Part 9.1C-HTN-CLASSES OF DRUGS part 2

[Vasodilators]

Arteriolar Vasodilators or Mixed Arterial and Venous Dilators

Hydralazine =_____

Hydralazine =_____

Nitrovasodilators =_____

Diazoxide =_____

Minoxidil =_____

Sodium Nitroprusside =_____

Hydralazine = Arteriolar Vasodilators

Hydralazine = Arteriolar Vasodilators

Nitrovasodilators = Mixed Arterial and Venous Dilators

Diazoxide = Arteriolar Vasodilators

Minoxidil = Arteriolar Vasodilators

Sodium Nitroprusside = Mixed Arterial and Venous Dilators

[Arteriolar Vasodilators]

Hydralazine MOA

a. Nitric oxide-mediated vasodilation

b. Opening of potassium channels leading to hyperpolarization of arteriolar smooth muscle membranes

c. Activation of D1 receptors in arterioles leading to arteriolar dilation and natriuresis

a. Nitric oxide-mediated vasodilation

[Arteriolar Vasodilators]

Minoxidil MOA

a. Nitric oxide-mediated vasodilation

b. Opening of potassium channels leading to hyperpolarization of arteriolar smooth muscle membranes

c. Activation of D1 receptors in arterioles leading to arteriolar dilation and natriuresis

b. Opening of potassium channels leading to hyperpolarization of arteriolar smooth muscle membranes

[Arteriolar Vasodilators]

Diazoxide MOA

a. Nitric oxide-mediated vasodilation

b. Opening of potassium channels leading to hyperpolarization of arteriolar smooth muscle membranes

c. Activation of D1 receptors in arterioles leading to arteriolar dilation and natriuresis

b. Opening of potassium channels leading to hyperpolarization of arteriolar smooth muscle membranes

[Arteriolar Vasodilators]

Fenoldepam MOA

a. Nitric oxide-mediated vasodilation

b. Opening of potassium channels leading to hyperpolarization of arteriolar smooth muscle membranes

c. Activation of D1 receptors in arterioles leading to arteriolar dilation and natriuresis

c. Activation of D1 receptors in arterioles leading to arteriolar dilation and natriuresis

[Arteriolar Vasodilators]

Hydralazine uses in HTN:

a. Resistance Hypertensive

b. White Coat Hypertensive

c. Hypertensive Crisis

d. Masked Hypertensive

c. Hypertensive Crisis

[Arteriolar Vasodilators]

Hydralazine uses in HTN:

a. Resistance Hypertensive

b. Hypertension in pregnancy

c. Renal Hypertension

d. Masked Hypertensive

b. Hypertension in pregnancy

[Arteriolar Vasodilators]

Minoxidil uses in HTN:

a. Resistance Hypertensive

b. White Coat Hypertensive

c. Hypertensive Crisis

d. Masked Hypertensive

c. Hypertensive Crisis

[Arteriolar Vasodilators]

Diazoxide uses in HTN:

a. Resistance Hypertensive

b. White Coat Hypertensive

c. Hypertensive Crisis

d. Masked Hypertensive

c. Hypertensive Crisis

[Arteriolar Vasodilators]

Fenoldepam uses in HTN:

a. Resistance Hypertensive

b. White Coat Hypertensive

c. Hypertensive Crisis

d. Masked Hypertensive

c. Hypertensive Crisis

[Arteriolar Vasodilators]

Hydralazine ADR

a. Hirsutism/ hypertrichosis

b. Drug-induced lupus

c. Increased intraocular pressure

d. Hypoglycemia

b. Drug-induced lupus

[Arteriolar Vasodilators]

Minoxidil ADR

a. Hypertrichosis

b. Drug-induced lupus

c. Increased intraocular pressure

d. Hypoglycemia

a. Hypertrichosis aka Hirsutism

[Arteriolar Vasodilators]

Diazoxide ADR

a. Hypertrichosis

b. Drug-induced lupus

c. Increased intraocular pressure

d. Hypoglycemia

d. Hypoglycemia

[Arteriolar Vasodilators]

