NUR641E ADVANCED PHARMACOLOGY FINAL
EXAM STUDY GUIDE: CARDIOVASCULAR,
RESPIRATORY, ENDOCRINE & INFECTIOUS
DISEASES
Section 1: Cardiovascular Pharmacology
1. A 68-year-old male with a history of chronic heart failure with reduced ejection
fraction (HFrEF, EF 30%), hypertension, and stage 3 chronic kidney disease presents
to the clinic for routine follow-up. He currently takes furosemide 40 mg daily,
lisinopril 20 mg daily, and metoprolol succinate 50 mg daily. Despite this regimen,
he continues to experience dyspnea on exertion and has bilateral pitting edema. His
blood pressure is 110/70 mmHg, heart rate is 72 bpm, and potassium is 4.2 mEq/L.
The provider decides to initiate sacubitril/valsartan. Which of the following is the
most critical consideration regarding the transition from lisinopril to
sacubitril/valsartan in this patient?
[ ] A. The patient must stop lisinopril for 12 hours before starting sacubitril/valsartan
to reduce the risk of angioedema.
[ ] B. The patient must stop lisinopril for 24 hours before starting sacubitril/valsartan
to reduce the risk of angioedema.
[✓] C. The patient must stop lisinopril for 36 hours before starting
sacubitril/valsartan to reduce the risk of angioedema.
[ ] D. The patient can transition immediately from lisinopril to sacubitril/valsartan
without a washout period.
Answer and Rationale: C
The correct answer is C. Sacubitril/valsartan is an angiotensin receptor-neprilysin inhibitor
(ARNI) that significantly reduces morbidity and mortality in HFrEF. Neprilysin is an enzyme
,that breaks down natriuretic peptides, bradykinin, and other vasoactive substances. When
combined with an ACE inhibitor, the dual inhibition of neprilysin and the renin-angiotensin-
aldosterone system (RAAS) dramatically increases the risk of life-threatening angioedema
due to bradykinin accumulation. Therefore, a strict washout period of 36 hours is required
between the last dose of an ACE inhibitor (lisinopril) and the first dose of
sacubitril/valsartan. Option A (12 hours) and Option B (24 hours) are insufficient and would
put the patient at high risk for angioedema. Option D is incorrect because an immediate
transition is absolutely contraindicated. If the patient were transitioning from an ARB to the
ARNI, no washout period is strictly required, but transitioning from an ACE inhibitor
mandates the 36-hour gap.
2. A 55-year-old female is initiated on amiodarone 400 mg daily for the management of
persistent atrial fibrillation. She has a past medical history significant for
hypothyroidism and mild liver enzyme elevations. Which of the following monitoring
parameters is most specific to the unique pharmacokinetic profile of amiodarone
and must be conducted prior to and periodically during therapy?
[ ] A. Monthly complete blood counts (CBC) to monitor for drug-induced bone
marrow suppression.
[✓] B. Baseline and serial pulmonary function tests (PFTs) and chest X-rays to
monitor for pulmonary toxicity.
[ ] C. Continuous telemetry monitoring for the first 72 hours to assess for QT
shortening.
[ ] D. Weekly vital capacity measurements using a spirometer at home to detect
early neuromuscular blockade.
Answer and Rationale: B
The correct answer is B. Amiodarone is a class III antiarrhythmic with a highly complex
pharmacokinetic profile, including extensive tissue distribution and a long half-life (up to
100 days). One of its most severe adverse effects is pulmonary toxicity, which can manifest
as interstitial pneumonitis or pulmonary fibrosis. This risk necessitates baseline and
periodic chest X-rays and pulmonary function tests (PFTs), specifically checking the
diffusing capacity for carbon monoxide (DLCO). Option A is incorrect because bone
marrow suppression is not a common adverse effect of amiodarone. Option C is incorrect
because amiodarone prolongs the QT interval, it does not shorten it, and continuous
telemetry for 72 hours is not standard for outpatient oral initiation. Option D is incorrect
because amiodarone does not cause neuromuscular blockade; home spirometry is not the
standard monitoring approach for its pulmonary toxicity. The provider must also monitor
thyroid and liver function, given this patient's history, but the pulmonary monitoring is
uniquely tied to its severe and potentially fatal respiratory complications.
, 3. A 62-year-old male with a history of hypertension and gout presents with resistant
hypertension. His current regimen includes amlodipine 10 mg daily and lisinopril 40
mg daily. His blood pressure remains 152/94 mmHg. The provider considers adding
a thiazide diuretic. Which of the following thiazide diuretics would be the most
appropriate choice for this patient to minimize the risk of exacerbating his gout,
while effectively managing his blood pressure?
