NUR 557 Module 2 Case Paper Example

Pressure, Salt and Angiotensin: Joining the Pathophysiology of Hypertension to Two Drugs in a 68-Year-Old

[Student Name]

Southern New Hampshire University

NUR 557: Advanced Pathophysiology and Pharmacology Across the Lifespan

Case Paper

[Instructor Name]

[Date]

The organization, setting and figures below are a composite written as a model document. No real employer, client, colleague or patient is described.

Pressure, Salt and Angiotensin: Joining the Pathophysiology of Hypertension to Two Drugs in a 68-Year-Old

Blood pressure is the product of cardiac output and systemic vascular resistance, and chronic hypertension reflects a sustained shift in the systems that set both. In older adults, stiffening arteries and changes in how the kidneys handle sodium are especially important. This paper explains the hypertension of a composite 68-year-old woman and joins each treatment to the part of the mechanism it targets. It argues that combining a thiazide-like diuretic with an ACE inhibitor makes sense because each drug blocks a different step in the same loop, and each offsets a weakness of the other, while her age and kidney findings determine both the choice and the monitoring.

The Case

Our composite patient, 68 years old and female, manages type 2 diabetes on metformin alone. Two weeks of home blood pressure readings averaged 156/94 mm Hg, confirming the elevated clinic readings. Kidney tests show an estimated filtration rate of 58 and 60 mg of albumin per gram of creatinine in her urine, with potassium 4.4 mmol/L and sodium 139 mmol/L. She has no heart failure or coronary disease. She lives alone and walks daily.

Why Her Pressure Is High

Three processes combine. First, with age the large arteries lose elasticity as elastin fragments and collagen increases, so they buffer each heartbeat less and systolic pressure rises. Second, the kidneys set long-term pressure through sodium balance; when they excrete sodium less readily, as often happens with age, diabetes and early kidney disease, blood volume and pressure rise until enough sodium is excreted to restore balance. Third, the renin-angiotensin-aldosterone system amplifies both processes. Renin from the kidney converts angiotensinogen to angiotensin I, which angiotensin-converting enzyme turns into angiotensin II. Angiotensin II constricts arterioles, raising resistance, and stimulates aldosterone, which signals the collecting ducts to hold on to salt and the water that follows it (Rosenthal & Burchum, 2021).

Her albuminuria adds a fourth consideration. By tightening the small outflow vessel of each glomerulus, angiotensin II keeps pressure inside the filter high, and that pressure drives albumin into the urine and injures the kidney over time.

Placing the Drugs on the Mechanism

Current guidance defines her readings as stage 2 hypertension and recommends starting two first-line drugs from different classes, aiming for a target below 130/80 mm Hg (Whelton et al., 2018). Table 1 shows where each chosen drug acts.

Table 1

Where Each Drug Acts and What It Should Do

The two drugs complement each other. Chlorthalidone lowers blood volume, which on its own would trigger more renin release and blunt its effect; lisinopril blocks the angiotensin II that renin would produce. Chlorthalidone tends to lower potassium; lisinopril, by reducing aldosterone, tends to raise it, so the net change is usually small. The ACE inhibitor also addresses her albuminuria directly: by reducing angiotensin II's constriction of the efferent arteriole, it lowers pressure inside the glomerulus. That same effect explains why creatinine often rises slightly after starting it, a change that reflects lower filtration pressure rather than kidney damage, provided the rise is modest (Rosenthal & Burchum, 2021).

The cough some patients develop on ACE inhibitors has its own mechanism. The enzyme also breaks down bradykinin, and when it is blocked, bradykinin accumulates in the airways. If cough occurs, an angiotensin receptor blocker acts at the next step, the receptor, without affecting bradykinin.

Why Not the Other First-Line Classes

Guidelines list calcium channel blockers alongside thiazides and ACE inhibitors as first-line choices (Whelton et al., 2018), so the selection needs a reason. A dihydropyridine calcium channel blocker such as amlodipine relaxes arterial smooth muscle and lowers resistance effectively, and it would be a reasonable second or third drug, but it does nothing for the glomerular pressure driving her albuminuria and often causes ankle swelling. Beta-blockers are not first-line for uncomplicated hypertension and are reserved for patients with a compelling reason, such as coronary disease or heart failure, neither of which she has. An angiotensin receptor blocker would protect her kidneys as well as an ACE inhibitor and is the substitute if cough develops, but combining the two adds risk without benefit. The choice therefore follows her mechanism and her kidneys, not habit.

Age and This Patient

Age changes both how the drugs are handled and how the patient tolerates their effects. Older adults have blunted baroreceptor reflexes, so a drop in pressure on standing is compensated less quickly, raising the risk of dizziness and falls; she lives alone, so this matters. Thiazide-type diuretics cause low sodium more often in older adults, particularly women of low body weight. Declining kidney function reduces clearance of lisinopril, which is eliminated by the kidney (Mangoni & Jackson, 2004). These considerations explain the low starting doses and the emphasis on early monitoring.

Monitoring Derived From the Mechanism

Each monitoring step follows from the table. Potassium, sodium and creatinine are checked one to two weeks after starting, because the drugs push potassium in opposite directions, the thiazide can lower sodium and the ACE inhibitor lowers glomerular pressure. A creatinine rise of up to about 30% can be accepted if it stabilizes, while a larger rise calls for review. Standing and sitting blood pressures are checked at the follow-up visit because of her blunted reflexes. Home readings continue, aiming for below 130/80 mm Hg. Urine albumin is rechecked in three months to see whether the ACE inhibitor is protecting her kidneys, and she is taught to stop lisinopril and seek care at once if her lips or tongue swell.

Conclusion

This patient's hypertension arises from stiff arteries, impaired sodium excretion and an active renin-angiotensin-aldosterone system, with angiotensin II also raising pressure inside her glomeruli. Chlorthalidone removes sodium at the distal tubule, and lisinopril blocks the angiotensin II that would otherwise counteract it, lowering pressure and albuminuria together. Age explains the cautious doses, and the mechanisms explain every laboratory check. Treating her pressure well means understanding exactly where each drug meets the disease.

References

Mangoni, A. A., & Jackson, S. H. D. (2004). Age-related changes in pharmacokinetics and pharmacodynamics: Basic principles and practical applications. British Journal of Clinical Pharmacology, 57(1), 6-14. https://doi.org/10.1046/j.1365-2125.2003.02007.x

Rosenthal, L. D., & Burchum, J. R. (2021). Lehne's pharmacotherapeutics for advanced practice nurses and physician associates (2nd ed.). Elsevier.

Whelton, P. K., Carey, R. M., Aronow, W. S., Casey, D. E., Collins, K. J., Dennison Himmelfarb, C., DePalma, S. M., Gidding, S., Jamerson, K. A., Jones, D. W., MacLaughlin, E. J., Muntner, P., Ovbiagele, B., Smith, S. C., Spencer, C. C., Stafford, R. S., Taler, S. J., Thomas, R. J., Williams, K. A., . . . Wright, J. T. (2018). 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension, 71(6), e13-e115. https://doi.org/10.1161/HYP.0000000000000065