Part 9.1C-HTN-CLASSES OF DRUGS part 1

[DIURETICS]

The mechanism of action of diuretics is to:
a. Promote urinary excretion of water ± electrolytes
b. Increase platelet aggregation
c. Block pain perception
d. Increase cholesterol synthesis

a. Promote urinary excretion of water ± electrolytes

[DIURETICS]

Diuretics are classified mainly based on:
a. Chemical structure only
b. Site of action in the renal tubule
c. Color of the drug
d. Duration of sleep

b. Site of action in the renal tubule

[DIURETICS]

Osmotic diuretics site of action

a. Proximal convoluted tubule

b. Early Portion of Loop of Henle

c. Late Portion of Loop of Henle

d. Distal convoluted tubule

e. Collecting duct/tubule

a. Proximal convoluted tubule &

b. Early Portion of Loop of Henle

[DIURETICS]

Carbonic anhydrase inhibitors site of action

a. Proximal convoluted tubule

b. Early Portion of Loop of Henle

c. Late Portion of Loop of Henle

d. Distal convoluted tubule

e. Collecting duct/tubule

a. Proximal convoluted tubule

[DIURETICS]

Xanthines site of action

a. Proximal convoluted tubule

b. Early Portion of Loop of Henle

c. Late Portion of Loop of Henle

d. Distal convoluted tubule

e. Collecting duct/tubule

a. Proximal convoluted tubule

[DIURETICS]

Acidifying salts site of action

a. Proximal convoluted tubule

b. Early Portion of Loop of Henle

c. Late Portion of Loop of Henle

d. Distal convoluted tubule

e. Collecting duct/tubule

a. Proximal convoluted tubule

[DIURETICS]

Loop diuretic site of action

a. Proximal convoluted tubule

b. Early Portion of Loop of Henle

c. Late Portion of Loop of Henle

d. Distal convoluted tubule

e. Collecting duct/tubule

c. Late Portion of Loop of Henle

[DIURETICS]

Thiazides site of action

a. Proximal convoluted tubule

b. Early Portion of Loop of Henle

c. Late Portion of Loop of Henle

d. Distal convoluted tubule

e. Collecting duct/tubule

d. Distal convoluted tubule

[DIURETICS]

Potassium-sparring diuretic site of action

a. Proximal convoluted tubule

b. Early Portion of Loop of Henle

c. Late Portion of Loop of Henle

d. Distal convoluted tubule

e. Collecting duct/tubule

e. Collecting duct/tubule

[DIURETICS]

Loop diuretics are also known as:
a. Potassium-sparing diuretics
b. Carbonic anhydrase inhibitors
c. High ceiling diuretics
d. Osmotic diuretics

c. High ceiling diuretics

[DIURETICS: Loop]

Sulfonamide
a. Furosemide
b. Ethacrynic acid
c. Torsemide only
d. Spironolactone

a. Furosemide

[DIURETICS: Loop]

Sulfonamide
a. Hydrochlorothiazide
b. Ethacrynic acid
c. Torsemide only
d. Bumetanide

d. Bumetanide

[DIURETICS: Loop]

Sulfonylurea
a. Furosemide
b. Ethacrynic acid
c. Torsemide only
d. Spironolactone

c. Torsemide only

[DIURETICS: Loop]

Phenoxyacetatic acid
a. Furosemide
b. Ethacrynic acid
c. Torsemide only
d. Spironolactone

b. Ethacrynic acid

[DIURETICS]

Loop diuretics MOA
a. NCC (Na-Cl cotransporter)
b. NKCC2 (Na-K-2Cl cotransporter)
c. ENaC channel
d. Na/H exchanger

b. NKCC2 (Na-K-2Cl cotransporter)

[DIURETICS]

Loop diuretics exert their action mainly at the:
a. Proximal convoluted tubule
b. Collecting duct
c. Distal convoluted tubule
d. Thick ascending limb of the loop of Henle

d. Thick ascending limb of the loop of Henle

[DIURETICS]

The initial vascular effect of loop diuretics is:
a. Peripheral vasoconstriction
b. Peripheral venodilation
c. Bronchodilation
d. Platelet aggregation

b. Peripheral venodilation

[DIURETICS]

produced by loop diuretics
a. Diuresis
b. Natriuresis
c. Kaliuresis
d. All of the above

d. All of the above

[DIURETICS]

