Pharmacology Test 3 Guide 2023 PDF

Pharmacology 1014 Test 3 Review -Fall 2023 Covers Weeks 8-10 Forma?ng 2 Select all that apply 5 Dosage calculaFons- like previous tests Ch 23: AnFhypertensive drugs • Categories: goal of therapy, mechanism of ac5ons contraindica5ons, adverse eﬀects, therapeu5c eﬀects, nursing considera5ons, comparison between ACE inhibitors and ARBS Mechanism of Action • • • • • • Inhibits ACE which is responsible for converting angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor and causes aldosterone secretion from the adrenal glands. Blocks ACE, thus preventing the formation of angiotensin 2 Prevents the breakdown of the vasodilating substance (bradykinin) Ability to decrease SVR and preload. Can stop the progression of left ventricular hypertrophy Lowers BP Contraindications • Pregnancy Adverse Side Effects • • • • • Fatigue, dizziness, headache, impaired taste Mood changes First dose can cause a hypotensive effect Dry cough Angioedema Therapeutic Effects • Lower blood pressure Nursing Considerations • • • • • • • • • • • • Before therapy obtain a health history and head to toe assessment Assess for contraindications to antihypertensive drugs Assess for conditions that require cautious use of these drugs Educate patients about the importance of not missing doses Tell patient to report to physician if dose is missed Monitor BP daily and record Do not abruptly discontinue these meds Oral forms should be given with food IV administration extreme caution and needs to use IV pump Encourage patients to watch their diet, decrease stress, weigh and alcohol intake Change positions slowly Avoid hot tubs, saunas, steam showers and hot weather climates of prolonged sun sitting Comparison between ACE inhibitors and ARBS • Ace is the first line of defence and ARBS are the second line of defence. Both only effect the blood pressure not the heart rate. Special Considerations • • • • Older Patients – Low-dose thiazide diuretics remain first-line therapy for older patients Renal and Cardio Protective Effects – Can elevate potassium levels. Which can elevate blood pressure and kidney toxicity Male Patients – May cause impotency Black Patients – hydralazine/isosorbide should be used • Special considera5ons: older pa5ents, renal and cardio protec5ve eﬀects, male pa5ents, black pa5ents, nonblack pa5ents Special ConsideraFons Ch 24: AnFanginal drugs • Classes of drugs (3 classes): therapeu5c objec5ves, mechanism of ac5on, routes of administra5ons and instruc5ons for pa5ents, indica5ons, adverse eﬀects, tolerance nursing considera5ons health teachings 3 classes of An5anginal Drugs include: 1. Beta Blockers 2. Calcium Channel Blockers 3. Nitrate & Nitrites Beta Blockers Therapeu5c Objec5ves: Mechanism of Ac5on: Beta blockers also slow conduc5on through the (AV) node and reduce myocardial contrac5lity (nega5ve inotropic eﬀect). Both of these eﬀects serve to slow the heart rate (nega5ve chronotropic eﬀect). These eﬀects reduce myocardial oxygen demand, which aids in the treatment of angina by reducing the heart’s workload. Slowing the heart rate is also beneﬁcial in pa5ents with ischemic heart disease because the coronary arteries have more diastolic 5me to ﬁll with oxygen- and nutrient-rich blood and deliver these substances to the myocardial 5ssues. Routes of Administra5ons: Atenolol is available in oral form Metoprolol is available in oral for (immediate-release and long-ac5ng) as well in Parenteral forms. Intravenous metoprolol is commonly administered to pa5ents who are hospitalized a]er an MI and for those with hypertension who cannot take oral medica5on. Indica5ons: Beta blockers are most eﬀec5ve in the treatment of exer5onal angina. They are also approved for treatment of MI, hypertension, cardiac dysthymias. Adverse Eﬀects: Blocking of beta1 receptors can lead to a decrease in heart rate, cardiac output, and cardiac contrac5lity. Blocking of beta2 receptors can result in bronchoconstric5on and increased airway resistance in pa5ents with asthma or chronic obstruc5ve pulmonary disease. Beta blockers may lead to cardiac rhythm problems, decreased SA and AV nodal conduc5on, decrease in systolic and diastolic blood pressures, peripheral receptor blockade, and decreased renin release from the kidneys. Beta blockers can mask the tachycardia associated with hypoglycemia, and pa5ents with diabetes may not be able to tell when their blood sugar falls too low. Fa5gue, insomnia, and weakness may occur because of nega5ve eﬀects on the heart and the central nervous system. Beta blockers can also cause both hypoglycemia and hyperglycemia, which is of par5cular concern in pa5ents with diabetes. Tolerance: Nursing Considera5on: Health Teaching: Calcium Channel Blockers There are 3 chemical classiﬁca5ons of Calcium Channel Blockers: 1. Phenylalkylamines 2. Benzothiazepines 3. Dihydropyridines Therapeu5c Objec5ves: The therapeu5c beneﬁts of the CCBs are numerous. Because of their acceptable adverse eﬀect and safety proﬁles, they are considered ﬁrst-line drugs for the treatment of angina, hypertension, and supraventricular tachycardia. They are o]en eﬀec5ve for the treatment of coronary artery spasms Mechanism of Ac5on: Calcium plays an important role in the excita5on–contrac5on coupling process that occurs in the heart and vascular smooth muscle cells, as well as in skeletal muscle. Preven5ng calcium from entering this process thus prevents muscle contrac5on and promotes relaxa5on. Relaxa5on of the smooth muscles that surround the coronary arteries causes them to dilate. This dila5on increases blood ﬂow to the