Part 9.1C-HTN-CLASSES OF DRUGS part 1

Proverbs 16:3

a. Promote urinary excretion of water ± electrolytes

[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

b. Site of action in the renal tubule

[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

a. Proximal convoluted tubule &

b. Early Portion of Loop of Henle

[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

[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

c. Late Portion of Loop of Henle

[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

d. Distal convoluted tubule

[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

e. Collecting duct/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

c. High ceiling diuretics

[DIURETICS]

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

a. Furosemide

[DIURETICS: Loop]

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

d. Bumetanide

[DIURETICS: Loop]

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

c. Torsemide only

[DIURETICS: Loop]

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

b. Ethacrynic acid

[DIURETICS: Loop]

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

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

[DIURETICS]

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

d. Thick ascending limb of the loop of Henle

[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

b. Peripheral venodilation

[DIURETICS]

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

d. All of the above

[DIURETICS]

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

a. Calcium and magnesium

[DIURETICS]

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

a. Hypertensive emergency complicated by pulmonary edema

[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. Dehydration and hypotension

[DIURETICS]

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

a. Ototoxicity only

[DIURETICS]

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

a. Hypokalemia
c. Hypomagnesemia

d. Hyponatremia

[DIURETICS]

Electrolyte imbalance may occur with loop diuretics

a. Hypokalemia

b. Hypernatremia

c. Hypomagnesemia

d. Hyponatremia

e. Hyperkalemia

f. Hypercalcemia

g. Hypoglucemia

b. Hyperuricemia

h. Hyperglycemia

d. Dyslipidemia

[DIURETICS]

Metabolic imbalance may occur with loop diuretics

a. Hypokalemia

b. Hyperuricemia

c. Hypomagnesemia

d. Dyslipidemia

e. Hyperkalemia

f. Hypercalcemia

g. Hypoglycemia

h. Hyperglycemia

I. hypersensitivity

III. SJS-TEN

IV. dermatologic reactions

VI. aplastic anemia

VII. hematologic reactions

[DIURETICS: loop]

Sulfa-associated (sulfonamide, sulfonylurea):

I. hypersensitivity

II. SLE

III. SJS-TEN

IV. dermatologic reactions

V. hepatotoxicity

VI. aplastic anemia

VII. hematologic reactions

a. Benzothiadiazides and sulfonamide thiazide-like diuretics

[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. Hydrochlorothiazide (HCTZ)

[DIURETICS: Thiazide]

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

a. Chlorothiazide

[DIURETICS: Thiazide]

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

b. Chlorthalidone

[DIURETICS: Thiazide]

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

c. Metolazone

[DIURETICS: Thiazide]

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

d. Indapamide

[DIURETICS: Thiazide]

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

d. Inhibit Na⁺—Cl^- symporter at DCT

[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

a. Diuresis and natriuresis

[DIURETICS]

During the first 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]

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

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

d. Among the first-line therapies for hypertension

[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. Low doses to lower risk of hyponatremia

[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

c. 25 mg/day

[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

a. ≤5 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

b. Combined with other antihypertensives

[DIURETICS]

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

b. Loop diuretics

[DIURETICS]

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

b. Hyponatremia

[DIURETICS]

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

b. MOA

[DIURETICS]

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

I. Spironolactone

IV. Spironolactone

[DIURETICS: K+ sparring]

Aldosterone antagonists:

I. Spironolactone

II. Triamterene

III. Amiloride

IV. Spironolactone

II. Triamterene

III. Amiloride

[DIURETICS: K+ sparring]

Direct NaCl transport inhibitors

I. Spironolactone

II. Triamterene

III. Amiloride

IV. Spironolactone

a. Hyperaldosteronism

[DIURETICS]

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

c. Thiazide or loop diuretics

[DIURETICS]

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

b. To prevent or treat diuretic-induced hypokalemia

[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

a. Hyperkalemia

[DIURETICS]

