Ch 1 The Nursing Process and Drug therapyfive phases of the nursing process. 1. Assessment- Data collection involves both Subjective and Objective. Should be focused on symptoms & organs most likely to be affected by clients drug therapy - Subjective- Current Healthy history, client verbalized symptoms, current medications (dosage, route, frequency, & prescribing physician), clients knowledge of their medications, drug allergies, clients compliance of drug regimen, over the counter supplements, past medical history, clients environment, and their support system. - Objective Gross and fine motor movement, ROM, laboratory results, diagnostic studies, clients height weight and other physical assessment values temperature, pulse, blood pressure and respirations. 2. Diagnosis -human response to illness (actual or at risk) -related to -as evidenced by 3. Planning- Setting of the goals for the patient and developing interventions to help patient to accomplish them. 1. Goals should always follow SAME: 2. Specific for this patient 3. Action oriented 4. Measurable ( and in a specific time frame) 5. Evaluation- is able to continually be evaluated and revised as necessary. 4. Implementation- this would be our Nursing actions 5. Evaluation REMEMBER OUR NURSING RESPONSIBILITY IS TEACHING ! 5 Big Ones: each and every time Right Patient Right Drug Right Dose Right Time Right Route Right Documentation (the 6th) Right Rationale Right to Refuse Nursing responsibilities of medication administration One of key interventions in nursing care. Name of drug Intended use Effects on body Contraindications and precautions Special considerations Why it is prescribed How to administer the drug

Ch 2 Drug Action

Pharmacology: The study of drugs and their interactions with living systems Encompasses the study of the physical and chemical properties of drugs as well as their biochemical and physiological effects. Clinical Pharmacology: Study of drugs in humans (includes study of drugs in patients as well as healthy volunteers). DRUGS: Effectiveness: Most important! Elicits the response for which the drug is given. Current US law requires proof effectiveness prior to release for marketing. Safety: One that cannot produce harmful effects (there is no such thing as a SAFE drug) Selectivity: Elicits only the response for which it is given thus no side effects (No such thing as a selective drug). Pharmacotherapeutics: The medical use of drugs (use to dx, prevent or treat disease, or prevent pregnancy) Pharmacokinetics: The study of the movement of drugs through the body. Drugs that are taken by mouth go through three phases A PO drug has to become a solution so that it can pass through biological membrane. This process is called dissolution. If a drug is administered intravenously, intramuscularly or subcutaneously there is no dissolution Four Basic Processes 1. Absorption (think stomach) 2. Distribution (think blood flow) 3. Metabolism (think liver) 4. Excretion (think kidney) Movement through the body Absorption: the movement of a drug from its site of administration into the blood. -Enhanced absorption occurs by rapid drug dissolution, high lipid solubility, a large surface area, and high blood flow at the site of administration. Distribution: defined as the movement of drugs throughout the body. - In most tissues, drugs can easily leave the vasculature through spaces between the cells that compose the capillary wall. - Many drugs reversibly bind to albumin. While bound to albumin, drug molecules cannot leave the vascular system. Metabolism: Biotransformation. Enzymatic alteration of drug struction -most takes place in the liver and is catalyzed by cytochrome p450 system of enzymes. -Most important consequence of drug metabolism is promotion of renal drug excretion First-Pass Effect: rapid inactivation of some oral drugs as they pass through the liver after being absorbed. Essentially, how much drug is left available after passing through the liver. Used to determine dosage and intensity. Excretion: Most drugs are excreted by the kidney. -Renal drug exretion has 3-steps: glomerular filtration, passive tubular

reabsortion, and active tubular secretion. -Drugs that are highly lipid soluble cannot be reabsorbed back into the kidney -Drugs can be excreted into breast milk. Bioavailabilty: free-circulating drug system (post-first pass) even after binding. Half-Life: Time required for the amount of drug in the body to decline by 50%. Shorter the half-life, the more frequent the administration. Time to reach plateau about 4 half-lives. Drugs with a long half-life may need a loading dose to reach plateau. Pharmacokincetic tolerance: results from a accelerated drug metabolism. Pharmacodynamics: Is the study of drug concentration and its effect on body. Drug response can be primary effect or a secondary physiological effect. -Think Onset of action-Is the time it takes the drug to reach minimum effect concentration -Time of Peak effect of the drug -Time that it takes for drug to reach its highest blood or plasma level -Duration- The length of time the drug has a pharmacological effect. Agonist: Drugs that produce a response Antagonist: Drugs that inhibit/block a response Categories : There are four 1. Stimulation/or Depression- either the drug stimulates of depresses a cell or a glands activity. 2. Replacement- drug replaces an essential body compound like insulin 3. Inhibition or killing of Organism- think antibacterial or anti- fungal agents 4. Irritation-here think of laxatives causing intestinal irritation to stimulate peristalsis. Reducing risk of adverse interactions: minimize # of drugs the patient is on. Take a thorough drug history. Adjust dosages when using an inducing agent. Adjust timing of administration to reduce absorption problems. Monitor for early signs of toxicity. Be vigilant when a patient is on a drug with a low therapeutic index. Pharmacodynamic tolerance: results from adaptive changes that occur in response to prolonged exposure. It increases the MEC of a drug.

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Therapeutic Index: (LD50: ED50) A measure of a drugs safety. Drugs with a high TI are presumably safe. Enteral Drug Administration Advantages/Disadvantages Convenient and least costly Safe

Can be a fast absorption Sublingual has a rapid onset Swallowing difficulties can make it difficult in some people May be inactivated if tablets or capsules crushed or opened Can irritate mucosa Can be inactivated by enzymes or hepatic circulation Depends on client gastrointestinal motility and mobility Parenteral Drug Administration Advantages/Disadvantages Rapidly absorbed Rapid onset of action Not inactivated by enzymes or metabolized in liver Possibility of introduction of pathogenic microbes Once injected, cannot be retrieved Topical Drug Administration Advantages/Disadvantages Fewer side effects Absorbed slowly but consistently Rectal safe for comatose clients Unless ordered, not applied to compromised skin Rectal route may be difficult to retain Can work locally, or be absorbed for generalized body use Example triamcinolone vs. fentanyl Multidrug Therapy and Drug Interactions Additive effect : 1 + 1 = 2 Synergistic effect : 1 + 1 = 3 Antagonistic effect : 1 + 1 = 75% absorbed rapidly directly into the internal Jugular Vein Right Atrium. Topical Transderm Nitro Patch- slow absorption by the skin acts on the smooth muscle, blood vessel, causing relaxation & dilatation cardiac preload and after load( Peripheral vascular resistance) myocardial O2 demand. - Pharmacodynamics- SL- Onset- 1- 3 minutes, Peak- 4 min. Duration- 2030 min Slow Released Onset 20-45 min. Duration- 3-8 hrs. Ointment Onset 20 -60 min Peak 1-2 hrs. Duration 6-8hrs. Patch -

Onset 30- 60 min Peak 1-2 hrs. Duration20-24hrs. I.V. - Onset 1-3 min. Duration 3-5 min. - Side Effects nausea, vomiting, H/A, dizziness, syncope, weakness, flush, confusion, pallor, rash, dry mouth. d. Adverse Reactions: Hypotension, reflex tachycardia, paradoxical bradycardia. e. Drug-Lab-Food Interactions effect with alcohol, beta-blockers, calcium channel blockers, antihypertensives, effects of heparin. Beta Adrenergic Blockers Beta I and Beta II the effects of the Sympathetic nervous Systems by blocking catecholamines Epinepherine and Norepinepherine which heart rate and blood pressure. Used as an anti-anginal, anti-dysrhythmic, and antihypertensive. Patients should be told that they should NOT abruptly stop these medications. - Beta1- Atenolol ( Tenorium) - It can be used with asthmatic patients. -Metoprolol( Lopressor)- Beta1 . High dose can effect Beta2 Bronchoconstriction -Beta1 and Beta2 - used to treat Angina Pectoris and hypertension - Nadolol (Corgard) - Propanolol (Inderal) . Risk for Bronchospasms Calium Channel Blockers - myocardial contractions O2 demand by myocardial tissue. Relax coronary artery spasms and peripheral arterioles, cardiac oxygen demand. Amilodipine (Norvasc) - Angina and Hypertension 1. Diltiazem ( Cardizem) - Used for treatment of Angina Pectoris, its hypotensive effect is not as severe as with procardia. Kidney function should be monitored, 2. Nifedipine ( Procardia) - . It is used for to treat angina pectoris and hypertension. Suppresses contraction of cardiac and vascular smooth muscle. Increases heart rate and cardiac output. Decreases blood pressure. Three of the Calcium Channel Blockers are used for the long term treatment of Angina Verapamil( Calan), Nifedipine (Procardia), and Diltiazem (Cardizem). Procardia is the most potent. Side Effects H/A, hypotension ( more common with procardia) and less common with Diltiazem. calcium channel blockers Calan, ProCardia, Cardizem lowers myocardial contraction and eases workload, lowers HR and BP, raises blood flow to heart, lowers peripheral vasorestiction for HTN, angina, A-fib, migraines SE=HYPOtension, HA, "blah" feeling....monitor hepatic and renal function, assess BP and HR Antidysrhythmia - A dysrhythmia is any deviation from a normal rate or pattern of a heartbeat. 1. Dysrhythmia- disturbance of a heart rhythm. 2. Arrhythmia- absence of a heart rhythm 3. Aterial Dysrhythmia- prevents ventricular filling and. 4. Arrhythmia- absence of a heart rhythm 5. Aterial Dysrhythmia- prevents ventricular filling and cardiac output by 1/3 6. Ventricular Dysrhythmia- are life threatening because of ineffective filling of the ventricle resulting in or absence of cardiac output.

7. Cardiac Dysrhythmias commonly occur after a M.I.(myocardial infarct) or hypoxia or hypercapnia (level of CO2 in the blood) , thyroid disease, C.A.D., Cardiac Surgery, Excessive catecholamines, or electrolyte imbalances. 8. Action Potential- Remember when Na+ and Ca+ enter the mycocardial cells muscle contraction and depolarization occurs. Anti-dysrhythmia drugs- there are four class of anti-arrhythmic drug which effect the different phases of the action potential. Class I: Sodium Chanel Blockers: -Slow condition which prolongs Repolarization (Atrial and Ventricular such as PAT- Paroxysmal Atrial Tachycardia and SVT Supra Ventricular Tachycardia) -Slow conduction that shortens Repolarization(Acute Ventricular Dysrhythmias) -Prolong condition with little effect on Repolarization (Life threatening Ventricular dysrhythmias). Class II: Beta Blockers: Reduce Ca+ entry, conduction velocity ,automaticity and recovery time (refractory period) Used to treat (Atrial flutter & Fibrillation, tachydysrhythmias and Ventricular and Supraventricular dysryhthmias). Class II Beta-Adrenergic Blockers- (more frequently used prescription for dysrhythmias than Na+ channel blockers Acetbutolol (Sectral)-Beta1 blocker - Pharmocokinetics- Well absorbed from the GI tract. via -Metabolized in Liver to active metabolites- 50-60% is eliminated in bile feces. 30-40 is excreted in urine. Pregnancy class is B. Protein Bound: UK . -Metabolism: t : 3-4 hrs. Metabolites: 8-13 hrs. -Pharmocodynamics: Ventricular dysrhythmia: PO: Onset: 1 hr. -Peak: 4-6 hrs. -Duration: 10 hrs. For treatment of HTN duration = 20-24 hrs. Class III: Drugs that prolong Repolarization: Prolong repolarization during ventricular dysrhythmias, and prolong action potential duration. Used to treat (Life threatening Atrial & Ventricular dysrhythmias resistant to other drugs). Class IV: Calcium Channel Blockers: Block influx of Ca+, Slow conduction velocity, myocardial contractility (Negative Inotropic), and refraction in the AV node. Used to treat (Supraventricular tachdysrhythmias, prevention of Paroxysmal supraventricular tachycardia PSVT). Examples: - Na+ Channel Blockers: Class IA a. Napamide (Norpace) Adult dose PO: 100-200mg every 6 hrs. or if CR is used then PO 300mg every 12 hrs. b. Procainamide (Procanbid or Pronestyl)- Adult PO 250-500mg q 3-4

hrs., or if SR is used dose is 250mg 1 Gm. q 6 or q 12 hrs. -Na+ Class IB : a. Lidocaine (Xylocaine)- USE cautiously with patients who have Liver Failure or an AV Block. Given I.V. Bolus dose: 50-100mg over 23min.: then Continuous infusion at dose 20-50mcg/kg/min. b. Mexiletine (Mexitil)- Adult dose PO 200-400mg q 8hrs. c. Tocainide (Tonocard)- Adult loading dose is 600mg then 400mg q 8hrs. with a maximum dose of 2.4 Gm/day. - Na+ Class IC : -Flecainide (Tambor) Adult PO initial dose 50-100mg q 12hrs, dose by 50mg q 12hrs every 4 days; Maintenance dose of 150mg q 12hrs. Maximum dose of 300mg/day. Propafenone (Rythmol) Adult PO dose 150-300mg q 8hrs. Maximum dose is 900mg /day.