ischemic heart, which in turn increases the oxygen supply and helps shi] the supply-and-demand ra5o back to normal. Dila5on also occurs in the arteries throughout the body, which results in a decrease in the force (systemic vascular resistance) against which the heart has to exert when delivering blood to the body (a]erload). Decreasing the a]erload reduces the workload of the heart and therefore reduces myocardial oxygen demand. This is the primary beneﬁcial an5anginal eﬀect of the dihydropyridine CCBs, such as amlodipine and nifedipine. These drugs have a less nega5ve inotropic eﬀect than verapamil hydrochloride and dil5azem do Routes of Administra5ons: Indica5ons: angina, hypertension, and supraventricular tachycardia. They are o]en eﬀec5ve for the treatment of coronary artery spasms (vasospas5c or Prinzmetal’s angina). However, they may not be as eﬀec5ve as the beta blockers in blun5ng exercise-induced eleva5ons in heart rate and blood pressure. CCBs are also used for the short- term management of atrial ﬁbrilla5on and ﬂu`er, migraine headaches and Raynaud’s disease (a type of peripheral vascular disease). The dihydropyridine nimodipine is indicated solely as an adjunct for cerebral artery spasms associated with aneurysm rupture. Adverse Eﬀects: Limited and primarily relate to overexpression of their therapeu5c eﬀects Tolerance: Nursing Considera5on: A par5cular food interac5on of note is grapefruit juice. Health Teaching: Nitrate & Nitrites Therapeu5c Objec5ves: Mechanism of Ac5on: The nitrates dilate all blood vessels. They predominantly aﬀect venous vascular beds; however, they also have a dose-dependent arterial vasodilator eﬀect. These vasodilatory eﬀects are the result of relaxa5on of the vascular smooth muscle cells that are part of the wall structure of veins and arteries. Routes of Administra5ons: They are available in a wide variety of prepara5ons, including sublingual, chewable, and oral tablets; capsules; ointments; patches; a translingual spray; and intravenous solu5ons. The following nitrates are the rapid- and long-ac5ng nitrates available for clinical use: • nitroglycerin (both rapid and long ac5ng) • isosorbide (both rapid and long ac5ng) • isosorbide-5-mononitrate (long ac5ng) Indica5ons: Nitrates are used to treat stable, unstable, and vasospas5c angina. Long-ac5ng dosage forms are used more for preven5on of anginal episodes. Rapid-ac5ng dosage forms, most o]en sub- lingual nitroglycerin tablets or spray, or an intravenous drip in the hospital sedng, are used to treat acute anginal a`acks. Adverse Eﬀects: The most common undesirable eﬀects are headaches, dizziness, and fa5gue, which generally diminish in intensity and frequency soon a]er the start of therapy. Other cardiovascular eﬀects include tachycardia and orthosta5c hypotension. If nitrate-induced vasodila5on occurs too rapidly, the cardiovascular system overcompensates and increases the heart rate, a condi5on referred to as reﬂex tachycardia. Tolerance: Nursing Considera5on: Health Teaching: Ch 25: Heart failure drugs • • • • • Drug Therapy for Heart Failure: Drugs of Choice for Early Treatment of Heart Failure Cardiac Glycosides (Digoxin/lanoxin): Mechanism of Ac5on, Drug Eﬀects, Adverse Eﬀects, Digoxin Toxicity, Condi5ons that Predispose to Digoxin Toxicity ACE Inhibitors, ARBS, valsartan, β-Blockers, Aldosterone Antagonists, Miscellaneous Drugs to Treat Heart Failure, Phosphodiesterase Inhibitors, Milrinone, Heart Failure Drugs: Nursing Implica5ons What is heart failure? The physical defects producing heart failure are of two types: (1) a heart defect (myocardial deﬁciency such as myocardial infarc5on or valve insuﬃciency), which leads to inadequate cardiac contrac5lity and ventricular ﬁlling, and (2) a defect outside the heart (e.g., systemic defects such as coronary artery disease, pulmonary hypertension, or diabetes), which results in an over- load on an otherwise normal heart. Either or both of these defects may be present in a given pa5ent. The emphasis of this chapter is on systolic dysfunc5on or inadequate ventricular contrac5ons (systole) during the pumping of the heart. Drug Therapy for Heart Failure: • • • PosiFve Inotropic Drugs (which increases the force of myocardial contracFon) Posi5ve Chronotropic Drugs (which increases the heart rate) Posi5ve Dromotropic Drugs (which accelerates cardiac conduc5on) This chapter focuses on the positive inotropic drugs, phosphodiesterase inhibitors (PDIs), and cardiac glycosides. Although several other drugs are used in the treatment of heart failure, for example, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), beta blockers, the vasodilator nitroglycerin, in the form of patches, is used in acute and chronic heart failure, as and the mainstays of early treatment diuretics. Drugs of choice for Early Treatment of Heart Failure: The drugs of choice at the start of therapy are the: • ACE inhibitors (lisinopril, enalapril, captopril, and others) or the • ARBs (valsartan, candesartan, losartan, and others) and • Certain beta blockers (metoprolol or bisoprolol fumarate, cardio selec5ve beta blockers; carvedilol, a nonspeciﬁc beta blocker) to preserve LV func5on and reduce blood pressure throughout the progression of the illness. • Loop diuretics (furosemide) are used to reduce the symptoms of heart failure secondary to fluid overload, and the mineralocorticoid receptor antagonists (spironolactone, eplerenone) are added as the heart failure progresses. • Only after these drugs are used is digoxin added. • Dobutamine, a positive inotropic drug, has also been used to treat heart