Loop diuretics increase urinary excretion of:
a. Calcium and magnesium
b. Cholesterol
c. Glucose
d. Platelets

a. Calcium and magnesium

[DIURETICS]

Loop diuretics are used as an adjunct in management of:
a. Hypertensive emergency complicated by pulmonary edema
b. Viral fever complicated by pulmonary edema
c. Bacterial infection complicated by pulmonary edema
d. Hypercholesterolemia

a. Hypertensive emergency complicated by pulmonary edema

[DIURETICS]

excessive loop diuretic use
a. Dehydration and hypotension
b. Hypertension only
c. Hyperkalemia only
d. Bradycardia only

a. Dehydration and hypotension

[DIURETICS]

A serious toxicity associated with loop diuretics is:
a. Ototoxicity only
b. Hepatotoxicity only
c. Nephrotoxicity
d. Seizures only

a. Ototoxicity only

[DIURETICS]

Electrolyte imbalance may occur with loop diuretics

a. Hypokalemia

b. Hypernatremia

c. Hypomagnesemia

d. Hyponatremia

e. Hyperkalemia

f. Hypercalcemia

g. Hypoglucemia

a. Hypokalemia
c. Hypomagnesemia

d. Hyponatremia

[DIURETICS]

Metabolic imbalance may occur with loop diuretics

a. Hypokalemia

b. Hyperuricemia

c. Hypomagnesemia

d. Dyslipidemia

e. Hyperkalemia

f. Hypercalcemia

g. Hypoglycemia

h. Hyperglycemia

b. Hyperuricemia

h. Hyperglycemia

d. Dyslipidemia

[DIURETICS: loop]

Sulfa-associated (sulfonamide, sulfonylurea):

I. hypersensitivity

II. SLE

III. SJS-TEN

IV. dermatologic reactions

V. hepatotoxicity

VI. aplastic anemia

VII. hematologic reactions

I. hypersensitivity

III. SJS-TEN

IV. dermatologic reactions

VI. aplastic anemia

VII. hematologic reactions

[DIURETICS: Thiazide]

Thiazide diuretics primarily include:
a. Benzothiadiazides and sulfonamide thiazide-like diuretics
b. Sulfonylurea and Sulfonamide
c. Phenoxyacetatic Acid
d. Potassium-sparing diuretics

a. Benzothiadiazides and sulfonamide thiazide-like diuretics

[DIURETICS: Thiazide]

Benzothiadiazide
a. Hydrochlorothiazide (HCTZ)
b. Chlorthalidone
c. Metolazone
d. Indapamide

a. Hydrochlorothiazide (HCTZ)

[DIURETICS: Thiazide]

Benzothiadiazide
a. Chlorothiazide
b. Chlorthalidone
c. Metolazone
d. Indapamide

a. Chlorothiazide

[DIURETICS: Thiazide]

Sulfonamide thiazide-like
a. Chlorothiazide
b. Chlorthalidone
c. HCTZ
d. Furosemide

b. Chlorthalidone

[DIURETICS: Thiazide]

Sulfonamide thiazide-like
a. Chlorothiazide
b. HCTZ
c. Metolazone
d. Bumetanide

c. Metolazone

[DIURETICS: Thiazide]

Sulfonamide thiazide-like
a. Chlorothiazide
b. Torsemide
c. HCTZ
d. Indapamide

d. Indapamide

[DIURETICS]

Thiazide MOA

a.Inhibit NKCC2 (Na-K-2Cl cotransporter)

b. Inhibit vesicular uptake and storage of catecholamine

c. Inhibit exocytosis of norepinephrine

d. Inhibit Na⁺—Cl^- symporter

d. Inhibit Na⁺—Cl^- symporter at DCT

[DIURETICS]

During the first 2 weeks of thiazide diuretic therapy, the main effects are:
a. Diuresis and natriuresis
b. Vasoconstriction
c. Vasodilation
d. Bronchodilation

a. Diuresis and natriuresis

[DIURETICS]

Beyond 2 weeks of thiazide diuretic therapy, the main effects are:

a. Diuresis and natriuresis
b. Vasoconstriction
c. Vasodilation
d. Bronchodilation

c. Vasodilation

increased vascular compliance → vasodilation

[DIURETICS]

