Pathology Overview Quiz

Pathogenesis

• Pathogenesis describes the mechanisms by which a causative agent produces pathological changes in tissues, specifically how a lesion forms.

Prognosis

• Prognosis predicts the course and outcome of a disease.

Pathological Investigations

• Biopsy: Examining a specimen from a lesion during life.
• Autopsy: Post-mortem examination of a cadaver. Samples are immediately placed in a fixative solution, typically 10% formalin, to prevent autolysis.

Histological Staining

• Routine histological staining methods are used to identify pathological changes.
• If specific identification of the disease isn't possible with routine staining, immunohistochemistry, electron microscopy, or molecular tests are used.

Electron Microscopy

• Electron microscopy provides detailed insights into the fine structure of cells and tissues, as well as the function of subcellular organelles.

Molecular Tests

• Various molecular tests are used in pathology to identify and diagnose diseases.

Staining Results

• Nuclei stain blue.
• Cytoplasm stains pink.

Fixation Not Used In

• Fixation is not used in frozen sections, immunofluorescence, electron microscopy, cultures, or chromosome studies.

Terms to Describe Pathological Conditions

• Gross pathology: Pathological changes visible with the naked eye.
• Ulcer: Loss of surface epithelium
• Nodule: Small, rounded, irregular, distinct lump
• Cavity: Space filled by a content
• Microscopic pathology: Pathological changes in cells and tissue visible only under a microscope.

Sectioning of Tissues

• Tissues are sectioned with a microtome.
• Sections are then floated on a 37°C water bath.
• Sections are placed on glass slides.
• Paraffin sections are placed on slides overnight at room temperature to bond.
• Sections are then stained.

Clearing and Paraffin Infiltration

• Xylene is used to dissolve alcohol present in the specimen for 1 hour.
• The specimen is then immersed in paraffin wax at 58°C for 1 hour to displace the xylene.

Embedding Tissues in Paraffin Blocks

• Infiltrated tissues are embedded in wax blocks.
• Paraffin wax is commonly used, it is solid at room temperature but melts at up to 70°C

Necrosis Types

• Coagulative necrosis: Characterized by infarction in most solid organs, except the brain.
• Liquefactive necrosis: Dead tissue decomposes into a viscous liquid, often appearing creamy yellow due to pus formation; characteristic of brain infarction.
• Caseous necrosis: Seen in tuberculous infections; necrotic tissue has a cheesy appearance.
• Fat necrosis: Characterized by white, chalky deposits of calcium and fatty acids, often seen in pancreatitis.
• Fibrinoid necrosis: Typically associated with autoimmune diseases.

Fate of Necrosis

• Small areas of necrosis heal.
• Large areas of necrosis are surrounded by fibrous capsules.

Macroscopic Examination of Inflammation

• Redness
• Swelling
• Hotness
• Pain
• Loss of function

Vascular Changes in Inflammation

• Vasodilation: Increased diameter of arterioles, capillaries, and post-capillary venules, resulting in increased blood flow; exhibited clinically by redness and heat. Vasodilation is caused by histamine.

Increased Capillary Permeability

• Endothelial changes cause leakage of protein-rich fluid (exudate), resulting in inflammatory edema.
• Histamine and kinin are causes of this increased permeability.

Abscess Fate

• If not evacuated: Can become a chronic abscess, spread through blood or lymph.
• If evacuated: Heals via granulation tissue, forms a sinus ( blind-ended tract to the surface), or a fistula (tract connecting two surfaces), or ulcer formation in the damaged surface.

Systemic Effects of Acute Inflammation

• Fever: Caused by pyrogens (exogenous from bacteria and fungi, endogenous from cytokines like interleukin-1 (IL-1) and tumor necrosis factor (TNF)).
• Leucocytosis: IL-1 and TNF stimulate the release of leukocytes from bone marrow.

Edema

• Edema is abnormal fluid accumulation in interstitial tissue or body cavities.
• Causes of edema: Increased vascular hydrostatic pressure; increased tissue osmotic pressure; decreased blood osmotic pressure.

Hyperemia and Congestion

• Both indicate increased blood volume in a tissue.
• Hyperemia: Increased blood flow due to arteriolar dilation (physiological: exercise, emotion; pathological: inflammation, fever). The tissue appears red due to oxygenated blood.
• Congestion: Passive hyperemia due to obstructed venous flow (pathological, often right-sided heart failure). The affected tissue appears blue-red due to increased non-oxygenated blood.