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

a. Spironolactone

anti-androgenic effects→ gynecomastia

[DIURETICS]

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

b. Spironolactone

[DIURETICS]

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

c. Triamterene

[DIURETICS]

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

a. Sulfonamides

[DIURETICS]

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

a. Acetazolamide

[DIURETICS]

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

II. Acetazolamide

III. Brinzolamide

IV. Dorzolamide

V. Methazolamide

VII. Dichlorphenamide

I and VI are sulfonamides also but classified as Loop diuretics

[DIURETICS]

carbonic anhydrase inhibitor

I. Furosemide

II. Acetazolamide

III. Brinzolamide

IV. Dorzolamide

V. Methazolamide

VI. Bumetanide

VII. Dichlorphenamide

b. Inhibiting carbonic anhydrase enzyme

[DIURETICS]

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

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

[DIURETICS]

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

I. Natriuresis
III. Diuresis
V. Bicarbonaturia

[DIURETICS]

produced by carbonic anhydrase inhibitors

I. Natriuresis

II. Hyponatremia

III. Diuresis

IV. Ototoxicity

V. Bicarbonaturia

c. Ciliary body of the eye

[DIURETICS]

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

a. Glaucoma (Open-angle glaucoma)

[DIURETICS]

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

a. Acute mountain sickness

[DIURETICS]

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

a. Certain seizure disorders/epilepsy

[DIURETICS]

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

a. Metabolic alkalosis

[DIURETICS]

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

d. AOTA

[DIURETICS]

Hematologic ADR of Acetazolamide

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

a. SJS-TEN only

[DIURETICS]

Dermatologic ADR of Acetazolamide

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

a. Lithium

[DIURETICS]

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

c. Methenamine mandelate

[DIURETICS]

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

a. Metabolic acidosis

[DIURETICS]

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

d. COPD

[DIURETICS]

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

a. Mannitol

[DIURETICS]

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

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

[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

c. Proximal convoluted tubule and early loop of Henle

[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

a. Intracerebral edema and increased intracranial pressure

[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. Poisoning and rhabdomyolysis

[DIURETICS]

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

d. Platinum or cisplatin

[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. Hypovolemic Hypernatremia

[DIURETICS]

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

c. Increased risk of Pulmonary edema

[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

a. Reserpine

[SYMPATHOPLEGICS: Peripherally acting]

Adrenergic neuron blockers

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

d. Guanethidine

[SYMPATHOPLEGICS: Peripherally acting]

Adrenergic neuron blockers

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

b. Inhibiting vesicular uptake and storage of catecholamines

[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

a. Inhibit exocytosis of norepinephrine

[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. Management of hypertension

[SYMPATHOPLEGICS: Peripherally acting]

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

c. Postural hypotension

[SYMPATHOPLEGICS: Peripherally acting]

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

b. No longer commonly used

[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. β1 receptors

[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. 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]

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

a. Cardiac output (CO)

• 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

b. Juxtaglomerular (JG) apparatus

• 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. Decreased renin release

• 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

d. CAD, anxiety episodes, hypersympathetic stimulation

[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

c. Esmolol

[SYMPATHOPLEGICS: Peripherally acting]

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

c. Labetalol

[SYMPATHOPLEGICS: Peripherally acting]

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

a. Rebound hypertension and tachycardia

[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. Prazosin

[SYMPATHOPLEGICS: Peripherally acting]

Alpha blocker

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

a. Phentolamine

[SYMPATHOPLEGICS: Peripherally acting]

Alpha blocker

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

b. Blocking α1 receptors in blood vessels causing vasodilation

[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

a. Pheochromocytoma

[SYMPATHOPLEGICS: Peripherally acting]

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

c. BPH

[SYMPATHOPLEGICS: Peripherally acting]

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

d. First-dose phenomenon

[SYMPATHOPLEGICS: Peripherally acting]

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

c. Central α2 agonist

[SYMPATHOPLEGICS: Centrally acting]

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

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

[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