Antihypertensives

Antihypertensives US Medical PG Question 1: An investigator is comparing the risk of adverse effects among various antiarrhythmic medications. One of the drugs being studied primarily acts by blocking the outward flow of K+ during myocyte repolarization. Further investigation shows that the use of this drug is associated with a lower rate of ventricular tachycardia, ventricular fibrillation, and torsades de pointes when compared to similar drugs. Which of the following drugs is most likely being studied?

• A. Verapamil
• B. Procainamide
• C. Esmolol
• D. Amiodarone (Correct Answer)
• E. Sotalol

Antihypertensives Explanation: ***Amiodarone*** - Amiodarone is a **Class III antiarrhythmic drug** that primarily blocks **potassium channels**, thereby prolonging repolarization and the effective refractory period in cardiac myocytes. - While it has properties of all four Vaughn-Williams classes, its dominant action as a potassium channel blocker makes it highly effective in preventing and treating various arrhythmias, including **ventricular tachycardia (VT)** and **ventricular fibrillation (VF)**, and it has a relatively lower risk of **torsades de pointes (TdP)** compared to other Class III drugs due to its broader ion channel effects. *Verapamil* - Verapamil is a **Class IV antiarrhythmic drug (non-dihydropyridine calcium channel blocker)** that primarily blocks **L-type calcium channels**, slowing conduction through the AV node. - It is mainly used for **supraventricular tachycardias** and rate control in atrial fibrillation, not typically for ventricular arrhythmias like VT/VF. *Procainamide* - Procainamide is a **Class IA antiarrhythmic drug** that blocks **sodium channels** and also prolongs repolarization by blocking some potassium channels, but its primary effect is on sodium channels. - Class IA drugs are known to **increase the QT interval** and carry a significant risk of **torsades de pointes**, making them less favorable for preventing VT/VF with adverse effect concerns. *Esmolol* - Esmolol is a **Class II antiarrhythmic drug (beta-blocker)** that primarily acts by **blocking beta-adrenergic receptors**, thereby reducing heart rate, contractility, and AV nodal conduction. - While useful in some arrhythmias, its main mechanism is not potassium channel blockade, and it is not typically preferred for the direct prevention of VT/VF in situations with concerns about TdP. *Sotalol* - Sotalol is a **Class III antiarrhythmic drug** that primarily acts as a **potassium channel blocker**, prolonging the action potential duration and effective refractory period, and also has **beta-blocking properties**. - While it blocks potassium channels, sotalol carries a **higher risk of torsades de pointes** compared to amiodarone, especially at higher doses and in patients with underlying heart conditions.

Antihypertensives US Medical PG Question 2: A 65-year-old male with a history of hypertension presents to his primary care physician complaining of multiple episodes of chest pain, palpitations, and syncope. Episodes have occurred twice daily for the last week, and he is asymptomatic between episodes. Electrocardiogram reveals a narrow-complex supraventricular tachycardia. He is treated with diltiazem. In addition to its effects on cardiac myocytes, on which of the following channels and tissues would diltiazem also block depolarization?

• A. L-type Ca channels in skeletal muscle
• B. T-type Ca channels in bone
• C. P-type Ca channels in Purkinje fibers
• D. N-type Ca channels in the peripheral nervous system
• E. L-type Ca channels in smooth muscle (Correct Answer)

Antihypertensives Explanation: ***L-type Ca channels in smooth muscle*** - **Diltiazem** is a **calcium channel blocker** that acts on **L-type calcium channels**, which are extensively found in both cardiac muscle and vascular **smooth muscle**. - By blocking these channels in smooth muscle, diltiazem induces **vasodilation**, contributing to its use in hypertension, as seen in the patient's history. *L-type Ca channels in skeletal muscle* - While skeletal muscle does contain L-type calcium channels (also known as dihydropyridine receptors), their primary role is in **excitation-contraction coupling**, acting as voltage sensors rather than directly regulating calcium influx for contraction. - **Skeletal muscle contraction** is primarily triggered by calcium release from the sarcoplasmic reticulum, not direct calcium influx through L-type channels, making them largely **insensitive to calcium channel blockers** like diltiazem at therapeutic doses. *T-type Ca channels in bone* - **T-type calcium channels** are found in various tissues, including neurons and cardiac pacemaker cells, but they are generally **not the primary target of diltiazem**, which preferentially binds to L-type channels. - Furthermore, **bone tissue** is not known to have a significant physiological role mediated by T-type calcium channels that would be relevant to diltiazem's action or clinical effects. *P-type Ca channels in Purkinje fibers* - **Purkinje fibers** primarily rely on **L-type calcium channels** for phase 2 of their action potential and are sensitive to diltiazem, but **P-type calcium channels** are mainly found in neurons. - P-type calcium channels are involved in **neurotransmitter release** at the presynaptic terminal, and diltiazem does not typically block these channels clinically. *N-type Ca channels in the peripheral nervous system* - **N-type calcium channels** are predominantly located in the **peripheral and central nervous systems**, where they are crucial for **neurotransmitter release** at nerve terminals. - Diltiazem's primary mechanism of action is on **L-type calcium channels**, and it has **minimal to no clinically significant effect** on N-type calcium channels.

