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Questions and Answers
What is the primary mechanism behind the edema observed in congestive heart failure (CHF)?
What is the primary mechanism behind the edema observed in congestive heart failure (CHF)?
Which drug class is typically considered to reduce water retention in heart failure patients?
Which drug class is typically considered to reduce water retention in heart failure patients?
In a patient with CHF, which of the following is NOT a compensatory response observed?
In a patient with CHF, which of the following is NOT a compensatory response observed?
What is the most common cause of congestive heart failure in the United States?
What is the most common cause of congestive heart failure in the United States?
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What left ventricular ejection fraction (LVEF) percentage is considered normal?
What left ventricular ejection fraction (LVEF) percentage is considered normal?
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What is the primary clinical use of digoxin in patients with atrial fibrillation?
What is the primary clinical use of digoxin in patients with atrial fibrillation?
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Why is plasma monitoring necessary for digoxin therapy?
Why is plasma monitoring necessary for digoxin therapy?
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What effect does digoxin NOT have on cardiac function?
What effect does digoxin NOT have on cardiac function?
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How does quinidine affect digoxin levels in the body?
How does quinidine affect digoxin levels in the body?
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What is a common adverse effect of digoxin toxicity?
What is a common adverse effect of digoxin toxicity?
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What role do azoles, such as itraconazole, play in drug interactions involving digoxin?
What role do azoles, such as itraconazole, play in drug interactions involving digoxin?
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What is the average half-life of digoxin?
What is the average half-life of digoxin?
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Which statement regarding the dosage of digoxin is correct?
Which statement regarding the dosage of digoxin is correct?
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What is the primary way digoxin is eliminated from the body?
What is the primary way digoxin is eliminated from the body?
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Which of the following actions of itraconazole poses a risk when taken with digoxin?
Which of the following actions of itraconazole poses a risk when taken with digoxin?
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What is considered a narrow therapeutic index concentration range for digoxin?
What is considered a narrow therapeutic index concentration range for digoxin?
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Which of the following symptoms is NOT associated with digoxin toxicity?
Which of the following symptoms is NOT associated with digoxin toxicity?
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What is one of the first steps in treating digoxin overdose?
What is one of the first steps in treating digoxin overdose?
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How does Digibind® function in the treatment of digoxin overdose?
How does Digibind® function in the treatment of digoxin overdose?
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Based on historical data, how many documented cases of fatalities were reported due to digoxin overdose in 1996?
Based on historical data, how many documented cases of fatalities were reported due to digoxin overdose in 1996?
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What is the approximate amount of digoxin that one vial of Digibind® can bind?
What is the approximate amount of digoxin that one vial of Digibind® can bind?
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What was the primary focus of William Withering's work in relation to digoxin?
What was the primary focus of William Withering's work in relation to digoxin?
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What was the primary historical significance of Withering's text on digoxin published in 1785?
What was the primary historical significance of Withering's text on digoxin published in 1785?
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Which component is primarily affected by the action of digoxin in cardiac muscle cells?
Which component is primarily affected by the action of digoxin in cardiac muscle cells?
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What is the primary outcome of digoxin's inhibition of the Sodium-Potassium ATPase pump?
What is the primary outcome of digoxin's inhibition of the Sodium-Potassium ATPase pump?
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What physiological change occurs as a result of increased intracellular sodium due to digoxin use?
What physiological change occurs as a result of increased intracellular sodium due to digoxin use?
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How is digoxin primarily excreted from the body?
How is digoxin primarily excreted from the body?
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Which prominent society was William Withering a member of that contributed to his work with digoxin?
Which prominent society was William Withering a member of that contributed to his work with digoxin?
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Which of the following best describes the pharmacological effect of digoxin?
Which of the following best describes the pharmacological effect of digoxin?
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What is the primary form of digoxin that exhibits pharmacological activity?
What is the primary form of digoxin that exhibits pharmacological activity?
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Which of the following drugs is NOT classified as an inotropic agent used in congestive heart failure?
Which of the following drugs is NOT classified as an inotropic agent used in congestive heart failure?
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What is the role of phosphodiesterase (PDE) inhibitors in heart failure treatment?
What is the role of phosphodiesterase (PDE) inhibitors in heart failure treatment?
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How does angiotensin II affect the body in the context of heart failure?