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-Therapuetic : to help in treatment of recurrent stable ventricular dsyrhythmias. - Side Effects: Dizziness, H/A , B//P, diaphoresis, fatigue, constipation, contraindicated in 2 or 3rd degree heart blocks, and severe bradycardia, severe HF, or in cardiogenic shock. Adverse Reactions: Palpitations with abrupt withdrawal . Life Threatening: agranulocytosis, bronchospasm with high doses. Teach patients that they should avoid alcohol, smoking and caffeine.

Propanolol ( Inderal Beta1& 2 Blockers- . , IV bolus, Used for treatment of Ventricular dysrhythmia, angina, and hypertension. Sotalol (Betapace) Beta1&2 Blockers - Adult PO 80 mg B.I.D. with a Maximum dose of 240mg-320mg/day 1. Pharmocokinetics- Well absorbed from the GI tract. 2. Metabolized in Liver to active metabolites- 50-60% is eliminated in bile via feces. 30-40 is excreted in urine. Pregnancy class is B. 5. Class III- Drugs that prolong Repolarizationa. Adenosine (Adenocard)- Adult IV initial dose is 6mg rapid bolus May repeat the dose at 12 mg IV x 2 more doses. b. Amiodarone (Cordarone) Adult loading dose is 400mg-1600mg/day. Be-aware of the photosensitivity it causes. c. Bretylium Tosylate (Bretylol)- . d. Sotalol (Betapace)- Adult PO dose is same as Class II . 6. Calcium Channel Blockers- Contraindicated in 2nd & 3rd degree heart blocks a. Verapamil (Calan Isoptin)- Adult dose 240-480 mg/day in 3 to 4 divided doses. IV 5- 10 mg IV push. b. Diltiazem (Cardizem)- 7. Other

a. Phenytoin (Dilantin)-Adult IV 100mg q 5-10 min until dysrhythmia ceases. Maximum dose 1000mg. Used for digitalis induced dysrhythmia. b. Digoxin (Lanoxin) - Adult IV loading dose 0.6-1mg/d in 24hrs.

"statin" meds given for high cholesterol change diet exercise REPORT CRAMPS TO DR LABS: AST/ALT 0-35,4-36 give at NITE except LIPITOR IN MORNINGDiuretics- Two main purposes 1. Blood Pressure;& 2. Edema (peripheral/pulmonary). Diuretics work by inhibiting Na+ and H2O re-absorption from the kidneys in the tubules thus promoting their loss through excretion in the form of urine. Five Categories of Diuretics: 1. * Thiazide and Thiazide like 2. * Loop or high ceiling diuretics 3. Osmotic 4. Carbonic anhydrase inhibitor 5. * Potassium sparing (* Most frequently prescribed for HTN, edema associated with Heart failure) 6. Combination Diuretics- (Both K+ sparing and K+ wasting) used for the treatment of HTN Thiazide- Diuretics used primarily in patients with normal renal functions. Thiazide drugs cause not only loss of Na+, K+, and magnesium they also cause calcium reabsorption, which may lead to Hypercalcemia, another consideration that it cause glucose intolerance or possible Hyperglycemia so it should be used with caution in patients with diabetes mellitus. Drug -Lab/Food Interactions: Drugs: digitalis toxicity with digitalis and hypokalemia; K+ loss with steroids; antidiabetic effect; thiazide effect with cholestramine and colestipol. Lab: serum calcium, glucose, uric acid, serum potassium, sodium & magnesium. Pharmacokinetics- Readily absorbed from the GI tract 1. 65% Protein bound 2. Metabolism: t = 6-15 hrs. 3. Excretion in the urine Pharmacodynamics- PO Onset : 2 hr 1. Peak: 3-6 hrs 2. Duration: 6- 12 hrs 3. Therapeutic Effects: to urine output, to treat: HTN, edema from HF, hepatic cirrhosis, renal dysfunction. Mode of action to Na+, K+, and H2O excretion and preload and cardiac output. 4. Side Effects: dizziness, vertigo, weakness, N/V, diarrhea, hyperglycemia, constipation, rash, and photosensitivity. 5. Adverse Reaction: Severe dehydration, hypotension, severe hypokalemia,

uremia, aplastic anemia, hemolytic anemia, thrombocytopenia,& agranulocytosis. 2. Loop (High Ceiling) Diuretics: act in the thick ascending Loop of Henle to inhibit chloride transport of Na+ into the circulation. They inhibit passive re-absorption of Na+ which leads to loss of Na+ , water, K+, Ca+, Mg+ . They can also effect blood sugar levels and uric acid levels. These groups of drugs are extremely potent causing a marked electrolyte and water depletion. Less effective as anti hypertensive agents than the Thiazides. They can renal blood flow up to 40%. Frequently prescribed when pt.s creatinine clearance is < 30ml/min. & for end stage renal disease. This group of diuretics cause Ca+ excretion where as the Thiazides inhibit Ca+ loss. Example: Furosemide (Lasix) Both Lasix and Bumex are sulfonamide derivatives for patients who are allergic to Sulfa (use Ethancrynic Acid) Lasix should never be prescribed with another loop diuretic. It should be administered in the AM when taken orally or administered IV when the clients condition warrants immediate removal of body fluid. Pharmacokinetics: PO readily absorbed from the GI tract. . 3. Excretion: In urine, some in feces: crosses the placenta. 4. Drug-Lab/Food Interactions : Drug- orthostatic hypotension with alcohol; ototoxicity with aminoglycosides; bleeding with anticoagulants; K+ loss with steroids; digitalis toxicity with digoxin and hypokalemia; lithium toxicity;amphotericin B ototoxicity and nephrotoxicity. Side Effects: dizziness, electrolyte imbalances, vertigo, cramping, rash, headache, weakness, ECG changes, blurred vision, photosensitivity. Adverse Reactions: Severe dehydration; marked hypotension. e. Life threatening: Renal failure, thrombocytopenia, and agranulocytosis. Transient deafness. Prolonged use could cause Thiamine deficiency. f. Aloe K+ level especially when taken with K+ wasting diuretics and licorice can K+ loss. Osmotic Diuretics: osmolality & Na+ re-absorption in proximal tubules and in Loop of Henle. This group of drugs are used to prevent kidney failure, Intracranial pressure, Intraocular pressure (glaucoma). Mannitol potent osmotic K+ wasting diuretic frequently used in Emergency situations. It can also be used with Chemotherapy drugs Crisplatin and Caboplatin to induce diuresis common side effect of these drugs fluid retention). Diuresis with Mannitol occurs in 1-3 hrs. for IV route. Side Effects: Fluid and Electrolyte Imbalances, pulmonary edema from rapid fluid shift, N/V, tachycardia, acidosis, crystallization of Mannitol may occur in the vial due to exposure to lower temperatures. Vial may be warmed to dissolve the crystals. CRYSTALS MUST BE DISOLVED BEFORE DRUG CAN BE GIVEN IV. MUST BE GIVEN WITH EXTREME CAUTION in Patients with Heart Disease & Heart Failure Osmotic diuretic Mannitol increases osmotic pressure, prevents water reabsorption; raises Na and Cl excretion. For:oliguria, edema, raises intracranial pressure-cerebral edema, raisesintraocular

pressure(glaucoma) . Potassium WASTER! Used in ICU/trauma setting. Assess serum osmality. SE; dry mouth, cellular dehydration, fluid and electrolyte imbalance, pulmonary edema, circulatory overload. Oliguria, Stops water, Mannitol, Output of urine(monitor), Tissue dehydration, Increased urinating, Circulatory overloadCarbonic Anhydrase Inhibitors: Acetazolamide, Dichlorphenamide, Ethoxzolamide, Methazolamide block the action of the enzyme carbonic anhydrase (needed to maintain acid/base). Inhibition of this enzyme causes Na+, K+, HCO3 excretion. These groups of drugs are used to intraocular pressure in patients with open angle (chronic) glaucoma. Other uses are for diuresis, treatment of Epilepsy, and treatment of high altitude or acute mountain sickness. Side Effects: Acetazolamide can cause fluid and electrolyte imbalance, metabolic acidosis, N/V, anorexia, confusion, orthostatic hypotension, hemolytic anemia,& renal calculi. Potassium Sparing Diuretics: Weaker drugs than the Thiazides and Loop Diuretics( daily K+ supplements are not used when patients is taking K+ sparing diuretics). Monitor : K+ levels if > 5.3 Meq/L while on these drugs, stop drugs and restrict diet of foods K+. Area of action is in the collecting ducts and distal tubules to promote Na+ and H2O excretion and K+ retention. Spironolactone ( Aldactone)- An Aldosterone antagonist. First K+ sparing diuretic. Remember Aldosterone is a mineralocorticoid secreted by Adrenal Cortex. Other examples are : Amiloride(Midamor), Triamterene(Dyrenium) Eplerenone(Inspra). They are used in treatment of edema caused by HF or cirrhosis of the liver.None of the K+ sparing drugs should be taken with ACE inhibitors & Angio II Recptor Blockers (ARBs) because they also can K+ levels. Side Effects- K+ especially with patient with poor renal function. Urine output should be @ least 600ml/day. GI disturbances like N/V, diarrhea, numbness & tingling of hands and feet. Triameterene ( Dyrenium)- Adult dose for edema 100mg/day in 2 divided doses p.c., not to exceed 300mg/day. Contraindications severe kidney or hepatic disease severe K+. Use with Caution : In patients with renal ,hepatic dysfunction and those who have diabetes mellitus. Pharmacokinetics: PO rapidly absorbed from GI tract 1. Distribution : 67 % Protein Bound 2. Metabolism: t = 1.5 2.5 hrs 3. Excretion: in urine; mostly as metabolites and bile Pharmacodynamics: PO Onset : 2-4 hr 1. Peak: 6-8 hrs 2. Duration: 12-16 hrs Drug-Lab/Food Interactions: Drug- Serum K+ level with K+ supplements; effects of antihypertensive and lithium; Life threatening: Hyperkalemia if given with ACE inhibitor. Lab- Increase serum K+ level; may BUN, AST, alkaline phosphatase levels; serum sodium chloride.