Antihypertensives US Medical PG Question 3: A 66-year-old man with congestive heart failure presents to the emergency department complaining of worsening shortness of breath. These symptoms have worsened over the last 3 days. He has a blood pressure of 126/85 mm Hg and heart rate of 82/min. Physical examination is notable for bibasilar crackles. A chest X-ray reveals bilateral pulmonary edema. His current medications include metoprolol succinate and captopril. You wish to add an additional medication targeted towards his symptoms. Of the following, which statement is correct regarding loop diuretics?

• A. Loop diuretics can cause metabolic acidosis
• B. Loop diuretics can cause ammonia toxicity
• C. Loop diuretics can cause hyperlipidemia
• D. Loop diuretics decrease sodium, magnesium, and chloride but increase calcium
• E. Loop diuretics inhibit the action of the Na+/K+/Cl- cotransporter (Correct Answer)

Antihypertensives Explanation: ***Loop diuretics inhibit the action of the Na+/K+/Cl- cotransporter*** - Loop diuretics, like furosemide, directly block the **Na+/K+/2Cl- cotransporter** in the **thick ascending limb of the loop of Henle**, preventing the reabsorption of these ions. - This inhibition leads to increased excretion of water, sodium, potassium, and chloride, which is beneficial in conditions like **pulmonary edema** due to **congestive heart failure**. *Loop diuretics can cause metabolic acidosis* - Loop diuretics typically cause **metabolic alkalosis**, not acidosis, because they increase the excretion of hydrogen ions and potassium, leading to a compensatory increase in bicarbonate. - The increased delivery of sodium to the collecting duct can also stimulate potassium and hydrogen secretion, contributing to alkalosis. *Loop diuretics can cause ammonia toxicity* - Loop diuretics do not directly cause **ammonia toxicity**; this is more commonly associated with conditions like **hepatic encephalopathy** or certain other medications. - Their primary mechanism of action is on renal ion transport, not ammonia metabolism. *Loop diuretics can cause hyperlipidemia* - While some diuretics like **thiazide diuretics** can cause mild increases in **lipid levels**, loop diuretics are not typically associated with significant **hyperlipidemia**. - The most common metabolic side effects of loop diuretics include electrolyte imbalances. *Loop diuretics decrease sodium, magnesium, and chloride but increase calcium* - Loop diuretics decrease the reabsorption of **sodium**, **magnesium**, and **chloride**, leading to their increased excretion. - They also increase **calcium excretion** (cause hypocalcemia), rather than increasing serum calcium levels, by inhibiting its reabsorption in the thick ascending limb of the loop of Henle.

Antihypertensives US Medical PG Question 4: A 34-year-old man is being evaluated in an emergency clinic for dizziness and headache after a stressful event at work. He also reports that his face often becomes swollen and he occasionally has difficulty breathing during these spells. Family history is significant for his father who died of a stroke and his mother who often suffers from similar facial swelling. The patient’s blood pressure is 170/80 mm Hg. On physical examination, the patient appears well. Which of the following medications is most likely contraindicated in this patient?

• A. The patient has no contraindications.
• B. Enalapril (Correct Answer)
• C. Sulfadiazine
• D. Penicillin
• E. Losartan

