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Immuno LEC

This document defines cellular injury, adaptation, and the inflammatory response. It discusses how cells can adapt through atrophy, hypertrophy, hyperplasia, dysplasia, or metaplasia. Inflammation is the body's response to injury and involves vascular changes, increased permeability, and cellular events. The goals of inflammation are to neutralize the injurious agent, control the damage, and eliminate it. Healing and repair begin during inflammation through regeneration of the same cell type or replacement with connective tissue.

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0% found this document useful (0 votes)
53 views9 pages

Immuno LEC

This document defines cellular injury, adaptation, and the inflammatory response. It discusses how cells can adapt through atrophy, hypertrophy, hyperplasia, dysplasia, or metaplasia. Inflammation is the body's response to injury and involves vascular changes, increased permeability, and cellular events. The goals of inflammation are to neutralize the injurious agent, control the damage, and eliminate it. Healing and repair begin during inflammation through regeneration of the same cell type or replacement with connective tissue.

Uploaded by

Menggay SanDiego
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© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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DEFINITION AND CAUSE OF CELLULAR INJURY AND ADAPTATION

HOMEOSTASIS

HANDLE NORMAL PHYSIOLOGIC STRESS Adaptive Pumping iron Enlargement of muscle Exceed - Cell injury Prolonged Irreversible cell injury Cell Death Causes of Cell Injury and Cell Death A. Hypoxia 1. Loss of blood supply (ischemia) i. When arterial flow is impeded by atherosclerosis or thrombi 2. Inadequate blood supply due to cardio-respiratory failure 3. Loss of the oxygen carrying capaci ty of the blood as in anemia B. Physical Agents 1. extremes of high temperature 2. Extremes of temperature

i. Vasoconstriction ii. Blood flow become sluggish iii. Clot formation iv. Also causes cell crystallization to bursting of cell 3. Radiation and electrical shock 4. mechanical Trauma i. mass hits body, collision leading to destruction of cell integrity, blood supply and blood loss C. Nutritional Imbalance 1. deficiency or excess D. Infectious agents 1. viruses, bacteria, fungi 2. Viruses E. Disordered immune response 1. functions include: i. detecting foreign bodies ii. distinguishes self from non self iii. destroying the non self F. Chemical agents 1. acids, heavy metals, poisons G. Genetic disorder 1. sickle cell 2. cystic fibrosis 3. hemophilia CELLULAR ADAPTATION A. ATROPHY  Shrinkage in the size of the cell by loss of cell substance resulting to decrease in organ size  Possible causes: i. Decrease workload or use ii. Loss of inervation o Poliomyelitis, paralysis iii. Diminished blood supply

iv. Inadequate nutrition v. Loss of endocrine stimulation o Menopause vi. Aging  Common affected structures i. Skeletal muscles ii. Secondary sex organs iii. Heart brain B. Hyperthrophy  Refers to the increase in the size of the cells  Resulting in increase in the size of the organ  Hyperthrophied Organ i. No new cells, just larger cells ii. NOT to an increased intake of fluid o Cellular swelling iii. Synthesis of more structural components  Common Sites i. Skeletal muscles ii. Cardiac muscles  Physiologic uterus and athlete  Pathologic diseases C. Hyperplasia  Is the increase in the number of cells in an organ or tissue  Cell mitosis  Can occur if the cellular population is capable of synthesizing DNA  Not all have the property  CAN: i. Epidermis ii. Intestinal epithelium iii. Hepatocytes iv. Bone marrow  CANT:

i. Nerve cells ii. Cardiac and skeletal muscles  Hormonal hyperplasia i. Breast in adolescence  Compensatory hyperplasia i. Blood loss ii. Liver is removed D. Dysplasia  Is the change in the appearance of the cell after they have been subjected to chronic irritation  Tendency to become malignant  Not an adaptive process but considered because it is closely related to hyperplasia E. Metaplasia  Is a cell transformation in which a highly specialized cell is replaced or changed to a less specialized cell Ex: Ciliated columnar epithelium lining of the bronchi Squamous epithelium (more resistant) Loss of mucous and cilia CELLULAR RESPONSE TO INJURY Inflammation o Is the reaction of vascularized living tissue to an injury Purpose: 1. neutralize 2. Control 3. Eliminate the offending agent o For the preparation of repair Without Inflammation

