This document provides an outline and notes for a pathology lecture covering general pathology topics over two days. Day 1 will discuss introduction to pathology, cellular adaptation, tissue injury, inflammation, hemostasis, thrombosis and infarcts, and neoplasia. Day 2 will cover common systemic diseases and radiologic correlation for diagnostic radiology. The notes provide definitions and explanations of key pathology terms including disease, etiology, pathogenesis, diagnosis, prognosis, epidemiology, and clinical manifestations. Cellular responses such as atrophy, hypertrophy, hyperplasia, dysplasia and metaplasia are also explained. Mechanisms of cellular injury including necrosis, types of necrosis, and causes of cell injury are detailed. An overview of the
This document provides an outline and notes for a pathology lecture covering general pathology topics over two days. Day 1 will discuss introduction to pathology, cellular adaptation, tissue injury, inflammation, hemostasis, thrombosis and infarcts, and neoplasia. Day 2 will cover common systemic diseases and radiologic correlation for diagnostic radiology. The notes provide definitions and explanations of key pathology terms including disease, etiology, pathogenesis, diagnosis, prognosis, epidemiology, and clinical manifestations. Cellular responses such as atrophy, hypertrophy, hyperplasia, dysplasia and metaplasia are also explained. Mechanisms of cellular injury including necrosis, types of necrosis, and causes of cell injury are detailed. An overview of the
This document provides an outline and notes for a pathology lecture covering general pathology topics over two days. Day 1 will discuss introduction to pathology, cellular adaptation, tissue injury, inflammation, hemostasis, thrombosis and infarcts, and neoplasia. Day 2 will cover common systemic diseases and radiologic correlation for diagnostic radiology. The notes provide definitions and explanations of key pathology terms including disease, etiology, pathogenesis, diagnosis, prognosis, epidemiology, and clinical manifestations. Cellular responses such as atrophy, hypertrophy, hyperplasia, dysplasia and metaplasia are also explained. Mechanisms of cellular injury including necrosis, types of necrosis, and causes of cell injury are detailed. An overview of the
This document provides an outline and notes for a pathology lecture covering general pathology topics over two days. Day 1 will discuss introduction to pathology, cellular adaptation, tissue injury, inflammation, hemostasis, thrombosis and infarcts, and neoplasia. Day 2 will cover common systemic diseases and radiologic correlation for diagnostic radiology. The notes provide definitions and explanations of key pathology terms including disease, etiology, pathogenesis, diagnosis, prognosis, epidemiology, and clinical manifestations. Cellular responses such as atrophy, hypertrophy, hyperplasia, dysplasia and metaplasia are also explained. Mechanisms of cellular injury including necrosis, types of necrosis, and causes of cell injury are detailed. An overview of the
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PATHOLOGY LECTURE
SERIES Butch Dumdum
Outline Day 1 (General Pathology) Introduction, Cellular Adaptation,Tissue Injury Inflammation (Acute and Chronic) Hemostasis,Thrombosis, and Infarct Neoplasia
Day 2 (Systemic Pathology)
Common systemic diseases (Pathological basis of disease) Radiologic Correlation (Diagnostic Radiology)
Introduction, Cell & Tissue
Damage
Pathology Definition Pathology is the study (logos) of suffering/diseases (pathos) Involves basic medical sciences and clinical practice to investigates of the causes (etiology) of the diseases and the mechanism (pathogenesis)
Disease / dis-ease Disease is a condition in which the presence of an abnormality of the body causes a loss of normal health Idiopathic no identifiable causes Iatrogenic occur as a result from medical treatment Congenital disease existing at birth or before birth, involves in the development of fetus Acquired - develops post fetally Nosocomial due to being in a hospital environments 6
Etiology Refers to the study of the cause of the disease General categories of etiological agents; genetic abnormalities, infective agents, chemical, radiation, mechanical trauma, malnutrition
Pathogenesis Is a mechanism of the disease which etiology operates to produce the pathological and clinical manifestation For examples inflammation, degeneration, immune response
Diagnosis Refers to the process of attempting to determine or identify a possible disease or disorder.
