Human Health & Disease – NEET Biology Study Notes
(Prepared for NEET‑M (Medical) – Biology Section)
1. Simple Explanation
| Concept | Definition | Why It Matters |
|---|---|---|
| Health | A state of complete physical, mental, and social well‑being, not merely the absence of disease (WHO 1948). | Sets the baseline for understanding disease and prevention. |
| Disease | A pathological condition that disrupts normal body functions, usually with identifiable signs, symptoms, and laboratory/clinical findings. | Understanding disease mechanisms helps in diagnosis, treatment, and public‑health planning. |
| Pathogenesis | The series of events that lead from an insult to the establishment of disease. | Provides insight into how to intervene early. |
2. Key Points – Classification of Diseases
| Category | Main Features | Example |
|---|---|---|
| A. Infectious (Communicable) Diseases | Caused by pathogens (bacteria, viruses, fungi, parasites). Spread via direct/indirect routes. | Tuberculosis, Malaria, COVID‑19 |
| B. Genetic / Hereditary Diseases | Inherited mutations in nuclear or mitochondrial DNA. | Cystic fibrosis, Sickle‑cell anemia |
| C. Congenital Diseases | Abnormalities present at birth due to genetic or environmental factors. | Down syndrome, Congenital heart disease |
| D. Metabolic / Endocrine Disorders | Dysregulation of metabolism/ hormone production. | Diabetes mellitus, Hyperthyroidism |
| E. Neoplastic (Cancer) Diseases | Uncontrolled cell proliferation. | Breast cancer, Leukemia |
| F. Nutritional Deficiencies | Lack of essential nutrients. | Iodine deficiency (goiter), Vitamin D deficiency (rickets) |
| G. Trauma / Mechanical Injury | Physical damage to tissues. | Fractures, Burns |
| H. Radiation‑Induced Disease | Damage due to ionising or non‑ionising radiation. | Radiation sickness, Cancer from UV exposure |
| I. Chemical / Toxic Exposure | Injury from foreign chemicals. | Lead poisoning, Asbestos‑related lung disease |
Etiological agents
- Bacteria – Mycobacterium tuberculosis, Streptococcus pneumoniae
- Viruses – Influenza, HIV, Hepatitis B/C
- Fungi – Candida albicans
- Parasites – Plasmodium falciparum, Schistosoma
- Others – Prions (Creutzfeldt‑Jakob disease)
3. Pathophysiology Basics (Common Themes)
| Step | Typical Process | Key Cells / Molecules |
|---|---|---|
| 1. Initiation | Exposure to pathogen/ toxin | Receptors, pathogen‑associated molecular patterns (PAMPs) |
| 2. Recognition | Innate immune system detects danger | Toll‑like receptors (TLRs), complement |
| 3. Amplification | Inflammatory response | Cytokines (IL‑1, TNF‑α), chemokines |
| 4. Effector Response | Elimination of the insult | Neutrophils, macrophages, NK cells, adaptive immunity |
| 5. Resolution / Repair | Tissue healing | Fibroblasts, collagen deposition, angiogenesis |
| 6. Complications | Chronic inflammation or auto‑immunity | Fibrosis, autoimmune disease |
Note: The same framework applies to many disorders—e.g., in diabetes, hyperglycaemia triggers oxidative stress → inflammation → micro‑vascular damage.
4. Worked Example – Type 2 Diabetes Mellitus (T2DM)
4.1 Clinical Scenario
A 52‑year‑old male presents with increased thirst, frequent urination, and blurred vision. He reports a sedentary lifestyle and a family history of diabetes.
| Investigation | Result | Interpretation |
|---|---|---|
| Fasting Plasma Glucose (FPG) | 140 mg/dL | Normal < 100 mg/dL; 100–125 mg/dL pre‑diabetes; > 126 mg/dL diabetes |
| HbA1c | 7.2 % | > 6.5 % confirms diabetes |
| Post‑load glucose (OGTT) | 200 mg/dL | > 200 mg/dL indicates diabetes |
| Lipid profile | TG = 200 mg/dL, LDL = 130 mg/dL | Dyslipidaemia typical in T2DM |
4.2 Pathogenesis (Simplified)
- Insulin Resistance – Peripheral tissues (muscle, adipose) respond poorly to insulin.
- Compensatory Hyperinsulinemia – Pancreatic β‑cells secrete more insulin to maintain glucose homeostasis.
- β‑Cell Dysfunction –