Graves’ Disease

Graves’ disease is a chronic autoimmune disorder characterized by hyperthyroidism, diffuse

thyroid enlargement, and the presence of extrathyroidal manifestations such as Graves’
orbitopathy and pretibial myxedema. It is the most common cause of hyperthyroidism.

Epidemiology
• Age: Commonly presents between 20–50 years.
• Gender: Affects women more than men (female-to-male ratio of 5:1).
• Prevalence: Higher in regions with adequate iodine intake.
• Family History: Strong genetic predisposition with familial clustering.

Pathophysiology
Graves’ disease is caused by autoimmune activation of the thyroid gland.
• Thyroid-stimulating antibodies (TSAb) bind to and activate the thyrotropin
receptor (TSH receptor), leading to:
o Increased synthesis and release of thyroid hormones (T3 and T4).
o Thyroid gland hypertrophy and hyperplasia (diffuse goiter).
• Extrathyroidal manifestations are due to autoimmune inflammation mediated by T-
cells and cytokines, particularly in the orbit and dermis.

Clinical Features
1. Hyperthyroid Symptoms:
o Weight loss despite increased appetite.
o Heat intolerance and excessive sweating.
o Tachycardia, palpitations, and arrhythmias (e.g., atrial fibrillation).
o Nervousness, irritability, tremors, and anxiety.
o Fatigue, muscle weakness, and diarrhea.
2. Thyroid Gland Enlargement:
o Diffuse, symmetrical, and non-tender goiter.
3. Extrathyroidal Manifestations:
o Graves’ orbitopathy:
▪ Eye symptoms include proptosis, lid lag, lid retraction, redness, and
diplopia.
▪ Severe cases may lead to exposure keratitis or optic neuropathy.
o Pretibial myxedema: Localized dermopathy with thickened, hyperpigmented
skin over the shins.
o Acropachy: Clubbing and soft tissue swelling of the fingers and toes.
4. Others:
o Menstrual irregularities.
o Osteopenia/osteoporosis due to increased bone resorption.
o Rarely, thyroid storm (life-threatening exacerbation).
Investigations
1. Thyroid Function Tests:
o Elevated free T4 and/or T3 levels.
o Suppressed TSH levels due to negative feedback on the pituitary.
2. Autoantibody Tests:
o Positive thyroid-stimulating immunoglobulins (TSI) or thyrotropin receptor
antibodies (TRAb) confirms autoimmune etiology.
3. Radioactive Iodine Uptake (RAIU) Scan:
o Increased diffuse uptake in the thyroid gland.
4. Thyroid Ultrasound:
o Useful in assessing gland size and vascularity (increased vascular flow on
Doppler).
5. Eye Examination:
o Assessment for orbitopathy using clinical scoring systems or imaging (e.g., CT
or MRI of the orbit).

Differential Diagnosis
• Toxic multinodular goiter: Patchy thyroid uptake on RAIU scan.
• Thyroiditis: Hyperthyroidism with low RAIU.
• Toxic adenoma: Solitary “hot nodule” on RAIU scan.
• Factitious thyrotoxicosis: Exogenous thyroid hormone use.

Management
1. Antithyroid Drugs:
o Carbimazole or methimazole: Inhibit thyroid hormone synthesis.
o Propylthiouracil (PTU): Preferred in the first trimester of pregnancy or
thyroid storm.
o Side effects include rash, agranulocytosis, and hepatotoxicity.
2. Beta-Blockers:
o Propranolol: Provides symptomatic relief by controlling tachycardia, tremors,
and anxiety.
3. Radioactive Iodine Therapy:
o Administered orally to ablate thyroid tissue.
o Not used in pregnant or breastfeeding women.
4. Surgery (Thyroidectomy):
o Indicated for large goiters, compressive symptoms, or when other treatments
are contraindicated.
o Complications include hypocalcemia and recurrent laryngeal nerve injury.
5. Graves’ Orbitopathy Management:
o Mild cases: Lubricating eye drops and selenium supplementation.
oSevere cases: Glucocorticoids (e.g., IV methylprednisolone) or orbital
decompression surgery.
6. Smoking Cessation:
o Smoking worsens orbitopathy and increases relapse risk.

Complications
• Thyroid storm: A medical emergency with severe hyperthyroidism, fever, and
cardiovascular instability.
• Heart complications: Atrial fibrillation, high-output heart failure.
• Osteoporosis: Due to chronic bone resorption.
• Relapse or treatment-related hypothyroidism.
Hyperthyroidism

Hyperthyroidism is a clinical condition caused by excessive production of thyroid hormones

(T3 and T4), leading to an increased metabolic rate and hypermetabolic state.

Etiology
1. Primary Hyperthyroidism (Thyroid gland overactivity):
o Graves’ disease: Autoimmune stimulation of the thyroid gland.
o Toxic multinodular goiter: Autonomous functioning thyroid nodules.
o Toxic adenoma: A single hyperfunctioning nodule.
o Iodine-induced hyperthyroidism: Due to excess iodine intake (Jod-Basedow
phenomenon).
o Thyroid carcinoma (rare).
2. Secondary Hyperthyroidism (Increased TSH production):
o TSH-secreting pituitary adenoma.
3. Transient Hyperthyroidism:
o Subacute thyroiditis (e.g., viral or postpartum thyroiditis).
o Exogenous thyroid hormone use (factitious thyrotoxicosis).

Pathophysiology
• Excess thyroid hormones enhance metabolic activity by upregulating beta-
adrenergic receptors and increasing the basal metabolic rate.
• Hyperthyroidism affects nearly all systems, resulting in sympathetic overactivity and
increased tissue oxygen demand.

Clinical Features
1. General Symptoms:
o Weight loss despite normal or increased appetite.
o Heat intolerance, sweating.
o Fatigue, weakness.
2. Cardiovascular System:
o Tachycardia, palpitations.
o Atrial fibrillation, high-output heart failure.
3. Neuromuscular System:
o Tremors, nervousness, irritability.
o Hyperreflexia.
4. Gastrointestinal System:
o Increased bowel movements or diarrhea.
5. Reproductive System:
o Oligomenorrhea or amenorrhea.
o Infertility.
6. Ocular Signs:
o Lid lag, lid retraction (due to sympathetic overactivity).
o Graves’ orbitopathy in Graves’ disease.
7. Thyroid Gland:
o Diffuse or nodular goiter.

Investigations
1. Thyroid Function Tests:
o Increased free T4 and/or T3 levels.
o Suppressed TSH levels (primary hyperthyroidism).
o Elevated TSH in secondary hyperthyroidism.
2. Thyroid Autoantibodies:
o Thyroid-stimulating immunoglobulins (TSI) or TSH receptor antibodies
(TRAb) in Graves’ disease.
3. Radioactive Iodine Uptake (RAIU):
o Diffuse uptake: Graves’ disease.
o Patchy uptake: Toxic multinodular goiter.
o Low uptake: Thyroiditis or exogenous hormone use.
4. Imaging:
o Ultrasound: Helps differentiate nodular goiters from diffuse goiters.
o MRI/CT orbit: To assess Graves’ orbitopathy.

Management
1. Antithyroid Drugs:
o Carbimazole or Methimazole: Inhibit thyroid hormone synthesis.
o Propylthiouracil (PTU): Preferred in pregnancy (first trimester) and thyroid
storm.
o Monitor for side effects like rash, agranulocytosis, and hepatotoxicity.
2. Beta-Blockers:
o E.g., Propranolol: Controls tachycardia, tremors, and anxiety.
3. Radioactive Iodine Therapy:
o Used to ablate thyroid tissue in non-pregnant adults.
4. Surgery:
o Total or subtotal thyroidectomy for large goiters, compressive symptoms, or
malignancy.
5. Treatment of Specific Causes:
o Graves’ disease: Combination of antithyroid drugs and symptomatic relief.
o Thyroiditis: Supportive care, as it is often self-limiting.

Complications
• Thyroid storm: Life-threatening exacerbation of hyperthyroidism.
• Atrial fibrillation and thromboembolism.
• Osteoporosis due to increased bone turnover.
• Relapse or progression to hypothyroidism post-treatment.
Hypothyroidism

Hypothyroidism is a clinical condition resulting from reduced production of thyroid

hormones (T3 and T4), leading to a generalized slowing of metabolic processes.

Etiology
1. Primary Hypothyroidism (Intrinsic thyroid gland dysfunction):
o Chronic autoimmune thyroiditis (Hashimoto’s thyroiditis): Most common
cause.
o Iodine deficiency: Common in developing countries.
o Post-treatment hypothyroidism: After thyroidectomy or radioactive iodine
therapy.
o Drug-induced: Lithium, amiodarone, antithyroid drugs.
o Congenital hypothyroidism: Thyroid dysgenesis or dyshormonogenesis.
2. Secondary Hypothyroidism (Central hypothyroidism):
o Pituitary disease: Tumors, trauma, surgery, or radiation.
o Hypothalamic dysfunction: Rare causes like tumors or infiltrative diseases.
3. Transient Hypothyroidism:
o Postpartum thyroiditis.
o Subacute thyroiditis (de Quervain’s).

Pathophysiology
• Inadequate thyroid hormone levels impair cellular metabolism, affecting nearly
every organ system.
• TSH levels are elevated in primary hypothyroidism due to loss of negative feedback,
while they are low or normal in central causes.

