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📚 MUHS 2nd Year MBBS Pharmacology — Hormones Chapter

Exam-Ready Answers (Simple Language)

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1. THYROID HORMONES & SYNTHESIS

Q. Name the thyroid hormones and describe their synthesis.

• Thyroxine (T4)
• Triiodothyronine (T3)
• Calcitonin

• Iodide is oxidized to iodine by peroxidase enzyme
• Iodine attaches to tyrosine residues of thyroglobulin → forms MIT (monoiodotyrosine) and DIT (diiodotyrosine)

• MIT + DIT → T3
• DIT + DIT → T4

• TSH controls release
• Thyroglobulin is taken back into cells (endocytosis) → proteolysis → T3, T4, MIT, DIT released

• Most hormone released is T4 (less potent)
• T4 → T3 conversion occurs mainly in liver and kidney

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2. ANTITHYROID DRUGS

Q. Classify antithyroid drugs with examples. Write mechanism, uses, and adverse effects.

Classification:

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A. THIOAMIDES

1. Inhibit thyroid peroxidase enzyme → iodide not converted to iodine
2. Block iodination of tyrosine residues in thyroglobulin
3. Block coupling of MIT and DIT

• Well absorbed orally
• PTU is most rapidly absorbed
• Carbimazole is a prodrug → converted to methimazole after absorption
• Accumulate in thyroid gland

• Skin rashes (most common)
• Joint pain, fever
• Hepatitis, nephritis
• Agranulocytosis (rare but serious)

1. Long-term treatment of hyperthyroidism (Graves' disease, toxic nodular goitre) where surgery/radioiodine not possible
2. Preoperatively before thyroidectomy (carbimazole used to achieve euthyroid state)
3. Along with radioactive iodine (for initial control)
4. Thyrotoxic crisis — PTU used with iodide and propranolol

• Carbimazole/methimazole preferred for long-term (long-acting, not hepatotoxic)

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B. IODINE AND IODIDES

• Oldest antithyroid agents; most rapid acting

1. Lugol's iodine (5% iodine in 10% KI solution)
2. Ipodate sodium, Iopanoic acid

• Given orally preoperatively before thyroidectomy and in thyroid storm
• Make gland firm, less vascular, smaller → easier surgery with less bleeding
• Other uses: Expectorant (KI), Antiseptic (Tincture of iodine), Prophylaxis of endemic goitre (iodized salt)

• Type III hypersensitivity: Angioedema, laryngeal oedema, arthralgia, fever, eosinophilia, lymphadenopathy

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C. RADIOACTIVE IODINE (¹³¹I)

• Half-life: 8 days (therapeutic)
• ¹²³I (half-life 13 hours) → used for diagnostic scan

• Hyperthyroidism due to toxic nodular goitre / Graves' disease (especially elderly, cardiac patients)
• Adenoma or carcinoma when surgery not feasible

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3. THYROTOXIC CRISIS (THYROID STORM)

Q. What is thyroid storm? How is it treated?

• All usual features of hyperthyroidism PLUS
• Hyperpyrexia (high fever)
• Cardiac arrhythmias (atrial fibrillation)
• Nausea, vomiting, diarrhoea
• Mental confusion

1. Hospitalization
2. Supportive care — cooling blankets, hydration, sedation, antibiotics for infection
3. Propranolol — 1-2 mg IV slowly every 4 hours → controls palpitations, tremors, tachycardia; also inhibits peripheral T4→T3 conversion
4. Propylthiouracil — via nasogastric tube (blocks synthesis + T4→T3 conversion)
5. Sodium ipodate — 0.5 g orally → inhibits hormone release + T4→T3 conversion
6. Diltiazem — if propranolol is contraindicated
7. Hydrocortisone — 100 mg IV every 8 hours → inhibits T4→T3 conversion; corrects adrenal insufficiency

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4. INSULIN

Q. Describe insulin — its mechanism, preparations, uses, and complications.

• Two chains: A chain and B chain connected by two disulphide bridges

• ↑ Glucose uptake into cells
• ↑ Glycogen synthesis in liver and muscle
• ↑ Protein synthesis
• ↑ Lipogenesis
• ↓ Gluconeogenesis, glycogenolysis, lipolysis

• Binds to tyrosine kinase receptor on cell membrane
• Receptor has 2α + 2β subunits
• α subunit: extracellular (binds insulin)
• β subunit: transmembrane, has tyrosine kinase activity
• Binding activates tyrosine kinase → phosphorylation cascade → glucose enters cell

• Destroyed by gut enzymes → NOT effective orally
• Given by subcutaneous (SC) route usually
• Emergencies: IV route (regular insulin only)
• Half-life after IV: ~6 minutes (metabolized by liver and kidney)

1. Type 1 DM (all patients)
2. Diabetic ketoacidosis (DKA)
3. Non-ketotic hyperglycaemic coma
4. Diabetes during pregnancy
5. Stress of surgery, infections, trauma in diabetics
6. Type 2 DM not controlled by oral drugs