Thiazide diuretics are considered:
a. Second-line therapy
b. Used in emergencies
c. Contraindicated in HTN
d. Among the first-line therapies for hypertension

d. Among the first-line therapies for hypertension

[DIURETICS]

Thiazide diuretics in hypertension are commonly given at:
a. High doses to maximize natriuresis
b. Intermittent weekly doses
c. Toxic doses only
d. Low doses to lower risk of hyponatremia

d. Low doses to lower risk of hyponatremia

[DIURETICS]

The usual low dose of hydrochlorothiazide (HCTZ) in HTN management is:
a. 15mg/day
b. 100 mg/day
c. 25 mg/day
d. 50 mg/day

c. 25 mg/day

[DIURETICS]

The recommended dose of indapamide in HTN management is:
a. ≤5 mg/day
b. 25 mg/day
c. 50 mg/day
d. 100 mg/day

a. ≤5 mg/day

[DIURETICS]

Thiazide diuretics are commonly used:
a. Alone only and never combined
b. Combined with other antihypertensives

b. Combined with other antihypertensives

[DIURETICS]

Thiazide diuretics have adverse effects similar to:
a. Opioids
b. Loop diuretics
c. Antimalarials
d. Anticoagulants

b. Loop diuretics

[DIURETICS]

Electrolyte abnormality is more prominent with thiazides, especially at higher doses
a. Hypernatremia
b. Hyponatremia
c. Hyperkalemia
d. Hypercalcemia

b. Hyponatremia

[DIURETICS]

Potassium-sparing diuretics are classified based on:
a. Structure
b. MOA
c. Duration of action
d. Onset of action

b. MOA

[DIURETICS: K+ sparring]

Aldosterone antagonists:

I. Spironolactone

II. Triamterene

III. Amiloride

IV. Spironolactone

I. Spironolactone

IV. Spironolactone

[DIURETICS: K+ sparring]

Direct NaCl transport inhibitors

I. Spironolactone

II. Triamterene

III. Amiloride

IV. Spironolactone

II. Triamterene

III. Amiloride

[DIURETICS]

Potassium-sparing diuretics are useful in resistant hypertension associated with:
a. Hyperaldosteronism
b. Hyperglycemia
c. Hyperthyroidism
d. Hypercholesterolemia

a. Hyperaldosteronism

[DIURETICS]

Potassium-sparing diuretics are commonly given with:
a. Osmotic diuretics
b. CAI
c. Thiazide or loop diuretics
d. Xanthines

c. Thiazide or loop diuretics

[DIURETICS]

Why are potassium-sparing diuretics combined with thiazide or loop diuretics?
a. To prevent or treat diuretic-induced hypoglycemia
b. To prevent or treat diuretic-induced hypokalemia
c. To prevent or treat diuretic-induced hypernatremia
d. To prevent or treat diuretic-induced HTN

b. To prevent or treat diuretic-induced hypokalemia

[DIURETICS]

A major adverse effect of potassium-sparing diuretics is:
a. Hyperkalemia
b. Hypokalemia
c. Respiratory depression
d. Hyperuricemia

a. Hyperkalemia

[DIURETICS]

Potassium-sparing diuretic that may cause anti-androgenic effects
a. Spironolactone
b. Amiloride
c. Triamterene
d. Eplerenone

a. Spironolactone

anti-androgenic effects→ gynecomastia

[DIURETICS]

Gynecomastia is a known adverse effect of:
a. Hydrochlorothiazide
b. Spironolactone
c. Furosemide
d. Metolazone

b. Spironolactone

[DIURETICS]

Potassium-sparing diuretic may cause renal stone formation due to drug precipitation
a. Eplerenone
b. Amiloride
c. Triamterene
d. Spironolactone

c. Triamterene

[DIURETICS]

Carbonic anhydrase inhibitors are structurally classified as:
a. Sulfonamides
b. Opioids
c. Benzodiazepines
d. Macrolides

a. Sulfonamides

[DIURETICS]

