CCPP Module 13, Section 4: Clinical Scenarios by Specialty
Module 13: Pharmacotherapeutic Management and Optimization

Section 4: Clinical Scenarios by Specialty

Apply your skills in real-world case studies. This section will walk through complex patient scenarios in common disease states, challenging you to make and justify therapeutic decisions from initiation to optimization.

SECTION 13.4

The Clinical Simulator: From Theory to Therapy

Applying Your Comprehensive Skillset to Complex, Real-World Patient Cases.

13.4.1 The “Why”: Where Knowledge Becomes Judgment

The previous sections of this module have equipped you with the foundational skills of a collaborative practice pharmacist. You have learned the systematic frameworks for initiating, adjusting, and discontinuing medications. You have mastered the proactive mindset of safety monitoring and the art of deprescribing. You have, in essence, assembled a powerful toolkit of clinical capabilities. But a toolkit, no matter how sophisticated, is only as good as the artisan who wields it. This section is the workshop where you will learn to use those tools in concert to create masterpieces of clinical care. This is where abstract knowledge transforms into applied clinical judgment.

Real patients are never as neat as textbook examples. They do not present with a single disease state. They arrive with a tangled web of comorbidities, a long list of medications prescribed by multiple specialists, variable adherence, socioeconomic barriers, and personal beliefs that shape their health. A patient with diabetes also has chronic kidney disease and heart failure. A patient with hypertension also has hyperkalemia and gout. It is in this crucible of complexity that a CCPP pharmacist truly proves their worth. Your value is not in simply knowing the diabetes guidelines; it is in knowing how to apply them to a patient whose renal function limits your first-line choices and whose cardiovascular risk demands a specific, evidence-based agent.

The “Why” of this section is to simulate this complexity. We will move beyond single-drug or single-disease-state thinking and dive into holistic, patient-centered case management. The following clinical scenarios are designed to be challenging. They will force you to integrate multiple guidelines, weigh competing risks and benefits, anticipate problems, and formulate a comprehensive plan that is safe, effective, and tailored to the individual. This is the final and most important step in your training: moving from knowing the “what” and “how” to mastering the “why” and “for whom.” This is the clinical simulator where you will earn your wings as a true therapeutic decision-maker.

Pharmacist Analogy: The Chess Grandmaster

Learning the rules of pharmacotherapy is like learning how the pieces move in chess. You learn that a bishop moves diagonally (an ACE inhibitor is good for diabetic kidney disease), a knight moves in an “L” shape (metformin can cause GI upset), and a rook moves in straight lines (a statin lowers cholesterol). The previous sections taught you these moves. You can now look at any single piece and know its function perfectly.

A complex patient case, however, is not about a single piece. It is a mid-game chessboard, filled with pieces from both sides, each exerting pressure and controlling different squares. A novice player only sees their next move. A Grandmaster sees the entire board. They don’t just think, “I can move my knight here.” They think, “If I move my knight here, it will attack his rook, but it will expose my bishop to his queen and weaken my pawn structure on the left side of the board. Is that trade-off worth it in the long run?”

This is the level of thinking required in these scenarios.

  • “Attacking his rook” is choosing an SGLT2 inhibitor to lower the A1c.
  • “Exposing my bishop” is recognizing that the patient’s eGFR is near the cutoff for that SGLT2 inhibitor, creating a risk of acute kidney injury.
  • “Weakening my pawn structure” is acknowledging the potential for genitourinary side effects and the high cost of the medication, which could impact adherence.

Your job in this section is to stop playing checkers—making simple, one-for-one moves—and start playing chess. You must assess the entire board (the patient’s full clinical picture), anticipate your opponent’s moves (potential adverse effects and drug interactions), and make strategic decisions that best position you for a long-term win (improved patient outcomes). This is the transition from tactician to strategist, from pharmacist to clinical grandmaster.

13.4.2 Diabetes Masterclass: The Patient with Triple Comorbidity

This case is designed to test your ability to navigate the complex, overlapping guidelines for type 2 diabetes (T2DM), atherosclerotic cardiovascular disease (ASCVD), heart failure with reduced ejection fraction (HFrEF), and chronic kidney disease (CKD). Your decision will have profound implications for the patient’s cardiovascular, renal, and metabolic future.

Case Presentation: Mr. Chen

Patient: Mr. Chen is a 68-year-old man presenting to your pharmacist-led chronic care management clinic for a follow-up on his T2DM.

History of Present Illness: He reports feeling more fatigued than usual and notes his shoes feel tight at the end of the day. He checks his blood glucose “a few times a week,” with fasting values ranging from 150-180 mg/dL. He denies chest pain but does admit to getting short of breath more easily when walking up the single flight of stairs to his apartment.

