Pathology Chapter: Inflammation and Abscesses

Cell Injury

• Causes of cell injury include: hypoxia (lack of oxygen), infectious agents, physical agents (trauma, radiation), chemical agents, immunologic reactions, and nutritional imbalances.
• Types of cell injury include reversible cell injury (degeneration) and irreversible cell injury (necrosis and apoptosis).
• Reversible cell injury includes hydropic degeneration (cloudy swelling) - a type of cell swelling due to water accumulation.
• Other forms of reversible cell injury include fatty change (steatosis) - excess fat in parenchymal cells (liver, frequently).
• Irreversible cell injury includes necrosis, characterized by cell death in a group of cells in a living body.
• Different types of necrosis include coagulative necrosis (occurs in various organs except the brain), liquefactive necrosis (in brain and abscess), and caseous necrosis (in tuberculosis).

Fat Necrosis

• Types include enzymatic and traumatic fat necrosis.
  • Enzymatic fat necrosis forms calcium soaps in acute pancreatitis.
  • Traumatic fat necrosis occurs in the female breast due to trauma.

Fibrinoid Necrosis

• Fibrinoid necrosis occurs in autoimmune diseases like rheumatic myocarditis.

Apoptosis

• Is a programmed cell death, often involving few or single cells.
• It is regulated by the Bcl-2 gene.
• It does not involve release of chemical mediators or inflammation.
• Can be physiological (normal) such as during embryogenesis or menstruation, or pathological.
• Examples: Liver cells in hepatitis, and some malignant tumour cells.

Morphological features of Apoptosis

• Shrinkage of cell size
• Nuclear chromatin condensation, followed by DNA fragmentation
• Formation of apoptotic bodies
• The apoptotic bodies consist of a dark nuclear fragmented cytoplasm. They become engulfed by phagocytic cells.

Intracellular Accumulation & Extracellular Deposition

• Cells may accumulate water, fat, glycogen, protein (in hyalinosis), and pigments (endogenous and exogenous).
• Melanin is a naturally occurring pigment in skin and hair, increased melanin exposure can occur due to sun exposure or pregnancy, decreased melanin is present in albinism.
• Hemosiderin is a form of iron deposition sometimes resulting in hemosiderosis (localized) and haemochromatosis(generalized).
• Lipochromes are yellow-brown pigments that increase in older tissues.
• Examples of Haemoglobin derived pigment include hemosiderin and haemoglobin.

Exogenous Pigments

• Inhalation of carbon particles can result in black lung pigment (anthracosis).
• Chronic lead ingestion results in lead deposition in gum mucosa.

Calcium

• Dystrophic calcification is the deposition of calcium salts in injured/necrotic tissue.
• Metastatic calcification is the deposition of calcium salts in normal tissues due to high blood calcium.

Amyloidosis

• Extracellular deposition of abnormal protein (amyloid), mainly in walls of blood vessels and basement membranes.
• Examples include systemic amyloidosis (amyloid deposited in many organs) & localized amyloidosis (amyloid deposited in one organ).

Tuberculosis (TB)

• A chronic granulomatous inflammation caused by tubercle bacilli.
• The basic lesion is a tubercle, which is a granuloma containing caseous necrosis.
• Grossly, tubercles fuse to form small (1-2mm) follicles.
• Microscopically, the tubercles contain epithelioid cells, giant cells, lymphocytes, and caseous necrosis.
• Pathologically, a primary TB complex develops containing Ghon's focus (initial TB lung lesion), tuberculous lymphangitis (lymph vessel involvement), and lymphadenitis (enlarged lymph nodes).

Acute and Chronic Inflammation

• Inflammation: A protective response to tissue injury that aims to localize and destroy the injury and start repair.
• Acute inflammation: Rapid onset, short duration (minutes or hours), mild injury, self-limiting.
• Chronic inflammation: Gradual onset, prolonged duration (weeks to years), severe, prolonged.
• Local vascular events (steps in acute inflammation):
  • Temporary vasoconstriction (first to occur).
  • Arteriolar vasodilation.
  • Increased vascular permeability
  • Vascular slowing.
  • Inflammatory fluid exudate formation.

Types of Acute Inflammation

• Suppurative (pus formation): abscess, boil, carbuncle, cellulitis, acute suppurative appendicitis, peritonitis.
• Non-suppurative: Serous, fibrinous, serofibrinous, catarrhal, pseudomembranous, and allergic inflammation.

Healing by Fibrosis

• The replacement of damaged tissue by granulation tissue, which matures into fibrous tissue (scar).

Types of Wound Healing

• Healing by primary union (intension) - clean wound, minimal tissue damage, shorter healing time, less granulation tissue, small pale scar.
• Healing by secondary union (second intention) - infected, gapping wound, longer healing time, more granulation tissue, larger scar.

Complications of Wound Healing

• Cosmetic deformities (scarring).
• Function loss (contractures).
• Keloid formation.
• Chronic ulcer, sinus, fistula.

