NR 565 - Advanced Pharmacology Midterm – Chamberlain
Complete Study Guide with 200+ Questions with Answers &
Rationales
1. 1st line treatment of osteoporosis – ANSWER alendronate
Rationale: Alendronate is a bisphosphonate that is considered first-line therapy
for osteoporosis in most patients. It reduces bone resorption, increases bone
mineral density, and decreases fracture risk. It is preferred due to its efficacy,
once-weekly dosing, and extensive clinical evidence supporting its use.
2. **A 41-year-old patient comes into the clinic complaining of increased
heart rate after starting nitro patches for stable angina. What would an
appropriate response be?
let’s lower the dose and frequency of use
I will prescribe a BB to help with this
Next time this happens, lie down and practice deep breathing, this will bring your
heart rate down –
ANSWER2- I will prescribe a BB to help with this**
Rationale: Nitroglycerin causes vasodilation, which lowers blood pressure and
triggers a reflex tachycardia via the baroreceptor reflex. This tachycardia increases
myocardial oxygen demand, counteracting the therapeutic benefit of nitroglycerin.
Beta-blockers (BB) suppress this reflex tachycardia by blocking sympathetic
activation of beta-1 adrenergic receptors on the heart, thereby reducing heart rate
and myocardial oxygen demand. This is the most appropriate pharmacological
intervention.
3. **A 55-year-old male comes into the clinic with a gouty arthritis. He states
that he has one flareup a year. Your response is:
, I will prescribe you glucocorticoids to help with inflammation
Let’s start you on prophylactic therapy colchicine.
4. It will be helpful to take an NSAID to start with to help relieve some inflammation.
I'll prescribe naproxen. - ANSWER3- in patients with infrequent flareups, being
less than three per year, treatment of symptoms is all that’s needed. NSAIDS are
the first line agent for relieving pain of an acute gout attack. **
Rationale: For patients with infrequent gout flares (less than three per year), acute
symptomatic treatment is appropriate. NSAIDs (like naproxen) are first-line for
acute gout attacks due to their rapid anti-inflammatory and analgesic effects.
Prophylactic therapy with colchicine is indicated only for patients with frequent
flares (three or more per year) or those with tophi or joint damage. Glucocorticoids
are second-line or reserved for patients with contraindications to NSAIDs.
2. 12 CDC guidelines for prescribing opioids - ANSWEROpioids are not first
line therapy; establish goals for pain and function; Discuss risks and benefits;
Use immediate release opioids when starting; Use the lowest effective dose;
Prescribe short durations for acute pain; Evaluate benefits and harms
frequently; Use strategies to mitigate risk; Review PDMP data; Use urine
drug testing; Avoid concurrent opioid and benzo prescribing; Offer treatment
for opioid use disorder
Rationale: These guidelines from the CDC (2016, updated 2022) are designed to
improve the safety and effectiveness of opioid prescribing for chronic pain outside
of active cancer treatment, palliative care, and end-of-life care. They emphasize
non-opioid therapies first, careful risk-benefit assessment, starting with the lowest
effective dose of immediate-release opioids, frequent monitoring, and using
prescription drug monitoring programs (PDMPs) and urine drug testing to reduce
the risk of misuse, diversion, and overdose.
,5. **A patient comes in stating that he tried NSAIDS to relieve a gouty attack but it
hasnt helped. He asks, "what are my options?" He further states that he has attacks
every few years but when he does NSAIDS do not help. Your response is:
6. I can prescribe a glucocorticoid (prednisone) and that will bring down the
inflammation and pain.
7. Have your tried increasing your dosage of NSAIDS and drink plenty of water?
8. Lets start by making some changes in your diet, can you tell me what you eat
regularly? - ANSWER1**
Rationale: When NSAIDs are ineffective or contraindicated for an acute gout
attack, glucocorticoids (e.g., prednisone) are a highly effective alternative due to
their potent anti-inflammatory effects. While dietary changes (option 3) are
important for long-term management, they are not appropriate as the primary acute
intervention. Increasing NSAID dosage (option 2) is not advised if the current dose
has failed and could increase toxicity.