Clinical Features
1. General Symptoms:
o Fatigue, lethargy.
o Cold intolerance.
o Weight gain despite reduced appetite.
2. Skin and Hair:
o Dry, coarse skin.
o Hair thinning or hair loss (including outer third of eyebrows).
o Brittle nails.
3. Neurological:
o Depression, poor memory, and cognitive impairment (“mental slowing”).
o Hoarseness of voice.
4. Cardiovascular:
o Bradycardia, hypotension.
o Pericardial effusion (in severe cases).
5. Musculoskeletal:
o Myopathy, muscle stiffness.
o Arthralgia.
6. Gastrointestinal:
o Constipation.
7. Reproductive:
o Menorrhagia, infertility in women.
o Reduced libido in men and women.
8. Facial Features:
o Puffy face with periorbital edema.
o Macroglossia (enlarged tongue).

Specific Forms
• Myxedema: Severe hypothyroidism characterized by mucopolysaccharide
deposition in the skin and other tissues, leading to thickened, non-pitting edema.
• Cretinism: Congenital hypothyroidism causing growth retardation and
developmental delays.

Investigations
1. Thyroid Function Tests:
o Primary hypothyroidism: Low T3 and T4, elevated TSH.
o Secondary hypothyroidism: Low T3, T4, and TSH.
2. Thyroid Autoantibodies:
o Anti-thyroid peroxidase (TPO) antibodies: Positive in Hashimoto’s
thyroiditis.
o Anti-thyroglobulin antibodies: Supportive evidence in autoimmune thyroid
disease.
3. Imaging:
o Ultrasound of the thyroid: For structural abnormalities.
o MRI brain: If central hypothyroidism is suspected.
4. Other Tests:
o Lipid profile: Hypercholesterolemia is common.
o Anemia: Normocytic or macrocytic anemia.

Management
1. Thyroid Hormone Replacement:
o Levothyroxine (T4): Mainstay of treatment.
▪ Dose: 1.6 μg/kg/day, adjusted based on TSH levels.
▪ Start with a lower dose in elderly or cardiac patients to avoid
complications.
o Liothyronine (T3): Rarely used except in acute cases like myxedema coma.
2. Monitoring:
o TSH levels are rechecked 6–8 weeks after initiating or adjusting therapy.
o Target TSH: Normal range (0.5–4.0 mU/L).
3. Myxedema Coma:
o A medical emergency requiring IV levothyroxine, supportive care, and
treatment of precipitating factors.

Complications
• Cardiovascular: Hyperlipidemia, atherosclerosis, and heart failure.
• Neurological: Cognitive dysfunction and peripheral neuropathy.
• Myxedema Coma: Life-threatening decompensated hypothyroidism.

Adrenal Insufficiency

Adrenal insufficiency is a condition caused by the inadequate production of glucocorticoids,

mineralocorticoids, or both from the adrenal cortex, resulting in impaired stress response and
metabolic dysfunction.

Classification
1. Primary Adrenal Insufficiency (Addison’s Disease):
o Caused by direct damage to or dysfunction of the adrenal glands.
o Common causes:
▪ Autoimmune adrenalitis (most common).
▪ Infectious diseases: Tuberculosis, fungal infections, HIV.
▪ Adrenal hemorrhage (e.g., Waterhouse-Friderichsen syndrome).
▪ Infiltrative disorders: Metastases, amyloidosis, sarcoidosis.
▪ Genetic disorders: Congenital adrenal hyperplasia (CAH),
adrenoleukodystrophy.
2. Secondary Adrenal Insufficiency:
o Caused by reduced adrenocorticotropic hormone (ACTH) production from
the pituitary gland.
o Common causes:
▪ Pituitary tumors, surgery, or radiation.
▪ Long-term glucocorticoid therapy causing suppression of the
hypothalamic-pituitary-adrenal (HPA) axis.
3. Tertiary Adrenal Insufficiency:
o Due to hypothalamic dysfunction and reduced corticotropin-releasing
hormone (CRH).

Pathophysiology
• Primary adrenal insufficiency: Deficiency of cortisol and aldosterone, leading to
electrolyte imbalances (e.g., hyponatremia, hyperkalemia) and impaired stress
response.
• Secondary and tertiary insufficiency: Isolated glucocorticoid deficiency as
aldosterone secretion remains intact (regulated by the renin-angiotensin system).

Clinical Features
1. General Symptoms:
o Fatigue, weakness.
o Weight loss.
o Poor appetite.
2. Skin Changes:
o Hyperpigmentation (specific to primary adrenal insufficiency due to elevated
ACTH stimulating melanocytes).
o Vitiligo (in autoimmune conditions).
3. Cardiovascular:
o Hypotension (postural or persistent).
o Shock in adrenal crisis.
4. Electrolyte Imbalance:
o Hyponatremia (common).
o Hyperkalemia (specific to primary adrenal insufficiency).
o Hypoglycemia.
5. Gastrointestinal:
o Nausea, vomiting, abdominal pain.
6. Neuropsychiatric:
o Depression, irritability, or confusion.

Adrenal Crisis
• A medical emergency caused by acute glucocorticoid deficiency, often triggered by
stress (e.g., infection, surgery).
• Symptoms: Severe hypotension, shock, hypoglycemia, and electrolyte imbalances.

Investigations
1. Biochemical Tests:
o Serum cortisol: Low levels (<100 nmol/L in acute cases).
o ACTH levels:
▪ High in primary adrenal insufficiency.
▪ Low/normal in secondary or tertiary causes.
2. Stimulation Tests:
o Short Synacthen Test: Failure of cortisol to rise after synthetic ACTH
administration confirms adrenal insufficiency.
3. Electrolytes:
o Hyponatremia, hyperkalemia (in primary cases).
4. Plasma Renin and Aldosterone:
o High renin and low aldosterone in primary insufficiency.
5. Autoantibodies:
o Anti-21-hydroxylase antibodies in autoimmune adrenalitis.
6. Imaging:
o CT/MRI of the adrenals for structural abnormalities (e.g., infection,
hemorrhage).
o MRI of the pituitary for secondary causes.

Management
1. Glucocorticoid Replacement:
o Hydrocortisone: Preferred agent.
▪ Dosage: 15–30 mg/day in divided doses (morning and afternoon).
o Adjust doses during stress (e.g., illness, surgery).
2. Mineralocorticoid Replacement:
o Fludrocortisone: For primary adrenal insufficiency to correct aldosterone
deficiency.
3. Patient Education:
o Stress dosing of steroids.
o Emergency glucocorticoid self-injection kits (e.g., hydrocortisone).
o Medical alert identification.
4. Adrenal Crisis Management:
o IV hydrocortisone (100 mg stat, then 50 mg every 6 hours).
o IV fluids (normal saline with dextrose).
o Electrolyte correction.

Complications
• Adrenal crisis.
• Chronic fatigue and impaired quality of life if untreated.
• Osteoporosis from long-term glucocorticoid therapy.

Addison’s Disease
Addison’s disease, also known as primary adrenal insufficiency, is a chronic condition caused
by destruction or dysfunction of the adrenal cortex, leading to insufficient production of
glucocorticoids (cortisol), mineralocorticoids (aldosterone), and adrenal androgens.

Etiology
1. Autoimmune Adrenalitis (70–90%):
o Most common cause in developed countries.
o Often associated with polyglandular autoimmune syndromes.
2. Infections:
o Tuberculosis (TB): Most common cause in developing countries.
o Fungal infections: Histoplasmosis, coccidioidomycosis.
o HIV-related adrenal insufficiency.
3. Adrenal Hemorrhage or Infarction:
o Waterhouse-Friderichsen syndrome (meningococcal septicemia).
o Antiphospholipid syndrome.
4. Infiltrative Diseases:
o Metastatic carcinoma (lung, breast, melanoma).
o Sarcoidosis, amyloidosis, hemochromatosis.
5. Genetic Causes:
o Congenital adrenal hyperplasia.
o Adrenoleukodystrophy (X-linked).
6. Other Causes:
o Bilateral adrenalectomy.
o Drugs: Ketoconazole, etomidate, rifampicin.

Pathophysiology
• Adrenal cortex damage leads to deficiency of cortisol, aldosterone, and
androgens.
• Loss of cortisol impairs stress response, metabolism, and immune regulation.
• Aldosterone deficiency causes hyponatremia, hyperkalemia, and volume
depletion.
• Elevated ACTH levels result from loss of negative feedback, causing
hyperpigmentation.

Clinical Features
1. General Symptoms:
o Fatigue, weakness.
o Weight loss, anorexia.
2. Skin Changes:
o Hyperpigmentation: Seen in exposed and unexposed areas, especially in
palmar creases, gums, and scars.
o Vitiligo (in autoimmune cases).
3. Cardiovascular:
o Hypotension (postural and persistent).
o Dizziness, syncope.
4. Electrolyte Abnormalities:
o Hyponatremia: Causing confusion and lethargy.
o Hyperkalemia.
o Hypoglycemia.
5. Gastrointestinal:
o Nausea, vomiting, abdominal pain.
o Diarrhea or constipation.
6. Neuropsychiatric Symptoms:
o Depression, irritability, apathy.

Investigations
1. Biochemical Tests:
o Serum cortisol: Low levels (<100 nmol/L in acute cases).
o Plasma ACTH: Elevated in primary adrenal insufficiency.
2. Stimulation Test:
o Short Synacthen Test: Failure of cortisol to rise after administration of
synthetic ACTH confirms adrenal insufficiency.
3. Electrolyte Abnormalities:
o Hyponatremia, hyperkalemia.
4. Autoantibodies:
o Anti-21-hydroxylase antibodies in autoimmune adrenalitis.
5. Imaging:
o CT Abdomen: To detect adrenal calcifications (TB), hemorrhage, or
metastases.
o MRI brain: If secondary causes are suspected.