Side Effects: N/V, diarrhea, rash, dizziness, H/A, weakness, dry mouth, photosensitivity. Adverse reactions: - Life threatening severity hyperkalemia, thrombocytopenia, megaloblastic anemia. Monitor signs and symptoms of K+ peaked T wave, Bradycardia, oliguria. Teach patient to avoid exposure to direct sunlight.

Ch 28 Coagulation modifier drugsThrombosis - Formation of a clot in an arterial or venous vessel. Arterial clots could be caused by stasis of blood, platelet aggregation (clumping) on vessel wall. They are usually made up of white & red clots. White clots: - (Platelets) initiating the process followed by fibrin formation trapping red blood cells into fibrin. Blood clots of the veins are from platelet aggregation with fibrin that attaches to red blood cells. Both kinds of thrombosis formation can become dislodged from the wall of the vessel and lead to embolus. Platelets dont usually stick together unless there is a break in the endothelial lining of the blood vessel. When platelets do stick to the lining they synthesize Thromboxane A2 (product of prostaglandins and protein synthesis). Platelet receptor protein glycoprotein IIb & IIIa. Thromboxane A2, and adenosine diphosphate (ADP) the activation of this receptor. As thrombus inhibits blood flow, fibrin, platelets and red blood cells surround the clot building the clots size and structure. As clots occludes the vessel, tissue ischemia occurs. The venous thrombus usually develops because of slow blood flow. Venous clots can occur rapidly. Heparin & Warfrin: Act primarily to prevent venous thrombosis whereas Anti-platelet drugs act to prevent ARTERIAL thrombosis. Both groups of drugs suppress thrombosis in general. Anticoagulants: Used to inhibit clot formation. They DO NOT dissolve clots like Thrombolytics. They are used in clients with venous & arterial vessel disorders that put them at high risk for clot formation. They can be administered Orally, Intravenously, or Subcutaneous. Venous- deep vein thrombosis, Pulmonary Emboli Arterial Coronary artery thrombosis (MI) presence of artificial valves, CVA/Strokes Heparin: Introduced in 1938, it is a natural substance found in the liver. It was used with blood transfusions to prevent clotting. Is indicated for a rapid anti-coagulant effect when thrombus occurs d/t DVT, Pulmonary Emboli, or an evolving stroke and for open heart surgery to prevent blood from clotting & in Disseminated Intravascular Coagulopathy. Heparin works with anti-thrombin III to inactivate Xa thus preventing thrombus formation. Poorly absorbed through the GI tract and much is destroyed by Heparinase (a Liver enzyme). IV bolus and or IV fluid for continuous drip Heparin prolongs clotting time. Heparin affects Partial Thromboplastin Time - (PTT). Heparin can platelet count causing Thrombocytopenia. ANTIDOTE: PROTAMINE SULFATE. Low Molecular Weight Heparin( LMWH) - Lowers the risk for DVT, Pulmonary Emboli after abdominal or orthopedic surgeries. Commonly used to prevent Pulmonary Emboli. LMWHs produce more stable responses at recommended doses, therefore frequent monitoring of PTT is not required. LMWH inactivates factor Xa , but it is less able to

inactivate thrombin like Heparin is able to. 1. 4 Types of LMWH are: All can be given subcutaneously and do not require monitoring of aPTT. Treatment is injection in the abdomen for 7-14 days. It is usually started in the hospital 24 hrs. post-operatively. The half life of LMWH are 2 to 4 times longer than that of heparin. Instruct clients not to take aspirin or other anti-platelet drugs while on LMWH. Bleeding with these drugs is less likely to occur than with Heparin. If bleeding dose occur Protamine Sulfate is the anti-dote.(dose would be 1mg of Protamine S. for every 1mg of LMWH given.) Contra-Indications: Pt. whom have had a stroke, peptic ulcers, or other blood anomolies Enoxaparin Sodium: (Lovenox) Dalteparin Sodium: (Fragmin) Danaparoid : ( Orgaran) - **It is considered LMWH but actually does not have Heparin in its structure. d. Tinzaparin Sodium: (Innohelp)

low molecular weight heparin....Lovenox used to prevent DVT for post-op, prevents acute event, lowers risk of bleeding.HIGH ALERT DRUG!!! SE: fever, confusion,nausea, thrombocytopenia,bleeding.DONT MIX WITH OTHER DRUGS=increase risk of blleding...ASSESS for bleeding. SUBCUT ONLY.Teach soft toothbrush.leave bubble in syringe.LOVE handles

Direct Thrombin Inhibitors: Anticoagulants II There are 4 new parental anti-coagulants that directly inhibit thrombin from converting fibrinogen to fibrin. Three are given Intravenously and are very costly! Argotroban ( Acova) Bivalirudin (Angiomax) binds with inhibitors free flowing thrombin Lepirudin (Refludan) The 4th Drug is given Subcutaneously Desirudin (Iprivask) C. Oral AntiCoagulants- Examples would be Warfrin/Coumadin before it was used on humans it was used on rodenticides to kill rats by causing them to hemorrhage. Oral anti-coagulants inhibit hepatic synthesis of Vitamin K thus affecting clotting factors II, VIII, IX, and X. Warfrin is used mainly to prevent thromboembolic conditions such as: 1. Thrombophlebitis 2. Pulmonary Embolism 3. Embolisms formation caused by Aterial Fibrillation which can lead to CVA Prolong clotting time and monitoring of Prothrombin Time . INR = International Normalized Ratio is used to account for the varibilities in reported levels from different labatories. Normal INR is 1.3 to 2 however patients on Warfrin therapeutic range is 2-3 INR and for patients with Mechanical Heart Valves INR is maintained at 2.5-3.5 and could go as high as 4 on the INR.

Coumadin PO inhibits hepatic synthesis of VIT k dependent factors .Use for chronic A-Fib, prosthetic heart valves, CHRONIC anticoagulation needs:prevents or slows the action of blood

clots. LABS:PT & INR(2-3) ANTIDOTE: Vit K. SE: anorexia, bleeding, heamaturia, thrombocytopenia, hemmorrhage. assess for bleeding-stools & GI. AVOID foods rich in VIT K(leefy greens)no ASA and NSAIDSCoumadin has a long t and a very long duration. Drug accumulation can occur and lead to external and internal bleeding. Teach patients to watch for signs of bleeding(petechiae, ecchymosis, tarry stools, & hematemsis. ANTIDOTE FOR COUMADIN IS VITAMIN K or Aquamephyton-but it takes 24-48 hrs to be effective. Usually a low dose of oral Vitamin K is recommended for patient with INR of 5.5. ** If excessive Vitamin K is given it may take Warfrin 1- 2 weeks before it can be effective again. If patient with acute bleeding give Fresh Frozen Plasma. D. Anti- Platelet Drugs: are used to prevent thrombosis in the arteries by suppressing platelet aggregation. (Heparin and Warfrin are used to prevent thrombosis in the veins). Anti- platelet drug therapy is mainly for prophylactic use in : 1. Prevention of myocardial infarction or stroke for patients who have a family history. 2. Prevention of a repeat M.I. 3. Prevention of a stroke in patients who have had a transient ischemic attack. Long term therapy of a low dose aspirin has been found to be both an effective and cheap treatment for suppressing platelet aggregation. Aspirin works by inhibiting cyclooxyganase, an enzyme needed by the platelets to synthesize thromboxane (A2). Because aspirin has a prolonged anti-platelet activity it should be stopped/discontinued for at least 7 days prior to surgery. 1. Other Examples of anti-platelets: a. Dypridamole (Persantine) b. Ticlopidine (Ticlid) c. Clopidogrel (Plavix) Prototype It may be prescribed by itself or in combination with Aspirin. Tirofiban (Aggrastat) Clopidogrel, dypridamole and ticlopidine have similar effects as aspirin but they are known as Adenosine Diphosphate antagonists affecting platelet aggregation. 2. Clopidogrel (Plavix) Anti- Platelet Used to prevent recurrence of MI, CVA, vascular death. Pregnancy Category: B Usual PO dose is a loading dose of 3oomg then 75 mg. A. Pharmacokinetics: 1. Absorption: Rapid 2. Distribution: (Protein Bond) 94%-98% 3. Metabolism: t : 8 hours 4. Excretion : 50% in urine and 50% in feces B. Pharmacodynamics: PO: Onset- 12 hrs. Peak- 2 -3 Duration: 3 days or longer. Side Effects- Upper Resp. Tract Infection, flu-like symptoms, dizziness, headaches, fatigue, chest pain, diarrhea Adverse Reactions: None of significance May cause hypertension, bronchitis. Thrombolytic: Remember that normally it takes about 1-2 weeks for a blood clot to disintegrate by natural fibrinolytic mechanisms. Our goal with thrombolytic therapy is for this to occur much quicker thus preventing ischemia & then tissue necrosis. These drugs work by promoting the mechanism of converting plasminogen to plasmin, which destroys the fibrin in blood clot. The thrombosis will disintegrate within 4 hours after the administration of a thrombolytic drug. These drugs should be administered within 3 hours of a thrombolytic

stroke. They are also used in treatment of Pulmonary Emboli, & Deep Vein thrombosis. 1. Five Types of Thrombolytics: 1. Steptokinase- enzyme 2.Urokinase- enzyme c. Alteplase- alos know as a tissue plasminogen activator(tPA) Prototype) d. Reteplase (Retavase) e. Tenecteplase(TNKase) *** all five of these drugs induce Fibrinolysis (fibrin breakdown) ** Anticoagulants and Anti-platelets increase the risk of hemorrhage Alteplase: promotes the conversion of plasminogen to plasmin. Thrombolytic agent. It Initiates fibrinolysis Trade name: tPA, Activase Adult Dose: IV Bolus 15mg, then 50mg infused over 30 minutes, then 35mg infused over 60min. Maximum; 100 mg Drug- Lab Food Interactions: Drug: Increase bleeding when taken with oral anticoagulants, NSAIDS, cefotetan, plicamycin Lab; Decreases in plasminogen, fibrinogen, hematocrit, and hemogloblin 1. Pharmacokinetics: a. Absorption: IV b. Distribution: Protein Bind Unknown c. Metabolism: t1/2- 5min d. Excretion: Urine 2. Pharmacodynamics: PO Onset: immediate Peak: 5-10 min. Duration: 3hrs 3. Side Effects: Bleeding 4. Adverse Reactions: Life-threatening: Intracerebral hemorrhage, stroke, atrial or ventricular dysrhythmias. 5. The Antithrombolytic drug Aminocaproic Acid(Amicar) is used to stop bleeding by inhibiting plasminogen activation, which inhibits thrombolysis.

