Hyperaldosteronism: Diagnosis and Management

• Hyperaldosteronism is characterized by excess aldosterone secretion, leading to sodium retention, potassium and hydrogen ion excretion.
• Hypertension with hypokalemic alkalosis is the hallmark of hyperaldosteronism.

Primary Hyperaldosteronism

• Primary hyperaldosteronism (PA) includes solitary adrenocortical adenoma, which can be associated with a genetic link.

Secondary Hyperaldosteronism

• Secondary hyperaldosteronism is caused by increased aldosterone levels due to nonadrenal factors.
• Renal artery stenosis, renin-secreting tumors, and chronic kidney disease can lead to secondary hyperaldosteronism.

Clinical Manifestations

• Hyperaldosteronism results in increased aldosterone.
• Sodium retention, hypernatremia, hypertension, and headache occur without edema.
• Potassium excretion leads to hypokalemia and muscle weakness.
• Fatigue, dysrhythmias, glucose intolerance, and metabolic alkalosis leading to tetany can occur.

Diagnostic Studies

• Diagnosis of primary aldosteronism includes increased plasma aldosterone levels, increased sodium levels, and decreased potassium levels.
• Decreased plasma renin activity, CT scan or MRI, and plasma 18-hydroxycorticosterone levels are used in diagnosis.

Treatment

• Adrenalectomy is the preferred treatment to remove the adenoma.
• Preoperative care involves potassium-sparing diuretics like spironolactone and eplerenone.
• Antihypertensives, oral potassium supplements, and sodium restrictions may be necessary before surgery.
• Treatment for bilateral adrenal hyperplasia includes potassium-sparing diuretics.
• Calcium channel blockers control BP, and dexamethasone decreases adrenal hyperplasia.

Nursing Management

• Nursing management involves careful assessment.
• Monitoring fluid and electrolyte balance and cardiovascular status are important.
• Patient teaching includes medications and their side effects, signs and symptoms of hypo- and hyperkalemia.
• Frequent monitoring and continued health care are part of nursing management.

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Etiology and Pathophysiology

• SIADH involves overproduction or sustained release of ADH despite normal or low plasma osmolarity.
• Hormone-secreting tumors (e.g., lung cancer) commonly cause SIADH,.
• SIADH is characterized by fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine with normal or increased intravascular volume, and normal renal function.

Clinical Manifestations

• Low urine output and increased body weight are clinical manifestations.
• Early symptoms include thirst, dyspnea on exertion, and fatigue.
• Mild hyponatremia causes muscle cramping, irritability, and headache.
• Sodium levels of less than 120 mEq/L cause severe vomiting, abdominal cramps, and muscle twitching
• Continued decline leads to cerebral edema, lethargy, confusion, seizures, and coma.

Diagnostic Studies

• Diagnosis involves urine and serum osmolality tests.

Treatment

• Treat the underlying cause to restore normal fluid and volume osmolality.
• Avoid medications that stimulating ADH release.
• Fluid restriction if serum Na is greater than 125 mEq/L will result in gradual weight loss, rise in serum Na concentration & osmolality.
• Loop diuretics and 3% IV hypertonic saline solution can be used with caution.
• Instruct on self-management with chronic SIADH.

Nursing Management

• Monitor I&O, vital signs, heart and lung sounds, and conduct daily weights test.
• Neuro checks and seizure precautions are necessary for signs of hyponatremia.
• Severe hyponatremia must be corrected slowly (no more than 8-12 mEq/L in first 24 hours).
• Teach patients about self-management.

Diabetes Insipidus

Etiology and Pathophysiology

• Diabetes insipidus (DI) involves deficient production or secretion of ADH or decreased renal response to ADH.
• It can be transient, chronic, or lifelong.
• Types of include central (most common), nephrogenic, and primary forms.

Clinical Manifestations

• Common manifestations include polydipsia, polyuria (2-20L/day) with dilute urine (greater than 200mL/h).
• Lethargy and generalized weakness may occur.
• If volume deficit is not replaced, hypotension, tachycardia, & hypovolemic shock can develop.
• Brain shrinkage and intracranial bleeding may occur with uncorrected hypernatremia.

Diagnostic Studies

• Diagnostic studies show urine specific gravity less than 1.005, urine osmolality less than 100 mOsm/kg.
• Serum osmolality is greater than 295 mOsm/kg, and serum sodium is greater than 145 mg/dL.

Treatment & Nursing Management

• Early detection to identify the cause
• Central & nephrogenic DI require water deprivation test
• Maintain fluid and electrolyte balance
• Central DI treated with fluid and hormone therapy
• Nephrogenic DI treated with low-sodium diet, thiazide diuretics, or indomethacin if prior therapies are ineffective.
• Provide long-term management patient teaching

Pheochromocytoma

Etiology and Pathophysiology

• A pheochromocytoma is a rare adrenal medulla tumor producing excess catecholamines.
• Excess epinephrine and norepinephrine cause severe hypertension.
• It is inherited by persons with multiple endocrine neoplasia (MEN).
• If undiagnosed or untreated, pheochromocytoma can lead to encephalopathy, diabetes, cardiomyopathy, multiple organ failure, and death.

Clinical Manifestations

• Attacks are provoked by direct trauma to tumor or mechanical pressure or stress (surgery, exercise, defecation, sexual intercourse, alcohol, smoking)
• Drugs such as antihypertensives, opioids, radiologic contrast media, or tricyclic antidepressants can cause attacks.
• Severe episodic hypertension is accompanied by a classic triad of severe, pounding headache.
• Tachycardia with palpitations and profuse sweating may occur.
• Unexplained abdominal or chest pain are clinical manifestations.
• Episodes last few minutes to several hours.

Diagnostic Studies

• Use a 24-hour urine collection to diagnose.
• CT or MRI can be applied for tumor detection.

Treatment and Nursing Management

• Treatment involves surgical removal of the tumor.
• Pre-op care includes administering alpha and beta-adrenergic receptor blockers 10-14 days before surgery.
• Monitor blood pressure and orthostatic hypotension.
• Post-op care: keep patient comfortable with rest, proper nutrition, and emotional support.
• Carefully monitor BP and blood glucose levels.
• Follow-up care is important.

Explore hyperaldosteronism, differentiating primary and secondary forms. Learn how hormonal imbalances, such as renal artery stenosis, impact aldosterone secretion. Understand the importance of managing potassium levels preoperatively before adrenalectomy.