Pharmacology Diuretics Slides: Nursing Practice Questions PDF

NUR 328/Pharmacology Dr. Cheryl VerStrate DIURETICS  ANATOMY & PHYSIOLOGY REVIEW Nephron Glomerulus Proximal tubule Loop of Henle Distal tubule 3 Functions: _____________ _______________ ______________ ANA...

NUR 328/Pharmacology Dr. Cheryl VerStrate DIURETICS  ANATOMY & PHYSIOLOGY REVIEW Nephron Glomerulus Proximal tubule Loop of Henle Distal tubule 3 Functions: _____________ _______________ ______________ ANATOMY & PHYSIOLOGY: REABSORPTION REABSORPTION Proximal Convoluted Tubule HIGH reabsorptive capacity Sodium, chloride, bicarbonate, and potassium; water passively follows. Loop of Henle Descending limb freely permeable to water (promotes urine concentration). Ascending limb additional sodium and chloride reabsorption. Distal Convoluted Tubule Early -Additional sodium & chloride reabsorption, water passively follows. Late -Exchange of sodium for potassium (regulated by aldosterone) -Final concentration of urine (regulated by ADH)  INTRO TO DIURETICS HOW DIURETICS WORK Blockade of _________ and _________ reabsorption; ultimately results in increased water excretion. A D V E R S E I M PA C T S O N E X T R A C E L LU L A R F LU I D Diuretics interfere with normal kidney function. Hypovolemia, acid-base imbalance, and electrolyte abnormalities. CLASSIFICATION OF DIURETICS Loop Diuretics Thiazide Diuretics Osmotic Diuretics Potassium-sparing Diuretics  LOOP DIURETICS PROTOTYPE DRUG: FUROSEMIDE Generic Name: Furosemide Trade Name: Lasix Mechanism of Action: Acts on the ascending Loop of Henle to block sodium and chloride reabsorption and prevents passive water reabsorption. Diuresis with furosemide is less dependent on kidney function; can promote diuresis even in patients with severe renal impairment. Therapeutic Uses: Pulmonary edema associated with CHF, CHF, edema not responsive to less powerful diuretics, hypertension not controlled by other diuretics  THIAZIDE DIURETICS PROTOTYPE DRUG: HYDROCHLOROTHIAZIDE Generic Name: Hydrochlorothiazide Trade Name: Microzide Mechanism of Action: Acts on the early segment of the distal convoluted tubule; inhibits sodium reabsorption which results in increased secretion of sodium and water. Diuresis is dependent on kidney function; will be less effective in patients with GFR < 20 mL/min. Therapeutic Uses: Essential HTN, edema related to CHF Adverse Effects: Dehydration, hypokalemia, hypotension.  POTASSIUM-SPARING DIURETICS PROTOTYPE DRUG: SPIRONOLACTONE Generic Name: Spironolactone Trade Name: Aldactone Mechanism of Action: Blocks the action of aldosterone in the distal nephron.  Aldosterone normally facilitates exchange of sodium for potassium (potassium excretion); aldosterone inhibition results in potassium retention and sodium excretion. Therapeutic Uses: HTN, edema, CHF Adverse Effects: Hyperkalemia, endocrine effects  OSMOTIC DIURETICS PROTOTYPE DRUG: MANNITOL Generic Name: Mannitol Trade Name: Osmitrol Mechanism of Action: Diuresis through osmotic force, inhibits passive reabsorption of water. Therapeutic Uses: Reduction in intracranial pressure, reduction of intraocular pressure Adverse Effects: Edema, precipitation of CHF and pulmonary PRACTICE QUESTIONS The nurse knows that diuretics mostly affect which function of the kidneys? a. Cleansing and maintenance of extracellular fluid volume b. Maintenance of acid-base balance c. Excretion of metabolic waste d. Elimination of foreign substances The nurse knows that diuretics mostly affect which function of the kidneys? a. Cleansing and maintenance of extracellular fluid volume Rationale: Most diuretics block sodium and chloride reabsorption, thus affecting the maintenance of extracellular fluid volume. The nurse plans to closely monitor for which clinical manifestation after administering furosemide [Lasix]? a. Decreased pulse b. Decreased temperature c. Decreased blood pressure d. Decreased respiratory rate The nurse plans to closely monitor for which clinical manifestation after administering furosemide [Lasix]? c. Decreased blood pressure Rationale: Loop diuretics, (i.e. furosemide), are the most effective diuretic agents. They produce more loss of fluid and electrolytes than any others. A sudden loss of fluid can result in decreased blood pressure. When blood pressure drops, the pulse probably will