Management
1. Hormonal Replacement:
o Glucocorticoids:
▪ Hydrocortisone: 15–30 mg/day in divided doses (higher dose in the
morning).
o Mineralocorticoids:
▪ Fludrocortisone: 50–200 μg/day (in primary adrenal insufficiency).
2. Patient Education:
o Stress dosing during illness or surgery.
o Medical alert identification.
3. Treatment of Adrenal Crisis:
o IV hydrocortisone (100 mg stat, followed by 50 mg every 6 hours).
o IV fluids (normal saline ± dextrose).
4. Monitor:
o Electrolytes, blood pressure, and symptoms.

Complications
• Adrenal Crisis: Life-threatening event triggered by stress, infection, or abrupt
withdrawal of steroids.
• Chronic fatigue and quality-of-life impairment.

Adrenal Crisis

Adrenal crisis, also known as acute adrenal insufficiency, is a life-threatening medical

emergency caused by a sudden and severe deficiency of cortisol. It commonly occurs in
individuals with undiagnosed or poorly managed adrenal insufficiency, especially during
physiological stress.

Etiology
1. Primary Causes:
o Addison’s disease (autoimmune adrenalitis, tuberculosis, adrenal
hemorrhage).
o Abrupt withdrawal of long-term glucocorticoid therapy.
o Adrenal infarction or metastasis.
2. Secondary Causes:
o Pituitary dysfunction (e.g., tumors, surgery, radiation).
3. Triggers in Known Adrenal Insufficiency:
o Infections (e.g., sepsis, pneumonia).
o Surgery, trauma, or major stress.
o Severe dehydration.

Pathophysiology
• Severe cortisol deficiency disrupts stress response, leading to:
o Hypoglycemia due to impaired gluconeogenesis.
o Electrolyte imbalances: Hyponatremia, hyperkalemia.
o Hypovolemia: Due to aldosterone deficiency and dehydration.
o Hypotension and shock: Resulting from cortisol’s role in vascular tone
maintenance.

Clinical Features
1. General:
o Severe fatigue, weakness.
o Confusion, irritability, or altered mental state.
2. Gastrointestinal:
o Nausea, vomiting, abdominal pain.
3. Cardiovascular:
o Severe hypotension (unresponsive to fluids).
o Shock (cold, clammy skin, tachycardia).
4. Electrolyte Imbalance:
o Hyponatremia, hyperkalemia.
o Hypoglycemia.
5. Other Features:
o Fever (infections as a precipitating factor).

Diagnosis
1. Biochemical Tests:
o Low serum cortisol (<100 nmol/L).
o High ACTH levels (in primary adrenal insufficiency).
2. Electrolytes:
o Hyponatremia, hyperkalemia, metabolic acidosis.
3. Glucose Levels:
o Hypoglycemia.
4. Plasma Renin and Aldosterone:
o Elevated renin, low aldosterone in primary adrenal insufficiency.
5. ACTH Stimulation Test:
o If the patient is stable, confirm diagnosis by failure of cortisol to rise after
ACTH administration.

Management
1. Immediate Management:
o IV Hydrocortisone: 100 mg bolus, followed by 50 mg every 6 hours.
o IV Fluids:
▪ Normal saline to restore volume.
▪ Dextrose-containing solutions if hypoglycemia is present.
o Correct Electrolyte Imbalances: Monitor and manage hyperkalemia and
hyponatremia.
2. Identify and Treat Underlying Cause:
o Treat infections or other precipitating factors.
3. Transition to Maintenance Therapy:
o Oral hydrocortisone (15–30 mg/day in divided doses).
o Fludrocortisone if aldosterone deficiency is present.

Prevention
• Education on stress dosing during illness or surgery.
• Regular follow-up to adjust glucocorticoid therapy.
• Emergency self-injection kits for glucocorticoids.
• Medical alert identification.
Complications
• Hypovolemic shock.
• Organ failure from prolonged hypotension.
• Death if untreated.

Thyroid Storm

Thyroid storm is a rare, life-threatening condition characterized by severe hyperthyroidism with

systemic decompensation. It occurs due to excessive release of thyroid hormones, leading to
multisystem dysfunction and can be fatal without prompt treatment.

Etiology
1. Triggers in Hyperthyroid Patients:
o Infections (e.g., sepsis, pneumonia).
o Surgery or trauma.
o Emotional or physical stress.
o Acute iodine load (e.g., contrast agents, amiodarone).
o Discontinuation of antithyroid drugs.
2. Underlying Conditions:
o Graves’ disease (most common).
o Toxic multinodular goiter.
o Toxic adenoma.

Pathophysiology
• Excess thyroid hormones increase metabolic activity and catecholamine sensitivity,
leading to:
o Hyperthermia and tachycardia.
o Increased oxygen consumption and metabolic rate.
o Multiorgan dysfunction due to hypermetabolic state.

Clinical Features
1. General:
o High-grade fever (>39°C).
o Profuse sweating.
2. Cardiovascular:
o Severe tachycardia, palpitations.
o Arrhythmias (e.g., atrial fibrillation).
o Congestive heart failure.
3. Neurological:
o Agitation, restlessness, delirium.
o Seizures or coma in severe cases.
4. Gastrointestinal:
o Nausea, vomiting, diarrhea.
o Abdominal pain, potential jaundice (hepatic dysfunction).
5. Other Features:
o Tremors, weight loss, muscle weakness.

Diagnosis
1. Clinical Diagnosis:
o Based on signs of severe hyperthyroidism with systemic decompensation.
2. Laboratory Findings:
o Elevated free T3 and T4 levels.
o Suppressed TSH levels.
o Electrolyte disturbances: Hypercalcemia, hypokalemia.
3. Supporting Tests:
o ECG: Sinus tachycardia or atrial fibrillation.
o Liver function tests: Elevated transaminases or bilirubin.
4. Scoring System:
o Burch-Wartofsky Point Scale: Used to assess likelihood of thyroid storm.

Management
1. Supportive Care:
o Admit to ICU.
o Aggressive cooling (cooling blankets, antipyretics).
o IV fluids to correct dehydration.
o Electrolyte correction.
2. Control of Thyroid Hormones:
o Antithyroid Drugs:
▪ Propylthiouracil (PTU): Blocks hormone synthesis and peripheral
conversion of T4 to T3.
▪ Methimazole: Alternative if PTU is contraindicated.
o Iodine Therapy (after antithyroid drugs):
▪ Lugol's iodine or potassium iodide to inhibit thyroid hormone release.
3. Reduce Peripheral Effects of Thyroid Hormones:
o Beta-blockers:
▪ Propranolol: Reduces tachycardia and tremors.
▪ Esmolol (short-acting) in unstable patients.
4. Inhibit Peripheral Conversion of T4 to T3:
o High-dose glucocorticoids (e.g., hydrocortisone): Also helps manage adrenal
insufficiency.
5. Treat Precipitating Factors:
o Antibiotics for infections.
o Stop iodine-containing drugs.
Complications
• Cardiac arrhythmias and failure.
• Shock and multiorgan dysfunction.
• Mortality: High if untreated.

Cushing Syndrome

Cushing syndrome is a clinical condition resulting from prolonged exposure to excess

glucocorticoids, either endogenous (due to adrenal or pituitary disorders) or exogenous (from
corticosteroid therapy).

Etiology
1. Exogenous Causes:
o Prolonged use of corticosteroid medications (most common).
2. Endogenous Causes:
o ACTH-Dependent:
▪ Cushing’s disease (pituitary adenoma secreting ACTH).
▪ Ectopic ACTH production (e.g., small cell lung carcinoma, carcinoid
tumors).
o ACTH-Independent:
▪ Adrenal adenoma or carcinoma.
▪ Adrenal hyperplasia.

Pathophysiology
Excess glucocorticoids lead to:
• Increased gluconeogenesis causing hyperglycemia.
• Protein catabolism resulting in muscle wasting and skin thinning.
• Lipolysis with abnormal fat distribution (central obesity, buffalo hump).
• Immune suppression and impaired wound healing.

Clinical Features
1. General Appearance:
o Central obesity.
o Moon face.
o Buffalo hump (fat pad over the upper back).
2. Skin Changes:
o Thin, fragile skin with easy bruising.
o Purple striae (abdomen, thighs, breasts).
o Hyperpigmentation (in ACTH-dependent cases).
3. Musculoskeletal:
o Proximal muscle weakness.
o Osteoporosis with increased fracture risk.
4. Metabolic:
o Hyperglycemia (diabetes mellitus).
o Dyslipidemia.
o Hypertension.
5. Neuropsychiatric:
o Depression, anxiety, or cognitive dysfunction.
o Insomnia.
6. Immune and Reproductive:
o Increased susceptibility to infections.
o Menstrual irregularities in women.
o Reduced libido in men.

Diagnosis
1. Initial Screening Tests:
o 24-hour urinary free cortisol: Elevated cortisol excretion.
o Low-dose dexamethasone suppression test: Failure of cortisol
suppression.
o Late-night salivary cortisol: Elevated cortisol levels.
2. Confirmatory Tests:
o ACTH Levels:
▪ Low: Suggests adrenal source (adenoma, carcinoma).
▪ High: Suggests ACTH-dependent causes.
3. Imaging:
o MRI of the pituitary (for Cushing’s disease).
o CT/MRI of adrenal glands (for adrenal tumors).
o CT chest/abdomen (for ectopic ACTH-producing tumors).

