Pharmacological Treatments for Heart Failure and Hypertension, Exams of Nursing

Download Pharmacological Treatments for Heart Failure and Hypertension and more Exams Nursing in PDF only on Docsity! 1 NR 508 Midterm Exam Consist of 50 Questions From a Random Test Bank of Questions from Chapters 1-4 (including Week 4 Content) and All Embedded Recorded Lectures. Information is taken from the following Areas: Highlighted areas are areas to help you understand the concepts better they are in NO way an indication of what you are guaranteed to see on the exam. Remember these are random some of your classmates may not have the same question that appear on your exam. PLEASE NOTE that this study guide may not be inclusive of all topics you may see on the exam 1 NP Practice 1-2 Questions 2 Birth Control Contraindications 1-2 Questions 3 Treatment of CHF 5-15 Questions • Know First Line Treatment in CHF • Side Effects of Diuretics • Side Effects of Ace Inhibitors 4.Treatment of Hypertension 5-6 Questions • Know First Line Treatment in Hypertension • Side Effects of Diuretics • Side Effects of Ace Inhibitors 2 5. Treatment of Fungal infections 3-5 Questions • Know How to Treat Various Fungal Infections • Common Uses 6. Treatment of Abnormal Heart Rhythms 4-5 Questions • Know Treatment of Arrhythmia 7. Treatment of Depression& Anxiety 4-5 Questions 8. Treatment of Parkinson 4-5 Questions • Know Treatment of Parkinson Disease 5 ▪ Ventricular dilation helps to maintain cardiac output to an extent (due to Starling's Law), but past a certain point it can no longer help. o Factors affecting cardiac performance: ▪ Higher preload: due to increased blood volume and venous tone. ▪ Higher afterload: due to hypertension, increased arterial tone. ▪ Lower contractility ------- > lower inotropic state ▪ Higher heart rate, due to reflex tachycardia o Edema: Especially pulmonary edema, but also peripheral. Results from decreased Cardiac Output, by two mechanisms: ▪ Decreased CO ------> impaired venous return ------- > higher capillary hydrostatic pressure ▪ Decreased CO ------> decreased renal perfusion ------- > activate renin angiotensin system RAS ------ > aldosterone causes higher Na+ and fluid retention. • TREATMENT: o CARDIAC GLYCOSIDES: See CHF PowerPoint Slides : o MECHANISM: Inhibit Na+/K+-ATPase Pump ------------ > increased intracellular Na+ in myocardium ------> decreased expulsion of Ca+2 in myocardium ------ > 6 tonically higher levels of intracellular Ca+2 ------ > increased myocardial contractility o MECHANICAL ACTION on HEART: ▪ Increased myocardial contractility ▪ Bradycardia, due to reduced sympathetics. ▪ Increased Cardiac Output, due to reduced TPR (from reduced sympathetics) and increased inotropic state. o ELECTRICAL ACTION on HEART: 7 ▪ Direct Effect on AV Node: Increase risk of heart block ▪ Decrease the rate of rise of Phase-0 depolarization at AV node. ▪ Prolong refractory period at AV-Node ▪ Decrease conduction velocity at AV-Node. ▪ Direct Effect on Purkinje Fibers: ▪ Increase automaticity ------> increased risk of arrhythmias. This occurs by two mechanisms: ▪ Increase the slope of Phase-4 depolarization. ▪ Elevate the resting membrane potential of the SA-Node, as a consequence of inhibiting the Na+/K+-ATPase ▪ Decrease conduction velocity ▪ Parasympathomimetic Effects: Digitalis increases vagal stimulation, by three mechanisms: ▪ Baroreceptor Sensitization ▪ Central Vagal Stimulation ▪ Facilitate muscarinic transmission at myocardial cells 10 LOOP DIURETICS: • MECHANISM: They inhibit the Na+/K+/2Cl- transporter, essentially shutting down the counter-current multiplier ----- > profuse natriuresis. • INDICATIONS: o Edema, caused by CHF, cirrhosis, or nephrosis. 