Fenoldepam ADR

a. Hypertrichosis

b. Drug-induced lupus

c. Increased intraocular pressure

d. Hypoglycemia

c. Increased intraocular pressure

[Arteriolar Vasodilators]

ADRs common to all Arteriolar Vasodilators:

reflex tachycardia or bradycardia?

slow heartbeat or palpitations?

peripheral edema or central edema?

reflex tachycardia

palpitations

peripheral edema

[Arterial and Venous Dilators]

Sodium nitroprusside lowers blood pressure mainly by:
a. Blocking nitric oxide synthetase
b. Stimulating nitric oxide synthetase
c. Blocking α1 receptors
d. Stimulating α1 receptors

b. Stimulating nitric oxide synthetase

Stimulating nitric oxide synthetase → NO → guanylyl cyclase → cGMP → PKG → vasodilation

[Arterial and Venous Dilators]

The antihypertensive effect of sodium nitroprusside is mediated by:
a. Nitric oxide (NO) pathway
b. Renin inhibition only
c. COX inhibition
d. Calcium channel blockade

a. Nitric oxide (NO) pathway

Stimulating nitric oxide synthetase → NO → guanylyl cyclase → cGMP → PKG → vasodilation

[Arterial and Venous Dilators]

Sodium nitroprusside stimulates guanylyl cyclase, resulting in increased:
a. ATP
b. cGMP
c. cAMP
d. Dopamine

b. cGMP

Stimulating nitric oxide synthetase → NO → guanylyl cyclase → cGMP → PKG → vasodilation

[Arterial and Venous Dilators]

Increased cGMP produced by sodium nitroprusside activates:
a. Protein kinase G (PKG)
b. Protein kinase A (PKA)
c. Cyclooxygenase
d. Renin

a. Protein kinase G (PKG)

Stimulating nitric oxide synthetase → NO → guanylyl cyclase → cGMP → PKG → vasodilation

[Arterial and Venous Dilators]

The final vascular effect of sodium nitroprusside is:
a. Vasoconstriction
b. Vasodilation

b. Vasodilation

Stimulating nitric oxide synthetase → NO → guanylyl cyclase → cGMP → PKG → vasodilation

[Arterial and Venous Dilators]

Sodium nitroprusside is considered the drug of choice (DOC) for:
a. Hypertensive emergencies
b. Hyperlipidemia
c. Chronic gout
d. Stable angina

a. Hypertensive emergencies

[Arterial and Venous Dilators]

Sodium nitroprusside is metabolized or degraded by:
a. Hemoglobin, oxygen, and light
b. Liver enzymes, CO2, and light
c. Kidney, CO2, and O2
d. Gastric acid, WBC, protein

a. Hemoglobin, oxygen, and light

[Arterial and Venous Dilators]

A toxic metabolite of sodium nitroprusside is:
a. Thiocyanate
b. Cyanide
c. Dopamine
d. Both a and b

d. Both a and b

[Arterial and Venous Dilators]

Toxicity from sodium nitroprusside is due to [cyanide or thiocyanate]

Psychosis =_______

Metabolic acidosis =_______

Arrhythmias =_______

Weakness =_______

Convulsions =_______

Muscle spasms =_______

Severe hypertension =_______

Death =_______

Disorientation =_______

Psychosis = Thiocyanate

Metabolic acidosis = Cyanide

Arrhythmias = Cyanide

Weakness = Thiocyanate

Convulsions = Thiocyanate

Muscle spasms = Thiocyanate

Severe hypertension = Cyanide

Death = Cyanide

Disorientation = Thiocyanate

[Arterial and Venous Dilators]

Sodium nitroprusside preparations should be:
a. Exposed to sunlight for activation
b. Protected from light
c. Frozen before use
d. Mixed with alcohol

b. Protected from light

[Arterial and Venous Dilators]

Sodium nitroprusside solution should ideally be used within:
a. 1 hour of preparation
b. 12 hours of preparation
c. 24 hours of preparation
d. 72 hours of preparation

c. 24 hours of preparation

[Arterial and Venous Dilators]