Management
1. Exogenous Cushing Syndrome:
o Gradual tapering of corticosteroid therapy.
2. Endogenous Cushing Syndrome:
o Surgical Management:
▪ Transsphenoidal resection of pituitary adenoma (Cushing’s disease).
▪ Adrenalectomy for adrenal tumors.
▪ Resection of ectopic ACTH-secreting tumors.
o Medical Therapy:
▪ Steroidogenesis Inhibitors: Ketoconazole, metyrapone.
▪ Glucocorticoid Receptor Antagonists: Mifepristone (for refractory
cases).
o Radiotherapy:
▪ For pituitary adenomas not amenable to surgery.
3. Supportive Measures:
o Treat hypertension, diabetes, and osteoporosis.
o Infection prophylaxis.

Complications
• Cardiovascular disease (hypertension, myocardial infarction).
• Diabetes mellitus.
• Opportunistic infections.
• Osteoporotic fractures.

Tetany

Tetany is a clinical syndrome characterized by involuntary muscle contractions and spasms,

primarily due to hypocalcemia or other electrolyte imbalances that increase neuromuscular
excitability.

Etiology
1. Electrolyte Imbalances:
o Hypocalcemia: Most common cause (e.g., hypoparathyroidism, vitamin D
deficiency).
o Hypomagnesemia: Impairs parathyroid hormone (PTH) secretion and action.
o Alkalosis: Causes increased binding of calcium to albumin, reducing ionized
calcium levels.
2. Endocrine Disorders:
o Hypoparathyroidism (post-surgical, idiopathic, or autoimmune).
o Pseudohypoparathyroidism (resistance to PTH).
3. Vitamin Deficiency:
o Vitamin D deficiency or resistance.
4. Renal and Gastrointestinal Causes:
o Chronic kidney disease (CKD) causing secondary hyperparathyroidism.
o Malabsorption syndromes (e.g., celiac disease, chronic pancreatitis).
5. Other Causes:
o Respiratory alkalosis (e.g., hyperventilation).
o Post-thyroidectomy or parathyroidectomy.

Pathophysiology
• Hypocalcemia lowers the threshold potential, increasing neuromuscular
excitability.
• Involuntary muscle contractions occur due to hyperexcitable nerves and muscles.

Clinical Features
1. Neuromuscular Symptoms:
o Muscle cramps and spasms (especially in hands and feet).
o Paresthesia (tingling or numbness) in extremities and around the mouth.
o Carpopedal spasm (classic feature).
2. Signs:
o Chvostek’s Sign: Facial muscle twitching upon tapping the facial nerve.
o Trousseau’s Sign: Carpal spasm induced by inflating a blood pressure cuff
above systolic pressure for 3 minutes.
3. Severe Cases:
o Laryngospasm leading to stridor.
o Seizures.
4. Associated Features (Depending on Cause):
o Dry skin, brittle nails, and hair loss (hypoparathyroidism).
o Signs of vitamin D deficiency (e.g., bone pain, rickets in children).

Diagnosis
1. Laboratory Tests:
o Serum Calcium: Low total and ionized calcium.
o Serum Magnesium: To rule out hypomagnesemia.
o Serum Phosphate: Elevated in hypoparathyroidism.
o PTH Levels: Low in hypoparathyroidism; high in secondary
hyperparathyroidism.
o Vitamin D Levels: Deficiency or insufficiency.
2. Arterial Blood Gas (ABG):
o Alkalosis in hyperventilation-induced tetany.
3. ECG Findings:
o Prolonged QT interval in hypocalcemia.

Management
1. Acute Management:
o Calcium Replacement:
▪ Intravenous calcium gluconate for severe symptoms.
o Magnesium Replacement: If hypomagnesemia is present.
o Correct Underlying Alkalosis: Treat hyperventilation or other causes.
2. Chronic Management:
o Oral Calcium Supplements: Calcium carbonate or citrate.
o Vitamin D Supplementation: Cholecalciferol or calcitriol.
o Magnesium Replacement: Oral magnesium salts if deficiency persists.
o Parathyroid Hormone (PTH) Therapy: In cases of refractory
hypoparathyroidism.
3. Treat Underlying Cause:
o Address malabsorption, vitamin D deficiency, or kidney disease.

Complications
• Prolonged untreated tetany can result in seizures, respiratory distress, or cardiac
arrhythmias.

Acromegaly

Acromegaly is a rare endocrine disorder caused by excessive secretion of growth hormone

(GH), usually due to a pituitary adenoma, leading to abnormal growth of soft tissues and bones,
primarily in adults after epiphyseal plate closure.

Etiology
1. Pituitary Causes:
o Growth hormone-secreting pituitary adenoma (most common).
o Pituitary hyperplasia (secondary to hypothalamic dysfunction).
2. Extra-pituitary Causes:
o Ectopic secretion of growth hormone-releasing hormone (GHRH) (e.g.,
neuroendocrine tumors of the pancreas or lungs).
o Rare ectopic production of GH (e.g., bronchial carcinoma).

Pathophysiology
• Excess GH stimulates the liver to produce insulin-like growth factor 1 (IGF-1), which
mediates the tissue growth and metabolic effects of GH.
• Elevated GH and IGF-1 levels cause soft tissue hypertrophy, increased bone growth,
and metabolic derangements, including insulin resistance.

Clinical Features
1. Gradual Onset of Symptoms:
o Coarse facial features: Enlarged nose, lips, and jaw (prognathism).
o Enlargement of hands and feet: Rings and shoes may no longer fit.
o Thickened skin with increased sweating and oiliness.
2. Musculoskeletal Symptoms:
o Arthralgia and joint pain.
o Increased bone size, especially in the skull, jaw, hands, and feet.
3. Neurological Symptoms:
o Headaches (due to mass effect of the pituitary tumor).
o Visual disturbances (e.g., bitemporal hemianopia due to optic chiasm
compression).
4. Metabolic Effects:
o Insulin resistance, leading to diabetes mellitus.
o Hypertension.
5. Other Features:
o Deepened voice (due to vocal cord hypertrophy).
o Sleep apnea (due to soft tissue enlargement in the airway).
o Enlargement of internal organs (e.g., cardiomegaly, hepatomegaly).
Diagnosis
1. Biochemical Tests:
o Serum IGF-1: Elevated levels (most reliable marker).
o Oral Glucose Tolerance Test (OGTT): Failure of GH suppression (<1 ng/mL)
after oral glucose load confirms acromegaly.
2. Imaging:
o MRI of the Pituitary: To detect pituitary adenoma.
o CT Scan: For ectopic GHRH/GH-secreting tumors if pituitary imaging is
normal.
3. Other Investigations:
o Assess for complications (e.g., fasting glucose, HbA1c for diabetes;
echocardiography for cardiac involvement).

Management
1. Surgical Treatment:
o Transsphenoidal Surgery: First-line treatment for pituitary adenomas.
2. Medical Therapy:
o Somatostatin Analogues: Octreotide, lanreotide (reduce GH secretion).
o GH Receptor Antagonists: Pegvisomant (blocks GH action).
o Dopamine Agonists: Cabergoline, bromocriptine (inhibit GH in some cases).
3. Radiotherapy:
o Reserved for cases where surgery and medical therapy fail.
4. Management of Complications:
o Treat associated diabetes, hypertension, or cardiac issues.
o Continuous positive airway pressure (CPAP) for sleep apnea.

Complications
• Cardiovascular disease: Hypertension, cardiomyopathy.
• Insulin resistance or overt diabetes mellitus.
• Increased risk of colorectal cancer.
• Sleep apnea and respiratory problems.
• Visual impairment or blindness (from tumor compression).

Diabetes Insipidus

Diabetes insipidus (DI) is a disorder characterized by excessive urination (polyuria) and thirst
(polydipsia) due to the inability of the kidneys to concentrate urine, resulting in the excretion of
large volumes of dilute urine. It is caused by either a deficiency of antidiuretic hormone (ADH,
also known as vasopressin) or a resistance to its action.

Types of Diabetes Insipidus

1. Central Diabetes Insipidus (CDI):
o Caused by insufficient secretion of ADH from the pituitary gland or
hypothalamus.
o Common causes: Pituitary tumors, head trauma, infections, genetic
mutations, or idiopathic.
2. Nephrogenic Diabetes Insipidus (NDI):
o Caused by the kidneys' inability to respond to ADH.
o Common causes: Genetic mutations, chronic kidney disease, drugs (e.g.,
lithium, demeclocycline), hypercalcemia, or hypokalemia.
3. Dipsogenic Diabetes Insipidus:
o Due to an abnormal thirst mechanism, resulting in excessive fluid intake that
suppresses ADH secretion.
4. Gestational Diabetes Insipidus:
o Occurs during pregnancy due to the breakdown of ADH by placental enzymes,
leading to decreased ADH activity.

Pathophysiology
• ADH Mechanism: ADH acts on the kidneys' collecting ducts, promoting water
reabsorption, thus concentrating urine.
• In central DI, the hypothalamus or pituitary gland fails to release adequate ADH,
leading to excessive water loss in urine.
• In nephrogenic DI, despite normal or high levels of ADH, the kidneys do not
respond due to receptor defects or renal dysfunction, causing water loss.

Clinical Features
1. Polyuria: Excessive urination (3-20 liters of urine per day), often dilute and
colorless.
2. Polydipsia: Excessive thirst and increased water intake, which may be difficult to
satisfy.
3. Nocturia: Frequent urination during the night.
4. Dehydration: Can lead to hypovolemia, hypernatremia, and symptoms like dry
mouth, dizziness, and confusion in severe cases.
5. Fatigue: Due to disrupted sleep and dehydration.

