Relationships btwn drugs/extra questions Flashcards
Why do loop diuretics cause hypokalemia, but potassium-sparing diuretics do not?
Loop diuretics increase sodium and water excretion, leading to potassium loss in the distal tubule.
Potassium-sparing diuretics block aldosterone, preventing potassium excretion.
Compare the mechanisms of heparin and low-molecular-weight heparin (LMWH).
Heparin: Binds antithrombin III, inhibiting thrombin and Factor Xa.
LMWH: Primarily inhibits Factor Xa with less effect on thrombin.
What is the difference between non-dihydropyridine and dihydropyridine calcium channel blockers?
Non-dihydropyridines (e.g., verapamil) reduce heart rate and contractility.
Dihydropyridines (e.g., amlodipine) primarily cause vasodilation
Describe the physiological role of the RAAS system in blood pressure regulation.
The renin-angiotensin-aldosterone system (RAAS) is activated in response to low blood pressure or sodium levels. Renin converts angiotensinogen to angiotensin I, which is then converted by ACE to angiotensin II. Angiotensin II causes vasoconstriction and stimulates aldosterone release, increasing sodium and water retention to raise blood pressure.
How do antithrombotic, anticoagulant, and fibrinolytic drugs differ in their mechanisms?
Antithrombotic drugs (e.g., aspirin) prevent platelet aggregation.
Anticoagulants (e.g., warfarin, heparin) inhibit the coagulation cascade to prevent clot formation.
Fibrinolytics (e.g., tPA) break down existing clots by activating plasmin
A patient with a history of myocardial infarction is prescribed aspirin and clopidogrel. How do these drugs work together to prevent another event?
Aspirin inhibits cyclooxygenase (COX), reducing thromboxane and preventing platelet aggregation.
Clopidogrel blocks ADP receptors on platelets, preventing further activation and aggregation.
The combination provides a dual antiplatelet effect.
Compare the effects of beta-blockers and ACE inhibitors on cardiac remodeling.
Beta-blockers reduce myocardial oxygen demand and slow disease progression by decreasing heart rate and contractility.
ACE inhibitors prevent angiotensin II-mediated vasoconstriction and reduce myocardial fibrosis, slowing remodeling.
How does the mechanism of action of loop diuretics differ from that of thiazide diuretics in managing hypertension?
Loop diuretics (e.g., furosemide) inhibit Na⁺-K⁺-2Cl⁻ co-transporter in the loop of Henle, leading to significant fluid loss.
Thiazide diuretics (e.g., hydrochlorothiazide) inhibit the Na⁺-Cl⁻ symporter in the distal tubule, producing a more moderate diuresis.
Evaluate the pharmacokinetics of catecholamines versus noncatecholamines in adrenergic pharmacology.
Catecholamines (e.g., epinephrine) are rapidly metabolized by MAO and COMT, have a short half-life, and are ineffective orally.
Noncatecholamines (e.g., phenylephrine) lack hydroxyl groups, making them less susceptible to metabolism and allowing oral administration.
Design a treatment algorithm for a patient newly diagnosed with heart failure, considering first-line and adjunct therapies.
First-line: ACE inhibitors/ARBs, beta-blockers, diuretics if fluid overload.
Adjunct: Aldosterone antagonists (spironolactone), digoxin if symptomatic.
Advanced: Ivabradine, neprilysin inhibitors, implantable devices.
Propose a strategy for reducing the risk of stroke in a high-risk patient, integrating pharmacologic and lifestyle interventions.
Pharmacologic: Antiplatelet therapy (aspirin, clopidogrel), anticoagulation if indicated (warfarin, DOACs).
Lifestyle: Blood pressure control, smoking cessation, weight management, physical activity
Why do patients taking alpha-1 antagonists like prazosin experience orthostatic hypotension?
Alpha-1 blockers reduce vascular tone, leading to vasodilation. Upon standing, reduced venous return causes a drop in blood pressure due to impaired baroreceptor reflex compensation.
Explain the role of baroreceptors in the short-term regulation of blood pressure.
Baroreceptors in the carotid sinus and aortic arch detect changes in blood pressure and send signals to the medulla, which adjusts sympathetic and parasympathetic output to stabilize blood pressure.
A patient with diabetes and hypertension is prescribed an ACE inhibitor. What are the benefits of this drug in diabetic patients?
ACE inhibitors reduce diabetic nephropathy progression by decreasing glomerular pressure and protecting kidney function.
What is the relationship between renal function and the effectiveness of loop diuretics?
Loop diuretics act on the Na⁺-K⁺-2Cl⁻ symporter in the loop of Henle and remain effective in renal impairment, whereas thiazide diuretics lose efficacy as kidney function declines.
A 60-year-old patient presents with a blood pressure of 180/100 mmHg and signs of organ damage. What class of drugs should be initiated for hypertensive emergency?
IV antihypertensives such as nitroprusside, labetalol, or nicardipine should be used to lower BP gradually
Compare and contrast the pharmacodynamics of heparin and warfarin in anticoagulation.
Heparin: Activates antithrombin III, inhibiting thrombin immediately (IV administration).
Warfarin: Inhibits vitamin K-dependent clotting factors, with a delayed onset.
Explain how the pharmacokinetics of hydrophilic and lipophilic beta-blockers affect their clinical use.
Lipophilic beta-blockers (e.g., propranolol) cross the BBB, causing CNS effects.
Hydrophilic beta-blockers (e.g., atenolol) remain in circulation, reducing CNS side effects.
Why might a patient on warfarin require a dosage adjustment after starting an antibiotic like erythromycin?
Erythromycin inhibits CYP enzymes, decreasing warfarin metabolism, increasing INR and bleeding risk.
If a patient has a history of stroke and atrial fibrillation, how would you decide between using aspirin or an oral anticoagulant?
Aspirin is for low-risk patients; oral anticoagulants (e.g., warfarin, DOACs) are for high-risk patients