At high doses, infusion of sodium nitroprusside should be limited to:
a. <1 hour
b. 6 hours
c. 12 hours
d. 24 hours

a. <1 hour

[ANGIOTENSIN MODIFIERS]

ACE inhibitors and ARBs lower blood pressure mainly by:
a. Blocking prostaglandin synthesis
b. Blocking effects of angiotensin II
c. Blocking β1 receptors
d. Increasing renin release

b. Blocking effects of angiotensin II → ↓ vasoconstriction, ↓ catecholamines, ↓ aldosterone

[ANGIOTENSIN MODIFIERS]

The normal RAAS pathway is:
a. Angiotensin II → Angiotensin I → ACE
b. Angiotensin I → Angiotensin II (by ACE) → AT1 receptors
c. Renin → Bradykinin → AT1 receptors
d. Aldosterone → ACE → Angiotensin II

b. Angiotensin I → Angiotensin II (by ACE) → AT1 receptors

[ANGIOTENSIN MODIFIERS]

Activation of AT1 receptors results in:
a. Direct vasoconstriction, ↑ catecholamines, ↑ aldosterone
b. Direct vasodilation, ↑ catecholamines, ↑ aldosterone
c. Direct vasodilation, ↑ catecholamines, ↓ aldosterone
d. Direct vasoconstriction, ↑ catecholamines, ↓ aldosterone

a. Direct vasoconstriction, ↑ catecholamines, ↑ aldosterone

[ANGIOTENSIN MODIFIERS]

ACE is involved in the metabolism of:
a. Dopamine
b. Bradykinin
c. Histamine
d. Serotonin

b. Bradykinin

[ANGIOTENSIN MODIFIERS]

Bradykinin is considered a powerful:
a. Vasoconstrictor
b. Vasodilator

b. Vasodilator

[ANGIOTENSIN MODIFIERS]

ACE inhibitors and ARBs are considered:
a. First-line drugs in hypertension management
b. Contraindicated in HTN
c. Drugs for acute gout
d. Second-line only for emergencies

a. First-line drugs in hypertension management

[ANGIOTENSIN MODIFIERS]

ACE inhibitors and ARBs should:
a. Always be combined together
b. Replace diuretics completely
c. Be used only during pregnancy
d. Never be combined together

d. Never be combined together

[ANGIOTENSIN MODIFIERS]

ACE inhibitors and ARBs are first-line in the management of:
a. Congestive heart failure (CHF)
b. Acute poisoning only
c. Osteoarthritis only
d. Acute mountain sickness

a. Congestive heart failure (CHF)

[ANGIOTENSIN MODIFIERS]

In CHF, ACE inhibitors and ARBs act as:
a. Loaders
b. Unloaders
c. Platelet activators
d. Bronchodilators

b. Unloaders

[ANGIOTENSIN MODIFIERS]

ACE inhibitors and ARBs are first-line in the management of:
a. Viral fever
b. Hyperthyroidism
c. Proteinuria
d. Seizures

c. Proteinuria

[ANGIOTENSIN MODIFIERS]

Which electrolyte abnormality may occur with ACE inhibitors and ARBs?
a. Hyperkalemia
b. Hypokalemia
c. Hypercalcemia
d. Hyponatremia

a. Hyperkalemia

[ANGIOTENSIN MODIFIERS]

A common adverse effect of ACE inhibitors and ARBs is:
a. Hypotension
b. Ototoxicity
c. Respiratory depression
d. Hyperglycemia

a. Hypotension

[ANGIOTENSIN MODIFIERS]

Hypotension with ACE inhibitors is minimized by:
a. Abrupt withdrawal
b. Giving maximum dose immediately
c. Combining with another ACE inhibitor
d. Starting low then gradually increasing dose

d. Starting low then gradually increasing dose

[ANGIOTENSIN MODIFIERS]

Which adverse effect is specifically associated with ACE inhibitors?
a. Idiosyncratic cough
b. Hyperuricemia
c. Gynecomastia
d. Ototoxicity

a. Idiosyncratic cough aka Dry cough

[ANGIOTENSIN MODIFIERS]