Diagnosis
1. Water Deprivation Test:
o Diagnostic test to differentiate between types of DI. Water is withheld for
several hours, and urine volume, osmolality, and plasma osmolality are
measured.
o In central DI, urine continues to be dilute despite dehydration, and ADH
administration improves urine concentration.
o In nephrogenic DI, urine remains dilute despite dehydration and ADH
administration does not improve urine concentration.
2. Plasma and Urine Osmolality:
o Plasma osmolality is elevated, and urine osmolality is low.
o In central DI, ADH levels are low; in nephrogenic DI, ADH levels may be
normal or high.
3. MRI of the Brain:
o To detect pituitary abnormalities, especially in central DI.
4. Blood Tests:
o Serum sodium (hypernatremia in severe cases).
o Renal function tests to rule out nephrogenic causes.

Management
1. Central Diabetes Insipidus (CDI):
o Desmopressin (DDAVP): Synthetic ADH analog that can be given intranasally,
orally, or parenterally. It reduces urine output and increases water
reabsorption in the kidneys.
o Fluid Management: Maintain proper hydration, especially in acute cases or
during periods of high water loss.
2. Nephrogenic Diabetes Insipidus (NDI):
o Thiazide Diuretics: They paradoxically reduce urine output by decreasing
renal filtration.
o Indomethacin: Can increase the kidney’s sensitivity to ADH.
o Low-Salt, Low-Protein Diet: To reduce the kidney's burden of excreting
solute.
o Adequate Fluid Intake: Patients need to be vigilant about drinking enough
water to prevent dehydration.
3. Dipsogenic Diabetes Insipidus:
o Treatment of Underlying Cause: Addressing the cause of abnormal thirst
(e.g., psychiatric disorders or lesions in the hypothalamus).
4. Gestational Diabetes Insipidus:
o Desmopressin: Can be used to replace the lost ADH activity.
o Monitoring: Frequent monitoring of fluid balance and electrolytes during
pregnancy.

Complications
• Dehydration: Can result in hypovolemia, hypernatremia, and subsequent
neurological deficits.
• Hypernatremia: High serum sodium levels, which can cause confusion, seizures,
or coma.
• Kidney Damage: Chronic nephrogenic DI can lead to renal impairment over time.

Myxoedema Coma
Myxoedema coma is a life-threatening, severe form of hypothyroidism that occurs when there is
a significant, prolonged deficiency of thyroid hormone. It is characterized by a reduced level of
consciousness, hypothermia, respiratory depression, bradycardia, and multiple organ
dysfunction, and it is often triggered by acute illness or stress in patients with pre-existing
hypothyroidism.

Etiology
1. Primary Hypothyroidism:
o Most cases of myxoedema coma are due to untreated or inadequately treated
primary hypothyroidism.
o Common causes: Hashimoto’s thyroiditis, iodine deficiency, thyroidectomy,
radioactive iodine treatment, or medications (e.g., amiodarone, lithium).
2. Exacerbating Factors:
o Infections (e.g., pneumonia, sepsis).
o Cold exposure, trauma, or surgery.
o Use of sedatives, narcotics, or central nervous system depressants.
o Acute stress (e.g., heart failure, stroke).
3. Secondary or Tertiary Hypothyroidism:
o Dysfunction of the pituitary or hypothalamus leading to insufficient thyroid
hormone production.

Pathophysiology
• Thyroid Hormone Deficiency: Leads to a generalized slowing of metabolic
processes. The body’s thermoregulatory and cardiovascular systems are affected,
resulting in hypothermia, bradycardia, and reduced cardiac output.
• Myxoedema: Refers to the accumulation of glycosaminoglycans
(mucopolysaccharides) in the skin and other tissues, leading to edema (swelling),
thickened skin, and a characteristic puffy appearance.
• End-Organ Effects: Reduced function of multiple organs due to the lack of thyroid
hormone's regulatory effect on metabolism, including the heart (decreased
contractility), kidneys (reduced renal perfusion), and gastrointestinal system
(slowed peristalsis).

Clinical Features
1. Neurological Symptoms:
o Lethargy, confusion, or stupor.
o Coma in severe cases.
o Psychosis or depression may be present in milder forms of hypothyroidism.
2. Cardiovascular:
o Bradycardia (slow heart rate).
o Hypotension (low blood pressure).
o Decreased cardiac output, leading to hypoperfusion of vital organs.
3. Respiratory:
o Hypoventilation due to reduced respiratory drive, leading to respiratory
acidosis.
o Shallow breathing and decreased tidal volume.
4. Thermoregulatory:
o Hypothermia (temperature < 35°C).
o Cold intolerance.
5. Gastrointestinal:
o Constipation, abdominal bloating, and delayed gastric emptying.
o In severe cases, paralytic ileus may develop.
6. Other:
o Puffy face, periorbital edema.
o Hoarseness due to laryngeal edema.
o Dry, coarse skin and hair.
o Non-pitting edema, particularly in the lower extremities.

Diagnosis
1. Clinical Diagnosis:
o Based on a combination of clinical features (e.g., lethargy, hypothermia,
bradycardia, and edema) and a known history of hypothyroidism.
2. Laboratory Tests:
o Thyroid Function Tests:
▪ Serum TSH (elevated in primary hypothyroidism).
▪ Free T4 (low in myxoedema coma).
▪ Free T3 (also low in severe cases).
o Electrolyte Imbalance:
▪ Hyponatremia (due to impaired water excretion).
▪ Hypoglycemia (due to decreased metabolic rate).
o ABG:
▪ Respiratory acidosis due to hypoventilation.
3. Imaging:
o Chest X-ray or CT scan if there is suspicion of infection or other precipitating
conditions (e.g., pneumonia).

Management
1. Thyroid Hormone Replacement:
o Intravenous Levothyroxine (T4): The initial treatment for myxoedema coma.
Higher doses of IV levothyroxine (loading dose of 300-500 µg) are often
required in severe cases, followed by daily maintenance doses.
o Liothyronine (T3) may be used if there is poor response to T4 alone.
2. Supportive Therapy:
o Hypothermia Management: Gradual rewarming of the patient to prevent
shock or arrhythmias (avoid rapid warming).
o Ventilatory Support: Assisted ventilation if respiratory failure occurs.
o Monitoring and Stabilization: Continuous monitoring of vital signs,
electrolytes, glucose levels, and urine output.
o Management of Precipitating Factors: Treat infections (antibiotics for sepsis
or pneumonia), control blood pressure, and support other organ systems as
needed.
3. Fluid Management:
o Careful fluid resuscitation to avoid overhydration, as these patients are prone
to heart failure and pulmonary edema.
4. Corticosteroids:
o Hydrocortisone should be given as a precautionary measure because
adrenal insufficiency may coexist with myxoedema coma and can worsen the
condition.

Complications
• Cardiac Arrest: Due to bradycardia and decreased cardiac output.
• Respiratory Failure: Due to hypoventilation and respiratory acidosis.
• Hypoglycemia: Resulting from the reduced metabolic rate.
• Electrolyte Imbalances: Particularly hyponatremia and hyperkalemia.
• Shock: Due to reduced perfusion of vital organs.

Cretinism

Cretinism is a severe form of hypothyroidism that occurs in infants and young children,
resulting from a deficiency of thyroid hormones. It leads to physical and mental developmental
delays, growth failure, and characteristic features of thyroid hormone deficiency.

Etiology
1. Congenital Hypothyroidism:
o Primary (Thyroid-related): The most common cause, where the thyroid gland
is either absent or underdeveloped (thyroid dysgenesis), or there is a defect in
thyroid hormone synthesis (e.g., defects in iodine metabolism).
o Secondary (Pituitary-related): Rare and occurs due to pituitary failure to
produce TSH (thyroid-stimulating hormone).
o Tertiary (Hypothalamic-related): Rare and occurs due to hypothalamic
failure to produce TRH (thyrotropin-releasing hormone), leading to low TSH
and low thyroid hormones.
2. Iodine Deficiency:
o The most common cause of cretinism worldwide, especially in areas where
iodine deficiency is prevalent.
3. Maternal Thyroid Disease:
o Insufficient maternal thyroid hormone levels during pregnancy (e.g., untreated
hypothyroidism or iodine deficiency) can lead to fetal thyroid dysfunction.
4. Genetic Factors:
o Inherited defects in thyroid hormone biosynthesis or metabolism can also
lead to congenital hypothyroidism, though they are less common than iodine
deficiency.

Pathophysiology
• Thyroid Hormone Deficiency: Inadequate thyroid hormone results in impaired
growth, abnormal bone development, and delayed intellectual development.
Thyroid hormones are essential for normal development of the central nervous
system, skeletal system, and metabolic processes.
• Neurological Effects: Lack of thyroid hormone during critical periods of brain
development leads to irreversible cognitive impairment, poor motor development,
and speech delay.
• Physical Effects: Growth retardation, coarse features, a protruding tongue, and a
distended abdomen can be seen. The child may also develop a hoarse cry and
lethargy.

Clinical Features
1. Growth Failure:
o Short stature due to stunted physical development.
o Failure to thrive in infancy.
2. Mental Retardation:
o Intellectual disability ranging from mild to severe.
o Delayed milestones such as crawling, walking, and speech development.
3. Characteristic Facial Features:
o Coarse, dry skin.
o Puffy face with a flattened nose and wide-set eyes.
o Enlarged tongue (macroglossia).
o Thickened skin.
4. Skeletal Abnormalities:
o Short limbs and abnormal bone development.
o Large fontanelles, delayed closure of sutures.
5. Other Symptoms:
o Constipation, poor feeding, and low energy levels.
o Hoarse cry and sluggish movements.
o Umbilical hernia due to abdominal distension.
o Delayed puberty if not treated.
Diagnosis
1. Newborn Screening:
o Most developed countries now screen all newborns for congenital
hypothyroidism.
o High TSH levels and low T4 levels in the blood confirm the diagnosis.
2. Thyroid Function Tests:
o Elevated TSH and low Free T4 or total T4.
o Free T3 may also be low.
3. Neuroimaging:
o In severe cases, neuroimaging may reveal delayed myelination and other
structural abnormalities in the brain.
4. Iodine Deficiency:
o Urinary iodine levels can help identify iodine deficiency as the cause of
cretinism.