failure. • A combination of hydralazine and isosorbide dinitrate is recommended specifically for use in patients who are Black. Cardiac Glycosides (Digoxin/Lanoxin) Mechanism of Ac5on: Increase in myocardial contrac5lity (posi5ve inotropic eﬀect). Which occurs secondarily to the inhibi5on of the sodium-potassium adenosine triphosphatase pump. When this is inhibited completely contrac5ons of cellular sodium and calcium concentra5ons increase. This results in an enhanced myocardial contrac5lity. Digoxin changes the electrical conduc5on proper5es of the heart by decreasing the velocity (rate) and prolonging the refractory period (an area in between the atria and the ventricles [SA to AV node]). This allows the cardiac cells to remain in a state of depolariza5on for longer thus reducing the heart rate. Drug Eﬀects: • A posi5ve inotropic eﬀect—> an increase in the force and velocity of myocardial contrac5on without a corresponding increase in oxygen consump5on • A nega5ve chronotropic eﬀect—> reduced heart rate • A nega5ve dromotropic eﬀect—> decreased automa5city at the SA node, decreased AV nodal conduc5on, reduced conduc5vity at the bundle of His, and prolonga5on of the atrial and ventricular refractory periods • An increase in stroke volume • A reduc5on in heart size during diastole • A decrease in venous blood pressure and vein engorgement • An increase in coronary circula5on • Promo5on of 5ssue perfusion and diuresis as a result of improved blood circula5on • A decrease in exer5onal and paroxysmal nocturnal dyspnea, cough, and cyanosis • Improved symptom control, quality of life, and exercise tolerance, but no apparent reduc5on in mortality Adverse Eﬀects: The common undesirable eﬀects associated with digoxin use are cardiovascular, CNS, ocular, and gastrointes5nal (GI) eﬀects. Digoxin Toxicity: • • • Hyperkalemia (a serum potassium level higher than 5 nmol/L) in a pa5ent with digoxin toxicity Life-threatening cardiac dysrhythmias, sustained ventricular tachycardia or ﬁbrilla5on, and severe sinus bradycardia or heart block unresponsive to atropine treatment or cardiac pacing Life-threatening digoxin overdose—more than 10 mg of digoxin in adults; more than 4 mg of digoxin in children Condi5ons that Predispose to Digoxin Toxicity: Ch 26: AnFdysrhythmic drugs • Classes: indica5on, contraindica5ons, adverse eﬀects, drug interac5ons, nursing implica5ons, pa5ent teaching Class 1a Drugs: Mechanism of Ac.on: Membrane-stabilizing drugs as they possess local anaesthe5c proper5es. They work by stabilizing the membrane and have depressant eﬀects on phase 0 of the ac5on poten5al. Drugs in 1a include procainamide, quinidine, and disopyramide. Indica.on for use of Class 1a Drugs: Atrial ﬁbrilla5on, premature atrial contrac5ons, premature ventricular contrac5ons, ventricular tachycardia, Wolﬀ-Parkinson-White syndrome. Adverse Eﬀects: Procainamide: Hypotension, rash, diarrhea, nausea, vomi5ng, agranulocytosis, SLE-like syndrome Quinidine: Hypotension, QT prolonga5on, light-headedness, diarrhea, bi`er taste, anorexia, blurred vision, 5nnitus, angina Drug Interac.ons: Class 1b Drugs: Mechanism of Ac.on: Share similar characteris5cs to class 1a drugs but act preferen5ally on ischemic myocardial 5ssue and li`le eﬀects on conduc5on velocity in normal 5ssue. These drugs have weak depressive eﬀect in phase 0 depolariza5on, the APD, and the ERP. Drugs in 1b include lidocaine hydrochloride and phenytoin. Indica.on for use of Class 1b Drugs: Ventricular dysrhythmias only (premature ventricular contrac5ons, ventricular tachycardia, ventricular ﬁbrilla5on) Adverse Eﬀects: Lidocaine Hydrochloride: Bradycardia, dysrhythmia, hypotension, anxiety, metallic taste Drug Interac.ons: Nursing Implica.ons: With lidocaine, vials of clear solu5on are labelled as either for cardiac use or not for cardiac use. This is important to remember when reading the vial’s label so that the wrong drug is not given. It is also important to remember that lidocaine solu5ons need to be used with extreme cau5on and that it is the plain solu5on that is used to treat various cardiac condi5ons. Parenteral solu5ons of these drugs are usually stable for only 24 hours. Lidocaine is also used as an anaesthe5c, so the diﬀerent concentra5ons of the drug need to be double-checked, if not triple-checked. In addi5on, lidocaine comes in a solu5on with epinephrine, a potent vasoconstrictor. This combined solu5on is indicated when the surgeon or physician is suturing or repairing wounds, with the lidocaine ac5ng as an anaesthe5c and the epinephrine causing vasoconstric5on of the local blood vessels and helping to control bleeding of the area, or in dental or oral situa5ons. The solu5on with epinephrine must never be used intravenously, but only as a topical anaesthe5c. With lidocaine, document vital signs prior to ini5a5on of and during therapy, and closely monitor the ECG. O]en, when pa5ents are receiving this drug, they are in a cardiac step-down unit, telemetry unit, or intensive care sedng. Class 1c Drugs: Mechanism of Ac.on: They produce a more pronounced blockage of the sodium channel than class 1a and 1b but have li`le eﬀects on repolariza5on or the APD. Drugs in this class signiﬁcantly slow conduc5on in the atria, AV node and ventricles. Because of their marked eﬀects on conduc5on, they strongly suppress PVCs, reducing or elimina5ng them. Drugs in this class include ﬂecainide acetate and propafenone hydrochloride. Indica.on for use of Class 1c Drugs: Ventricular tachycardia and supraventricular tachycardia dysrhythmias, atrial ﬁbrilla5on, and ﬂu`er; Wolﬀ-Parkinson-White