Past Medical History:

  • Type 2 Diabetes (12-year history)
  • Hypertension
  • Hyperlipidemia
  • Coronary Artery Disease (CAD) s/p Percutaneous Coronary Intervention (PCI) with stent to LAD 3 years ago
  • Heart Failure with Reduced Ejection Fraction (HFrEF), last known EF 35%

Current Medications:

  • Metformin 1000 mg PO BID
  • Glipizide 10 mg PO BID
  • Lisinopril 40 mg PO daily
  • Carvedilol 25 mg PO BID
  • Atorvastatin 80 mg PO daily
  • Aspirin 81 mg PO daily
  • Clopidogrel 75 mg PO daily
  • Furosemide 40 mg PO daily

Vitals & Physical Exam:

  • BP: 138/84 mmHg
  • HR: 68 bpm
  • Weight: 95 kg (up 3 kg from 3 months ago)
  • Exam: Notable for 1+ bilateral lower extremity pitting edema.

Recent Labs:

  • HbA1c: 8.4%
  • SCr: 1.6 mg/dL (baseline was 1.4 mg/dL 6 months ago)
  • eGFR: 42 mL/min/1.73m²
  • K+: 4.8 mEq/L
  • Lipid Panel: TC 150, TGs 180, HDL 35, LDL 79
  • Urine Albumin-to-Creatinine Ratio (UACR): 150 mg/g

The Central Clinical Challenge

Mr. Chen has uncontrolled T2DM (A1c 8.4%) despite being on two agents, including one (glipizide) that poses a significant hypoglycemia risk. More importantly, his current regimen is not optimized according to current guidelines for a patient with established ASCVD, HFrEF, and CKD with albuminuria. Your task is to completely overhaul his diabetes regimen to simultaneously improve glycemic control and, more critically, reduce his risk of cardiovascular and renal disease progression.

Pharmacist’s Systematic Workup
1. Initial Assessment & Problem List Synthesis:
  • Uncontrolled T2DM: A1c of 8.4% is well above the goal of <7%.
  • High-Risk Medication Use: Glipizide carries a significant risk of hypoglycemia and provides no cardiovascular or renal benefit. It is a PIM per the Beers Criteria due to its long action.
  • Guideline-Care Gap (Major): Patient has three compelling indications (ASCVD, HFrEF, CKD) for specific classes of glucose-lowering therapy that he is not currently receiving.
  • Progressive CKD: His eGFR has declined, and he has albuminuria, placing him at high risk for progression to ESRD.
  • Worsening HF: His weight gain, edema, and increased dyspnea suggest his fluid status is not optimized.
  • Sub-optimal BP Control: BP of 138/84 mmHg is above the goal of <130/80 mmHg.
2. Guideline Application & Goal Setting:
  • ADA/KDIGO Guidelines: For a T2DM patient with CKD and albuminuria, a first-line agent after metformin should be an SGLT2 inhibitor shown to reduce CKD progression and cardiovascular events.
  • ACC/AHA/HFSA Guidelines: For a T2DM patient with HFrEF, an SGLT2 inhibitor (specifically empagliflozin, dapagliflozin, or sotagliflozin) is now considered foundational, guideline-directed medical therapy (GDMT) independent of A1c, as it reduces HF hospitalizations and cardiovascular death.
  • ADA/ACC Guidelines: For a T2DM patient with established ASCVD, an agent with proven cardiovascular benefit (a GLP-1 RA or SGLT2 inhibitor) must be part of the regimen.
  • Patient-Specific Goals: A1c < 7.0%, BP < 130/80 mmHg, prevent further decline in eGFR, improve HF symptoms, and eliminate high-risk medications.
The Guideline Convergence Point

Notice the power of the evidence: all three major guidelines—diabetes, kidney, and heart failure—are pointing to the exact same drug class as the mandatory next step. The use of an SGLT2 inhibitor in Mr. Chen is not just a good idea for his glucose; it is the single most important intervention you can make to treat his heart failure and protect his kidneys. This is the epitome of “two-for-one” (or in this case, “three-for-one”) prescribing.

3. Therapeutic Plan Formulation:

Your plan must be decisive and address the highest-risk issues first.

Step A: Deprescribe the Harmful Agent.

The glipizide provides no organ protection and poses a significant risk of hypoglycemia, which could lead to a fall and devastating injury in this patient. It must be discontinued.

Step B: Initiate the Most Beneficial Agent.

An SGLT2 inhibitor is the clear choice. Which one? We need to check the evidence and the patient’s renal function.