Which ARB is associated with hyperuricemia?
a. Olmesartan
b. Irbesartan
c. Telmisartan
d. Losartan

d. Losartan

[ANGIOTENSIN MODIFIERS]

ACE inhibitors and ARBs are contraindicated in:
a. Bilateral renal artery stenosis
b. Hyperlipidemia
c. Osteoarthritis
d. Migraine

a. Bilateral renal artery stenosis

[ANGIOTENSIN MODIFIERS]

ACE inhibitors and ARBs are contraindicated during:
a. Fever
b. Lactation only
c. Pregnancy
d. Acute pain

c. Pregnancy

[ANGIOTENSIN MODIFIERS]

ACE inhibitors lower blood pressure mainly by:
a. Blocking ACE/Kininase II
b. Blocking β1 receptors
c. Blocking α1 receptors only
d. Stimulating renin release

a. Blocking ACE/Kininase II → ↓ angiotensin II and ↑ bradykinin

[ANGIOTENSIN MODIFIERS]

Bradykinin contributes to ACE inhibitor action by causing:
a. Vasoconstriction
b. Vasodilation

b. Vasodilation

[ANGIOTENSIN MODIFIERS]

ACE inhibitor contains a sulfhydryl Zn-binding moiety
a. Captopril only
b. Fosinopril only
c. Losartan only
d. All the rest of ACE inhibitors

a. Captopril

• Sulfhydryl - Captopril

• Phosphinyl - Fosinopril

• Carboxyl - all the rest

[ANGIOTENSIN MODIFIERS]

ACE inhibitor contains a carboxyl Zn-binding moiety
a. Captopril only
b. Losartan only
c. Fosinopril only
d. All the rest of ACE inhibitors

d. All the rest of ACE inhibitors

• Sulfhydryl - Captopril

• Phosphinyl - Fosinopril

• Carboxyl - all the rest

[ANGIOTENSIN MODIFIERS]

ACE inhibitor contains a phosphinyl Zn-binding moiety
a. Captopril only
b. Losartan only
c. Fosinopril only
d. All the rest of ACE inhibitors

c. Fosinopril only

• Sulfhydryl - Captopril

• Phosphinyl - Fosinopril

• Carboxyl - all the rest

[ANGIOTENSIN MODIFIERS]

ARBs lower blood pressure by:
a. Blocking binding of angiotensin II to AT1 receptors
b. Increasing angiotensin II synthesis
c. Blocking β1 receptors only
d. Increasing renin release

a. Blocking binding of angiotensin II to AT1 receptors

[ANGIOTENSIN MODIFIERS]

Blocking AT1 receptors with ARBs results in:
a. Vasoconstriction to increase angiotensin II activity
b. Vasodilation due to decreased angiotensin II activity
c. Increased catecholamine release
d. Platelet aggregation

b. Vasodilation due to decreased angiotensin II activity

[ANGIOTENSIN MODIFIERS]

Which statement about vasodilating effect is correct?
a. ARBs > ACE inhibitors
b. ACE inhibitors > ARBs

b. ACE inhibitors > ARBs

[ANGIOTENSIN MODIFIERS]

Aliskiren is classified as a:
a. Renin inhibitor
b. ACE inhibitor
c. Beta blocker
d. Alpha blocker

a. Renin inhibitor

[ANGIOTENSIN MODIFIERS]

Aliskiren lowers blood pressure by:

a. Blocking ACE directly and preventing renin from binding to angiotensinogen
b. Blocking AT1 receptors and preventing renin from binding to angiotensinogen
c. Binding to the S3 binding protein and preventing renin from binding to angiotensinogen
d. Blocking β1 receptors and preventing renin from binding to angiotensinogen

c. Binding to the S3 binding protein and preventing renin from binding to angiotensinogen

[ANGIOTENSIN MODIFIERS]

Which statement correctly describes aliskiren MOA?
a. Prevents renin from binding to angiotensinogen
b. Increases angiotensin II formation
c. Blocks α1 receptors
d. Stimulates bradykinin metabolism

a. Prevents renin from binding to angiotensinogen

[ANGIOTENSIN MODIFIERS]

