Pathology Vocabulary

Pathology Disciplines

• Histopathology & Cytology: Study structural abnormalities in tissues/cells via biopsy/autopsy.

  • Biopsy: Tissue sample during life.

  • Autopsy: Examination post-mortem.

• Haematology: Detect blood/bone marrow abnormalities.

• Biochemistry: Detect abnormalities in body chemistry (e.g., glucose, urea levels).

• Microbiology: Detect infectious diseases.

• Immunoserology: Detect immune/infectious diseases via antigen/antibody reactions.

• Molecular Pathology: Detect abnormalities at the molecular level (genes).

• Medical Genetics: Detect inherited diseases; prenatal diagnosis.

• Medical Radiations: Aid in diagnosis/treatment (X-rays, CT, MRI).

Diagnostic Procedure

• Patient presents with symptoms.

• Clinician examines and detects signs.

• Differential diagnosis: List possible diseases.

• Presumptive diagnosis: Initial diagnosis.

• Definitive diagnosis: Final diagnosis after tests.

• Prognosis: Forecast of disease course/outcome.

• Remission: Absence of disease activity (possibility of return).

• Relapse: Renewed disease activity post-remission.

Classifying Disease

• Eponymous term (e.g., "Bright’s disease").

• Descriptive term (e.g., glomerulonephritis).

Aetiology & Pathogenesis

• Aetiology: Cause of disease (e.g., Staph. aureus).

• Pathogenesis: How aetiology causes the disease.

Aetiology of Disease

• Genetically determined: Gene defects/DNA anomalies, may be influenced by environment, present at birth.

• Acquired: Environmental factors.

Genetically Determined Disease

• Cytogenetic Disorders: Chromosomal defects.

  • Down's syndrome: 47, XY+21

  • Klinefelter's Syndrome: 47, XXY

• Mendelian Disorders: Gene defects.

  • Phenylketonuria (PKU): Enzyme gene defect.

• Multifactorial Inheritance Disorders: Many genes + environment.

  • Hypertension: Genes + salt intake/stress.

• Congenital Malformations: DNA expression errors.

  • Heart defects, Thalidomide phocomelia, Rubella virus infection.

Acquired Disease (Environmental Factors)

• Causative agent (e.g., Streptococcus pneumoniae).

• Predisposing factors (e.g., smoking).

• Contributory factors (e.g., malnutrition).

Acquired Disease (Pathological Stimuli)

• Physical Agents: Trauma, heat, cold, radiation.

• Chemical Agents: Synthetic/natural chemicals, toxins.

• Biological/Infective Agents: Worms, bacteria, viruses.

• Immune factors: Allergies, autoimmunity, immunodeficiency.

• Deficiency/Excess Factors: Vitamins, minerals.

• Psychogenic factors: Psychological state.

• Iatrogenic factors: Medical intervention (e.g., Aspirin overdose).

• Idiopathic factors: Unknown cause (e.g., Sarcoidosis).

Injury & Response

• Injury: Disrupts normal structure/function.

• Trauma: Injury due to mechanical/physical agent.

• Sublethal (mild) injury: Parenchymal cells -> Sublethal changes; Connective tissue cells -> Inflammation.

Sublethal/Reactive Changes

• Hydropic change: Membrane ion pumps failing.

• Fatty Change: SER damaged, fat accumulation.

• Glycogen depletion: Mitochondria damaged, ATP produced anaerobically.

• Protein synthesis ↓: Ribosomes/GER damaged.

• Autophagy: Lysosomes damaged, lytic enzymes released.

Response to Injury (Lethal)

• Lethal (severe) injury: Parenchymal & connective tissue cells -> Necrosis.

• Angina Pectoris: Mild injury (hypoxia).

• Myocardial Infarction: Severe injury (anoxia).

Processes Leading to Myocardial Infarction

• Aetiology: Ischaemia (blocked blood supply).

• Pathogenesis:

  • Acute anoxia.

  • Oxidative phosphorylation stops.

  • Anaerobic glycolysis generates ATP.

  • Membrane ion pumps fail, cell swells.

  • Biochemical necrosis (irreversible).

  • Intracellular membrane rupture.

    • Autolysis: Cytoplasm dissolves.

    • Coagulation: Cytoplasm solidifies.

Nuclear Changes in Necrosis

• Pyknosis: Nucleus shrinks and condenses.

• Karyorrhexis: Nucleus fragments.

• Karyolysis: Nuclear fragments dissolve.

Myocardial Infarction (Histological Necrosis)

• Cellular proteins coagulate.

• Diagnosis: Coagulative necrosis due to ischaemia.

Reaction to Necrotic Tissue

• In vital organs -> death may occur.

• If patient survives:

  • Inflammation & removal by phagocytes.

  • Replaced by scar tissue (fibrosis/gliosis).

  • Calcium deposits (dystrophic calcification).

Types of Necrosis

• Coagulative Necrosis: Common in solid organs (e.g., heart, kidney); ischaemia -> protein coagulation.

• Colliquative (Liquefactive) Necrosis:

  • Brain: Autolysis.

  • Suppuration: Neutrophils lyse bacteria (heterolysis).

• Caseous Necrosis: Tuberculosis (Mycobacterium tuberculosis); hypersensitivity reaction.

• Haemorrhagic Necrosis: Ischaemia -> necrotic tissue w/ extravasated RBCs.

• Gummatous Necrosis: Tertiary syphilis (Treponema pallidum).

• Fat Necrosis:
  * Enzymatic: Pancreatic lipases (alcoholics).
  * Traumatic: Injury to adipose tissue.

• Fibrinoid Necrosis: Connective tissue/blood vessel walls; collagen degenerates.

• Gangrenous Necrosis: Ischaemia & infection with anaerobic bacteria.

Sequelae of Necrosis

• Coagulative -e.g ischaemia; coagulation of proteins (myocardial infarction)

• Colliquative - e.g stroke

• Colliquative - e.g pyogenic infection; heterolysis of cells (abscess)

• Haemorrhagic -e.g ischaemia; extravasated RBCs

• Caseous - e.g Mycobacterium tuberculosis infection (tuberculosis)

• Gangrenous-e.g ischaemia; gas gangrene

• Gummatous - e.g Treponema pallidum infection

• Fat-e.g adipose cell injury (Pancreatitis)

• Fibrinoid - e.g. degeneration of collagen

Apoptosis

• "Shrinkage necrosis" (no inflammation).

• Controlled cell death, programmed.

• Death-inducing signals > cell-surviving signals.

Apoptosis - Seen In:

• Embryogenesis (separating digits).

• Withdrawal of hormonal growth stimulus (uterus after childbirth).

• Removal of cells with high turnover (gastric mucosal cells).

• Removal of cells w/ DNA damage (viral infection, irradiation).

• Removal of neoplastic cells in tumours.

Key Terms:

• Ischaemia: Interrupted blood supply.

• Infarction: Necrosis due to ischaemia.