Adrenal and Pituitary Gland Disorders Study Notes Ch.48
Hyperpituitarism
Cause- Excess hormone production in the anterior pituitary gland, most commonly due to a benign adenoma (tumor) of the pituitary gland.
Hormones commonly affected: growth hormone (GH) causing Acromegaly in adults or Gigantism in children; prolactin (PRL) causing Hyperprolactinemia; less commonly, follicle-stimulating hormone (FSH), luteinizing hormone (LH), or adrenocorticotropic hormone (ACTH) causing Cushing's disease.
Signs and symptoms-
Neurological: Visual problems (e.g., bitemporal hemianopsia due to optic chiasm compression) and persistent headache (often the first indications).
Skeletal/Musculoskeletal (Acromegaly): Enlargement of hands and feet (requiring larger shoe/ring sizes), deformities of the spine (kyphosis) and mandible (prognathism, dental malocclusion).
Soft Tissue/Organ Enlargement: Enlargement of tongue (macroglossia), skin (thickening), liver (hepatomegaly), and spleen (splenomegaly); visceral enlargement leading to abdominal distention.
Respiratory: Sleep apnea (due to soft tissue growth in the pharynx).
Integumentary: Diaphoresis (excessive sweating), oily skin (seborrhea), acne.
Metabolic: Hyperglycemia/DM symptoms (e.g., polyuria, polydipsia, polyphagia) due to growth hormone's anti-insulin effects.
Gastrointestinal: Dysphagia (difficulty swallowing) due to tongue enlargement.
Voice: Deepening of voice due to vocal cord enlargement.
Reproductive (Hyperprolactinemia): Galactorrhea (milky nipple discharge in non-pregnant, non-nursing individuals), hypogonadism (decreased libido, erectile dysfunction in men, amenorrhea/oligomenorrhea in women).
Medical diagnosis-
Radiographic studies: MRI or CT scan of the brain/sella turcica to identify pituitary tumors.
Sella Turcica may also show structural abnormalities that could affect pituitary function, contributing to the symptoms of hyperprolactinemia.
Angiography: Cerebral angiography may be performed to assess blood supply to the tumor, especially prior to surgery.
Lab tests: Measurement of anterior pituitary hormones (e.g., elevated GH or prolactin levels). Random GH levels are often elevated. IGF-1 (Insulin-like Growth Factor-1) is a more stable indicator of average GH levels.
GH suppression test (Oral Glucose Tolerance Test - OGTT): The most reliable diagnostic test for acromegaly. Normally, GH levels decrease to less than after the administration of of oral glucose. In hyperpituitarism (acromegaly), GH levels fail to suppress (remain elevated).
Medical treatment-
Surgery: Transsphenoidal hypophysectomy (surgical removal of the pituitary tumor through the nasal cavity) is the primary treatment.
Radiation therapy: May be used as an adjunct to surgery or for patients who are not surgical candidates. Types include conventional external beam radiation or stereotactic radiosurgery (e.g., Gamma Knife).
Drug therapy:
Somatostatin analogs: e.g., Octreotide (Sandostatin) and Lanreotide. These drugs reduce GH secretion and tumor size.
Sandostatin (Octreotide): Administered subcutaneously (SubQ) every 8 hours.
Sandostatin Depot (Octreotide LAR): Administered intramuscularly (IM) every 4 weeks.
Dopamine agonists: e.g., Bromocriptine, Cabergoline. Primarily used for prolactinomas but can also be effective in some GH-secreting tumors.
GH receptor antagonists: e.g., Pegvisomant (Somavert). Blocks GH action at target tissues for patients unresponsive to somatostatin analogs.
Nursing care-
Assessment: Ongoing assessment of energy level, height (baseline and changes over time, though minimal in adults with acromegaly), weight, vital signs (especially BP due to potential hypertension), head/face contours (documenting changes), visual acuity (using Snellen chart), speech/voice quality, and abdominal distention.
Patient problems/diagnoses:
Altered body image related to physical changes.
Reduced activity tolerance related to joint pain, muscle weakness, and fatigue.
Chronic pain related to joint changes and nerve compression.
Ineffective self-health management due to complex medication regimens or disease process.
Post-hypophysectomy specific care:
Monitor for cerebrospinal fluid (CSF) leak: Halo sign on dressing (clear ring around blood), persistent clear nasal drainage, headache. Test drainage for glucose.