Hemorrhage

• Hemorrhage is blood escape outside the cardiovascular system.
• Causes: Trauma, bleeding disorders.
• Types: External (outside the body), internal (within serous sacs), interstitial (within tissue spaces).

Interstitial Hemorrhage Types

• Petechiae: 1-2mm diameter spots; often on skin.
• Purpura: Larger (3-5mm) spots.
• Ecchymosis: Larger subcutaneous hematomas (1-2cm)

Effects of Hemorrhage

• Chronic external blood loss: Iron deficiency.
• Acute or chronic loss of 20% total blood volume: Does not affect healthy individuals
• Acute loss more than 25% total blood volume: Produces hypovolemic shock

Shock

• Acute peripheral circulatory failure due to reduced cardiac output.
• Types: Neurogenic, cardiogenic, hypovolemic, septic (endotoxic).

Thrombosis

• Formation of a blood clot inside a blood vessel or heart cavity during life.
• Causes (Virchow's triad): Roughness of the vessel intima (endothelial injury); slowing of blood flow (stasis); blood composition changes (hypercoagulability).

Thrombosis Types

• According to site: Venous thrombosis (deep vein, lower limb); arterial thrombi (coronary, cerebral, femoral); mural thrombi (heart chambers, aortic lumen).
• According to presence/absence of organism (infection): Septic, aseptic.

Embolism

• Circulation of insoluble material (solid, liquid, or gas) and its lodging in a narrow blood vessel.
• Types: Thromboembolism (99%, including fat emboli, parasitic emboli, air emboli, tumor emboli).

Infarction

• Area of necrosis due to acute ischemia in an organ with end arteries (e.g., brain, retina, heart, spleen, kidney, intestine).
• End arteries have little to no anastomosis with neighboring arteries.

Infarction Types

• Red (hemorrhagic) infarct: In soft, vascular organs like lung & intestine; due to hemorrhage in the infarct tissues.
• Pale (anemic) infarct: In firm, less vascular organs like kidneys & heart.

Infarction Characteristics

• Size of infarct is related to the size of the obstructed artery & tissue susceptibility to ischemia.
• Wedge-shaped (pyramidal) distribution, with the base towards the organ surface and apex deeper.
• Surrounded by a red zone of hyperemia.

Microscopic Infarction

• Area of coagulative necrosis, sometimes liquefactive (in brain); surrounded by acute inflammation (hyperemia).

Bacterial infection

• The invasion of living tissue with pathogenic microorganisms.
• Exogenous: Skin/mucous membranes, ingestion, inhalation, injection, blood transfusion, sexual, transplacental.
• Endogenous: Commensal bacteria.

Methods of Spread of Infection

• Direct contact: Touching infected area.
• Lymphatic: Spread via lymphatic channels.
• Blood: Spread through the bloodstream.
• Along natural passages: Spread along openings such as the gastrointestinal or respiratory tracts.

Toxaemia

• The circulation of bacterial toxins in the blood, leading to clinical and pathological manifestations.
• Sources: Directly produced by organisms or released by necrotic tissue.
• Types: Acute and chronic.

Bacteraemia

• Circulation of relatively few bacteria.
• Sources: Endogenous, exogenous.

Septicaemia

• Wide spread circulation and multiplication of virulent microorganisms and their toxins throughout the body, resulting in significant clinical complications and structural changes.
• Causes: Strept. Haemolyticus, Staph. aureus.

Pyemia

• Circulation of detached septic thrombi with localization in organs.
• Cause: Staph. aureus.

Tuberculosis

• Chronic infective granulomatous disease, primarily affecting the lungs.
• Predisposing factors: Environmental and personal.
• Causative agents: T.B. bacilli (human type and bovine type).

Primary Tuberculosis (Childhood Type)

• Methods of infection: Inhalation, ingestion, and direct contact.
• Primary complex sites: Lung, intestine, tonsils, and skin.

Tubercle Characteristics

• Gross: Small (1-3mm) with central yellow caseation and peripheral gray areas.
• Microscopic: Central caseating material, surrounded by epithelioid cells, macrophages, Langhan's giant cells, lymphocytes, and peripheral fibroblastic reaction.

