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PBBSC FY MEDICAL SURGICAL NURSING UNIT 8

  • Nursing management of patients with endocrine problems

Nursing Management of Patients with Endocrine Problems

Endocrine disorders involve dysfunctions of the glands that regulate hormones, affecting growth, metabolism, reproduction, and homeostasis. Nursing care focuses on symptom management, patient education, and preventing complications.

Common Endocrine Disorders

  1. Diabetes Mellitus:
    • Types: Type 1, Type 2, Gestational diabetes.
  2. Thyroid Disorders:
    • Hypothyroidism, hyperthyroidism, goiter, thyroid nodules.
  3. Adrenal Disorders:
    • Addison’s disease, Cushing’s syndrome, pheochromocytoma.
  4. Pituitary Disorders:
    • Diabetes insipidus, syndrome of inappropriate antidiuretic hormone (SIADH), acromegaly.
  5. Parathyroid Disorders:
    • Hypoparathyroidism, hyperparathyroidism.
  6. Other Disorders:
    • Polycystic ovary syndrome (PCOS), menopause, metabolic syndrome.

Nursing Assessment

  1. History Taking:
    • Evaluate symptoms like fatigue, weight changes, polyuria, polydipsia, mood alterations, and skin changes.
    • Assess family history, lifestyle factors, and medication adherence.
  2. Physical Examination:
    • Observe for signs like:
      • Goiter, tremors, exophthalmos (thyroid disorders).
      • Hyperpigmentation, edema, hirsutism (adrenal disorders).
      • Weight loss or gain, skin changes, and vital sign abnormalities.
  3. Laboratory and Diagnostic Tests:
    • Blood glucose levels (for diabetes).
    • TSH, T3, T4 (for thyroid function).
    • Serum cortisol and ACTH levels (for adrenal function).
    • Serum calcium and phosphate (for parathyroid function).

Nursing Diagnoses

  1. Imbalanced Nutrition:
    • Related to hormonal imbalances (e.g., hyperthyroidism, diabetes).
  2. Fluid Volume Deficit or Excess:
    • Related to conditions like diabetes insipidus or SIADH.
  3. Risk for Injury:
    • Due to complications like hypoglycemia, fractures, or hypertension.
  4. Body Image Disturbance:
    • Due to physical changes like moon face (Cushing’s syndrome) or goiter.
  5. Knowledge Deficit:
    • Regarding disease management, medications, or lifestyle changes.

General Nursing Interventions

1. Monitoring and Assessment

  • Regular monitoring of vital signs, blood glucose, fluid and electrolyte balance.
  • Watch for signs of complications like diabetic ketoacidosis (DKA), thyroid storm, adrenal crisis, or hypoglycemia.

2. Administering Medications

  • Diabetes:
    • Insulin therapy, oral hypoglycemics (e.g., metformin).
  • Thyroid Disorders:
    • Levothyroxine for hypothyroidism; antithyroid drugs (propylthiouracil, methimazole) for hyperthyroidism.
  • Adrenal Disorders:
    • Corticosteroid replacement for Addison’s disease; inhibitors (ketoconazole) for Cushing’s syndrome.
  • Calcium or Vitamin D:
    • For hypoparathyroidism or osteoporosis.

3. Fluid and Electrolyte Management

  • Encourage hydration for patients with polyuria (e.g., diabetes insipidus).
  • Restrict fluid intake in SIADH to prevent hyponatremia.

4. Nutritional Support

  • Encourage a balanced diet tailored to the disorder:
    • Low-carbohydrate diet for diabetes.
    • High-protein, high-calorie diet for hyperthyroidism.
    • Sodium restriction for Cushing’s syndrome or SIADH.

5. Preventing Complications

  • Teach patients with diabetes about proper insulin administration, foot care, and hypoglycemia management.
  • Prevent infection in immunocompromised patients (e.g., adrenal insufficiency, uncontrolled diabetes).

6. Patient Education

  • Emphasize adherence to medications and lifestyle modifications.
  • Educate on the importance of regular follow-ups and self-monitoring of symptoms.
  • Provide psychological support for patients with chronic endocrine conditions.

Specific Nursing Care for Common Disorders

1. Diabetes Mellitus

  • Monitor blood glucose levels and signs of hypo-/hyperglycemia.
  • Educate on diet, exercise, and medication compliance.
  • Administer insulin or oral hypoglycemic agents as prescribed.

2. Thyroid Disorders

  • Hypothyroidism:
    • Administer levothyroxine and monitor for signs of improvement (e.g., reduced fatigue, normalized heart rate).
    • Watch for signs of myxedema coma.
  • Hyperthyroidism:
    • Administer antithyroid drugs and beta-blockers (for symptom relief).
    • Provide a cool environment for heat intolerance.

3. Adrenal Disorders

  • Addison’s Disease:
    • Administer corticosteroids and monitor for signs of adrenal crisis (e.g., hypotension, fatigue).
    • Encourage salt intake if sodium levels are low.
  • Cushing’s Syndrome:
    • Monitor for hypertension, edema, and hyperglycemia.
    • Provide emotional support for physical changes.

4. Pituitary Disorders

  • Diabetes Insipidus:
    • Administer desmopressin (synthetic ADH) and encourage hydration.
    • Monitor urine output and specific gravity.
  • SIADH:
    • Restrict fluids and monitor for signs of hyponatremia (e.g., confusion, seizures).

5. Parathyroid Disorders

  • Hyperparathyroidism:
    • Monitor calcium levels and administer fluids to reduce hypercalcemia.
  • Hypoparathyroidism:
    • Administer calcium and vitamin D supplements.

Complications to Monitor

  1. Diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS).
  2. Thyroid storm or myxedema coma.
  3. Adrenal crisis in Addison’s disease.
  4. Electrolyte imbalances in parathyroid disorders.
  5. Hypertension or fractures in Cushing’s syndrome.

Patient Education

  • Importance of regular medication and lifestyle compliance.
  • Monitoring symptoms and reporting changes promptly.
  • Encouraging support groups for chronic endocrine disorders.

Prognosis

  • Prognosis depends on early diagnosis and effective management.
  • Many endocrine disorders can be managed well with medication and lifestyle adjustments.
  • Review of anatomy and physiology and patho-physiology of patients with Thyroid disorders

Review of Anatomy and Physiology of the Thyroid Gland

Anatomy of the Thyroid Gland

  1. Location:
    • The thyroid gland is a butterfly-shaped organ located in the neck, anterior to the trachea, and inferior to the larynx.
  2. Structure:
    • Comprised of two lobes (right and left) connected by an isthmus.
    • Composed of follicles, which are the functional units.
  3. Blood Supply:
    • Highly vascularized; supplied by the superior and inferior thyroid arteries.
  4. Innervation:
    • Innervated by the sympathetic and parasympathetic branches of the autonomic nervous system.