6. A patient with HF develops fibrotic changes, what should the provider do
next? - ANSWERensure that a patient is on an ARB (valsartan) as this
inhibits fibrosis (aldosterone antagonist)
Rationale: In heart failure, aldosterone promotes myocardial fibrosis and
remodeling. ARBs (angiotensin receptor blockers) like valsartan, along with ACE
inhibitors and aldosterone antagonists (spironolactone/eplerenone), help prevent
and reverse fibrotic changes by blocking the renin-angiotensin-aldosterone system
(RAAS). Ensuring the patient is on an ARB is a key step in managing HF and
limiting fibrotic progression.
, 7. A person who is depend on a pure opioid agonist should NEVER receive an
opioid agonist antagonist - ANSWERtrue
Rationale: Opioid agonist-antagonists (e.g., buprenorphine, pentazocine) can
precipitate acute withdrawal in a patient who is physically dependent on a pure
opioid agonist (like morphine or oxycodone). These drugs have partial agonist
activity and can displace full agonists from opioid receptors, leading to withdrawal
symptoms. They should be avoided or used with extreme caution in such patients.
8. **ACE inhibitors MOA - ANSWERAngiotensin Converting Enzyme Inhibitors
(ACE-I) prevent the conversion of angiotensin I to angiotensin II, which disrupts
the renin-angiotensin-aldosterone system (RAAS).
9. reduce levels of angiotensin II (through inhibition of ACE)
10.increasing levels of bradykinin (through inhibition of kinase 11)
End in -pril**
Rationale: ACE inhibitors work by blocking the ACE enzyme, which converts
angiotensin I to the potent vasoconstrictor angiotensin II. This reduces blood
pressure, decreases aldosterone secretion, and increases sodium/water excretion.
They also inhibit kinase II, which breaks down bradykinin, leading to increased
bradykinin levels (which contributes to vasodilation but also to side effects like
cough and angioedema).
9. adverse effects for bisphosphonates - ANSWERosteonecrosis of the jaw and
hip fracture, Esophagitis
Rationale: Bisphosphonates can cause esophagitis and esophageal ulcers if not
taken properly (with a full glass of water and remaining upright). Long-term use is
associated with osteonecrosis of the jaw (ONJ), especially after dental procedures,
Complete Study Guide with 200+ Questions with Answers &
Rationales
1. 1st line treatment of osteoporosis – ANSWER alendronate
Rationale: Alendronate is a bisphosphonate that is considered first-line therapy
for osteoporosis in most patients. It reduces bone resorption, increases bone
mineral density, and decreases fracture risk. It is preferred due to its efficacy,
once-weekly dosing, and extensive clinical evidence supporting its use.
2. **A 41-year-old patient comes into the clinic complaining of increased
heart rate after starting nitro patches for stable angina. What would an
appropriate response be?
let’s lower the dose and frequency of use
I will prescribe a BB to help with this
Next time this happens, lie down and practice deep breathing, this will bring your
heart rate down –
ANSWER2- I will prescribe a BB to help with this**
Rationale: Nitroglycerin causes vasodilation, which lowers blood pressure and
triggers a reflex tachycardia via the baroreceptor reflex. This tachycardia increases
myocardial oxygen demand, counteracting the therapeutic benefit of nitroglycerin.
Beta-blockers (BB) suppress this reflex tachycardia by blocking sympathetic
activation of beta-1 adrenergic receptors on the heart, thereby reducing heart rate
and myocardial oxygen demand. This is the most appropriate pharmacological
intervention.
3. **A 55-year-old male comes into the clinic with a gouty arthritis. He states
that he has one flareup a year. Your response is:
, I will prescribe you glucocorticoids to help with inflammation
Let’s start you on prophylactic therapy colchicine.
4. It will be helpful to take an NSAID to start with to help relieve some inflammation.
I'll prescribe naproxen. - ANSWER3- in patients with infrequent flareups, being
less than three per year, treatment of symptoms is all that’s needed. NSAIDS are
the first line agent for relieving pain of an acute gout attack. **
Rationale: For patients with infrequent gout flares (less than three per year), acute
symptomatic treatment is appropriate. NSAIDs (like naproxen) are first-line for
acute gout attacks due to their rapid anti-inflammatory and analgesic effects.