syndrome. Adverse Eﬀects: Flecainide Acetate: Dizziness, visual disturbances, dyspnea, palpita5ons, nausea, vomi5ng, diarrhea, weakness Propafenone Hydrochloride: Prodysrhythmic eﬀect, angina, tachycardia, syncope, AV block, dizziness, fa5gue, dyspnea Drug Interac.ons: Class 2 Drugs: Mechanism of Ac.on: These are beta blockers; they work by blocking the sympathe5c nervous system s5mula5on to the heart and the hearts conduc5on system. This prevents catecholaminemediated ac5ons on the heart. The results of class 2 drugs include decreased heart rate, delayed AV node conduc5ons, reduced myocardial contrac5lity and decreased myocardial automa5city. Drugs in this class speciﬁcally for an5dysrhythmic include acebutolol hydrochloride, esmolol, metoprolol, propranolol hydrochloride and sotalol Sotalol has class 3 proper5es along with class 2. *Saved by the suﬃx: -olol Indica.on for use of Class 2 Drugs: Both supraventricular and ventricular dysrhythmias (act as a general myocardial depressants). Adverse Eﬀects: β-blockers: Bradycardia, hypotension, dizziness, fa5gue, AV block, heart failure, hyperglycemia, mask the symptoms of hypoglycemia, bronchospasm, wheezing, dry mouth, erec5le dysfunc5on. Class 3 Drugs: Mechanism of Ac.on: These increase the APD by prolonging repolariza5on in phase 3. The primary role of potassium channels in cardiac ac5on poten5als is cell repolariza5on; these drugs are also referred to as calcium channel blockers. They aﬀect fast 5ssue and are most used to manage dysrhythmias that are diﬃcult to treat and use for those where other therapies have failed Drugs In this class include amiodarone, dronedarone hydrochloride and sotalol. Indica.on for use of Class 3 Drugs: Life-threatening ventricular tachycardia or ﬁbrilla5on. Atrial ﬁbrilla5on or ﬂu`er resistant to other drugs. Adverse Eﬀects: Amiodarone Hydrochloride: Pulmonary toxicity, thyroid disorders, bradycardia, hypotension, SA node dysfunc5on, AV block, ataxia, QT prolonga5on, torsades de pointes, vomi5ng, cons5pa5on, photosensi5vity, abnormal liver func5on test results, jaundice, visual disturbances, hyperglycemia or hypoglycemia, and dermatologic reac5ons including rash, toxic epidermal necrolysis, vasculi5s, blue–grey colouring of the skin (face, arms, neck) Ibu5lide Fumarate: Nonsustained ventricular tachycardia, ventricular extrasystoles, tachycardia, hypotension, AV block, headache, nausea Sotalol Hydrochloride: Bradycardia, chest pain, palpita5ons, fa5gue, dizziness, light-headedness, weakness, dyspnea Drug Interac.ons: Class 4 Drugs Mechanism of Ac.on: They are calcium channel blockers; these drugs are also useful for those with hypertension and angina. The drugs in this class work on preven5ng the ventricles from bea5ng as fast as the atria. They do this by blocking and slowing the inward ﬂow of calcium ions into the slow calcium channels in cardiac conduc5on 5ssues. Drugs in this class 4 include dil5azem hydrochloride and verapamil hydrochloride. Indica.on for use of Class 4 Drugs: Paroxysmal supraventricular tachycardia; rate control for atrial ﬁbrilla5on and ﬂu`er. Adverse Eﬀects: Calcium channel blockers: Cons5pa5on, bradycardia, heart block, hypotension, dizziness, dyspnea Drug Interac.ons: Nursing Implica.ons: Beta blockers, dil5azem, and verapamil may all be used to manage abnormal rhythms and are to be given only a]er checking and documen5ng pulse rates and blood pressures. Contact the health care provider and withhold the drug—if supported by facility policy and the health care provider’s guidelines—if the pulse rate is 60 beats per minute or lower or 100 beats per minute or higher or if the systolic blood pressure is 90 mm Hg or lower. Unclassiﬁed AnFdysrhythmic Mechanism of Ac.on: It works by slowing the electrical conduc5on 5me through the AV node and is indicated for the conversion of paroxysmal supraventricular tachycardia to sinus rhythm, especially when it has failed to respond to the medica5on verapamil. Other uses include coexis5ng condi5ons such as heart failure, hypotension, or le] ventricular dysfunc5on which limits the use of verapamil. Because of its short life of 10 seconds, it is only be administered IV rapidly, as it can commonly cause asystole. If given in the parenteral form, the pa5ent must have heart monitoring. Drugs in this class include adenosine. Nursing Implica.ons: Amiodarone may lead to GI upset, which may be pre- vented or decreased by taking the drug with a meal or a snack. Photosensi5vity (sunburn and other exaggerated skin reac5ons to the sunlight) and photophobia (light sensi5vity) are other concerns with this drug. With photosensi5vity, protec5ve clothing, a hat, and sunscreen are needed. Emphasize the importance of eye protec5on, such as with sunglasses or 5nted contact lenses, to pa5ents taking this medica5on. Encourage consump5on of ﬂuids and a high-ﬁbre diet to minimize the cons5pa5on that is a common adverse eﬀect of an5dysrhythmic drugs. When beta blockers are used with an an5dysrhythmic, any shortness of breath, weight gain, changes in baseline blood glucose levels, or excessive fa5gue must be reported to the health care provider immediately. General General An.dysrhythmic Contraindica.on: Drug allergy to a speciﬁc product. Other contraindica5ons may include second- or third-degree AV block, bundle branch block, cardiogenic shock, sick sinus syndrome, or any other major ECG changes General An.dysrhythmic Nursing Implica.ons: When antidysrhythmics are administered, monitor vital signs, especially pulse rate and blood pressure, before administering the drug; if pulse rate is lower