Ch 29Anti-Lipidemics And Peripheral VasodilatorsThere are 4 major categories of lipoproteins: 1High Density Lipoproteins= HDL AKA Friendly or Good lipoproteins. It is responsible for removing cholesterol from the blood stream and sending it to the liver for excretion in the bile. 2. Low Density Lipoproteins= LDL= Bad Cholesterol contains 50- 60% of the cholesterol in the blood stream. With an elevated LDL there is a greater risk for developing atherosclerotic plaques and heart disease. 3. Very Low- Density Lipoprotein= VLDL- they carry mostly triglycerides & less cholesterol. 4. The first treatment for hyperlipodemia should be a reducing the intake of saturated fats and cholesterol in the patients diet. The plan is to reduce total intake of fats to 3040% of intake and reduce cholesterol intake to 300mg/day. **Remember that 75-80% of our total cholesterol is produced Endogenously. ** Diet modification will only reduce cholesterol levels by 10%- 30%. Exercise is another important non-pharmacuetical way to work on for lowering cholesterol levels. Exercise will increase the HDL and lower cholesterol levels.

Smoking increase the LDL, cholesterol and decreases the HDL. Antilipidemics: Drugs that lower lipoproteins. Lipids (Cholesterol, triglycerides, and phospholipids) are bound in the inner shell of protein, which is a carrier that transports lipids into the blood stream. Hyperlipidemia is defined as an excess amount of one or more lipids in the blood stream. Drugs that lower lipid levels include bile-acid sequestrants, fibrates (fibric acid), nicotinic acid, cholesterol absorption inhibitors and hepatic 3 hydroxy-3methylglutarycoenzyme A reductase inhibitors (statins). The statins have fewer adverse effects and are tolerated well. Clients need to be educated that if they stop Antilipidemic therapy that their cholesterol levels will go back to pretreatment levels. Questran One of the first bile sequestrants, which reduces LDL. It binds with bile salts in the intestines. It can be used with Statin drugs .It is a gritty powder that must be dilated in liquid like water or juice. Clofibtate (Atromid- S) & Gemfibrizol( Lopid)- are fibratic acid derivatives that are more effective in lowering triglcerides and VLDL. They are highly protein bond and should not be taken with anticoagulants. It is not suggested for long term use d/t many side effects like cardiac dysrhythmias, angina, thromboembolism, and gall stones. Nictotinic Acid-(Niacin)or (Vitamin B2)- reduces VLDL& LDL. Because of its numerous side effects and need for larger doses ( al low as 20% of clients can tolerate it. Ezetimibe (Zetia)- is a cholesterol absorption inhibitor that acts on the cells in the small intestine to inhibit cholesterol absorption. It lowers levels of cholesterol and lipids from the foods that are ingested. It lowers LDL, triglycerides, and ApoB levels. It also causes small increase to the HDL. It MUST be combined with statins for optimum effect. Statins- first introduced in 1987, inhibits the enzyme HMG CoA reuctase in cholesterol synthesis in the liver. These drugs decrease the concentration of cholesterol, decreases the LDL, and slightly increased HDL. May see a decrease in LDL in as early as 2 weeks. All statins should be monitoring Liver enzymes and yearly eye examinations because of risk of cataract formation and rhabdomyolysis. 1. Atorvastitin Calcium (Lipitor) Prototype 2. Fluvastain (Lescol) 3. Lovastatin (Mevacor)- 1st statin to be used . Side effects: GI disturbances, H/A, muscle cramps, and tiredness . 4. Pravastatin Sodium ( Pravachol) 5. Simvastatin (Zocor) 6. RosuvastatinCalcium (Crestor) Atrovastatin( Lipitor)- Decreases LDL by 25% with lower doses and 55% with higher doses. It inhibits HMG-CoAreductase, the enzyme necessary for hepatic production of cholesterol. Adult PO : 10mg/day may increase up to 80mg/day. Drug Lab-Food Interactions: Drug: Decrease effect with antiacids, propanolol. May increase digoxin level, oral contraceptives. Increases effects with macrolide antiobiotics, and antifungals. 1. Pharmacokinetics; a. Absorption: rapid b.

Distribution: Protein bond 98% c. Metabolism: t1/2 14 hours: metabolites 20-30 hrs. d. Excretion: to primarily in bile; some in urine Pharmacodynamics: PO onset: 2 week for decreasing cholesterol Peak: 1-2 h. 2-4 weeks to be effective Duration: 24 hrs. 3. Side effects: Rare H/A, rash/pruitus, constipation/diarrhea, sinusitis, pharyngitis 4. Adverse Reactions: Rhabdomyolysis, myalgia, photosensitivity, cataracts It can be used and tolerated by some whom concomitant use of Aspirin.

Ch 25Antihypertensive drugs Ch 26Diuretic drugs Hypertension is defined as an increase in systolic B/P > 140 and the diastolic > 90 mmHg.Essential HTN: affecting 90 % of persons with HTN exact origin of essential HTN is unknown. A. Contributing Factors- Family Hx of HTN Hyperlipidemia African American background- Diabetes Obesity Aging Stress Excessive smoking and alcohol Secondary HTN- it is the other 10% of HTN cases are related to Renal & Endocrine disorders Kindeys regulate the Reni- Angiotension I to Angiotension II-(causes release of Aldosterone from the Adrenal glands). Baro-receptors in the Aorta and Carotid Sinus and the vasomotor in center of the medulla assist in regulating B/P. Catecholamines Norepinepherine released from sympathetic nerve terminals and Epinepherine released from the Adrenal Medulla B/P through vasoconstriction activity on the blood vessels. Anti- Diuretic Hormone (produced by hypothalamus by stored and ANP (atrial naturetic peptide and Brain Naturetic Peptide) released by the posterior pituitary gland. Non- Pharmacologic Control for HTN : If systolic is > 140 anti hypertension drugs are generally necessary. A. Stress reduction techniques B. Exercise C. Salt restriction D. Alcohol ingestion E. Weight reduction Most Clients may need two or more Anti - hypertensive drugs to achieve a goal Blood pressure reading: 1. Six Categories of drugs to treat HTN: 1. Diuretics- ** see chapter 41 2. Sympatholytics-(Beta Adrenergic Blockers) 3. Direct- acting Arteriolar Vasodilators4. Angiotension Convert Enzyme inhibitors5. Angiotension II receptor Blockers 6. Calcium Channel Blockers Beta Adrenergic Blocker : Beta ( 1 & 2) Adrenergic Blockers reduce cardiac output by

diminishing the sympathetic nervous system response to basal sympathetic tone. They reduce heart rate, contractility, and Renin release. African Americans with HTN do NOT respond as well to Beta blockers for HTN control so they are given beta blockers combined with diuretics. 1. Metroprolol (Lopressor, Toprol SR)- Beta1 {Prototype}PO Adult dose for HTN 50-100mg/d in 1-2 divided doses Maintenance dose is 450mg/day in divided doses. Elderly- PO 25mg/day Maintenance dose of 25300mg/day Myocardial Infarction- PO: 100mg B.I.D. IV: 5mg q 2 min X 3 doses. Drug- Lab/Food Interactions: Drug- bradycardia with digitalis: Hypotensive effect with other anti-hypertensive, alcohol, anesthetics. a. Pharmacokinetics : 1. Absorption: PO 95% 2. Distribution: Protein Bound is 12% 3. Metabolism: t1/2= 3-7 hrs. 4. Excretion : in urine b. Pharmacodynamics: PO : Onset 15 min IV Onset: Immediate Peak: 1.5 hrs IV Peak : 20 min Duration: 10-19 hrs. IV Duration: 5-10 hrs. c. Side Effects: Fatigue, weakness, dizziness, nausea, vomiting, diarrhea, mental changes, nasal stuffiness, impotence, libido, depression. d. Adverse Reaction: Bradycardia, thrombocytopenia e. Life Threatening: Complete heart block, bronchospasm, and agranulocytosis. Cardioselective Beta-blockers- are preferred Beta Blockers because they act mainly on the cardiac Beta1 receptors rather than Beta2 so bronchoconstriction is less likely to occur. Medications in this group are: Acebutolol ( Sectral), Atenolol ( Tenormin), Betaxolol( Kerlone), Bisoprolol (Zebeta). 2. Centrally Acting Alpha2- Centrally acting alpha2 agonists the sympathetic response from the brainstem to the peripheral vessels. By stimulating the alpha2 receptors which in turn sympathetic activity: vagus activity, cardiac output and serum epinephrine, norepinepherine, & renin release. All actions result in reducing peripheral vascular resistance and vasodilation. This group of drugs has minimal effect on cardiac output and kidney perfusion. Beta Blockers are NOT given with centrally acting sympatholytics, because of bradycardia during therapy and rebound hypertension on discontinuing therapy that can occur. Example: Of these types of drugs is Methyldopa (Aldomet). In higher doses Methyldopa & clonidine can cause water retention therefore they should be used with a diuretic. Potential side effects: drowsiness, dry mouth, dizziness, and slow heart rate(bradycardia). Methyldopa should NOT be used in clients with impaired liver functions & serum liver enzymes should be monitored periodically. These drugs must not be stopped abruptly d/t rebound hypertensive crisis. 3. Alpha-Adrenergic Blockers: - These drugs block the alpha receptor sites resulting in vasodilation B/P. Useful in treat of HTN in patients with Hyperlipidemia. They the very low density lipoproteins (VLDL) and the low density lipoproteins (LDL) which cause plaque buildup leads to artherosclerosis, they also build up the good lipoproteins High

density ones (HDL). They are also good for diabetic patients because they do not effect Glucose metabolism. 4. Examples of Alpha Adrenergic Blockers: Prazosin (Minipres) {Prototype}, Terazosin( Hytrin), Doxazosin( Cardura) are mainly used for HTN but can also be used for treatment of Ben usually are given once/day. They do cause NA+ & water retention therefore a diuretic is also given concomitantly to fluid accumulation. More potent medications like Phenoxybenzamine and Tolazoline are used to treat HTN Crisis & vere HTN resulting from catecholamine secreting tumors of the adrenal medulla like (phenochromocytomas). Prazosin HCL (Minipres) Alpha Adrenergic Blocker PO Adult dose 1mg B.I.D. or T.I.D. With a maintenance dose of 3-15mg/day. Drug- lab/ Food Interactions: Hypotension effect with other anti-hypertensives, nitrates and alcohol. a. Pharmacokinetics : Absorption in G.I. 60%, 5% in circulation 1. Distribution: Protein Bond 95% 2. Metabolism: 3 Hours 3. Excretion: in bile & Feces 10% in urine. 4. Mode of Action: Dilation of peripheral blood vessels via blocking Alpha Adrenergic receptors. 2. Pharmacodynamics: P.O. Onset o.5 2 hrs. Peak: 2-4 hrs. Duration: 10 hrs. a. Adverse Reactions: Orthostatic Hypotension, palpitations, Tachycardia, pancreatitis b. Side Effects: Drowsiness, H/A, N/V, diarrhea, impotence, vertigo, urinary frequency, tinnitus. c. Drug Interactions: when Alpha Adrenergics Blockers are taken with Antiinflammatory drugs and nitrates Fluid Retention peripheral edema Nitrates - Lower B/P as do Alpha-Adrenergic which leads to syncope/fainting. Adrenergic Neuron Blockers are potent antihypertensive drugs that block Norepinepherine. Release from the Sympathetic nerve endings, causing a decrease in B/P, & decrease in Cardiac output & in peripheral vascular resistance. Reserpine, Guanethidine, Guanadrel (are 3 very potent drugs) that are used to treat severe HTN. Adrenergic Neuron Blockers are the LAST drugs considered for treatment of HTN because of the orthostatic hypotension. Reserpine can cause nightmares and suicidal tendencies. Alpha1, Beta1, Adrenergic Blockers : Labetalol( Normodyne) & Carteolol(Cartrol) are examples of Alpha/Beta blockers. When the Alpha1 receptor sites are blocked it causes Vasodilation. , which decreases the resistance of the blood flow. The blocking of effect on the Alpha receptor site is stronger than that on the Beta receptor therefore B/P is lowered and pulse rate is moderately decreased. Common side Effects: Orthostatic Hypotension, GIdistrubances, nervousness, dry mouth, fatigue. *** Large doses of Labetalol may cause Atrial Ventricular Heart Block. (Property of Beta blockers that slows Atrial Ventricular conduction which in turn slows heart rate). Direct Acting Arteriolar Vasodilators: This group of drugs act by relaxing the smooth muscle of mainly the arterioles. Vasodilatation leads to blood flow to the Brain and kidneys, with a decrease in B/P Na and water are retained leading to edema. This is why a diuretic would be given with these drugs. Examples would be Hydralazine and Minoxidil both can be