1. Hypoglycaemia — most common and dangerous; prolonged hypoglycaemia → permanent brain damage
2. Allergic reactions — local skin reactions (swelling, redness); rare
3. Lipodystrophy — atrophy or hypertrophy at injection site; avoid by rotating sites, using purified insulin
4. Oedema — salt and water retention

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5. DIABETIC KETOACIDOSIS (DKA)

Q. What is DKA? How is it managed?

• Anorexia, nausea, vomiting
• Polyuria, abdominal pain
• Hypotension, tachycardia
• Hyperventilation (Kussmaul breathing)
• Altered consciousness or coma

1. Insulin replacement:
   • IV bolus: 0.2–0.3 U/kg followed by 0.1 U/kg/hour IV infusion
   • Blood glucose should fall by 10% in first hour
   • Once conscious → shift to SC insulin
2. Fluid replacement:
   • Normal saline 1 L/hour initially; reduce gradually
   • When blood glucose falls to ~250 mg/dL → give 5% dextrose in normal saline (prevents hypoglycaemia and cerebral oedema)
3. Potassium:
   • After insulin + correction of acidosis → K⁺ shifts into cells → hypokalaemia
   • Give KCl 10-20 mEq/hour after 4 hours of insulin therapy
   • Monitor serum K⁺ and ECG
4. Sodium bicarbonate — IV if required (for severe acidosis)
5. Phosphate — replacement if severe hypophosphataemia
6. Antibiotics — to treat associated infection

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6. ORAL ANTIDIABETIC DRUGS

Q. Classify oral antidiabetic drugs. Describe mechanism, uses, and adverse effects.

Classification:

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A. SULPHONYLUREAS

• Well absorbed orally
• Highly bound to plasma proteins
• Metabolized in liver, excreted in urine

1. Hypoglycaemia (most common, especially with glibenclamide and chlorpropamide due to long action) — glibenclamide avoided in elderly
2. GI disturbances (nausea, vomiting, diarrhoea, flatulence)
3. Weight gain (stimulates appetite)
4. Allergic reactions (skin rashes, itching, photosensitivity)
5. Teratogenicity — NOT safe in pregnancy

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B. BIGUANIDES — METFORMIN

1. Activates AMPK (AMP-dependent protein kinase):
   • ↓ Hepatic gluconeogenesis (major action)
   • ↑ Peripheral glucose utilization in muscle and fat
   • ↑ Glycogen storage, fatty acid oxidation
   • ↓ Lipogenesis
2. Inhibits alimentary absorption of glucose
3. Does NOT affect insulin release → improves insulin sensitivity

• Metallic taste, anorexia, nausea, vomiting, diarrhoea, weight loss, skin rashes
• Lactic acidosis — most serious (rare)
• Prolonged use → Vitamin B12 deficiency (malabsorption)
• Does NOT cause hypoglycaemia

• Type 2 DM (alone or combined)
• Protects against vascular complications of diabetes
• Drug of choice in obese Type 2 DM

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C. THIAZOLIDINEDIONES — PIOGLITAZONE

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D. α-GLUCOSIDASE INHIBITORS — ACARBOSE

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7. CORTICOSTEROIDS

Q. Classify corticosteroids. Describe pharmacological actions, adverse effects, and therapeutic uses.

Classification:

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PHARMACOLOGICAL ACTIONS:

• ↑ Glycogen deposition in liver
• ↑ Gluconeogenesis (glucose from amino acids)
• ↓ Peripheral utilization of glucose
• → Hyperglycaemia

• Redistribution of body fat → Moon face, buffalo hump, fish mouth with thin limbs (Cushingoid appearance)

• ↑ Protein breakdown and amino acid mobilization from muscle, bone, skin, lymphoid tissue
• → Muscle wasting, thinning of skin, osteoporosis, growth retardation
• ↓ Wound healing and fibrosis

• Weak mineralocorticoid action → Na⁺ and water retention, K⁺ excretion → oedema, hypertension
• (Dexamethasone, betamethasone, triamcinolone — NO sodium-retaining property)

• ↓ Calcium absorption from gut
• ↑ Renal calcium excretion
• ↑ Osteoclast activity → osteoporosis, pathological fractures of vertebrae

• Na⁺ and water retention → hypertension
• Permissive effect on pressor action of adrenaline and angiotensin
• Chronic use → hypertension, worsening of CCF

• Required for normal function
• Weakness in both hypocorticism (poor circulation) and hypercorticism (hypokalaemia)

• ↑ Gastric acid and pepsin secretion (by inhibiting PGs)
• ↓ Local immune response against H. pylori
• → May aggravate peptic ulcer

• Inhibit phospholipase A₂ enzyme (via lipocortin) → ↓ arachidonic acid → ↓ PGs and LTs
• Suppress redness, heat, pain, swelling