[ ] A. Hydrochlorothiazide 25 mg daily
[ ] B. Chlorthalidone 25 mg daily
[✓] C. Indapamide 2.5 mg daily
[ ] D. Metolazone 5 mg daily
Answer and Rationale: C
The correct answer is C. Thiazide and thiazide-like diuretics are first-line agents for
hypertension, but they can increase serum uric acid levels by reducing renal clearance of
urate, potentially precipitating gout attacks. Indapamide is a thiazide-like diuretic that has
been shown in clinical studies to have a significantly lower impact on serum uric acid
levels compared to traditional thiazides like hydrochlorothiazide and chlorthalidone.
Therefore, in a patient with a history of gout who requires a diuretic for resistant
hypertension, indapamide is the preferred agent. Option A (hydrochlorothiazide) and
Option B (chlorthalidone) are both known to elevate uric acid levels significantly.
Chlorthalidone is more potent and longer-acting than HCTZ, but it carries a higher risk of
metabolic disturbances, including hyperuricemia. Option D (metolazone) is typically
reserved for severe edema or resistant hypertension when profound diuresis is needed,
often in combination with loop diuretics, and it also carries a substantial risk of electrolyte
and uric acid disturbances.
4. A 45-year-old male with a history of familial hypercholesterolemia presents for a
follow-up. He is currently taking atorvastatin 80 mg daily. His recent lipid panel
shows an LDL of 135 mg/dL, HDL of 40 mg/dL, and triglycerides of 150 mg/dL. The
provider decides to add evolocumab, a PCSK9 inhibitor. What is the mechanism of
action of evolocumab and how does it affect LDL receptor trafficking?
[ ] A. It inhibits the synthesis of PCSK9 in the liver, thereby increasing the
degradation of LDL receptors.
[✓] B. It binds to circulating PCSK9, preventing it from degrading LDL receptors, thus
increasing hepatic LDL clearance.
[ ] C. It acts as a bile acid sequestrant, increasing the excretion of cholesterol and
upregulating PCSK9 production.
[ ] D. It inhibits microsomal triglyceride transfer protein (MTP), reducing the hepatic
assembly of VLDL.
, Answer and Rationale: B
The correct answer is B. Evolocumab is a monoclonal antibody that binds to proprotein
convertase subtilisin/kexin type 9 (PCSK9) in the circulation. PCSK9 normally binds to LDL
receptors on the hepatocyte surface, and the complex is internalized and degraded in the
lysosome. By binding to PCSK9, evolocumab prevents PCSK9 from binding to the LDL
receptors. This preserves the LDL receptors, allowing them to recycle back to the cell
surface and continue clearing LDL cholesterol from the blood, resulting in a profound
reduction in LDL levels (often by 50-60%). Option A is incorrect because evolocumab does
not inhibit the synthesis of PCSK9, nor does it increase the degradation of LDL receptors;
rather, it prevents LDL receptor degradation. Option C describes the mechanism of bile
acid sequestrants, not PCSK9 inhibitors. Option D describes the mechanism of lomitapide,
an MTP inhibitor used in homozygous familial hypercholesterolemia, not evolocumab.
5. A 72-year-old female with a history of atrial fibrillation and a previous ischemic
stroke is brought to the emergency department with an acute onset of right-sided
weakness and aphasia. A CT scan of the head reveals an acute ischemic stroke. Her
medication list includes warfarin, but her INR on arrival is 1.2. The stroke team
decides to administer intravenous alteplase (tPA). Which of the following is an
absolute contraindication to the administration of alteplase in this patient based on
standard guidelines?
[ ] A. The patient took her prescribed dose of warfarin 12 hours ago.
[ ] B. The patient's blood pressure has been consistently 150/90 mmHg for the past
hour.
[✓] C. The patient's symptoms began approximately 6 hours prior to arrival.
[ ] D. The patient has a history of a transient ischemic attack (TIA) 6 months ago.
Answer and Rationale: C
The correct answer is C. The standard time window for the administration of intravenous
alteplase in acute ischemic stroke is 4.5 hours from the onset of symptoms. Since this
patient's symptoms began 6 hours prior to arrival, she is outside the therapeutic window,
and administering alteplase would significantly increase the risk of intracranial
hemorrhage without proven benefit. Option A is incorrect because while taking oral
anticoagulants is a contraindication if the INR is elevated, her INR is 1.2 (within normal
limits), meaning the anticoagulant effect is negligible. Option B is incorrect because a
blood pressure of 150/90 mmHg is below the strict threshold required for alteplase
administration (typically must be consistently below 185/110 mmHg prior to and below
180/105 mmHg after the infusion). Option D is incorrect because a remote history of TIA is
not a contraindication to alteplase.