Management
1. Thyroid Hormone Replacement:
o Levothyroxine (T4) is the standard treatment.
o Early initiation of therapy (preferably within the first few weeks of life) is crucial
to prevent irreversible cognitive impairment.
o The dosage should be adjusted according to age, weight, and thyroid function
tests.
2. Iodine Supplementation:
o If the cause is iodine deficiency, iodine supplementation should be given to
the mother during pregnancy and to the child.
3. Regular Monitoring:
o Thyroid function tests should be performed regularly to ensure that
appropriate thyroid hormone levels are maintained.
4. Supportive Care:
o Early educational intervention and therapies to address developmental
delays.
o Special education and rehabilitation may be required for cognitive and motor
impairments.

Hirsutism

Hirsutism refers to excessive or abnormal hair growth in women in areas where men typically
grow terminal hair, such as the face, chest, abdomen, and back. It is typically associated with
elevated androgen (male hormones) levels or an increased sensitivity of hair follicles to normal
levels of androgens.
Etiology
1. Polycystic Ovary Syndrome (PCOS):
o The most common cause of hirsutism in women.
o Associated with elevated levels of androgens (testosterone) due to ovarian
dysfunction.
o Other features include menstrual irregularities, obesity, and acne.
2. Androgen-Secreting Tumors:
o Tumors of the ovaries or adrenal glands that secrete excess androgens.
o Sudden onset of severe hirsutism, often accompanied by virilization signs
(e.g., deepening of the voice, clitoromegaly).
3. Cushing's Syndrome:
o Excess cortisol levels can lead to increased androgen production.
o Characterized by central obesity, moon face, and other features of
hypercortisolism.
4. Congenital Adrenal Hyperplasia (CAH):
o A group of inherited disorders where enzyme deficiencies in the adrenal
glands lead to excessive production of androgens.
o Classic forms can present in infancy or adolescence, while non-classic forms
may be diagnosed later.
5. Medications:
o Drugs that can increase androgen levels, such as anabolic steroids,
testosterone, and some anticonvulsants.
6. Idiopathic Hirsutism:
o No identifiable underlying cause; occurs in genetically predisposed women
with mildly elevated androgen levels.

Pathophysiology
• Androgens and Hair Follicles:
o The growth of terminal hair in hirsutism is stimulated by androgens,
specifically testosterone.
o These hormones bind to androgen receptors in hair follicles, increasing hair
growth in areas that are androgen-sensitive.
• Increased Androgen Production or Sensitivity:
o The underlying cause of hirsutism could be either an increase in androgen
production (e.g., in PCOS or adrenal tumors) or an increased sensitivity of hair
follicles to normal androgen levels.

Clinical Features
1. Excessive Hair Growth:
o Common sites: Upper lip, chin, jawline, chest, abdomen (linea alba), back,
and thighs.
o The hair is typically coarse and dark in contrast to the fine, vellus hair seen in
women without hirsutism.
2. Virilization:
o In severe cases, hirsutism may be associated with other signs of virilization,
including:
▪ Deepening of the voice.
▪ Clitoromegaly (enlargement of the clitoris).
▪ Male-pattern baldness (alopecia).
▪ Increased muscle mass or body habitus.
3. Menstrual Irregularities:
o Seen in conditions like PCOS, where irregular periods, anovulation, and
infertility may be present.
4. Acne and Seborrhea:
o Due to the increased activity of sebaceous glands in response to androgens.
5. Obesity:
o Particularly associated with PCOS and Cushing's syndrome.

Diagnosis
1. Clinical Evaluation:
o A detailed history and physical examination to assess the onset, severity, and
associated symptoms (e.g., menstrual irregularities, voice changes, acne).
o Ferriman-Gallwey scoring system: A scale used to assess the severity of
hirsutism, scoring hair growth in nine body areas.
2. Hormonal Assessment:
o Serum testosterone levels: Elevated in PCOS, adrenal tumors, and Cushing's
syndrome.
o DHEA-S (dehydroepiandrosterone sulfate): Elevated in adrenal causes of
hirsutism.
o 17-hydroxyprogesterone: Elevated in congenital adrenal hyperplasia (CAH).
o LH, FSH (for PCOS): An elevated LH/FSH ratio is suggestive of PCOS.
3. Imaging:
o Ultrasound of ovaries: To look for features of PCOS (e.g., ovarian cysts).
o CT or MRI of abdomen/pelvis: In case of suspected androgen-secreting
tumors (e.g., adrenal or ovarian).

Management
1. Medical Treatment:
o Oral Contraceptives: First-line treatment for hirsutism, especially in women
with PCOS. They reduce ovarian androgen production and increase sex
hormone-binding globulin (SHBG), which binds free testosterone.
o Anti-androgens:
▪ Spironolactone: A potent anti-androgen that blocks androgen
receptors and reduces hair growth.
▪ Finasteride: Inhibits 5-alpha reductase, reducing the conversion of
testosterone to dihydrotestosterone (DHT), a more potent androgen.
o Insulin Sensitizers: In PCOS, drugs like metformin may help reduce
androgen levels and improve ovulatory function.
2. Cosmetic Treatments:
o Laser hair removal: A long-term solution for hair removal that works by
targeting and destroying hair follicles.
o Electrolysis: Permanent hair removal technique.
o Waxing, shaving, or plucking: Temporary solutions for hirsutism
management.
3. Treatment of Underlying Conditions:
o For conditions like Cushing's syndrome or androgen-secreting tumors,
specific treatments such as surgery, chemotherapy, or radiation may be
required.
4. Psychological Support:
o Hirsutism can have significant psychological effects, especially in severe
cases. Counseling and support groups can help women cope with the
emotional and social aspects of the condition.

Turner Syndrome

Turner syndrome (TS) is a chromosomal disorder affecting females, characterized by the partial
or complete absence of one of the X chromosomes (45,X karyotype). This condition leads to a
variety of physical and developmental abnormalities.

Etiology
• Chromosomal Abnormality: Turner syndrome results from the loss or structural
abnormalities of one of the X chromosomes in females. It typically presents as a
45,X karyotype (only one X chromosome instead of the normal two).
• Mosaicism: Some women with Turner syndrome may have a mosaic karyotype,
where some cells have the normal 46,XX chromosome complement, and others
have 45,X.

Clinical Features
1. Short Stature:
o A hallmark feature, with an average adult height of about 4'8" to 4'10" (142–
147 cm). Growth hormone therapy may help improve final height.
2. Primary Amenorrhea:
o Due to ovarian dysgenesis (underdeveloped ovaries), girls with Turner
syndrome typically do not undergo puberty unless treated with hormone
replacement therapy (HRT).
3. Webbed Neck:
o A characteristic feature, which may appear as extra folds of skin around the
neck. It is often present at birth or develops early in childhood.
4. Cardiovascular Abnormalities:
o Bicuspid aortic valve: Seen in up to 30% of patients.
o Coarctation of the aorta: Narrowing of the aorta, present in 10–20% of
patients.
o Hypertension: May develop secondary to the coarctation or other
cardiovascular issues.
5. Renal Anomalies:
o Renal abnormalities, such as horseshoe kidney, renal agenesis, or
hydronephrosis, are common in Turner syndrome.
6. Lymphedema:
o Swelling of the hands and feet at birth or in early childhood due to abnormal
lymphatic drainage.
7. Facial Features:
o Low-set ears, wide-set eyes, low hairline, and broad, shield-shaped chest
with widely spaced nipples are characteristic features.
8. Intellectual and Developmental Delays:
o Most individuals with Turner syndrome have normal intelligence, but learning
difficulties, particularly in mathematics and spatial relationships, are
common.
9. Infertility:
o Due to ovarian failure, infertility is almost universal in females with Turner
syndrome. However, assisted reproductive technologies like egg donation are
options for some women.
10. Endocrine Abnormalities:
o Hypothyroidism: Common in Turner syndrome and should be monitored
regularly.
o Diabetes and other metabolic issues may also be more common in
adulthood.

Diagnosis
1. Clinical Suspicion:
o Turner syndrome is often suspected based on physical features such as short
stature, webbed neck, and primary amenorrhea.
2. Karyotyping:
o A definitive diagnosis is made by chromosomal analysis showing the presence
of a 45,X karyotype or other chromosomal abnormalities affecting the X
chromosome.
3. Ultrasound and Imaging:
o Cardiac ultrasound: To assess for structural heart defects, including bicuspid
aortic valve or coarctation of the aorta.
o Renal ultrasound: To detect renal anomalies such as horseshoe kidneys or
other malformations.
4. Hormonal Studies:
o FSH, LH, and estrogen levels to assess ovarian function. Elevated FSH and LH
with low estrogen are suggestive of ovarian insufficiency.

