NSG 5240 Advanced Pharmacology: Ultimate
Midterm Prep (100 Q&A with Rationales) 2026/2027
section 1: Autonomic Nervous System (ANS)
1. A patient with open-angle glaucoma is prescribed Timolol (Timoptic) ophthalmic drops. The
nurse practitioner educates the patient that despite it being an eye drop, it can cause which
systemic side effect due to its mechanism of action?
A) Tachycardia and bronchodilation
B) Bradycardia and bronchoconstriction
C) Hypertension and hyperglycemia
D) Diarrhea and excessive salivation
Answer>> B
Rationale: Timolol is a non-selective beta-blocker (blocks both Beta-1 and Beta-2 receptors).
Blocking Beta-2 in the lungs causes bronchoconstriction (dangerous for asthmatics/COPD
patients). Blocking Beta-1 in the heart causes bradycardia. Ophthalmic drops can drain into the
nasolacrimal duct and be systemically absorbed.
2. A patient with myasthenia gravis is taking Pyridostigmine (Mestinon). The NP notices the
patient has new onset severe muscle weakness, excessive salivation, and abdominal cramping.
The NP recognizes this as a cholinergic crisis. What is the underlying pharmacological cause?
A) Under-medication leading to profound muscle fatigue
B) Over-medication causing excessive acetylcholine accumulation at the neuromuscular junction
,C) Destruction of the acetylcholine receptors by an autoimmune response
D) Interaction with a new beta-blocker medication
Answer>> B
Rationale: Pyridostigmine is an acetylcholinesterase inhibitor; it prevents the breakdown of ACh.
If over-medicated, ACh builds up to toxic levels, causing a "cholinergic crisis" (SLUDGE:
Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis) and paradoxical muscle
weakness due to depolarizing blockade. (Note: Under-medication causes a myasthenic crisis,
which lacks the SLUDGE symptoms).
3. A patient is admitted with organophosphate pesticide poisoning. The NP anticipates
administering which of the following medications to reverse the life-threatening muscarinic
effects (excessive secretions, bronchoconstriction)?
A) Propranolol
B) Atropine
C) Edrophonium
D) Neostigmine
Answer>> B
Rationale: Organophosphates are irreversible acetylcholinesterase inhibitors. Atropine is a
competitive antagonist at muscarinic receptors. It is given in high doses to dry up secretions,
stop bronchoconstriction, and block the muscarinic effects of the poisoning. It does not reverse
the nicotinic effects (muscle weakness), which require pralidoxime (2-PAM).
4. A patient with hypertension is prescribed Clonidine (Catapres), a central-acting alpha-2
agonist. If this medication is abruptly discontinued, what is the most dangerous adverse effect
the NP must warn the patient about?
A) Severe bradycardia
B) Rebound severe hypertension
C) Profuse diarrhea
D) Acute renal failure
,Answer>> B
Rationale: Clonidine stimulates central alpha-2 receptors, which decreases sympathetic outflow
from the CNS, lowering blood pressure. If stopped abruptly, there is a sudden surge in
sympathetic release (catecholamine rebound), causing severe, potentially fatal hypertension. It
must be tapered slowly over 2-4 days.
5. An NP is considering prescribing an alpha-1 blocker (e.g., Prazosin) for a patient with benign
prostatic hyperplasia (BPH). What adverse effect requires specific patient education before the
first dose?
A) Dry mouth
B) First-dose syncope (severe orthostatic hypotension)
C) Tachycardia
D) Urinary retention
Answer>> B
Rationale: Alpha-1 blockers relax smooth muscle in the bladder neck/prostate (good for BPH)
AND in the blood vessels (causing vasodilation). The first dose causes a rapid, profound drop in
blood pressure, particularly when moving from sitting to standing. Patients should take the first
dose at bedtime to prevent injury from fainting.