Physiology of the Thyroid Gland

  1. Hormones Produced:
    • Thyroxine (T4): The inactive form, converted to T3 in tissues.
    • Triiodothyronine (T3): The active form, responsible for most physiological effects.
    • Calcitonin: Regulates calcium levels by inhibiting bone resorption.
  2. Hormone Synthesis:
    • Requires iodine, which is absorbed from the diet.
    • Thyroglobulin in the follicles binds iodine to produce T3 and T4.
  3. Regulation of Thyroid Function:
    • Controlled by the hypothalamic-pituitary-thyroid axis:
      • Hypothalamus: Secretes thyrotropin-releasing hormone (TRH).
      • Pituitary: Releases thyroid-stimulating hormone (TSH) in response to TRH.
      • Thyroid Gland: Releases T3 and T4 in response to TSH.
  4. Functions of Thyroid Hormones:
    • Metabolism: Increases basal metabolic rate (BMR).
    • Growth and Development: Critical for brain development in infants and children.
    • Cardiovascular: Increases heart rate and cardiac output.
    • Thermogenesis: Regulates body temperature.
    • Protein and Lipid Metabolism: Influences synthesis and degradation.

Pathophysiology of Thyroid Disorders

1. Hypothyroidism

  • Definition:
    • A condition where the thyroid gland produces insufficient thyroid hormones.
  • Causes:
    • Autoimmune thyroiditis (Hashimoto’s thyroiditis).
    • Iodine deficiency.
    • Post-thyroidectomy or radioactive iodine therapy.
    • Congenital hypothyroidism.
    • Pituitary or hypothalamic dysfunction (secondary or tertiary hypothyroidism).
  • Pathophysiology:
    1. Reduced T3 and T4 levels result in decreased metabolic activity.
    2. Increased TSH (in primary hypothyroidism) due to loss of negative feedback.
    3. Accumulation of glycosaminoglycans in tissues causes non-pitting edema (myxedema).
  • Symptoms:
    • Fatigue, weight gain, cold intolerance, bradycardia.
    • Dry skin, hair thinning, depression.
    • Myxedema in severe cases.

2. Hyperthyroidism

  • Definition:
    • Excessive production of thyroid hormones, leading to increased metabolism.
  • Causes:
    • Graves’ disease (autoimmune condition).
    • Toxic multinodular goiter.
    • Thyroiditis (transient hyperthyroidism due to inflammation).
    • Excessive iodine intake or thyroid hormone supplementation.
  • Pathophysiology:
    1. Overproduction of T3 and T4 leads to excessive stimulation of target organs.
    2. Negative feedback suppresses TSH in primary hyperthyroidism.
    3. In Graves’ disease, thyroid-stimulating immunoglobulins (TSIs) mimic TSH, causing excessive hormone release.
  • Symptoms:
    • Weight loss, heat intolerance, tachycardia, palpitations.
    • Tremors, anxiety, hyperreflexia, exophthalmos (in Graves’ disease).
    • Goiter.

3. Goiter

  • Definition:
    • Enlargement of the thyroid gland due to various causes.
  • Causes:
    • Iodine deficiency (endemic goiter).
    • Autoimmune diseases (Graves’ disease, Hashimoto’s thyroiditis).
    • Thyroid nodules or cancer.
  • Pathophysiology:
    1. Prolonged TSH stimulation (due to low T3/T4 or TSI in Graves’ disease) causes thyroid hypertrophy.
    2. Chronic inflammation leads to fibrosis in Hashimoto’s thyroiditis.
  • Symptoms:
    • Visible swelling in the neck.
    • Dysphagia, dyspnea, or hoarseness if the goiter compresses adjacent structures.

4. Thyroid Storm (Thyrotoxic Crisis)

  • Definition:
    • A life-threatening complication of untreated or poorly controlled hyperthyroidism.
  • Pathophysiology:
    1. Sudden release of large amounts of thyroid hormones.
    2. Exaggerated metabolic effects, leading to severe hyperthermia, tachycardia, and agitation.
  • Symptoms:
    • High fever, severe tachycardia, delirium, dehydration.
    • Hypotension, heart failure, and coma in severe cases.

5. Thyroid Cancer

  • Definition:
    • Malignant growth in the thyroid gland.
  • Types:
    • Papillary (most common and least aggressive).
    • Follicular, medullary, and anaplastic (most aggressive).
  • Pathophysiology:
    1. Genetic mutations cause uncontrolled cell growth in thyroid tissue.
    2. Cancerous cells invade surrounding tissues or metastasize.
  • Symptoms:
    • A hard, painless nodule in the thyroid.
    • Enlarged lymph nodes, hoarseness, or difficulty swallowing.

Diagnosis of Thyroid Disorders

  1. Laboratory Tests:
    • TSH: Elevated in hypothyroidism, suppressed in hyperthyroidism.
    • T3 and T4: Low in hypothyroidism, high in hyperthyroidism.
    • Thyroid Antibodies:
      • Anti-TPO antibodies (Hashimoto’s thyroiditis).
      • TSI (Graves’ disease).
  2. Imaging:
    • Ultrasound: Detects nodules, goiters, or tumors.
    • Radioactive Iodine Uptake (RAIU): Differentiates causes of hyperthyroidism.
    • CT/MRI: Evaluates large goiters or suspected malignancies.
  3. Biopsy:
    • Fine-needle aspiration for thyroid nodules to assess malignancy.

Management of Thyroid Disorders

Hypothyroidism:

  • Medication:
    • Levothyroxine (synthetic T4).
  • Lifestyle:
    • Adequate iodine intake, weight management.

Hyperthyroidism:

  • Antithyroid Drugs:
    • Methimazole, propylthiouracil (PTU).
  • Beta-Blockers:
    • Propranolol for symptom relief.
  • Radioactive Iodine Therapy:
    • Destroys overactive thyroid tissue.
  • Surgery:
    • Thyroidectomy for severe cases or cancer.

Goiter and Cancer:

  • Surgery to remove nodules or the entire thyroid.
  • Radioactive iodine or chemotherapy for cancer.
  • Diabetes mellitus

Diabetes Mellitus: Overview

Definition:
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia (high blood glucose levels) due to defects in insulin secretion, insulin action, or both.

Types of Diabetes Mellitus

  1. Type 1 Diabetes Mellitus (T1DM):
    • Autoimmune destruction of pancreatic beta cells.
    • Insulin deficiency.
    • Common in younger individuals.
  2. Type 2 Diabetes Mellitus (T2DM):
    • Insulin resistance and relative insulin deficiency.
    • Associated with obesity and sedentary lifestyle.
    • Common in adults but increasingly seen in children.
  3. Gestational Diabetes Mellitus (GDM):
    • Hyperglycemia diagnosed during pregnancy.
    • Increases the risk of developing T2DM later in life.
  4. Other Specific Types:
    • Monogenic diabetes syndromes (e.g., MODY).
    • Secondary diabetes due to medications (e.g., steroids) or conditions like pancreatitis.

