New ppt template ENDOCRINE DISORDERS PPT

ENDOCRINE

1. (Course name Course code ) Title: Pathophysiology of Endocrine Disorders Subtitle: A Comprehensive Guide for Medicine and Pharmacy Students Presented by: [Your Name or Institution] Date: [Insert Date]

2. Title Learning Objectives Understand the role and anatomy of the endocrine system Learn hormonal signaling pathways and feedback mechanisms Explore major endocrine disorders (thyroid, adrenal, pituitary, pancreas, etc.) Examine clinical signs, diagnostic tests, and underlying pathophysiology Apply knowledge through case studies and summaries

3. Endocrine System Definition: The endocrine system is a network of glands that secrete hormones into the bloodstream to regulate body functions. Key Glands: Hypothalamus & Pituitary: Central regulators of other glands Thyroid & Parathyroids : Metabolism and calcium control Adrenals: Stress response, blood pressure, metabolism Pancreas (Islets of Langerhans): Glucose homeostasis Gonads: Reproduction (testes & ovaries) Functions: Growth & development Metabolism regulation Reproduction & sexual differentiation Fluid and electrolyte balance Response to stress and injury

4. Types of Hormones 1. Peptide Hormones (hydrophilic, act via surface receptors): Examples: Insulin, GH, ACTH, ADH Stored in vesicles and released via exocytosis 2. Steroid Hormones (lipophilic, act via intracellular receptors): Derived from cholesterol Examples: Cortisol, Aldosterone, Estrogen , Testosterone Synthesized on demand, not stored 3. Amino Acid-Derived Hormones: From tyrosine or tryptophan Examples: Thyroxine (T4), Epinephrine, Dopamine Clinical Note: Peptide hormones act quickly, while steroid hormones have delayed but long-lasting effects.

5. Hormonal Signaling Mechanisms Endocrine Signaling : Hormone travels through bloodstream to distant targets. Example: TSH secreted from pituitary → stimulates thyroid gland. Paracrine Signaling : Hormones act locally on nearby cells. Example: Somatostatin in pancreas inhibits insulin/glucagon nearby. Autocrine Signaling : Hormone acts on the same cell that secreted it. Example: Interleukins in immune cells. Juxtacrine Signaling (less common): Contact-dependent signaling . Receptors: Cell membrane receptors for peptide hormones Intracellular receptors for steroid/thyroid hormones Second messengers: cAMP , IP3, calcium ions

6. Feedback Regulation in Endocrinology Negative Feedback: The most common hormonal control loop Prevents overproduction of hormones Maintains homeostasis Example: Hypothalamic-Pituitary-Thyroid Axis Hypothalamus → TRH (Thyrotropin-releasing hormone) Anterior Pituitary → TSH (Thyroid-stimulating hormone) Thyroid → T3/T4 hormones T3/T4 inhibit both TRH and TSH secretion when elevated Positive Feedback (less common): Example: Oxytocin during childbirth → uterine contractions → more oxytocin 🧠 Clinical Note: Dysfunction in feedback loops leads to hypo- or hyper-function of glands.

7. Pituitary Gland Overview Location: Base of the brain in the sella turcica Divisions: Anterior Pituitary ( Adenohypophysis ) – regulated by hypothalamic releasing hormones Posterior Pituitary ( Neurohypophysis ) – direct neural connection to hypothalamus Hormone Source Target Function GH Anterior pituitary Liver, muscle, bone Growth, metabolism ACTH Anterior pituitary Adrenal cortex Stimulates cortisol release TSH Anterior pituitary Thyroid gland Stimulates T3/T4 production FSH & LH Anterior pituitary Gonads Regulate reproduction Prolactin Anterior pituitary Breast tissue Milk production ADH & Oxytocin Posterior pituitary Kidneys, uterus, breast Water balance, labor , lactation

8. Hyperpituitarism Definition: Excess secretion of pituitary hormones, usually due to a pituitary adenoma Common Types: Prolactinoma (most common) ↑ Prolactin → galactorrhea, amenorrhea, infertility In males: ↓ libido, impotence Growth Hormone-secreting tumor → Acromegaly Adults: Acromegaly (enlarged jaw, hands, feet) Children: Gigantism ↑ IGF-1, abnormal glucose tolerance ACTH-secreting tumor → Cushing’s Disease Central obesity, moon face, hypertension 🧠 Diagnostic Tip: Measure hormone levels + MRI of sella turcica

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10. Hypopituitarism Definition : Partial or complete deficiency of anterior pituitary hormones Causes: Pituitary tumor (mass effect or surgery/radiation) Ischemia (e.g., Sheehan’s syndrome post-partum hemorrhage ) Infiltrative diseases: sarcoidosis , hemochromatosis Hormone Deficient Symptoms GH Fatigue, decreased muscle mass, poor growth ACTH Weakness, hypotension, hypoglycemia TSH Cold intolerance, bradycardia FSH/LH Amenorrhea, infertility, loss of libido Prolactin Inability to lactate post-partum