Aliskiren is used in hypertension:
a. Only during pregnancy
b. As the only therapy for all patients
c. Only in hypertensive emergency
d. Combined with ACE inhibitor or ARB

d. Combined with ACE inhibitor or ARB

[ANGIOTENSIN MODIFIERS]

Compared with ACE inhibitor or ARB alone, aliskiren combination therapy causes:
a. Greater blood pressure lowering
b. Lower efficacy
c. No antihypertensive effect
d. Immediate tachycardia

a. Greater blood pressure lowering

[ANGIOTENSIN MODIFIERS]

Despite lowering BP, aliskiren:
a. Improves cardiovascular outcomes greatly
b. Does not improve cardiovascular outcomes
c. Replaces all antihypertensives
d. Eliminates heart failure risk

b. Does not improve cardiovascular outcomes

[ANGIOTENSIN MODIFIERS]

aliskiren ADR

a. Ototoxicity, nausea and vomiting
b. Hyperglycemia, constipation, and vomiting
c. Rash, diarrhea, nausea and vomiting
d. Severe thrombocytopenia

c. Rash, diarrhea, nausea and vomiting

[ANGIOTENSIN MODIFIERS]

A rare adverse effect of aliskiren is:
a. Nephrolithiasis
b. Cataracts
c. Angioedema
d. Hyperthyroidism

c. Angioedema

[ANGIOTENSIN MODIFIERS]

Aliskiren may increase which risk in diabetic patients?
a. Cardiovascular mortality and events
b. Pulmonary fibrosis
c. Renal stone formation only
d. Severe hypoglycemia only

a. Cardiovascular mortality and events

[CCB]

Calcium channel blockers are drugs that:
a. Increase calcium entry into cells
b. Disrupt the movement of calcium through calcium channels
c. Disrupt the movement of calcium through passive diffusion
d. Stimulate catecholamine release

b. Disrupt the movement of calcium through calcium channels

[CCB]

Calcium channel blockers are classified based on:
a. Duration of action
b. Structure
c. Color
d. Route of administration

a. Duration of action &

b. Structure

Structure

• DHP

• Non-DHP

DOA

• Intrinsically short-acting

• Intrinsically long-acting

• Modified long acting

[CCB]

Dihydropyridines (-dipines)

a. blocks the L-type Ca+ channels in arteriolar vascular smooth muscles and the heart

b. blocks the L-type Ca+ channels in arteriolar vascular smooth muscles

b. blocks the L-type Ca+ channels in arteriolar vascular smooth muscles

[CCB]

Non dihydropyridine

a. blocks the L-type Ca+ channels in arteriolar vascular smooth muscles and the heart

b. blocks the L-type Ca+ channels in arteriolar vascular smooth muscles

a. blocks the L-type Ca+ channels in arteriolar vascular smooth muscles and the heart

[CCB]

DHP or Non-DHP

Verapamil = ____

Amlodipine = ____

Nicardipine = ____

Diltiazem = ____

Nifedipine = ____

Nimodipine = ____

Felodipine = ____

Verapamil = Non-DHP

Amlodipine = DHP

Nicardipine = DHP

Diltiazem = Non-DHP

Nifedipine = DHP

Nimodipine = DHP

Felodipine = DHP

[CCB]

Dihydropyridine calcium channel blockers primarily act on:
a. Arteriolar vascular smooth muscle
b. Cardiac conduction system
c. Kidney tubules
d. Skeletal muscle

a. Arteriolar vascular smooth muscle

[CCB]

Blocking L-type calcium channels in arteriolar smooth muscle results in:
a. Vasoconstriction
b. Vasodilation

b. Vasodilation

[CCB]

DHP or Non-DHP

Arteriolar vasodilation = _____

Bradycardia = _____

Reflex tachycardia = _____

Inotropism = _____

Peripheral edema = _____

Intrinsically natriuretic and diuretic = ____

Arteriolar vasodilation = Both

Bradycardia = Non-DHP

Reflex tachycardia = DHP

Inotropism = Non-DHP

Peripheral edema = Both

Intrinsically natriuretic and diuretic = Both

[CCB]

