Pharmacology slides; spring term first year
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Complete list of Terms and Definitions for Pharmacology slides; spring term first year

Terms Definitions
HCTZ ADR digoxin NSAIDS
Ezetimibe adverse effects myopathy rhabdomyolysis hepatitis pancreatitis thrombocytopenia (watch platelets)  
Blocking agents Ezetimibe (Zetia) inhibits cholesterol absorption in small intestine  
revascularization therapy CABG Percutaneous transluminal coronary angioplasty (PTCA)
Nitro drug interactions hypotensive drugs phosphodiesterase type5 inhibitors BB's, verapamil, diltiazem
Calcium Channel blockers diltiazem(cardizem) and nifedipine(procardia) blocks calcium channels in VSM  
Variant angina (prinzmetal's-vasospastic) pathophysiology coronary artery spasm
apolipoprotiens recog. sites for cell-surface receptors activate enzyme that metabolize lipoprotiens increases structural stability of lipoprotiens
sodium lost at the PCT 60-65%
Chronic stable angina (exertional) pathophysiology emotional excitement large meals cold exposure coronary heart disease  
variant angina Tx inc. cardiac O2 supply
CCB adverse effects reflex tachycardia (from hypotension) dilation of peripheral arterioles hypotension bradycardia heart failure AV block
HMG-CoA reductase inhibitors (statins) Atorvastatin (Lipitor) most effective reduces LDL elevates HDL Reduces triglycerides Non lipid action: promotes plaque stability, reduces risk for CV event, inc. bone formation
acute corornary syndrome unstable angina or MI
Active secretion "pumps" organic acids and organic bases
Re-absorption key factor with diuretics What is reabsorbed and where is it re-absorbed?
Cholesterol component of all cell membranes and membranes of intracellular organisms required for synthesis of certain hormones (reproductive) and bile salts deposited in stratum corneum of skin
unstable angina Tx maintain O2 supply dec. O2 demand
determinants of O2 supply myocardial blood flow myocardial perfusion only in diastole
streptokinase therapeutic uses acute coronary thrombosis (acute MI) Large deep venous thrombosis massive pulmonary emboli
Spironolactone ADR ACE inhibitors (lisinopril): inc. K+ retention
Na+ lost at the DCT (early segment) 10%
HCTZ uses initial HTN Tx (mild - moderate) Vasodilation (diuretic effect dwindles but this stays) Ca++ spilling in urine (helps reabsorb higher rates of calcium) slows osteoporotic process
streptokinase (streptase) binds to plasminogen to form active complex
Gemfibrozil Therapeutic uses reduces high levels of plasma triglycerides and VLDLs less effective than statins in reducing LDL can raise HDL (not approved for this)
Ezetimibe therapeutic uses reducing total cholesterol, LDL, and apolipoprotien B approved for monotherapy and combonation with statins (slightly inc. risk for liver damage)
dietary cholesterol produces only small increase in blood levels inhibits endogenous cholesterol production
furosmide drug interactions Digoxin (potentiates toxicity due to low K+ levels) aminoglycosides (also produce ototoxicity) cephalosporins (compete in gut with lasix for transfer into body, Tx inc. lasix) NSAIDS (dec. effectiveness of lasix, Tx change pain med)  
diuretics that work at the early segment of the DCT thiazides (hydrochlorothiazide)
spironolactone cautions monitor serum and sodium levels no K+ salts or substitutes
LDL in atherosclerosis begins with transport of LDL's from arterial lumen into endothelial cells, then to the space underlying the arterial epithelium
Chronic stable angina Tx inc. cardiac O2 supply dec. O2 demand
Low density lipoprotiens (LDL) transport from liver to body periphery
adjunct Tx or High LDL cholesterol Therapeutic lifestyle changes TLC diet weight control excercise smoking cessation Drugs should be used only if these fail
diuretics that work at the PCT manitol osmotic diuretic carbonic anyhydrase inhibitor used for: mountain climbers - high altitude - swelling of the brain
diuretics that work at the ascending limb of loop of henle Loop diuretics (furosemide)
three families of antianginal agents 1. organic nitrates (e.g. nitro, isosorbide (isordil)) 2. CCB's (diltiazem, nifedipine) 3. BB's (propanolol, metoprolol)
diuretics that work at the late segment of the DCT Potasium sparing diuretics/aldosterone antagonist (spironolactone, aldactone)
Filtration non-selective process
thrombolytic drugs streptokinase(streptase): fibrinolytic, causes lysis of thrombus Altepase (tPa)