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ADVERSE EFFECTS:

1. Metabolic: Hyperglycaemia, aggravates diabetes
2. Cushing's habitus: Moon face, buffalo hump, thin limbs
3. GIT: Peptic ulceration (with haemorrhage or perforation)
4. Salt and water retention: Oedema, hypertension, CCF
5. Muscle: Hypokalaemia → weakness, steroid myopathy
6. Bone: Osteoporosis, pathological fractures, ischaemic necrosis of femoral head
7. Growth retardation: In children (especially dexamethasone and betamethasone)
8. Eye: Glaucoma, cataract (prolonged use)
9. CNS: Nervousness, insomnia, mood changes, psychosis
10. Immunosuppression: Opportunistic infections — fungal (candidiasis), viral (herpes), bacterial (reactivation of TB)

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THERAPEUTIC USES:

1. Rheumatoid arthritis — dramatic symptomatic relief (does not halt progression)
2. Osteoarthritis — intra-articular injection for acute episodes (1-2 joints)
3. Rheumatic fever — better than aspirin in cases with carditis and CCF
4. Gout — reserve drug when NSAIDs fail
5. Allergic diseases — hay fever, urticaria, contact dermatitis, angioedema, anaphylaxis (slow onset)
6. Bronchial asthma — IV hydrocortisone in acute severe asthma; inhalational (beclomethasone, budesonide, fluticasone) for chronic asthma → minimal systemic effects
7. Collagen diseases — polymyositis, polyarteritis nodosa, dermatomyositis
8. Renal disease — first-line in nephrotic syndrome
9. Ocular diseases — topical, subconjunctival, or systemic
10. Skin diseases — topical preferred to minimize systemic effects
11. Haematological disorders — autoimmune haemolytic anaemia; leukaemia, lymphomas, Hodgkin's disease, multiple myeloma
12. Cerebral oedema — effective in oedema due to brain tumours, metastasis, tubercular meningitis; least effective in head injury
13. Intestinal diseases — ulcerative colitis (methylprednisolone retention enema)
14. Septic shock — prompt IV glucocorticoids may be life-saving

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8. HORMONAL CONTRACEPTIVES

Q. Classify hormonal contraceptives. Describe mechanism, beneficial effects, and adverse effects.

Classification:

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MECHANISM OF ACTION (Combined Pill):

1. Inhibit ovulation — Oestrogen + Progestin inhibit FSH and LH via negative feedback on hypothalamic-pituitary axis
2. Inhibit fertilization — cause tubal and uterine contractions
3. Inhibit implantation — endometrium made less suitable
4. Block sperm penetration — progestin makes cervical mucus thick and viscid

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POSTCOITAL (EMERGENCY) PILL:

• Interferes with implantation + anti-ovulatory effect
• Levonorgestrel 0.75 mg × 2 doses — effective if taken within 72 hours ("morning after pill")
• Mifepristone 600 mg single dose (antiprogestin)
• Used after rape, unprotected intercourse, condom failure

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BENEFICIAL EFFECTS:

• Relieve dysmenorrhoea and premenstrual tension
• Prevent iron-deficiency anaemia (by reducing menstrual loss)
• Reduce pelvic inflammatory disease and endometriosis
• Protect against ovarian and endometrial carcinoma

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ADVERSE EFFECTS:

1. Nausea, vomiting, headache, breakthrough bleeding (initially, subside with continued use)
2. Weight gain, fluid retention, acne, skin pigmentation (later)
3. Impaired glucose tolerance, altered lipid profile (rare with low-dose pills)
4. Blood pressure increase on long-term use
5. Venous thromboembolic disease (especially in smokers)
6. Risk of MI and stroke in women with diabetes or hypertension
7. Increased risk of gallstones, benign liver tumours, breast cancer on prolonged use

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INJECTABLE CONTRACEPTIVES:

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9. UTERINE RELAXANTS (TOCOLYTICS)

Q. What are tocolytics? Classify with uses and adverse effects.

Classification:

Uses:

1. Delay preterm labour
2. Threatened abortion
3. Dysmenorrhoea

A. β-adrenergic agonists (selective β₂-agonists):

B. Prostaglandin synthesis inhibitors (NSAIDs):

• Indomethacin has tocolytic effect (inhibits PG synthesis)
• Not used for labour delay — risk of premature closure of ductus arteriosus → pulmonary hypertension
• Can be used for dysmenorrhoea

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10. UTERINE STIMULANTS (OXYTOCICS / ECBOLICS)

Q. Classify uterine stimulants. Describe oxytocin in detail.

Classification:

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OXYTOCIN (Important drug!)