Agent eGFR Cutoff for Initiation Proven Benefit in HFrEF & CKD
Empagliflozin (Jardiance) ≥ 20 mL/min/1.73m² Yes (EMPEROR-Reduced, EMPA-KIDNEY)
Dapagliflozin (Farxiga) ≥ 25 mL/min/1.73m² Yes (DAPA-HF, DAPA-CKD)
Canagliflozin (Invokana) ≥ 30 mL/min/1.73m² Yes (CANVAS, CREDENCE)

Mr. Chen’s eGFR is 42. Therefore, either empagliflozin or dapagliflozin would be an excellent, evidence-based choice. Let’s select Empagliflozin.

Step C: Create the Dosing, Monitoring, and Counseling Plan.

  • Dosing:
    • Discontinue Glipizide 10mg BID immediately.
    • Initiate Empagliflozin 10 mg PO daily. (Standard starting dose, does not require titration for HF/CKD benefit).
    • Continue Metformin 1000mg BID.
  • Monitoring:
    • Expect a small, transient dip in eGFR (around 5-10%) upon initiation of an SGLT2i. This is a normal hemodynamic effect and a sign the drug is working. Do not panic and stop the drug. Check a BMP in 1-2 weeks to ensure the dip is not >30% and to monitor potassium.
    • Patient to monitor for signs of genitourinary infections.
    • Patient to monitor for symptoms of hypotension, especially given the diuretic effect.
    • Recheck A1c in 3 months.
  • Counseling:
    • Explain the “why”: “Mr. Chen, we are stopping your glipizide because it carries a risk of low blood sugar and isn’t the best option for you. We are starting a new medication called Jardiance. While it will help your blood sugar, the main reason we are using it is that it has been proven to protect your heart and your kidneys from further damage. It is one of the most important medications you can be on.”
    • Explain the side effects: Counsel on the risk of yeast infections and the importance of good hygiene. Explain the “sick day” protocol: if he develops vomiting or diarrhea and can’t stay hydrated, he should temporarily hold the SGLT2 inhibitor.
4. Address Secondary Problems:
  • Heart Failure: The SGLT2i will also act as a mild osmotic diuretic and will likely help his fluid status. However, his dose of furosemide may need adjustment based on his daily weights and symptoms.
  • Hypertension: The SGLT2i will also have a modest blood-pressure-lowering effect. This may be enough to get him to goal. If his BP remains elevated after 4 weeks, consider adding a mineralocorticoid receptor antagonist (MRA) like spironolactone, which is also GDMT for HFrEF, but would require very close monitoring of his K+ and eGFR.

13.4.3 Hypertension Masterclass: The Resistant Hypertension Puzzle

This case challenges you to think like a detective to uncover the root causes of resistant hypertension and to use a systematic, evidence-based approach to select and monitor the appropriate fourth-line agent in a patient with complicating factors.

Case Presentation: Ms. Washington

Patient: Ms. Washington is a 72-year-old woman with a long history of difficult-to-control hypertension. She is referred to your clinic for management of “resistant hypertension.”

History of Present Illness: She diligently checks her blood pressure at home, bringing you a log showing morning BPs consistently in the 150s/90s. She feels frustrated, stating “I take all my pills, I don’t add salt to my food, I don’t know what else to do.” She also complains of chronic knee pain from osteoarthritis, for which she takes “something from the drug store.”

Past Medical History:

  • Hypertension (20+ year history)
  • Gout (last flare 1 year ago)
  • Stage 3b CKD
  • Osteoarthritis of the knees

Current Medications (Confirmed via Reconciliation):

  • Lisinopril 40 mg PO daily
  • Amlodipine 10 mg PO daily
  • Chlorthalidone 25 mg PO daily
  • Allopurinol 300 mg PO daily
  • Ibuprofen 600 mg PO TID PRN knee pain (reports taking it “most days”)

Vitals & Physical Exam:

  • BP: 158/92 mmHg (taken in both arms, proper technique)
  • HR: 76 bpm

Recent Labs:

  • SCr: 1.5 mg/dL
  • eGFR: 38 mL/min/1.73m²
  • K+: 5.1 mEq/L
  • Na+: 137 mEq/L

The Central Clinical Challenge

Ms. Washington meets the definition of resistant hypertension: uncontrolled BP despite the use of three antihypertensive agents from different classes, including a diuretic, at maximally tolerated doses. Your job is twofold: first, to investigate and eliminate potential exacerbating factors, and second, to choose and safely implement a fourth-line agent in the context of her CKD and borderline hyperkalemia.

Pharmacist’s Systematic Workup
1. Confirm True Resistance & Investigate Exacerbating Factors:

Before adding a fourth drug, you must play detective. The mnemonic “ABCDE” can help.