Pathophysiology

  1. Type 1 DM:
    • Autoimmune attack on pancreatic beta cells → complete insulin deficiency.
    • Glucose uptake by cells decreases → hyperglycemia.
    • Increased lipolysis → ketogenesis → diabetic ketoacidosis (DKA).
  2. Type 2 DM:
    • Insulin resistance in peripheral tissues (e.g., muscle, liver).
    • Compensatory hyperinsulinemia initially.
    • Progressive beta-cell dysfunction → relative insulin deficiency.
    • Chronic hyperglycemia leads to complications.
  3. Gestational Diabetes:
    • Pregnancy hormones induce insulin resistance.
    • Pancreatic beta cells fail to compensate.

Symptoms

  1. Classic Symptoms:
    • Polyuria (frequent urination).
    • Polydipsia (excessive thirst).
    • Polyphagia (increased hunger).
    • Unexplained weight loss (common in Type 1 DM).
  2. Other Symptoms:
    • Fatigue, blurred vision, slow wound healing.
    • Recurrent infections (e.g., urinary tract, skin).

Complications

Acute Complications:

  1. Diabetic Ketoacidosis (DKA):
    • More common in Type 1 DM.
    • Symptoms: Nausea, vomiting, abdominal pain, fruity breath, Kussmaul respirations, altered consciousness.
  2. Hyperosmolar Hyperglycemic State (HHS):
    • More common in Type 2 DM.
    • Severe hyperglycemia without significant ketosis.
    • Symptoms: Severe dehydration, confusion, coma.
  3. Hypoglycemia:
    • Symptoms: Sweating, trembling, confusion, dizziness, seizures.

Chronic Complications:

  1. Microvascular Complications:
    • Retinopathy: Can lead to blindness.
    • Nephropathy: Progresses to chronic kidney disease (CKD).
    • Neuropathy: Peripheral, autonomic, or focal nerve damage.
  2. Macrovascular Complications:
    • Cardiovascular disease (CVD): Myocardial infarction, stroke.
    • Peripheral arterial disease (PAD): Can lead to limb amputation.

Diagnosis

  1. Blood Tests:
    • Fasting Plasma Glucose (FPG) ≥ 126 mg/dL.
    • 2-hour Plasma Glucose (OGTT) ≥ 200 mg/dL.
    • HbA1c ≥ 6.5%.
    • Random Plasma Glucose ≥ 200 mg/dL with symptoms.
  2. Urine Tests:
    • Glucose and ketones in urine (indicates hyperglycemia or DKA).
  3. Additional Tests:
    • C-peptide: Differentiates Type 1 from Type 2 DM.
    • Autoantibodies (GAD, ICA): Present in Type 1 DM.

Management

1. Medical Management

  1. Lifestyle Modifications:
    • Diet:
      • Low glycemic index foods.
      • Controlled carbohydrate intake.
      • Regular meals to avoid hypoglycemia.
    • Exercise:
      • Regular aerobic and resistance exercise.
      • Avoid during episodes of hypoglycemia or poorly controlled hyperglycemia.
  2. Medications:
    • Type 1 DM:
      • Insulin (mandatory):
        • Basal insulin (long-acting): Glargine, Detemir.
        • Bolus insulin (short/rapid-acting): Lispro, Aspart.
    • Type 2 DM:
      • Oral Hypoglycemic Agents (OHAs):
        • Metformin: First-line treatment.
        • Sulfonylureas (e.g., glimepiride): Stimulate insulin secretion.
        • DPP-4 inhibitors (e.g., sitagliptin): Increase incretin levels.
        • SGLT-2 inhibitors (e.g., empagliflozin): Promote glucose excretion in urine.
        • GLP-1 agonists (e.g., liraglutide): Improve insulin secretion and delay gastric emptying.
      • Insulin: Added in advanced stages or during acute illness.
    • Gestational Diabetes:
      • Lifestyle modifications.
      • Insulin (preferred over OHAs).
  3. Monitoring:
    • Self-Monitoring of Blood Glucose (SMBG) for glycemic control.
    • Regular HbA1c testing (goal: <7% for most patients).

2. Preventing and Managing Complications

  1. Eye Care:
    • Annual dilated eye exams for retinopathy.
  2. Kidney Care:
    • Regular urine albumin-to-creatinine ratio tests.
    • ACE inhibitors/ARBs for nephropathy.
  3. Foot Care:
    • Regular foot exams.
    • Educate on proper foot hygiene and footwear.
  4. Cardiovascular Risk Reduction:
    • Blood pressure control (<140/90 mmHg).
    • Lipid management with statins.
    • Smoking cessation.

Nursing Management

  1. Assessment:
    • Monitor for signs of hyperglycemia or hypoglycemia.
    • Assess for complications (retinopathy, neuropathy, nephropathy).
  2. Interventions:
    • Administer prescribed medications.
    • Educate on insulin administration and SMBG.
    • Promote adherence to diet and exercise.
  3. Patient Education:
    • Recognize symptoms of hypo-/hyperglycemia and seek timely care.
    • Emphasize the importance of routine follow-ups and screenings.
    • Teach foot care to prevent ulcers and infections.

Prognosis

  • With proper management, patients with diabetes can live long, healthy lives.
  • Poor control increases the risk of acute and chronic complications.
  • Diabetes insipidus

Diabetes Insipidus (DI): Overview

Definition:
Diabetes insipidus (DI) is a condition characterized by excessive thirst (polydipsia) and excretion of large amounts of dilute urine (polyuria) due to a deficiency of antidiuretic hormone (ADH) or the kidney’s inability to respond to ADH.

Types of Diabetes Insipidus

  1. Central (Neurogenic) DI:
    • Caused by a deficiency of ADH secretion from the hypothalamus or posterior pituitary.
    • Common causes:
      • Brain injury, surgery, or tumors.
      • Infections (e.g., meningitis, encephalitis).
      • Congenital abnormalities.
  2. Nephrogenic DI:
    • Caused by the kidney’s resistance to ADH.
    • Common causes:
      • Genetic mutations.
      • Chronic kidney disease.
      • Medications (e.g., lithium, demeclocycline).
  3. Dipsogenic DI:
    • Excessive water intake due to a defect in thirst regulation.
    • Often associated with psychiatric conditions.
  4. Gestational DI:
    • Occurs during pregnancy due to increased metabolism of ADH by placental enzymes.

