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Endocrine Physiology II — Complete Viva Notes

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1. CALCIUM METABOLISM: PTH, Calcitonin & Vitamin D3

Normal Calcium Balance

• Normal plasma calcium: 9–10.5 mg/dL (ionized Ca²⁺ ≈ 4.5–5.2 mg/dL)
• 99% calcium is in bones; 1% in body fluids — but this 1% is critical for nerve function, muscle contraction, blood clotting, and enzyme activity.

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Parathormone (PTH)

Think of PTH as the "bone breaker, calcium saver" — it breaks bone to raise blood calcium.

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Calcitonin

• Inhibits osteoclasts → decreases bone resorption
• Increases Ca²⁺ excretion by kidney
• Works opposite to PTH

Calcitonin = "calm" + "toning down" calcium. It lowers what PTH raises.

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Vitamin D3 (Calcitriol — 1,25-dihydroxycholecalciferol)

1. Skin: UV light converts 7-dehydrocholesterol → Cholecalciferol (Vitamin D3)
2. Liver: 25-hydroxylation → 25-hydroxycholecalciferol
3. Kidney: 1α-hydroxylation (activated by PTH) → Calcitriol (active form)

• Intestine (main role): ↑ Ca²⁺ and PO₄³⁻ absorption (makes calbindin protein)
• Bone: Supports mineralization; also works with PTH in bone resorption
• Kidney: Mild ↑ Ca²⁺ reabsorption

• Children → Rickets (soft, deformed bones)
• Adults → Osteomalacia (weak, painful bones)
• Elderly → Osteoporosis (brittle bones)

Vitamin D is the "calcium absorber" — without it, you can eat all the calcium you want and still be deficient.

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2. PANCREATIC HORMONES: Insulin & Glucagon

Islets of Langerhans

• Beta cells (60%) → Insulin
• Alpha cells (25%) → Glucagon
• Delta cells (10%) → Somatostatin (inhibits both insulin & glucagon)

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INSULIN

Insulin Effects on Carbohydrate Metabolism

• ↑ Glucose uptake into cells (GLUT-4 in muscle & fat)
• ↑ Glycogen synthesis in liver and muscle
• ↓ Gluconeogenesis
• ↓ Glycogenolysis
• Net result: ↓ Blood glucose

Insulin Effects on Fat Metabolism

• ↑ Fat synthesis (lipogenesis) in adipose
• ↑ Uptake of triglycerides into fat cells
• ↓ Lipolysis (inhibits hormone-sensitive lipase)
• Net result: Promotes fat storage
• Deficiency → lipolysis ↑ → free fatty acids → ketone bodies → ketoacidosis

Insulin Effects on Protein Metabolism

• ↑ Amino acid uptake into cells
• ↑ Protein synthesis
• ↓ Protein catabolism
• Net result: Anabolic — builds muscles
• Deficiency → muscle wasting

Insulin is the "storage hormone" — after a meal, it stores everything: glucose as glycogen, fat in adipose, amino acids as protein.

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GLUCAGON

Actions:

Glucagon is the "fasting hormone" — it keeps blood glucose up when you haven't eaten.

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3. ADRENAL CORTEX — MINERALOCORTICOIDS (Aldosterone)

Zones of Adrenal Cortex (GFR rule)

• Glomerulosa → Mineralocorticoids (Aldosterone)
• Fasciculata → Glucocorticoids (Cortisol)
• Reticularis → Sex steroids (androgens)

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Aldosterone Actions

• ↑ Na⁺ reabsorption (conserves Na⁺, water follows → ECF volume ↑)
• ↑ K⁺ excretion into urine (prevents hyperkalemia)
• ↑ H⁺ secretion (mild metabolic alkalosis)

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Regulation of Aldosterone Secretion (RAAS)

1. ↓ Blood volume/Na⁺ → Renin from JGA → Angiotensin I → II → stimulates aldosterone
2. ↑ K⁺ → directly stimulates aldosterone release
3. ACTH — minor role
4. Na⁺ ↓ also stimulates directly

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"Aldosterone Escape" (Very Important Viva Topic!)

• Initial Na⁺ retention → ECF volume expands → BP rises
• Elevated BP → pressure natriuresis (kidney excretes more Na⁺ simply because of higher arterial pressure)
• Also, ANP (atrial natriuretic peptide) is released by stretched atria → inhibits Na⁺ reabsorption in collecting ducts

Think: In Conn's syndrome — high BP + low K⁺ + no edema = aldosterone escape.

