Muhs university exams answers in easy language

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🧪 AUTACOIDS — MUHS Pharmacology (Easy Language Notes)

📌 What are Autacoids?

Autacoids = "Local Hormones"

They are chemicals produced by body cells that act locally (near where they are made).
Examples: Histamine, Serotonin (5-HT), Prostaglandins, Leukotrienes, Angiotensin, Kinins, PAF (Platelet Activating Factor), Bradykinin

1️⃣ HISTAMINE & ANTIHISTAMINES

What is Histamine?

A biogenic amine found in mast cells of skin, lungs, liver, gastric mucosa, placenta
Released during allergic/inflammatory reactions

Histamine Receptors (Remember: H1 to H4)

Receptor	Action
H1	↑ Ca²⁺ → Smooth muscle contraction, ↑ capillary permeability
H2	↑ cAMP → ↑ Gastric acid secretion
H3 (presynaptic)	↓ cAMP → ↓ Histamine in brain, lungs, skin
H4	↑ cAMP → Chemotaxis, cytokine secretion

H1 Antihistamines (Classify them!)

🔴 First Generation (cross BBB → cause drowsiness)

Sedation Level	Drugs
Highly sedative	Diphenhydramine, Dimenhydrinate, Promethazine, Hydroxyzine
Moderately sedative	Pheniramine, Cyproheptadine, Meclizine, Cinnarizine
Mildly sedative	Chlorpheniramine, Dexchlorpheniramine, Triprolidine, Clemastine

🟢 Second Generation (do NOT cross BBB → non-sedating)

Loratadine, Cetirizine, Levocetirizine, Fexofenadine, Azelastine, Mizolastine, Ebastine

Key difference of 2nd generation:

❌ No anticholinergic effects
❌ No antiemetic effect
❌ Do NOT cross BBB → no drowsiness
✅ Do not impair psychomotor performance

H1 Blocker — Mechanism

Competitive antagonism at H1 receptors → block histamine effects

Uses of First Generation H1 Blockers

Allergic diseases — urticaria, pruritus, rhinitis, conjunctivitis, angioedema
Common cold — symptomatic relief (sedation + anticholinergic)
Pre-anaesthetic — Promethazine for sedation + anticholinergic
Antiemetic — Promethazine, Diphenhydramine, Dimenhydrinate → motion sickness, post-op vomiting, chemo vomiting
Parkinsonism — Promethazine, Diphenhydramine, Orphenadrine (control tremor, rigidity, sialorrhoea)
Transfusion reactions — mild blood transfusion/saline infusion reactions
Sedation — Promethazine, Diphenhydramine to induce sleep (especially in children)

2️⃣ SEROTONIN (5-HT)

What is Serotonin?

Made from Tryptophan (hydroxylation → decarboxylation, similar to catecholamines)
Stored in vesicles; action terminated by reuptake
Acts on 5-HT1 through 5-HT7 receptors
5-HT3 receptors are present in the GIT (ionotropic/fast)

5-HT Antagonists (Classify!)

Class	Drugs
Non-selective / partial agonist-antagonists	Ergotamine, LSD, Methysergide, Cyproheptadine, 2-Bromocriptine, Cinnarizine
5-HT2 antagonists	Ketanserin, Ritanserin, Risperidone
5-HT3 antagonists (antiemetics)	Ondansetron, Granisetron, Tropisetron, Palonosetron, Ramosetron

3️⃣ ERGOT ALKALOIDS

Naturally found in fungus Claviceps purpurea
Act on multiple receptors (serotonin, dopamine, adrenergic)
Uses: Migraine, bleeding (oxytocic), Parkinson's (Bromocriptine)

4️⃣ PROSTAGLANDINS (PGs)

How made?

Membrane phospholipids → (Phospholipase A₂) → Arachidonic acid → (COX enzyme) → Prostaglandins

Also: Arachidonic acid → (Lipoxygenase) → Leukotrienes

COX-1 vs COX-2

	COX-1	COX-2
Type	Constitutive (always present)	Inducible (appears during inflammation)
Location	Most tissues: BV, kidney, stomach, platelets	Brain, kidney (constitutive) + inflammatory sites
Function	Gastric protection, homeostasis, platelet aggregation	Pain, inflammation

Main PGs: PGE2, PGF2α, PGI2 (prostacyclin)

Prostaglandin Analogues — Uses in Obstetrics

Abortion:
- Dinoprostone (PGE2, vaginal) → mid-trimester abortion, missed abortion, hydatidiform mole
- Misoprostol (oral/vaginal) + mifepristone → early pregnancy abortion
- Carboprost (IM) → 2nd trimester abortion
- Gemeprost (PGE1), Dinoprost (PGF2α) → abortion
Induction of labour: PGs soften cervix
PPH (Post-Partum Haemorrhage):
- Carboprost (IM) + Misoprostol (oral) → control PPH

5️⃣ NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)

Mechanism

Block COX (cyclooxygenase) → reduce prostaglandins → less pain, fever, inflammation

Main adverse effect: Gastric irritation/ulceration

How to prevent GI side effects of NSAIDs:

a) Take NSAIDs after food
b) Use buffered aspirin (aspirin + antacid)
c) Take PPI / H2 blockers / Misoprostol with NSAIDs
d) Use selective COX-2 inhibitors