Prognosis Refers to the expected outcome of a disease. 9
Complication and sequalae
Complication is the onset of the disease in a person who is already coping with another existing disease. Sequalae unwanted outcomes of having disease or are the result of trauma
10
Clinical Manifestation Are the signs and symptoms or evidence of disease Signs objective alteration that can be observe or measured by another person; pulse rate, blood pressure, Temperature etc Symptoms subjective experiences reported by the person, complains such as pain, nausea, vomiting etc 11
Epidemiology Is the study of tracking patters of disease occurrence and transmission among populations and by geographic areas. Incidence of a disease is the number of new cases occurring in specific time of period Prevalence of a disease is the number of existing cases within a populations during the specific time
12
Prefixes and Suffixes and
Roots Root- the foundation of the word Prefix place before the root to modify its meaning Suffix places after root to modify and give essential meaning to the root 1. Hyperlipoproteinemia Prefix : hyper (higher) Roots : lipoprotein Suffix : -emia (blood condition) 13
Cells degeneration, Cell Death CELLS ADAPTATION Injuries
NORMAL CELLS
Injurie s
CELLS DEGENERATION
Injuries CELLS DEATH (NECROSIS/APOPTOSI S 15
Cellular Adaptation Under normal conditions, cells must constantly adapt to changes is their environment (physiological, pathological). Atrophy Hypertrophy Hyperplasia Dysplasia Metaplasia 16
Atrophy
Shrinkage of the size of the
cells by the lost of the cells substance. The entire tissue or organs diminishes in size and function May be due to decrease in workload, lost of nerve innervations, Lack of blood supply, inadequate nutrition, lost of endocrine stimulation and aging process.
17
Hypertrophy Increase the size of the cells and consequently the size of the organs Increased the synthesis of structural protein and organelles Can be physiologic (ex;increase workload during exercise, uterine myometrium during pregnancy) and pathologic (hypertrophy of myocardium hypertension/aortic valve disease)
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Hyperplasia Increase the number of cells in an organ or tissue. (increase rate of cellular division) Hypertrophy and hyperplasia are closely related (exp : gravid uterus) Can be compensatory hyperplasia (exp: liver), hormonal hyperplasia (exp: uterus, breast) and pathological (exp: endometrium) 19
Metaplasia Is a reversible change in which one adult cell type is replaced by another cell type. Adaptation of cells that sensitive to particular stress to cell types better able to withstand the adverse of environment
20
21
Dysplasia Not a true cellular adaptation Atypical hyperplasia Abnormal change in the size, shape and organization of mature cells Strongly associated with common neoplastic growth Exp: CIN cervical intraepithelial neoplasia, hip dysplasia 22
Nonlethal injury may produce cell degeneration Manifested as a abnormality of biochemical function, structural changes or combination. Its reversible but may become irreversible (necrosis/apoptosis) May produce clinical disease. 25
Necrosis (Lethal Injury)
Definition unprogrammed cell death and living tissues. (opposite to apoptosis) Irreversible Accompanied with by biochemical and morphological changes Due to hypoxia, chemical substances, free radical, immunologic response, infections etc 26
Stages of Necrosis Early changes : morphologically normal Nuclear changes : pyknosis chromatin clumps into coarse strands, nucleus become shrunken Cytoplasmic changes : denaturation of cytoplasmic protein and lost of ribosomes, swelling of mitochondria and disruption of organelle membranes and autolysis occur via lysosomes 27
Type of Necrosis Different cells shows different morphologic changes after they undergo necrosis. Base on that necrosis can be classified into: 1. Coagulative necrosis 2. Liquefactive necrosis 3. Caseous / gummatous necrosis 4. Fat necrosis 5. Gangrenous Necrosis 29
Coagulative Necrosis Typically occur in solid organ; heart, kidney, adrenal glands Due to hypoxia (maybe from severe ischemia or chemical) Normally, this necrotic cells retains its cellular outline. Denaturation of protein albumin causes coagulation.
30
Liquefactive Necrosis Normally occurs in CNS which affects neuron and neuroglia cells Associated with focal bacterial and fungus infections The affected cells completely digest by hydrolytic enzymes thus changes the tissue into liquid viscous mass. 31
Caseous Necrosis Caseous cheese like appearance Associated with tuberculous pulmonary (TB) infection, esp by Mycobacterium Tuberculosis 32
Fat Necrosis Occur in pancreas, breast and other abdominal structures Caused by lipases enzymes which break down triglycerides (lipid) into fatty acids and glycerol Fatty acids and glycerol then combine with Ca, Mg, Na to form Calcium Soaps (Saponification) The necrotic tissue appears opaque and chalk white.
33
Gangrenous Necrosis (gangrene)
Extensive tissue necrosis Divide into two; dry and wet Dry occurs in extremities as a results of ischemic coagulative necrosis due to arterial obstruction Wet occurs in extremities and internal organ as a results of liquefactive necrosis due to bacterial infection. Gas necrotic tissue infected by clostridium perfringes 34
Oxygen deprivation Hypoxia oxygen deficiency Due to ischemia lost/lack of blood supply (due to arterial blockage or reduce venous drainage) Hypoxia also can occurs via: Lack of oxygen inside blood Reduction in oxygen carrying capacity in RBC (anemia) Carbon monoxide poisoning 36
Chemical agents Most of the chemical substances can cause cell injury For example : poisons, air pollutants, insecticides, CO, asbestos, ethanol, therapeutics drugs etc This agents can cause cell death by: Altering membrane permeability Altering osmotic homeostasis Altering integrity of an enzyme 37
Immunologic Reactions Autoimmune disease immunity against its own tissues . For examples SLE, Rheumatoid Arthritis etc
39
Genetic Defects Abnormalities to the genomes mutation This chromosome anomaly is associated with missing, or irregularities or extra in portion of chromosomal DNA Syndrome Down, Alzheimer's Disease, Huntingtons Disease etc 40
Nutritional Imbalance Cause by directly or indirectly lack of essential nutrients (malnutrition) Or it maybe related to excessive of food intake (Diabetic Mellitus) For example protein deficiency Kwashiorkor, Marasmus Calcium deficiency osteoporosis Vitamin C - Scurvy 41
Physical Agents Trauma, extremes of temperature, radiation, electrical shock all have wide ranging effects on cells.