Bilharziasis

• An infective parasitic granuloma, involving several species (S. haematobium, S. mansoni, S. japonicum).
• Eggs can be detected in urine or stool samples.
• Biopsy of infected tissue is also used for diagnosis.

Bilharzial Lesions of Hollow Organs

• Ulcers
• Hemorrhagic spots
• Polyps
• Sandy patches
• Fissures
• Secondary bacterial infections

Polyp (characteristics)

• Gross: Small or large pedunculated or compound, intact or ulcerated mucosa, soft, varying numbers.
• Microscopic: Connective tissue core with bilharzial reaction, intact or hyperplastic/ulcerated mucosa.

Urinary Bilharziasis Complications

• Hypochromic anemia
• Stone formation
• Obstructive uropathy
• Carcinoma
• Pulmonary bilharziasis

Bilharziasis Diagnosis

• Clinical evaluation
• Detection of ova in urine, stool
• Biopsy (rectum, bladder wall, demonstrating terminal or lateral spines for differentiation)
• Serological testing (ELISA)
• Radiological imaging

Innate Immunity

• Defensive mechanisms present before infection, protecting against infection. Includes: epithelial barriers; phagocytic cells (neutrophils, macrophages); natural killer cells; and plasma proteins (complement system).

Adaptive Immunity

• Cell-mediated immunity: Targets intracellular microbes (e.g. mycobacterium, viruses, tumor cells, parasites). Mediated by T lymphocytes.
• Humoral immunity: Targets extracellular bacteria and toxins. Mediated by B lymphocytes and antibodies (immunoglobulins).

Disorders of the Immune System

• Hypersensitivity reactions: Exaggerated immune responses to antigens (e.g., dust, pollens, foods, drugs, microbes, chemicals, blood).
• Autoimmune diseases: Immune system attacks self-antigens.
• Immunodeficiency syndromes: Genetic or acquired defects in immune system components; can result in chronic infections, recurrent infections, unusual infections, and failures to clear infections with treatment.

Hypersensitivity Reactions Overview

• Exaggerated immune responses triggered by encounters with antigens such as dust, pollen, foods, drugs, microbes, chemicals, and blood.

Types of Hypersensitivity

• Type I (immediate): Rapid immunologic reaction (minutes post-antigen exposure) in previously sensitized individuals; allergens are antigens that trigger this response.
• Type II (antibody-mediated): Antibody-mediated disorders.
• Type III (immune complex): Immune complex-mediated disorders.
• Type IV (cell-mediated or delayed): Cell-mediated or delayed-type hypersensitivity.

Character of Infection Associated with Immunodeficiency (ID) Diseases

• Chronic infection: Prolonged duration.
• Recurrent infection: More frequent than expected.
• Unusual/opportunist infection: Infections by organisms usually not virulent.
• Incomplete clearing or incomplete response to treatment: Infections persist or do not resolve following treatments.

Types of Infections Suggestive of ID Disease

• Recurrent bacterial otitis media & pneumonia: Suggestive of hypogammaglobulinemia.
• Fungal, protozoal, or viral infections (especially chronic): Suggestive of cell-mediated immunodeficiency.
• Recurrent Neisseria infection: Suggestive of complement deficiency (MAC).
• Systemic infections by uncommon bacterial organisms (normally low virulence): Suggestive of chronic granulomatous disease, a phagocytic disorder.

Secondary (Acquired) Immunodeficiencies

• Viral infections: Examples include HIV.
• Therapeutic drugs: Medications like those used after transplant surgery
• Lifestyle factors: Certain lifestyle choices, for example, heavy alcohol use
• Chronic conditions: Diseases like diabetes or aging processes that affect the immune system

Acquired Immunodeficiency Syndrome (AIDS)

• Etiology: RNA retroviruses (HIV-1 and HIV-2).
• Clinical features: Latent period (6 months to 4 years); acute infection phase (influenza-like); antibody production (3-20 weeks), AIDS-related complex (ARC) phase with opportunistic infections, malignancies (Kaposi's sarcoma, malignant lymphoma); and nervous system complications. A significant drop below 200 cells/mm³ in CD4+ T cells is a significant marker of AIDS development.

This quiz covers fundamental concepts in pathology, including the mechanisms of pathogenesis, methods of diagnosis through biopsy and autopsy, and various staining techniques used in histology. Test your understanding of electron microscopy and molecular tests that play a crucial role in pathological investigations.