Selective COX-2 Inhibitors

Parecoxib (IV/IM), Etoricoxib (oral), Celecoxib (oral)
Parecoxib is a prodrug of Valdecoxib

Nonselective COX inhibitors	Selective COX-2 inhibitors
Block COX-1 + COX-2	Block only COX-2
Cause gastric ulcers	Less gastric side effects
Antiplatelet effect present	No antiplatelet effect → ↑ thrombosis risk

6️⃣ PARACETAMOL (Acetaminophen)

Pharmacology

Routes: Oral & parenteral
Well absorbed, widely distributed
Metabolized in liver: sulphate + glucuronide conjugation
Metabolites excreted in urine

Uses

Antipyretic — reduce fever
Analgesic — headache, toothache, myalgia, dysmenorrhoea
Preferred in: peptic ulcer, haemophilia, bronchial asthma, children

Adverse Effects

Skin rashes, nausea (occasional, rare at normal doses)
Hepatotoxicity — acute overdose or chronic use ⚠️
Nephrotoxicity — chronic use

⚠️ Acute Paracetamol Poisoning

Toxic metabolite: NAPQI (N-acetyl-p-benzoquinone imine) — formed when normal GSH pathway is saturated

Symptoms: Nausea, vomiting, diarrhoea, abdominal pain, hypoglycaemia, hypotension, hypoprothrombinaemia → Liver failure

Treatment:

N-Acetylcysteine (NAC) — replenishes glutathione (antidote)
Activated charcoal (if early)
Supportive care

Aspirin (Salicylate) — Special Note

Reye's Syndrome: Aspirin given to children with viral infection (flu, chickenpox) can cause:

Fatty liver
Encephalopathy
Therefore: Aspirin is CONTRAINDICATED in children with viral infections

Aspirin adverse effects: Rhinitis, bronchospasm, angioneurotic oedema, anaphylactoid reactions

7️⃣ GOUT TREATMENT

Acute Gout

Colchicine — inhibits microtubule polymerisation → prevents WBC migration → anti-inflammatory
NSAIDs — indomethacin, naproxen
Corticosteroids

Chronic Gout / Uric Acid Lowering

Uricosuric drugs (increase uric acid excretion):

Probenecid, Sulfinpyrazone

Uric acid synthesis inhibitors:

Allopurinol → inhibits xanthine oxidase → reduces uric acid synthesis → reduces plasma urate
- Active metabolite: Alloxanthine (non-competitive inhibitor of xanthine oxidase)
- Reduces urate crystals in kidney, joints, soft tissue
- Drug of choice for asymptomatic gout
- Also used in cancer chemotherapy-related hyperuricaemia, kala-azar
- ⚠️ Do NOT start within 3 weeks of acute attack (may precipitate another attack)

8️⃣ RHEUMATOID ARTHRITIS (RA) Treatment

RA = Chronic autoimmune disease → inflammatory synovitis of peripheral joints

Cause	Mediator
Pain + swelling	Prostaglandins
Joint damage/deformity	Cytokines

Drug Classes

1. DMARDs (Disease-Modifying Antirheumatic Drugs)

(i) Non-biologic: Methotrexate, Azathioprine, Cyclophosphamide, Hydroxychloroquine, Sulphasalazine, Leflunomide, D-Penicillamine, Gold compounds
(ii) Biologic:
- TNF-α antagonists: Etanercept, Infliximab, Adalimumab
- IL-1 antagonist: Anakinra
- T-cell modulator: Abatacept
- B-cell depleter: Rituximab

Mnemonic for DMARDs: MEDIC ALS R Gold

M-Methotrexate, E-Etanercept, D-D-Penicillamine, I-Infliximab, C-Chloroquine/Hydroxychloroquine, A-Anakinra/Abatacept, L-Leflunomide, S-Sulphasalazine, R-Rituximab, Gold

2. NSAIDs — Aspirin, Diclofenac, Naproxen, Piroxicam, Etoricoxib

3. Glucocorticoids — Prednisolone, Triamcinolone, Methylprednisolone

Sulphasalazine

Used alone in mild RA or in combination in severe RA
Also used in chronic inflammatory bowel disease (IBD)

🔑 Quick Exam Points to Remember

Topic	Key Fact
Autacoids =	Local hormones
H2 receptor →	↑ Gastric acid (blocked by ranitidine, cimetidine)
Most sedating antihistamine	Diphenhydramine, Promethazine
Non-sedating antihistamine	Loratadine, Fexofenadine, Cetirizine
5-HT3 blockers	Ondansetron — antiemetic in chemo
COX-2 =	Inducible (inflammation)
Aspirin contraindicated in	Children with viral fever (Reye's syndrome)
Paracetamol antidote	N-Acetylcysteine
Gout drug of choice (asymptomatic)	Allopurinol
Allopurinol inhibits	Xanthine oxidase
RA biologics: TNF-α blockers	Etanercept, Infliximab, Adalimumab
PPH drug	Carboprost, Misoprostol
Paracetamol metabolized in	Liver (sulphate + glucuronide conjugation)

These notes cover the complete Autacoids chapter from your MUHS Pharmacology PDF in easy, exam-ready language. All major topics — Histamine, Serotonin, Prostaglandins, NSAIDs, Paracetamol, Gout, and Rheumatoid Arthritis — are included with mechanisms, uses, and adverse effects.

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