42
Aging Aged cells become larger, less able to divide and multiply Lose their ability to functions, or function abnormally.
43
Inflammation Acute vs Chronic
SEQUENCE OF EVENTS NORMAL HISTOLOGY VASODILATATION INCREASED VASCULAR PERMEABILITY LEAKAGE OF EXUDATE MARGINATION, ROLLING, ADHESION TRANSMIGRATION (DIAPEDESIS) CHEMOTAXIS PMN ACTIVATION PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion) TERMINATION 100% RESOLUTION, SCAR, or CHRONIC INFLAMMATION are the three possible
INFECTIOUS PHYSICAL CHEMICAL Tissue Necrosis Foreign Bodies (FBs) Immune responses, or complexes
Vascular Changes Changes in Vascular Flow and Caliber Increased Vascular Permeability
INCREASED PERMEABILITY
DILATATION Endothelial gaps Direct Injury Leukocyte Injury Transocytosis (endo/exo)
LEAKAGE OF PROTEINACEOUS FLUID (
EXUDATE,
NOT TRANSUDATE)
EXTRAVASATION of PMNs
MARGINATION (PMNs go toward wall) ROLLING (tumbling and HEAPING) ADHESION TRANSMIGRATIO N (DIAPEDESIS)
ADHESION MOLECULES (glycoproteins) affecting ADHESION and TRANSMIGRATION
SECRETINS (from endothelial cells) INTEGRINS (from many cells)
CHEMOTAXIS PMNs going to the site of injury AFTER transmigration
LEUKOCYTE ACTIVATION triggered by the offending stimuli for PMNs to: 1) Produce eicosanoids (arachidonic acid derivatives) Prostaglandin (and thromboxanes) Leukotrienes Lipoxins
Lipoxins INHIBIT chemotaxis Vasodilatation Counteract actions of leukotrienes
Platelet-Activating Factor (PAF) Phospholipid From MANY cells, like eicosanoids ACTIVATE PLATELETS, powerfully
CYTOKINES/CHEMOKIN ES CYTOKINES are PROTEINS produced by MANY cells, but usually LYMPHOCYTES and MACROPHAGES, numerous roles in acute and chronic inflammation
TNF, IL-1, by macrophages
CHEMOKINES are small proteins
which are attractants for PMNs (>40)
NITRIC OXIDE Potent vasodilator Produced from the action of nitric oxide synthetase from arginine
LYSOSOMAL SECONDARY CONSTITUENTS PRIMARY Also called AZUROPHILIC, or NONspecific Myeloperoxida se Lysozyme (Bact.) Acid Hydrolases
Increased Platelet Count and their adhesiveness. Decreased coagulation inhibitots Antithrombin III
Alteration in the Blood flow
Turbulance and Stasis Platelets near endothelial lining.
Morphology Sites Heart , Arteries, Veins, Capillaries. Arterial Thrombi Effect is Ischemia Venous Thrombi Effect is Embolism
Gross Various shapes n
sizes. Arterial thrombi White and mural Venous thrombi Red and occlusive M/E : Lines of Zahn Arterial Vs Venous thrombi
Fates of Thrombi Resolution Organisation Propagation Embolism
Predisposing factors : Genetic Deficiency of Antithrombin, Protein C and S , Fibrinolysis . Acquired Old age , Prolonged Bed rest ,Immobilisation , oral contraceptives , smoking , Trauma fracture burns , Atherosclerosis , Varicose veins, Cancers
NEOPLASIA
Neoplasia:
Neo + Plasia New + Growth.
Tumour Swelling any swelling* Clinically tumour = neoplasm (technically incorrect..!)
Willis definition: A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissue and persists in the same manner after cessation of the stimuli which evoked the change
Cell division without control
Irreversible DNA damage, resulting in autonomous growth of abnormal cells *
Cell population / Growth Control:
Proliferation Differentiation Apoptosis *
Normal Neoplasia Stem cell
Benign - Malignant Carcinogen Initiator + Promotor C