Monitor for diabetes insipidus (DI): Sudden onset of polyuria with low urine specific gravity. May require vasopressin replacement.
Monitor for SIAHD: Less common, but possible due to manipulation of posterior pituitary.
Assess neurological status frequently (LOC, visual fields, pupillary response).
Elevate head of bed to to reduce intracranial pressure and promote venous drainage.
Avoid coughing, sneezing, bending, straining (Valsalva maneuvers) to prevent increased intracranial pressure and CSF leak. Educate patient on open-mouth sneezing.
Administer corticosteroids as prescribed to prevent adrenal insufficiency.
Monitor fluid and electrolytes closely.
Anxiety related to diagnosis, treatment, and potential body changes.
Visual disturbance related to tumor compression.
Acute pain related to surgical incision.
Impaired oral mucous membrane integrity related to transsphenoidal approach.
Potential for injury due to vision changes or balance issues.
Fluid volume excess or deficit (especially post-surgery, risk for DI or SIADH).
Potential for infection (meningitis, sinusitis) related to surgical site.
Patient education: Comprehensive teaching on disease process, medication therapy, post-operative care, signs of complications, and importance of adherence to follow-up.
Hypopituitarism
Cause and pathophysiology- Decreased secretion of one or more pituitary hormones, most commonly growth hormone (GH) and gonadotropins (FSH, LH).
Can be hereditary (congenital deficiencies) or acquired due to damage to the gland or hypothalamus (e.g., tumors, infarction, radiation, trauma, infection, autoimmune processes, severe blood loss during childbirth - Sheehan's syndrome).
Panhypopituitarism may occur, involving a deficiency of all anterior pituitary hormones, leading to severe metabolic and endocrine dysfunction.
Signs and symptoms-
General: Fatigue, weakness, malaise, cold intolerance, lethargy, decreased energy levels.
If tumor is the cause: Headaches (due to mass effect), vision disturbances (e.g., visual field defects), seizures, and loss of smell (anosmia).
Specific symptoms depend on which hormone deficiency occurs and at what age:
Early deficiency of GH (in childhood): Short stature (dwarfism) with proportional body characteristics, often with delayed bone age.
GH deficiency in adults: Reduced muscle strength, increased adipose tissue, reduced bone density, decreased exercise tolerance.
Panhypopituitarism: Widespread effects including muscle and organ wasting, significant problems with digestion and metabolism, severe fatigue.
No ACTH (adrenocorticotropic hormone): Adrenal insufficiency leading to hypoglycemia (due to lack of cortisol), decreased sodium, increased potassium, weakness, weight loss, hypotension, and risk of adrenal crisis.
No TSH (thyroid-stimulating hormone): Secondary hypothyroidism leading to cold intolerance, bradycardia, lethargy, constipation, weight gain, dry skin, hair loss.
No MSH (melanocyte-stimulating hormone): Decreased skin pigmentation (e.g., pale skin, reduced tanning ability).
No gonadotropins (FSH, LH): Gonads atrophy, decreased libido, decreased body hair (axillary and pubic), sexual dysfunction (erectile dysfunction in men, amenorrhea in women, infertility in both genders).
No ADH (vasopressin): Can lead to secondary diabetes insipidus (posterior pituitary involvement).
Medical diagnosis-
Panhypopituitarism: Comprehensive health history, thorough physical examination to identify signs of hormone deficiencies, and extensive diagnostic tests.
Imaging: MRI, CT scan of the brain, or cerebral angiography to identify pituitary or hypothalamic lesions.
Serum pituitary hormones levels: Direct measurement of baseline pituitary hormone levels (e.g., GH, ACTH, TSH, FSH, LH, prolactin) and target gland hormones (e.g., cortisol, thyroid hormones, testosterone/estrogen).
Stimulation tests: Used to assess the functional reserve of the pituitary:
ACTH stimulation test: To assess adrenal response (cortisol production).
Insulin tolerance test (ITT): Gold standard for GH and ACTH deficiency, though rarely used due to risk of severe hypoglycemia.
GnRH stimulation test: To assess gonadotropin reserve.
TRH stimulation test: To assess TSH and prolactin reserve.
Medical and surgical treatment-
Hormone replacement therapy: The cornerstone of treatment, replacing deficient hormones lifelong.
Corticosteroids (e.g., hydrocortisone, prednisone) for ACTH deficiency.
Thyroid hormone (e.g., levothyroxine) for TSH deficiency.