Pathophysiology

  1. ADH Deficiency (Central DI):
    • Decreased ADH → reduced water reabsorption in the collecting ducts of the kidneys → excessive water loss → dilute urine and dehydration.
  2. ADH Resistance (Nephrogenic DI):
    • Normal ADH secretion, but kidney cells fail to respond → reduced water reabsorption.
  3. Dipsogenic and Gestational DI:
    • Excessive water intake or increased ADH degradation leads to similar effects.

Symptoms

  1. Classic Symptoms:
    • Polyuria (excretion of 3–20 liters/day of dilute urine).
    • Polydipsia (intense thirst, craving for cold water).
    • Nocturia (frequent urination at night).
    • Dehydration symptoms:
      • Dry skin, fatigue, dizziness, hypotension.
  2. Severe Cases:
    • Electrolyte imbalances (e.g., hypernatremia).
    • Confusion, irritability, muscle weakness.

Diagnosis

  1. History and Physical Examination:
    • History of excessive urination and thirst.
    • Assess for potential causes (e.g., trauma, medications).
  2. Laboratory Tests:
    • Serum Osmolality:
      • High (>295 mOsm/kg) in DI.
    • Urine Osmolality:
      • Low (<300 mOsm/kg) in DI.
    • Serum Sodium:
      • Hypernatremia may be present.
  3. Water Deprivation Test:
    • Restrict fluids and monitor urine output and osmolality.
    • Distinguishes central from nephrogenic DI:
      • Central DI: Urine osmolality increases with desmopressin.
      • Nephrogenic DI: No response to desmopressin.
  4. ADH Levels:
    • Low in central DI.
    • Normal or high in nephrogenic DI.
  5. MRI:
    • Evaluates the hypothalamus and pituitary for structural abnormalities in central DI.

Management

1. Central Diabetes Insipidus

  1. Desmopressin (DDAVP):
    • Synthetic ADH analog.
    • Administered orally, intranasally, or parenterally.
  2. Fluid Intake:
    • Encourage adequate hydration.
  3. Treatment of Underlying Causes:
    • Treat brain tumors, infections, or trauma.

2. Nephrogenic Diabetes Insipidus

  1. Medications:
    • Thiazide Diuretics:
      • Reduce urine output by causing mild volume depletion.
    • Amiloride:
      • Used in lithium-induced DI.
    • NSAIDs (e.g., Indomethacin):
      • Enhance renal response to ADH.
  2. Dietary Modifications:
    • Low-salt, low-protein diet to reduce urine output.
  3. Fluid Management:
    • Maintain hydration to prevent dehydration.

3. Dipsogenic DI

  • Address underlying psychiatric or behavioral issues.
  • Restrict excessive water intake.

4. Gestational DI

  • Desmopressin is the treatment of choice as it is safe during pregnancy.

Complications

  1. Dehydration:
    • Severe fluid loss leading to hypotension, shock.
  2. Electrolyte Imbalance:
    • Hypernatremia, which can cause confusion, seizures, and coma.
  3. Kidney Damage:
    • Chronic overwork of kidneys may lead to nephropathy.

Nursing Management

Assessment:

  1. Monitor urine output and characteristics.
  2. Assess for signs of dehydration and electrolyte imbalance.
  3. Evaluate fluid intake and weight changes.

Interventions:

  1. Administer prescribed medications (desmopressin, thiazides).
  2. Maintain strict intake and output records.
  3. Encourage adequate hydration, but avoid overhydration.
  4. Monitor laboratory values (serum sodium, osmolality).
  5. Educate on symptoms of dehydration and medication use.

Patient Education:

  1. Importance of adherence to prescribed medications (e.g., desmopressin).
  2. Recognizing signs of dehydration and hypernatremia.
  3. Encourage regular follow-ups to monitor electrolyte levels and overall health.

Prognosis

  • Central DI: Managed well with desmopressin and regular monitoring.
  • Nephrogenic DI: Requires lifestyle adjustments and medication; prognosis depends on the underlying cause.
  • Adrenal tumour

Adrenal Tumors: Overview

Definition:
Adrenal tumors are abnormal growths in the adrenal glands, located above each kidney. These can be benign (non-cancerous) or malignant (cancerous) and may be functional (hormone-producing) or non-functional (non-hormone-producing).

Types of Adrenal Tumors

  1. Benign Tumors:
    • Adenomas:
      • Non-functional or functional (e.g., producing cortisol, aldosterone, or androgens).
      • Commonly found incidentally during imaging (incidentalomas).
    • Myelolipomas:
      • Non-functional and composed of fat and bone marrow-like tissues.
  2. Malignant Tumors:
    • Adrenocortical Carcinoma:
      • Rare, aggressive, and often functional.
    • Metastases to Adrenal Glands:
      • Secondary tumors from cancers like lung, breast, or kidney cancer.
  3. Functional Tumors:
    • Pheochromocytoma:
      • Arises from the adrenal medulla; produces catecholamines (e.g., adrenaline).
    • Aldosteronoma:
      • Produces aldosterone, causing primary hyperaldosteronism (Conn’s syndrome).
    • Cortisol-Secreting Tumor:
      • Leads to Cushing’s syndrome.
  4. Non-Functional Tumors:
    • Do not produce hormones but may grow and compress adjacent structures.

Causes

  • Genetic Syndromes:
    • Multiple endocrine neoplasia type 2 (MEN2).
    • Von Hippel-Lindau disease.
    • Li-Fraumeni syndrome.
    • Neurofibromatosis type 1 (NF1).
  • Sporadic Mutations:
    • Most adrenal adenomas and cancers are due to sporadic mutations.

Pathophysiology

  1. Hormone-Producing Tumors:
    • Excess hormone production (e.g., cortisol, aldosterone, catecholamines) leads to systemic effects:
      • Hypercortisolism → Cushing’s syndrome.
      • Hyperaldosteronism → Hypertension, hypokalemia.
      • Catecholamine excess → Pheochromocytoma.
  2. Non-Functional Tumors:
    • May cause local symptoms due to mass effect or remain asymptomatic.

Symptoms

  1. Functional Tumors:
    • Cortisol-Secreting Tumor (Cushing’s Syndrome):
      • Weight gain, moon face, abdominal striae, muscle weakness.
      • Hypertension, hyperglycemia, osteoporosis.
    • Aldosteronoma (Conn’s Syndrome):
      • Persistent hypertension, hypokalemia (muscle weakness, cramps).
      • Polydipsia, polyuria.
    • Pheochromocytoma:
      • Episodic headaches, sweating, palpitations.
      • Severe hypertension, tremors, anxiety.
    • Androgen-Producing Tumor:
      • Virilization in women (e.g., deep voice, hirsutism).
      • Precocious puberty in children.
  2. Non-Functional Tumors:
    • Often asymptomatic, detected incidentally during imaging.
    • Large tumors may cause abdominal pain or compression of nearby organs.