o Infections would go unchecked o Wounds would never heal Inflammation is Harmful o Rheumatoid arthritis, hypersensitivity reaction , asthma o Can lead to scars, to obstruction and limit mobility Inflammatory Response (3 changes that occurs) 1. Changes in the micocirculation Constrciction 3-5 seconds Vasodilatation Increased blood flow Heat (calor)and redness (rubor) Increased hydrostatic pressure Transudation of Fluid Slowing of circulation Increase viscosity of blood 2. Increased vascular permeability Leaking plasma fluids Swelling (Tumor) Pain (Pressure of fluid or swelling on nerve
Endings, irritation of nerve endings by bradykinin)

Loss of Function Chemical Mediators: a. Histamine and kinins o Is present in many tissues but concentrated in the mast cells

o Responsible for vasodilation and increase vascular permeability o Kinins attract neutrophils b. Prostaglandins o Increase permeability Plasma fluids o Liquid portion of the blood o 90% water o 10% plasma proteins, fibrinogen, clotting factors, nutrients and enzymes Plasma Proteins: Albumin main component of plasma proteins - Maintain colloidal osmotic pressure Globulins alpha- transport of globulins and clotting factor The liver Beta Gamma- immunoglobulins or antibodies 3. Cellular Events o Leukocytic exudation and phagocytosis o Principally the neutrophils and monocytes PROCESS: a. Margination central - stagnation - in contact with endothelium b. Adhesion c. emigration and chemotaxis o Uni directional migration of cells towards an attractant d. Phagocytosis d.1. recognition and attachement o Involves the coating of IgG antibody (Opsonins) d.2. engulfment o Enclosure of the particle

SYSTEMIC RESPONSE TO INFLAMMATION - Inflammatory response occur at the site of injury but systemic response can occur 1. Fever o Endogenous pyrogens o Substances that cause fever released by neutrophils 2. Leukocytosis o Increase in the neutrophils 4. Non specific symptoms o Malaise, decrease appetite, weakness TYPES OF INFLAMMATION A. Acute Inflammation o Usually last less than 2 weeks o 2 characteristic of inflammation  Local vascular and exudative changes PLUS emigration of leukocytes (STEREOTYPIC) b. Chronic Inflammation o Longer and less uniform o Can take months to years 3 Ways Which They Arise a. It may follow acute inflammation - Persistence of the stimulus (Infection) - Interference in the normal process of healing b. Repeated bout of acute inflammation inflammation necrosis fibrosis - repair c. Chronic inflammation may begin insidiously lowgrade does not initiate the normal acute inflammatory response - Tubercle bacilli, viral infection

HEALING AND REPAIR o BEGINS in the process of inflammation o END RESULTS IN, repair, replacement of dead or damaged cells Two Distinct Process 1. regeneration 2. replacement of connective tissue REGENERATION o Replacement of the injured cell/ tissue by parenchymal cells of the same type o Residual trace or no trace of previous injury Cells 3 Division Groups a. LABILE o Continue to proliferate throughout life o Worn out- replaced Ex: Stratified squamous surface of the skin, oral cavity, vagina and cervix Excretory glands: Salivary glands, pancreas, biliary tract Columnar epithelium of the gastric mucosa, uterus, fallopian tube and the Urinary tract b. Stable Cells o Demonstrate a low normal level of replication o But can undergo rapid division in response to variety of stimulus Ex: Parenchymal cells of all grandular organs (liver, kidney, pancreas) o Does not follow normal restitution of the normal structure o Framework destroyed disorganized proliferation

c. Permanent o Cannot reproduce o Ex. Skeletal and cardiac muscles, neurons Healing by Replacement o Repair by Connective tissue, GRANULATION o 24 hours- macrophages digest invading organism (survived from neutrophils) o 3 days fibroblast and vascular and endothelial cells to form Granulation Angiogenesis (Neurovascularization) TYPES OF WOUND HEALING 1. Primary Union/ first intention o Wound is clean and dry and edges are approximated o Little scar is formed, healing within a week o Dry sterile dressing 2. Secondary Union/ Secondary Intention o The wound is larger and gaping and has necrosis or dead materials o Ulcerations and abscess formation o Longer time, more scar formation loss of special function o Cicatrix 3. Third intention IMMUNE SYSTEM

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