How does angiotensin II affect the body in the context of heart failure?
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Which enzyme initiates the conversion of angiotensinogen to Angiotensin I?
Which enzyme initiates the conversion of angiotensinogen to Angiotensin I?
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What is the potential impact of increased cAMP and cGMP levels due to PDE inhibitors?
What is the potential impact of increased cAMP and cGMP levels due to PDE inhibitors?
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What is the typical dosage range for captopril in the management of heart failure?
What is the typical dosage range for captopril in the management of heart failure?
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Which form of digoxin can be neutralized by Digibind antibodies?
Which form of digoxin can be neutralized by Digibind antibodies?
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What is a common side effect experienced by 30% of patients taking ACE inhibitors?
What is a common side effect experienced by 30% of patients taking ACE inhibitors?
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Which drug class acts antagonistically to the renin-angiotensin system by blocking Angiotensin II receptor?
Which drug class acts antagonistically to the renin-angiotensin system by blocking Angiotensin II receptor?
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What is the primary action of BNP and ANP in relation to blood pressure?
What is the primary action of BNP and ANP in relation to blood pressure?
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What is the half-life of Nesiritide when administered IV?
What is the half-life of Nesiritide when administered IV?
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How does norepinephrine (NE) affect B1 receptors in the heart?
How does norepinephrine (NE) affect B1 receptors in the heart?
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What is the consequence of renal damage due to ACE inhibitors and Angiotensin II receptor blockers during pregnancy?
What is the consequence of renal damage due to ACE inhibitors and Angiotensin II receptor blockers during pregnancy?
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What natural peptide hormone is synthesized in the ventricles and plays a role in heart failure treatment?
What natural peptide hormone is synthesized in the ventricles and plays a role in heart failure treatment?
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Which receptors are primarily affected by norepinephrine to cause an increase in oxygen demand?
Which receptors are primarily affected by norepinephrine to cause an increase in oxygen demand?
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Study Notes
Pharmacology I, Chapter 13: CHF
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Case Study 1: A 65-year-old man presents with shortness of breath, edema in feet/ankles, and crackles in the lungs following a viral illness. Blood pressure is 110/70 mmHg, pulse is 105 bpm, and left ventricular ejection fraction is 20% (normal ~60%). The diagnosis is Stage C, Class III heart failure, with cardiomyopathy secondary to viral infection. What treatment?
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Case Study Treatments: Initial treatment includes a low-sodium diet and a diuretic (furosemide). An ACE inhibitor (enalapril) is added, followed by digoxin to manage continued shortness of breath. Beta blockers and eplerenone (aldosterone antagonist) are potential additional treatments.
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CHF Overview: CHF affects approximately 5 million patients in the US. It's characterized by decreased cardiac contractility and inadequate cardiac output to meet body needs. Coronary artery disease is the most common cause in the US.
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Homeostatic Response to CHF:
- Tachycardia: Increased sympathetic tone.
- Increased peripheral vascular resistance: Resulting from increased sympathetic tone.
- Salt and water retention: Mediated by the renin-angiotensin-aldosterone system, causing blood volume increases and edema.
- Cardiomegaly: A compensatory response to sympathetic discharge.
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Drug Treatments for CHF:
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(1) Positive Inotropic Drugs:
- Cardiac glycosides.
- PDE inhibitors.
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(2) Vasodilators:
- Nitrates (nitroprusside).
- Loop diuretics.
- Angio antagonists.
- Nesiritide (BNP).
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(3) Miscellaneous:
- Beta blockers.
- Spironolactone.
- Thiazides.
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(1) Positive Inotropic Drugs:
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Normal Cardiac Contractility: Involves decreased sensitivity of contractile proteins to calcium, amount of calcium released from the SR (sarcoplasmic reticulum), amount of trigger calcium, movement of calcium against its sodium gradient, and alteration of sodium/potassium ATPase (digoxin).
Digoxin
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Description: Digoxin (Lanoxin®), a cardiac glycoside, is the most commonly used glycoside derived from foxglove.
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Mechanism of Action: Digoxin inhibits the Na+/K+ ATPase pump, increasing intracellular calcium, thus strengthening cardiac muscle contractions.
