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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.Hypoxia1. Loss of blood supply (ischemia)

i. When arterial flow is impeded by atherosclerosisor thrombi

2. Inadequate blood supply due to cardio-respiratoryfailure

3. Loss of the oxygen carrying capacity of the blood as inanemia

B.Physical Agents1. extremes of high temperature2. Extremes of temperature

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i. Vasoconstrictionii. Blood flow become sluggishiii. Clot formationiv. Also causes cell crystallization to bursting of cell

3. Radiation and electrical shock4. mechanical Trauma

i. mass hits body, collision leading to destruction ofcell integrity, blood supply and blood loss

C. Nutritional Imbalance1. deficiency or excess

D.Infectious agents1. viruses, bacteria, fungi2.

VirusesE.Disordered immune response

1. functions include:i. detecting foreign bodiesii. distinguishes self from non selfiii. destroying the non self

F. Chemical agents1. acids, heavy metals, poisons

G.Genetic disorder1. sickle cell2. cystic fibrosis3. 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 useii. Loss of inervation

o Poliomyelitis, paralysisiii. Diminished blood supply

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iv. Inadequate nutritionv. Loss of endocrine stimulation

o Menopausevi. Aging

Common affected structuresi. Skeletal musclesii. Secondary sex organsiii. 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 cellsii. NOT to an increased intake of fluido Cellular swelling

iii. Synthesis of more structural components Common Sites

i. Skeletal musclesii. 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. Epidermisii. Intestinal epitheliumiii. Hepatocytesiv. Bone marrow

CANT:

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i. Nerve cellsii. Cardiac and skeletal muscles

Hormonal hyperplasiai. Breast in adolescence

Compensatory hyperplasiai. Blood lossii. 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 isclosely 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 injuryPurpose:1. neutralize2. Control3. Eliminate the offending agent

o For the preparation of repairWithout Inflammation

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o Infections would go uncheckedo Wounds would never heal

Inflammation is Harmful

o Rheumatoid arthritis, hypersensitivity reaction, asthmao Can lead to scars, to obstruction and limit mobility

Inflammatory Response (3 changes that occurs)

1. Changes in the micocirculation

Constrciction Vasodilatation

3-5 seconds 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 nerveEndings, irritation of nerve endings by bradykinin)

Loss of Function

Chemical Mediators:

a. Histamine and kinins

o Is present in many tissues but concentrated in themast cells

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o Responsible for vasodilation and increase vascularpermeability

o Kinins attract neutrophilsb. Prostaglandins

o Increase permeabilityPlasma fluids

o Liquid portion of the bloodo 90% watero 10% plasma proteins, fibrinogen, clotting factors,

nutrients and enzymes

Plasma Proteins:

Albumin main component of plasma proteins- Maintain colloidal osmotic pressureGlobulins alpha- transport of globulins and clotting factor

The liver

Beta

Gamma- immunoglobulins or antibodies

3. Cellular Events

o Leukocytic exudation and phagocytosiso Principally the neutrophils and monocytesPROCESS:

a. Margination

central - stagnation - in contact with endothelium

b. Adhesion

c. emigration and chemotaxis

o Uni directional migration of cells towards anattractant

d. Phagocytosis

d.1. recognition and attachement

o Involves the coating of IgG antibody (Opsonins)d.2. engulfment

o Enclosure of the particle

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SYSTEMIC RESPONSE TO INFLAMMATION

- Inflammatory response occur at the site of injury but systemic

response can occur

1. Fever

o Endogenous pyrogenso Substances that cause fever released by

neutrophils

2. Leukocytosis

o Increase in the neutrophils4. Non specific symptoms

o Malaise, decrease appetite, weakness

TYPES OF INFLAMMATIONA. Acute Inflammation

o Usually last less than 2 weekso 2 characteristic of inflammation

Local vascular and exudative changes PLUSemigration of leukocytes (STEREOTYPIC)

b. Chronic Inflammation

o Longer and less uniformo Can take months to years3 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 insidiouslylowgrade does not initiate the normal acute

inflammatory response

- Tubercle bacilli, viral infection

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HEALING AND REPAIR

o BEGINS in the process of inflammationo END RESULTS IN, repair, replacement of dead or

damaged cells

Two Distinct Process

1. regeneration2.replacement of connective tissue

REGENERATION

o Replacement of the injured cell/ tissue by parenchymalcells of the same type

oResidual trace or no trace of previous injury

Cells 3 Division Groups

a. LABILE

o Continue to proliferate throughout lifeo Worn out- replacedEx:

Stratified squamous surface of the skin, oral cavity,

vagina and cervix

Excretory glands: Salivary glands, pancreas, biliarytract

Columnar epithelium of the gastric mucosa, uterus,

fallopian tube and the Urinary tract

b. Stable Cells

o Demonstrate a low normal level of replicationo 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 normalstructure

o Framework destroyed disorganized proliferation

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c. Permanent

o Cannot reproduceo Ex. Skeletal and cardiac muscles, neurons

Healing by Replacemento Repair by Connectivetissue,GRANULATIONo 24 hours- macrophages digest invading organism

(survived from neutrophils)

o 3 days fibroblast and vascular and endothelial cells toform

Granulation

Angiogenesis (Neurovascularization)

TYPES OF WOUND HEALING

1. Primary Union/ first intention

o Wound is clean and dry and edges are approximatedo Little scar is formed, healing within a weeko Dry sterile dressing

2. Secondary Union/ Secondary Intention

o The wound is larger and gaping and has necrosis or deadmaterials

o Ulcerations and abscess formationo Longer time, more scar formation loss of special functiono Cicatrix

3. Third intention

IMMUNE SYSTEM