11 o Management of hyponatremia or hypercalcemia. Given in combination with saline infusion. o Increase K- and H+ excretion in patients with distal renal tubular acidosis. • PHARMACOKINETICS: o Furosemide is secreted by a probenecid-sensitive transport mechanism into proximal tubule. Thus indomethacin or NSAID's decrease its effectiveness. o Bioavailability 50-70%. Extensively binds to plasma albumin. • ADVERSE EFFECTS: o Metabolic effects: ▪ Hyponatremia, hypomagnesemia, metabolic acidosis. ▪ Hypokalemia: can be counteracted with K+-sparing diuretic, or with supplemental K+. ▪ Hypochloremic Alkalosis: Increased delivery of Na+ to distal tubules ------> increased RAS and aldosterone ------ > increased secretion of K+ and H+ ------ > hypokalemic alkalosis. o Hyperuricemia, hypercholesterolemia o Ototoxicity, especially in patients with impaired renal function. 12 THIAZIDE DIURETICS: • MECHANISM: They inhibit Na+/Cl- antiport ---------- > natriuresis. • ADVERSE EFFECTS: Also see thiazides under Anti-HTN o Metabolic Effects: ▪ Marked hyponatremia. ▪ Hypokalemia and Hypomagnesemia: can be particularly bad in folks with CHF (taking glycosides), cirrhosis, MI, arrhythmias. ▪ Slight hypercalcemia 15 ▪ Anti-Arrhythmics stop reentry excitation by prolonging the refractory period at the ectopic site. In this way the unidirectional block becomes a bidirectional block, and the cycle is stopped. • GENERAL EFFECTS of ANTI-ARRHYTHMICS: Anti-arrhythmics also cause arrhythmias. All anti-arrhythmics also have local anesthetic effects. o Reduce the slope of Phase-4 Depolarization ------ > reduce automaticity. o Decrease conduction velocity. o Reduce threshold potential. o Terminate reentrant excitation, by prolonging the refractory period of the initiation point. ANTI-HYPERTENSIVE DRUGS: • ORAL DIURETICS: o SUBTYPES: ▪ THIAZIDE DIURETICS: Most commonly used for HTN. Hydrochlorothiazide, Chlorthalidone, Indapamide ▪ ACTION: Lowers blood volume by depleting body Na+ stores, by increasing Na+ excretion in the kidney. ▪ LOOP DIURETICS: Rarely used for HTN, often used for CHF. 16 ▪ POTASSIUM-SPARING DIURETICS: Weak; used in conjunction with thiazides to help alleviate hypokalemia. o PATIENT POPULATION: Thiazides can be used as monotherapy. ▪ Old, black males respond best to Thiazide diuretics. ▪ Cheap drug ▪ For patients with moderate HTN, and normal kidney and cardiac function. o SIDE EFFECTS: 17 ▪ Sexual impotence, as is potentially true with any anti-hypertensive ▪ Hyperuricemia, gout ▪ Reflex increase in renin secretion (can be counteracted with ACE Inhibitor) ▪ Potassium depletion: Can be potentially countered with (1) supplemental potassium, or (2) potassium-sparing diuretic ▪ Muscle cramps ▪ Arrhythmias ▪ Impaired glucose tolerance, hyperinsulinemia. ▪ Atherogenesis: Thiazides increase LDL and increase the LDL/HDL ratio. ▪ Hyperlipidemia o DOSING: Very low dose (6-12 mg/day) is required for lowering blood pressure, as compared to that which is required for diuresis (100-200 mg/day). This helps to alleviate side-effects. • SYMPATHOLYTICS: o CENTRALLY ACTING: alpha2-agonists. Clonidine, Guanabenz, Guanfacine, Methyldopa. ▪ ADVERSE EFFECTS: Not recommended for monotherapy. 20 o ADVERSE EFFECTS: Mainly GI and CNS ▪ GI: Diarrhea, constipation, nausea, vomiting ▪ CNS: Insomnia, lassitude, nightmares, depression. ▪ Atherogenesis: Increase plasma triglycerides and decrease HDL ▪ Hypoglycemia: beta-blockers impair the epinephrine-mediated response to hypoglycemia, thus they should not be used with insulin and should be used with caution in Diabetics. ▪ Arrhythmias, especially heart-block, can be caused by overdose. 21 o CONTRAINDICATIONS: Diabetes, Congestive Heart Failure, Heart Block, Asthma • alpha-BLOCKERS: Only alpha1-selective blockers (Prazosin, Terazosin, Doxazosin) are used to treat HTN. o MECHANISM: Block alpha1 receptors --------- > decreased vasomotor tone. ▪ alpha1-selective: reflex tachycardia is mitigated, because alpha2- receptors are not also blocked. o ADVERSE EFFECTS: Orthostatic Hypotension is the only big one ▪ Orthostatic Hypotension: It may be particularly pronounced with first dose ▪ CNS: Drowsiness, dizziness, headache ▪ Palpitations ▪ Easy fatigability • ACE-INHIBITORS: o ACTIONS: They inhibit ACE----------- > reduce vascular tone and blood pressure. ▪ They work well, despite the fact that Angiotensin levels are not always changed appreciably in patients taking the drug. 22 o PATIENT POPULATION: Recommended for monotherapy for mild to moderate hypertension in any population. ▪ The drugs are expensive. ▪ They are less effective in elderly black man. Use thiazides for them. o ADVERSE EFFECTS: ▪ Dry Cough: 5-20% of patients. Thought to be due to bradykinin. ▪ ACE also catalyzes the breakdown of bradykinin. Inhibit ACE ------> increase levels of bradykinin. 