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PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 3. 1000mL PNSS to infuse over 4 hours Antagonists block receptor activation by agonists. 4. 250mL PNSS over 5 hours. Tubing drop facto...

PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 3. 1000mL PNSS to infuse over 4 hours Antagonists block receptor activation by agonists. 4. 250mL PNSS over 5 hours. Tubing drop factor of 10gtt/mL Alpha 1 ○ abundant in the blood vessels VASOCONSTRICTION Alpha 2 ○ blood vessels VASODILATION W2&3: CARDIOVASCULAR DRUGS Beta 1 ○ heart muscles increases Heart rate ( Tachycardia) ○ High RR and BP ANTIHYPERTENSIVE MEDICATIONS Beta 2 ○ Widens the airway smooth muscles of the airway A. ANTI ANGINAL BRONCHODILATION B. GLYCOSIDES (Ex. Asthma)Salbutamol C. C. DIURETICS famous If you use antagonist it does the opposite Agonists and Antagonists effect Agonists - Drugs that occupy receptors and Alpha 1 Antagonist: activate them. Antagonists - Drugs that occupy receptors blocking them with an antagonist but do not activate them. would lead to vasodilation (widening of blood vessels). This could lower PAGE 19  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 blood pressure because the blood given sublingual every vessels stay relaxed. 15 mins *check bp and hr Alpha 2 Antagonist: High doses: Na & H20 Retention ○ *peripheral edema blocking would result in ○ *diuretics vasoconstriction(narrowing of blood X given with beta-blockers: severe vessels), which could raise blood bradycardia pressure. ALPHA - ADRENERGIC BLOCKERS Beta 1 Antagonist: Vasodilation = decreased BP maintains renal blood flow An antagonist would block this effect, lowers VLDL (very low density leading to a reduced heart rate and lipoprotein) & LDL + increases HDL possibly a weaker heartbeat. Beta no effect on glucose(safe to give to blockers, which are Beta 1 diabetic clients) & respiratory antagonists, are commonly used to function treat high blood pressure and heart Selective (Alpha 1): Prazosin conditions by slowing the heart down. X take with alcohol & other anti-HPN Beta 2 Antagonist: Taken with Diuretics: Na & H,0 Retention (Edema) If blocked by an antagonist, it would cause bronchoconstriction More potent: Phentolamine (narrowing of the airways). This could Hypertensive Crisis make it harder to breathe, which is ○ higher than 180 systolic why Beta 2 antagonists are generally pressure. avoided in conditions like asthma. reflex tachycardia ○ when bp is low causing to pump more blood. BETA - ADRENERGIC BLOCKERS Reduce HR, contractility & renin release. ○ Non-selective: Beta 1 & 2 Propranolol (Inderal) ○ Selective: Beta 1 Atenolol (Tenormin) Metoprolol (Lopressor) CENTRALLY - ACTING ALPHA2, AGONISTS Decrease sympathetic response: Vasodilation ○ Methyldopa (Aldomet) (pregnant women) ○ Clonidine (Catapres) PAGE 20  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 ADRENERGIC NEURON BLOCKERS Block norepinephrine release: decreased BP Severe HPN: very potent ○ Reserpine / Guanethidine / Guanadrel Epinephrine ○ Last choice: Orthostatic If di na makahinga patient, kapag di Hypotension na kaya ng nebulizer. IM It causes Na & H20 administration Retention A1 SYMPATHETIC NERVOUS SYSTEM ALPHA-1 & BETA-1 ADRENERGIC BLOCKERS Blocks both: Alpha-1 & Beta-1 Labetalol (Normodyne) ○ Vasodilation: slowed HR & decreased BP ○ Large doses: bronchoconstriction / Atrioventricular Block (AV Block) **detected through ECG Contraindications: ○ 2nd or 3rd-degree AV Block ○ Bradycardia ○ Hypotension ○ Renal / Liver impairment ○ COPD emphysema bronchitis asthma PAGE 21  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 Notes: Drug History Baseline & Monitoring of VS, labs Compliance X Do not discontinue (D/C) abruptly: rebound HPN Drug Interactions (herbal & OTC) ○ If there is intake of herbal tell the doctor immediately. Pinapatigil ung herbs for 1 week ○ Why? :Some herbal medicines neutralize/buffer (pinapawalang bisa) A1 RENIN - ANGIOTENSIN SYSTEM cardiovascular medicines. Self-administration: take PR & BP (daily record) renin (kidney) + angiotensin (liver) = S/E & A/R: Report angiotensin 1 Non-pharmacologic measures (diet modifications) ○ Low cholesterol and salt diet DIRECT - ACTING ARTERIOLAR VASODILATORS Relax smooth muscles of blood vessels = Vasodilate Na & H20 Retention = edema Hydralazine ( HPN for pregnant patients) & Minoxidil: reflex **HPN is not ideal for renin - angiotensin tachycardia system Nitroprusside & Diazoxide: Acute HPN emergency ACE (angiotensin converting enzyme) S/E & A/R: INHIBITORS Hydralazine: Neurologic symptoms Captopril (Capoten) Minoxidil: Excess hair growth Enalapril / Quinapril *anginal attack ○ suffix: PRIL (Ace inhibitors) Nitroprusside: Reflex Tachycardia 1st line HPN therapy Diazoxide: Hyperglycemia X pregnant: reduce placental blood flow X taken with K-sparing diuretics / salt substitutes Renal disease: decreased dose Taken with food PAGE 22  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 Additional Information B Calcium Channel Blockers S/E: Constant, irritated cough A/R: N/V + Diarrhea Headache / Dizziness / Fatigue / Insomnia Tachycardia Major A/R: 1st-dose hypotension + hyperkalemia NURSING RESPONSIBILITY Drug History ○ ask patient’s maintenance Baseline VS, Labs **Hypoglycemic reaction in DM patients Report: bruising / bleeding = severe A/R calcium: increases contractility ANGIOTENSIN-II RECEPTOR BLOCKERS vasoconstriction. Direct at receptor site: Vasodilation Verapamil / Diltiazem / Nifedipine Losartan (Cozaar) / Telmisartan (Common in the PH) (Micardis) ○ Reflex Tachycardia ○ suffix:SARTAN ○ + hydrochlorothiazide (diuretic): X Calcium: activates myocardial contraction Potassium wasting = potassium (-) inotropic (muscle contraction) loss ○ afterload Potassium is still ○ workload of heart = moderately needed if the decreases Oxygen demand patient has HPN Verapamil ○ 1st-line TX for HPN Nifedipine Diltiazem DIRECT RENIN INHIBITOR Aliskiren (Tekturna) ○ Binds with Renin = decreased slows the heart rate Angiotensin | and 11 & aldosterone decreases heart muscle contractions. ○ Effective: mild to moderate HPN relax the blood vessels ○ alone or with another anti-HPN ○ Amlodipine, Diltiazem ○ additive effect: thiazide diuretic or SE: ARB Bradycardia Hypotension Dizziness Flushing of skin Reflex Tachycardia PAGE 23  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 Need to oxygenate insufficient ___ to prevent cellular PATHOPHYSIOLOGY death PATHOPHYSIOLOGY a. HYPERTENSION b. MYOCARDIAL INFARCTION A ANTI-ANGINALS c. ANGINA Increase in blood flow Increase in oxygen supply Decrease in oxygen demand Nitrates Beta-blockers Calcium Channel blockers NITRATES 1st anti-anginals Vasodilation = Increase in blood flow *hypotension SL tablet Q5 mins = max. 3 doses ○ Nitroglycerin (NTG) wear gloves to prevent contact to skin that can cause dizziness and Atherosclerosis headache ○ deposition of blood ○ Isosorbide dinitrate (Isordil) Arteriosclerosis ○ Isosorbide mononitrate (Imdur) ○ thickening/hardening of blood vessels due to age S/E: HEADACHE Polycythemia vera Hypotension ○ many red blood cells but doesn’t carry Dizziness oxygen or no oxygen at all. Weakness Thromoangitis Obliterans/Buerger’s Faintness Disease ○ bluish peripheries NTG transdermal patch: taper doses (do not discontinue abruptly) Reflex tachycardia=rapid administration Drug interactions A1 PHARMACOLOGIC THERAPY Nitroglycerine - mainstay of treatment. Vasodilation >> veins Venous pooling resulting to decrease in Preload and BP. PAGE 24  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 Vasodilation of arteries results to Alcohol Eliminates the decreased BP and decrease in effect of Transdermal afterload. patch. Side effect : Hypotension ○ Protect SL tablet from light 1400 111800 ○ Transdermal patch ○ Headache: Acetaminophen Nitroglycerin Tablet, 1 tablet every after 5 ○ Hypotension: Trendelenberg min x 3 doses ○ Take PR prior = Dilates coronary