Pharmacological Actions:

• Stimulates contraction of pregnant uterus
• Sensitivity increased by oestrogens, decreased by progestins
• Oestrogens increase oxytocin receptors

• Contracts myoepithelial cells → milk ejection

• High doses → ADH-like action → ↓ urine output → water intoxication

• High doses → vasodilation and transient hypotension → reflex tachycardia and flushing

Mechanism of Action:

• Binds to G-protein-coupled receptors on myometrium
• → Generation of IP₃ (inositol triphosphate)
• → Release of Ca²⁺ from intracellular stores
• → ↑ PG production by endometrium
• → Contraction of pregnant uterus

Uses:

1. Induction of labour — drug of choice
   • Given by IV infusion
   • Start with low dose, adjust according to response
   • Monitor: uterine contractions, maternal BP, fetal and maternal heart rate
2. Postpartum haemorrhage (PPH)
   • Used for prevention (IM or IV infusion) and treatment (IV infusion)
   • Contracts uterine smooth muscle → compresses blood vessels → arrests bleeding
   • Preferred over ergot derivatives (fewer side effects)
3. Uterine inertia — IV infusion to increase intensity, frequency, duration of contractions if labour is not progressing
4. Breast engorgement — intranasal oxytocin → milk let-down

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✅ Quick Revision Table — All Topics at a Glance

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Exam Tip: For 10-mark questions write: Definition/Classification → Mechanism → Pharmacokinetics → Uses → Adverse Effects. For 5-mark questions: Classification + Mechanism + Key Uses. For short notes (2 marks): definition + 3-4 key points.All 10 main topics from your PDF are covered above. Here's what's included:

• The memory mnemonics from your notes (like PYARA PATI, SITA ALOK LINA, BMW) are already incorporated
• For 10-mark questions: write headings clearly — Classification → MOA → PK → Uses → ADR
• The "Quick Revision Table" at the end is perfect for last-minute reading before the exam

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📝 HORMONES PHARMACOLOGY — IMPORTANT POINT NOTES

MUHS 2nd Year MBBS

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🔵 TOPIC 1: THYROID HORMONES

• T — Trapping (iodide taken into follicular cells via NIS — sodium/iodide symporter)
• O — Oxidation (iodide → iodine by peroxidase)
• I — Iodination (iodine + tyrosine → MIT and DIT)
• H — Hormone formation / Coupling (MIT+DIT = T3 / DIT+DIT = T4) — by thyroid peroxidase
• R — Release (controlled by TSH; endocytosis + proteolysis of thyroglobulin)

• Most hormone released from thyroid is T4 (less potent)
• T4 → T3 conversion occurs in liver and kidney
• T3 is more potent than T4

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🔵 TOPIC 2: ANTITHYROID DRUGS

Classification (easy):

• Block synthesis → Thioamides (PTU, Methimazole, Carbimazole)
• Block iodide trapping → Ionic inhibitors (Thiocyanate, Perchlorate, Nitrate)
• Block hormone release → Iodine/Iodides (Lugol's iodine, KI)
• Destroy thyroid tissue → Radioactive iodine (¹³¹I)

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A) THIOAMIDES — PTU, Methimazole, Carbimazole

1. Iodide → Iodine conversion blocked
2. Iodination of tyrosine blocked
3. Coupling of MIT + DIT blocked

• Also blocks peripheral T4 → T3 conversion (that's why PTU used in thyroid storm)

• All well absorbed orally
• Carbimazole is a prodrug → converted to methimazole in body
• Accumulate in thyroid gland

• Skin rashes — most common
• Agranulocytosis — rare but dangerous
• Joint pain, fever, hepatitis, nephritis

1. Long-term hyperthyroidism (Graves' disease, toxic nodular goitre)
2. Preoperatively before thyroidectomy → to make patient euthyroid
3. With radioactive iodine → for initial control (¹³¹I is slow)
4. Thyroid storm (PTU preferred)

• Carbimazole/Methimazole preferred for long-term → long acting, not hepatotoxic
• PTU preferred in thyroid storm and pregnancy (crosses placenta less)

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B) IODINE AND IODIDES

• Oldest antithyroid agents
• Most rapid acting antithyroid drugs
• Preparations: Lugol's iodine (5% iodine + 10% KI), Ipodate sodium, Iopanoic acid

• Preoperatively before thyroidectomy (makes gland firm, small, less vascular → less bleeding during surgery)
• Thyroid storm
• KI as expectorant (mucolytic)
• Tincture of iodine as antiseptic
• Iodized salt → prophylaxis of endemic goitre

• Type III hypersensitivity → angioedema, laryngeal oedema, arthralgia, fever, eosinophilia

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C) RADIOACTIVE IODINE (¹³¹I)

• ¹³¹I half-life = 8 days → therapeutic use
• ¹²³I half-life = 13 hours → diagnostic scan

• Hyperthyroidism (Graves' disease, toxic nodular goitre) — especially elderly + cardiac patients
• Adenoma/carcinoma when surgery not feasible

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🔵 TOPIC 3: THYROID STORM (THYROID CRISIS)