used to treat mild to moderate HTN. Also because of the vasodilatation that these drugs cause Reflex Tachycardia and Renin is released. Beta Blockers are frequently prescribed with D.A.A. V. to decrease the Heart rate (counter act the Reflex Tachycardia). Nitroprusside & Diazoxide : These are 2 very potent vasodilators used for acute HTN emergency. Nitroprusside acts on both arterial & venous blood vessels, whereas Diazoxide acts on only arteries. Common side effects: Hydralazine side effects are tachycardia, palpitations, edema, nasal congestion, H/A, dizziness, bleeding, and Lupus like symptoms. Minoxidil & Diazoxide : Refex Tachycardia, palpitation, restlessness, agitation, nausea, and confusion. Diazoxide: hyperglycemia due to its action of inhibiting release of insulin from the Pancreatic Beta cells. Angiotension Converting Enzyme Inhibitors: They inhibit the formation of Angiotension II and blocks the release of Aldesterone. When aldesterone is blocked Na and water are not retained but are excerted. K + is retained. ACE inhibitors cause little change in Cardiac Output or HR but do peripheral vascular resistance. These drugs can be used in patients with renin levels. They are primarily used to treat HTN , some are effective in treatment of Heart Failure. There are 10 drugs in this category: 1. First one discovered in 1970s is Captopril (Capoten) 7. Moexipril(Univasc) 2. Benzepril (Lotension) 8. Perindopril (Aceon) 3. Enalapril (Vasotec) 9. Fosinopril (Monopril) 4. Ramipril(Altace) 10. Quinapril (Accupril) 5. Trandolapril(Mavik) 6. Lisinopril (Prinavil Zestril) These drugs can be used as the first line Anti Hypertensive agents but the use of Thiazide diuretics are also recommended. ****** African Americans and Older Adults DO NOT RESPOND TO ACE inhibitors until diuretics are added. SHOULD NOT PRESCRIPED/ADMINISTERED DURING PREGNANCY (D/T the effect they have of reducing Placental blood flow). Side Effects: Constant irritating cough; Nausea/Vomiting, diarrhea, H/A, dizziness, fatigue, insomnia, Hyperkalemia, and tachycardia. Contraindications: Should not be administered while pregnant will cause fetal harm d/t decrease placental blood flow. Should not be taken with K+ sparing diuretics or salt substitutes (those that use K instead of Na). Angiotension II Receptor Blockers (ARBs): They are similar to the ACE drugs except ARBs block Angiotension II from Angiotension receptors found in many tissues. ARBs cause vasodilatation and peripheral resistance. They do not cause the constant irritating cough. ARBs should not be taken during pregnancy either. Examples: Losartan (Cozaar), Valsartan (Diovan) Irbesartan (Atacand), Olmesaran Medoxomil (Benecar)- these agents block the vasoconstrictor effects of Angiotension II at the receptor sites. ARBs can be used as a first line Treatment for HTN. Pharmacokinestics: Cozaar is used primarily to manage HTN and to form active metabolites. 1. Distribution: They are Highly Protein Bond 2. Metabolism: t 1.2- 2 hours & metabolite half life is 6- 9 hrs. 3. Excretion: In the Urine and Feces

Pharmacodynamics: Losartan (Cozaar) is a potent vasodilator which blocks the binding of Angiotension II to the Angiotension receptors found in many tissues. PATIENTS WITH MILD HEPATIC INSUFFICENCY CAN TAKE THESE DRUGS. The Peak time is 6 hrs., Duration is 24 hrs. THEY ARE LESS EFFECTIVE IN AFRICAN AMERICAN and may cause Angioedema Direct Renin Inhibitors: Aliskiren ( Tekturna) 1st FDA approved Renin inhibitor. Aliskiren binds with Renin causing a in Angiotension, Angiotension II and Aldesterone levels. Effective for the treatment of mild to moderate HTN. Can be used alone or with another antihypertensive agent. Has an added effect in B/P when combined with Thiazide diuretics or ARBs. Losartan ( Cozaar) Angiotension II receptor Blockers . Pregnancy C ( First Trimester), D (2nd or 3rd Trimester can use Hyzaar). PO: For HTN- 25- 50 mg/day in single or divided doses. Maxium dose is 100mg/ day. Contraindicated: During Pregnancy and while Breastfeeding Caution: Renal & Hepatic Impairment. Pharmacokinestic: 1. Absorption: Rapidly absorbed in blood in 25-30 minutes. 2. Distribution: Protein bond 90-95% 3. Metabolism: t 1.2- 2 hrs. metabolites in 6-9hrs. 4. Excretion: 35% in the urine. 5. Side Effects: Dizziness, diarrhea, insomnia, & occ. Cough 6. Drug & Lab Interactions: Phenobarbital effect of Cozaar & its metabolites May increase ALT, AST, ALP ,Bilirubin , Creatinine , Hbg. and Hct. 7. Adverse: Upper Respiratory Infections. Pharmacodynamic: Onset: < 1 hr. Peak : 6 hrs. Duration: 24 hrs. Calicum Channel Blockers: These are a group of drugs that are slow channels found only in myocardium & vascular smooth muscle. Free Ca+ muscle contractility, peripheral resistance, & B/P. Ca+ channel blockers also called Calcium anti-agonist promote vasodilation. Large central arteries are not as sensitive to Ca+ as the coronary, Cerebral and peripheral arteries are. They are highly protein bond but have a short half- life. 3 groups of Ca+ blockers. Calcium Channel Blockers lower B/P better in African Americans than drugs in other categories. 1. Verapamil (Calan): is used for treatment of chronic HTN, angina pectoris & cardiac dysrhythmias. Verapamil and Diltiazem act on the arterioles & the heart. Nifedopine is used to prevent ischemic brain injury due to vasospasm that often accompanies subarachnoid hemorrhage. Also used as treatment of choice in Variant angina (Prentz Metal ) also thought to be caused by vasospasm of the coronary arteries. 2. Nifedipine (Procardia): Decreases B/P in older adults & in those with low serum Renin values. In the immediate released capsules (10-20mg) it has been associated with increased incident of sudden Cardiac Death especially when prescribed for outpatient at high doses d/t the fact that Ca+ channel blockers cause reflex tachycardia. This tachycardia is more prevalent with Procardia. 3. Amlodipine (Norvasc) : It is used to treat mild to mod. HTN, and Angina Pectoris. Mode of action: Decreases peripheral vascular resistance (vasodilation),

promoting in B/P. PO 5- 10mg/day or for Elderly 2.5- 5mg/day. Lotrel is a combination of Amlodipine with Benzepril. Contra-Indications: Severe hypotension. Cautious Use: Liver Disease, Heart Failure, Aortic Stenosis, pregnancy & lactation. Drug- Lab Interactions: Drugs bradycardia with Adenosine Labs: May Amlodipine with Grapefruit juice. 1. Pharmacokinetics: a. Absorption: > 90% is absorbed; gradually absorbed from the G.I. tract. b. Distribution: Highly Protein Bond > 95% c. Metabolism: t 30- 50 hrs. Elderly: t : 50100 hrs. d. Excretion: in urine & feces as inactive metabolites. 2. Pharmacodynamics: Onset is gradual Peak: 6-9 hrs. Duration 24 hrs. Usually only prescribed once a day. 4. Side Effects : Peripheral edema may occur because of its vasodilator effect, flushing, dizziness and nausea. 5. Adverse: Reflex Tachycardia

Ch 27 Fluid and electrolytes Ch 30 Pituitary drugs Ch 31 Thyroid and antithyroid rugs Ch 32 Antidiabetic drugs Ch 33 Adrenal drugs Ch 34 Womens health drugs Ch 11 Analgesic drugs Ch 12 General and local anesthetics Ch13 CNS depressants and muscle relaxants

Sedatives/Hypnotics: Often are prescribed for treatment of insomnia Remember that dreams occur during Rapid Eye Movement stage of sleep. A. They are the mildest form of CNS depressants are our sedative drugs. B. They do not affect the consciousness. Barbiturates 1900s were introduced as a sedative. A. Long acting - Phenobarbital B. Intermediate Acting- Butabarbital (Butisol) C. Short- Acting Secobarbital ( Seconal) & Pentobarbital (Nembutal) {Prototype} D. Ultra Short Acting- Barbiturate, Thiopental (Na Pentothal) Benzodiazepines minor tranquilizer or anxiolytic. Class IV according to Controlled Substances Act. They the action of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) to the GABA receptors. Neuron excitability is . Also of the Benzodiazepines except temezepam can cause vivid dreams/nightmares. Should not be used for longer than 3 to 4 weeks. Remember that it is recommended that with renal or hepatic dysfunction smaller

doses A. Chlordiazepoxide (Librium) class IV. Used also for treatment of alcohol withdrawl syndrome DTs, anxiety and tension. For anxiety usual PO dose is 5-25mg t.i.d. or q.i.d. For alcohol withdrawl PO/IM/IV 50-100mg max. 300mg/d B. Flurazepam (Dalmane) {Prototype} C. Temazepam (Restoril) D. Triazolam ( Halicon) E. Lorazepam (Ativan) {Prototype} used for treatment of mild to moderate anxiety. PB 85-95%, t 3.5- 21 hr. F. Diazepam (Valium) used to manage anxiety, muscle spasms status post epilepticus. PO/IM/IV 2-10mg b.i.d.- q.i.d. For Post epilepticus IV 5-10mg q 10-20 min. 30mg

max.

Non benzodiazepines Used for short term insomonia (< 10 days duration) a. Zolpidem (Ambien) .Duration is 6-8 hrs. with a short t1/2 of 2 to 2.5 hrs. M a. Metabolized in the liver to 3 inactive metabolites and excreted in bile, urine, and feces. Chloral Hydrate- It is used to induce sleep and decrease nocturnal awakenings. Fewer occurrences of hang-over, resp. depression, and tolerance. Effective in older clients. It can be given to patients with mild hepatic dysfunction, but should be avoided if liver or renal failure is severe. Anesthetics - Two classifications 1. General Anesthetic depresses the CNS, alleviates pain, and causes loss of consciousness. One of the first ones used was Nitrous Oxide (laughing gas) 1. Four Stages of Anesthesia1st stage is Analgesia (induction stage) (consciousness and goes to loss of consciousness. Loss of sensation of smell and pain occur. 2. 2nd stage is Excitement Or Delirium produces loss of consciousness caused by depression of the cerebral cortex. Confusion, excitement or delirium occurs. 3. 3rd stage Surgical Surgical procedure is performed during this stage. 4. 4th stage Medullary Paralysis Toxic stage of anesthesia Resp. are lost & circulatory collapse occurs. Must be on Ventilator. 2. Inhalation Anesthetics- used during the 3rd stage, inhalation gases are used. Some like Nitrous Oxide are absorbed quickly, have rapid action but also eliminated quickly. Some examples in the 1950s and later are Halothane, Methoxyflurane, Enflurane ,Isoflurane, Desflurane, and in 1995 Seroflurane. Inhalation agents are usually combined with a barbiturate, a strong analgesic like morphine, and a muscle relaxant like pancuronium. Potential adverse effects are respiratory depression, hypotension, dysrhythmias,& hepatic dysfunction.ould be used. 3. Intravenous Anesthetics May be used for induction with addition of inhalation anesthesia or in an outpatient setting for procedures with an anticipated short surgical time. a. Midazolam (Versed) b. Propofol (Diprivan)- this drug supports microbial growth & may risk for infections. Open vials should be discarded after 6 hours to prevent sepsis.