increase rather than decrease. Lasix should not affect respiration or temperature. The nurse should also closely monitor the patient’s potassium level. The nurse is caring for a patient with heart failure who needs a diuretic. Which agent is likely to be chosen, because it has been shown to greatly reduce mortality in patients with heart failure? a. Furosemide [Lasix] b. Hydrochlorothiazide [HydroDIURIL] c. Spironolactone [Aldactone] d. Mannitol [Osmitrol] The nurse is caring for a patient with heart failure who needs a diuretic. Which agent is likely to be chosen, because it has been shown to greatly reduce mortality in patients with heart failure? c. Spironolactone [Aldactone] Rationale: Spironolactone is a potassium-sparing diuretic used to treat both hypertension and edema. It is a preferred drug in heart failure, because it has been shown to have a cardioprotective effect, reducing mortality in patients with heart failure. HEMODYNAMI CS NUR 328/Pharmacology Dr. Cheryl VerStrate Overview of Circulatory System 18  HEMODYNAMICS: REGULATION OF CARDIAC OUTPUT Cardiac Output = ___________ x __________ CARDIAC OUTPUT HEART RATE STROKE VOLUME Average CO is 5L/minute Primarily controlled by Volume of blood Factors effecting CO are the autonomic nervous expelled from the left Heart Rate & Stroke system ventricle during systole. Volume Normal 60 – 100 bpm Determined by: Myocardial Example #1: Heart rate 70 bpm and stroke volume 70 mL contractility Cardiac afterload AFTER the heart 70bpm x 70mL = 4,900 mL/minute or 4.9 L/minute Cardiac preload PRE heart Example #2: Heart rate 140 bpm and stroke volume 70 Normal 60 - 100mL mL 140bpm x 70mL = 9,800 mL/minute or 9.8 L/minute Example #3: Heart rate 70 bpm and stroke volume 40 mL 70bpm x 40mL = 2,800 mL/minute or 2.8 L/minute 19 HEMODYNAMICS: STARLING'S LAW When ____________ increases, ___________ increases. 20 HEMODYNAMICS: MAINTAINING PULMONARY-SYSTEMIC BALANCE 21 HEMODYNAMICS: REGULATION OF ARTERIAL PRESSURE Arterial Pressure = Peripheral Resistance x Cardiac Output Peripheral Resistance regulated primarily by vasodilation and vasoconstriction or arterioles. Arterial Pressure is regulated by 3 systems: 1. Autonomic Nervous System  Steady-state sympathetic tone  Baroreceptor reflexes 2. Renin-Angiotensin-Aldosterone System (RAAS)  Constriction of arterioles & veins  Retention of water by the kidneys 3. Kidneys 4. **Natriuretic Peptides  During volume overload 22 Practice Questions Which statements accurately reflect Starling’s law as applied to a healthy heart? (Select all that apply.) a) When venous return increases, stroke volume decreases. b) The right and left ventricles pump the same amount of blood. c) Cardiac output is equal to the volume of blood delivered by the veins. d) When venous return increases, cardiac output increases. e) As cardiac muscle fibers increase in length, their contractile force decreases. Which statements accurately reflect Starling’s law as applied to a healthy heart? (Select all that apply.) b) The right and left ventricles pump the same amount of blood. c) Cardiac output is equal to the volume of blood delivered by the veins. d) When venous return increases, cardiac output increases. Rationale: Starling’s law states that the force of ventricular contraction is proportional to muscle fiber length. Therefore, as muscle fibers increase in length, the force of the heart contraction increases. In this situation, the right and left ventricles pump the same amount of blood, and overall cardiac output is equivalent to the volume delivered by the veins. As venous return increases, stroke volume increases What are the primary regulatory systems of arterial pressure? (Select all that apply.) a) Autonomic nervous system b) Renin-angiotensin-aldosterone system c) Renal system d) Pulmonary system e) P450 enzyme system What are the primary regulatory systems of arterial pressure? (Select all that apply.) a) Autonomic nervous system b) Renin-angiotensin-aldosterone system c) Renal system Rationale: Arterial pressure is regulated primarily by the autonomic nervous system (provides short-term tone and control), the renin- angiotensin-aldosterone system (constriction and volume), and the renal system (long-term volume control). A patient is taking a beta1-adrenergic drug to improve the stroke volume of the