Pharmacology Exam 1
Practice Questions &
Answers
Comprehensive Explanations
& Rationales
Key Concepts • Review
Questions • Exam Preparation
,Equation for Blood Pressure BP = CO × SVR (Cardiac Output × Systemic Vascular Resistance).
Equation for Cardiac Output CO = HR × SV (Heart Rate × Stroke Volume).
Renal Compensation for High Blood Pressure Kidneys increase urine output to reduce blood volume and lower blood pressure.
Cardiovascular Compensation for High Blood Pressure Promotes vasodilation, decreased stroke volume, and reduced heart rate.
Trigger for Renin Release Low blood pressure triggers the kidneys to release renin.
Function of Renin Converts angiotensinogen into angiotensin I.
Source of Angiotensinogen Produced and released into circulation by the liver.
Enzyme Converting Angiotensin I to II Angiotensin-converting enzyme (ACE).
Primary Site of ACE Conversion Conversion of angiotensin I to angiotensin II occurs primarily in the lungs.
Major Physiological Effects of Angiotensin II Causes systemic vasoconstriction and stimulates aldosterone release.
Site of Aldosterone Release Released from the adrenal glands.
Physiological Action of Aldosterone Promotes sodium and water reabsorption to increase blood pressure.
Prototype Direct Renin Inhibitor Aliskiren.
Mechanism of Action: Aliskiren Blocks renin directly, preventing conversion of angiotensinogen to angiotensin I.
Clinical Indication for Aliskiren Hypertension only.
, Adverse Effects of Aliskiren Diarrhea (at high doses), fetal injury, and risks of stroke, blindness, kidney disease,
and death.
Pregnancy Consideration for Aliskiren Contraindicated during pregnancy due to high risk of fetal injury.
Advantage of ACEIs/ARBs Over Aliskiren They do not carry aliskiren's specific risks of stroke, blindness, kidney disease, and
death.
Mnemonic for Aliskiren "Alice and Kiren walk in the Rainin; Alice can't get pregnant."
Prototype ACE Inhibitors Captopril and lisinopril.
Mechanism of Action: ACE Inhibitors Inhibit ACE, blocking conversion of angiotensin I to angiotensin II.
Major Indications for ACE Inhibitors Hypertension, heart failure, myocardial infarction, and diabetic nephropathy.
Cause of ACE-Inhibitor-Induced Cough Accumulation of bradykinin in the lungs.
Cause of ACE-Inhibitor-Induced Angioedema Accumulation of bradykinin.
Cause of Hyperkalemia with ACE Inhibitors Inhibition of aldosterone secretion reduces renal potassium excretion.
Major Adverse Effects of ACE Inhibitors First-dose hypotension, angioedema, cough, hyperkalemia, and fetal injury.
Potentially Fatal Adverse Effect of ACE Inhibitors Angioedema.
Management of Severe ACE-Inhibitor Angioedema Discontinue the drug immediately; severe cases may be treated with subcutaneous
epinephrine.
Pregnancy Consideration for ACE Inhibitors Causes severe fetal injury; must be discontinued during pregnancy.
What is the prototype ARB? Losartan.
Practice Questions &
Answers
Comprehensive Explanations
& Rationales
Key Concepts • Review
Questions • Exam Preparation
,Equation for Blood Pressure BP = CO × SVR (Cardiac Output × Systemic Vascular Resistance).
Equation for Cardiac Output CO = HR × SV (Heart Rate × Stroke Volume).
Renal Compensation for High Blood Pressure Kidneys increase urine output to reduce blood volume and lower blood pressure.
Cardiovascular Compensation for High Blood Pressure Promotes vasodilation, decreased stroke volume, and reduced heart rate.
Trigger for Renin Release Low blood pressure triggers the kidneys to release renin.
Function of Renin Converts angiotensinogen into angiotensin I.
Source of Angiotensinogen Produced and released into circulation by the liver.
Enzyme Converting Angiotensin I to II Angiotensin-converting enzyme (ACE).
Primary Site of ACE Conversion Conversion of angiotensin I to angiotensin II occurs primarily in the lungs.
Major Physiological Effects of Angiotensin II Causes systemic vasoconstriction and stimulates aldosterone release.
Site of Aldosterone Release Released from the adrenal glands.
Physiological Action of Aldosterone Promotes sodium and water reabsorption to increase blood pressure.
Prototype Direct Renin Inhibitor Aliskiren.
Mechanism of Action: Aliskiren Blocks renin directly, preventing conversion of angiotensinogen to angiotensin I.
Clinical Indication for Aliskiren Hypertension only.
, Adverse Effects of Aliskiren Diarrhea (at high doses), fetal injury, and risks of stroke, blindness, kidney disease,
and death.
Pregnancy Consideration for Aliskiren Contraindicated during pregnancy due to high risk of fetal injury.
Advantage of ACEIs/ARBs Over Aliskiren They do not carry aliskiren's specific risks of stroke, blindness, kidney disease, and
death.
Mnemonic for Aliskiren "Alice and Kiren walk in the Rainin; Alice can't get pregnant."
Prototype ACE Inhibitors Captopril and lisinopril.
Mechanism of Action: ACE Inhibitors Inhibit ACE, blocking conversion of angiotensin I to angiotensin II.
Major Indications for ACE Inhibitors Hypertension, heart failure, myocardial infarction, and diabetic nephropathy.
Cause of ACE-Inhibitor-Induced Cough Accumulation of bradykinin in the lungs.
Cause of ACE-Inhibitor-Induced Angioedema Accumulation of bradykinin.
Cause of Hyperkalemia with ACE Inhibitors Inhibition of aldosterone secretion reduces renal potassium excretion.
Major Adverse Effects of ACE Inhibitors First-dose hypotension, angioedema, cough, hyperkalemia, and fetal injury.
Potentially Fatal Adverse Effect of ACE Inhibitors Angioedema.
Management of Severe ACE-Inhibitor Angioedema Discontinue the drug immediately; severe cases may be treated with subcutaneous
epinephrine.
Pregnancy Consideration for ACE Inhibitors Causes severe fetal injury; must be discontinued during pregnancy.
What is the prototype ARB? Losartan.