• Hyperpyrexia (very high fever)
• Cardiac arrhythmias (atrial fibrillation)
• Nausea, vomiting, diarrhoea
• Mental confusion / coma

1. Hospitalization + supportive care (cooling, hydration, sedation, antibiotics)
2. Propranolol IV 1-2 mg every 4 hours → controls tachycardia, tremors; blocks T4→T3 conversion
3. PTU via nasogastric tube → blocks synthesis + T4→T3 conversion
4. Sodium ipodate 0.5 g orally → blocks hormone release + T4→T3 conversion
5. Diltiazem → if propranolol is contraindicated
6. Hydrocortisone 100 mg IV every 8 hrs → blocks T4→T3; corrects adrenal insufficiency

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🔵 TOPIC 4: INSULIN

Basic Facts:

• Made by β-cells of pancreatic islets
• Route: preproinsulin → proinsulin → insulin (C-peptide removed)
• Structure: A chain + B chain connected by 2 disulphide bridges

Actions:

• ↑ glucose uptake, glycogen synthesis, protein synthesis, lipogenesis
• ↓ gluconeogenesis, glycogenolysis, lipolysis, ketogenesis

Mechanism of Action:

• Receptor = Tyrosine kinase receptor (2α + 2β subunits)
• α subunit = extracellular (binds insulin)
• β subunit = transmembrane with tyrosine kinase activity
• Binding → tyrosine kinase activation → phosphorylation cascade → glucose enters cell

Pharmacokinetics:

• Destroyed in gut → NOT oral
• Route: SC (subcutaneous) usually; IV only in emergencies (regular insulin)
• Half-life after IV = ~6 minutes (liver + kidney metabolize)

Insulin Preparations (by duration):

Indications:

1. Type 1 DM (all patients, always)
2. DKA
3. Non-ketotic hyperglycaemic coma
4. Diabetes in pregnancy
5. Stress (surgery, infection, trauma) in diabetics
6. Type 2 DM when oral drugs fail

Site of Injection (SC): Abdomen, buttock, anterior thigh, dorsal arm

Complications:

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🔵 TOPIC 5: DIABETIC KETOACIDOSIS (DKA)

• Anorexia, nausea, vomiting
• Polyuria, abdominal pain
• Hypotension, tachycardia
• Kussmaul breathing (hyperventilation)
• Altered consciousness → coma

1. Insulin — Regular insulin IV bolus 0.2–0.3 U/kg → then 0.1 U/kg/hr infusion
   • Blood glucose should ↓ by 10% in first hour
   • Once conscious → shift to SC insulin
2. Fluids — Normal saline 1 L/hr → reduce gradually
   • When blood glucose reaches ~250 mg/dL → switch to 5% dextrose + normal saline (prevents hypoglycaemia + cerebral oedema)
3. Potassium — After insulin, K⁺ shifts into cells → hypokalaemia
   • Give KCl 10–20 mEq/hr after 4 hours of insulin
   • Monitor serum K⁺ and ECG
4. Sodium bicarbonate — IV if severe acidosis
5. Phosphate — If severe hypophosphataemia
6. Antibiotics — For associated infection

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🔵 TOPIC 6: ORAL ANTIDIABETIC DRUGS

Classification (Simple):

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A) SULPHONYLUREAS

1. Hypoglycaemia — MC complication (especially glibenclamide, chlorpropamide — long acting); avoid glibenclamide in elderly
2. GI disturbances (nausea, vomiting, flatulence)
3. Weight gain
4. Skin rashes, photosensitivity
5. Teratogenic — NOT safe in pregnancy

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B) METFORMIN (Biguanide)

1. Activates AMPK → ↓ hepatic gluconeogenesis (main action)
2. ↑ peripheral glucose utilization in muscle and fat
3. ↓ intestinal absorption of glucose

• Does NOT stimulate insulin secretion → improves insulin sensitivity

• Metallic taste, nausea, vomiting, diarrhoea, weight loss
• Lactic acidosis — most serious (rare)
• Vitamin B12 deficiency — on prolonged use (malabsorption)
• Does NOT cause hypoglycaemia ✅

• Drug of choice in obese Type 2 DM
• Protects against vascular complications
• No hypoglycaemia

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C) PIOGLITAZONE (Thiazolidinedione)

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D) ACARBOSE (α-Glucosidase inhibitor)

• Must be taken just before food
• Best for obese Type 2 DM patients
• Side effects: flatulence, fullness, diarrhoea (all GI — because undigested carbs ferment in colon)

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🔵 TOPIC 7: CORTICOSTEROIDS

Classification:

• Short acting: Hydrocortisone (Cortisol)
• Intermediate acting: Prednisolone, Methylprednisolone, Triamcinolone, Deflazacort
• Long acting: Dexamethasone, Betamethasone
• Mineralocorticoids: Aldosterone, Fludrocortisone, DOCA

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Pharmacological Actions:

• Dexamethasone, betamethasone, triamcinolone → NO Na⁺ retention

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Adverse Effects — Remember "COME BUGS":

• C — Cushing's (moon face, buffalo hump)
• O — Osteoporosis + fractures
• M — Muscle weakness, myopathy
• E — Electrolyte changes (Na⁺↑, K⁺↓), oedema
• B — Blood sugar ↑ (diabetes aggravated)
• U — Ulcer (peptic)
• G — Growth retardation in children; Glaucoma + cataract
• S — Suppression of immunity → infections (TB reactivation, candidiasis, herpes)

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Therapeutic Uses — All 14:

1. Rheumatoid arthritis — symptomatic relief (doesn't stop progression)
2. Osteoarthritis — intra-articular injection
3. Rheumatic fever with carditis + CCF
4. Gout — reserve drug (when NSAIDs fail)
5. Allergic diseases — hay fever, urticaria, angioedema, anaphylaxis
6. Bronchial asthma — IV hydrocortisone (acute); inhaled beclomethasone/budesonide (chronic)
7. Collagen diseases — polymyositis, polyarteritis nodosa, dermatomyositis
8. Nephrotic syndrome — first-line drug
9. Ocular diseases — topical/subconjunctival/systemic
10. Skin diseases — topical preferred
11. Haematological — autoimmune haemolytic anaemia; lymphomas, leukaemia, Hodgkin's, myeloma
12. Cerebral oedema — very effective for brain tumours, metastasis, TB meningitis; least effective in head injury
13. Ulcerative colitis — methylprednisolone retention enema
14. Septic shock — prompt IV glucocorticoids may be life-saving

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🔵 TOPIC 8: HORMONAL CONTRACEPTIVES

Types:

• Combined pill (Oestrogen + Progestin)
• Mini pill (Progestin only)
• Emergency/Postcoital pill
• Injectable

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Combined Pill — Schedule:

• 1 tablet daily for 21 days → 7-day gap → repeat
• Efficacy: 98–99.9%

Mini Pill — Schedule:

• 1 tablet daily continuously (no gap)
• Efficacy: 96%

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Mechanism of Combined Pill — 4 ways:

1. ↓ FSH + LH by negative feedback on hypothalamus-pituitary → no ovulation (main action)
2. Tubal + uterine contractions → interfere with fertilization
3. Endometrium made unsuitable for implantation
4. Progestin → thick cervical mucus → blocks sperm penetration

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Emergency Contraception (Morning After Pill):

• Used within 72 hours of unprotected intercourse
• Levonorgestrel 0.75 mg × 2 doses (most common)
• Mifepristone 600 mg single dose (antiprogestin)
• Ulipristal — can be used up to 120 hours
• Mechanism: interferes with implantation + anti-ovulatory

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Beneficial Effects:

• ↓ Dysmenorrhoea + premenstrual tension
• ↓ Iron deficiency anaemia (less menstrual loss)
• ↓ Pelvic inflammatory disease + endometriosis
• ↓ Risk of ovarian and endometrial cancer ✅

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Adverse Effects:

• Early: Nausea, vomiting, headache, breakthrough bleeding
• Late: Weight gain, fluid retention, acne, skin pigmentation, BP ↑
• Serious (long-term): Venous thromboembolism (especially smokers), risk of MI + stroke (in diabetes/hypertension), gallstones, breast cancer, benign liver tumours
• Impaired glucose tolerance (rare with low-dose)

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Injectable Contraceptives:

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🔵 TOPIC 9: UTERINE RELAXANTS (TOCOLYTICS)

Classification:

• β₂-agonists: Ritodrine, Salbutamol, Terbutaline, Isoxsuprine
• Calcium channel blockers: Nifedipine
• Oxytocin antagonist: Atosiban
• Others: Magnesium sulfate, Progesterone, Nitrates, Halothane

Uses:

1. Preterm labour — to delay it
2. Threatened abortion
3. Dysmenorrhoea

β₂-agonists — Key Points:

• Adverse effects: Tachycardia, palpitations, arrhythmias, pulmonary oedema, hyperglycaemia, hypokalaemia
• Avoid in: Pregnant women with diabetes or heart disease

NSAIDs (Indomethacin) as tocolytic:

• Blocks PG synthesis → uterine relaxation
• NOT used for preterm labour → risk of premature closure of ductus arteriosus → pulmonary hypertension
• OK for dysmenorrhoea only

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🔵 TOPIC 10: UTERINE STIMULANTS (OXYTOCICS)

Classification:

• Posterior pituitary: Oxytocin, Desamino-oxytocin
• Ergot alkaloids: Ergometrine, Methylergometrine
• Prostaglandins: PGE₂ (Dinoprostone), PGF₂α (Dinoprost), Carboprost (15-methyl PGF₂α), Misoprostol
• Others: Ethacridine, Quinine