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12. Diabetes Insipidus (DI) Definition : A disorder of water balance due to ADH deficiency or resistance Types : Diagnosis: Water deprivation test (fails to concentrate urine) ADH administration: response in central DI only Treatment: Central: Desmopressin (synthetic ADH) Nephrogenic : Thiazides, low-salt diet Type Cause Key Features Central DI ↓ ADH secretion (e.g., trauma, tumor) Polyuria, polydipsia, dilute urine Nephrogenic DI Kidney unresponsive to ADH (e.g., drugs, lithium) Similar symptoms but ADH levels normal/high

13. Syndrome of Inappropriate Antidiuretic Hormone (SIADH ) Definition : Excessive release of ADH → water retention → hyponatremia Causes: CNS: Stroke, trauma, infection Pulmonary: Pneumonia, TB, small cell lung carcinoma Drugs: SSRIs, carbamazepine, cyclophosphamide Ectopic ADH production ( paraneoplastic ) Pathophysiology: ↑ ADH → ↑ water reabsorption in collecting ducts → ↓ serum sodium ( dilutional hyponatremia ) Urine remains concentrated despite low plasma osmolality Clinical Features: Nausea, headache, confusion, seizures, coma (if rapid ↓ Na⁺) 🧪 Labs: Serum Na⁺ < 135 mmol /L Urine osmolality > 100 mOsm /kg Serum osmolality < 275 mOsm /kg Euvolemic hyponatremia Treatment: Fluid restriction Demeclocycline or vasopressin antagonists (e.g., tolvaptan )

14. Pituitary disorders –Summary Table Disorder Hormone Affected Key Features Diagnosis Acromegaly GH ↑ Enlarged hands, feet, jaw; ↑ IGF-1 IGF-1, OGTT, MRI Prolactinoma Prolactin ↑ Galactorrhea, amenorrhea, ↓ libido Serum prolactin, MRI Cushing’s Disease ACTH ↑ Central obesity, striae, hypertension Dexamethasone suppression test Hypopituitarism Multiple ↓ Fatigue, amenorrhea, hypotension Hormonal profile, stimulation test Central DI ADH ↓ Polyuria, polydipsia, low urine osm Water deprivation test SIADH ADH ↑ Hyponatremia, concentrated urine Serum/urine osmolarity , ADH level

15. Thyroid Hormone Synthesis Steps in Synthesis (in thyroid follicular cells): Iodide uptake : via sodium-iodide symporter Oxidation of iodide to iodine (via thyroid peroxidase, TPO ) Iodination of tyrosine residues in thyroglobulin → MIT & DIT Coupling : MIT + DIT → T3 DIT + DIT → T4 Storage in colloid , then release upon TSH stimulation Regulation: TRH (hypothalamus) → TSH (pituitary) → stimulates all steps of T3/T4 synthesis Negative feedback : T3 and T4 inhibit TRH & TSH 🧠 Clinical Pearl: TPO is the target of antibodies in Hashimoto’s thyroiditis

16. Hyperthyroidism (Graves’ Disease ) Definition : Excess production of thyroid hormones → ↑ metabolic rate Graves' Disease: Autoimmune (TSI antibodies stimulate TSH receptor) Most common cause of hyperthyroidism in young women Clinical Features: Weight loss, heat intolerance, sweating Tachycardia, palpitations Tremors, anxiety, insomnia Goiter with bruit Exophthalmos & pretibial myxedema (Graves' specific) 🧪 Diagnostics: ↓ TSH, ↑ T3/T4 Positive TSI antibodies Radioactive iodine uptake: diffuse uptake Treatment: Antithyroid drugs: Methimazole , PTU Beta-blockers for symptom control Radioiodine therapy or surgery

17. Hypothyroidism (Hashimoto’s Thyroiditis ) Definition : Deficient thyroid hormone production → ↓ metabolic rate Hashimoto’s Thyroiditis: Autoimmune destruction of thyroid Most common cause of hypothyroidism in iodine-sufficient areas Pathophysiology: Autoantibodies: anti-TPO , anti-thyroglobulin Lymphocytic infiltration → fibrosis Clinical Features: Weight gain, cold intolerance Fatigue, depression Bradycardia, constipation Dry skin, hair thinning, facial puffiness May present with painless goiter 🧪 Diagnostics: ↑ TSH, ↓ T3/T4 Positive anti-TPO antibodies Ultrasound: heterogeneous, hypoechoic gland Treatment: Levothyroxine (synthetic T4)

18. Subclinical Thyroid Dysfunction 🔹 Subclinical Hypothyroidism: ↑ TSH , normal T3/T4 Often asymptomatic, may progress to overt hypothyroidism Causes: Early Hashimoto’s Post-thyroidectomy Iodine deficiency Management: Treat if TSH >10 mIU /L Consider in pregnancy, infertility, or symptomatic patients 🔹 Subclinical Hyperthyroidism: ↓ TSH , normal T3/T4 May increase risk for atrial fibrillation and osteoporosis Causes: Early Graves' disease Toxic nodular goiter Management: Observation vs. treatment depending on age, risk, and TSH suppression level