artery → good blood flow ○ D/C: taper doses →reduce the pain. Beta-Blockers Advice: Anti-anginal Avoid activities that precipitate Anti-dysrhythmic Angina (ex. Smoking) Anti-HPN Severe physical movement Take Nitroglycerin for chest pain ⬇ HR & myocardial contractility: Take maintenance drugs for ⬇O2 consumption Hypertension ⬇anginal pain A plan for regular exercise *classic (stable) angina ○ Best: walking Loss excess weight, recommend high OLOL ( A suffix used to designated beta Fiber diet blocker) Propanolol (Inderal) Nadolol Anti-Anginal Atenolol Metoprolol Notes: S/E: ⬇PR ⬇JBP ○ Baseline VS A/E: Bronchospasm orthostatic hypotension Psychotic response kapag nakahiga Impotence lang patient: as a ○ reproductive system issue for nurse elevate mo male muna by 30 degrees until 90 *taper doses bago ipalakad ○ Health and Drug History ○ Sit or lie down: rise slowly ○ Sips of water prior to SL tablet ○ Ointment: X use fingers to apply ○ Transdermal patch: chest Client Teaching ○ Report persistent angina: >15 mins ○ Avoid alcohol PAGE 25  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 GOALS of Medical Management Relieve the acute pain Restore coronary blood flow Opiate Analgesics - reduces pain ○ Vasodilators: Nitroglycerin: ⬆ Diameter of Cardiac arteries. ⬆ Supply of O2 Beta adrenergic blockers: ⬇workload, + ⬇O2 demand. + ⬇angina attacks Calcium Channel blocker: dilate the arteries. ⬆O2 Anti platelet: inhibit platelet **Oxygenate the area aggregation, prevents clot formation Medical Management: Prevent further attacks: education and Aspirin at onset of Manifestation counseling elevated clients head, loosen tight clothing O2. Connect to heart ANTI PLATELET AND ANTICOAGULATION monitor. Defibrillation if possible MEDICATIONS ○ As a nurse prepare it but not in Prevents platelet aggregation front of the patient. Aspirin: 1 tablet= 4 mg but if for Reduce chest pain - Iv Morphine emergency 325 mg. H2Blockers may ECG, Echocardiogram, use of be given in combination betablockers and IV nitroglycerin ○ H2 receptor- increase gastric Thrombolytic agents (ex. acid production Streptokinase) give within a hour Clopidogrel and Ticlodipine. If after onset pain, Alteplase and allergic to aspirin. reteplase HEPARIN: prevents the formation of Anti Dysrythmic agents New Blood clots. (betablockers): ACE inhibitors (RAAS) OXYGEN ADMINISTRATION >> greater than 93 percent saturation In patients: bed rest. ○ Bedside commode Portable toilet for adult MYOCARDIAL INFARCTION patient. NOT RELIEVED by NITROGLYCERINE ○ ⬇Na intake. Medical management: ○ Passive exercises, ○ Aim: Minimize myocardial ○ gradual approach to regain damage preserve myocardial ADL. function prevent complication to avoid muscle constriction decorticate decerebrate PAGE 26  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 Outpatient Home: adequate help. Conducive to rest Digitalis Toxicity Sexual activity: Resume: 4-8 weeks after M.I. Most able to climb 2 flights CARDIOTOXICITY of stars before resuming sexual bradycardia activity Dysrhythmia: PVCs (Premature ○ May take nitroglycerine before Ventricular Contractions) sex activity to ⬇Angina ○ di maririnig through XXXXXX not together with auscultation madetect lang Viagra( causes vasoconstriction through ECG leading to no effect), smoking, Heart block and strenuous exercise NAVDA - Nausea, Return to work in 8 to 9 weeks Headaches Malaise Visual illusions:halos CARDIAC GLYCOSIDES Confusion/delirium Nursing Responsibilities: Congestive Heart Failure (CHF) Drug and Herbal history ○ Heart Failure: Left-sided VS Baseline VS Right-sided s/sx of digitalis toxicity Read drug label carefully DIGITALIS Glycosides Check serum drug & potassium level inhibit sodium-potassium pump Client Teaching: increase Calcium = muscle Compliance contractility OTC medications ○ (+) Inotropic Check PULSE prior ○ (-)Chronotropic Child safety ○ (-)Dromotropic Report S/E Potassium-rich foods Drug interactions Diuretics KIDNEY: purpose 2 main purposes: Decrease: HPN and EDEMA ○ Pre eclampsia high blood pressure in pregnant women Mechanism of Action: DIURESIS increased urine flow inhibit Na & H20 reabsorption from kidney tubules PAGE 27  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 Anti-hypertensive effect: Increase in aldosterone because liver cannot sodium + water loss activate anymore the steroid hormone, so Decreased fluid volume increase in salt and water reabsorption lowered BP + edema leading to fluid accumulation Sodium retention Water retention = increased BP C. NEPHROTIC SYNDROME loss of protein from plasma reduces Loss of electrolytes: K, Mg, Cl, HCO3 the colloidal osmotic pressure (Bisodium Carbonate) resulting to edema. Sparing VS Wasting plasma volume is low as aldosterone is stimulated so more water and COLLECTING TUBULES AND DUCTS sodium reabsorption resulting to Responsible for: edema. sodium, potassium exchange hydrogen secretion potassium reabsorption ALDOSTERONE LIST OF DRUGS Released by the adrenal gland, ingfg 1. PROXIMAL CONVOLUTED TUBULES result to : ACETAZOLAMIDE Na reabsorption 2. DESCENDING LOOP OF HENLE K secretion 3. ASCENDING LOOP OF HENLE ○ Inversely proportional BEFT-LOOP: ADH (vasopressin) : BUMETANIDE promote water reabsorption from ○ most common diuretic collecting tubules and ducts ETHACRYNIC ACID mediated by C A mp FUROSEMIDE ○ most important: do not give In kidney disease, na reabsorption is if the BP is less than 100/60. abnormally High. ALWAYS CHECK THE BP OF Result: THE PATIENT 1. increase in water retention TORSEMIDE 2. Increase in blood volume 4. DISTAL CONVOLUTED TUBULES 3. Expansion of extracellular fluid (edema) THIAZIDES 5. COLLECTING TUBULES causes STA-R A. CHF : more salt, more water, but heart SPIRONOLACTONE cannot increase the output results to TRIAMTERENE edema AMILORIDE Na - extracellular fluid B. ASCITES: Fluid in the abdominal cavity CARBONIC ANHYDRASE INHIBITORS complication of the cirrhosis of the liver a. Increase in portal blood pressure as it ACETAZOLAMIDE is obstructed inhibits the Carbonic anhydrase b. Hyperaldosteronism intracellularly and in the membrane Measure abdominal girth. of the proximal tubules. PAGE 28  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 USES : For Glaucoma: What are the adverse effects of LOOP If acute: use pilocarpine Diuretics ? If chronic: use Acetazolamide 1. ototoxicity (in the ears=ear pain) ○ decrease intraocular pressure. specially if combined with amino 1. decreases IOP glycosieds 2. Antiepileptic medication 2. Hyperurecemia: more gouty effects 3. acute Mountain sickness if with furosemide and ethacdrynic acid AE : 3. acute Hypovolemia if there is a severe metabolic acidosis reduction of blood volume calcium depletion 4. Potassium depletion as adverse effect. KIND OF ACIDOSIS AND ALKALOSIS Give potassium ** wala lang sa medsurg daw use : potassium sparing diuretics (STAR) Pharmacodynamics Carbonic anhydrase inhibition THIAZIDES causes significant HCO, losses and Most widely used diuretic may lead to hyperchloremic greater effect than acetazolamide metabolic acidosis. all affects the distal tubules The diuretic efficacy of acetazolamide decreases CHLOROTHIAZIDES significantly with use over several prototype days because HCO3- depletion decreases the reabsorption of sodium leads to enhanced NaCl by inhibiting the sodium chloride reabsorption by the remainder of cotransport on the luminal the nephron. membrane decreases sodium reabsorption LOOP OR HIGH CEILING DIURETICS Cont:thiazides Most effective Action : BEFT - LOOP 1. Increases excretion of sodium and ○ Bumetarate (more potent than chloride furosemide) 2. Loss of potassium ○ Ethacrynic acid 3. decrease In calcium excretion ○ Furosemide 4. Reduce peripheral vascular ○ Torsemide resistance MOA: inhibits the na/ k/ Cl transport of USES OF THIAZIDES: luminal membrane in the ascending loop of 1. Mainstay in hypertensive nedication henle so its reabsorption is decreased. 