6. A patient with asthma is prescribed Albuterol (ProAir), a short-acting beta-2 agonist (SABA).
The NP explains that this medication relieves bronchospasm by:
A) Blocking parasympathetic impulses to the lungs
B) Stimulating beta-2 receptors, causing bronchial smooth muscle relaxation
C) Reducing histamine release from mast cells
D) Decreasing mucosal edema in the airways
Answer>> B
Rationale: SABAs bind to Beta-2 adrenergic receptors in the lungs, activating adenylate cyclase,
increasing cAMP, and causing relaxation of bronchial smooth muscle. Mast cell stabilizers (like
Cromolyn) reduce histamine release. Anticholinergics (like Ipratropium) block parasympathetic
impulses.
, Section 2: Cardiovascular System
7. A patient is started on Lisinopril, an ACE inhibitor. The patient calls the clinic 2 weeks later
complaining of a persistent, dry, hacking cough. The NP explains that this cough is caused by:
A) Allergic reaction to the medication
B) Accumulation of bradykinin in the lungs
C) Direct irritation of the respiratory mucosa
D) Increased pulmonary blood pressure
Answer>> B
Rationale: ACE inhibitors not only block the conversion of Angiotensin I to Angiotensin II, but
they also block the breakdown of bradykinin (a potent vasodilator). The accumulation of
bradykinin in the respiratory tract causes a dry, non-productive cough in up to 20% of patients.
If it occurs, the patient should be switched to an ARB (which does not affect bradykinin).
8. A 32-year-old female patient of childbearing age is diagnosed with hypertension. Which of
the following medications is absolutely contraindicated due to teratogenicity (fetal toxicity)?
A) Lisinopril (ACE Inhibitor)
B) Amlodipine (Calcium Channel Blocker)
C) Hydralazine (Vasodilator)
D) Labetalol (Beta Blocker)
Answer>> A
Rationale: ACE inhibitors and ARBs are highly teratogenic, especially in the 2nd and 3rd
trimesters. They can cause fetal renal agenesis, oligohydramnios, pulmonary hypoplasia, and
fetal death. They are strictly contraindicated in pregnancy.
9. A patient with heart failure is prescribed Spironolactone (Aldactone), a potassium-sparing
diuretic. The NP knows that Spironolactone is beneficial in heart failure specifically because it:
A) Causes profound diuresis, rapidly reducing pulmonary edema
Midterm Prep (100 Q&A with Rationales) 2026/2027
section 1: Autonomic Nervous System (ANS)
1. A patient with open-angle glaucoma is prescribed Timolol (Timoptic) ophthalmic drops. The
nurse practitioner educates the patient that despite it being an eye drop, it can cause which
systemic side effect due to its mechanism of action?
A) Tachycardia and bronchodilation
B) Bradycardia and bronchoconstriction
C) Hypertension and hyperglycemia
D) Diarrhea and excessive salivation
Answer>> B
Rationale: Timolol is a non-selective beta-blocker (blocks both Beta-1 and Beta-2 receptors).
Blocking Beta-2 in the lungs causes bronchoconstriction (dangerous for asthmatics/COPD
patients). Blocking Beta-1 in the heart causes bradycardia. Ophthalmic drops can drain into the
nasolacrimal duct and be systemically absorbed.
2. A patient with myasthenia gravis is taking Pyridostigmine (Mestinon). The NP notices the
patient has new onset severe muscle weakness, excessive salivation, and abdominal cramping.
The NP recognizes this as a cholinergic crisis. What is the underlying pharmacological cause?
A) Under-medication leading to profound muscle fatigue
B) Over-medication causing excessive acetylcholine accumulation at the neuromuscular junction
,C) Destruction of the acetylcholine receptors by an autoimmune response
D) Interaction with a new beta-blocker medication
Answer>> B
Rationale: Pyridostigmine is an acetylcholinesterase inhibitor; it prevents the breakdown of ACh.
If over-medicated, ACh builds up to toxic levels, causing a "cholinergic crisis" (SLUDGE:
Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis) and paradoxical muscle
weakness due to depolarizing blockade. (Note: Under-medication causes a myasthenic crisis,
which lacks the SLUDGE symptoms).
3. A patient is admitted with organophosphate pesticide poisoning. The NP anticipates
administering which of the following medications to reverse the life-threatening muscarinic
effects (excessive secretions, bronchoconstriction)?