Growth hormone (somatropin) for GH deficiency (especially in children, but also increasingly in adults).
Sex hormones (e.g., testosterone for men, estrogen/progesterone for women) for gonadotropin deficiency.
Surgical treatment: Removal of pituitary tumors or other lesions causing the hypofunction.
Radiation therapy: May be used for tumors if surgery is not feasible or effective.
Nursing care-
Patient education: Crucial for long-term management.
Importance of lifelong hormone replacement therapy and strict adherence.
Proper administration of medications (e.g., injectable GH, oral steroids).
Recognition of signs and symptoms of under- or over-replacement of hormones.
Importance of carrying medical identification (e.g., MedicAlert bracelet) indicating hormone deficiencies, especially for adrenal insufficiency (risk of adrenal crisis).
Stress management techniques, as stress can increase hormone requirements.
Regular follow-up appointments and lab tests.
Assessment: Monitor vital signs, energy levels, weight, signs of hormone imbalance.
Fluid and electrolyte balance: Especially with ACTH deficiency.
Psychosocial support: Addressing body image issues (e.g., stunted growth), fatigue, and sexual dysfunction.
Diabetes Insipidus (DI)
Cause- Insufficient ADH (vasopressin) or the kidneys' inability to respond to ADH.
Classifications:
Neurogenic (Central or Hypothalamic) DI: Most common. Caused by a deficiency in ADH production or release from the posterior pituitary, often due to damage to the hypothalamus or pituitary gland (e.g., head trauma, brain tumors, neurosurgery, infections, idiopathic).
Nephrogenic DI: Kidneys are unable to respond to ADH, despite normal ADH levels. Can be inherited (genetic mutations affecting vasopressin receptors) or acquired (e.g., chronic kidney disease, certain drugs like lithium, hypercalcemia, hypokalemia).
Dipsogenic DI: Caused by excessive intake of water due to a defect in the thirst mechanism, leading to suppression of ADH. This is a primary polydipsia rather than true DI.
Gestational DI: Occurs during pregnancy due to increased vasopressinase activity (an enzyme that breaks down ADH).
Pathophysiology- Lack of effective ADH action leads to impaired water reabsorption in the renal tubules and collecting ducts. This causes massive polyuria (excessive urination), leading to intense thirst (polydipsia) as the body tries to compensate. If fluid intake cannot keep up with the diuresis, severe dehydration and hypernatremia occur.
Signs and symptoms-
Massive diuresis: Excretion of large volumes of dilute urine, often 4 to 30 liters per day or even more (normal is 1.5-2 L/day). This occurs day and night (nocturia).
Dehydration: If fluid intake is inadequate, leading to hypotension (especially orthostatic), tachycardia (compensatory), dizziness, decreased skin turgor, dry mucous membranes, weakness, and possible syncope.
Thirst: Intense, unquenchable thirst (polydipsia), usually for cold water.
Neurological: Malaise, lethargy, irritability, altered mental status, confusion, and seizures (due to hypernatremia and cellular dehydration of the brain).
Cardiovascular: Possible irregular heartbeat due to electrolyte imbalances.
Weight loss despite adequate food intake.
Medical diagnosis-
Initial diagnosis: High suspicion with urine output (U.O.) greater than .
Urine specific gravity: Very low (typically <1.005 or even <1.001), indicating very dilute urine.
Decreased urine osmolality: Low urine osmolarity (usually <200 \text{ mOsm/kg}).
Increased serum osmolality: Blood becomes concentrated (often >295 \text{ mOsm/kg}) due to water loss.
Hypernatremia: Serum sodium levels often elevated (>145 \text{ mEq/L}).
Water Deprivation Test (Fluid Deprivation Test): A definitive diagnostic test used to differentiate between neurogenic and nephrogenic DI.
Procedure: Patient is deprived of water for 8–16 hours or until of body weight is lost or plasma osmolality reaches >295 \text{ mOsm/kg}. During the test, monitor vital signs (especially BP for orthostatic changes), body weight, and urine osmolality, urine specific gravity, and plasma osmolality every hour.
Stopping criteria: Test is stopped if urine osmolality stabilizes (meaning no further increase), if the patient loses >5\% of body weight, or if they develop significant orthostatic hypotension.
After water deprivation: Exogenous ADH (desmopressin or vasopressin) is administered. Urine osmolality is checked 1 hour later.
Neurogenic DI: Urine osmolality significantly increases (>50\%) after ADH administration, indicating the kidneys can respond, but central ADH is deficient.