2. Use in CHF if loop is not succesful = decreased renal vascular resistance and 3. Renal impairment increase in renal blood flow 4. Hypercalceuria: calcium excretion is inhibited What are the uses of LOOP? DOC for acute pulmonary edema of CHF PAGE 29  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 5. Diabetes insipidus: has the ability to aldosterone antagonists competeing produce hyperosmolar urine. aldosterone in the receptor sites. Antidiuretic effect action: For edematous states. TAKEN ORALLY USES : 1. For Retention of potassium. Adverse Effects of thiazides: 2. For secondary hyper aldosteronism A. Hypokalemia ORALLY ABSORBED it will cause ventricular. AE: Arrythmia ○ Gynecomastia ( enlargement ○ To counteract: use of breast) in male potassium sparing ○ Menstrual anomalies in diuretics female Spirinolactone : ○ interferse with the action of TRIAMTERENE AND AMILORIDE aldosterone BLOCKS THE Na transport channel Triamterene: resulting in decrease in NA/K ○ retains Potassium exchange and has potassium sparing B. Hyperurecemia diuretics. C. Volume depletion ○ use in combination e=with D. hypercalcemia : Thiazides and furosemide. E. hypersensitivity AE: Leg cramps, increased BUN - Blood, urea, nitrogen. Hydrochlorothiazide ○ more potent OSMOTIC DIURETICS : Chlorotalidone Thiazide analogue Mannitol ○ Metalazone ○ used in patients with more potent and causes Increased intracranial pressure. Na excretion unlike ○ These are more on water thiazide excretion than sodium excretion. PRIMARY SPARING DIURETICS ○ increases urine flow after acute use primarily when aldosterone is in toxic ingestion of substances excess that can caus renal failure, acts in collecting tubules to : shock, > toxicity and trauma. ○ Inhibit sodium reabsorption Mannitol: IV ONLY ○ potassium excretion ○ hydrogen secretion For treatment of hypertension with SUMMARY thiazides you have just learned: Again: what are the potassium sparing The principles involved in lowering diuretics? the blood pressure with the use of Spirinolactone different types of anti hypertensive Triamterene medications. Amiloride The different anti Anginal drugs, its main effects and the nursing SPIRINOLACTONE : PAGE 30  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 responsibility in the pre and post medications, the MOA, Intended drug administration. conditions The glycosides and its main Adverse effects of these actions medications The principles of decreasing the Discuss the medications for the body fluids and blood pressure treatment of bleeding. with the use of Diuretic Discuss the mechanism of action of medications. commonly prescribed anti-lipidemic and peripheral A. Anti coagulants vasodilators. B. Antiplatelet Explain the effects of C. Antithrombotic Drugs antidysrhythmic drugs, its purpose, D. Antilipidemic Medication and side effects in relation to the management of irregularity of heartbeat. INTRODUCTION Integrate knowledge of This module will give you an idea about cardiovascular agents with the the following: nursing process as the core of Anti-coagulants achieving quality nursing care. Antiplatelets Thrombolytic agents Anti-lipidemic agents and Blood clot Formation Peripheral intrinsic - internal/inside Vasodilators extrinsic - external/outside Antidysrhythmic drugs Clotting Factors Application of Nursing Process in 2, 5, 7, 9, 10, 11, 12 Pharmacology for clients taking Cardiovascular ANTICOAGULANT, ANTI- PLATELET, Agents THROMBOLYTIC >>BLOOD >>CLOTTING FACTORS >> DECREASES FAT THROMBOSIS PLAGUES/CHOLESTEROL LEARNING OBJECTIVES localized Differentiate a thrombus from an unwanted clot formation within the embolus blood vessels and the heart ○ Embolus most common thromboembolic movable disease ○ Thrombus Bleeding disorders Discuss the differences in the A. hemophilia properties and mechanisms a. Males action of Anti-coagulants: Heparin B. vitamin k deficiency and Warfarin. Present the other anti-platelet, CLOT FORMATION anti-coagulants and thrombolytic PAGE 31  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 Platelet activation >> platelet Aggregation ○ Go disintegrate within 4 hours >>> Thrombin formation of administration > Protease catalysis production of Fibrin >> Should be given within 3 hours of cross links >> stabilizes the Clot.. thrombolic stroke ○ aneurysm Trombus clot adheres to the wall Prognosis Embolus positive outcome ( patient is better Floats The doctor gives Mannitol to decrease ICP. THROMBOSIS FORMATION Lysis cell swelling burst Crenation cell shrinking Thrombosis ○ formation of a clot in a blood Apoptosis vessel Programmed cell death can be dislodged & move through bloodstream:Embolus Mechanism of action: Platelets aggregate as a result of: conversion of plasminogen to break in blood vessel plasmin As thrombus inhibits blood flow: Plasmin: digests fibrin in the clot ○ Fibrin + Platelets + RBCs = clot ○ degrades fibrinogen, size & structure prothrombin & clotting factors Induce fibrinolysis Venous thrombus: slow blood flow Streptokinase: ○ can occur rapidly may cause hypotension (1st ○ can detach & travel administration) = pulmonary embolus ○ drug dosage may need to be adjusted Anticoagulants Urokinase ○ Venous thrombosis Anti-platelets Alteplase: tPA ○ Arterial thrombosis Tissue plasminogen activator: but both suppress thrombosis in general identical to human tPA S/E & A/R: Allergic reactions Thrombolytics ○ Anaphylaxis ○ Streptokinase ○ Dysrhythmias Thromboembolism = ischemia Major complication (happens when there’s no oxygen) = ○ Hemorrhage tissue necrosis ○ Aminocaproic acid (Amicar): 1-2 weeks: for blood clot to anti-thrombolytic disintegrate naturally inhibits plasminogen ○ basis for thrombolytic therapy activation PAGE 32  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 TICLODIPINE Thrombin Inhibitor of platelet aggregation key role in coagulation inhibits ATD pathway decreases thrombotic stroke Platelet aggregation Inhibitors: ○ AE: NEUTROPENIA Aspirin decrease number of Ticlodipine neutrophil Dipyridamole first line of defense against Contraindications: infection Peptic ulcer / active bleeding / intracranial hemorrhage DYPIRIDAMOLE : Coronary vasodilation for angina Parietal cell- increase gastric acid. can be given together with aspirin Salicylic acid triggers leukotrienes Inhibits synthesis of tromboxane A 2 leading to allergic reaction. Inhibits embolization in Prosthetic (Important to know if the patient is Bypass (Bypass Graft) allergic to aspirin) ○ to reduce/prevent embolus Leukotrienes- lessen the symptom of allergy ANTICOAGULANT : thromboxane - substance produced 1. HEPARIN by platelets 2. VITAMIN K (ANTAGONIST is Warfarin) WATCH THE ASPIRIN VIDEO!! Difference Heparin-IV (safest), Subq Aspirin Warfarin-Oral Inhibits cyclooxygenase HEPARIN ○ As a result: Arachnidonic is Rapidly acting injectable not thromboxane A2 anticoagulant ○ Uses with Histamine in mast cells a. Transient cerebral acidic ischemia acts directly on the Antithrombin 3 b. Reduce MI c. Prophylactic use: MI / USES : CVA 1. For deep vein thrombosis and ○ Long term: low-dose Aspirin Pulmonary embolism therapy = effective 2. in Dialysis machines to prevent ○ Aspirin: prolonged thrombosis anti-platelet effect 3. For patients with Prosthetic valves ○ D/C at least 7 days prior to (can provide bypass graft) Pulmonary surgery Embolism / Stroke Warning ○ Increase bleeding time ENOXAPINE ○ Be careful: Gl Bleeding to prevent DVT with HIP replacement ○ Hemorrhagic stroke PAGE 33  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 ○ Never administer IM. It will MOA result to Hematoma ○ Vitamin Dependent factors: formation (bruise) 2,7,9 and 10 Adverse effects: Vitamin K epoxide reductase HEMORRHAGE inhibitor Contraindicated with : This is the one inhibited by warfarin PROTAMINE SULFATE ○ if you give too much warfarin Hypersensitivity Reaction give vitamin K (vice versa) Thrombocytopenia ○ decrease amount of platelets WARFARIN(Coumadin) ○ less than 150,000 prolong Prothrombin Time (PT) Thrombocytosis Performed