Prophylactic therapy with colchicine is indicated only for patients with frequent
flares (three or more per year) or those with tophi or joint damage. Glucocorticoids
are second-line or reserved for patients with contraindications to NSAIDs.
2. 12 CDC guidelines for prescribing opioids - ANSWEROpioids are not first
line therapy; establish goals for pain and function; Discuss risks and benefits;
Use immediate release opioids when starting; Use the lowest effective dose;
Prescribe short durations for acute pain; Evaluate benefits and harms
frequently; Use strategies to mitigate risk; Review PDMP data; Use urine
drug testing; Avoid concurrent opioid and benzo prescribing; Offer treatment
for opioid use disorder
Rationale: These guidelines from the CDC (2016, updated 2022) are designed to
improve the safety and effectiveness of opioid prescribing for chronic pain outside
of active cancer treatment, palliative care, and end-of-life care. They emphasize
non-opioid therapies first, careful risk-benefit assessment, starting with the lowest
effective dose of immediate-release opioids, frequent monitoring, and using
prescription drug monitoring programs (PDMPs) and urine drug testing to reduce
the risk of misuse, diversion, and overdose.
,5. **A patient comes in stating that he tried NSAIDS to relieve a gouty attack but it
hasnt helped. He asks, "what are my options?" He further states that he has attacks
every few years but when he does NSAIDS do not help. Your response is:
6. I can prescribe a glucocorticoid (prednisone) and that will bring down the
inflammation and pain.
7. Have your tried increasing your dosage of NSAIDS and drink plenty of water?
8. Lets start by making some changes in your diet, can you tell me what you eat
regularly? - ANSWER1**
Rationale: When NSAIDs are ineffective or contraindicated for an acute gout
attack, glucocorticoids (e.g., prednisone) are a highly effective alternative due to
their potent anti-inflammatory effects. While dietary changes (option 3) are
important for long-term management, they are not appropriate as the primary acute
intervention. Increasing NSAID dosage (option 2) is not advised if the current dose
has failed and could increase toxicity.
6. A patient with HF develops fibrotic changes, what should the provider do
next? - ANSWERensure that a patient is on an ARB (valsartan) as this
inhibits fibrosis (aldosterone antagonist)
Rationale: In heart failure, aldosterone promotes myocardial fibrosis and
remodeling. ARBs (angiotensin receptor blockers) like valsartan, along with ACE
inhibitors and aldosterone antagonists (spironolactone/eplerenone), help prevent
and reverse fibrotic changes by blocking the renin-angiotensin-aldosterone system
(RAAS). Ensuring the patient is on an ARB is a key step in managing HF and
limiting fibrotic progression.
, 7. A person who is depend on a pure opioid agonist should NEVER receive an
opioid agonist antagonist - ANSWERtrue
Rationale: Opioid agonist-antagonists (e.g., buprenorphine, pentazocine) can
precipitate acute withdrawal in a patient who is physically dependent on a pure
opioid agonist (like morphine or oxycodone). These drugs have partial agonist
activity and can displace full agonists from opioid receptors, leading to withdrawal
symptoms. They should be avoided or used with extreme caution in such patients.
8. **ACE inhibitors MOA - ANSWERAngiotensin Converting Enzyme Inhibitors
(ACE-I) prevent the conversion of angiotensin I to angiotensin II, which disrupts
the renin-angiotensin-aldosterone system (RAAS).
9. reduce levels of angiotensin II (through inhibition of ACE)
10.increasing levels of bradykinin (through inhibition of kinase 11)
End in -pril**
Rationale: ACE inhibitors work by blocking the ACE enzyme, which converts
angiotensin I to the potent vasoconstrictor angiotensin II. This reduces blood
pressure, decreases aldosterone secretion, and increases sodium/water excretion.
They also inhibit kinase II, which breaks down bradykinin, leading to increased
bradykinin levels (which contributes to vasodilation but also to side effects like
cough and angioedema).
9. adverse effects for bisphosphonates - ANSWERosteonecrosis of the jaw and
hip fracture, Esophagitis
Rationale: Bisphosphonates can cause esophagitis and esophageal ulcers if not
taken properly (with a full glass of water and remaining upright). Long-term use is
associated with osteonecrosis of the jaw (ONJ), especially after dental procedures,