Chapter 4 Cellular adaptation

• Atrophy: Decrease in cell size due to decreased anabolism and/or increased catabolism.
  • Physiological atrophy (e.g. thymus after puberty, mammary glands, or ovaries after menopause).
  • Pathological atrophy (e.g., disuse atrophy or nerve injury related atrophy).
• Hypertrophy: Increase in cell size due to increased protein synthesis
• Physiological hypertrophy (e.g. pregnancy uterus, muscle builders).
• Pathological hypertrophy (e.g. left ventricular hypertrophy due to hypertension).

Chapter 4. Cellular Adaptation and Growth Disturbances - Hyperplasia

• Hyperplasia: Increase in the number of cells leading to an increase in tissue/organ size.
  • Physiological hyperplasia (e.g., mammary glands at puberty, endometrial hyperplasia, or compensatory hyperplasia after partial hepatectomy).
  • Pathologic hyperplasia (e.g., endometrial hyperplasia due to excessive estrogen stimulation).

Chapter 4. Cellular Adaptation and Growth Disturbances - Metaplasia

• Metaplasia: Transformation of one mature cell type into another mature cell type of the same lineage.
  • Epithelial metaplasia: Columnar or transitional cells transform into stratified squamous epithelium (e.g., bronchial or respiratory epithelium in smokers).
  • Mesenchymal metaplasia: Transformation of fibroblasts into chondroblasts or osteoblasts resulting in bone or cartilage formation (e.g., local myositis ossificans).

Chapter 4 Cellular Adaptation and Growth Disturbances - Dysplasia

• Dysplasia: Non-neoplastic proliferation of cells characterized by cell atypia/pleomorphism.
• Cellular atypia - variations in cell morphology or shape.
• Enlarged hyperchromatic nuclei and increased mitotic activity

Chapter 5 Neoplasia

• Benign tumors: Slow growth rate, expansive growth pattern, well-defined margins, no metastasis, encapsulated/non-encapsulated.
• Malignant tumors: Rapid growth rate, infiltrative growth pattern, irregular margins, potential for metastasis, and often lack encapsulation.
• Carcinomas (epithelial origin), sarcomas (mesenchymal origin)

Chapter 6 Infections - Bacteremia and Septicemia

• Bacteremia: low number of low-virulence bacteria in the blood
• Septicemia: a fatal condition caused by substantial numbers of high-virulence bacteria in the blood
• Pyaemia: development of multiple small abscesses in different organs due to a septic embolus.

Chapter 6 Infections - Parasitic Infections (Bilharziasis)

• Bilharziasis: chronic granulomatous inflammation.
• Etiology: Parasitic infection.
• Pathogenesis: formation of granulomas containing macrophages, lymphocytes, plasma cells, eosinophils, and fibroblasts.

Chapter 6 Infections - Fungal Infections (Candidiasis)

• Candidiasis (moniliasis): fungal infection with Candida albicans
  • Superficial candidiasis (e.g., thrush, vaginal lesions).
  • Invasive/disseminated candidiasis (usually in patients with low immunity).

Chapter 6 Infections - Viral Infection (HPV)

• Human papillomavirus (HPV) is a family of over 100 types.
• Some HPV types (low-risk) cause warts, others (high-risk) are associated with cancer development.
• HPV is linked to cervical, anal, and other cancers.

Chapter 6 Hemodynamic Disturbances - Hyperemia and Congestion

• Hyperemia: Active process (increase in blood flow to tissue).
• Congestion: Passive process (venous outflow obstruction).
• Types include local (single organ e.g. venous obstruction, or systemic) venous congestion (heart failure).

Chapter 6 Hemodynamic Disturbances - Thrombosis

• Thrombosis: Abnormal blood clot (thrombus) inside the cardiovascular system.
• Virchow's Triad: Three factors for thrombus formation: endothelial injury, alterations in blood flow (stasis/turbulence), and hypercoagulability.

Chapter 6 Hemodynamic Disturbances - Embolism

• Embolism: Obstruction of a blood vessel by an embolus (solid, liquid, or gaseous).
• Types of emboli include thromboemboli (most common), fat emboli, amniotic fluid emboli, gas emboli, tumor emboli, and septic emboli.

Chapter 6 Hemodynamic Disturbances - Ischemia and Infarction

• Ischemia: Reduced blood supply to a tissue.
• Infarction: Ischemic necrosis of tissue, often due to complete arterial occlusion (e.g. thrombosis or embolism).
• Types of infarction, pale (e.g. heart, kidney), red (e.g. venous obstruction).

Chapter 6.6 Gangrene

• Gangrene is massive tissue necrosis followed by putrefaction by saprophytic bacteria or organisms.
• Types of gangrene: Dry, moist, and gas gangrene.
• Differentiating characteristic features between dry and moist gangrene.