than 60 beats per minute, notify the health care provider. During the initiation of therapy, closely monitor the ECG and vital signs because of possible prolongation of the QT interval by more than 50%. The result may be the occurrence of a variety of conduction disturbances. Advise patients that oral dosage forms are better tolerated if taken with food and fluids to help minimize GI upset, unless otherwise ordered. During treatment with quinidine (or with any of the antidysrhythmics), immediately report to the health care provider any patient report of angina, hypotension, lightheaded- ness, loss of appetite, tinnitus, or diarrhea. An infusion pump is recommended for intravenous dosing of any of the classes of antidysrhythmics, with proper solution and dilution. Pa.ent Teaching: Ch 27: CoagulaFon modiﬁers • • • Coagula5on Modiﬁer Drugs classiﬁca5on Types of drugs in each class Treatment goals, indica5on, mechanisms of ac5on, adverse eﬀects, contraindica5on, therapeu5c eﬀects, route of administra5on and pa5ent teaching, toxicity, lab values monitoring, nursing implica5ons, pa5ent educa5on Anticoagulants inhibit the action or formation of clotting factors, thereby preventing clots from forming. Mechanism of Ac5on: Indica5on: The ability of an5coagulants to prevent clot forma5on is of beneﬁt in certain condi5ons where there is a high likelihood of clot forma5on. These include MI, unstable angina, atrial ﬁbrilla5on, presence of indwelling devices such as mechanical heart valves, and condi5ons in which blood ﬂow may be slowed and blood may pool, such as major orthopedic surgery, prolonged periods of immobility, or even long plane rides. Treatment Goals: The ul5mate consequence of a clot can be a stroke, an MI, a DVT, or a pulmonary embolism; therefore, the ul5mate beneﬁt of these drugs is the preven5on of these serious events. Warfarin is indicated for preven.on of any of these events, whereas unfrac5onated heparins, LMWHs, direct thrombin inhibitors, and the factor Xa inhibitor are used for both preven5on and treatment. Adverse Eﬀects: Bleeding is the main complica5on of an5coagula5on therapy, and the risk increases with increasing dosage May be localized (e.g., hematoma at the site of injec5on) or systemic. It also depends on the nature of the pa5ent’s underlying clinical disorder and is increased in pa5ents taking high doses of aspirin or other drugs that impair platelet func5on Contraindica5on: Contraindica5ons to the use of an5coagulants are generally similar for all of the diﬀerent drugs within this class. They include known drug allergy to a speciﬁc product and usually include any acute bleeding, as well as thrombocytopenia. Warfarin is strongly contraindicated in pregnancy, whereas the other an5coagulants are rated in lower pregnancy categories, where beneﬁts of taking the drug during pregnancy may override poten5al risks. LMWHs are contraindicated in pa5ents with an indwelling epidural catheter; they can be given 2 hours a]er the epidural is removed. This is important to remember because giving an LMWH with an epidural has been associated with epidural hematoma. Route of Administra5on: Toxicity: In the event of heparin or warfarin toxicity, the drug is to be stopped immediately. In the case of heparin, simply stopping the drug may be enough to reverse the toxic eﬀects because of the drug’s short half-life (1 to 2 hours). In severe cases or when large doses have been given inten5onally (i.e., during cardiopulmonary bypass for heart surgery), intravenous (IV) injec5on of protamine sulphate is indicated. This drug is a speciﬁc heparin an5dote and forms a complex with heparin, completely reversing its an5coagulant proper5es. This occurs in as few as 5 minutes. In general, 1 mg of protamine sulphate can reverse the eﬀects of 100 units of heparin. Protamine sulphate may also be used to reverse the eﬀects of LMWHs. A 1-mg dose of protamine sulphate is administered for each milligram of LMWH given (e.g., 1 mg protamine sulphate for 1 mg enoxaparin). Antiplatelet drugs prevent platelet plugs from forming by inhibiting platelet aggregation, which can be beneficial in preventing heart attacks and strokes. Adverse Eﬀects: Contraindica5on: Contraindica5ons to the use of an5platelet drugs include known drug allergy to a speciﬁc product, thrombocytopenia, ac5ve bleeding, leukemia, trauma5c injury, GI ulcer, vitamin K deﬁciency, and recent stroke. Therapeu5c Eﬀects: In the event of heparin or warfarin toxicity, the drug is to be stopped immediately. In the case of heparin, simply stopping the drug may be enough to reverse the toxic eﬀects because of the drug’s short half-life (1 to 2 hours). In severe cases or when large doses have been given inten5onally (i.e., during cardiopulmonary bypass for heart surgery), intravenous (IV) injec5on of protamine sulphate is indicated. This drug is a speciﬁc heparin an5dote and forms a complex with heparin, completely reversing its an5coagulant proper5es. This occurs in as few as 5 minutes. In general, 1 mg of protamine sulphate can reverse the eﬀects of 100 units of heparin. Protamine sulphate may also be used to reverse the eﬀects of LMWHs. A 1-mg dose of protamine sulphate is administered for each milligram of LMWH given (e.g., 1 mg protamine sulphate for 1 mg enoxaparin). Route of Administra5on: Hemorheological drugs alter platelet function without preventing the platelets from working. Sometimes clots form and totally block a blood vessel. When this happens in one of the coronary arteries, a heart attack occurs, and the clot must be lysed to prevent or minimize damage to