heart. The nurse caring for this patient knows that this drug acts by increasing: a) cardiac afterload. b) cardiac preload. c) myocardial contractility. d) venous return. A patient is taking a beta1-adrenergic drug to improve the stroke volume of the heart. The nurse caring for this patient knows that this drug acts by increasing: c) myocardial contractility Rationale: Beta-1 adrenergic stimulation increases the force of heart muscle contraction. By enhancing contractility, beta-1 adrenergic drugs improve cardiac output, which is particularly useful in conditions where stroke volume is compromised, like heart failure. DRUGS ACTING ON RAAS NUR 328/Pharmacology Dr. Cheryl VerStrate ANATOMY & PHYSIOLOGY REVIEW ANATOMY & PHYSIOLOGY REVIEW: THE BASICS 1. Renin Release Released by the _______ when ______ is low. 2. Angiotensin Activation Renin converts angiotensinogen into angiotensin I, which is then converted into angiotensin II by the angiotensin-converting-enzyme (aka ACE) 3. Angiotensin II 1) Narrows the blood vessels to raise BP 2) Stimulate the release of aldosterone from the adrenal glands 4. Aldosterone Trigger sodium and water retention in the kidneys -> increases ____________-> increases 34 _____________ ANATOMY & PHYSIOLOGY REVIEW Renin Angiotensinogen -> Angiotensin I Angiotensin-Converting Enzyme (aka ACE or Kinase II) Angiotensin I -> Angiotensin II Formation of Angiotensin II is influenced by Renin and Angiotensin-Converting Enzyme  PHYSIOLOGY OF THE RAAS Renin catalyzing angiotensin I from angiotensinogen is the rate- limiting step in angiotensin II formation. Renin release is stimulated by:  BP  Blood Volume  plasma sodium content  renal perfusion pressures Stimulation of beta1 adrenergic receptors in the juxtaglomerular cells Renin release is suppressed by opposite factors Negative feedback loop 36  PHYSIOLOGY OF THE RAAS Types of Angiotensin: 1. Angiotensin I 2. Angiotensin II – VERY active physiologically 3. Angiotensin III Actions of Angiotensin II Vasoconstrictor Stimulates release of aldosterone Alteration of cardiac and vascular structure Actions of Aldosterone Regulation of BP and blood volume Pathologic cardiovascular effects 37  ACTIONS OF ANGIOTENSIN II & ALDOSTERONE ANGIOTENSIN II ALDOSTERONE POWERFUL vasoconstrictor Regulation of Blood Volume & Acts directly on vascular smooth Blood Pressure muscle Acts on the distal tubules of the Acts indirectly on: kidney to cause retention of Na+ SNS to promote release of and excretion of K+ norepinephrine Adrenal medulla to promote Pathologic CV eff ects include: release of epinephrine Promotes cardiac remodeling & CNS to  sympathetic outflow to fibrosis blood vessels Activate SNS and suppress uptea of Structural changes to the heart & NE in the heart  promotes blood vessels dysrhythmias Results in cardiac remodeling and Promotion of vascular fibrosis hypertrophy, HTN, HF, MI and atherosclerosis Disruption of baroreceptor reflex38 ANATOMY & PHYSIOLOGY REVIEW Drug Classes Acting on the RAAS Angiotensin-Converting Enzyme Inhibitors (ACEIs) Angiotensin II Receptor Blockers (ARBS) Aldosterone Antagonists Direct Renin Inhibitors 39  PROTOTYPE DRUGS Angiotensin-Converting Enzyme Inhibitors (ACEIs) Captopril Angiotensin II Receptor Blockers (ARBS) Losartan Aldosterone Antagonists Eplerenone Direct Renin Inhibitors Aliskiren Pitch Deck 40  ACE INHIBITORS Captopril – PROTOTYPE Enalapril Lisinopril Ramipril Benazepril Fosinopril Moexipril Perinodpril Quinapril Trandolapril 41 MECHANISM OF ACTION OF ACE INHIBITORS ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE INHIBITORS) MECHANISM OF ACTION  levels of angiotensin II by inhibiting ACE  levels of bradykinin by inhibition of kinase II (ACE) THERAPEUTIC USES Hypertension Heart Failure Acute MI Left Ventricular Dysfunction Diabetic & nondiabetic nephropathy Prevention of MI, stroke, and death in patients at high risk for CV events 44  ACE INHIBITORS: ADVERSE EFFECTS 1ST Dose Hypotension Greatest risk in those with severe hypotension, on diuretics or who have Na+/volume depletion Minimize by starting with lower doses, temporarily stopping diuretics a few days before starting ACE inhibitors. Hyperkalemia Renal Failure Risk of severe renal insufficiency in those with bilateral renal artery stenosis Cough  risk with older age, women, and those of Asian