25 ▪ Best treated with combination of nitrates and calcium-channel blockers. Do not use beta-blockers! o Unstable Angina: Crushing chest pain while at rest. MI is imminent. • MYOCARDIAL OXYGEN SUPPLY: Oxygen extraction is already maximal in the heart. o Coronary Blood-flow can be increased to relieve angina: ▪ Increase perfusion pressure (diastolic pressure) ▪ Increase the duration of diastole (slower heart rate) o Lower preload relieves angina. Increase venous capacitance ------ > decrease myocardial oxygen demand. ▪ Throbbing headache, due to increased blood volume in cranium. ANTI-DEPRESSANTS: • TRI-CYCLIC ANTIDEPRESSANTS (TCA'S): o PHARMACODYNAMICS: The therapeutic effect is to block reuptake of Norepinephrine and Serotonin in the CNS ------- > prolonged and heightened effects of those two neurotransmitters. o EFFECTS: Very efficacious, but effect are delayed ----- 1-2 week of therapy required before therapeutic effect. 26 o ADVERSE EFFECTS: Anti-Histaminic, Anti-Cholinergic, Anti-alpha- Adrenergic ▪ Anti-Histaminic: Sedation, weight gain, possible hypotension. ▪ Anti-Cholinergic: urinary retention, constipation, dry mouth, blurred vision, anti-cholinergic psychosis. ▪ Use caution in patients with glaucoma or BPH, because of anti- cholinergic effects. ▪ CV: Can be seriously cardiotoxic. ▪ Orthostatic Hypotension, myocardial depression. 27 ▪ Arrhythmias: Can make worse or precipitate AV heart-block. Prolonged QRS or QT intervals, and ST-T wave changes. ▪ Tachycardia can progress to CHF, death. ▪ Can precipitate seizures, although incidence is low. ▪ Sexual dysfunction: Impaired erection, impotence, priapism, lost libido. ▪ Hypersensitivity: Rash, leukopenia, cholestatic jaundice. o TOXICITY: Overdose results in death. Tricyclics are the leading cause of drug- overdose death in the United States. • MAO-INHIBITORS: Phenylzine, Isocarboxazid, Tranylcypromine o EFFECTS: ▪ Delayed Therapeutic Effect: several weeks of therapy required for anti- depressants to take effect. Significant inhibition of MAO is required before effects are seen. o SIDE-EFFECTS: ▪ Concomitant use of tyramine can lead to hypertensive crisis. ▪ Treat the crisis with IV phentolamine (alpha-antagonist) until pressure stabilizes. ▪ Myoclonus. 30 ▪ They are excreted unchanged, in both the kidneys(passive filtration) and feces. Enterohepatic circulation concentrates the drugs in the bile. o INDICATIONS: Broad-spectrum of activity against both gram-positives and gram-negatives. ▪ Rickettsiae, Chlamydia, Mycoplasma: Tetracyclines are especially indicated for the intracellular bacteria, as they readily can enter both the human host-cells and the bacterial cells. ▪ Lyme Disease is also treated with tetracycline. 31 ▪ Syndrome of Inappropriate ADH Secretion (SIADH): Tetracyclines block ADH in the kidney. Demeclocycline can be used to treat SIADH. o RESISTANCE: Due to decreased absorption of the drug, either active or passive. ▪ Pseudomonas, Proteus, coliforms are especially prone to resistance. o ADVERSE EFFECTS: ▪ Calcium Chelation: Tetracyclines chelate calcium, as well as Mg+2, Fe+2, Al+3. As a result you see discoloration and dysplasia. ▪ Do not take tetracycline with food or milk. The calcium will sequester the drug and block its absorption. ▪ Never use with pregnancy. The drugs get into the placenta, and chelate calcium in teeth and bones, leading to deformity, growth inhibition, weakness in the fetus. ▪ Never give to growing children. Can result in deformities or inhibited growth. ▪ GI: Direct irritation to GI tract (nausea, vomiting, anorexia) will be evident after the very first dose of drug, if it is going to occur. ▪ GI Superinfection: A GI Superinfection is fairly common and can produce similar patient complaints as above, but with a delayed onset (2-4 days after starting drug). If there are delayed GI complaints in someone taking tetracycline, a GI superinfection should be considered. 