EXAM STUDY GUIDE: CARDIOVASCULAR,
RESPIRATORY, ENDOCRINE & INFECTIOUS
DISEASES
Section 1: Cardiovascular Pharmacology
1. A 68-year-old male with a history of chronic heart failure with reduced ejection
fraction (HFrEF, EF 30%), hypertension, and stage 3 chronic kidney disease presents
to the clinic for routine follow-up. He currently takes furosemide 40 mg daily,
lisinopril 20 mg daily, and metoprolol succinate 50 mg daily. Despite this regimen,
he continues to experience dyspnea on exertion and has bilateral pitting edema. His
blood pressure is 110/70 mmHg, heart rate is 72 bpm, and potassium is 4.2 mEq/L.
The provider decides to initiate sacubitril/valsartan. Which of the following is the
most critical consideration regarding the transition from lisinopril to
sacubitril/valsartan in this patient?
[ ] A. The patient must stop lisinopril for 12 hours before starting sacubitril/valsartan
to reduce the risk of angioedema.
[ ] B. The patient must stop lisinopril for 24 hours before starting sacubitril/valsartan
to reduce the risk of angioedema.
[✓] C. The patient must stop lisinopril for 36 hours before starting
sacubitril/valsartan to reduce the risk of angioedema.
[ ] D. The patient can transition immediately from lisinopril to sacubitril/valsartan
without a washout period.
Answer and Rationale: C
The correct answer is C. Sacubitril/valsartan is an angiotensin receptor-neprilysin inhibitor
(ARNI) that significantly reduces morbidity and mortality in HFrEF. Neprilysin is an enzyme
,that breaks down natriuretic peptides, bradykinin, and other vasoactive substances. When
combined with an ACE inhibitor, the dual inhibition of neprilysin and the renin-angiotensin-
aldosterone system (RAAS) dramatically increases the risk of life-threatening angioedema
due to bradykinin accumulation. Therefore, a strict washout period of 36 hours is required
between the last dose of an ACE inhibitor (lisinopril) and the first dose of
sacubitril/valsartan. Option A (12 hours) and Option B (24 hours) are insufficient and would
put the patient at high risk for angioedema. Option D is incorrect because an immediate
transition is absolutely contraindicated. If the patient were transitioning from an ARB to the
ARNI, no washout period is strictly required, but transitioning from an ACE inhibitor
mandates the 36-hour gap.
2. A 55-year-old female is initiated on amiodarone 400 mg daily for the management of
persistent atrial fibrillation. She has a past medical history significant for
hypothyroidism and mild liver enzyme elevations. Which of the following monitoring
parameters is most specific to the unique pharmacokinetic profile of amiodarone
and must be conducted prior to and periodically during therapy?
[ ] A. Monthly complete blood counts (CBC) to monitor for drug-induced bone
marrow suppression.
[✓] B. Baseline and serial pulmonary function tests (PFTs) and chest X-rays to
monitor for pulmonary toxicity.
[ ] C. Continuous telemetry monitoring for the first 72 hours to assess for QT
shortening.
[ ] D. Weekly vital capacity measurements using a spirometer at home to detect
early neuromuscular blockade.
Answer and Rationale: B
The correct answer is B. Amiodarone is a class III antiarrhythmic with a highly complex
pharmacokinetic profile, including extensive tissue distribution and a long half-life (up to
100 days). One of its most severe adverse effects is pulmonary toxicity, which can manifest
as interstitial pneumonitis or pulmonary fibrosis. This risk necessitates baseline and
periodic chest X-rays and pulmonary function tests (PFTs), specifically checking the
diffusing capacity for carbon monoxide (DLCO). Option A is incorrect because bone
marrow suppression is not a common adverse effect of amiodarone. Option C is incorrect
because amiodarone prolongs the QT interval, it does not shorten it, and continuous
telemetry for 72 hours is not standard for outpatient oral initiation. Option D is incorrect
because amiodarone does not cause neuromuscular blockade; home spirometry is not the
standard monitoring approach for its pulmonary toxicity. The provider must also monitor
thyroid and liver function, given this patient's history, but the pulmonary monitoring is
uniquely tied to its severe and potentially fatal respiratory complications.
, 3. A 62-year-old male with a history of hypertension and gout presents with resistant
hypertension. His current regimen includes amlodipine 10 mg daily and lisinopril 40
mg daily. His blood pressure remains 152/94 mmHg. The provider considers adding
a thiazide diuretic. Which of the following thiazide diuretics would be the most
appropriate choice for this patient to minimize the risk of exacerbating his gout,
while effectively managing his blood pressure?