Antihypertensives Explanation: **Enalapril** - The patient's presentation with recurrent facial swelling, occasional difficulty breathing, and a family history of similar symptoms in his mother and stroke in his father is highly suggestive of **hereditary angioedema (HAE)**. - **ACE inhibitors**, such as enalapril, are absolutely contraindicated in patients with HAE because they increase bradykinin levels, which can precipitate or worsen angioedema attacks. *The patient has no contraindications.* - The patient's history of recurrent angioedema episodes and a significant family history strongly suggest an underlying condition, likely HAE, which has clear contraindications for certain medications. - Dismissing contraindications without further investigation into the cause of his angioedema would be unsafe and medically negligent. *Sulfadiazine* - **Sulfonamide antibiotics** are not directly contraindicated in HAE. - While some individuals may have allergies to sulfa drugs, there is no specific link between sulfadiazine and triggering HAE attacks. *Penicillin* - Penicillin is a **beta-lactam antibiotic** and is not known to exacerbate or be contraindicated in hereditary angioedema. - Allergic reactions to penicillin are common, but this is a Type I hypersensitivity, distinct from bradykinin-mediated angioedema. *Losartan* - **Angiotensin Receptor Blockers (ARBs)** like losartan generally do not significantly increase bradykinin levels and are typically considered a safer alternative to ACE inhibitors in patients who might develop ACE inhibitor–induced angioedema. - While rare cases of ARB-induced angioedema have been reported, the risk is considerably lower than with ACE inhibitors, making it a less likely contraindication in this context.

Antihypertensives US Medical PG Question 5: A 53-year-old man presents to the office for a routine examination. The medical history is significant for diabetes mellitus, for which he is taking metformin. The medical records show blood pressure readings from three separate visits to fall in the 130–160 mm Hg range for systolic and 90–100 mm Hg range for diastolic. Prazosin is prescribed. Which of the following are effects of this drug?

• A. Vasodilation, decreased heart rate, bronchial constriction
• B. Vasodilation, increased peristalsis, bronchial dilation
• C. Vasoconstriction, bladder sphincter constriction, mydriasis
• D. Vasoconstriction, increase in AV conduction rate, bronchial dilation
• E. Vasodilation, bladder sphincter relaxation (Correct Answer)

Antihypertensives Explanation: ***Vasodilation, bladder sphincter relaxation*** - **Prazosin** is an **alpha-1 adrenergic receptor antagonist**, which blocks the effects of norepinephrine on vascular smooth muscle, leading to **vasodilation** and decreased blood pressure. - Blocking alpha-1 receptors in the bladder neck and prostate causes **bladder sphincter relaxation**, which can improve urine flow and is also useful in benign prostatic hyperplasia (BPH). - These are the two primary clinically relevant effects of alpha-1 blockade with prazosin. *Vasodilation, decreased heart rate, bronchial constriction* - While prazosin causes **vasodilation**, it does not typically decrease heart rate directly; alpha-1 blockade can lead to **reflex tachycardia** due to decreased blood pressure. - Prazosin has no significant effect on bronchial smooth muscle and does not cause **bronchial constriction**; bronchial effects are primarily mediated by beta-2 receptors or muscarinic (M3) receptors. *Vasodilation, increased peristalsis, bronchial dilation* - Prazosin does cause **vasodilation** but does not directly cause **increased peristalsis**; gastrointestinal motility is mainly regulated by the autonomic nervous system via muscarinic receptors and the enteric nervous system. - Prazosin does not cause **bronchial dilation**; this effect is mediated by beta-2 adrenergic receptor stimulation. *Vasoconstriction, bladder sphincter constriction, mydriasis* - Prazosin is an alpha-1 antagonist, meaning it *blocks* **vasoconstriction** and instead causes vasodilation. - Similarly, it causes **bladder sphincter relaxation**, not constriction. - Prazosin has minimal effects on pupil size; mydriasis would be caused by alpha-1 agonists or muscarinic antagonists, not alpha-1 antagonists. *Vasoconstriction, increase in AV conduction rate, bronchial dilation* - Prazosin causes **vasodilation**, not vasoconstriction. - It does not significantly affect **AV conduction rate** or directly cause **bronchial dilation**.

Antihypertensives US Medical PG Question 6: A 70-year-old Caucasian male visits your office regularly for treatment of New York Heart association class IV congestive heart failure. Which of the following medications would you add to this man's drug regimen in order to improve his overall survival?