4. Topical Anesthetics- Available in many different forms. Decrease the sensitivity of the nerve endings to the affected/injured area. 5. Local Anesthetics These drugs block pain at the site where the drug is administered, allowing for consciousness to be maintained. Beneficial in many minor procedures. Consist of two main groups Esters and Amides. a. Esters Short Acting - Chloroprocaine (Nesacaine), Procaine HCl (Novacain) which both is effective for (1/2-1hr.). Long Acting -Tetracaine (Pontocaine), which is effective for (3-10 hr.) b. Amides Low incident of allergic reactions. Lidocaine Hydrochloride (Xylocaine) has a rapid onset and long duration of action. Labeled as Moderate acting (1-3 hr.) Another example would be Prilocaine (Citanest). Long Acting Bupivacaine (Marcaine & Sensorcaine) 6. Spinal Anesthesia use of local anesthetics injected in the subarachnoid space at L3-4. Potential complications could be respiratory distress if anesthetic is injected or travels to high in the spinal column, headaches due to leak of cerebral spinal fluid. a. Spinal Nerve Block local anesthetics is injected into the 2nd layer of the spinal column subarachnoid membrane b. Epidural Block- local anesthetic is injected into the outer covering of the spinal column the dura mater. c. Caudal Block- anesthetic is placed near the sacral area. A d. Saddle Block anesthetic placed near the lower end of the spinal column to numb the perineal area.Ch 30 - 32

The endocrine System consists of ductless glands that secrete hormones in the blood stream. Endocrine glands include: Pituitary (Hypophysis), Thyroid, Parathyroid, Adrenal , gonads, and the Pancreas. Hormones are chemicals synthesized from amino acids & cholesterol that act on body tissue, organs & affect cellular activity. Glands- A. Pituitary Gland- Located at the base of the brain. Divided into 2 lobes Anterior and Posterior. 1. Anterior Lobe: (Adenohypophysis) Often called the Master Gland D/T its function of secretions of hormones that stimulate the release of other hormones from target glands like the thyroid. Parathyroid, adrenals, and gonads. It secretes a total of 6 hormones a. Thyroid Stimulating Hormone (TSH) also called Thyrotropic Hormone - is secreted in response to the Hypothalmus releasing Thyroid Releasing Hormone. When this hormone is over secreted (hypersecretion) can cause Hyperthyroidism. b. Adrenocorticotropic Hormone ( ACTH)- Hormone secreted to stimulate Adrenal Cortex to release Glucocorticoid (cortisol), Mineralcorticoid hormone( Aldesterone). More ACTH is secreted in the AM then in the PM c. Gondtropins- Follicle stimulating hormone (FSH), & Luteinizing Hormone (LH) these hormones control the release of hormones from the Thyroid and Adrenal, and ovaries. Regulate hormone secretion from the ovaries & testes. d. Growth Hormone (GH)or the Somatotrophic Hormone acts on body tissues, particularly the bones & skeletal muscles. Regulated by the amount of Growth Hormone Releasing Hormone & Growth Hormone

Inhibiting Hormone (Somatostatin) that is released from the Hypothalamus. Sympathomimetics drugs, Serotinin, glucocorticoids can inhibit the secretion of Growth Hormone. e. Prolactin (PL)- stimulates milk formation in the glandular breast tissue after childbirth f. Melanocyte Stimulating Hormone (MSH) Remember the amount of each hormone is regulated by negative feedback system to the Anterior Pituitary Gland. Posterior Lobe: (Neurohypophysis) secretes 2 Neurohormones: A. Antidiuretic Hormone- Increases the reabsorbtion of water in the tubules, returning it to the systemic circulation. Secretion of ADH is regulated by serum Osmolality .If serum osmolality is increased so is the production of ADH. (Vasopressin). B. Oxytocin- Stimulates the contraction of the smooth muscles of the Uterus. Thyroid Gland- It also has 2 lobes and is located on either side of the anterior Trachea. It secretes two hormones: A. Thyroxine (T4) B. Triiodothyronine( T3) These hormones affect nearly every tissue & organ by controlling their metabolic rate. Stimulation by the Thyroid hormone results in cardiac output, O2 consumption, carbohydrate use, protein synthesis, & the breakdown of fats (Lipolysis). These hormones also affect body heat regulation and womens menstrual cycles.\ . Parathyroid Gland: There are 4 parathyroid glands 2 pairs that lie on the dorsal surface of the thyroid gland. It secretes 2 hormones A. Parathyroid Hormone/PTH - this hormone regulates serum Ca+ levels. When there is a in serum Ca+ (Hypocalcemia)the PTH is release from the parathyroid gland. PTH will serum Ca+ levels by: 1) Mobilizing Ca+ from the bone. Remember PTH P for PTH pulls Ca+ from the bone and puts it back into the blood stream; 2).Promotes Ca+ absorption from the intestines; 3) Promotes Ca+ re-absorption from the renal tubules. B. Calicitonin- Hormone that primarily is produced by Thyroid (and to a lesser extent the Parathyroid & Thymus Glands). Its purpose is to inhibits Ca+ re-absorption by the bone & renal excretion of Ca+ . Think Calcitonin Keeps Calcium in the bone, which is the opposite effect of P.T.H. Adrenal Glands: Located at the top of each Kidney. There are two separate sections: A. Medulla or Center secretes catechlomanines Epinephrine and Norepinephrine. B. Cortexor known as the outer portion of the gland. Secretes 2 major hormones: 1. Glucocorticoids- Principal hormone is Cortisol 2. Mineralcorticoid- Aldersterone which acts in the kidney telling the kidney to reabsorb Na+ and then water back in the systemic circulation. Some other hormones to a smaller extent would be Androgen, Estrogen, and Progestin. Pancreas: Located to the left and behind the stomach is both an Exocrine and Endocrine gland. A. Exocrine property would be the secretion of digestive enzymes into the duodenum of the small intestines. B. Endocrine- hormones are secreted by cluster of cells called Islets of Langerhans There are 2 types of cells the Alpha islet cells produce

glucagon(which breaks glycogen down into glucose in the liver). The Beta islet cells secrete Insulin (Regulates glucose metabolism). Growth Hormones: There are 2 which are secreted from the Hypothalamic Hormones: A. Growth Hormone- releasing Hormone and Growth Hormone Inhibiting Hormone (Somatostatin). Growth Hormone doesnt have a specific target gland but it does affect body tissues and bones. Synthetic Growth Hormone Drugs cannot be given orally due to them being inactivated by gastric enzymes. They are given subcutaneously or intramuscularly. G.H. replacement therapy is very expensive. G.H. acts on newly forming bone and it must be administered before the epiphyses are fused. Prolonged G. H. therapy can antagonize Insulin secretion and eventually cause Diabetes Mellitus. A. G. H. Deficiencies Drug Therapy: Drugs used to treat growth failure in children are : 1. Somatrem (Protropin)- Has identical amino acid plus an additional amino acid. 2. Somatropin (Humatrope) has identical amino acid sequences as Human G Hormone (contraindicated in children with Prader Willi Syndrome and those children who are severely obese or who have Respiratory impairment. B. Growth Hormone Excess- Gigantism- excessive growth during childhood or Acromegaly (excessive growth after puberty) can occur with Hypersecretion of G.H. and is associated with Pituitary tumors. If the treatment with radiation is ineffective the Prolactin- Release Inhibitor: Bromocriptine can inhibit the release of G. H. C. Octreotide(Sandostatin) : is a potent synthetic Somatostatin used to suppress G.H. release. It can be used alone or with Surgery and or Radiation. This drug is expensive. G.I. side effects are common. This drug can also be used for severe diarrhea resulting from carcinoid tumors. Thyroid Stimulating Hormone: Adenohypophysis secretes T.S.H. in response to ThyroidReleasing Hormone from the Hypothalamus. TSH stimulates the thyroid to secrete: Thyroxine (T4)& Triiodothyronine(T3). A. Excessive or Deficiency in production of TSH: 1. Excessive Production of TSH causes Hyperthyroidism: 2. Deficiency of TSH causes Hypothyroidism: Primary Hypothyroidism caused by Thyroid gland disorder. Secondary Hypothyroidism caused by decrease amount of TSH. B. Thyrotropin(Thytropur): is a purified extract of TSH used as a diagnostic agent to differentiate between primary and secondary hypothyroidism. Adrenocorticotrophic Hormone: Corticotropin Releasing Factor (CRF) stimulates the Pituitary corticotrophs to secrete (ACTH) secretion stimulates the release o Glucocorticoids(Cortisol) and Mineral Corticoids (Aldesterone) and Androgens from the Adrenal cortex. Usually ACTH & Cortisol secretions are in the morning versus lower in the evening , also stressors like Surgery , Sepsis, and trauma override diurnal rhythm. A. ACTH Corticotropin (Acthar) - Is used to diagnosis Adrenal disorders; treat Adrenal Insufficiency and as an anti-inflammatory drug in treatment of allergic response, if it is administered I.V. Should see in serum cortisol levels in 30-60 min. ACTH the symptoms of Multiple Sclerosis during its exacerbation phase. Pregnancy- C. Dosage: As a diagnostic test 10- 25 Units IV in 500 ml of D5W q 8 Hr. Acute MS: - Sub Q/IM 80-120 Units/day for 2-3 weeks