Diagnosis

  1. History and Physical Examination:
    • Symptoms of hormone excess (e.g., hypertension, weight changes).
    • Family history of endocrine tumors.
  2. Laboratory Tests:
    • Cortisol Levels:
      • 24-hour urinary free cortisol or dexamethasone suppression test.
    • Aldosterone and Renin Ratio:
      • Elevated aldosterone with suppressed renin in primary hyperaldosteronism.
    • Catecholamines and Metanephrines:
      • Measured in plasma or urine for pheochromocytoma.
    • Androgens and Estrogens:
      • Abnormal levels in virilizing or feminizing tumors.
  3. Imaging:
    • CT/MRI:
      • Characterizes tumor size, location, and composition.
      • Helps differentiate benign from malignant tumors.
    • Functional Imaging:
      • MIBG scan for pheochromocytomas.
      • PET scan for malignant tumors.
  4. Biopsy:
    • Rarely done due to the risk of spreading malignant cells.
    • Contraindicated in pheochromocytomas.

Management

1. Surgical Management

  • Adrenalectomy:
    • Indicated for functional tumors and large or suspicious non-functional tumors.
    • Performed laparoscopically for benign tumors; open surgery for malignant ones.
  • Preoperative Preparation for Pheochromocytoma:
    • Alpha-blockers (e.g., phenoxybenzamine) to control blood pressure.
    • Beta-blockers added after adequate alpha blockade to manage tachycardia.

2. Medical Management

  1. Hormone-Specific Treatments:
    • Cushing’s Syndrome:
      • Ketoconazole or metyrapone to inhibit cortisol production.
    • Hyperaldosteronism:
      • Spironolactone or eplerenone to block aldosterone effects if surgery is not an option.
    • Pheochromocytoma:
      • Long-term alpha and beta-blockade if inoperable.
  2. Supportive Care:
    • Antihypertensives for blood pressure control.
    • Potassium supplements for hypokalemia in Conn’s syndrome.
  3. Chemotherapy/Radiotherapy:
    • Used for adrenocortical carcinomas or metastatic disease.

Complications

  1. Tumor-Specific:
    • Hormonal imbalances causing systemic effects.
  2. Surgical:
    • Bleeding, infection, or adrenal insufficiency post-adrenalectomy.
  3. Malignant Tumors:
    • Local invasion or metastasis to lungs, liver, or bones.

Nursing Management

Preoperative Care:

  1. Prepare the patient for imaging and laboratory evaluations.
  2. Monitor blood pressure and electrolyte levels (especially in pheochromocytoma and Conn’s syndrome).
  3. Educate the patient on the importance of preoperative medication adherence.

Postoperative Care:

  1. Monitor for signs of adrenal insufficiency (hypotension, fatigue, hypoglycemia).
  2. Assess for wound healing and infection.
  3. Monitor hormone levels to evaluate for recurrence or residual disease.

Patient Education:

  1. Importance of regular follow-ups to monitor hormone levels.
  2. Recognizing symptoms of adrenal insufficiency or recurrence.
  3. Adherence to lifelong hormone replacement therapy if both adrenal glands are removed.

Prognosis

  • Benign Tumors: Excellent prognosis after surgical removal.
  • Malignant Tumors: Depends on the stage at diagnosis; early detection improves outcomes.
  • Pituitary disorders

Pituitary Disorders: Overview

The pituitary gland, often called the “master gland,” regulates various hormones essential for growth, metabolism, reproduction, and homeostasis. Disorders of the pituitary gland arise due to hypersecretion, hyposecretion, or physical abnormalities like tumors.

Anatomy and Physiology of the Pituitary Gland

  1. Location:
    • A small, pea-shaped gland located at the base of the brain in the sella turcica, beneath the hypothalamus.
  2. Structure:
    • Anterior Pituitary (Adenohypophysis): Produces hormones such as:
      • Growth hormone (GH).
      • Thyroid-stimulating hormone (TSH).
      • Adrenocorticotropic hormone (ACTH).
      • Prolactin (PRL).
      • Luteinizing hormone (LH) and Follicle-stimulating hormone (FSH).
    • Posterior Pituitary (Neurohypophysis): Stores and releases:
      • Antidiuretic hormone (ADH).
      • Oxytocin.
  3. Regulation:
    • Controlled by hypothalamic releasing and inhibiting hormones via the hypothalamic-pituitary axis.

Common Pituitary Disorders

  1. Hyperpituitarism:
    • Excess production of one or more pituitary hormones.
    • Examples: Acromegaly, gigantism, Cushing’s disease, hyperprolactinemia.
  2. Hypopituitarism:
    • Deficient production of one or more pituitary hormones.
    • Can lead to secondary hypothyroidism, adrenal insufficiency, or growth failure.
  3. Pituitary Tumors (Adenomas):
    • Benign tumors of the anterior pituitary.
    • May be functional (hormone-secreting) or non-functional.
  4. Posterior Pituitary Disorders:
    • Diabetes insipidus (ADH deficiency).
    • Syndrome of Inappropriate Antidiuretic Hormone (SIADH; excess ADH).

Pathophysiology of Pituitary Disorders

1. Hyperpituitarism

  • Acromegaly/Gigantism:
    • Overproduction of GH.
    • Gigantism: Occurs before epiphyseal plate closure in children → abnormal height.
    • Acromegaly: Occurs after epiphyseal plate closure in adults → bone thickening, organ enlargement.
  • Cushing’s Disease:
    • Excess ACTH stimulates the adrenal glands to produce cortisol.
    • Leads to symptoms like central obesity, moon face, and hyperglycemia.
  • Hyperprolactinemia:
    • Elevated prolactin levels.
    • Symptoms: Galactorrhea, menstrual irregularities, infertility.

2. Hypopituitarism

  • Partial or complete failure of the anterior pituitary to secrete hormones.
  • Causes: Tumors, trauma, infections, radiation.
  • Symptoms depend on the deficient hormone(s):
    • GH deficiency: Growth retardation, fatigue.
    • TSH deficiency: Hypothyroidism.
    • ACTH deficiency: Adrenal insufficiency.
    • LH/FSH deficiency: Infertility, loss of secondary sexual characteristics.

3. Pituitary Tumors

  • Can cause hormone overproduction (functional tumors) or compression effects (non-functional tumors).
  • Compression symptoms:
    • Visual disturbances (due to proximity to the optic chiasm).
    • Headaches, nausea, vomiting.