• A. Spironolactone (Correct Answer)
• B. Furosemide
• C. Amiloride
• D. Acetazolamide
• E. Hydrochlorothiazide

Antihypertensives Explanation: ***Spironolactone*** - **Spironolactone** is an **aldosterone antagonist** that has been shown to reduce mortality and morbidity in patients with **NYHA Class III and IV heart failure**. - It works by blocking the harmful effects of **aldosterone** on the heart, such as **fibrosis** and remodeling, improving cardiac function and survival. *Furosemide* - **Furosemide** is a **loop diuretic** primarily used to relieve **symptoms of congestion** (edema, dyspnea) in heart failure by promoting fluid excretion. - While it improves symptoms, **furosemide** alone does not significantly improve long-term survival in patients with heart failure. *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that works by blocking sodium channels in the collecting duct, leading to modest diuresis. - It is often used to prevent **hypokalemia** caused by other diuretics but does not have the same proven mortality benefit in heart failure as spironolactone. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** primarily used for glaucoma, metabolic alkalosis, and altitude sickness. - It has a weaker diuretic effect and is not a commonly used or recommended medication for improving long-term survival in patients with heart failure. *Hydrochlorothiazide* - **Hydrochlorothiazide** is a **thiazide diuretic** primarily used for hypertension and mild to moderate edema. - While it can help manage fluid retention, it does not offer the same mortality benefit in advanced heart failure as aldosterone antagonists like spironolactone.

Antihypertensives US Medical PG Question 7: A 56-year-old Caucasian male presents to the clinic to establish care. He has never seen a physician and denies any known medical problems. Physical examination is notable for central obesity, but the patient has regular heart and lung sounds. He has a blood pressure of 157/95 mm Hg and heart rate of 92/min. He follows up 2 weeks later, and his blood pressure continues to be elevated. At this time, you diagnose him with essential hypertension and decide to initiate antihypertensive therapy. Per the Joint National Committee 8 guidelines for treatment of high blood pressure, of the following combinations of drugs, which can be considered for first-line treatment of high blood pressure in the Caucasian population?

• A. ACE inhibitor, ARB, CCB, or thiazide (Correct Answer)
• B. ACE inhibitor, angiotensin receptor blocker (ARB), beta-blocker (BB), or thiazide
• C. ACE inhibitor, ARB, CCB, or loop diuretic
• D. ACE inhibitor, ARB, alpha-blocker, or loop diuretic
• E. ACE inhibitor, ARB, alpha-blocker, or direct vasodilator

Antihypertensives Explanation: **ACE inhibitor, ARB, CCB, or thiazide** - The **JNC 8 guidelines** recommend **ACE inhibitors**, **ARBs**, **calcium channel blockers (CCBs)**, and **thiazide diuretics** as first-line agents for essential hypertension in the general non-Black population. - These drug classes have demonstrated efficacy in reducing cardiovascular events and are generally well-tolerated. *ACE inhibitor, angiotensin receptor blocker (ARB), beta-blocker (BB), or thiazide* - While **ACE inhibitors**, **ARBs**, and **thiazides** are first-line, **beta-blockers** are generally not considered first-line for uncomplicated hypertension unless there are specific compelling indications (e.g., post-MI, heart failure). - **Beta-blockers** are less effective than other first-line agents in preventing stroke in the elderly and may have more side effects in some populations. *ACE inhibitor, ARB, CCB or loop diuretic* - **ACE inhibitors**, **ARBs**, and **CCBs** are first-line options, but **loop diuretics** are typically reserved for patients with fluid overload or chronic kidney disease, not for initial management of essential hypertension. - **Loop diuretics** have a shorter duration of action and a greater electrolyte-wasting effect compared to thiazide diuretics, making them less suitable for long-term monotherapy. *ACE inhibitor, ARB, alpha-blocker, or loop diuretic* - **Alpha-blockers** and **loop diuretics** are not considered first-line agents for essential hypertension. **Alpha-blockers** are typically used for benign prostatic hyperplasia or as add-on therapy for resistant hypertension. - **Alpha-blockers** can cause significant orthostatic hypotension, particularly with the first dose, and have not shown the same cardiovascular protective benefits as true first-line agents. *ACE inhibitor, ARB, alpha-blocker, or direct vasodilator* - **Alpha-blockers** and **direct vasodilators** (e.g., hydralazine, minoxidil) are not first-line treatments for essential hypertension. - **Direct vasodilators** are potent but often cause reflex tachycardia and fluid retention, requiring co-administration with other agents, and are typically reserved for severe or resistant hypertension.

Antihypertensives US Medical PG Question 8: A 57-year-old otherwise healthy male presents to his primary care physician for a check-up. He has no complaints. His blood pressure at the previous visit was 160/95. The patient did not wish to be on any medications and at the time attempted to manage his blood pressure with diet and exercise. On repeat measurement of blood pressure today, the reading is 163/92. His physician decides to prescribe a medication which the patient agrees to take. The patient calls his physician 6 days later complaining of a persistent cough, but otherwise states that his BP was measured as 145/85 at a local pharmacy. Which of the following is a contraindication to this medication?