19. Myxedema Coma Definition : A life-threatening complication of severe, untreated hypothyroidism. Precipitating Factors: Infection, trauma, cold exposure Sedatives, anesthesia Noncompliance with levothyroxine Clinical Features: Altered mental status, coma Hypothermia Hypoventilation, bradycardia Hypoglycemia , hyponatremia 🧪 Labs: ↑ TSH, ↓ T4 Hypoglycemia , hyponatremia Treatment: IV levothyroxine Hydrocortisone (in case of concomitant adrenal insufficiency) Supportive care (warmth, fluids, respiratory support)

20. Thyroid Storm Definition : An acute, life-threatening exaggeration of hyperthyroidism Triggers: Surgery, trauma, infection Iodine load (contrast) Withdrawal of antithyroid drugs Clinical Features: High fever Severe tachycardia, arrhythmias Agitation, delirium, coma Nausea, vomiting, diarrhea CHF or shock in severe cases 🧪 Labs: ↓ TSH, ↑ T3/T4 Diagnosis is clinical — use Burch- Wartofsky scoring system Treatment (4 Ps): Propranolol – for adrenergic symptoms PTU – inhibits hormone synthesis Prednisone – reduces T4 to T3 conversion Potassium iodide – blocks release of hormones (after PTU)

21. Goiter and Nodular Thyroid Disease Goiter = Enlargement of thyroid gland Diffuse goiter : uniform (e.g., Graves’, Hashimoto’s) Multinodular goiter : irregular, often euthyroid Nodules: May be solitary or multiple Risk of malignancy with solitary “cold” nodules Test Purpose TSH Initial screening Ultrasound Nodule size, features (solid, cystic) Fine Needle Aspiration Malignancy evaluation Radioiodine scan Functional activity ("hot" vs. "cold")

22. Summary Table – Thyroid Disorders Disorder TSH T3/T4 Antibodies Key Features Graves’ ↓ ↑ TSI Goiter, exophthalmos, tremor Hashimoto’s ↑ ↓ Anti-TPO, anti-Tg Fatigue, weight gain, goiter Subclinical Hypo ↑ Normal Often positive Asymptomatic, may progress Subclinical Hyper ↓ Normal ± TSI Often asymptomatic Thyroid storm ↓ ↑↑ ± TSI Fever, agitation, tachycardia Myxedema coma ↑ ↓↓ Anti-TPO Coma, hypothermia, hypotension

23. Parathyroid Hormone (PTH) & Calcium Regulation Function of PTH: Secreted by chief cells in the parathyroid glands Regulates serum calcium & phosphate Feedback Loop: ↓ Serum Ca²⁺ → ↑ PTH ↑ Serum Ca²⁺ → ↓ PTH (via negative feedback) Organ Action Bone Stimulates osteoclasts → ↑ bone resorption → ↑ serum Ca²⁺ Kidney ↑ Ca²⁺ reabsorption, ↓ phosphate reabsorption (phosphaturia) Kidney Stimulates 1 α- hydroxylase → ↑ active Vitamin D (calcitriol) GI tract Indirect ↑ calcium absorption via calcitriol

24. Primary Hyperparathyroidism Autonomous overproduction of PTH → ↑ serum calcium 🔹 Causes: Parathyroid adenoma (most common) Hyperplasia or carcinoma MEN 1 or 2A syndromes 🔹 Clinical Features: “ Stones, bones, groans, psychiatric overtones ” Nephrolithiasis, bone pain, fractures Abdominal pain, constipation, pancreatitis Depression, confusion 🧪 Labs: ↑ PTH ↑ Ca²⁺, ↓ phosphate ↑ urine cAMP , ↑ ALP Treatment: Surgery ( parathyroidectomy ) Hydration, bisphosphonates if surgery not feasible

25. Secondary Secondary Hyperparathyroidism: Cause: Chronic hypocalcemia → compensatory ↑ PTH Common in chronic kidney disease (CKD) ↓ 1,25(OH)₂D → ↓ Ca²⁺ → ↑ PTH 🧪 Labs: ↑ PTH ↓ or normal Ca²⁺ ↑ phosphate (CKD patients) Treatment: Phosphate binders Vitamin D analogs ( calcitriol ) Dialysis

26. Tertiary Hyperparathyroidism Tertiary Hyperparathyroidism: Long-standing secondary hyperparathyroidism → autonomous PTH secretion (after kidney transplant) 🧪 Labs: ↑ PTH ↑ Ca²⁺ Often ↑ phosphate Treatment: Parathyroidectomy

27. Hypoparathyroidism Deficient PTH secretion → hypocalcemia 🔹 Causes: Post-surgical (thyroidectomy or parathyroidectomy ) Autoimmune DiGeorge syndrome (22q11 deletion) Clinical Features: Tetany , muscle cramps, perioral numbness Chvostek’s & Trousseau’s signs Seizures, prolonged QT 🧪 Labs: ↓ PTH ↓ Ca²⁺, ↑ phosphate Normal or low calcitriol Treatment: Calcium & vitamin D supplementation Recombinant PTH in resistant cases