Prototype carbonic anhydrase inhibitor
a. Acetazolamide
b. Dorzolamide
c. Methazolamide
d. Brinzolamide

a. Acetazolamide

[DIURETICS]

carbonic anhydrase inhibitor

I. Furosemide

II. Acetazolamide

III. Brinzolamide

IV. Dorzolamide

V. Methazolamide

VI. Bumetanide

VII. Dichlorphenamide

II. Acetazolamide

III. Brinzolamide

IV. Dorzolamide

V. Methazolamide

VII. Dichlorphenamide

I and VI are sulfonamides also but classified as Loop diuretics

[DIURETICS]

Carbonic anhydrase MOA
a. Blocking NKCC2 transporter
b. Inhibiting carbonic anhydrase enzyme
c. Blocking aldosterone receptors
d. Stimulating carbonic anhydrase enzyme

b. Inhibiting carbonic anhydrase enzyme

[DIURETICS]

Inhibition of carbonic anhydrase results in:
a. Increased bicarbonate reabsorption
b. Increased glucose reabsorption
c. Inhibition of bicarbonate resorption
d. Potassium retention

c. Inhibition of bicarbonate resorption by tubular cells leading to bicarbonate retention in tubules

[DIURETICS]

produced by carbonic anhydrase inhibitors

I. Natriuresis

II. Hyponatremia

III. Diuresis

IV. Ototoxicity

V. Bicarbonaturia

I. Natriuresis
III. Diuresis
V. Bicarbonaturia

[DIURETICS]

Carbonic anhydrase inhibitors lower aqueous humor production at the:
a. Retina
b. Cornea
c. Ciliary body
d. Optic nerve

c. Ciliary body of the eye

[DIURETICS]

Carbonic anhydrase inhibitors are used in the management of:
a. Glaucoma
b. Hypercholesterolemia
c. Acute MI
d. Gout

a. Glaucoma (Open-angle glaucoma)

[DIURETICS]

Acetazolamide is specifically used in the management of:
a. Acute mountain sickness
b. Hyperthyroidism
c. Diabetes mellitus
d. Acute diarrhea

a. Acute mountain sickness

[DIURETICS]

Acetazolamide may also be used for:
a. Certain seizure disorders/epilepsy
b. Platelet inhibition
c. Hyperlipidemia
d. Anticoagulation

a. Certain seizure disorders/epilepsy

[DIURETICS]

Acetazolamide is useful in the management of:
a. Metabolic alkalosis
b. Metabolic acidosis

a. Metabolic alkalosis

[DIURETICS]

Hematologic ADR of Acetazolamide

a. Aplastic anemia
b. Thrombocytopenia
c. Leukopenia
d. All of the above

d. AOTA

[DIURETICS]

Dermatologic ADR of Acetazolamide

a. SJS-TEN only
b. Acne only
c. Alopecia only
d. Vitiligo only

a. SJS-TEN only

[DIURETICS]

Carbonic anhydrase inhibitors may reduce the efficacy of:
a. Lithium
b. Aspirin
c. Morphine
d. Atropine

a. Lithium

[DIURETICS]

Carbonic anhydrase inhibitors reduce activation of:
a. Digoxin
b. Warfarin
c. Methenamine mandelate
d. Clopidogrel

c. Methenamine mandelate

[DIURETICS]

A metabolic adverse effect of carbonic anhydrase inhibitors is:
a. Metabolic acidosis
b. Metabolic alkalosis

a. Metabolic acidosis

[DIURETICS]

Carbonic anhydrase inhibitors are contraindicated in patients with:
a. Migraine
b. Hypertension
c. Hyperlipidemia
d. COPD

d. COPD

[DIURETICS]

osmotic diuretic
a. Mannitol
b. Furosemide
c. Hydrochlorothiazide
d. Spironolactone

a. Mannitol

[DIURETICS]

Mannitol acts primarily by:
a. Blocking NKCC2 transporter across the renal tubule to prevent sodium reabsorption
b. Increasing osmotic gradient across the renal tubule to prevent water reabsorption
c. Blocking aldosterone receptors across the renal tubule to prevent potassium reabsorption
d. Inhibiting carbonic anhydrase across the renal tubule to prevent potassium reabsorption

b. Increasing osmotic gradient across the renal tubule to prevent water reabsorption

[DIURETICS]