[ ] A. Hydrochlorothiazide 25 mg daily
[ ] B. Chlorthalidone 25 mg daily
[✓] C. Indapamide 2.5 mg daily
[ ] D. Metolazone 5 mg daily
Answer and Rationale: C
The correct answer is C. Thiazide and thiazide-like diuretics are first-line agents for
hypertension, but they can increase serum uric acid levels by reducing renal clearance of
urate, potentially precipitating gout attacks. Indapamide is a thiazide-like diuretic that has
been shown in clinical studies to have a significantly lower impact on serum uric acid
levels compared to traditional thiazides like hydrochlorothiazide and chlorthalidone.
Therefore, in a patient with a history of gout who requires a diuretic for resistant
hypertension, indapamide is the preferred agent. Option A (hydrochlorothiazide) and
Option B (chlorthalidone) are both known to elevate uric acid levels significantly.
Chlorthalidone is more potent and longer-acting than HCTZ, but it carries a higher risk of
metabolic disturbances, including hyperuricemia. Option D (metolazone) is typically
reserved for severe edema or resistant hypertension when profound diuresis is needed,
often in combination with loop diuretics, and it also carries a substantial risk of electrolyte
and uric acid disturbances.
4. A 45-year-old male with a history of familial hypercholesterolemia presents for a
follow-up. He is currently taking atorvastatin 80 mg daily. His recent lipid panel
shows an LDL of 135 mg/dL, HDL of 40 mg/dL, and triglycerides of 150 mg/dL. The
provider decides to add evolocumab, a PCSK9 inhibitor. What is the mechanism of
action of evolocumab and how does it affect LDL receptor trafficking?
[ ] A. It inhibits the synthesis of PCSK9 in the liver, thereby increasing the
degradation of LDL receptors.
[✓] B. It binds to circulating PCSK9, preventing it from degrading LDL receptors, thus
increasing hepatic LDL clearance.
[ ] C. It acts as a bile acid sequestrant, increasing the excretion of cholesterol and
upregulating PCSK9 production.
[ ] D. It inhibits microsomal triglyceride transfer protein (MTP), reducing the hepatic
assembly of VLDL.
, Answer and Rationale: B
The correct answer is B. Evolocumab is a monoclonal antibody that binds to proprotein
convertase subtilisin/kexin type 9 (PCSK9) in the circulation. PCSK9 normally binds to LDL
receptors on the hepatocyte surface, and the complex is internalized and degraded in the
lysosome. By binding to PCSK9, evolocumab prevents PCSK9 from binding to the LDL
receptors. This preserves the LDL receptors, allowing them to recycle back to the cell
surface and continue clearing LDL cholesterol from the blood, resulting in a profound
reduction in LDL levels (often by 50-60%). Option A is incorrect because evolocumab does
not inhibit the synthesis of PCSK9, nor does it increase the degradation of LDL receptors;
rather, it prevents LDL receptor degradation. Option C describes the mechanism of bile
acid sequestrants, not PCSK9 inhibitors. Option D describes the mechanism of lomitapide,
an MTP inhibitor used in homozygous familial hypercholesterolemia, not evolocumab.
5. A 72-year-old female with a history of atrial fibrillation and a previous ischemic
stroke is brought to the emergency department with an acute onset of right-sided
weakness and aphasia. A CT scan of the head reveals an acute ischemic stroke. Her
medication list includes warfarin, but her INR on arrival is 1.2. The stroke team
decides to administer intravenous alteplase (tPA). Which of the following is an
absolute contraindication to the administration of alteplase in this patient based on
standard guidelines?
[ ] A. The patient took her prescribed dose of warfarin 12 hours ago.
[ ] B. The patient's blood pressure has been consistently 150/90 mmHg for the past
hour.
[✓] C. The patient's symptoms began approximately 6 hours prior to arrival.
[ ] D. The patient has a history of a transient ischemic attack (TIA) 6 months ago.
Answer and Rationale: C
The correct answer is C. The standard time window for the administration of intravenous
alteplase in acute ischemic stroke is 4.5 hours from the onset of symptoms. Since this
patient's symptoms began 6 hours prior to arrival, she is outside the therapeutic window,
and administering alteplase would significantly increase the risk of intracranial
hemorrhage without proven benefit. Option A is incorrect because while taking oral
anticoagulants is a contraindication if the INR is elevated, her INR is 1.2 (within normal
limits), meaning the anticoagulant effect is negligible. Option B is incorrect because a
blood pressure of 150/90 mmHg is below the strict threshold required for alteplase
administration (typically must be consistently below 185/110 mmHg prior to and below
180/105 mmHg after the infusion). Option D is incorrect because a remote history of TIA is
not a contraindication to alteplase.
