Introduction to GI, Joint Disorders & Cancer
Unit 4 focuses on diseases of the gut and joints, plus a fundamental introduction to Cancer. Gastrointestinal diseases (IBD, Hepatitis, Jaundice) are heavily linked to Biochemistry. Joint disorders (Rheumatoid Arthritis, Gout) are important pharmacology targets. Cancer principles are essential for understanding oncology and chemotherapy.
Syllabus & Topics
- 1Inflammatory Bowel Diseases: Crohn’s Disease vs Ulcerative Colitis (differences).
- 2Jaundice: Types (Pre-hepatic/Hemolytic, Hepatic/Hepatocellular, Post-hepatic/Obstructive).
- 3Hepatitis: Types A, B, C, D, E, F (routes of transmission, clinical significance).
- 4Alcoholic Liver Disease: Fatty Liver → Alcoholic Hepatitis → Cirrhosis.
- 5Disease of Bones and Joints: Rheumatoid Arthritis (RA) – Autoimmune pathogenesis, Pannus formation.
- 6Osteoporosis: Mechanism (imbalance of osteoblast/osteoclast activity), risk factors.
- 7Gout: Hyperuricemia → Monosodium Urate crystal deposition → Inflammation.
- 8Principles of Cancer: Definition, differences between Benign and Malignant tumors.
- 9Classification of Cancer: Carcinoma, Sarcoma, Lymphoma, Leukemia.
- 10Etiology of Cancer: Chemical carcinogens, Physical (radiation), Viral, Hereditary.
- 11Pathogenesis of Cancer: Proto-oncogenes, Tumor suppressor genes, Metastasis.
Learning Objectives
Frequently Asked Questions (FAQs)
Q1. What is the difference between Crohn’s Disease and Ulcerative Colitis?
- Crohn’s Disease: Affects any part of the GI tract (mouth to anus), shows skip lesions, has transmural inflammation, and may form granulomas.
- Ulcerative Colitis: Affects only the colon and rectum, has continuous lesions, and inflammation is confined to mucosa and submucosa.
Q2. What is the difference between Benign and Malignant Tumors?
Benign Tumors: Slow-growing, well-encapsulated, do not invade surrounding tissues or metastasize, Malignant Tumors (Cancer): Invasive, can metastasize (spread to distant sites via blood or lymph), and may cause death.
Q3. What are the types of Jaundice?
- Pre-hepatic (Hemolytic): Excess RBC destruction increases bilirubin.
- Hepatic (Hepatocellular): Liver cell damage (e.g., Hepatitis B).
- Post-hepatic (Obstructive/Cholestatic): Bile duct obstruction (e.g., gallstones).
Q4. What is the mechanism of Rheumatoid Arthritis?
Rheumatoid Arthritis is an autoimmune disease where T-cells and B-cells attack the synovial membrane. TNF-α and IL-1 drive joint inflammation and pannus formation (destructive granulation tissue), leading to joint erosion.
Q5. What are Proto-oncogenes and Tumor Suppressor Genes?
Proto-oncogenes (e.g., ras, myc) normally promote cell growth. Mutations convert them into oncogenes, causing uncontrolled proliferation, Tumor Suppressor Genes (e.g., p53, Rb) normally inhibit cell growth. Loss of function leads to cancer development.