Management
1. Growth Hormone Therapy:
o Human growth hormone (hGH) can be given to promote growth in children
with Turner syndrome. Early initiation, ideally before the age of 2, is associated
with better outcomes.
2. Estrogen Replacement Therapy:
o Estrogen therapy is given to induce puberty in individuals with Turner
syndrome, typically starting between the ages of 11-13 years. Progesterone is
added later to induce menstruation and protect the endometrium.
3. Cardiovascular Management:
o Monitoring and treatment of any cardiovascular abnormalities, including
surgical correction of aortic coarctation or repair of the bicuspid aortic valve,
are essential.
o Regular blood pressure monitoring is also crucial to detect early signs of
hypertension.
4. Fertility Options:
o While natural conception is generally not possible, assisted reproductive
technologies such as egg donation can help some women with Turner
syndrome achieve pregnancy.
5. Psychological Support:
o Counseling may be necessary to address the social and emotional aspects of
Turner syndrome, especially regarding body image, fertility, and cognitive
challenges.
6. Regular Screening:
o Lifelong monitoring for associated conditions such as hypothyroidism,
diabetes, and cardiovascular disease is recommended.
o Bone density screening may be required due to the risk of osteoporosis,
especially after estrogen therapy.
Klinefelter Syndrome

Klinefelter syndrome (KS) is a genetic condition in males where an individual has at least one
extra X chromosome in addition to the normal male XY chromosomal pattern, resulting in a
karyotype of 47,XXY (or variants like 48,XXXY, 49,XXXXY). This condition can lead to a
variety of physical, developmental, and hormonal abnormalities.

Etiology
• Klinefelter syndrome results from a random error in the division of sex
chromosomes during the formation of sperm or egg cells, leading to males
inheriting an extra X chromosome. The presence of an extra X chromosome in males
disrupts the normal male development, leading to various physical and
psychological changes.
• The condition is not inherited but arises due to non-disjunction during meiosis,
which occurs by chance. The additional X chromosome can be passed down to the
next generation in rare cases.

Clinical Features
1. Physical Features:
o Tall Stature: Males with Klinefelter syndrome tend to be taller than average,
with long arms and legs and a lack of muscular build.
o Gynecomastia: Enlargement of breast tissue is common in affected males
due to an imbalance between estrogen and testosterone.
o Hypogonadism: Small testes with reduced testosterone production are a
hallmark, leading to incomplete puberty and low libido.
o Infertility: Due to underdeveloped testes, most men with Klinefelter
syndrome are infertile.
o Sparse Facial and Body Hair: Reduced body and facial hair growth due to low
testosterone levels.
o Wide Hips: Some males may show a wider pelvic shape and less muscular
build.
2. Developmental and Cognitive Features:
o Learning Disabilities: Some individuals with Klinefelter syndrome may have
mild intellectual disabilities or learning difficulties, especially with language
development and executive functions (e.g., reading, writing, and
mathematics).
o Speech and Language Delay: Delayed speech development and difficulty
with language skills are common, particularly in early childhood.
o Social and Behavioral Issues: Males with Klinefelter syndrome may have
social adjustment difficulties and higher rates of anxiety and depression,
though the cognitive impairment is generally mild.
3. Endocrine Abnormalities:
o Low Testosterone Levels: As a result of testicular dysfunction, testosterone
levels are typically low.
o Elevated LH and FSH: Secondary to the failure of the testes to produce
testosterone, leading to a feedback increase in gonadotropins (luteinizing
hormone (LH) and follicle-stimulating hormone (FSH)).
o Possible Development of Osteoporosis: Due to reduced testosterone levels,
individuals are at higher risk for developing osteoporosis later in life.
4. Metabolic Abnormalities:
o Increased Risk of Obesity: Klinefelter syndrome is associated with a higher
risk of developing obesity, particularly around the abdomen.
o Insulin Resistance and Diabetes: Increased prevalence of metabolic
syndrome, including insulin resistance and type 2 diabetes, is observed in
some individuals with Klinefelter syndrome.

Diagnosis
1. Clinical Suspicion:
o Clinical diagnosis is often suspected in adolescence or adulthood when the
characteristic signs like gynecomastia, infertility, or tall stature become
apparent.
2. Karyotyping:
o A chromosomal analysis (karyotype) confirms the diagnosis by detecting the
presence of the extra X chromosome(s). The most common pattern is 47,XXY,
but other variants (e.g., 48,XXXY, 49,XXXXY) can also occur.
3. Hormonal Studies:
o Low testosterone levels and high levels of LH and FSH help in diagnosing the
syndrome.
4. Imaging:
o Testicular ultrasound can help assess the size of the testes and detect any
associated structural abnormalities.

Management
1. Testosterone Replacement Therapy:
o Early treatment with testosterone replacement therapy (TRT) is important to
help initiate and maintain puberty, improve muscle mass, and increase bone
density.
o TRT can help improve mood, energy, and overall well-being, as well as prevent
the complications of hypogonadism such as osteoporosis and sexual
dysfunction.
2. Fertility Management:
o Most men with Klinefelter syndrome are infertile, but sperm retrieval
techniques such as testicular sperm extraction (TESE) can be considered for
those seeking fatherhood. Assisted reproductive technologies, including IVF
with ICSI, may be options for some individuals.
3. Psychosocial Support:
o Individuals may benefit from counseling or therapy to address social and
emotional challenges, particularly related to self-esteem, social skills, and
mental health (anxiety, depression).
o Speech and language therapy can help with communication skills.
4. Educational Support:
o Early intervention programs, special education services, and tutoring may be
helpful in managing the learning difficulties associated with Klinefelter
syndrome.
5. Regular Monitoring:
o Monitoring for the development of osteoporosis, diabetes, and other
metabolic issues should be ongoing.
o Regular cardiovascular health assessments and screening for other metabolic
abnormalities are essential for long-term management.

Pseudohypoparathyroidism

Pseudohypoparathyroidism (PHP) is a rare inherited disorder characterized by resistance to the

action of parathyroid hormone (PTH), despite normal or elevated levels of the hormone. This
results in hypocalcemia (low calcium levels) and hyperphosphatemia (elevated phosphate
levels) similar to hypoparathyroidism. However, in pseudohypoparathyroidism, the parathyroid
glands are functioning normally and producing adequate amounts of PTH; the problem lies in
the target tissues' inability to respond to the hormone.

Etiology
• Pseudohypoparathyroidism is usually caused by genetic mutations that affect the
signaling pathways of PTH in its target tissues. These mutations are often associated
with defects in the G protein-coupled receptor system, particularly the Gs alpha
subunit (Gαs).
• The condition is inherited in an autosomal dominant manner and can occur due to
mutations in the GNAS gene (which codes for Gαs), leading to impaired intracellular
signaling following PTH receptor activation.
There are two main forms:
1. Type 1 (PHP1):
o Divided into subtypes 1a and 1b, Type 1 is the most common form and results
from mutations affecting the GNAS gene.
o Subtype 1a is typically associated with both PTH resistance and end-organ
resistance to other hormones such as TSH (thyroid-stimulating hormone),
LH (luteinizing hormone), and FSH (follicle-stimulating hormone), leading to
features of Albright's hereditary osteodystrophy (AHO).
o Subtype 1b primarily causes isolated PTH resistance without AHO features.
2. Type 2 (PHP2):
o A rare form, typically caused by mutations in the GNAS gene as well, but
without the features of AHO. PHP2 is associated with resistance to PTH but
without the skeletal, adiposity, and developmental features seen in Type 1.

Clinical Features
• Hypocalcemia: The hallmark feature, leading to symptoms such as muscle
cramps, tetany, and Chvostek's sign (twitching of the facial muscles when tapping
the facial nerve).
• Hyperphosphatemia: Elevated phosphate levels due to defective renal excretion of
phosphate in response to normal or elevated PTH.
• Albright's Hereditary Osteodystrophy (AHO): Common in PHP1a, which may
include:
o Short stature: Affected individuals are often shorter than their peers.
o Round face: Characteristic facial features with a broad, round face.
o Obesity: Adiposity, particularly around the trunk.
o Brachydactyly: Shortened fingers and toes.
o Mental retardation: Mild cognitive impairments are seen in some cases,
especially in the context of AHO.
• Skeletal Abnormalities: Mild to moderate developmental defects, including
shortened metacarpals and metatarsals.
• Ovarian Dysfunction: In females, there may be resistance to LH and FSH, leading
to delayed puberty or infertility.

Diagnosis
1. Laboratory Tests:
o Serum calcium: Low serum calcium levels (hypocalcemia) are observed.
o Serum phosphate: Elevated phosphate levels (hyperphosphatemia) occur
due to the kidneys' inability to excrete phosphate.
o Serum PTH: Elevated or normal PTH levels, indicating that the parathyroid
glands are functional.
o Genetic Testing: Detection of mutations in the GNAS gene confirms the
diagnosis.
2. Radiological Features:
o X-ray findings: In individuals with AHO, X-rays may show characteristic
features such as shortened metacarpals and metatarsals.

Management
1. Calcium and Vitamin D Supplementation:
oTreatment of hypocalcemia with calcium salts (oral or intravenous) and
vitamin D (such as calcitriol) to promote calcium absorption and restore
normal calcium levels.
2. Phosphate Binders:
o Since individuals with pseudohypoparathyroidism often have
hyperphosphatemia, phosphate binders such as calcium carbonate or
sevelamer may be used to reduce phosphate levels and prevent
complications such as soft tissue calcification.
3. Management of Associated Conditions:
o Growth hormone therapy: In cases of short stature, growth hormone
treatment may be considered, especially for patients with AHO features.
o Thyroid and Gonadal Hormone Replacement: In females or individuals with
resistance to gonadotropins, hormone replacement may be necessary to treat
fertility and menstrual dysfunction.
4. Regular Monitoring:
o Regular monitoring of serum calcium, phosphate, and PTH levels is essential
to guide therapy and ensure that patients maintain normal mineral
metabolism.