  • A (Adherence): You’ve already done a reconciliation, but you probe further. Her frustration suggests she is likely adherent, but it’s always worth confirming.
  • B (Bad Lifestyle/White Coat): Her home BP log rules out white coat hypertension. She reports a low-salt diet, but you provide more specific education.
  • C (Contributing Drugs): This is the red flag. Her near-daily use of ibuprofen, a potent NSAID, is almost certainly contributing to her resistant hypertension. NSAIDs cause sodium and water retention and interfere with the action of most antihypertensives, especially diuretics and ACE inhibitors.
  • D (Dosing): Her current three agents are at appropriate maximum doses.
  • E (Etiology – Secondary Causes): While less common, you keep secondary causes like primary aldosteronism or renal artery stenosis in the back of your mind.
The Number One Rule of Resistant HTN

Always look for the offending agent first. More often than not, resistant hypertension is being caused or significantly worsened by an interfering substance. NSAIDs are the most common culprit, followed by decongestants, excessive alcohol, and certain herbal supplements. Stopping the offending agent is a more powerful intervention than adding a fourth antihypertensive.

2. Therapeutic Plan – Part 1 (Subtraction):
  • The Primary Intervention: Your first and most important action is to address the ibuprofen. You must counsel Ms. Washington on the impact it’s having on her blood pressure and kidneys.
    • The Script: “Ms. Washington, I think I’ve found a major reason why your blood pressure is so stubborn. The ibuprofen you’re taking for your arthritis, while good for pain, is known to work against your blood pressure pills and can be hard on the kidneys. My first goal is to find a safer way to manage your pain so we can stop the ibuprofen. This single change might make a huge difference for your blood pressure.”
  • Provide Alternatives for Pain:
    • Scheduled acetaminophen up to 3g/day.
    • Topical diclofenac gel applied directly to the knees.
    • Referral to physical therapy.
    • Intra-articular steroid injections.
  • The Plan: You will have her stop the ibuprofen completely, start scheduled acetaminophen, and try topical diclofenac. You will ask her to monitor her BP closely for the next 2 weeks and then return for follow-up.
3. Therapeutic Plan – Part 2 (Addition, If Still Needed):

Let’s assume Ms. Washington returns in 2 weeks. She has stopped the ibuprofen. Her knee pain is managed with acetaminophen and topical gel. However, her home BPs are still averaging 145/88. You have removed the exacerbating factor, but she still has true resistance. Now, you must choose a fourth agent.

  • Guideline Application (2017 ACC/AHA): For resistant hypertension, the preferred fourth-line add-on therapy is a mineralocorticoid receptor antagonist (MRA).
  • The Agent of Choice: Spironolactone.
  • The “Gotcha”: Her baseline potassium is 5.1 mEq/L and her eGFR is 38. This makes initiating spironolactone a high-risk maneuver that requires extreme caution and a robust monitoring plan.
The Spironolactone Safety Checklist

Before initiating spironolactone in a patient with CKD, you must go through a mental safety checklist.

  1. Is the eGFR > 30? Yes, hers is 38. (Most experts avoid use if eGFR < 30).
  2. Is the baseline K+ < 5.0? No, hers is 5.1. This is a relative contraindication. You must first take action to lower her potassium.
  3. Are they on other drugs that raise K+? Yes, an ACE inhibitor (lisinopril). This is an expected interaction but increases the risk. Are they on potassium supplements or using salt substitutes (potassium chloride)? You must confirm they are not.

4. The Final, Refined Plan:
  • Address the Hyperkalemia: You will provide dietary counseling to strictly limit high-potassium foods (bananas, potatoes, oranges). You will recheck her potassium in one week.
  • The Recheck: She returns in one week, having followed the diet, and her K+ is now 4.8 mEq/L. You can now proceed cautiously.
  • Initiate Spironolactone: Start with a very low dose: 12.5 mg PO daily.
  • The Critical Monitoring Plan:
    • Check a BMP (for K+ and SCr) in 3-7 days. This is non-negotiable.
    • If K+ remains ≤ 5.5 and SCr is stable, check BMP again in 2-4 weeks.
    • If BP is still not at goal after 4 weeks and labs are stable, you can consider titrating to 25 mg daily, followed by the same intense lab monitoring.
  • Counseling: “Ms. Washington, we are going to add a new water pill called spironolactone. It works differently and is very effective when other pills aren’t enough. However, it can affect your potassium levels, so it is absolutely critical that you get your bloodwork done exactly when we schedule it so I can make sure it’s safe for you. We also need to be careful with your diet.” You also counsel her on the potential for gynecomastia.