before administering the ○ increase amount of platelets next drug dose ○ greater than 450,000 until the therapeutic level has been SQ/IV reached Prolongs clotting time + Can 1.25 to 2.5 times the control level decrease platelet count International Normalized Ratio (INR) Partial thromboplastin time (PTT) Reagents used in PT test are compared with ○ Activated partial international reference standard & reported thromboplastin time (aPTT) as INR N: 1.3 - 2 Antidote: Protamine Sulfate on Warfarin therapy: 2 - 3 seconds before D/C: begin oral warfarin monitoring at regular intervals therapy Low-Molecular-Weight Heparins (LMWH) Types of Coagulation Tests lower risk of bleeding more stable responses inactivates Xa factor Prothrombin Time (PT) Enoxaparin Sodium (Lovenox) ○ Evaluates ability to clot International Normalized Ratio WARFARIN(Coumadin) (INR) this a common anticoagulant for ○ Ensures that results from a PT Long term therapy test are the same from one lab a. Warfarin to another b. Dicumarol Partial Thromboplastin Time (PTT) ○ Determines if blood-thinning Warfarin therapy is effective Action ○ antagonizes the cofactor Warfarin (Coumadin) function of Vitamin K Antidote: Vitamin K (phytonadione) Oral anticoagulant takes 24-48 hours to be effective ○ Mostly confined to vascular if given in excess: may take 1-2 weeks system for Warfarin can be effective again ○ used primarily to prevent acute bleeding: FFP (Fresh Frozen thromboembolic conditions Plasma) PAGE 34  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 ○ contains high concentration of platelets AE : Hemorrhage STREPTOKINASES Warning: Never use WARFARIN in Extra protein purified cultures from b pregnancy. It is teratogenic and can hemolytic streptococci cause abortion Hydrolytic A/R: ○ Catalyzes the degradation Hemorrhage fibrinogen and clotting factor 5 ○ Monitor for signs of bleeding and 7 Reminder: Uses: Heparin works against anti thrombin ○ MI DVT, Occluded shunts and WARFARIN: works against Vitamin K etc AE : ○ Bleeding dissolves the THROMBOLYTIC AGENTS hematopoietic plug give in cases of emergency: (ASSU )Anesteplase Aminocaproic acid Alteplace ○ Hypersensitivity reaction ( urokinase protein) streptokinase Actions: UROKINASE Directly or indirectly acts to convert directly degrades Fibrin and plasminogen to plasmin which fibrinogen cleaves fibrin thus lysing thrombi Expensive : used if a patient is ○ clots are more resistant to lysis sensitive to streptokinase. as they age this is non antigenic ( antigenic is ○ Avoids: plasminogen + plasmin streptokinases) (formation) = fibrin for DVT and pulmonary embolism Fibrin - will create blood complications: bleeding clot USES: Deep vein thrombosis Pag nag blood thinner watch out for pulmonary embolism bleeding Mi - acute Arterial thrombosis Drugs to treat Bleeding unclotting catheters and shunts AE: Hemorrhage Contraindication: 1. aminocaproic acid Peptic ulcer. Healing wound controls fibrinolytic states pregnancy 2. Tranexamic acid Synthetic and inhibit ALTEPLASE (PA): Tissue plasmin activators plasminogen activators Fibrin selective in thrombosis and ○ AE : Intramuscular hemostatic plug thrombosis USES: MI 3. Protamine sulfate ○ Pulmonary embolism antagonizes the the anticoagulant ○ Acute ischemic str effects of Heparin PAGE 35  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 ○ AE: Hypersensitivity, flushing 4. Vitamin K: response is after 24 hours so if in a ERYTHROPOIETIN hurry: use Fresh Frozen plasma Regulate the red cell proliferation in (FFP) the bone marrow ○ produced in the kidney ○ good for anemia caused by kidney failure Drugs to treat ANEMIA ○ IV and sub Q AE : Increased BP Anemia ○ Blood viscosity Below normal level of plasma hemoglobin concentration due to decrease in the number of circulating B1 NURSING RESPONSIBILITIES RBC. ○ iron-RBC an abnormally total hemoglobin History of abnormal clotting / health content per unit of blood volume problems causes: blood loss, infection, Bone Drug & Herbal