Insulinoma

Insulinoma is a rare, usually benign tumor of the pancreas that originates from the insulin-
producing beta cells of the islets of Langerhans. It results in an excessive release of insulin,
leading to hypoglycemia (low blood sugar) and its associated symptoms. Insulinomas are
typically small, with most being less than 2 cm in size, and are generally solitary, though
multiple tumors can sometimes occur.

Etiology
• Insulinomas are typically sporadic, but in some cases, they can be associated with
multiple endocrine neoplasia type 1 (MEN1), a hereditary disorder that
predisposes individuals to tumors in multiple endocrine glands.
• The tumor arises from the beta cells of the pancreas, leading to excessive insulin
secretion, independent of blood glucose levels. The insulin secretion is not
suppressed by the normal feedback mechanisms that control insulin release in
response to blood glucose.

Clinical Features
The most common symptom of insulinoma is hypoglycemia, which occurs when insulin levels
are inappropriately high in relation to blood glucose. Symptoms of hypoglycemia include:
• Sweating
• Tremors
• Palpitations
• Anxiety
• Dizziness
• Confusion
• Headache
• Weakness
• Severe cases can lead to seizures or loss of consciousness.
Patients may experience whipple's triad, which includes:
1. Hypoglycemia (low blood sugar levels)
2. Symptoms of hypoglycemia that are relieved by glucose administration
3. A blood glucose level < 45-50 mg/dL during episodes of symptoms
Associated Symptoms:
• Weight gain: May occur in some cases, due to the increased insulin levels
promoting fat storage.
• Hyperinsulinism-related symptoms: Prolonged episodes of hypoglycemia may
result in cognitive dysfunction, and long-term hypoglycemia can lead to neuronal
injury and mental confusion.
• Gastrointestinal complaints: Such as nausea, vomiting, and abdominal
discomfort.

Diagnosis
1. Clinical Diagnosis:
o Diagnosis is often based on the presence of whipple's triad (as noted above).
o Patients may be treated for hypoglycemia with glucose administration, which
promptly alleviates symptoms.
2. Laboratory Tests:
o Fasting Test: A prolonged fast (usually 72 hours) is typically performed to
induce hypoglycemia and confirm the diagnosis. The insulin levels are
measured during hypoglycemic episodes.
o Insulin Levels: Elevated insulin levels in the presence of hypoglycemia are
characteristic of insulinomas.
o C-peptide Levels: Elevated C-peptide levels alongside insulin confirm
endogenous insulin production.
o Proinsulin Levels: Proinsulin levels may also be elevated.
3. Imaging:
o CT scan or MRI of the abdomen can help locate the tumor, especially in cases
where the tumor is larger.
o Endoscopic ultrasound: More sensitive than CT and MRI for detecting
smaller insulinomas, especially in the head of the pancreas.
o Selective Arterial Calcium Stimulation Test: This test is used in cases where
imaging fails to locate the tumor. It involves injecting calcium into the arterial
supply of the pancreas and measuring the insulin response to determine the
tumor's location.
4. Differential Diagnosis:
o Factitious hypoglycemia: Caused by exogenous insulin or sulfonylurea
administration, often in patients who deliberately induce hypoglycemia.
o Other causes of hypoglycemia, such as insulin resistance, adrenal
insufficiency, or liver disease, need to be excluded.

Management
1. Surgical Treatment:
o Surgical resection is the definitive treatment for insulinoma. The tumor is
typically located and removed surgically. In most cases, surgical resection
leads to complete resolution of hypoglycemic symptoms.
o Partial pancreatectomy: If the tumor is located in a specific area of the
pancreas, a partial resection may be performed.
2. Medical Management:
o Diazoxide: A medication that inhibits insulin release and is used as an
adjunct in managing symptoms, especially in patients who are not candidates
for surgery or in those with inoperable tumors.
o Octreotide: A somatostatin analog can sometimes be used, as it may help
reduce insulin secretion.
o Glucocorticoids: Can be used in some cases, as they increase blood glucose
levels by stimulating gluconeogenesis.
3. Management in MEN1:
o Patients with insulinoma due to MEN1 require surveillance for other endocrine
tumors and may need surgical management of multiple tumors.

Hyperprolactinemia

Hyperprolactinemia refers to an elevated level of prolactin in the blood. Prolactin is a hormone

produced by the pituitary gland, and its primary function is to promote lactation (milk
production) in women after childbirth. In men and non-lactating women, prolactin levels are
typically low, and elevated levels can be indicative of various underlying conditions.

Etiology
Hyperprolactinemia can result from physiological, pathological, or pharmacological causes:
1. Physiological Causes:
o Pregnancy: Prolactin levels increase significantly during pregnancy to prepare
the breasts for lactation.
o Breastfeeding: Prolactin is elevated in lactating women to maintain milk
production.
o Sleep: Prolactin levels can increase during sleep, particularly during the REM
stage.
o Stress: Emotional or physical stress can lead to transient increases in
prolactin.
o Exercise: Intense physical activity may transiently elevate prolactin.
2. Pathological Causes:
o Prolactin-secreting tumors (Prolactinomas): Benign tumors of the pituitary
gland (usually microadenomas) that produce excess prolactin.
o Hypothyroidism: Low thyroid hormone levels can lead to increased prolactin
secretion due to reduced negative feedback on the hypothalamus, causing
increased TRH (thyrotropin-releasing hormone), which stimulates prolactin
release.
o Pituitary stalk compression: Any mass lesion (such as a tumor or cyst)
affecting the pituitary stalk can disrupt the hypothalamo-pituitary connection,
impairing dopamine inhibition of prolactin secretion.
o Chronic renal failure: Impaired clearance of prolactin can lead to elevated
levels in the blood.
o Polycystic ovary syndrome (PCOS): Hyperprolactinemia can occasionally
occur in women with PCOS.
3. Pharmacological Causes:
o Dopamine antagonists (e.g., antipsychotic drugs like haloperidol and
risperidone): These medications block the action of dopamine, a natural
inhibitor of prolactin.
o Antidepressants: Certain drugs such as SSRIs (selective serotonin reuptake
inhibitors) can elevate prolactin levels.
o Opiates: Chronic use of opiates like morphine can increase prolactin
secretion.
o Antihypertensives: Some medications, like verapamil, may elevate prolactin
levels.
o Estrogens: Oral contraceptives and hormone replacement therapy can
increase prolactin levels.

Clinical Features

1. In Women:
o Galactorrhea: Spontaneous milk production not associated with childbirth or
breastfeeding.
o Menstrual irregularities: Often presents as oligomenorrhea (infrequent
periods) or amenorrhea (absence of periods).
o Infertility: Due to anovulation caused by elevated prolactin levels interfering
with gonadotropin secretion.
o Decreased libido and vaginal dryness: Elevated prolactin can affect
estrogen levels, leading to hypoestrogenism.
2. In Men:
o Erectile dysfunction: Hyperprolactinemia can impair normal testosterone
production, leading to reduced libido and erectile difficulties.
o Gynecomastia: Development of breast tissue in men, which may be
associated with increased prolactin levels.
o Infertility: Low testosterone and sperm production can result due to impaired
gonadal function.
3. General Symptoms:
o Headaches and visual disturbances: Often seen in patients with large
prolactinomas due to compression of surrounding structures like the optic
chiasm.
o Pituitary apoplexy: In rare cases, a prolactinoma can bleed, leading to
sudden and severe headaches, visual impairment, and pituitary insufficiency.

Diagnosis

1. Elevated Serum Prolactin:

The initial diagnostic test is a blood test to measure prolactin levels. An elevation greater
than 200 ng/mL is typically suggestive of a prolactinoma. However, levels of less than
200 ng/mL may indicate other causes, such as physiological conditions or medications.
2. Further Evaluation:
o Thyroid function tests: To rule out hypothyroidism, which is a common cause
of secondary hyperprolactinemia.
o Pregnancy test: To rule out pregnancy as a physiological cause of
hyperprolactinemia.
o MRI of the brain: To detect prolactinomas and assess their size and impact
on surrounding structures. MRI is critical in evaluating the pituitary gland and
identifying any potential tumors.
3. Other Tests:
o Serum estradiol (in women) and testosterone (in men): To evaluate for
hypoestrogenism or hypogonadism, which can result from
hyperprolactinemia.
o Visual field examination: To assess for any defects that might indicate
compression of the optic chiasm by a large prolactinoma.

Management
Treatment depends on the underlying cause of the hyperprolactinemia:
1. For Prolactinomas:
o Dopamine agonists (first-line treatment):
▪ Cabergoline and bromocriptine are the primary drugs used to reduce
prolactin secretion and shrink the tumor. These drugs mimic the action
of dopamine, which inhibits prolactin release.
▪ Cabergoline is preferred due to its better side effect profile and once-
weekly dosing.
o Surgical treatment: If the tumor is large, causing symptoms like visual
disturbances, or if medical therapy fails, transsphenoidal surgery may be
necessary to remove the tumor.
2. For Hypothyroidism:
o Thyroid hormone replacement: Treating the underlying thyroid disorder may
normalize prolactin levels.
3. For Medication-induced Hyperprolactinemia:
o Discontinuing or switching medications: If the hyperprolactinemia is due to
medication use (such as antipsychotics), reducing or switching the
medication may lower prolactin levels.
4. For Other Causes:
o Addressing underlying causes like chronic kidney disease or stress can also
reduce prolactin levels.