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Pharmacological Effects: Specifically, it increases cardiac contractility, ventricular ejection volume, cardiac output, and renal perfusion. Additionally, it can cause early and toxic responses, as seen in the electrical effects.
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Clinical Uses: Digoxin is used to reduce symptoms of CHF and atrial fibrillation.
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Drug Interactions: Quinidine displaces digoxin from tissue binding sites, increasing digoxin levels. Itraconazole inhibits the P-glycoprotein pump, leading to an increased risk of digoxin toxicity.
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Toxicity: Digoxin toxicity includes nausea, vomiting, diarrhea, visual disturbances (color changes), arrhythmias, and potentially life-threatening CNS effects.
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Overdose Treatment: Includes correction of any potassium deficiency, use of digoxin antibodies (Digibind®) to bind digoxin, and close monitoring of serum digoxin concentrations.
Digoxin in the Body
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Forms of Digoxin:
- Free form (70%): Active form.
- Inactive bound to albumin: Not pharmacologically active.
- Bound to tissue receptors (Na+/K+ ATPase pumps): Where Digibind® antibodies bind.
PDE Inhibitors
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Description: These drugs are inotropic agents used in CHF. Milrinone is a specific example of an IV-only PDE inhibitor that can be used in acute heart failure. Examples include theophylline, amrinone, and milrinone.
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Mechanism of Action: PDE inhibitors inhibit the phosphodiesterase (PDE) enzyme, resulting in increased intracellular calcium and improved contractility.
ACE Inhibitors
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Mechanism of Action: ACE inhibitors decrease blood pressure by blocking the conversion of angiotensin I to angiotensin II. This reduces vasoconstriction and aldosterone secretion. They also increase renal blood flow.
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Examples: Examples include captopril, enalapril, and benazepril.
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Clinical Significance: Approximately 30% of patients experience a cough, and they are contraindicated during pregnancy due to potential fetal renal damage.
Angiotensin Antagonists
- Mechanism of Action: A second class of drugs used in CHF, acting antagonistically to the renin-angiotensin system. This can be accomplished by two different types of drugs:
- block Angio II formation (ACE inhibitors)
- Block Angio II receptor
Angio II Receptor Blockers
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Mechanism of Action: Specifically block the receptor for Angio II, reducing its effects.
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Examples: Losartan is an example.
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Clinical Significance: Similar clinical effects to ACE inhibitors, but with a lower incidence of cough. Fetal kidney damage is still a risk, and these agents should never be used during pregnancy.
BNP Agonist
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Description: BNP is a naturally occurring peptide hormone synthesized in the ventricles that counteracts the renin-angiotensin-aldosterone system and lowers blood pressure. ANP is a similar, but the atria synthesizes this peptide hormone.
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Function: These hormones are natriuretic, meaning they increase sodium excretion.
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Examples: Nesiritide (Natrecor®)
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Clinical Significance: The drug form, nesiritide, is used intravenously (IV) in acute heart failure cases. Serum levels of the natural BNP are often utilized as a screening tool to detect cardiac disease.
Beta Receptors
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Mechanism of Action: Beta-1 receptors in the heart increase heart rate, blood pressure, and oxygen demand. Beta-2 receptors in the periphery trigger vasoconstriction. When NE binds to beta 1 receptors, Ca++ flows into the cardiac cells, strengthening their contractions.
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Examples: NE (norepinephrine), metoprolol (Lopressor®), bisoprolol, and carvedilol.
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Clinical Significance: Beta blockers are used to slow down the heart rate in patients with heart issues. By blocking the stimulation of beta receptors by catecholamines, these medications offer a different mechanism of action to manage patients with congestive heart failure (CHF).
Case Study Treatment summary
- Drug treatments are tailored in CHF depending on disease severity (mild, moderate, severe).
- This case involves a moderate presentation of the disorder.
- For the moderate case detailed in the example case study, the treatment involves digoxin and ACE inhibitors, and diuretics.
- Use of beta blockers and other medications such as vasodilators may be added to moderate CHF management based on disease progression and the specific condition of the patient.
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Description
This quiz explores the complexities of Congestive Heart Failure (CHF) through case studies, focusing on symptoms, diagnostic criteria, and treatment options. Learners will evaluate appropriate pharmacological interventions based on patient presentations and current guidelines. Prepare to deepen your understanding of managing heart failure.