4. Posterior Pituitary Disorders

  • Diabetes Insipidus:
    • ADH deficiency → excessive urination and thirst.
  • SIADH:
    • Excess ADH → water retention, hyponatremia.

Symptoms of Pituitary Disorders

  1. General Symptoms:
    • Headaches, vision problems.
    • Hormonal imbalances leading to systemic effects.
  2. Specific Symptoms by Disorder:
    • Acromegaly: Enlarged hands, feet, coarse facial features.
    • Cushing’s Disease: Moon face, truncal obesity, purple striae.
    • Hyperprolactinemia: Milky nipple discharge (galactorrhea), infertility.
    • Diabetes Insipidus: Polyuria, polydipsia, dehydration.
    • SIADH: Fluid retention, hyponatremia, confusion.

Diagnosis

  1. History and Physical Examination:
    • Assess for signs of hormonal excess or deficiency.
    • Evaluate vision changes and headache severity.
  2. Laboratory Tests:
    • Hormone levels:
      • GH, IGF-1 for acromegaly.
      • ACTH and cortisol for Cushing’s.
      • Prolactin for hyperprolactinemia.
      • TSH, free T4 for hypothyroidism.
      • LH/FSH for reproductive dysfunction.
    • Water deprivation test for diabetes insipidus.
    • Serum sodium and osmolality for SIADH.
  3. Imaging:
    • MRI of the pituitary to detect tumors or structural abnormalities.
  4. Dynamic Hormone Testing:
    • Dexamethasone suppression test for Cushing’s disease.
    • Glucose suppression test for acromegaly.

Management

1. Medical Management

  • Hyperpituitarism:
    • Dopamine agonists (e.g., cabergoline, bromocriptine) for prolactinomas.
    • Somatostatin analogs (e.g., octreotide) for acromegaly.
    • Ketoconazole, metyrapone for Cushing’s.
  • Hypopituitarism:
    • Hormone replacement therapy:
      • Levothyroxine for TSH deficiency.
      • Hydrocortisone for ACTH deficiency.
      • Growth hormone replacement.
      • Estrogen/progesterone or testosterone for LH/FSH deficiency.
  • Diabetes Insipidus:
    • Desmopressin (synthetic ADH).
  • SIADH:
    • Fluid restriction.
    • Hypertonic saline for severe hyponatremia.
    • Demeclocycline to inhibit ADH action.

2. Surgical Management

  • Transsphenoidal surgery to remove pituitary tumors.

3. Radiation Therapy

  • Used for residual or inoperable tumors.

Complications

  1. Compression Effects:
    • Visual loss or blindness.
    • Cranial nerve damage.
  2. Hormonal Imbalances:
    • Untreated hormonal excess or deficiency can lead to systemic complications.
  3. Post-Surgical Complications:
    • Hypopituitarism.
    • Cerebrospinal fluid (CSF) leaks.

Nursing Management

Assessment:

  1. Monitor for signs of hormone excess or deficiency.
  2. Evaluate neurological status (vision, headache).
  3. Assess fluid balance in diabetes insipidus or SIADH.

Interventions:

  1. Administer prescribed hormone replacements or inhibitors.
  2. Provide post-operative care:
    • Monitor for CSF leaks.
    • Assess for signs of infection.
  3. Educate patients on recognizing symptoms of hormone imbalances.

Patient Education:

  1. Importance of medication adherence.
  2. Lifestyle modifications to manage complications (e.g., diet in Cushing’s disease).
  3. Regular follow-ups for hormone level monitoring and imaging.

Prognosis

  • Early diagnosis and treatment improve outcomes.
  • Hormone replacement therapy ensures a near-normal quality of life for hypopituitarism.
  • Aggressive tumors require long-term follow-up and comprehensive care.
  • Diagnostic procedures

Diagnostic Procedures for Pituitary Disorders

Diagnosing pituitary disorders involves clinical evaluation, laboratory tests, imaging studies, and sometimes dynamic endocrine testing. These procedures help determine the type, severity, and cause of the disorder.

1. Clinical Evaluation

  • Detailed medical history:
    • Symptoms of hormonal imbalances (e.g., fatigue, growth abnormalities, menstrual irregularities).
    • Family history of endocrine or genetic disorders.
  • Physical examination:
    • Assessment of body proportions, facial features, and other physical changes.
    • Neurological examination, including vision testing (visual fields, acuity).

2. Laboratory Tests

A. Hormonal Assessments

  1. Growth Hormone (GH) and IGF-1:
    • Elevated levels in acromegaly/gigantism.
    • Dynamic testing:
      • Oral Glucose Suppression Test: GH levels should suppress after glucose administration. Failure to suppress indicates acromegaly.
  2. Adrenocorticotropic Hormone (ACTH) and Cortisol:
    • 24-Hour Urinary Free Cortisol: Elevated in Cushing’s disease.
    • Low-Dose Dexamethasone Suppression Test:
      • Cortisol should suppress with dexamethasone; failure to suppress suggests Cushing’s syndrome.
    • High-Dose Dexamethasone Suppression Test:
      • Differentiates between pituitary and ectopic ACTH production.
  3. Prolactin (PRL):
    • Elevated in prolactinomas or due to medications, pregnancy, or hypothyroidism.
    • Levels >200 ng/mL strongly suggest a prolactinoma.
  4. Thyroid-Stimulating Hormone (TSH) and Free T4:
    • Assess for secondary hypothyroidism or TSH-secreting tumors.
  5. Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH):
    • Evaluate for hypogonadism or gonadotropin-secreting adenomas.
  6. Antidiuretic Hormone (ADH):
    • Low in diabetes insipidus.
    • High in SIADH.
  7. Serum Sodium and Osmolality:
    • Hypernatremia in diabetes insipidus.
    • Hyponatremia in SIADH.

B. Special Tests

  1. Water Deprivation Test (For Diabetes Insipidus):
    • Differentiates central DI from nephrogenic DI.
    • Central DI: Urine osmolality increases after desmopressin administration.
    • Nephrogenic DI: No significant change in urine osmolality.
  2. Stimulation or Suppression Tests:
    • CRH Stimulation Test: Differentiates between Cushing’s disease and ectopic ACTH secretion.
    • GnRH Stimulation Test: Evaluates gonadotropin deficiencies.

3. Imaging Studies

A. Magnetic Resonance Imaging (MRI)

  • Preferred imaging modality for pituitary disorders.
  • Detects:
    • Microadenomas (<10 mm) and macroadenomas (>10 mm).
    • Structural abnormalities like empty sella syndrome or pituitary enlargement.

B. Computed Tomography (CT)

  • Alternative if MRI is contraindicated.
  • Useful for detecting calcifications, bony erosion, or large tumors.

C. Functional Imaging

  • Positron Emission Tomography (PET):
    • Used in cases of metastatic disease or ectopic hormone production.
  • Octreotide Scans:
    • For somatostatin receptor-positive tumors.