Nephrogenic DI: Urine osmolality shows little or no increase (<10\%) after ADH administration, indicating kidney resistance to ADH.
Medical treatment-
Managing symptoms and maintaining fluid balance:
Fluid replacement: Oral preferred; IV fluids (hypotonic saline or D5W) given if oral intake is insufficient, to replace lost volume and correct hypernatremia slowly.
Vasopressors: Not typically used for DI itself, but IV fluids and sometimes vasopressin replacement are the primary treatments.
Desmopressin acetate (DDAVP): Synthetic analog of ADH. The primary treatment for neurogenic DI.
Available as nasal spray (common), oral tablets, or subcutaneous/intravenous injection.
Frequency varies (e.g., daily to three times a day).
Dosage is titrated to control thirst and polyuria without causing fluid overload.
Aqueous vasopressin: Short-acting ADH replacement given subcutaneously.
For Nephrogenic DI: Sodium restrictions and thiazide diuretics (e.g., hydrochlorothiazide) are used Paradoxically, thiazide diuretics reduce polyuria in nephrogenic DI by inducing mild hypovolemia, which increases proximal tubular water reabsorption.
NSAIDs: Can sometimes be used to reduce urine output in nephrogenic DI.
Nursing care-
Assessment: Strict intake and output (I&O) monitoring, daily weights, vital signs (BP, heart rate), neurological status, skin turgor, mucous membranes, thirst level.
Patient problems/diagnoses:
Anxiety related to frequent urination and thirst.
Altered body image (less common, but significant in chronic cases).
Fluid volume deficit (or risk for) related to uncontrolled diuresis.
Risk for decreased activity tolerance due to fatigue from frequent voiding or dehydration.
Ineffective self-health management related to complex medication regimen or understanding of disease.
Patient education: Critical for self-management.
Proper administration of DDAVP (nasal spray technique, importance of regular dosing).
Monitoring for signs of fluid overload (headache, confusion, weight gain) from too much DDAVP.
Importance of adequate fluid intake, but not excessive (listen to thirst mechanism).
Wearing medical identification (MedicAlert bracelet).
Understanding the disease process and differentiating from diabetes mellitus.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Cause- Characterized by excessive ADH secretion or action inappropriate to plasma osmolality.
Common causes include:
Malignancies: Especially small cell lung carcinoma (most common ectopic source).
Central Nervous System (CNS) disorders: Head injury, stroke, brain tumors, meningitis, encephalitis.
Pulmonary diseases: Pneumonia, tuberculosis, acute respiratory failure.
Drugs: Certain medications like SSRIs, tricyclic antidepressants, carbamazepine, ecstasy (MDMA), vincristine, cyclophosphamide.
Surgery: Post-operative stress, especially neurosurgery.
Idiopathic.
Pathophysiology- Too much ADH leads to increased water reabsorption by the kidneys, resulting in dilutional hyponatremia and fluid retention. This causes intracellular fluid shifts, particularly into brain cells (cerebral edema), without peripheral edema (as total body sodium is usually near normal, but diluted). Water intoxication affects the nervous system and can cause severe neurological symptoms.
Signs and symptoms-
Hyponatremia and water retention: Symptoms are often related to the severity and rapidity of hyponatremia.
Early/Mild: Weakness, muscle cramps/twitching, anorexia, nausea, diarrhea, irritability, headache, weight gain without visible edema (due to fluid shift into cells rather than interstitial space).
Moderate/Severe (especially with rapid drops in Na+ or levels < ):
Water intoxication affects the nervous system: leading to lethargy, confusion, disorientation, changes in mental status.
Progressive signs: Seizures (due to cerebral edema and cellular swelling), coma, and potentially respiratory arrest due (often secondary to severe neurological compromise).
Decreased urine output despite fluid retention.
Medical diagnosis-
Serum & urine electrolytes and osmolality: Key diagnostic indicators.
Low serum sodium (Hyponatremia): Levels typically <135 \text{ mEq/L}.
Low serum osmolality: Blood dilution (typically <280 \text{ mOsm/kg}).
High urine sodium: Inappropriately concentrated urine (urine Na+ >20 \text{ mEq/L} despite hyponatremia).
High urine osmolality: Inappropriately concentrated urine (urine osmolality >100 \text{ mOsm/kg} despite low serum osmolality).
Other labs showing blood dilution: Low BUN (Blood Urea Nitrogen), low creatinine clearance, low uric acid.