myocardial muscle. Thrombolytic drugs lyse clots, or thrombi, that have already formed. This characteristic creates an important distinction between thrombolytics and anticoagulants, which can only pre- vent the formation of a clot. Indica5on: The purpose of the thromboly5c drugs is to ac5vate the con- version of plasminogen to plasmin, the enzyme that breaks down a thrombus. The presence of a thrombus that interferes signiﬁcantly with normal blood ﬂow on either the venous or the arterial side of the circula5on is an indica5on for the use of thromboly5c therapy. An excep5on may be a thrombus that has formed in blood vessels that connect directly with the CNS. The indica5ons for thromboly5c therapy include acute MI, arterial thrombosis, DVT, occlusion of shunts or catheters, pulmonary embolism, and acute ischemic stroke. Adverse Eﬀects: The most common undesirable eﬀect of thromboly5c therapy is internal, intracranial, and superﬁcial bleeding. Other problems include hypersensi5vity, anaphylactoid reac5ons, nausea, vomi5ng, and hypotension. These drugs can also induce cardiac dysrhythmias. Contraindica5on: Contraindica5ons to the use of thromboly5c drugs include known drug allergy to the speciﬁc product and any preserva5ves, as well as concurrent use of other drugs that alter clodng. Any history of recent major surgery, trauma, or bleeding (e.g., hemorrhagic stroke) are also contraindica5ons to their use. Route of Administra5on: Toxicity: Acute toxicity primarily causes an extension of the adverse eﬀects of the thromboly5c drug. Treatment is symptoma5c and suppor5ve, as thromboly5c drugs have a rela5vely short half-life and no speciﬁc an5dotes. Antifibrinolytic drugs, also known as hemostatic drugs, have the opposite effect of these other classes of drugs—they actually promote blood coagulation and are helpful in the management of conditions in which excessive bleeding would be harmful. Indica5on: An5ﬁbrinoly5cs are useful in both the preven5on and treatment of excessive bleeding resul5ng from systemic hyperﬁbrinolysis or surgical complica5ons. They have been proven to be successful in arres5ng excessive oozing from surgical sites such as chest tubes, as well as in reducing total blood loss and the dura5on of bleeding in the postopera5ve period. Desmopressin may also be used in pa5ents who have hemophilia A or type I von Willebrand disease. As stated earlier, recombinant factors VII, VIII, and IX are used to treat hemophilia or to stop bleeding caused by excessive warfarin therapy. Adverse Eﬀects: Contraindica5on: Contraindica5ons to the use of an5ﬁbrinoly5c drugs include known drug allergy to a speciﬁc product and disseminated intravascular coagula5on, which could be worsened by these drugs. Route of Administra5on: Lab Results: Nursing Considera5ons: Pa5ent Teaching Tips: Ch 28: Lipid modiﬁers • Diﬀerent classes: mechanism of ac5ons, indica5on, adverse eﬀects, pa5ent teaching, nursing considera5ons, rhabdomyolysis Four Classes of Drugs 1. 2. 3. 4. Fatty acids (saturated and unsaturated Glycerides (glycerol-containing lipids) Nonglyceride lipids (sphingolipids, steroids, waxes) Complex lipids (lipoproteins, glycolipids) Mechanism of Action • • Inhibit HMG-CoA reductase, which is used by the liver to produce cholesterol Lower the rate of cholesterol production Adverse Side Effects • • • • • Mild, Transient Gastrointestinal Disturbances Rash Headache Myopathy (muscle pain), possibly leading to rhabdomyolysis, a serious condition Do not use for patients with elevated liver enzymes or liver disease Therapeutic Uses • Treatment of type IIa and IIb Patient Education • • • • • • • Counsel patient concerning diet and nutrition on an ongoing basis Instruct patient on proper procedure for taking the medications Powder forms must be taken with a liquid, mixed thoroughly but not stirred, and never taken dry Other medications should be taken 1 hour before or 4 to 6 hours after meals to avoid interference with absorption Instruct patients to report persistent gastrointestinal upset, constipation, abnormal or unusual bleeding, and yellow discoloration of the skin Monitor for adverse effects, including increased liver enzyme studies Reduced cholesterol and triglyceride levels Nursing Considerations • • • Before beginning therapy, obtain a thorough health and medication history Assess dietary patterns, exercise level, weight, height, vital signs, tobacco and alcohol use, and family history Assess for contraindications, conditions that require cautious use, and drug interactions Rhabdomyolysis à Break down of muscle protein, myoglobinuria (urinary elimination of the muscle protein myoglobin. Can lead to acute kidney injury and death. When caught early it can be reversible with the discontinuation of statin drug Ch 29: DiureFcs • Types of diure5cs: indica5on, common side eﬀects, adverse eﬀects, Assessments, health teaching, lab results to consider, ﬂuid and electrolyte status/ imbalance, nursing considera5ons Classifications of Diuretics Carbonic Anhydrase Inhibitors Acetazolamide Methazolamide Loop Diuretics Bumetanide Ethacrynic acid (rarely used clinically) Furosemide Osmotic Diuretics Mannitol Potassium-Sparing Diuretics Amiloride Eplerenone Spironolactone Triamterene (available only in combination with hydrochlorothiazide) Thiazide and Thiazide-Like Diuretics Chlorthalidone Hydrochlorothiazide Indapamide Metolazone Carbonic Anhydrase Inhibitors – Acetazolamide & Methazolamide Form of Administration • • Oral Parenteral Therapeutic Uses • • Treatment of glaucoma Edema • • • • Epilepsy High-Altitude Sickness CAI’s are also