4. Ophthalmological Tests

  • Visual Field Testing:
    • Assesses for compression of the optic chiasm by pituitary tumors.
    • Common finding: Bitemporal hemianopia (loss of peripheral vision).
  • Visual Acuity Tests:
    • Evaluates overall visual sharpness and changes caused by tumor pressure.

5. Genetic Testing

  • Conducted for hereditary pituitary disorders:
    • Multiple Endocrine Neoplasia (MEN) types 1 and 2.
    • Familial isolated pituitary adenomas.

6. Biopsy and Histopathology

  • Rarely needed but may be performed for:
    • Confirmation of malignancy in suspected pituitary carcinoma.
    • Unusual lesions or infiltrative diseases like sarcoidosis.

7. Electrolyte and Fluid Balance Testing

  • Serum and Urine Osmolality:
    • Helps diagnose DI and SIADH.
  • Electrolyte Panels:
    • Assesses sodium levels for signs of hypo- or hypernatremia.

8. Dynamic Testing Summary

TestPurposeInterpretation
Glucose Suppression TestDiagnose acromegalyFailure of GH suppression confirms acromegaly.
Dexamethasone Suppression TestDiagnose Cushing’s syndromeLack of cortisol suppression indicates Cushing’s syndrome.
Water Deprivation TestDifferentiate types of DICentral DI: Increased urine osmolality after desmopressin. Nephrogenic: No change.
GnRH Stimulation TestEvaluate gonadotropin secretionAbnormal response indicates pituitary dysfunction.

Key Considerations

  1. Combine clinical findings with diagnostic results to confirm the diagnosis.
  2. Use imaging for tumor localization and to guide surgical planning.
  3. Reassess hormonal function post-treatment to evaluate therapy efficacy or recurrence.
  • Nursing management of patient with above problems

Nursing Management of Patients with Pituitary Disorders

Nursing care for patients with pituitary disorders focuses on managing hormonal imbalances, providing pre- and post-operative care, educating the patient, and preventing complications. The management depends on the specific pituitary condition (e.g., hyperpituitarism, hypopituitarism, or posterior pituitary disorders).

General Nursing Assessment

  1. History Taking:
    • Assess for symptoms related to hormonal imbalances, such as growth abnormalities, menstrual irregularities, polyuria, or polydipsia.
    • Evaluate visual changes, fatigue, or unexplained weight changes.
  2. Physical Examination:
    • Monitor for signs of hormone excess or deficiency:
      • Acromegaly: Enlarged hands, coarse facial features.
      • Cushing’s disease: Moon face, truncal obesity, striae.
      • Diabetes insipidus: Dehydration, low urine osmolality.
      • SIADH: Fluid retention, confusion, hyponatremia.
    • Neurological assessment: Vision testing, headaches.
  3. Diagnostic Monitoring:
    • Monitor lab values: hormone levels (GH, ACTH, prolactin, TSH), serum sodium, osmolality.
    • Record vital signs: blood pressure, pulse, temperature for early detection of complications.

Nursing Interventions

1. Hyperpituitarism (e.g., Acromegaly, Cushing’s Disease, Hyperprolactinemia)

  1. Symptom Management:
    • Administer prescribed medications:
      • Dopamine agonists (cabergoline, bromocriptine) for prolactinomas.
      • Somatostatin analogs (octreotide) for acromegaly.
      • Ketoconazole for Cushing’s disease.
    • Monitor blood glucose and manage hyperglycemia as needed.
  2. Preventing Complications:
    • Watch for signs of hypertension, hyperglycemia, or cardiovascular complications.
    • Educate the patient on maintaining a healthy weight and blood pressure.

2. Hypopituitarism

  1. Hormone Replacement:
    • Administer prescribed replacement hormones:
      • Levothyroxine for TSH deficiency.
      • Hydrocortisone or prednisone for ACTH deficiency.
      • Estrogen, progesterone, or testosterone for reproductive hormone deficiencies.
    • Monitor for signs of hormone overdose or insufficiency.
  2. Dietary Support:
    • Encourage a balanced diet rich in calcium and vitamin D to prevent osteoporosis.
  3. Emotional Support:
    • Address psychological impacts such as infertility or body image concerns.

3. Pituitary Tumors

  1. Pre-Operative Care:
    • Prepare the patient for transsphenoidal surgery:
      • Educate about the surgical procedure and its risks.
      • Monitor and stabilize hormonal levels before surgery.
  2. Post-Operative Care:
    • Assess for signs of complications:
      • Cerebrospinal fluid (CSF) leak: Clear nasal drainage.
      • Meningitis: Fever, neck stiffness.
      • Diabetes insipidus: Polyuria, polydipsia.
    • Prevent increased intracranial pressure:
      • Avoid coughing, sneezing, or straining.
    • Administer hormone replacements if pituitary function is impaired post-surgery.

4. Diabetes Insipidus

  1. Fluid Management:
    • Ensure adequate hydration to prevent dehydration.
    • Administer prescribed desmopressin (synthetic ADH).
    • Monitor urine output and serum sodium levels.
  2. Patient Education:
    • Teach the importance of regular medication use.
    • Instruct on recognizing early signs of dehydration or medication overdose.

5. SIADH

  1. Fluid Restriction:
    • Restrict fluid intake to manage hyponatremia.
    • Monitor for fluid overload (e.g., weight gain, edema).
  2. Medications:
    • Administer demeclocycline or vasopressin antagonists as prescribed.
    • Treat underlying causes, such as infections or tumors.
  3. Electrolyte Management:
    • Monitor serum sodium levels.
    • Administer hypertonic saline cautiously for severe hyponatremia.

Patient Education

  1. Medication Adherence:
    • Explain the purpose, dosage, and side effects of prescribed medications.
  2. Self-Monitoring:
    • Teach how to monitor for signs of hormonal imbalance (e.g., fatigue, visual changes, excessive urination).
  3. Lifestyle Modifications:
    • Encourage a healthy diet and regular exercise to manage weight and improve overall health.
  4. Follow-Up Care:
    • Emphasize the importance of regular follow-ups for lab monitoring and imaging.

Complications to Watch For

  1. Pituitary Apoplexy:
    • Sudden headache, vision loss, altered consciousness due to hemorrhage in a pituitary tumor.
    • Requires immediate medical attention.
  2. Adrenal Crisis:
    • Severe hypotension, shock due to ACTH deficiency.
    • Administer emergency hydrocortisone.
  3. Post-Surgical Complications:
    • Infection, CSF leak, or permanent hormone deficiencies.