Fluid excess with no edema: Patients typically present with weight gain but without overt peripheral or pitting edema.
Radiographic studies: To identify the underlying cause (e.g., chest X-ray/CT scan for lung cancer, brain MRI for CNS lesions).
Medical treatment-
Treat the underlying cause: Essential for long-term resolution (e.g., surgical removal of a tumor, discontinuation of causative drugs, treatment of lung infection).
Fluid restriction: Primary treatment for mild to moderate SIADH (often or even less), aiming to increase serum sodium concentration.
Salt tablets or high sodium intake: May be combined with fluid restriction for mild cases.
Treat hyponatremia:
Hypertonic saline (e.g., : Used cautiously for severe symptomatic hyponatremia (Na+ <120 \text{ mEq/L} or with seizures/coma). Administered slowly to avoid rapid correction, which can cause osmotic demyelination syndrome.
Loop diuretics (e.g., Furosemide): May be used with hypertonic saline to promote water excretion, especially if hyponatremia is accompanied by significant fluid overload, but not typically as monotherapy.
Vasopressin receptor antagonists (Vaptans): e.g., Tolvaptan, Conivaptan. These drugs block the action of ADH on the renal tubules, promoting water excretion without electrolyte loss. Used for severe or chronic euvolemic hyponatremia resistant to fluid restriction.
SIADH → Drugs : Demeclocycline, which is a tetracycline antibiotic used off-label for the treatment of SIADH. This medication works by causing the kidneys to become less responsive to ADH, thus promoting water excretion and correcting hyponatremia. Other treatment options for SIADH include fluid restriction, hypertonic saline, and monitoring serum sodium levels closely to avoid rapid correction, which can lead to serious neurological complications.
Nursing care-
Assessment: Meticulous monitoring of neurological status (LOC, mental status, seizure precautions), vital signs, strict I&O, daily weights, signs of fluid overload (e.g., crackles in lungs, distended neck veins), and serum sodium levels.
Patient problems/diagnoses:
Potential for injury related to altered mental status and seizures.
Fluid volume excess (or risk for) related to inappropriate ADH secretion.
Inability to manage self-care related to symptoms and treatment regimen.
Patient education: Explain fluid restriction, importance of adhering to medication, signs/symptoms of worsening hyponatremia or fluid overload, and the need for regular follow-up.
Safety: Implement seizure precautions for patients with severe hyponatremia.
Oral hygiene: Provide frequent oral care due to fluid restriction.
Adrenal Hypofunction (Addison Disease)
Cause- Insufficiency of adrenocortical hormones.
Primary Adrenal Insufficiency (Addison Disease): Most commonly due to autoimmune destruction of the adrenal cortex (approximately of cases), leading to a deficiency of cortisol and aldosterone.
Secondary Adrenal Insufficiency: Dysfunction of the hypothalamus or pituitary gland, resulting in decreased ACTH secretion (e.g., pituitary tumors, sudden withdrawal of long-term corticosteroid therapy).
Pathophysiology- Deficiency of glucocorticoids (cortisol), mineralocorticoids (aldosterone, primarily in primary Addison's), and adrenal androgens.
Cortisol deficiency: Impaired stress response, hypoglycemia, decreased gluconeogenesis, impaired protein/fat/carbohydrate metabolism, reduced vascular tone.
Aldosterone deficiency (primary): Impaired sodium and water reabsorption, leading to hyponatremia, hyperkalemia, hypovolemia, hypotension, and acidosis.
Androgen deficiency: Decreased libido and pubic/axillary hair in women.
Signs and symptoms-
Gradual onset: Often insidious, developing over months or years.
Weakness and fatigue: Progressive and profound.
Weight loss and anorexia.
Hyperpigmentation: Characteristic bronze-colored skin (especially in sun-exposed areas, skin creases, pressure points, and mucous membranes) due to increased ACTH and MSH in primary adrenal insufficiency.
Hypotension: Orthostatic hypotension is common, can progress to shock.
Gastrointestinal: Nausea, vomiting, diarrhea, abdominal pain, cravings for salty foods.
Electrolyte imbalances: Hyponatremia, hyperkalemia, hypoglycemia.
Salt craving.
Dizziness, syncope.
Adrenal crisis (Addisonian crisis): A life-threatening emergency caused by insufficient adrenocortical hormones, triggered by stress (infection, trauma, surgery), or sudden withdrawal of corticosteroids. Manifests as severe hypotension, shock, profound weakness, pain (abdominal, back, leg), severe vomiting/diarrhea, and altered mental status.