32 ▪ Superinfection bugs = S. Aureus, C. Difficile, Candida, as well as Pseudomonas, Proteus. ▪ Hepatotoxic: Especially in pregnant women, in high dose, and in patients with liver disease. ▪ Nephrotoxic: In patients with diminished kidney function. ▪ Photosensitivity: Tetracyclines are broken down by sunlight. Outdated, deteriorated samples can cause a Fanconi-like syndrome (renal tubular acidosis). 35 ▪ Hepatotoxicity ▪ Anemia o NYSTATIN: Only used topically, because the adverse effects are too severe. ▪ Oral administration for the topical treatment of fungal GI infections. • IMIDAZOLES: o PHARMACODYNAMICS: They all work by blocking the Cytochrome-P450 synthesis of ergosterol, thus inhibiting fungal growth. ▪ Specifically, they interfere with conversion of lanosterol to ergosterol. ▪ There is some cross-reactivity with human Cyt-P450 enzymes. All these drugs interact with Cyt-P450 in the liver. o FLUCONAZOLE: Systemic agent. ▪ PHARMACOKINETICS: Given PO and readily absorbed systemically. Also IV. ▪ Readily enters CNS. ▪ Inhibitor of Cyt-P450 enzymes. ▪ 80% urinary excretion. 36 ▪ INDICATIONS: Most popular azol, used for disseminated dimorphic infections. ▪ Fluconazole is often used prophylactically in AIDS patients (indefinite treatment is required after exposure to a systemic pathogen). ▪ Fluconazole is the single best treatment for Cryptococcal Meningitis. ▪ RESISTANCE: It will kill Candida Albicans, but other species of Candida are resistant. Thus treatment with Fluconazole can result in a Candida non Albicans disseminated infection. 37 ▪ ADVERSE EFFECTS: Hepatotoxicity, increased liver enzymes. ▪ DRUG INTERACTIONS: Increases blood levels of phenytoin, cyclosporine, warfarin, hypoglycemic drugs. o CLOTRIMAZOLE: Topical agent. ▪ PHARMACOKINETICS: Topical use, with little systemic absorption. o ITRACONAZOLE: Systemic anti-fungal. Broader spectrum and fewer adverse effects than ketoconazole. o MICONAZOLE: ▪ PHARMACOKINETICS: Topical use, with little systemic absorption. Also IV. ▪ Extensively metabolized by liver Cyt-P450 enzymes. ▪ Biliary excretion. ▪ ADVERSE EFFECTS: Nausea and vomiting after IV administration. ▪ INDICATIONS: Topical-use only. over-the-counter athlete's foot preparations. ▪ DRUG-INTERACTIONS: It potentiates the effects of warfarin by preventing it from being degraded by Cyt-P450 enzymes. We must decrease warfarin dose in compensation. 40 ▪ Only works on superficial fungi, dermatophytes. o PHARMACOKINETICS: Given orally, even for skin infections. Absorption is facilitated by a high-fat meal. ▪ It is concentrated in skin and other tissues containing keratin, which binds to the drug. o INDICATIONS: Ringworm, athlete's foot. o ADVERSE EFFECTS: Allergic reactions, headache, GI disturbances. • POTASSIUM IODIDE: 41 o INDICATIONS: Singularly useful against Sporothrix Schenckii. It is only to toxic to the yeast form -- not the mold form. • FLUCYTOSINE: o INDICATIONS: Active against yeasts -- Cryptococcus Neoformans and Candida Albicans. ▪ SYNERGY: It is most often used in conjunction with Amphotericin-B, where it has synergistic effects. o PHARMACOKINETICS: Well absorbed and gets into brain. Actively secreted and concentrated into the urine. ▪ Administered as a pro-drug, which is then deaminated by a fungal enzyme to form the active metabolite, 5-fluorocytosine. o PHARMACODYNAMICS: 5-fluorocytosine is an analog of cytosine that blocks thymidylate synthetase, and ultimately blocks DNA synthesis. Fungistatic. o RESISTANCE occurs