Ezetimibe drug interactions statins fibrates bile-acid sequesterants cyclosporine
Gemfibrozil adverse effects rashes GI disturb. gallstones myopathy liver injury (hepatotoxic)
Beta Blockers propanolol(inderol) and metoprolol(lopressor) Dec. cardiac O2 demand
determinants of oxygen demand HR myocardial contractility intramyocardial wall tension (preload/afterload)  
Bile Acid Sequesterants Colesevelam (Welchol) previously first line drugs but now adjunt to statins reduction in LDL inc. in VLDL (in some Pts) not absorbed in GI, Binds with bile acids also lowers LDL by inc. LDL receptors on hepatocytes
variant angina therapeutic agents CCB's Organic nitrates
very low density lipoprotiens (VLDL) tryglycerides
CHD risk factors Diabetes inc. age HTN smoking dec. HDL, inc. LDL Family Hx
Hmg co-A reductase enzyme to sythesize cholesterol inhibited by statins
nitro therapeutic uses acute anginal therapy sustained anginal therapy IV for perioperative control of blood pressure, and Tx of heart failure with MI, unstable angina, and uncontrolled exacerbations of chronic angina
HMG-CoA R.I. therapeutic uses hypercholesterolemia primary and secondary prevention of CV events post MI therapy diabetes? dec. risk of stroke
Spironolactone SE steroid structure (inc. testosterone like effect) profound hyperkalemia  
diuretics work to... counter/alter normal renal Fx
spironolactone uses HF, MI (aldosterone antagonist properties) used with lasix?  
BB's adverse effects bradycardia and hypotension dec. AV conduction reduction of contractility asthmatic effects depression insomnia and bizzare dreams sexual dysfuntion
streptokinase adverse effects bleeding- excessive fibrinolysis can be reversed with aminocaproic acid (amicar) antibody production hypotension fever intercranial hemorrhage
Na+ lost at the DCT (late segment) 5%
HCTZ cautions FVD Hypokalemia (not as severe as lasix) all electrolyte deficit (except Ca++) inc. CBG's lipid changes ototoxicity hypercalcemia
the faster the diuresis the more complications arise
Nicotinic Acid adverse effects skin (flushing, itching): initially intense preTx w/ ASA Gastrointestinal: hepatotoxicity hyperglycemia gouty arthritis raise blood level of homocysteine (inc. risk for CHD)
unstable angina pathophysiology symptoms of angina at rest new-onset exertional angina intensification of existing angina
time is takes for myocardium to die 20 minutes
HMG-CoA R.I. dosing once daily in evening greatest impact when given in evening because endogenous cholesterol syn. goes up in the night
fursosemide cautions take in morning leg cramps are not RLS K+ supplement watch BP hyponatremia drug interactions
furosemide misc SE hyperglycemia inc. LDL and HDL (watch lipid profile) inc. uric acid (gouty attacks)
high density lipoprotiens (HDL) take cholesterol from periphery where it is stored
HMG-CoA R.I. adverse effects Common: HA, Rash, Gi disturb. Rare: myopathy(muscle pain, weakness, tenderness)/rhabdomyolysis(muscle dissolves) hepatotoxicity(monitor LFT, baseline, then 6-12 Months) peripheral neuropathy maybe connection with parkinsons
Angina pectoris O2 supply to heart is insufficient to meet O2 demand sudden pain beneath sternum, often radiating to left shoulder and arm
Bile Acid Sequesterants adverse effects Constipation does not decrease uptake of fat-soluble vitamins (as other bile sequesterants do) does not significantly reduce absorprtion of statins, warfarin, or digoxin
drugs used to prevent MI and death antiplatelet drugs cholesterol lowering drugs ACE inhibitors antianginal agents
organic nitrates (nitroglycerin) works directly on vasc. smooth muscle for Venodilation dec. cardiac workload dec. pre/afterload= dec. O2 demand inc. O2 supply
furosemide (lasix) action keeps sodium in lumen of tubule last around six hours PO: diuresis w/in 60 min IV: diuresis within 5-10 min
HMG-CoA R.I. drug interactions most lipid lowering drugs (except bile acid sequesterants) Drugs that inhibit CYP3A4 (macrolide antibx, antifungals,
Fibric acid Derivatives (fibrates) most effective drugs for lowering TG levels can raise HDL Little to no effect on LDL can inc. risk for bleeding for Pts on warfarin(watch PT-INR) can inc. risk for rhabdomyolysis in Pts taking statins
Na+ lost at the ascending limb of the loop of henle 20 %
nicotinic acid (niacin) Niaspan (long acting niacin) Reduces LDL and TG levels (better at dec. TG) inc. HDL more effectively than any other drug dec. production of VLDL