used as an adjunct drug in long-term management of open-angle glaucoma Used with mitotic’s to lower intraocular pressure before ocular surgery in certain cases Mechanism of Action • • • • Block the action of carbonic anhydrase, thus preventing the exchange of H+ ions with sodium and water Inhibition of carbonic anhydrase reduces H+ ion concentration in renal tubules As a result, there is increased excretion of bicarb, sodium, water, and potassium Resorption of water is decreased, and urine output is increased Contraindications • • • • • • Known drug allergy Hyponatremia Hypokalemia Severe Kidney or Liver Dysfunction Adrenal Gland Insufficiency Cirrhosis – Liver scarring or damage Interactions • • Adverse Side Effects • • • • • • • • • Respiratory or metabolic acidosis Hypokalemia Drowsiness Anorexia Paresthesia’s Hematuria Urticaria (Skin Rash & Itching) Photosensitivity Melena (Bloody Stool) Digoxin Corticosteroids Loop Diuretics – Bumetanide, Ethacrynic Acid & Furosemide Form of Administration • • Oral Parenteral Therapeutic Uses • • • • Manages edema associated with heart failure and liver or kidney disease Management of hypertension Increase the kidney excretion of calcium in patients with hypercalcemia May also be indicated in cases of heart failure resulting from diastolic dysfunction Mechanism of Action • • • • • Possess kidney, cardiovascular, and metabolic effects Act directly on the ascending limb of the Loop of Henle to block chloride and sodium resorption Increase kidney prostaglandins, resulting in the dilation of blood vessels and reduce kidney, pulmonary and systemic vascular resistance which makes it useful for the treatment of edema associated with heart failure, liver cirrhosis and kidney disease Due to fast onset – loop diuretics are useful when rapid urine output (diuresis) is needed This diuretic lasts at least 2 hours Contraindications • • • Known Drug Allergy Hepatic Coma Severe Electrolyte Loss ** Known to be contraindicated for those with sulfa allergies. However, analysis shows that cross-reaction is unlikely to occur. Loop diuretics are commonly given to patients with sulfa allergies with no problems; always be aware of the possibility of an allergy! Summary of Major Drug Effects of Loop Diuretics • • • • Loop diuretics produce potent diuresis and subsequent loss of fluid The resulting decreased fluid volume leads to a decreased return of blood to the heart, or decreased filling pressures The metabolic effects of loop diuretics are secondary to electrolyte losses resulting from potent diuresis Major electrolyte losses include sodium, potassium, and to a lesser extent calcium Cardiovascular Effects • • • • • Reduced blood pressure Reduced pulmonary vascular resistance Reduced systemic vascular resistance Reduced central venous pressure Reduced left ventricular end-diastolic pressure Adverse Side Effects CNS • • Hematological Dizziness Headache • • • Agranulocytosis Thrombocytopenia Neutropenia Metabolic • • • • Hypokalemia Hyperglycemia Hyperuricemia Hyponatremia • • Tinnitus Blurred Vision Cardiovascular • • Dehydration Hypovolemia • • Nausea Vomiting & Diarrhea GI Interactions • • Loop diuretics possess both nephrotoxic and neurotoxic properties Produce addictive effects when given with other medications that have similar toxicities Aminoglycosides and Vancomycin • • Addictive effect Increased Neurotoxicity (Especially Ototoxicity) Corticosteroids and Digoxin • • • Hypokalemia Addictive Hypokalemia Increased Digoxin Toxicity Lithium Carbonate • • Decrease in kidney excretion Increased lithium toxicity NSAID’s • • Inhibition of kidney prostaglandins Decreased diuretic activity Osmotic Diuretics: Mannitol Form of Administration • IV Infusion ONLY May crystallize when exposed to low temperatures and must be stored in warmer areas The use of a filter is required Therapeutic Uses • • • • Treatment of patients in the early, oliguric phase of acute kidney injury Promote excretion of toxic substances Reduce intracranial pressure Treatment of cerebral edema Mechanism of Action • • • • • Mannitol works along the entire nephron, but mostly in the proximal tubule and descending loop of Henle It is nonabsorbable, it increases osmotic pressure in the glomerular filtrate, which as a result pulls fluid (primarily water) into the renal tubules from the surrounding tissues This process also inhibits the tubular reabsorption of water and solutes, thus producing rapid diuresis Overall, this action reduces cellular edema and increases urine production, however it only produces a slight loss of electrolytes (sodium) Mannitol may also induce vasodilation, which increases glomerular filtration and kidney plasma flow which makes it a good drug for preventing kidney damage or acute kidney injury Contraindications • • • • Known Drug Allergy Severe kidney disease Pulmonary edema (loop diuretics are used instead) Active cranial bleeding Adverse Side Effects • • • • • • • • Convulsions Thrombophlebitis Pulmonary Congestion Headaches Chest pain Tachycardia Blurred Vision Chills / Fever Interactions • There are no drugs that significantly interact with mannitol Potassium – Sparing Diuretics – Amiloride, Eplerenone, Spironolactone & Triamterene Available only in combination with Hydrochlorothiazide – AKA Aldosterone-Inhibiting Diuretics Form of Administration • Oral Therapeutic Uses Spironolactone & Triamterene • • • • Hyperaldosteronism Hypertension Reversing potassium loss caused by potassium-wasting diuretics (loop and thiazide) Certain cases of heart failure: prevention of remodeling (permanent ventricular myocardial wall damage following MI) Amiloride • • • Similar to spironolactone and triamterene, but less effective long-term May be more effective than spironolactone and triamterene in the treatment of metabolic alkalosis Used primarily in the management of heart failure Mechanism of Action • • • • Act in the collecting duct and distal convoluted tubules where they interfere with sodium-potassium exchange Spironolactone competitively binds to aldosterone receptors and therefore blocks the reabsorption of sodium and water that is induced by aldosterone secretion Amiloride and triamterene DO NOT bind to aldosterone receptors; however, they inhibit both aldosterone-induced and basal sodium reabsorption They are often prescribed for children in heart failure because pediatric heart problems are frequently accompanied by excess secretion of aldosterone Contraindications • • • • • Known Drug Allergy Hyperkalemia Severe Kidney Failure Anuria (failure of the kidneys to produce urine) Triamterene may also be contraindicated in cases of severe liver failure Adverse Side Effects Other CNS • • Dizziness Headache • • • Urinary frequency Weakness Hyperkalemia Spironolactone • • • • Gynecomastia Amenorrhea (Absence of Menstruation) Irregular Menstrual Cycles Postmenopausal Bleeding GI • • • • Cramps Nausea Vomiting Diarrhea Interactions • • • • Lithium Angiotensin-Converting Enzyme inhibitors Potassium supplements NSAID’s Thiazide and Thiazide – Like Diuretics – Chlorthalidone, Hydrochlorothiazide, Indapamide, Metolazone Form of Administration • Oral Therapeutic Uses • • • • • Hypertension (one of the most prescribed groups of drugs for this) Edema Idiopathic hypercalciuria Diabetes insipidus Heart failure caused by diastolic dysfunction Mechanism of Action • • • • Primary site of action is the distal convoluted tubule, where they inhibit tubular reabsorption of sodium, chloride, and potassium ions Results in osmotic water loss Thiazides also cause direct relaxation of the arterioles causing dilation Decreased preload and afterload Contraindications • • • • • • Known Drug Allergy Hepatic Coma (Metolazone) Anuria Severe kidney failure Should NOT be used if creatinine clearance is less than 30-50 mL/min (normal is 125 mL/min) Metolazone remans effective to a creatinine clearance of 10 mL/min Adverse Side Effects Hematological CNS • • • • • • Dizziness Headache Blurred Vision Integumentary GI • • • • Anorexia Nausea Vomiting Diarrhea • • Erectile Dysfunction Low Libido Jaundice Leukopenia Agranulocytosis • • Urticaria Photosensitivity Metabolic • • • • • GI Hypokalemia Glycosuria Hyperglycemia Hyperuricemia Hypochloremic Alkalosis ** Associated with higher risk of falls with older adults, with the highest risk in the first 3 weeks after prescription is given Interactions • • • • • Corticosteroids Diazoxide Digoxin Oral hypoglycemics Excessive consumption of licorice can lead to an addictive hypokalemia in patients taking thiazides Overdose and Toxicity • • • • Symptoms include Anorexia Nausea Lethargy • • • • Muscle Weakness Mental Confusion Hypotension Can lead to electrolyte imbalance resulting from hypokalemia Assessments Related to Diuretics • Complete medication history • • • • • • • Physical assessment with emphasis to the body system affected by the disease process or the indication for the diuretic as well as potential drug related adverse effects Assessment of baseline vitals (lung & heart sounds) Neurological status Checking skin for pitting edema, moisture levels of mucous membranes and capillary refill Assess postural BP (sitting, standing, and lying) before and during drug therapy Diuretic–Induced fluid volume loss, which may lead to orthostatic hypotension Assess patients baseline fluid volume status (as indicated by weight, height, vitals, intake-output as fluid volume levels and electrolyte concentrations are affected by diuretics Patient Education • • • • • • • • • Eat foods rich in potassium, except when contraindicated for potassium-sparing diuretics Frequent lab testing may be indicated at the beginning and throughout therapy with diuretics (Electrolytes, Blood Gases & Uric Acid) Encourage patient to change positions slowly to prevent dizziness and possible fainting (Syncope) Patients may be encouraged to increase their fluid intake (if not contraindicated) to prevent dehydration and minimize constipation (increased fiber may also be required) Advise patient to keep a journal – includes daily weights, how they feel every day, dose of diuretic etc. Signs and symptoms of hypokalemia – anorexia, nausea, lethargy, muscle weakness, mental confusion, and hypotension Emphasize the importance of being cautious in hot climates, excessive sweating, fevers, and the use of saunas or hot tubs Rationale: heat raises core body temperature and causes further loss of potassium, sodium and water through sweat which will increase the risk of additional problems related to fluid-electrolyte imbalances and hypotension Educate patients with Diabetes Mellitus who are taking Thiazide or Loop Diuretics about the need to closely monitor their blood glucose levels If the patient is taking a diuretic WITH Digoxin educate any of the patient's family members or anyone involved in their care how to monitor pulse rate Warning Signs of Digoxin Toxicity • • • • • • Headache Dizziness Confusion Nausea Visual Disturbances Bradycardia (HR less than 60) SYMPTOMS THAT MUST BE REPORTED RIGHT AWAY • • • • Excessive Dizziness Syncope Weakness Muscle Aches

Pharmacology Test 3 Guide 2023 PDF

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