Mannitol mainly acts in which renal segments?
a. Distal convoluted tubule and late loop of Henle
b. Collecting duct and early loop of Henle
c. Proximal convoluted tubule and early loop of Henle
d. Thick ascending limb and late loop of Henle

c. Proximal convoluted tubule and early loop of Henle

[DIURETICS]

Mannitol is commonly used in the management of:
a. Intracerebral edema and increased intracranial pressure
b. Hypercholesterolemia and increased intracerebral edema
c. Acute gout and increased intracranial edema
d. Osteoarthritis and intracerebral edema

a. Intracerebral edema and increased intracranial pressure

[DIURETICS]

Mannitol may be used in certain cases of:
a. Poisoning and rhabdomyolysis
b. Open angle glaucoma
c. Osteoporosis
d. Rheumatoid arthritis

a. Poisoning and rhabdomyolysis

[DIURETICS]

Mannitol can induce urinary excretion of metals such as:
a. Potassium or cisplatin
b. Calcium or zinc
c. Iron or zinc
d. Platinum or cisplatin

d. Platinum or cisplatin

[DIURETICS]

A metabolic/electrolyte adverse effect of mannitol is:
a. Hypovolemic Hypoglycemia
b. Hypovolemic Hyperkalemia
c. Hypovolemic Hyponatremia
d. Hypovolemic Hypernatremia

d. Hypovolemic Hypernatremia

[DIURETICS]

ADR of mannitol

a. Increased risk of Hepatic necrosis
b. Increased risk of Respiratory depression
c. Increased risk of Pulmonary edema
d. Increased risk of Platelet aggregation

c. Increased risk of Pulmonary edema

[SYMPATHOPLEGICS: Peripherally acting]

Adrenergic neuron blockers

a. Reserpine
b. Propranolol
c. Prazosin
d. Atenolol

a. Reserpine

[SYMPATHOPLEGICS: Peripherally acting]

Adrenergic neuron blockers

a. Nebivolol
b. Propranolol
c. Prazosin
d. Guanethidine

d. Guanethidine

[SYMPATHOPLEGICS: Peripherally acting]

Reserpine and related agents MOA
a. Inhibit exocytosis of norepinephrine
b. Inhibiting vesicular uptake and storage of catecholamines
c. Blocking β1 receptors only in the heart
d. Stimulating norepinephrine release

b. Inhibiting vesicular uptake and storage of catecholamines

[SYMPATHOPLEGICS: Peripherally acting]

Guanethidine and related agents MOA
a. Inhibit exocytosis of norepinephrine
b. Inhibiting vesicular uptake and storage of catecholamines
c. Blocking β1 receptors only in the heart
d. Stimulating norepinephrine release

a. Inhibit exocytosis of norepinephrine

[SYMPATHOPLEGICS: Peripherally acting]

Adrenergic neuron blockers were primarily used for:
a. Management of hypertension
b. Acute pain relief
c. Hypercholesterolemia
d. Seizure disorders

a. Management of hypertension

[SYMPATHOPLEGICS: Peripherally acting]

A common adverse effect of adrenergic neuron blockers is:
a. Respiratory depression
b. Hyperglycemia
c. Postural hypotension
d. Ototoxicity

c. Postural hypotension

[SYMPATHOPLEGICS: Peripherally acting]

Ganglionic blockers are

a. First-line antihypertensives today
b. No longer commonly used
c. Used only in glaucoma
d. Used for acute gout

b. No longer commonly used

[SYMPATHOPLEGICS: Peripherally acting]

The antihypertensive effect of beta blockers is mainly due to blockade of:
a. α1 receptors
b. β1 receptors
c. D2 receptors
d. Muscarinic receptors

b. β1 receptors

[SYMPATHOPLEGICS: Peripherally acting]

Blocking cardiac β1 receptors causes:
a. Increased heart rate and inotropism
b. Decreased inotropism and HR
c. Increased vasoconstriction
d. Decreased dromotropism and HR

b. Decreased inotropism and heart rate leading to decreased cardiac output

• Block cardiac β1 receptors → ↓ inotropism and HR → ↓ CO

• Block β1 in JG apparatus → ↓ renin release

[SYMPATHOPLEGICS: Peripherally acting]

Beta blockers decrease blood pressure partly by reducing:
a. Cardiac output (CO)
b. Platelet count
c. Glucose uptake
d. Aqueous humor production

a. Cardiac output (CO)