• A. Congestive heart failure
• B. Black race
• C. Bilateral renal artery stenosis (Correct Answer)
• D. Chronic obstructive pulmonary disease
• E. Gout

Antihypertensives Explanation: ***Bilateral renal artery stenosis*** - The patient's developing **cough** after starting a new antihypertensive suggests he was likely prescribed an **ACE inhibitor**. - **Bilateral renal artery stenosis** is a strong contraindication for ACE inhibitors due to the risk of precipitating **acute kidney injury**, as these medications rely on efferent arteriolar vasodilation to maintain renal perfusion when there's reduced afferent flow. *Congestive heart failure* - **ACE inhibitors** are often a **first-line treatment** for heart failure due to their ability to improve cardiac remodeling and reduce mortality. - They are used to prevent ventricular remodeling and reduce afterload, making this an indication, not a contraindication. *Black race* - While ACE inhibitors may be **less effective as monotherapy** in black patients, they are not contraindicated and can be effectively used in combination with other antihypertensives, such as **thiazide diuretics** or **calcium channel blockers**. - **African Americans** often respond better to calcium channel blockers and diuretics for hypertension but ACE inhibitors are not absolutely contraindicated. *Chronic obstructive pulmonary disease* - **ACE inhibitors** are **not contraindicated** in COPD, as they do not affect bronchial smooth muscle tone. - **Beta-blockers**, not ACE inhibitors, are typically avoided or used with caution in patients with reactive airway diseases like asthma or severe COPD. *Gout* - **ACE inhibitors** do not significantly impact **uric acid levels** and are generally safe for use in patients with gout. - In contrast, **thiazide diuretics** can increase uric acid levels and worsen gout, but this is not the medication indicated by the patient's cough.

Antihypertensives US Medical PG Question 9: A physician is choosing whether to prescribe losartan or lisinopril to treat hypertension in a 56-year-old male. Relative to losartan, one would expect treatment with lisinopril to produce which of the following changes in the circulating levels of these peptides?

• A. Aldosterone increase; bradykinin decrease
• B. Angiotensin II increase; bradykinin decrease
• C. Renin decrease; angiotensin I increase
• D. Bradykinin increase; angiotensin II decrease (Correct Answer)
• E. Renin decrease; angiotensin II increase

Antihypertensives Explanation: ***Bradykinin increase; angiotensin II decrease*** - **Lisinopril** is an **ACE inhibitor**, which directly blocks the conversion of **angiotensin I** to **angiotensin II**, leading to a decrease in circulating **angiotensin II** levels. - ACE is also responsible for the breakdown of **bradykinin**, so inhibiting ACE with lisinopril will lead to an **increase in bradykinin** levels, contributing to vasodilation but also the characteristic cough. *Aldosterone increase; bradykinin decrease* - **Lisinopril** (an ACE inhibitor) decreases **angiotensin II**, which in turn leads to a **decrease in aldosterone** synthesis and release, not an increase. - **Bradykinin** levels would increase due to ACE inhibition, as ACE is involved in its degradation. *Angiotensin II increase; bradykinin decrease* - **Lisinopril** directly inhibits the enzyme responsible for producing **angiotensin II**, thus leading to its **decrease**, not an increase. - **Bradykinin** levels would increase because its degradation pathway (via ACE) is blocked, not decrease. *Renin decrease; angiotensin I increase* - **Lisinopril** reduces the negative feedback on **renin** release, leading to an **increase in renin** levels, not a decrease. - While ACE is inhibited by lisinopril, this leads to an accumulation of its substrate, **angiotensin I**, resulting in an increase of angiotensin I. *Renin decrease; angiotensin II increase* - As an ACE inhibitor, lisinopril would lead to an **increase in renin** due to reduced negative feedback from angiotensin II, not a decrease. - **Angiotensin II** levels would **decrease** because its production from angiotensin I is directly inhibited by lisinopril.

Antihypertensives US Medical PG Question 10: A 58-year-old woman presents to her physician complaining of a headache in the occipital region for 1 week. Past medical history is significant for essential hypertension, managed with lifestyle modifications and 2 antihypertensives for the previous 6 months. Her blood pressure is 150/90 mm Hg. Neurological examination is normal. A third antihypertensive drug is added that acts as a selective α2 adrenergic receptor agonist. On follow-up, she reports that she does not have any symptoms and her blood pressure is 124/82 mm Hg. Which of the following mechanisms best explains the therapeutic effect of this new drug in this patient?