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4. ADRENAL CORTEX — GLUCOCORTICOIDS (Cortisol)

Cortisol as the "Life-Protecting" Hormone

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Metabolic Effects of Cortisol

Carbohydrate Metabolism

• ↑ Gluconeogenesis in liver (6–10 fold!) — main effect
• ↓ GLUT-4 translocation → peripheral glucose utilization ↓ (insulin resistance)
• Net: ↑ Blood glucose → "Adrenal diabetes"

Protein Metabolism

• ↑ Protein catabolism in muscle, bone, skin, lymphoid tissue
• ↑ Amino acid delivery to liver for gluconeogenesis
• ↓ Protein synthesis in most tissues (except liver)
• Clinical: muscle wasting, thin skin, poor wound healing (in Cushing's)

Fat Metabolism

• ↑ Lipolysis → ↑ free fatty acids in blood
• Paradoxically, in Cushing's syndrome → redistribution: central obesity, buffalo hump, moon face
• ↑ Ketone body formation (if insulin also low)

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Anti-Inflammatory Effects of Cortisol

1. Stabilizes lysosomal membranes → prevents release of proteolytic enzymes
2. ↓ Capillary permeability → less tissue edema
3. ↓ WBC migration (neutrophils, eosinophils) to injury site
4. ↓ Prostaglandin and leukotriene synthesis (inhibits phospholipase A2 via lipocortin)
5. Suppresses immune system → ↓ T-lymphocyte proliferation, ↓ interleukin-1 (→ reduces fever)
6. Blocks allergic reactions (e.g., anaphylaxis)

Key: Cortisol works by "stabilizing membranes and suppressing immune signaling." Used clinically in asthma, rheumatoid arthritis, allergies.

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Other Effects of Cortisol

• ↑ RBCs (polycythemia), ↓ eosinophils/lymphocytes
• ↑ Sensitivity of blood vessels to catecholamines (permissive effect)
• ↑ Gastric acid (risk of peptic ulcer)
• Weak mineralocorticoid effect

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5. ADRENAL MEDULLA — Adrenaline & Noradrenaline

Synthesis (Catecholamine Synthesis Pathway)

• The enzyme PNMT (phenylethanolamine-N-methyltransferase) converts NA → A
• PNMT is found only in adrenal medullary cells and is induced by cortisol (explaining anatomical relationship of medulla and cortex)
• Adrenal medulla secretes: ~80% Adrenaline + ~20% Noradrenaline

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Cardiovascular Effects

• ↑ Blood glucose (glycogenolysis in liver)
• ↑ Lipolysis
• Bronchodilation (β2)
• ↑ Metabolic rate
• Dilates pupils

Adrenaline = "fight or flight" hormone. Noradrenaline = mainly a vasoconstrictor.

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6. ENDOCRINE DISORDERS II

Diabetes Mellitus: Type 1 vs Type 2

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Cushing Syndrome vs Addison Disease

Cushing = too much cortisol = fat, hypertensive, diabetic, purple striae. Addison = too little cortisol = thin, hypotensive, hyperpigmented, hypoglycemic.

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7. HORMONAL REGULATION OF HOMEOSTASIS

A. Regulation of Blood Glucose (Normal: 80–90 mg/dL fasting)

1. ↑ Glucose → β-cells secrete Insulin
2. Insulin → ↑ glucose uptake by liver, muscle, fat
3. Liver stores glucose as glycogen
4. Blood glucose returns to normal (within 2 hrs)

1. ↓ Glucose → α-cells secrete Glucagon
2. Glucagon → glycogenolysis + gluconeogenesis in liver
3. Sympathetic activation → Epinephrine → rapid glycogenolysis
4. Prolonged hypoglycemia → Cortisol + Growth Hormone → ↓ glucose utilization, ↑ fat use
5. Brain gets priority — uses only glucose; neurons have GLUT-3 (insulin-independent)

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B. Regulation of ECF Volume (Blood Volume Regulation)

1. ↓ Renal perfusion → Renin from JGA
2. Renin → Angiotensin I → II
3. Angiotensin II:
   • Stimulates Aldosterone → ↑ Na⁺ & water reabsorption
   • Causes vasoconstriction → ↑ BP
   • Stimulates ADH (vasopressin) → water reabsorption in collecting duct
4. Volume restored

1. Atria stretch → ANP (atrial natriuretic peptide) released
2. ANP → ↑ Na⁺ excretion, ↓ renin, ↓ aldosterone, vasodilation
3. Volume decreases

Key Axis: RAAS (Renin-Angiotensin-Aldosterone) raises volume. ANP lowers volume. ADH conserves water.

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Quick Revision Summary Table

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• Guyton & Hall Textbook of Medical Physiology, 14th Ed. — Chapters 78 & 79
• Sembulingam K & Sembulingam P — Essentials of Medical Physiology, 8th Ed. — Unit on Endocrinology