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OXYTOCIN — Most Important

• Binds to G-protein coupled receptor on myometrium
• → ↑ IP₃ → releases Ca²⁺ from intracellular stores
• → ↑ PG production by endometrium
• → Uterine contraction

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Uses of Oxytocin — 4 main:

• Given by IV infusion
• Start low dose, monitor and adjust
• Monitor: uterine contractions, BP, fetal + maternal heart rate

• Contracts uterine muscle → compresses blood vessels → stops bleeding
• Preferred over ergot derivatives (fewer side effects)
• Given IM (prevention) or IV infusion (treatment)

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⚡ SUPER QUICK REVISION — ALL TOPICS

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📌 Exam formula: Classification → Mechanism → Uses → Adverse Effects = full marks on any question

⚡ HORMONES PHARMACOLOGY — SHORT IMPORTANT POINTS

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🔵 1. THYROID HORMONES

• Thyroid makes T3, T4, Calcitonin
• Synthesis steps: Trapping → Oxidation → Iodination → Coupling → Release
• Iodide trapped by NIS (sodium/iodide symporter)
• Oxidation by peroxidase enzyme
• Coupling: MIT+DIT = T3, DIT+DIT = T4
• Most hormone released = T4 (less potent)
• T4 → T3 conversion in liver and kidney
• T3 is more potent than T4

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🔵 2. ANTITHYROID DRUGS

Thioamides (PTU, Methimazole, Carbimazole)

• Block thyroid peroxidase → no iodination, no coupling
• PTU only → also blocks peripheral T4→T3 conversion
• Carbimazole = prodrug → converts to methimazole
• All accumulate in thyroid gland
• ADR: Skin rashes (MC), agranulocytosis, hepatitis
• Carbimazole preferred for long-term (not hepatotoxic)
• PTU preferred in thyroid storm + pregnancy

Iodine/Iodides

• Oldest + most rapid acting antithyroid drugs
• Used preoperatively → makes gland firm, small, less vascular
• KI = expectorant; Tincture iodine = antiseptic; Iodized salt = endemic goitre prevention
• ADR: Type III hypersensitivity (angioedema, laryngeal oedema)

Radioactive Iodine (¹³¹I)

• Half-life = 8 days (therapeutic); ¹²³I = 13 hrs (diagnostic)
• Used in elderly + cardiac patients
• CI: Pregnancy, children, nursing mothers
• Advantage: Permanent cure, no surgery
• Disadvantage: Slow, high incidence of hypothyroidism

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🔵 3. THYROID STORM

• Severe hyperthyroidism with hyperpyrexia, atrial fibrillation, mental confusion
• Precipitants: infection, trauma, surgery, DKA, MI

Treatment:

1. Hospitalization + supportive care
2. Propranolol → controls tachycardia + blocks T4→T3
3. PTU via NG tube
4. Sodium ipodate → blocks release + T4→T3
5. Diltiazem if propranolol contraindicated
6. Hydrocortisone 100 mg IV 8 hrly → blocks T4→T3 + corrects adrenal insufficiency

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🔵 4. INSULIN

• Made by β-cells of pancreas; preproinsulin → proinsulin → insulin (C-peptide removed)
• A chain + B chain joined by 2 disulphide bridges
• Destroyed in gut → NOT oral; given SC (IV only in emergency)
• Receptor = Tyrosine kinase receptor (2α + 2β subunits)
• Half-life IV = ~6 min

Preparations:

Indications:

• Type 1 DM, DKA, pregnancy, stress (surgery/infection), Type 2 DM (oral drugs failed)

Complications:

• Hypoglycaemia — MC + most dangerous
• Lipodystrophy — rotate injection sites to prevent
• Allergic reactions, oedema

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🔵 5. DIABETIC KETOACIDOSIS (DKA)

• Complication of Type 1 DM
• Features: vomiting, polyuria, Kussmaul breathing, hypotension, coma

Management:

1. Regular insulin IV — 0.2-0.3 U/kg bolus → 0.1 U/kg/hr infusion
2. Normal saline 1 L/hr → when BG ~250 switch to 5% dextrose + NS
3. KCl 10-20 mEq/hr after 4 hrs (insulin causes hypokalaemia)
4. Sodium bicarbonate if severe acidosis
5. Antibiotics for infection

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🔵 6. ORAL ANTIDIABETIC DRUGS

Sulphonylureas (Glibenclamide, Glipizide, Glimepiride)

• Block K⁺-ATP channels → insulin secretion (secretagogue)
• ADR: Hypoglycaemia (MC — especially glibenclamide, avoid in elderly), weight gain, teratogenic
• NOT safe in pregnancy

Metformin (Biguanide)

• Activates AMPK → ↓ hepatic gluconeogenesis (main)
• No hypoglycaemia ✅
• ADR: Metallic taste, GI upset, lactic acidosis (rare), Vit B12 deficiency (long-term)
• DOC in obese Type 2 DM