• A. Vasodilation of peripheral arteries
• B. Vasodilation of peripheral arteries and peripheral veins
• C. Decreased peripheral sympathetic outflow (Correct Answer)
• D. Negative inotropic effect on the heart
• E. Vasodilation of peripheral veins

Antihypertensives Explanation: ***Decreased peripheral sympathetic outflow*** - Selective **α2 adrenergic receptor agonists** (e.g., clonidine, guanfacine, methyldopa) act **centrally in the brainstem** (nucleus tractus solitarius and rostral ventrolateral medulla) to reduce **sympathetic nervous system activity**. - This **central action** leads to a **decrease in peripheral sympathetic outflow**, resulting in reduced heart rate, decreased cardiac output, and peripheral vasodilation, all contributing to lower blood pressure. - This is the **primary mechanism** of antihypertensive action for central α2 agonists. *Vasodilation of peripheral arteries* - While central α2 agonists do cause some peripheral vasodilation, this is an **indirect effect** of **reduced sympathetic tone**, not a primary direct action on peripheral arteries. - Their main mechanism of action is **central**, decreasing the overall sympathetic drive to the vasculature. *Vasodilation of peripheral arteries and peripheral veins* - This option describes a broader effect, and while some vasodilation occurs, it doesn't pinpoint the **primary mechanism of action** of central α2 agonists. - Drugs like alpha-1 blockers (prazosin, doxazosin) or direct vasodilators (hydralazine, minoxidil) would have a more pronounced direct effect on both arterial and venous smooth muscle. *Negative inotropic effect on the heart* - While central α2 agonists can **reduce heart rate** (bradycardia) and cardiac output due to decreased sympathetic stimulation, a **negative inotropic effect** (decreased myocardial contractility) is not their primary or most significant mechanism. - **Beta-blockers** are primarily known for their negative inotropic and chronotropic effects on the heart. *Vasodilation of peripheral veins* - Similar to arterial vasodilation, this is an **indirect effect** of **reduced sympathetic tone**, not the primary mechanism of action of central α2 agonists. - Direct venodilators like **nitrates** would primarily target peripheral veins to reduce preload.

Antihypertensives Flashcard 1 of 10

Question: What effect does clonidine have on blood pressure? _____

Answer: Decreased (via reduced sympathetic tone)

Antihypertensives Flashcard 2 of 10

Question: ACE inhibitors are a first line agent in the treatment of primary _____

Answer: hypertension

Antihypertensives Flashcard 3 of 10

Question: First Aid Pharmacology: Cardiovascular/RenalACE inhibitors may cause angioedema due to increased _____

Answer: bradykinin

Antihypertensives Flashcard 4 of 10

Question: First Aid Pharmacology: Renal (Diuretics) The potent diuretic effects of loop diuretics may lead to significant volume loss and thus _____

Answer: dehydration

Antihypertensives Flashcard 5 of 10

Question: Selective 1 adrenergic antagonists (except tamsulosin) may be used to treat _____ (BP)

Answer: hypertension

Antihypertensives Flashcard 6 of 10

Question: IV Ca2+ channel blockers, such as nicardipine and clevidipine, cause _____ dilation, which is useful for the treatment of hypertensive emergency

Answer: arteriolar

Antihypertensives Flashcard 7 of 10

Question: ACE inhibitors

Answer: renal damage

Antihypertensives Flashcard 8 of 10

Question: What is the mechanism of action of minoxidil? _____

Answer: Direct arteriolar vasodilator

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Antihypertensives Flashcard 9 of 10

Question: _____-dilators (e.g. hydralazine) cause decreased after-load

Answer: Vaso

Extra Information:  Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/pressure-volume-loops?index=4] https://onlinemeded.org/spa/cardiology/heart-failure/acquire?ref=anki 

Antihypertensives Flashcard 10 of 10

Question: _____ channel blockers are useful for treating hypertension

Answer: Ca2+

Extra Information:   Sketchy Pharmacology: Cardiovascular Watch Calcium channel blockers [https://dashboard.sketchy.com/study/medical/courses/medical-pharmacology/units/medical-pharmacology-cardiovascular-renal/videos/medical-pharmacology-cardiovascular-and-renal-antihypertensives-calcium-channel-blockers?utm_source=anki&utm_medium=partnership&utm_campaign=february_update&utm_content=medical]Watch associated Bootcamp video [https://app.bootcamp.com/med-school/cardiology/videos/vasodilation-and-vasoconstriction?index=8] https://onlinemeded.org/spa/cardiac?ref=anki