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CELL INJURY

CELL INJURY. By Soheir Mahfouz. AIM OF COURSE. What are the types of injurious agents ( cause ) How they produce a lesion ( mechanism ) (2) the common ways the body responds to injury ( lesion/pathology ), (3) the common diseases & their complications ,

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CELL INJURY

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  1. CELL INJURY By Soheir Mahfouz

  2. AIM OF COURSE • What are the types of injurious agents (cause) • How they produce a lesion (mechanism) (2) the common ways the body responds to injury (lesion/pathology), (3) the common diseases & their complications, (4) how to predict the clinical implications of lesion. The key concepts in pathology will be the tunes that enable us to learn the "little details" that we need for patient care.

  3. Anatomy- Histology -Physiology NOrmal

  4. NORMAL LUNG- Anatomy

  5. NORMAL- Anatomy All the structures distal to the terminal bronchioles form the lung parenchyma which is made of functioning units known as Acinus (about 50.000). The exchange of gases between the blood and the alveolar air is done at the level of the acinus.

  6. NORMAL LUNG- Anatomy • Each acinus is composed of:A respiratory bronchiole • An alveolar duct • An alveolar sac and several alveoli  A cluster of 4 to 5 respiratory bronchioles and their acini form aPulmonary Lobule, each lobule is separated from the adjacent one by a thin septum of fibrous tissue, several lobules form a Pulmonary lobe, each lobe is demarcated from the adjacent one by intervening visceral pleura. 

  7. NORMAL LUNG- Histology The wall of the respiratory bronchioles is alternately thick and thin, the thick areas contain smooth muscle fibers and the thin areas form the wall of the alveolar sacs. The alveolar sacs are made of several alveoli separated from each other by the alveolar septum which is lined on either sides by epithelial cells, the pneumocytes.

  8. NORMAL LUNG The lining epithelial cells or pneumocytes are of two types:A layer of squamous cells, the more abundant pneumocytes type l, form a continuous lining interrupted only by the second type of cells - the septal cells or pneumocytes type ll (10%) that seem to be active in the production of surfactant and the repair mechanism of the damaged alveoli. In the alveolar septa are the capillaries. In areas the endothelial lining of the capillaries and the epithelial lining of the alveoli share a common basement membrane, in other areas, the two membranes are separated by a thin layer of loose connective tissue containing smooth muscle fibers, elastic fibers and few lymphocytes.

  9. NORMAL LUNG- Histology Macrophages, which in the lung are called dust cells, are also present within the alveolar spaces, they play an important role in the clearing of the alveolar spaces. The particulate matters that escape the protective mechanisms of the upper respiratory passages and reach the alveolar spaces are taken by the alveolar macrophages. The organic particles are digested by those macrophages but the inorganic material is transported by the macrophages in the interstitial tissue of the lungs where it is deposited.

  10. NORMAL LUNG- Histology The lymphatic drainage of the lung starts at the level of the respiratory bronchioles, the alveolar walls are devoid of lymphatic vessels.

  11. NORMAL LUNG- Histology P1 - Type I pneumocytes (large flat cells with a large surface area) P 2 - Type II pneumocytes (60% of cells in alveoli and secrete surfactant) E - Capillary endothelial cells C - Blood capillaries M - Alveolar macrophages

  12. alveoli BV BV Bronchiole

  13. Bronchus main

  14. Respiratory bronchiole

  15. NORMAL LUNG- Physiology The lungs, are not only the essential organs of respiration but they also perform few other cardinal functions in the general homeostasis of the human body. A metabolic function is exemplified by the production of surfactant. An endocrine function consists of secretion of certain hormone (ACE)  An excretory function that helps in the elimination of certain poisonous substances like alcohol and paraldehyde.

  16. 1- Injurious agents Etiology 2- Mechanism of injury Pathogenesis 3-Lesions Pathology Gross & microscopic 4-Diseases 5-Complications 6- Clinical presentation Cell Injury

  17. DAMAGE Normal cell +Injurious agent Damage—REVERSIBLE or IRREVE‎RSIBLE according to: +/- -Severity & type of injury Body Reaction -Cell type & extent of tissue injury -Duration

  18. CELL INJURY A) INTRACELLULAR ·REVERSIBLE: Adaptations-Degeneration - Metabolic accumulations & Storage disorders ·IRREVERSIBLE: Apoptosis & necrosis Neoplasms B)EXTRACELLULAR: Depositions-Abnormal pigmentation-Calcification

  19. INJURIOUS AGENTS A.ENVIRONMENTAL 1.Physical: heat –cold(frost bite) – Irradiation 2.Chemical: toxins – free radicals – acids – alkalis 3.Infections: bacteria, viruses, parasites 4.Immunological: self antigen(autoimmunity) – foreign proteins(antigens) 5.Circulatory: hypoxia or ischemia 6.Nutritional: protein calorie deficiency-vitamin deficiency 7.Mechanical: trauma 8.Hormonal

  20. INJURIOUS AGENTS B. GENETIC 1.Congenital : Down’s syndrome 2.Hereditary: metabolic enzyme disorders 3.Mutations: cancer C.MULTIFACTORIAL

  21. Mechanism of action of injurious agent: 1.Hypoxia: deficient oxygenation to tissues 2.Toxic: free radicals and other poisonous chemicals 3.Direct injury to cell

  22. Type of damage depends on tissue type, severity & duration of injurious agent 1.Type of tissue: • Labile (rapid regeneration e.g. bronchial epithelium) divide continuously producing reversible changes • Stable (parenchymatous organs & connective tissue) divide on injury producing reversible/irreversible damage • Permanent (never divides e.g. striated muscle –neurons) producing irreversible damage