Which group includes the rest of the “-dipines”?
a. Intrinsically short-acting
b. Intrinsically long-acting
c. Modified long-acting

a. Intrinsically short-acting

• rest of the “-dipines”

• Verapamil

• Diltiazem

[CCB]

Intrinsically short-acting
a. Lacidipine
b. Amlodipine
c. Verapamil
d. Lercanidipine

c. Verapamil

[CCB]

Intrinsically short-acting class
a. Nicardipine
b. Amlodipine
c. Felodipine
d. Diltiazem

d. Diltiazem

[CCB]

Amlodipine

a. Intrinsically short-acting
b. Intrinsically long-acting
c. Modified long-acting

b. Intrinsically long-acting

[CCB]

Lacidipine

a. Intrinsically short-acting
b. Intrinsically long-acting
c. Modified long-acting

b. Intrinsically long-acting

[CCB]

Tercanidipine

a. Intrinsically short-acting
b. Intrinsically long-acting
c. Modified long-acting

b. Intrinsically long-acting

[CCB]

Modified long-acting calcium channel blockers are:
a. Beta blockers combined with calcium channel blockers
b. Naturally long-acting drugs
c. Drugs with no extended-release formulation
d. Intrinsically short-acting drugs formulated as modified release products

c. Intrinsically short-acting drugs formulated as modified release products

[CCB]

Adalat GITS is a modified-release form of:
a. Verapamil
b. Diltiazem
c. Nifedipine
d. Felodipine

c. Nifedipine

[CCB]

Verapamil XR, Diltiazem XR, Plendil XR are classified as:
a. Intrinsically long-acting
b. Modified long-acting
c. Short-acting

b. Modified long-acting

[CCB]

Plendil XR is the modified-release formulation of:
a. Nifedipine
b. Verapamil
c. Felodipine
d. Diltiazem

c. Felodipine

[CCB]

Calcium channel blockers are considered:
a. First-line in the management of hypertension
b. Contraindicated in hypertension
c. Used only for gout
d. Reserved for emergencies

a. First-line in the management of hypertension

[CCB]

Given IV for hypertensive emergency
a. Amlodipine
b. Verapamil
c. Nicardipine
d. Felodipine

c. Nicardipine

[CCB]

The adverse effects of calcium channel blockers are mainly due to:
a. Arteriolar vasodilation
b. Platelet inhibition
c. Renin activation
d. Bronchodilation

a. Arteriolar vasodilation

[CCB]

Short- or fast-acting dihydropyridines (DHPs) may cause:
a. Reflex tachycardia
b. Bradycardia
c. Both

c. Both

[CCB]

Reflex cardia associated with short/fast-acting DHPs makes them contraindicated in:
a. CAD
b. Gout
c. Glaucoma
d. COPD

a. CAD

[CCB]

Common to all calcium channel blockers (CCBs)
a. Peripheral edema
b. Hyperkalemia
c. Dry cough
d. Ototoxicity

a. Peripheral edema

[CCB]

Peripheral edema caused by calcium channel blockers is mainly due to:
a. Decreased aldosterone
b. Capillary congestion
c. Increased uric acid
d. Renal vasoconstriction

b. Capillary congestion

[CCB]

Associated with myocardial depression
a. Dihydropyridines (DHPs)
b. Non-dihydropyridines (non-DHPs)

b. Non-dihydropyridines (non-DHPs)

[CCB]

non-DHP
a. Bradycardia
b. Reflex tachycardia
c. Hyperkalemia
d. Dry cough

a. Bradycardia

[CCB]

May occur with non-DHP
a. Hyperuricemia
b. Atrial fibrillation
c. Heart block
d. Pulmonary edema

c. Heart block

[CCB]

Non-DHP calcium channel blockers are contraindicated in patients with:
a. Heart failure (HF) and heart block
b. Hyperlipidemia and gout
c. COPD and asthma only
d. Renal stones only

a. Heart failure (HF) and heart block

[CCB]

Oral ADR associated with calcium channel blockers
a. Dental caries
b. Aphthous ulceration
c. Gingival hyperplasia
d. Tooth discoloration

c. Gingival hyperplasia