A) Propranolol
B) Atropine
C) Edrophonium
D) Neostigmine
Answer>> B
Rationale: Organophosphates are irreversible acetylcholinesterase inhibitors. Atropine is a
competitive antagonist at muscarinic receptors. It is given in high doses to dry up secretions,
stop bronchoconstriction, and block the muscarinic effects of the poisoning. It does not reverse
the nicotinic effects (muscle weakness), which require pralidoxime (2-PAM).
4. A patient with hypertension is prescribed Clonidine (Catapres), a central-acting alpha-2
agonist. If this medication is abruptly discontinued, what is the most dangerous adverse effect
the NP must warn the patient about?
A) Severe bradycardia
B) Rebound severe hypertension
C) Profuse diarrhea
D) Acute renal failure
,Answer>> B
Rationale: Clonidine stimulates central alpha-2 receptors, which decreases sympathetic outflow
from the CNS, lowering blood pressure. If stopped abruptly, there is a sudden surge in
sympathetic release (catecholamine rebound), causing severe, potentially fatal hypertension. It
must be tapered slowly over 2-4 days.
5. An NP is considering prescribing an alpha-1 blocker (e.g., Prazosin) for a patient with benign
prostatic hyperplasia (BPH). What adverse effect requires specific patient education before the
first dose?
A) Dry mouth
B) First-dose syncope (severe orthostatic hypotension)
C) Tachycardia
D) Urinary retention
Answer>> B
Rationale: Alpha-1 blockers relax smooth muscle in the bladder neck/prostate (good for BPH)
AND in the blood vessels (causing vasodilation). The first dose causes a rapid, profound drop in
blood pressure, particularly when moving from sitting to standing. Patients should take the first
dose at bedtime to prevent injury from fainting.
6. A patient with asthma is prescribed Albuterol (ProAir), a short-acting beta-2 agonist (SABA).
The NP explains that this medication relieves bronchospasm by:
A) Blocking parasympathetic impulses to the lungs
B) Stimulating beta-2 receptors, causing bronchial smooth muscle relaxation
C) Reducing histamine release from mast cells
D) Decreasing mucosal edema in the airways
Answer>> B
Rationale: SABAs bind to Beta-2 adrenergic receptors in the lungs, activating adenylate cyclase,
increasing cAMP, and causing relaxation of bronchial smooth muscle. Mast cell stabilizers (like
Cromolyn) reduce histamine release. Anticholinergics (like Ipratropium) block parasympathetic
impulses.
, Section 2: Cardiovascular System
7. A patient is started on Lisinopril, an ACE inhibitor. The patient calls the clinic 2 weeks later
complaining of a persistent, dry, hacking cough. The NP explains that this cough is caused by:
A) Allergic reaction to the medication
B) Accumulation of bradykinin in the lungs
C) Direct irritation of the respiratory mucosa
D) Increased pulmonary blood pressure
Answer>> B
Rationale: ACE inhibitors not only block the conversion of Angiotensin I to Angiotensin II, but
they also block the breakdown of bradykinin (a potent vasodilator). The accumulation of
bradykinin in the respiratory tract causes a dry, non-productive cough in up to 20% of patients.
If it occurs, the patient should be switched to an ARB (which does not affect bradykinin).
8. A 32-year-old female patient of childbearing age is diagnosed with hypertension. Which of
the following medications is absolutely contraindicated due to teratogenicity (fetal toxicity)?
A) Lisinopril (ACE Inhibitor)
B) Amlodipine (Calcium Channel Blocker)
C) Hydralazine (Vasodilator)
D) Labetalol (Beta Blocker)
Answer>> A
Rationale: ACE inhibitors and ARBs are highly teratogenic, especially in the 2nd and 3rd
trimesters. They can cause fetal renal agenesis, oligohydramnios, pulmonary hypoplasia, and
fetal death. They are strictly contraindicated in pregnancy.
9. A patient with heart failure is prescribed Spironolactone (Aldactone), a potassium-sparing
diuretic. The NP knows that Spironolactone is beneficial in heart failure specifically because it:
A) Causes profound diuresis, rapidly reducing pulmonary edema
