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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