rapidly, due to altered drug-permeability. Drug is usually given in combination with Amphotericin-B or other drugs. o ADVERSE EFFECTS: Relatively non-toxic, because it is specific for fungi. Occasional alopecia and bone-marrow suppression. OTHER ANTI-PROTOZOALS: • METRONIDAZOLE: Tissue amebicide. o PHARMACOKINETICS: Oral or IV. It does reach the CNS. 42 o PHARMACODYNAMICS: A nitro-imidazole, that is activated similar to Nitrofurantoin. Nitro group of the drug is reduced in the Amoeba, forming oxidative intermediates that do oxidative damage to the bugs. o INDICATIONS: Wide variety of intestinal and tissue parasitic infections. Trichomoniasis, Giardiasis, Intestinal Amebiasis. o ADVERSE EFFECTS: Common. Nausea, headache, dry mouth. ▪ Disulfiram-like effect: Do not use with alcohol. This can affect patient- compliance. 45 o PHARMACODYNAMICS: Given orally, Diloxanide is the active drug, released by gut bacteria. o INDICATIONS: Mild drug used to combat intestinal amebiasis. o ADVERSE EFFECTS: Well-tolerated. • COAGULATION: o INTRINSIC PATHWAY: XII, XI, IX, VIII, Kallikrein, Kininogen. Relatively slow. ▪ PHARMACOLOGY: ▪ Partial Thromboplastin Time (PTT) measures its integrity. ▪ It contains many intrinsic proteases and is therefore generally inhibited by Heparin. ▪ PATHWAY: ▪ Anionic Surfaces can activate one of three substances in order to start the Intrinsic Pathway: Pre-kallikrein, Kininogen, and Factor XII ▪ Factor XII ------> Factor XI ---------- > Factor IX ▪ Factor VIII, anionic phospholipid, and Ca+2 are then required to activate Factor X o EXTRINSIC PATHWAY: Tissue Factor, VII. Relatively fast. 46 ▪ PHARMACOLOGY: ▪ Prothrombin Time (PT) measures its integrity. ▪ It contains many Vitamin-K dependent factors and is therefore generally inhibited by Warfarin. ▪ PATHWAY: Tissue Factor ------> Factor VII ------------- > Factor X o COMMON PATHWAY: X, V, II, I 47 ▪ PATHWAY: One way or another, the common pathway starts when Factor X is activated. ▪ Factor X converts Prothrombin (II) > Thrombin ▪ Factor V, anionic phospholipid, and Ca+2 are required as cofactors. ▪ Thrombin converts Fibrinogen (I) -------- > Fibrin ▪ Fibrin cross-links platelets and forms cohesive plug. Parkinsonism: pg 505, 506 (1st line therapy) • Dopamine agonists: Pramexole and rompirinole -also used to tx restless leg syndrome o Carbidopa (Lodosyn) – blocks amino acid decarboxylase in the periphery (allows in plasma levels of levodopa) o Levodopa (L-dopa) o Carbidopa/l-dopa (Sinemet) 4 clinical symptoms: tremor @ rest, bradykinesia, rigidity, and postural instability. Slow dz progression—resting tremor 4/7 cycles per sec Rapid dz--- postural instability and gait w/ includes: dementia and bradykensia. 50 Stage II hypertension: Two first line drugs…ACE or ARB + thiazide For: CKD, acute stroke, HR acute ICH Blacks with no HR or CKD: CCB and thiazide. Know first line treatment Thiazide diuretics (ex-hydrochlorothizide, chlorthalidone, metolazone) MOA: thiazides enhance Na excretion, resulting in a reduced intravascular volume and reduced peripheral resistance (presumably by lowering intracellular Na in vascular smooth muscle cells. 51 SIDE EFFECTS: hypokalemia, hyponatremia, HYPERcalcemia, hyperglycemia, increase in LDL. Loop Diuretics (furosemide, torsemide) MOA: blocks sodium reabsorption LaSIX (short duration of action 3-6 hours) SIDE EFFECTS: volume depletion, hypokalemia, hypomagnesmia, urinary frequency. ***Loop diuretics not as effective in BP control but is in the decreasing fluid retention**** Lasix should be prescribed 3 to 4 times per day or as needed. Per video. In adults with HF who present with symptoms of volume overload, diuretics should be prescribed to control hypertension (AHA). Potassium-sparing diuretics (Spironolactone and eplerenone) These are preferred agents in primary aldosteronism and resistant hypertension. Spironolactone is associated with a risk of gynecomastia and impotence, risk for hyperkalemia. CCBs (calcium blockers) 52 MOA: impede the entry of calcium in heart and vascular smooth muscle cells, resulting in a decreased cellular calcium concentration, w/c reduces vascular smooth muscle contraction and lowers peripheral resistance. Nondihydropyridines (verapamil and diltiazem) ccbs SIDE EFFECTS: slowing the heart rate and causing atrioventricular (AV) conduction delays. Verapamil- constipation, HA, dizziness 55 SIDE EFFECTS: bradycardia, fatigue, decreased exercise tolerance, and increased airway resistance, sexual dysfunction (?). These agents should be avoided in persons with conduction system dz and active bronchospatic. Can use in asthmatics but should be carefully monitored. Alpha-blockers (“zosin”drugs- doxazosin, terazosin) MOA: act peripherally at vascular postsynaptic a-adrenerigc receptors, causing arteriolar and venous dilation SIDE EFFECTS: orthostatic hypotension Often used first line drug in older hypertensive men with concurrent prostatism had been popular b/c they provide symptomatic relief of obstructive urinary symptoms. Vasodilators (ex-hydralazine, minoxidil) MOA: act directly to relax arterial smooth muscle SIDE EFFECTS: orthostatic hypotension, edema Rarely, hydralazine can cause LUPUS LIKE REACTION Minoxidil can cause hypertrichosis and topical formulations are used for HAIR LOSS. CENTRALLY ACTING SYMPHATHOLYTICS MOA: reduce blood pressure by stimulating central a-adrenergic receptors, s/c in turn, reduces sympathetic outflow to the heart and vasculature 56 SIDE EFFECTS: sedation, dry mouth, and rebound hypertension with abrupt cessation Clonidine is a popular ER tx for hypertensive emergencies Pregnancy Methyldopa and labertalol are the traditional first line therapies Long acting CCBs and thiazide diuretics appear to be safe ACE/ARBs are contraindicated d/t decrease in placental blood flow 57 Elderly- Caution with orthostatis Take home message Increase in 20 SBP and 10 DBP doubles the pts risk of cardiovascular disease (CVD) 1st line: thiazide diuretics, CCBs, and ACE inhibitors and ARBs. For pts with CKD and proteinuria, ACE or ARB should be considered first. Spironolactone!! Inc alderstone. With ACE or ARB…CKD or to decrease protein in urine. Acne treatment Pg. 149, dosage 167 Corticosteroid – diflorisone diacetate (Psorcon) (stronger) and hydrocortisone Benzoyl peroxide effective for moderate acne • Topical clindamycin and erythromycin effective for inflammatory lesions in mild, moderate, or severe acne • Topical tretinoin effective for inflammatory and noninflammatory lesions in mild and moderate acne • Azelaic acid effective for inflammatory and noninflammatory lesions in mild to moderate acne • Estrogen-containing oral contraceptives can be useful in some women. Isotretinoin cyctic acne that doesn’t respond to regular tx. 60 -Furosemide 40 mg is equivalent to 1 mg of bumetanide and 20 mg of torsemide. This is important when the change is made from one loop diuretic to another. Diuresis is seen with doses of 10 mg furosemide and at 40 mg in patients with normal renal function -Except in patients with renal insufficiency (GFR <30 ml/min), thiazide diuretics are more efficacious than loop diuretics for the treatment of hypertension. -hypokalemia, hyponatremia, hypomagnesemia, hypocalcemia, hyperuricemia, metabolic alkalosis, and elevations in BUN and serum creatinine. Excessive sodium and water losses may also lead to volume depletion and hypotension. 