• Block cardiac β1 receptors → ↓ inotropism and HR → ↓ CO

• Block β1 in JG apparatus → ↓ renin release

[SYMPATHOPLEGICS: Peripherally acting]

This structure contains β1 receptors involved in renin release
a. Ciliary body
b. Juxtaglomerular (JG) apparatus
c. Synovium
d. Loop of Henle

b. Juxtaglomerular (JG) apparatus

• Block cardiac β1 receptors → ↓ inotropism and HR → ↓ CO

• Block β1 in JG apparatus → ↓ renin release

[SYMPATHOPLEGICS: Peripherally acting]

Blocking β1 receptors in the JG apparatus results in:
a. Increased renin release
b. Decreased renin release

b. Decreased renin release

• Block cardiac β1 receptors → ↓ inotropism and HR → ↓ CO

• Block β1 in JG apparatus → ↓ renin release

[SYMPATHOPLEGICS: Peripherally acting]

Beta blockers are beneficial in hypertensive patients with concurrent:
a. Hyperthyroidism, anxiety episodes, hypersympathetic stimulation
b. Acute gout, COPD, anxiety episodes
c. COPD, chronic gout, hypothyroidism
d. CAD, anxiety episodes, hypersympathetic stimulation

d. CAD, anxiety episodes, hypersympathetic stimulation

[SYMPATHOPLEGICS: Peripherally acting]

preferred in hypertensive crisis because of its very short half-life
a. Atenolol
b. Metoprolol
c. Esmolol
d. Nebivolol

c. Esmolol

[SYMPATHOPLEGICS: Peripherally acting]

preferred for hypertension during pregnancy
a. Propranolol
b. Atenolol
c. Labetalol
d. Esmolol

c. Labetalol

[SYMPATHOPLEGICS: Peripherally acting]

Abrupt withdrawal of beta blockers may result in:
a. Rebound hypertension and tachycardia
b. Severe hypoglycemia and tachycardia
c. Hypernatremia and bradycardia
d. Respiratory depression and bradycardia

a. Rebound hypertension and tachycardia

[SYMPATHOPLEGICS: Peripherally acting]

Alpha blocker

a. Prazosin
b. Atenolol
c. Propranolol
d. Metoprolol

a. Prazosin

[SYMPATHOPLEGICS: Peripherally acting]

Alpha blocker

a. Phentolamine
b. Hydrochlorothiazide
c. Furosemide
d. Labetalol

a. Phentolamine

[SYMPATHOPLEGICS: Peripherally acting]

Alpha blockers lower blood pressure mainly by:
a. Blocking α2 receptors in blood vessels causing vasodilation
b. Blocking α1 receptors in blood vessels causing vasodilation
c. Blocking α1 receptors in blood vessels causing vasoconstriction
d. Blocking α2 receptors in blood vessels causing vasoconstriction

b. Blocking α1 receptors in blood vessels causing vasodilation

[SYMPATHOPLEGICS: Peripherally acting]

Alpha blockers are useful in hypertension associated with:
a. Pheochromocytoma
b. Hyperlipidemia
c. Acute mountain sickness
d. Osteoarthritis

a. Pheochromocytoma

[SYMPATHOPLEGICS: Peripherally acting]

Which condition makes alpha blockers beneficial in hypertensive patients?
a. Glaucoma
b. Diabetes mellitus
c. BPH
d. Viral fever

c. BPH

[SYMPATHOPLEGICS: Peripherally acting]

Classically associated with alpha blockers
a. Hyperglycemia
b. Ototoxicity
c. Respiratory depression
d. First-dose phenomenon

d. First-dose phenomenon

[SYMPATHOPLEGICS: Centrally acting]

Clonidine is classified as a:
a. Central α1 agonist
b. Central α2 antagonist
c. Central α2 agonist
d. Central α1 antagonist

c. Central α2 agonist

[SYMPATHOPLEGICS: Centrally acting]

Clonidine lowers blood pressure mainly by:
a. Blocking α2 receptors
b. Stimulating central α2 receptors
c. Blocking α1 receptors
d. Stimulating central α1 receptors

b. Stimulating central α2 receptors → decreased release of central norepinephrine (NE)