1. Pharmacokinestics: Absorbed well Protein Bond - Unknown a. Metabolism: t - 5-20 min. b. Excretion: Excreted in the urine. 2. Pharmacodynamics: IM Onset: 6hr. Peak: 6- 18 hrs. Duration: 12- 24 hrs. IV Onset: UK Peak: 1 hr. Duration: UK a. Side Effects: Nausea/vomiting, appetite, mood swing, Euphoria to depression, petechiae, water and Na+ retention, hypokalemia and hypocalcemia b. Adverse: Edema, ecchymosis, osteoporosis, muscle atrophy, growth retardation, depressed wound healing, cataracts, glaucoma, menstrual irregularities. c. Life Threatening: Ulcer perforation, pancreatitis. d. Drug;Food and Lab: Drug- Increase in ulcer formation with aspirin; may increase effect of potassium- wasting diuretics; decrease effects of oral antidiabetics or insulin (hypoglycemia). Posterior Pituitary Gland: Secrets Antidiuretic Hormone (Vasopressin) and Oxytocin. When there is a deficiency of ADH large amounts of water is excreted by the Kidneys Diabetes Insipidus severe fluid volume defecit. Head injuries, Brain tumors can be some of the major causes of Sudden Inappropiate Appropiate Antidiuretic Hormone secretion. ADH prepartion Vasopressin (Pitressin), Desmopressin Acetate (DDAVP) can both be administered Intravascularly or by injections. Thyroid Gland: Hormones that it secretes are Thyroxine(T4) and Triiodothyronine(T3) both are to regulate protein synthesis & energy activity . 20% of circulating T3 is secreted from the Thyroid gland and the other 80% comes from the degradation of about 40% oof the T4 . Both are carried by the blood by the Thyroxine binding globulin(TBG) and Albumin. T3 is more potent than T4 and only free unbound T3 & T4 are active and produce a hormonal response. Hypothyroidism: Synthetic T4 & T3 may be prescribed and can have either primary cause (gland disorder) or 2nd cause (lack of TSH secretion). Primary occurs more f requently T4 & TSH = Primary HypoThyroidism. The causes can be either acute or chronic inflammation of the Thyroid gland, radioiodine therapy, excessive intake of a ntithyroid drug or surgery. Myxedema is a severe Hypothyroidism- symptoms are lethargy, apathy, memory impairement, emotional changes, slow speech, deep coarse voice, edema of eyelids and face, thick dry skin, cold intolerance, slow pulse, constipation, weight gain, and abnormal menses. In children Hypothyroidism can be congenital (Cretinism). Levothyroxine Sodium( Levothyroid, Synthyroid){Prototype} - If levels of T3 and T4 ; also used to treat a simple goiter and chronic Lymphocytic Thyroiditis (Hoshimoto). To treat Hypothyroidism,Myxedema and Crentinism. Mode of action is to metabolic rate, oxygen consumption and body growth. Highly Protein Bound . Pregnancy Catergory A. Dosages- PO intially 25-50mcg/day; maintance Dose: 50-200 mcg/day. IV 0.2- 0.5 mg initially then 0.1- 0.2 mg/day until stable then go to PO doses 1. Pharmacokinestics- a. Absorption- PO 50-75% b. Distribution- PB 99% c. Metabolism- t 1/2 : 6-7 days d. Excretion- in bile and feces 2. Pharmacodynamics- PO Onset: UK Peak : 24 hr.-1 week Duration: 1- 3 weeks IV Onset: 6-8 hrs. Peak: 24-48hrs. Duration: UK

Side Effects- Nausea, vomiting,diarrhea, cramps, tremors, nervousness, insomnia, H/A, and weight loss. b. Adverse- Tachycardia, hypertension, palpitations Life Threatening- Thyroid crisis, angina pectoris, cardiac dysrhythmias, and cardiovascular collapse. Drug;Food; Labs- cardiac insufficiency with epinepherine; effects of anticoagulants, tricyclic antidepressants, vasopressors, decongestants. effects of antidiabetics (oral and insulin), digitalis, and decrease absorption with cholestyramine, colestipol. Lithyronine (Cytonel)- Synthetic T3 short t life and duration of action; not recommended for maintain therapy. It is better absorbed from GI then Levothyroid. It is used for the initial treatment of myxedema. Liotrix( Euthroid, Thyrolar)- is a mixture of Levothyroxine & Liothyronine (4:1 ratio). No advantage to using this drug over Levothyroxine alone. Hyperthyroidism: in circulating T4 & T3 which results from an overactive thyroid gland. It may be mild or severe as in Thyroid Storm. Graves Disease or Thyrotoxicosis- most common type of Hyperthyroidism caused by Hyperfunction of thyroid gland. Characterized by Tachycardia, palpitations, excessive perspiration, heat intolerance, nervousness, irritability, Exophthaalmos(bulging eyes), and weight loss. Can be treated surgically where a portion of the thyroid gland is removed(subtotal thyroidectomy) , by administering radioactive Iodine therapy, or antithyroid medications. Any of these treatments can cause Hypothyroidism. Propanolol (Beta- Adrenergic Blocker) is used to control cardiac symptoms like the tachycardia and palpitations. A. Drugs- the purpose is to reduce excessive secretion of thyroid hormones T4 & T3 by inhibiting their secretions. Thiourea Derivatives (Thioamides) - are the drugs of choice. These drugs interfere with the synthesis of thyroid hormones. They DO NOT destroy the thyroid tissue. Propylthiouracil (PTU) and Methimazole(Tapazole)- are effective thiamide antithyroid drugs. Useful for treatment for Thyrotoxic Crisis. PTU does inhibit peripheral conversions of T4 & T3. Methimazole also doesnt inhibit peripheral conversion T4 & T3 but is 10 times more potent and has a longer half life then PTU. Prolong use of thioamides may cause a goiter to form. Stron Iodine solutions Lugols solution has been used to suppress thyroid function. Sodium Iodine administered IV is useful for the management of thyrotoxic crisis. Drug Interaction Digoxin and Lithium can the action of thyroid drugs. Dilantin serum T3 levels. Parathyroid Gland- Parathyroid Hormone is secreted from this gland and is important in serum Ca+ levels. The other hormone that is important in Ca+ levels is Calcitonin this hormone serum Ca+ levels. The treatment for Hypoparathyroidism is the administration of Parathyroid Hormone. The treatment of Hyperparathyroidism is with a synthetic form of Calcitonin. A. Calcitriol (Rocaltrol) is a Vitamin D analogue that promotes Ca+ absorption from the GI

tract & secretion of Ca+ from the bone into the blood stream. Mode of action enhancement of Calcium deposits in the bone. Pregnancy Category: C Dosage: PO 0.25 mcg/day Contraindication: Hypersensitivity, hypercalcemia, hyperphosphatemia, Hypervitaminosis D, malabsorption syndrome. Caution: Cardiovascular diseases, renal calculi 1.Pharmacokinestics: a. Absorption: PO well absorbed b. Distribution: PB UK, crosses the placenta c. Metabolism: t : 3-8 hrs. d. Excretion: mostly in the feces Pharmacodynamics: PO Onset: 2-6hrs. Peak: 10-12 hrs. Duration: 3-5 days Side EffectsAnorexia, nausea, vomiting, diarrhea, cramps, drowsiness, H/A, dizziness, lethargy, and photophobia. Adverse Effects- Hypercalciuria, hyperphosphatemia, and hematuria Drug; Food; Labs- Increase cardiac dysrhythmias with Digoxin and Verapamil. Decreases calcitriol absorption with cholestyramine. Lab- Increases serum Ca+ with thiazide diuretics and calcium supplements. Adrenal Glands- 2 types of Hormones produced in the cortex : Glucocorticoids and the Mineral Corticotoids. A. Glucocorticoids(Cortisol)- is secreted from the Adrenal gland in response to the hypothalamus pituitary adrenal axis as a result of feedback. They are influenced by ATCH(Adrenalocorticoid Hormone) which is released by the anterior Pituitary gland. They affect carbohydrate, protein, and fat metabolism. Cortisol is the main Glucocorticoid is has an anti-inflamatory, anti- allergic, and anti stress effect. Indications for their use are; trauma, surgery, infections, emotional stress and anxiety. Drugs in this class are mostly a synthetic form. Conditions that they would be used for are : Mutiple Sclerosis, Rheumatiod arthritis, Myasthesia Gravis, Ulcerative Cololitis, Glomerulonephritis, shock, ocular and vascular inflammations, cerebral edema, polyarteries nosa, Hepatitis, allergic conditions, drug reactions, contact dermatitis, and anaphylaxis. Maybe used to treat organ rejections by the reciepant. Dexamethasone(Decadron)- drug used to treat severe inflammatory response resulting from head injuries or allergic reactions Prednisone(Deltasone, Orasone, Meticorten) Class is Glucocorticoid. Mode of action is to suppress inflammation and adrenal function. Also used as an immunosuppressant. Pregnancy Category- C. Adult Dose- PO 5-60 mg/day in divided doses. Contraindications- Hypersensitivity, psychosis, fungal infections. Caution- Diabetes Mellitus. Pharmacokinetics a. Absorption - absorbed from the GI tract b. Distribution- PB 65-91% crosses the placenta c. Metabolism- t - 3-4 hr. d. Excretion- In urine Pharmacodynamics- PO Onset- UK Peak- 1-2 hr. Duration- 24-36 hrs. Side EffectsNausea, diarrhea, abdominal distention, appetite, sweating, H/A, depression, flush, and mood changes. Adverse Effects/ Reactions- Petechiae, ecchymosis, hypertension, tachycardia, osteoporosis, and muscle weakness.

Life Threatening- GI hemorrhage, pancreatitis, circulatory collapse, thrombophlebitis, and embolism. Drug; Food; Labs Interactions- Drugs- effect with barbiturates, phenytoin, rifampin, ephedrine, theophylline, effects of aspirin, anticonvulsants, Ioniazid (INH), antidiabetics, and vaccines. Mineral Corticosteriods- promote Na+ retention/reabsorption and K+ excretion . They influence electrolytes, carbohydrate, protein, and fat metabolism a deficiency in them can result in a serious illness or death. A decrease in their secretion is called Adrenal Hyposecretion or Addisons disease.

Ch 32 Anti Diabetic medicationsComplications from Diabetes are the 3rd leading cause of death. Ethnical groups more suspectable to Diabetes are Native Americans, Hispanics, African- Americans (2 to 3 times higher incidence) than Caucasians. Diabetes Mellitus is a disorder of the Pancreas Diabetes Insipidus- is a disorder of the Posterior Pituitary gland & Anti-Diuretic Hormone. There are 4 Forms of Diabetes: Type I Insulin- Dependent Diabetes Mellitus(Previously known as Juvenile onset Diabetes 2) Non- Insulin Dependent Diabetes Mellitus(previously known as Adult onset Diabetes)Most common occurrence of 85-90% of all diabetic cases. 3) Secondary Diabetes( due to medications such as Glucocorticoid cortisol or prednisone, thiazide diuretics like hydrochlothiazide, and epinepherine or hormonal changes) 4) Gestational Diabetes Mellitus (GDM)- during 2nd and 3rd trimesters levels of progesterone , cortisol and Human Placental Hormone increase and they can inhibit insulin usuage. There are 2 groups of Drug Therapies to treat Diabetes 1. Insulin it is a protein hormone secreted by the Beta cells in the Pancreas. They are needed for metabolism of carbohydrates, and play a role in protein and fat metabolism too. 2. Oral Hypoglycemic agents Insulin Is released from the Pancreatic Beta cells when there is an increase in serum glucose level. Normal serum glucose levels are from 70-11-mg/dl. When serum levels go above 180mg/dl then glucosuria (glucose in the urine) can occur. glucose in the blood acts as an osmotic diuretic polyuria, when blood serum glucose levels are > 200mg/dl Diabetes Mellitus occurs. Normally our bodies produce 0.2 to 0.5 units/kg/day of Insulin. Example pt weighs 154lbs which is approx. 70 kg he would produce 14-35 units of Insulin/day. Commercially prepared Insulin- Parental Insulin is obtained from either Pork or Beef . Pork Insulin is closely related to the Human Insulin, it has only one different amino acid than Humans. Therefore Pork Insulin is a weaker allergen then Beef. Beef Insulin has 4 different amino acids. Since 1983 Humulin Insulin was introduced. It has a very low incidence of causing an allergic reaction and an Insulin resistance. Subcutaneous Human (humulin) insulin is absorbed much faster and has a shorter duration than the animal insulins. This type of insulin is usually prescribed for newly diagnosed clients that are insulin dependent diabetics or in a