  23. Type of damage depends on tissue type, severity & duration of injurious agent 2. Severity of injury & its duration: • Mild-moderate injury /severe short = reversible damage • Severe or moderate & prolonged injury = irreversible damage

  24. Subcellular response to injury(reversible & irreversible) First line of injury A-Mitochondria: Are respiratory organelles (ATP energy source) +source of some lipids. They are altered in cell injury Hydropic change -Number = Hypertrophy (cell size) -Number = Atrophy (cell size) -Large size =Hydropic change or Oncocytoma B-Rough Endoplasmic Reticulum(RER) Injury causes loss of ribosomes affecting protein synthesis, whilst dilatation of the RER produces vacuolar change

  25. MITOCHONDRIA & RER

  26. Subcellular response to injury(reversible & irreversible) Second line of injury 1. Smooth Endoplasmic Reticulum(SER): important in cell adaptation, lipid synthesis & drug storage Fatty change ×Drug tolerance swelling of SER hypertrophy ×Injury releases heat & shock (stress) proteins these can protect from tissue damage i.e. limitation of damage ×Lipid accumulation: fatty change & storage disorders

  27. SER

  28. Subcellular response to injury(reversible & irreversible) 2.Cytoskeletal abnormalities: result in loss of support with change in cell shape +  Motility ×Defective cell movement with migration of inflammatory cells & Phagocytosis ×Defective organelle movement with ciliary action e.g. respiratory infection Mitotic spindle causing infertility ×Defective intracellular accumulation of fibrils e.g. Alzheimer neurofibrillary tangles

  29. Subcellular response to injury(reversible & irreversible) 3. Lysosomal catabolism: they contain digestive enzymes Soluble matter a- Pinocytosis b- Phagocytosis Insoluble matterResidual body e.g. a-undigested debris (lipochrome) b-undigested pigment (tattoo) (coal dust in lung)

  30. Subcellular response to injury(reversible & irreversible) Final step Plasma & nuclear membrane damage occurs in cell death i.e. necrosis • Nucleus is important in mitosis & protein synthesis • Plasma membrane is important in carrying receptors that recognize environment & is responsible for the passage of molecules to & from the cell (phagocytosis-pinocytosis-selective permeability)

  31. ACCUMULATIONS & DEPOSITIONS IntracellularExtra+intracellularExtracellular Water =hydropic/vacuolar Fat =fatty change lipid storage disease atherosclerosis CHO =mucoid change myxomatous change Glycogen storage disease Protein =hyaline change hyaline change Amyloid Pigment=lipochrome Carbon (tattoo) Melanin Hemosiderin/hemochromatosis Jaundice (bilirubin) Calcium (dystrophic & metastatic)

  32. Intracellular FAT Fatty change occurs when cells which ordinarily take up a lot of lipid (heart, liver) cannot process it

  33. Extra+intracellular HYALINE HYALINE: Any substance (intracellular or extracellular) that stains a homogeneous (say "homo-JEAN-yuss") pink on routine H&E stains. • Mallory's alcoholic hyaline • Collagen can hyalinize, especially in keloids / hypertrophic scars and other abnormal fibrous proliferations

  34. Extracellular AMYLOID

  35. I) Reversible cell changes Adaptations Intracellular & extracellular accumulations/depositions

  36. I) Reversible cell changesCELL ADAPTATION of growth & differentiation A) PHYSIOLOGIC Changes that occur under the effect of hormones e.g. breast enlargement during lactation  B) PATHOLOGIC 1) Synthesis of new proteins e.g. stress proteins 2) Over production of specific proteins e.g. in chronic inflammation with collagen & extracellular matrix proteins 3) Adaptation in cell growth

  37. ADAPTATIONS Atrophy =  cell size resulting in weight & size of organ senile / atrophic emphysema Hypertrophy = cell size resulting in organ weight & size muscle wall of arteries in pulm hypertension Hyperplasia = cell number resulting in organ weight & size mucous gland hyperplasia inbronchial asthma Metaplasia = cell number & change in cell type e.g. columnar cells changes to squamous or vice versa (see growth disturbances) bronchial epithelium in bronchiectasis Dysplasia= Disordered proliferation bronchial epithelium precancerous in chronic irritation

  38. ATROPHY A) Physiologic: aging results in  organ size & function e.g. Brown atrophy of heart (see lipochrome pigment) B) Pathologic: Mechanism & types 1)Hormonal atrophy(endocrinal) Pituitary deficiency hormone e.g. atrophy of thyroid, gonads & adrenals 2) Vascular atrophy Tumor causing pressure/narrow blood vesselblood & O2 leads to atrophy

  39. ATROPHY 3) Pressure atrophy: same mechanism as vascular atrophy 4) Neuropathic atrophy e.g. poliomyelitis Reflexes & activity with  function with atrophy of muscle 5)Disuse atrophy: e.g. Blocked duct of a gland Muscles after prolonged immobilization in fracture bone

  40. ATROPHY

  41. HYPERTROPHY HYPERTROPHY:  size & weight of organ due to  size of its cells Physiologic: Pregnant uterus due to hormone stimulation & muscle hypertrophy in athletes Pathologic: Cardiac muscle hypertrophy in hypertension & valve disease & urinary bladder hypertrophy in bladder neck obstruction BV of pulmonary hypertension

  42. HYPERTROPHY Hypertrophy

  43. HYPERPLASIA HYPERPLASIA:  size & weight of organ due to  number of its cells. Hyperplasia can occur in any cell type capable of division Physiologic 1-hormonal hyperplasia =endometrium after menstruation due to estrogen stimulation 2-compensatory = bone marrow hyperplasia after hemorrhage Pathologic 1-hormonal = endometrial hyperplasia in repeated anovulatory cycles & benign prostatic hyperplasia 2-lymphoid hyperplasia in response to antigenic stimulation

  44. HYPERPLASIA

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