61 Potassium-sparing diuretics work in the aldosterone-sensitive principal cells in the cortical collecting tubule. Should be used with great caution or should be avoided in patients with renal insufficiency because of their potential to induce life-threatening hyperkalemia -Sodium channel blocker: Commonly paired with a loop or a thiazide for refractory edema or to blunt potassium loss. -Aldosterone antagonist: Spironolactone and eplerenone competitively inhibit the aldosterone receptor. Eplerenone differs from spironolactone in that it is a more specific inhibitor of aldosterone and produces fewer endocrine side effects. -Spironolactone benefit in the treatment of severe CHF when added to an ACE inhibitor and a loop diuretic for severe CHF (NYHA Class IV), reducing mortality rates. Hyperkalemia appears to be dose dependent. -The net diuretic effect of the aldosterone antagonists is approximately 1% to 2% filtered sodium. -These drugs are particularly useful in the treatment of cirrhosis and ascites and have been shown to improve survival in patients with advanced heart failure. The loop diuretics, thiazide diuretics, and carbonic anhydrase inhibitors are sulfonamide derivatives, and the provider should pay close attention to the specific reaction of a patient who reports an allergy to a sulfonamide or a “sulfa” drug (e.g., Bactrim, Septra, generic) because individuals with sulfa allergies often have a predisposition to allergic reactions in general, as opposed to cross- reactivity with sulfonamide drugs Ethycrynic is used when there is a true allergic reaction (loop diuretics). Osmotic diuretics used in an inpatient setting (Mannitol)- used to decrease intracranial pressure. 62 Treatment of abnormal Heart Rhythm Ch. 23 pg. 281 TABLE 23-1 Antiarrhythmic Medication Indications pg. 282 TABLE 23-3 Suggested Treatment of Common Arrhythmias pg. 285 -Treatment of Arrhythmia Amiodarone and dronedarone 65 Serum digoxin levels should not exceed 1.0 ng/mL (1.3 nmol/mL), particularly in women. Because ACE inhibitors and ARBs may cause hyperkalemia in patients with renal failure, these drugs should be avoided or should be used only with great caution when serum creatinine levels are higher than 2.5 mg/dL (220 µmol/L), when glomerular filtration rates (GFRs) are less than 30 mL/minute/1.73 m2, or when potassium levels are higher than 5.0 mEq/L (5.0 mmol/L). Patient Education • Take a missed dose as soon as possible. Skip the missed dose if it is almost time for the next dose. Do not take two doses at the same time. • Common side effects include nonproductive cough, dizziness, and light-headedness. • The patient should call the practitioner immediately if any of these serious adverse effects occur: • Swelling (face, mouth, hands, tongue, or feet), difficulty breathing or swallowing, hives, severe itching, fainting, cloudy urine, sore throat, fever and sudden onset of abdominal pain, diarrhea, and vomiting (intestinal edema) in an adult • Signs of excess potassium in the body: irregular heartbeat, leg weakness, numbness or tingling of hands or feet, and extreme nervousness Withhold ACEIs 24 to 72 hours when starting a diuretic. TREATMENT OF DEPRESSION (dosage) AND ANXIETY (dosage 548) Depression ch. 47 pg. 517 SSRIs are first line therapy---Fluoxetine (Prozac), Citalopram (Celexa) Anxiety ch. 48 pg 538 Treatment: Acute-benzodiazepine; long term-SSRI, venlafaxine (SSRI is used in panic disorder), buspirone (lacks potential abuse) monitor for dizziness, Lorazepam (preferred) Many times it is necessary to add an antidepressant. 66 TCA- nortriptyline is suggested b/c of low side effects compared to other TCA’s. Titrate slow and low doses are preferred. Patient Education Benzodiazepines ie Diazepam • May cause drowsiness, dizziness, and fatigue and should be used with caution when driving or operating machinery that requires alert mental status. • Do not use alcoholic beverages or other CNS depressants while taking these medications. • Dependency can be a problem. • Do not stop the medication suddenly. Withdrawal symptoms (e.g., sweating, vomiting, muscle cramps, tremors, and seizures) may occur. Dosage must be reduced gradually under the supervision of the practitioner. • Do not take any medications, including OTC preparations, without the knowledge 67 of your provider. • Report the following symptoms to the provider: tremor, seizures, ataxia, dizziness, difficulty breathing, and chest tightness. • Rise slowly from a lying or sitting position because orthostatic hypotension caused by the medication may result in dizziness.