ancenstry Angioedema 45  ACE INHIBITORS: DRUG INTERACTIONS DIURETICS Can intensify first-dose hypotension ANTIHYPERTENSIVES Additive effects when on multiple medications effecting BP LITHIUM ACE Inhibitors may result in toxic accumulations of lithium NONSTEROIDAL ANTIINFLAMMATORY DRUGS  antihypertensive effects of ACE inhibitors 46  ACE INHIBITORS PROTOTYPE DRUG: CAPTOPRIL Generic Name: Captopril Mechanism of Action: Competitive inhibitor of angiotensin- converting enzyme Results in decreased levels of angiotensin II Therapeutic Uses: HTN, HF, left ventricular dysfunction after MI, diabetic nephropathy Adverse Effects: Acute kidney injury/renal failure, angioedema, cough, hyperkalemia, hematologic effects, dermatologic reactions 47  ACE INHIBITOR MNEMONICS Cough Angioedema Potassium Excess Turns down Angiotensin II levels Only ACE inhibitor approved for nephropathy tx Pregnancy Problems Renal Failure Increases Bradykinin Lowers Blood Pressure Pitch Deck 48  ACE INHIBITOR MNEMONICS Angioedema Cough Elevated potassium Pitch Deck 49  ACE INHIBITOR MNEMONICS CHAD likes taking ACE inhibitors because they: Control Hypertension And Diabetic Nephropathy CHAD does not like taking ACE inhibitors because they cause: Cough Hyperkalemia Angioedema Dose #1 Hypotension Pitch Deck 50 ANGIOTENSIN II RECEPTOR BLOCKERS (ARB S ) Losartan – PROTOTYPE Valsartan Azilsartan Candesartan Eprosartan Irbesartan Olmesartan Telmisartan 51 MECHANISM OF ACTION OF ARBS ANGIOTENSIN II RECEPTOR BLOCKERS (ARBS) MECHANISM OF ACTION Blocks angiotensin II from activating its receptors in blood vessels, adrenal glands, and other tissues ____________ of arterioles and veins Prevention of pathologic cardiac structure changes  release of aldosterone   excretion of Na+ and H2O Does NOT inhibit ACE (Kinase II) Should not  levels of bradykinin in the lung, should not have adverse effect of _________ 53  ARBS THERAPEUTIC USES Hypertension Heart failure (HF) Myocardial infarction (MI) Stroke prevention Diabetic nephropathy Patients unable to tolerate ACE inhibitors 54  ARBS: ADVERSE EFFECTS Renal Failure Risk of severe renal insufficiency in those with bilateral renal artery stenosis Cough Low incidence of cough Angioedema – very rare Fetal Injury: Black Box Warning 55  ARBS PROTOTYPE DRUG: LOSARTAN Generic Name: Losartan Brand Name: Cozaar Mechanism of Action: Selective and competitive blockade of angiotensin II Therapeutic Uses: HTN, stroke prevention, diabetic nephropathy Adverse Effects: Acute kidney injury/renal failure, hyperkalemia, angioedema, cough 56 Aldosterone Antagonists Spironolactone Eplerenone - PROTO  ALDOSTERONE ANTAGONIST PROTOTYPE DRUG: EPLERENONE Generic Name: Eplerenone Brand Name: Inspra Mechanism of Action: Selective blockade of aldosterone receptors Therapeutic Uses: Hypertension (HTN) and heart failure (HF) Adverse Effects: Hyperkalemia Drug Interactions: Inhibitors of CYP3A4   levels of eplerenone 58 Direct renin inhibitors Aliskiren - PROTOTYP  DIRECT RENIN INHIBITORS PROTOTYPE DRUG: ALISKIREN Generic Name: Aliskiren Brand Name: Tekturna Mechanism of Action: Binds tightly to renin to inhibit cleavage of angiotensinogen to angiotensin I Therapeutic Uses: Hypertension (HTN) Adverse Effects: Hyperkalemia, diarrhea, cough, angioedema Fetal Injury: Black Box Warning 60 PRACTICE QUESTION The nurse teaches a patient about Captopril. Which statement by the patient requires an intervention by the nurse? A. “I use NoSalt instead of salt to season foods.” B. “I eat sweet potatoes once or twice a week.” C. “I drink 4 ounces of prune juice each morning.” D. “I like asparagus because it’s high in vitamin K.” 61 PRACTICE QUESTION The nurse teaches a patient about Captopril. Which statement by the patient requires an intervention by the nurse? Answer: A Rationale: An adverse effect of angiotensin-converting enzyme (ACE) inhibitors (eg, captopril) is hyperkalemia. Significant potassium accumulation is usually limited to patients taking potassium supplements, salt substitutes (which contain potassium), or a potassium-sparing diuretic. Patients should be instructed to avoid potassium supplements and potassium- containing salt substitutes unless they are prescribed. Sweet potatoes and prune juice are foods high in potassium; asparagus is high in vitamin K. Foods high in vitamin K are restricted for 62