Pioglitazone (Thiazolidinedione)

• Activates PPAR-γ → ↑ insulin sensitivity
• ADR: Oedema, heart failure, bladder cancer (rare)

Acarbose (α-Glucosidase inhibitor)

• Blocks α-glucosidase → ↓ carbohydrate absorption → ↓ postprandial sugar
• Taken just before food
• ADR: Flatulence, diarrhoea (only GI)

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🔵 7. CORTICOSTEROIDS

Classification:

• Short: Hydrocortisone
• Intermediate: Prednisolone, Methylprednisolone
• Long: Dexamethasone, Betamethasone
• Mineralocorticoid: Aldosterone, Fludrocortisone

Key Actions:

• Carbohydrate → ↑ gluconeogenesis → hyperglycaemia
• Fat → Moon face, buffalo hump, thin limbs
• Protein → Catabolic → muscle wasting, osteoporosis, poor wound healing
• Electrolytes → Na⁺ + water retention, K⁺ loss (Dexamethasone has NO Na⁺ retention)
• Calcium → Anti-Vit D → osteoporosis, fractures
• Anti-inflammatory → via lipocortin → inhibits phospholipase A₂ → ↓ PGs + LTs

Adverse Effects (COME BUGS):

• C — Cushing's (moon face, hump)
• O — Osteoporosis
• M — Muscle weakness
• E — Electrolyte imbalance + oedema
• B — Blood sugar ↑
• U — Ulcer (peptic)
• G — Growth retardation; Glaucoma + cataract
• S — Suppressed immunity → TB reactivation, candidiasis, herpes

Important Uses:

• Nephrotic syndrome — first-line
• Bronchial asthma — IV hydrocortisone (acute); inhaled beclomethasone (chronic)
• Cerebral oedema — best for tumours/TB meningitis; least for head injury
• Septic shock — life-saving IV glucocorticoids
• Rheumatoid arthritis, allergic diseases, haematological malignancies

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🔵 8. HORMONAL CONTRACEPTIVES

Combined Pill (Oestrogen + Progestin)

• Mechanism: ↓ FSH + LH → no ovulation (main); thick cervical mucus; hostile endometrium
• Schedule: 21 days on → 7 days gap → repeat
• Efficacy: 98–99.9%

Mini Pill (Progestin only)

• Continuous — no gap; Efficacy: 96%

Emergency Pill (within 72 hrs):

• Levonorgestrel 0.75 mg × 2 doses
• Mifepristone 600 mg single dose
• Mechanism: interferes with implantation + blocks ovulation

Non-contraceptive Benefits:

• ↓ Dysmenorrhoea, ↓ anaemia, ↓ PID, ↓ ovarian + endometrial cancer

Adverse Effects:

• Early: Nausea, headache, breakthrough bleeding
• Late: Weight gain, acne, BP ↑
• Serious: Venous thromboembolism (smokers), MI, stroke, breast cancer

Injectable:

• DMPA — 150 mg IM every 3 months
• NET-EN — 200 mg IM every 2 months
• Fertility returns after 6–8 months delay

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🔵 9. UTERINE RELAXANTS (TOCOLYTICS)

• Uses: Preterm labour, threatened abortion, dysmenorrhoea

Drugs:

• β₂-agonists: Salbutamol, Ritodrine, Terbutaline — ADR: tachycardia, pulmonary oedema, hyperglycaemia, hypokalaemia; avoid in diabetes + heart disease
• Nifedipine (Ca²⁺ channel blocker)
• Atosiban (oxytocin antagonist)
• Magnesium sulfate, Progesterone

NSAIDs (Indomethacin):

• Tocolytic but NOT used for preterm labour
• Risk: premature closure of ductus arteriosus → pulmonary hypertension
• OK only for dysmenorrhoea

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🔵 10. UTERINE STIMULANTS (OXYTOCICS)

Classification:

• Posterior pituitary: Oxytocin
• Ergot alkaloids: Ergometrine, Methylergometrine
• Prostaglandins: Misoprostol, Dinoprostone, Carboprost

Oxytocin — Key Points:

• Made in hypothalamus, stored in posterior pituitary
• Mechanism: G-protein receptor → IP₃ → Ca²⁺ release → uterine contraction
• Oestrogen ↑ sensitivity; Progesterone ↓ sensitivity

4 Actions:

• Uterus → contracts pregnant uterus
• Breast → milk ejection (myoepithelial cells)
• Kidney (high dose) → ADH-like → water intoxication
• CVS (high dose) → vasodilation → hypotension → reflex tachycardia

Uses:

1. Induction of labour — DOC → IV infusion, low dose, monitor carefully
2. PPH — prevention (IM) + treatment (IV); preferred over ergot
3. Uterine inertia — strengthen weak contractions
4. Breast engorgement — intranasal → milk let-down

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🟡 FINAL FLASH POINTS