Medical diagnosis-
Hormone levels: Decreased serum cortisol (especially morning cortisol), elevated plasma ACTH (in primary disease), decreased aldosterone levels (in primary disease).
Electrolytes: Hyponatremia, hyperkalemia.
ACTH Stimulation Test (Cosyntropin Stimulation Test): The definitive diagnostic test.
Procedure: Baseline cortisol and ACTH levels are drawn. Synthetic ACTH (cosyntropin) is administered IV or IM. Cortisol levels are measured at 30 and 60 minutes post-injection.
Interpretation: In primary Addison's, cortisol levels fail to rise significantly, indicating adrenal gland failure. In secondary Addison's, cortisol levels may rise, but slowly, or ACTH levels are low at baseline.
Imaging: CT or MRI of the adrenal glands to identify atrophy, hemorrhage, or tumors. MRI of the pituitary/hypothalamus for secondary causes.
ECG: May show changes due to hyperkalemia (peaked T waves).
Medical treatment-
Hormone replacement therapy: Lifelong replacement is essential.
Glucocorticoids: Hydrocortisone (most common), prednisone, or dexamethasone. Doses are adjusted based on stress (increased in illness, surgery, trauma).
Mineralocorticoids: Fludrocortisone acetate (Florinef) for primary adrenal insufficiency, to replace aldosterone function. Dosage adjusted based on blood pressure and electrolyte levels.
Increased salt intake: Especially during hot weather or exercise, if taking fludrocortisone.
Management of Adrenal Crisis: IV hydrocortisone (high doses), IV fluids (normal saline and D5W) for volume and glucose replacement, electrolyte correction (hyperkalemia management).
Nursing care-
Assessment: Monitor vital signs (especially BP for hypotension), fluid and electrolyte status (sodium, potassium, glucose), weight, signs of dehydration or fluid overload, skin color, energy level, and mental status.
Fluid and electrolyte balance: Closely monitor I&O, administer IV fluids as prescribed, monitor for signs of hyponatremia and hyperkalemia.
Medication management: Emphasize strict adherence to lifelong hormone replacement therapy. Educate on dose adjustments during stress, illness, or surgery. Instruct patient to never abruptly stop corticosteroids.
Patient education: Teach signs and symptoms of adrenal crisis and the need for immediate medical attention. Advise wearing a MedicAlert bracelet. Provide stress management techniques. Dietary considerations (increased salt, adequate glucose).
Safety: Prevent falls due to orthostatic hypotension. Monitor for hypoglycemia.
Adrenal Hypersecretion (Cushing Syndrome)
Cause- Excessive secretion of corticosteroids, particularly glucocorticoids (cortisol).
Exogenous (Iatrogenic) Cushing Syndrome: Most common cause, due to prolonged administration of high-dose corticosteroids (e.g., for asthma, autoimmune diseases, organ transplant).
Endogenous Cushing Syndrome: Less common, caused by internal overproduction of cortisol.
Cushing Disease: Pituitary adenoma (tumor) producing excessive ACTH, which stimulates the adrenal glands to overproduce cortisol (approximately of endogenous cases).
Adrenal Tumors: Adrenal adenoma or carcinoma directly overproducing cortisol (ACTH levels will be low).
Ectopic ACTH Syndrome: Non-pituitary tumors (e.g., small cell lung cancer, pancreatic tumors, thymomas) secreting ACTH or CRH, leading to adrenal hyperplasia and cortisol excess.
Pathophysiology- Excess cortisol leads to widespread metabolic and systemic effects:
Carbohydrate metabolism: Increased gluconeogenesis, resulting in hyperglycemia and insulin resistance.
Protein metabolism: Increased protein catabolism, leading to muscle wasting (thin extremities), fragile skin, delayed wound healing, and osteoporosis.
Fat metabolism: Redistribution of fat to the face (moon face), trunk (truncal obesity), and back of neck (buffalo hump).
Immune suppression: Increased susceptibility to infection, poor inflammatory response.
Mineralocorticoid effects: Hypertension, hypokalemia, fluid retention (though aldosterone levels are often normal, cortisol has mineralocorticoid activity at high concentrations).
Androgen effects: Acne, hirsutism (excessive hair growth in women), menstrual irregularities.
Signs and symptoms-
Characteristic physical changes: