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INTRODUCTION
Pathology : The science which deals with the study of structural and functional changes that occur in body tissues and organs in diseases. Pathology is the scientific study of diseases. Disease : A state of ill-health resulting from structural and functional changes in any organ or tissue outside normal range. The study of General Pathology: Deals with the general principles of disease and responses of the living tissue to pathologic stimuli. CAUSES OF DISEASES: (A) Genetic : Mongolism, favism and thalassemia. (B) Acquired : 1 - Biological: Bacteria, viruses, parasites, protozoa, fungi. 2 - Physical: Heat, cold, trauma, radiation. 3 - Chemical: Acids, alkali, toxins, drugs. 4 - Immunological: hypersensitivity reactions and autoimmune diseases. 5 - Endocrinal: Hypopituitarism, Hyperthyroidism, hyper-adrenalism. 6 - Metabolic: Diabetes mellitus. 7 - Hemodynamic disorders: Ischemia, hypoxia, cerebral stroke, shock. 8 - Nutritional: Marasmus, scurvy, iron-deficiency anemia. 9 - Carcinogenic agents. ASPECTS OF DISEASE STUDY: I- Etiology: Means the cause of the disease, it includes: a) Predisposing factors: Help the development of the disease, e.g. immune deficiency, diabetes, old age increases the risk of infections. b) Exciting factors: The actual cause the disease. II- Pathogenesis: It is the mechanism of the disease process, by which the pathological changes of the cells and tissues in response to the etiological agents are produced. III- Morphological (structural) changes: The characteristic structural changes that occur in the organs, tissues and cells. Such changes include: a) Gross changes (Macroscopic, Naked-eye picture): It is the naked eye description of the affected organ or tissue regarding : Size, Weight, Shape, Surface, Color, Capsule, Cut section, Consistency, border. b) Microscopic picture: The structural changes in tissues and organs detected by microscopic examination. Different types of microscopes are used as:
- Light microscope: Sections stained by routine, histochemical and immunohistochemical stains.
- Special microscopes: Electron microscope (E/M), Flourescent microscope.
IV- Clinical Picture (functional changes) of the disease:
- Signs: Features of the disease detected by the physician.
- Symptoms: Complaints of the patient.
- Complications: Additional pathological changes which may occur during or after the usual course of the disease which may affect or modify the disease outcome. N.B: The clinical picture together with the results of the investigations helps in diagnosis of diseases. V- Prognosis (fate of the disease) : What is going to happen as regarding the course and termination of disease whether complete recovery, chronicity or fatal outcome. TYPES OF PATHOLOGICAL SPECIMENS: (A) Tissue specimens : 1 - Whole organ: nephrectomy and hysterectomy specimens. 2 - Biopsy: Tissue sample from the affected organ.
- Excisional biopsy: Sampling of the whole diseased tissue**.
- Incisional biopsy:** Sampling of a portion of the diseased tissue. It includes: Punch biopsy: in skin lesions. Endoscopic biopsy : GIT, respiratory tract and urinary tract. Core cut needle biopsy: A wide needle is introduced into a suspected area to obtain a core of tissue from organs e.g. liver or breast. 3 - Autopsy: Postmortem specimens taken from organs and tissues to determine the cause of death (Medico-Legal). (B) Fluid specimens (cytology): 1 - **Exfoliated cells: cells falling off tissues e.g.:
- in body fluids:** Sputum, urine, C.S.F. - in Effusion fluid: Ascetic fluid, pleural & pericardial effusions. - in Body discharges: Nipple and ear discharge.
- Brushing specimens: Cells collected from the lesion by brush as in cervicovaginal and buccal smears.
- Imprint smears. 2 - Fine needle aspirate (F.N.A): Taken from subcutaneous or deep- seated lesions of different organs for cytological examination e.g. breast, thyroid and lymph nodes.
CELL INJURY AND TISSUE DEPOSITS
The normal cell function requires a balance between physiologic demands and the limitations of cell structure and metabolic capacity. Maintenance of this steady physiological state is termed as homeostasis. More severe physiologic stress and some pathologic stimuli may lead to cellular adaptation, during which new but altered steady state is achieved. These changes include: hypertrophy, hyperplasia, atrophy and metaplasia. When the limits of adaptive response to stimuli are exceeded, or when the cell is exposed to more severe injurious agent, a sequence of pathologic events occurs, termed as cell injury. Cell injury is reversible up to a certain point, but if the stimulus is severe enough and prolonged, the cell suffers irreversible cell injury (cell death). Fig. (1-1): Cell response to stress and injurious stimuli.
- Cellular adaptation: New altered steady state in which the cells show increase or decrease in their number, size and function in response to prolonged stimuli. - Reversible cell injury (degeneration): The injury is not severe enough to kill the cell (sub-lethal stimuli). The cytoplasmic organelles are affected without affection of the nucleus. Such changes are reversible after cessation of the stimulus. - Irreversible cell injury (cell death): The injury is severe enough to kill the cell (lethal stimuli). It affects the cell organelles as well as the nucleus and leads finally to cell death. There are two morphologic patterns of cell death: a) Necrosis, and b) Apoptosis Definition: Biochemical, structural and morphological changes occurring in cells due to exposure to an injury. **The cell injury may be: 1 - Reversible (Degeneration). 2 - Irreversible (Cell death).
- Causes of cell injury: a-Genetic causes:** as thalassemia and inborn errors of metabolism. b-Acquired causes: Hypoxia: Important cause of cell injury and cell death due to reduction of aerobic oxidative respiration. Ischemia: Produce more rapid and severe injury than hypoxia due to reduction of both oxygen & glucose. Physical agents: Mechanical trauma, extremes of temperature (burns & deep cold), radiation and electric shock. Chemical agents: Strong acids & alkalis, glucose or salts in hypertonic concentration, poisons, air pollutants, insecticides, alcohol and drug abuse. Infectious agents: Viruses, bacteria, fungi and parasites. Immunological reaction: Hypersensitivity reactions and autoimmune diseases. Nutritional abnormalities: Both over- and under-nutrition lead to different types of cell injury. Metabolic diseases: e.g. diabetes mellitus.
A) CELL INJURY
**2) Disturbance of lipid metabolism: Fatty change.
- Disturbance of glycogen metabolism.
- Disturbance of mucopolysacraides metabolism.
- Hyaline change.**
1 - Disturbance of Water Metabolism
A) Cloudy Swelling : Definition: Common type of reversible cell injury characterized by mild intracellular accumulation of water. Causes: 1) Hypoxia and ischemia. 2) Exogenous toxins (like bacterial and chemical) and Endogenous toxins (like ketone bodies in diabetes mellitus). Usually affects the paranchymatous organs as liver, heart and kidney. These organs normally need high energy production so they will be the first to be affected. Pathogenesis: Damage of the mitochondria leads to decrease of ATP production. This leads to failure of Na/K pump (with intracellular accumulation of Na and water), and loss of K ions. Also, increase anaerobic metabolism leads to cell swelling. Pathology: Gross picture: The affected tissue or organ appears swollen, pale in color, soft in consistency with smooth surface and rounded borders. Microscopic picture: Cells are swollen showing pale eosinophilic granular cytoplasm due to accumulation of water and mitochondrial fragments. The nuclei are normal. Effects: kidney (Albuminuria), heart (Tachycardia), liver (Mild hepatomegaly). B) Hydropic (Vacuolar) Degeneration: Definition: Severe form of cloudy swelling with excessive accumulation of water in the cytoplasm and formation of large cytoplasmic vacuoles.
Examples: 1) Epidermal cells in burns. 2) Liver cells in viral hepatitis. 3) Beta cells of islets of Langerhans in early stage of D.M.
2 - Disturbance of Lipid Metabolism
A) FATTY CHANGE (steatosis): Definition: Abnormal excessive accumulation of triglycerides in the non fatty tissue, especially the parenchymatous organs. Causes: Hypoxia & ischemia. Bacterial toxins: e.g. diphtheria. Chemicals: CCL4, chloroform, Arsenic and alcohol. Malnutrition: Decrease lipotropic factors as choline and methionine which are essential for normal fat metabolism. 1 - Fatty change of liver: The liver is a major organ responsible for fat metabolism, so it is usually the first organ to be affected by fatty change. Pathogenesis of fatty change in the liver: 1) Excessive entry of free fatty acids in the cells. 2) Increased fatty acid synthesis from acetate. 3) Increased esterification of fatty acids to triglycerides due to increased activity of alpha- glycero-phosphate. 4) Decreased fatty acid oxidation. 5) Decreased apo-protein synthesis. 6) Impaired lipoprotein secretion from the liver.
3 - HEART:
Gross picture: The heart is soft, flabby and slightly dilated chambers. In early stages, some cardiac muscles bundles are affected by fatty change and appear yellow while other bundles are still normal and appear red in color giving the heart a mottled tigroid or tabby-cat appearance. In late stages (due to severe toxemia) the whole cardiac muscles appear yellow in color. Microscopic picture: Tiny fat globules are seen inside the sarcoplasm of cardiac muscle fibers. Effects: Weak contractility, tachycardia and heart failure.
3 - DISTURBANCE OF MUCOPOLYSACCHARIDES
(a) MUCOID DEGENERATION: Definition: Excessive accumulation of mucin in epithelial cells. Examples: In respiratory and intestinal mucosa in catarrhal inflammation. In cells of malignant tumors of stomach, colon, breast and ovaries (signet ring carcinoma). Microscopic picture: At first, mucin appears as multiple small vacuoles in the cytoplasm which later on accumulates into one large clear vacuole displacing the nucleus at one side of the cell membrane (signet-ring appearance). N.B: Alcian blue stain differentiates mucin from fat vacuoles.
(b) MYXOMATOUS DEGENERATION:
Definition : Excessive accumulation of muco-polysaccharides in the connective tissue stroma giving a soft gelatinous consistency. Examples : Skin in hypothyroidism (myxedema), Mesenchymal tumors as leiomyoma, fibroma and chondroma. Gross picture: The affected part is soft, transparent and gelly-like. Microscopic picture: Myxomatous tissue is formed of small oval, triangular, fusiform, elongated or star-shaped or stellate cells with intercommunicating long processes in a homogenous pale basophilic background.
4 - HYALINE CHANGE:
Definition: Any intracellular or extracellular alteration which gives a homogenous glassy pink appearance when the tissue sections are stained with Eosin.
Types:
A- Intracellular hyalinosis:
Russel bodies: Degenerated old plasma cells in chronic inflammation as rhinoscleroma. Corpora amylacia: In senile prostatic hyperplasia, the detached epithelial cells lining undergo hyaline degeneration and form pink structureless bodies in the acinar lumen. Beta cells of islets of Langerhans in late stages of D.M.
B- Extracellular hyalinosis:
Old scars, old thrombi and keloid. Blood vessels in benign hypertension and atherosclerosis. Mesenchymal tumors as leiomyoma and fibroma.
