Part 9.1C-HTN-CLASSES OF DRUGS part 2

Proverbs 16:3

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

[Vasodilators]

Arteriolar Vasodilators or Mixed Arterial and Venous Dilators

Hydralazine =_____

Hydralazine =_____

Nitrovasodilators =_____

Diazoxide =_____

Minoxidil =_____

Sodium Nitroprusside =_____

a. Nitric oxide-mediated vasodilation

[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

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

[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

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

[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. Hypertensive Crisis

[Arteriolar Vasodilators]

Hydralazine uses in HTN:

a. Resistance Hypertensive

b. White Coat Hypertensive

c. Hypertensive Crisis

d. Masked Hypertensive

b. Hypertension in pregnancy

[Arteriolar Vasodilators]

Hydralazine uses in HTN:

a. Resistance Hypertensive

b. Hypertension in pregnancy

c. Renal Hypertension

d. Masked Hypertensive

c. Hypertensive Crisis

[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

b. Drug-induced lupus

[Arteriolar Vasodilators]

Hydralazine ADR

a. Hirsutism/ hypertrichosis

b. Drug-induced lupus

c. Increased intraocular pressure

d. Hypoglycemia

a. Hypertrichosis aka Hirsutism

[Arteriolar Vasodilators]

Minoxidil ADR

a. Hypertrichosis

b. Drug-induced lupus

c. Increased intraocular pressure

d. Hypoglycemia

d. Hypoglycemia

[Arteriolar Vasodilators]

Diazoxide ADR

a. Hypertrichosis

b. Drug-induced lupus

c. Increased intraocular pressure

d. Hypoglycemia

c. Increased intraocular pressure

[Arteriolar Vasodilators]

Fenoldepam ADR

a. Hypertrichosis

b. Drug-induced lupus

c. Increased intraocular pressure

d. Hypoglycemia

reflex tachycardia

palpitations

peripheral edema

[Arteriolar Vasodilators]

ADRs common to all Arteriolar Vasodilators:

reflex tachycardia or bradycardia?

slow heartbeat or palpitations?

peripheral edema or central edema?

b. Stimulating nitric oxide synthetase

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

[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

a. Nitric oxide (NO) pathway

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

b. cGMP

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

a. Protein kinase G (PKG)

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

b. Vasodilation

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

a. Hypertensive emergencies

[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. Hemoglobin, oxygen, and light

[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

d. Both a and b

[Arterial and Venous Dilators]

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

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]

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

Psychosis =_______

Metabolic acidosis =_______

Arrhythmias =_______

Weakness =_______

Convulsions =_______

Muscle spasms =_______

Severe hypertension =_______

Death =_______

Disorientation =_______

b. Protected from light

[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

c. 24 hours of preparation

[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

a. <1 hour

[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

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

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

[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

a. Direct vasoconstriction, ↑ catecholamines, ↑ aldosterone

[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

b. Bradykinin

[ANGIOTENSIN MODIFIERS]

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

b. Vasodilator

[ANGIOTENSIN MODIFIERS]

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

a. First-line drugs in hypertension management

[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

d. Never be combined together

[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

a. Congestive heart failure (CHF)

[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

b. Unloaders

[ANGIOTENSIN MODIFIERS]

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

c. Proteinuria

[ANGIOTENSIN MODIFIERS]

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

a. Hyperkalemia

[ANGIOTENSIN MODIFIERS]

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

a. Hypotension

[ANGIOTENSIN MODIFIERS]

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

d. Starting low then gradually increasing dose

[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

a. Idiosyncratic cough aka Dry cough

[ANGIOTENSIN MODIFIERS]

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

d. Losartan

[ANGIOTENSIN MODIFIERS]

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

a. Bilateral renal artery stenosis

[ANGIOTENSIN MODIFIERS]

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

c. Pregnancy

[ANGIOTENSIN MODIFIERS]

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

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

[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

b. Vasodilation

[ANGIOTENSIN MODIFIERS]

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

a. Captopril

• Sulfhydryl - Captopril

• Phosphinyl - Fosinopril

• Carboxyl - all the rest

[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

d. All the rest of ACE inhibitors

• 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

c. Fosinopril only

• 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

a. Blocking binding of angiotensin II to AT1 receptors

[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

b. Vasodilation due to decreased angiotensin II activity

[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. ACE inhibitors > ARBs

[ANGIOTENSIN MODIFIERS]

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

a. Renin inhibitor

[ANGIOTENSIN MODIFIERS]

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

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

[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

a. Prevents 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

d. Combined with ACE inhibitor or ARB

[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

a. Greater blood pressure lowering

[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

b. Does not improve cardiovascular outcomes

[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

c. Rash, diarrhea, nausea and vomiting

[ANGIOTENSIN MODIFIERS]

aliskiren ADR

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

c. Angioedema

[ANGIOTENSIN MODIFIERS]

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

a. Cardiovascular mortality and events

[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

b. Disrupt the movement of calcium through calcium channels

[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

a. Duration of action &

b. Structure

Structure

• DHP

• Non-DHP

DOA

• Intrinsically short-acting

• Intrinsically long-acting

• Modified long acting

[CCB]

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

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

[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

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

[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

Verapamil = Non-DHP

Amlodipine = DHP

Nicardipine = DHP

Diltiazem = Non-DHP

Nifedipine = DHP

Nimodipine = DHP

Felodipine = DHP

[CCB]

DHP or Non-DHP

Verapamil = ____

Amlodipine = ____

Nicardipine = ____

Diltiazem = ____

Nifedipine = ____

Nimodipine = ____

Felodipine = ____

a. Arteriolar vascular smooth muscle

[CCB]

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

b. Vasodilation

[CCB]

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

Arteriolar vasodilation = Both

Bradycardia = Non-DHP

Reflex tachycardia = DHP

Inotropism = Non-DHP

Peripheral edema = Both

Intrinsically natriuretic and diuretic = Both

[CCB]

DHP or Non-DHP

Arteriolar vasodilation = _____

Bradycardia = _____

Reflex tachycardia = _____

Inotropism = _____

Peripheral edema = _____

Intrinsically natriuretic and diuretic = ____

a. Intrinsically short-acting

• rest of the “-dipines”

• Verapamil

• Diltiazem

[CCB]

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

c. Verapamil

[CCB]

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

d. Diltiazem

[CCB]

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

b. Intrinsically long-acting

[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

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

[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. Nifedipine

[CCB]

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

b. Modified long-acting

[CCB]

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

c. Felodipine

[CCB]

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

a. First-line in the management of hypertension

[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

c. Nicardipine

[CCB]

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

a. Arteriolar vasodilation

[CCB]

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

c. Both

[CCB]

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

a. CAD

[CCB]

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

a. Peripheral edema

[CCB]

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

b. Capillary congestion

[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. Non-dihydropyridines (non-DHPs)

[CCB]

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

a. Bradycardia

[CCB]

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

c. Heart block

[CCB]

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

a. Heart failure (HF) and 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

c. Gingival hyperplasia

[CCB]

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