pregnant clients whom develop hyperglycemia and those women who are diabetics and who become pregnant. The usual dose concentration of Insulin is 100 Units/ml and is packaged in a 10 ml vial. Syringes are also calibrated to match 100Units/ml to be used for the 100U/ml Insulin type. Before using a vial of Insulin the nurse and or client must be taught not to shake the vial but to roll the vial between their palms to mix contents. Remember that Insulin is a protein and can NOT be given orally because GI secretions destroy the insulin structure! Please also remember that REGULAR Insulin is the only type of insulin that can be administered INTRAVENOUSLY! Clients should be taught a site rotation pattern to help avoid Lipodystrophy (tissue atrophy or hypertrophy) which can interfere with insulin absorption. Insulin Absorption- > when given in the Deltoid & Abdominal areas. ( the use of heat and massage will absorption). Of course illness and stress increase the need for insulin. Types of InsulinsRapid Acting- clear Include Lispro Humalog, Novolog. Onset: 5-15min Peak 30-60 min D: 3-4h Short Acting- Regular Humulin R. Onset:30-60min. Peak:2-3h D: 4-8 h Intermediate Acting- cloudy. Humulin N. Onset:1-2h Peak:4-12h D: 18-24h It may contain protamine (protein that prolongs action of or zinc that slow the onset of action and prolongs the duration of action. Long Acting- Glargine Lantus. Onset:1h Peak: None D: 24h Combination-Humulin 70/30, Novolin 70/30, Humulin 50/50. A. Oral Anti Diabetic Medications Used mostly for Type II diabetics because these clients do produce some amounts of Insulin. First group of oral diabetics were Sulfonylureas. These drugs stimulate beta cells to secrete more insulin. In the first generation of this group : Short Acting Tolbetamide Orinase Intermediate Acting- Acetohexamide (Dymelor), Tolazamide(Tolinase)

oral antidiabetic Sulfamylurea class: Amaryl, Glucotrol, Glucotrol XL used for type 2 diabetes. pancreas still producing some insulin. stimulates pancreatic beta cells to secrete insulin SE: HYPOglycemiaLong Acting- Chlorpropamide (Diabinese) 2nd generation of Sulfonylureas- the tissue response to insulin& glucose production from the liver. They have greater hypoglycemic potency, longer duration and cause fewer side effects. They should not be used in clients with liver or kidney dysfunction is present. Glimepiride (Amaryl) Glipizide (Glucotrol, Glucotrol XL) {Prototype} side effects Nausea/vomiting, diarrhea and abdominal pain. Hypoglycemia is a major side effect. Adverse: Hematological disorders aplastic anemia, leucopenia, thrombocytopenia, seizures, coma Dose- Pharmacokinetics Pharmacodynamics Biguanides (Metformin, Glucophage) acts by hepatic production of glucose from the stored glycogen, and absorption of glucose in the small intestine & it insulin receptor sensitivity. It does not cause Hypoglycemia or Hyperglycemia. It is not recommended for clients with Renal impairment. Hold for 48 hrs. before and after the client has IV contrast d/t lactic acid build up or possible development of acute renal failure. Other Anti- Diabetic Agents- Exenatide (Byetta) from amylin .Improves Betta Cell responsivenessimproves glucose control in clients with Diabetes Type II. Action is to enhance insulin secretion ; beta cell responsiveness , suppress glucagon secretion, slows gastric emptying & food intake. It is not a substitute for Insulin & should be given to patient whom have Type I Diabetes, Diabetic Ketoacidosis, some renal

dysfunction, or severe GI disease. Available in injectable pens. Promlintide Acetate(Symlin) used to improve post prandial glucose control in diabetic clients who are using Insulin but areCh 14 CNS stimulants and related drugs Ch 15 Antiepileptic drugs Ch 50 Acid controlling drugs Ch 51 Ch 52 Bowl disorder drugs

GERD antacid sodium bicarbonate Alka Setzer GOOD SE" constipation. Systemically absorbed .treats metabolic acidosis. can cause HYPERNatremia GERD antacid Aluminum based Amphojel GOOD SE" constipation. Binds phosphate, used w/renal pts. to focally eliminate phosphorus GERD antacid calium based Calcium carbonate Tums GOOD SE: constipation. tms used to increase calcium for osteoporosis and in renal pts. BEWARE w/HYPERglycemia

antidiarrheals Immodium(OTC) Lomotil (prescription) for treating diarrhea decreasing peristalsis. assessment of hyperactive bowel sounds. important due to loss of fluid and electrolyte imbalances. try Gatorade and pedialyte. MD may want to test for culture and O&P=test for worms. Chemically related to OPIATES assess for ALLERGIES Lomotil/Immodium (prescript/OTC) used to treat diarrhea chemically related to opiate so assess for allergyAntiemetic and anti Nausea Ch 53 Vitamins and minerals Ch 54 Nutritional supplements

PHARMACOLOGY STUDY GUIDE 5 rights of medication administration

1. right PT 2.right ROUTE 3.right DOSE 4. right Time 5. right Medication

Cummulative Section Pharmacology: The study of drugs and their interactions with living systems Encompasses the study of the physical and chemical properties of drugs as well as their biochemical and physiological effects. Clinical Pharmacology: Study of drugs in humans (includes study of drugs in patients as well as healthy volunteers). DRUGS: Effectiveness: Most important! Elicits the response for which the drug is given. Current US law requires proof effectiveness prior to release for marketing. Safety: One that cannot produce harmful effects (there is no such thing as a SAFE drug) Selectivity: Elicits only the response for which it is given thus no side effects (No such thing as a selective drug). Pharmacotherapeutics: The medical use of drugs (use to dx, prevent or treat disease, or prevent pregnancy) Pharmacokinetics: The study of the movement of drugs through the body. Four Basic Processes 1. Absorption (think stomach) 2. Distrubution (think blood flow) 3. Metabolism (think liver) 4. Excretion (think kidney) Process is determined by the concentration of a drug at the site of action determines intensity and time course of responses. Movement through the body: drugs must cross membranes, most commonly by dissolving directly into the lipid bilayer of the membrane to cross (lipid soluble drugs can cross membranes, but polar or ionized cannot). Other pathways to cross membranes: 1) passing through the pores 2) undergoing transport 3) penetrating membrane directly (common) Absorption: the movement of a drug from its site of administration into the blood. -Enhanced absorption occurs by rapid drug dissolution, high lipid solubility, a large surface area, and high blood flow at the site of administration. Distribution: defined as the movement of drugs throughout the body. - In most tissues, drugs can easily leave the vasculature through spaces between the cells that compose the capillary wall. - Many drugs reversibly bind to albumin. While bound to albumin, drug molecules cannot leave the vascular system.

Metabolism: Biotransformation. Enzymatic alteration of drug struction -most takes place in the liver and is catalyzed by cytochrome p450 system of enzymes. -Most important consequence of drug metabolism is promotion of renal drug excretion Excretion: Most drugs are excreted by the kidney. -Renal drug exretion has 3-steps: glomerular filtration, passive tubular reabsortion, and active tubular secretion. -Drugs that are highly lipid soluble cannot be reabsorbed back into the kidney -Drugs can be excreted into breast milk. First-Pass Effect: rapid inactivation of some oral drugs as they pass through the liver after being absorbed. Essentially, how much drug is left available after passing through the liver. Used to determine dosage and intensity. Bioavailabilty: free-circulating drug system (post-first pass) even after binding. Half-Life: Time required for the amount of drug in the body to decline by 50%. Shorter the half-life, the more frequent the administration. Time to reach plateau about 4 half-lives. Drugs with a long half-life may need a loading dose to reach plateau. Pharmacokincetic tolerance: results from a accelerated drug metabolism. Pharmacodynamics: What drugs do to the body. The study of biochemical and physiologic effects of drugs and molecular mechanisms by which those drugs are produce. Reducing risk of adverse interactions: minimize # of drugs the patient is on. Take a thorough drug history. Adjust dosages when using an inducing agent. Adjust timing of administration to reduce absorption problems. Monitor for early signs of toxicity. Be vigilant when a patient is on a drug with a low therapeutic index. Pharmacodynamic tolerance: results from adaptive changes that occur in response to prolonged exposure. It increases the MEC of a drug. Allergic Drug Reaction: an immune response. Estimated 60 and LDL ,100 total ,200 inhibits HmG-CoA reductase-enzyme that produces LDL at night. TAKE at BEDTIME except LIPITOR. Cholesterol affects LIVER so assess CPK, AST, ALT. shrinks plaque to prevent stroke .has anti-inflammatory effects so may help COLON CANCER and ALZHEIMERS. SE: myalgia, rhabdomyolysis. NO grapefruit juice. LOW fat DIET UTI med Pyridium/analgesic relieves pain, burning sensation, and frequency and urgency. blood test to monitor

glucose levels. monitor for GI disturbances, HEMOLYTIC ANEMIA, NEPHROtoxicity, and HEPAtoxicity. SE: HEMOLYTIC ANEMIA, NEPHROtoxicity, HEPAtoxicity, urine will become redish orange colored SNS epinephrine Adrenaline Beta1=heart Beta2=lungs UTI meds macrodantin E. coli Tx of acute and chronic UTIs. CBC w/long term therapy... assess RENAL and HEPATIC function. monitor output and obtain culture before therapy....SE: anorexia, n.v, discoloration of urine, superinfection, HEPAtoxicity deltoid inj (IM) 1 ml of medication landmark: acromian process opiate w/narcan used to treat pain and prevent narcotic addiction Heparin subcut or IV used for prophylaxis or acute events. Prolongs clotting time. Labs: PTT(1.5-2.5) ANTIDOTE: Protamine Sulfate...assess for bleeding, use soft toothbrush, electric shaver. WBC range 4-10,000 Beta Blockers "OLOLS" Inderal(non-selective) all others selective. decreases contractibility in heart, lowers renin release in KIDNEYS, and sympathetic output. for HTN,angina,MI,dysrhthmias.SE=BRADYcardia,hyPOtension,bronch constriction,lowers blood sugar.Hold for BP less than 60 or systolic less than 90. Inderal can decrease test anxiety antitussive narcotic: CODEINE over the counter: DEXTROMETHORPHAN suppresses cough reflex. if cough is nonproductive and irritating:can give antitussive. productive cough may be useful. GIVE AFTER MEALS!!!! oral antidiabetic Biguanide class : Glucophage decreases hepatic production of glucose, increases insulin receptor sensitivity.May be combined with other hypoglycemia needs. WITHHOLD 48hrs before and after tests using IV contrast dye;LACTIC ACIDOSIS and RENAL FAILURE may DEVELOP!!!! LIVER NSAID aspirin(ASA) falls under multiple classes analgesic,antipyretic,antiplatelet,anti-inflammatory,menstrual pain. Check for ASA allergies.assess hx for GI upset,bleeding & lier disease. TAKE with FOOD or FULL glass of WATER. admin PPI to reduce risk of ulcr. SE: no PREGGOS LAST TRImester,n

alcohol,don't take w/other NSAIDS,kids with flu like sx cant tae(reye's syndrome) SE: GI upset, bleeding,renal failure, TINNITUS insulin injection subcut into fatty tissue abdomen the best orange insulin syringe only anticholinergic atropine dries you up, ups heart rate,slows diarrhea, contraindicated in:glaucoma and GI disorders. Monitor VS and HR, monitor constipation,oliguria.Take 30 min before food. eat high fiber and lots fluids IV heparin drip know PTT lab (2-4) if too high=bleeding if too low=clot check PTT every 6hrs heparin 90 degree inj DONT aspirate