Goals of Nursing Care

  • Maintain hormonal balance.
  • Prevent and manage complications.
  • Educate the patient to promote independence and adherence to treatment.
  • Support the patient physically and emotionally in managing a chronic condition.
  • Drugs used in endocrine problems.

Drugs Used in the Management of Endocrine Problems

The choice of drugs for endocrine disorders depends on whether the condition involves hormone excess, deficiency, or resistance. Below is a list of commonly used drugs categorized by endocrine disorders:

1. Pituitary Disorders

A. Hyperpituitarism

  • Acromegaly/Gigantism:
    • Somatostatin Analogs:
      • Octreotide, Lanreotide: Inhibit growth hormone (GH) secretion.
    • Dopamine Agonists:
      • Cabergoline, Bromocriptine: Suppress GH and prolactin secretion.
    • GH Receptor Antagonists:
      • Pegvisomant: Blocks GH action.
  • Hyperprolactinemia:
    • Dopamine Agonists:
      • Cabergoline, Bromocriptine: Reduce prolactin levels.
  • Cushing’s Disease (ACTH Overproduction):
    • Adrenal Enzyme Inhibitors:
      • Ketoconazole, Metyrapone: Inhibit cortisol synthesis.
    • Dopamine Agonists:
      • Cabergoline: Reduces ACTH secretion.
    • Somatostatin Analogs:
      • Pasireotide: Suppresses ACTH secretion.

B. Hypopituitarism

  • Hormone Replacement Therapy:
    • Growth Hormone (GH): Somatropin.
    • Thyroid Hormone: Levothyroxine (T4).
    • Corticosteroids: Hydrocortisone, Prednisone (for ACTH deficiency).
    • Sex Hormones:
      • Estrogen-Progesterone (for women).
      • Testosterone (for men).
  • Diabetes Insipidus:
    • Desmopressin (DDAVP): Synthetic ADH.
    • Thiazide Diuretics: Reduce urine output in nephrogenic DI.
    • NSAIDs: Indomethacin to reduce polyuria in nephrogenic DI.
  • SIADH:
    • Vasopressin Antagonists:
      • Tolvaptan, Conivaptan: Promote water excretion.
    • Demeclocycline: Reduces renal sensitivity to ADH.

2. Thyroid Disorders

A. Hypothyroidism

  • Thyroid Hormone Replacement:
    • Levothyroxine (T4): Standard treatment.
    • Liothyronine (T3): Occasionally used for rapid correction.

B. Hyperthyroidism

  • Antithyroid Drugs:
    • Propylthiouracil (PTU): Inhibits thyroid hormone synthesis and peripheral conversion of T4 to T3.
    • Methimazole: Preferred for long-term therapy.
  • Beta-Blockers:
    • Propranolol, Atenolol: Control tachycardia, tremors, and other symptoms.
  • Radioactive Iodine (I-131):
    • Destroys overactive thyroid tissue.
  • Potassium Iodide (Lugol’s Solution):
    • Used before surgery to reduce vascularity of the thyroid gland.

3. Adrenal Disorders

A. Cushing’s Syndrome

  • Adrenal Enzyme Inhibitors:
    • Ketoconazole, Metyrapone: Inhibit cortisol production.
  • Somatostatin Analogs:
    • Pasireotide: Reduces ACTH secretion.
  • Glucocorticoid Receptor Blockers:
    • Mifepristone: Blocks cortisol action.

B. Addison’s Disease (Adrenal Insufficiency)

  • Corticosteroids:
    • Hydrocortisone, Prednisone: Replace cortisol.
  • Mineralocorticoids:
    • Fludrocortisone: Replace aldosterone.
  • Emergency Treatment:
    • Intravenous Hydrocortisone: For adrenal crisis.

C. Hyperaldosteronism (Conn’s Syndrome)

  • Aldosterone Antagonists:
    • Spironolactone, Eplerenone: Reduce blood pressure and potassium loss.
  • Potassium Supplements:
    • To correct hypokalemia.

D. Pheochromocytoma

  • Alpha-Blockers:
    • Phenoxybenzamine: Controls hypertension by blocking catecholamines.
  • Beta-Blockers:
    • Propranolol: Used after alpha-blockade to manage tachycardia.
  • Calcium Channel Blockers:
    • Nifedipine: For blood pressure control.

4. Parathyroid Disorders

A. Hypoparathyroidism

  • Calcium Supplements:
    • Calcium carbonate or calcium citrate.
  • Vitamin D Analogs:
    • Calcitriol: Enhances calcium absorption.
  • Recombinant Parathyroid Hormone:
    • Natpara (parathyroid hormone replacement).

B. Hyperparathyroidism

  • Bisphosphonates:
    • Alendronate, Zoledronic Acid: Reduce bone resorption.
  • Calcimimetics:
    • Cinacalcet: Lowers calcium levels by increasing sensitivity of parathyroid receptors.

5. Pancreatic Endocrine Disorders (Diabetes Mellitus)

A. Type 1 Diabetes Mellitus

  • Insulin Therapy:
    • Rapid-Acting: Lispro, Aspart.
    • Long-Acting: Glargine, Detemir.
    • Premixed Insulin: Combines rapid- and intermediate-acting insulin.

B. Type 2 Diabetes Mellitus

  • Oral Hypoglycemics:
    • Biguanides: Metformin (first-line therapy).
    • Sulfonylureas: Glimepiride, Glipizide (stimulate insulin secretion).
    • Thiazolidinediones: Pioglitazone (reduce insulin resistance).
    • DPP-4 Inhibitors: Sitagliptin, Linagliptin (increase incretin levels).
    • SGLT-2 Inhibitors: Empagliflozin, Dapagliflozin (increase glucose excretion).
  • Injectable Agents:
    • GLP-1 Agonists: Liraglutide, Semaglutide (improve insulin secretion and delay gastric emptying).
    • Insulin: For advanced stages.

6. Gonadal Disorders

A. Hypogonadism

  • Hormone Replacement Therapy:
    • Testosterone: For men with androgen deficiency.
    • Estrogen and Progesterone: For women with estrogen deficiency.

B. Polycystic Ovary Syndrome (PCOS)

  • Oral Contraceptives:
    • Regulate menstrual cycles and reduce androgen levels.
  • Anti-Androgens:
    • Spironolactone: Reduces hirsutism.
  • Insulin Sensitizers:
    • Metformin: Improves insulin resistance.

Key Nursing Considerations

  1. Monitoring:
    • Regular assessment of hormone levels and side effects.
    • Monitor blood glucose in patients on steroids or insulin.
  2. Patient Education:
    • Adherence to medication schedules.
    • Recognize signs of hypo- or hyperhormonal states.
  3. Dietary Guidance:
    • High-calcium diets for hypoparathyroidism.
    • Low-sodium diets for Cushing’s syndrome.
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