History marrow abnormality, Dietary Prepare flow chart: monitoring of lab deficiency (problem with the iron) tests management: transfusion of whole ○ baseline values blood Monitor VS, lab tests : Baseline VS, ○ management: ferrous Sulfate CBC, PT, INR (consider the Gl Medical & Drug History disturbances) ○ taking herbal supplements Check for signs of bleeding ○ *Older adults: monitor closely CYANOCOBALAMIN (Vit B 12) prone to hematoma efficiency in the food absorption of Keep antidote at bedside vitamins to facilitate the gastric parietal cells to produce the intrinsic Contraindications: factor Recent CVA (cerebrovascular accident) For MEGALOBLASTIC Anemia: combine: Active bleeding / Severe Hypotension 1. FOLIC ACID and Anti- coagulant therapy 2. Vitamin b 12 cyanocobalamine Recent traumatic injury: head Folic Acid+ Vitamin B12 Combination Note use of Aspirin / NSAIDs = increase the production of RBC *usually given in first trimester* Folic acid deficiency results to : Monitor VS: Signs of Impending Shock Decreased amino acid synthesis Observe for Signs of active bleeding decreased Purine synthesis *up to 24 hours after D/C decreased pyramidine Synthesis thrombolytic therapy —>>MEGALOBLASTIC ANEMIA (KULANG Observe for Signs of Allergic reaction ANG VITAMIN B12!) X Aspirin (give Acetaminophen instead) PAGE 36  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 Monitor ECG ○ increase recovery time IA: Quinidine, Procainamide Active blood cell IB: Lidocaine bright red ○ anesthetic found in arteries ○ used for cardiac dysrhythmia increase oxygen IC: Flecainide Inactive Blood Cell dark red found in veins A1 TYPES OF PRIMARY decrease oxygen HYPERLIPOPROTEINEMIA Client Teaching: Explain treatment to client & family There are five types of primary ○ Report S/E: hyperlipoproteinemia: Lightheadedness / Type 1 dizziness / palpitations / ○ is an inherited condition. It nausea causes the normal breakdown Pruritus or Urticaria of fats in your body to be disrupted. A large amount of Inform dentist & HCPs fat builds up in your blood as a Use soft toothbrush result. ○ if patient is taking blood Type 2 runs in families. thinner, they are not allowed ○ It's characterized by an to floss increase of circulating Shave using electric razor cholesterol, either low-density X smoking lipoproteins (LDL) alone or X Aspirin (Acetaminophen instead) with very-low-density Consult with HCP: OTC meds & lipoproteins (VLDL). herbal supplements ○ These are considered the "bad Controlling bleeding cholesterols." Reporting of A/R: signs of bleeding Type 3 Diet: foods to avoid ○ is a recessively inherited ○ citrus disorder in which ○ spicy intermediate-density ○ coff lipoproteins (IDL) accumulate in your blood. IDL has a cholesterol-to-triglycerides CARDIAC DYSRHYTHMIAS ratio that's higher than that for Deviation from normal HR & pattern VLDL. This disorder results in Bradycardia high plasma levels of both Tachycardia cholesterol and triglycerides. Arrhythmia/Dysrhythmia ○ Triglycerides ECG Restore Cardiac rhythm to normal Type 4 Fast (Sodium) Channel Blockers ○ is a dominantly inherited ○ decrease conduction velocity disorder. It's characterized by ○ Suppression of automaticity high triglycerides contained in VLDL. The levels of cholesterol PAGE 37  PHARMACOLOGY NCM 106 Ciara & Andrea —BSN-2C– 9:30-12:30 and phospholipids in your LDL: 50-60% of cholesterol in blood usually remain within bloodstream normal Limits. VLDL: mostly triglycerides & less Type 5 runs in families. cholesterol ○ It involves high levels of LDL alone or together with VLDL Chylomicrons: mostly triglycerides ○ easy to manage ○ *large particles - transport fatty 8l acids & cholesterol to liver A1 BETA BLOCKERS Serum Cholesterol & Triglycerides: part of routine PE Decrease conduction velocity *Fasting lipid profile (12-14 hour) Suppression of automaticity Fasting sugar Decrease recovery time Elevation of Cholesterol, Triglycerides & LDL: Propanolol (Inderal) CV risks N: Cholesterol: