
* • PREVENTS VITAMIN K RE-ACTIVATION by inhibiting Vit K epoxidereductase * • Active Vitamin K is required for synthesis of clotting factors in both theintrinsic and extrinsic systems * • Delayed onset of action * • Teratogenic: avoid during pregnancy; Has many drug interactions * - • Genetic variation in CYP2C9 reduceswarfarin metabolism = increased bleedingrisk * • variation in the VKORC1 subunit reduces warfarin sensitivity = increased clotting risk |
|
Tirofiban
|
* PLATELET RECEPTOR ANTAGONISTS
* • Antagonize receptors on platelet cell membranes to prevent physicalinteraction of platelets with fibinogen and therefore platelet aggregation * • Administered parenterally for Percutaneous Coronary Interventions (PCIs;new term for angioplasty) to prevent reocclusion of coronary vessel * - GPIIb/IIa Antagonists * - given during PCI surgery |
|
Amiloride
|
* - Potassium sparing diuretic; 5% Na+
* - Blocker of Na+ channel on apical membrane * – Reduced Na+/K+ exchange in distal tubule and collecting duct results inreduced Na+ re-absorption and K+ retention * – Commonly too weak to be used alone but counteract hypokalemia associated with other diuretics in high-risk patients * - All diuretics have dehydration as a potential side effect |
|
hydralazine
|
* - direct vasodilator
* - oral drug: used for outpatient treatment of hypertension * - selective arterial dilator |
|
verapamil
|
- CARDIOACTIVE CCBs: relax vascular smooth muscle andreduce cardiac output (decrease heart rate, AVconduction, and force of contraction)
|
|
minoxidil
|
* - direct vasodilator
* - oral drug: used for outpatient treatment of hypertension * - highly effective with lots of side effects (fyi: hypertrichosis); reserved for severehypertension that does not respond to other drugs * - inc hair growth = rogaine |
|
diazoxide
|
* - PARENTERAL DRUGS: used for emergency situations (hypertension crises)Too efficacious for outpatient use: too many side effects for outpatient use
* - highly effective and long-acting = not a first choice-drug |