CELL Pathology Ppt

CELLCELL It is a structural & functional unit of bodyIt is a structural & functional unit of body Cellular physiology characterized by Cellular physiology characterized by Closed interdependence of various components & Closed interdependence of various components &

activities.activities. Balancing control mechanism aimed at maintaining Balancing control mechanism aimed at maintaining

constant condition.constant condition. Very efficient compensatory & repair mechanisms to Very efficient compensatory & repair mechanisms to

minimize the damageminimize the damage

CELL INJURYCELL INJURY EtiologyEtiology Hypoxia & ischemia- Reduced supply of blood.Hypoxia & ischemia- Reduced supply of blood. Physical agents- Mechanical trauma, thermal trauma.Physical agents- Mechanical trauma, thermal trauma. Chemicals & drugs- Poisons like cyanides, arsenic, Chemicals & drugs- Poisons like cyanides, arsenic,

strong acids & alkali's environmental pollutants.strong acids & alkali's environmental pollutants. Microbial agents- Fungi, bacteria & protozoa.Microbial agents- Fungi, bacteria & protozoa. Immunological agents- Hypersensitivity reaction, Immunological agents- Hypersensitivity reaction,

anaphylactic reaction.anaphylactic reaction. Nutritional agents- Deficiency of nutrients, excess of Nutritional agents- Deficiency of nutrients, excess of

nutriets. nutriets.

PATHOGENESIS PATHOGENESIS Of reversible cell injuryOf reversible cell injury If ischemia of short time effects are reversibleIf ischemia of short time effects are reversible Sequential changes in reversible cell injurySequential changes in reversible cell injury Decrease cellular ATP.Decrease cellular ATP. Damage to plasma membrane sodium pump.Damage to plasma membrane sodium pump. Reduced protein synthesis.Reduced protein synthesis. Ultra structural changes-Ultra structural changes-1)Endolasmic reticulum-distention of cisternae. 1)Endolasmic reticulum-distention of cisternae. 2)Mitochondria- swelling. 2)Mitochondria- swelling. 3)Plasma membrane- loss of microvilli & focal projection of 3)Plasma membrane- loss of microvilli & focal projection of

cytoplasm.cytoplasm.4)Nucleolus- segregation of granular fibrilar components & 4)Nucleolus- segregation of granular fibrilar components &

reduced RNA synthesis.reduced RNA synthesis.

PATHOGENESISPATHOGENESIS Of irreversible injuryOf irreversible injury Mitochondrial dysfunctionMitochondrial dysfunction Membrane damage-Membrane damage-1)Accelarated degradation of membrane phospholipids.1)Accelarated degradation of membrane phospholipids.2)Cytoskeletal damage.2)Cytoskeletal damage.3)Breakdown of lipid.3)Breakdown of lipid.4)Reperfusion damage.4)Reperfusion damage. Hydrolytic enzyme-damage to lysosomal membrane followed Hydrolytic enzyme-damage to lysosomal membrane followed

by liberation of hydrolytic enzyme which on activation causes by liberation of hydrolytic enzyme which on activation causes enzymatic digestion of cellular components & induce nuclear enzymatic digestion of cellular components & induce nuclear changes & hence cell death.changes & hence cell death.

Serum estimation of liberated intracellular enzyme.Serum estimation of liberated intracellular enzyme.

CELL DEATHCELL DEATH AutolysisAutolysis Disintegration of cell by its own hydrolytic enzyme Disintegration of cell by its own hydrolytic enzyme

liberated from lysosomes. It can occur in living body liberated from lysosomes. It can occur in living body surrounded by inflammatory reaction or postmortem surrounded by inflammatory reaction or postmortem change where complete absence of inflammatory change where complete absence of inflammatory response. It is rapid in some tissues e.g. Pancreas, response. It is rapid in some tissues e.g. Pancreas, gastric mucosa. Intermediate in tissues e.g. Heart, gastric mucosa. Intermediate in tissues e.g. Heart, liver & kidney. It is slow in fibrous tissue. liver & kidney. It is slow in fibrous tissue. Morphologically it is identified by homogenous & Morphologically it is identified by homogenous & eosinophilic cytoplasm with loss of cellular details & eosinophilic cytoplasm with loss of cellular details & remains of cell debris. remains of cell debris.

APOPTOSISAPOPTOSIS Programmed death of cell. In this process normal abnormal or Programmed death of cell. In this process normal abnormal or

unwanted cells are eliminated. It is different from necrosis.unwanted cells are eliminated. It is different from necrosis. Apoptosis in health-Apoptosis in health-1)metamorphosis of tadpole to frog. 1)metamorphosis of tadpole to frog. 2)loss of auto reactive response of T cells in thymus preventing 2)loss of auto reactive response of T cells in thymus preventing

autoimmune attack.autoimmune attack.3)atrophy & involution often in withdrawal of hormones.3)atrophy & involution often in withdrawal of hormones. Apoptosis in disease-Apoptosis in disease-1)Irradiation.1)Irradiation.2)virus infection.2)virus infection.3)Action of cytotoxic T cells e.g. in rejection of transplant organ.3)Action of cytotoxic T cells e.g. in rejection of transplant organ.4)in tumour apoptosis & proliferation rate control the rata of 4)in tumour apoptosis & proliferation rate control the rata of

tumour growth.tumour growth.

NECROSISNECROSIS It is focal death of cell along with degeneration of It is focal death of cell along with degeneration of

tissue by hydrolytic enzyme liberated by cells.tissue by hydrolytic enzyme liberated by cells. There are 5 types of Necrosis-There are 5 types of Necrosis-1)Coagulative necrosis 1)Coagulative necrosis 2)liquification (colliquative) necrosis.2)liquification (colliquative) necrosis.3)Caseous necrosis. 3)Caseous necrosis. 4)Fat necrosis 4)Fat necrosis 5)Fibrinoid necrosis.5)Fibrinoid necrosis.

Coagulative NecrosisCoagulative Necrosis It is most common type. It is most common type. Causes- mostly due to sudden cessation of blood flow & less Causes- mostly due to sudden cessation of blood flow & less

often from bacterial & chemical agents. Organs affected are often from bacterial & chemical agents. Organs affected are heart, kidney & spleenheart, kidney & spleen

Appearance of affected organ-Appearance of affected organ-Grossly-:Grossly-:In early stage pale firm & slightly swollen with progression In early stage pale firm & slightly swollen with progression

becomes yellowish softer & shrunken.becomes yellowish softer & shrunken.Microscopically-Microscopically-Cells swollen more eosinofillic conversion of normal cell to Cells swollen more eosinofillic conversion of normal cell to

tombstone i.e. outline retained but the nuclear details are tombstone i.e. outline retained but the nuclear details are lost. Those results from lost. Those results from

1)1) Denaturation of proteins &Denaturation of proteins &2)2) 2)Enzymatic digestion of cell2)Enzymatic digestion of cell

Liquefaction (colliquative) NecrosisLiquefaction (colliquative) Necrosis Causes- It occurs due to ischemic & hypoxic injury & Causes- It occurs due to ischemic & hypoxic injury &

bacterial agents as well as degradation tissue by action of bacterial agents as well as degradation tissue by action of hydrolytic enzymes.hydrolytic enzymes.

Organs affected- infarcts of brain. Abscess cavity.Organs affected- infarcts of brain. Abscess cavity. Appearance- Appearance- Grossly-Grossly- Affected organ is soft with liquefied center containing necrotic Affected organ is soft with liquefied center containing necrotic

debris. debris. Microscopically- Microscopically- Macrophages filled with phagocytosed material cell wall formed Macrophages filled with phagocytosed material cell wall formed

by proliferating capillaries inflammatory cells & gliosis in by proliferating capillaries inflammatory cells & gliosis in case of brain & proliferating fibroblast in case of abscess case of brain & proliferating fibroblast in case of abscess cavity.cavity.

Caseous NecrosisCaseous Necrosis Found in the center of foci of tubercular infection it has Found in the center of foci of tubercular infection it has

combine features of both above necrosis.combine features of both above necrosis. Appearance-Appearance-Grossly-Grossly- Dry cheese & soft granular & yellowish appearance partly Dry cheese & soft granular & yellowish appearance partly

attributed to histotoxic effect of lipopolyscchariedes present in attributed to histotoxic effect of lipopolyscchariedes present in capsule of tubercle bacilli.capsule of tubercle bacilli.

Microscopically-Microscopically- Foci are eosinophilic structure less & contain granular debris. Foci are eosinophilic structure less & contain granular debris.

Surrounding tissue shows inflammatory reaction consisting of Surrounding tissue shows inflammatory reaction consisting of epitheloid cells with interspersed giant cells of langerhans & epitheloid cells with interspersed giant cells of langerhans & foreign body & peripheral mantle of lymphocytes.foreign body & peripheral mantle of lymphocytes.

Fat NecrosisFat Necrosis Occurs in two types-Occurs in two types-1)Accute pancreatic necrosis-1)Accute pancreatic necrosis-there is liberation of pancreatic lipase from injured or inflamed there is liberation of pancreatic lipase from injured or inflamed

tissue results in necrosis. tissue results in necrosis. 2)Tramatic fat necrosis- 2)Tramatic fat necrosis- Damage adipose cells assume cloudy appearance when only free Damage adipose cells assume cloudy appearance when only free

fatty acids complex with Ca+ to form calcium soaps. fatty acids complex with Ca+ to form calcium soaps. Appearance –Appearance –Grossly- Yellowish white & firm deposits. Chalky white Grossly- Yellowish white & firm deposits. Chalky white

appearance. appearance. Microscopically- Cloudy appearance & surrounded by Microscopically- Cloudy appearance & surrounded by

inflammatory tissue. Formation of calcium soap as amorphous inflammatory tissue. Formation of calcium soap as amorphous granular & basophilic material.granular & basophilic material.

Fibrinoid NecrosisFibrinoid Necrosis Characterised by deposition of fibrinlike material Characterised by deposition of fibrinlike material

which has staining properties of fibrin. It occurs in which has staining properties of fibrin. It occurs in immunologic tissue injury. immunologic tissue injury.

E.g. Immune complex vasculitis.E.g. Immune complex vasculitis.Autoimmune diseases. Autoimmune diseases. Appearance – Appearance – Microscopically –Microscopically – Identified by brightly eosinophilic hyaline like Identified by brightly eosinophilic hyaline like

deposition in vessel wall or on luminal surface of deposition in vessel wall or on luminal surface of peptic ulcer. Local hemorrhage occur due to rupture peptic ulcer. Local hemorrhage occur due to rupture of these blood vessels.of these blood vessels.

GANGRENEGANGRENE It is form of necrosis of tissue with superadded putra It is form of necrosis of tissue with superadded putra

function. There are 3 types of gangrene:function. There are 3 types of gangrene: 1)Dry gangrene1)Dry gangrene 2)Wet gangrene 2)Wet gangrene 3)Gas gangrene3)Gas gangrene1)Dry gangrene-Begins in distal part of limb due to ischemia 1)Dry gangrene-Begins in distal part of limb due to ischemia

occurs in toes & feet of old patient. occurs in toes & feet of old patient. Causes -Atherosclerosis, thromboangitis obliterance, rayaund’s Causes -Atherosclerosis, thromboangitis obliterance, rayaund’s

disease, trauma, ergot poisoning. Line of separation present disease, trauma, ergot poisoning. Line of separation present between gangrenous & viable part. between gangrenous & viable part.

Pathologic changes-Dry, shrunken & dark black due to liberation Pathologic changes-Dry, shrunken & dark black due to liberation of Hb from hemolysed RBCs acted by H2S produced by of Hb from hemolysed RBCs acted by H2S produced by bacteria result in iron sulphied. Histologically- Line of bacteria result in iron sulphied. Histologically- Line of separation consist of inflammatory tissue.separation consist of inflammatory tissue.

Wet GangreneWet Gangrene Occurs in moist tissues & organs such as mouth, bowel, lungs, Occurs in moist tissues & organs such as mouth, bowel, lungs,

cervix, vulva etc. diabetic foot is an another example of wet cervix, vulva etc. diabetic foot is an another example of wet gangrene. It develops rapidly due to the blockage of venous & gangrene. It develops rapidly due to the blockage of venous & less commonly due to arterial flow from thrombosis & less commonly due to arterial flow from thrombosis & embolism. There is no line of demarcation between the embolism. There is no line of demarcation between the gangrenous & viable part.gangrenous & viable part.

Pathologic changes – Pathologic changes – organ becomes soft, swollen, putrid, rotten, dark. organ becomes soft, swollen, putrid, rotten, dark. Histologically- Histologically- Coagulative necrosis with shifting of affected part is with Coagulative necrosis with shifting of affected part is with

blood. There is ulceration of mucosa & intence inflammatory blood. There is ulceration of mucosa & intence inflammatory infiltration.infiltration.

Gas GangreneGas Gangrene It is the special form of gangrene caused by gas It is the special form of gangrene caused by gas

forming clostridia which gain entry in tissues through forming clostridia which gain entry in tissues through open contaminated wound. Clostridia produces open contaminated wound. Clostridia produces various toxins which produce necrosis & edema various toxins which produce necrosis & edema locally & also absorb producing profound systemic locally & also absorb producing profound systemic manifestation. manifestation.

Pathologic changes- Pathologic changes- Area is swollen edematous painful & crepitant due to Area is swollen edematous painful & crepitant due to

accumulation of gas bubbles within the tissues. accumulation of gas bubbles within the tissues. Affected tisse become dark, black, & foul smelling.Affected tisse become dark, black, & foul smelling.

CELLULAR ADAPTATIONSCELLULAR ADAPTATIONS For the sake of survival on exposure to stress the cells make For the sake of survival on exposure to stress the cells make

adjustment with the changes in their environment to the adjustment with the changes in their environment to the physiologic needs & nonlethal pathologic injury.physiologic needs & nonlethal pathologic injury.

Decreasing or increasing their size i.e. atrophy or hypertrophy.Decreasing or increasing their size i.e. atrophy or hypertrophy. By changing pathway of phenotypic differentiation of cells i.e. By changing pathway of phenotypic differentiation of cells i.e.

metaplasia or dysplasiametaplasia or dysplasia Various mechanisms in adaptive cellular responses include – Various mechanisms in adaptive cellular responses include – Altered cell surface receptor binding. Altered cell surface receptor binding. Alteration in the signal for protein synthesis.Alteration in the signal for protein synthesis. Synthesis of protein to the target cell such as heat-shock Synthesis of protein to the target cell such as heat-shock

protein.protein.

AtrophyAtrophy Reduction of number & size of cells. Reduction of number & size of cells. 1)Physiologic atrophy-occurs due to loss of endocrine stimulation 1)Physiologic atrophy-occurs due to loss of endocrine stimulation

or atherosclerosis e.g. appendix & thymus or atherosclerosis e.g. appendix & thymus 2)pathologic atrophy-2)pathologic atrophy-Causes Causes a)a) starvation, starvation, b)b) ischemic injury e.g. atrophy of brain ischemic injury e.g. atrophy of brain c)c) Disuse atrophy- diminished function e.g. pancreatic duct Disuse atrophy- diminished function e.g. pancreatic duct d)d) Neuropathic- Interruption in nerve e.g. polio myelitis Neuropathic- Interruption in nerve e.g. polio myelitis e)e) Endocrine atrophy- e.g. hypothyroidism Endocrine atrophy- e.g. hypothyroidism f)f) Pressure atrophy- pressure of benign tumour Pressure atrophy- pressure of benign tumour g)g) Ediopathic atrophy – No specific cause e.g .myopathies, Ediopathic atrophy – No specific cause e.g .myopathies,

testicular atrophy.testicular atrophy.

HypertrophyHypertrophy Increase in size of of parenchymal cell result in Increase in size of of parenchymal cell result in

enlargement of organ or tissue without change in enlargement of organ or tissue without change in number. There are 2 types of hypertrophy-number. There are 2 types of hypertrophy-1)physiologic hypertrophy 1)physiologic hypertrophy

e.g. hypertrophy of uterus in pregnancy.e.g. hypertrophy of uterus in pregnancy. 2)Pathologic hypertrophy 2)Pathologic hypertrophy e.g. Cardiac muscle in cardiovascular diseases. e.g. Cardiac muscle in cardiovascular diseases.

Compensatory hypertrophy when the organ removed. Compensatory hypertrophy when the organ removed. Pathologic changes –Pathologic changes –

Affected organ becomes heavy enlarged. Increase Affected organ becomes heavy enlarged. Increase synthesis DNA & RNA. Increase protein synthesis. synthesis DNA & RNA. Increase protein synthesis. Increase number of organelles like mitochondria, ER, Increase number of organelles like mitochondria, ER, & myofibrils.& myofibrils.

HyperplasiaHyperplasiaIncrease in no of parenchymal cells resulting in number of tissue. Increase in no of parenchymal cells resulting in number of tissue. Causes- Non-neoplastic disorders of growth. It has been divided Causes- Non-neoplastic disorders of growth. It has been divided

as as A. physiologic –A. physiologic – hormonal hyperplasia e.g. female breast at puberty. hormonal hyperplasia e.g. female breast at puberty. Compensatory hyperplasia-regeneration of epidermis of skin Compensatory hyperplasia-regeneration of epidermis of skin

after abrasion. after abrasion. B. Pathologic hyperplasia-B. Pathologic hyperplasia- Excessive stimulation of hormones or growth factors.Excessive stimulation of hormones or growth factors. e.g. formation of warts due to papilloma virus. e.g. formation of warts due to papilloma virus. Pathologic changes –Pathologic changes – Enlargement of organ & increase in number of cells. Enlargement of organ & increase in number of cells.

Increase in rate of DNA synthesis & hence mitosis Increase in rate of DNA synthesis & hence mitosis increases.increases.

MetaplasiaMetaplasia Reversible change of one type of epithelial or mesenchyamal cell into Reversible change of one type of epithelial or mesenchyamal cell into

another type in response to stimulus & reverts back after removal of another type in response to stimulus & reverts back after removal of stimulus. Stimulus persist for long time may persist cancer. stimulus. Stimulus persist for long time may persist cancer.

1)Epithelial metaplasia- 1)Epithelial metaplasia- a) squamous metaplasia-due to chronic irritation that may be mechanical, a) squamous metaplasia-due to chronic irritation that may be mechanical,

chemical, & infective in origin.chemical, & infective in origin. e.g. in uterine cervix prolapse of uterus.e.g. in uterine cervix prolapse of uterus. In renal pelvis & urinary bladder renal in chronic infection & stone.In renal pelvis & urinary bladder renal in chronic infection & stone. b) Columnar metaplasia- Interstitial metaplasia e.g. chronic gastric ulcer.b) Columnar metaplasia- Interstitial metaplasia e.g. chronic gastric ulcer. 2)Mesenchymal metaplasia-2)Mesenchymal metaplasia- a) osseous metaplasia- Formation of bone in fibrous tissue cartilage & a) osseous metaplasia- Formation of bone in fibrous tissue cartilage &

myxoid tissue myxoid tissue e.g. arterial wall in old age.e.g. arterial wall in old age. b) Cartilagenous metaplsia- in healing of fractures. It may occur where b) Cartilagenous metaplsia- in healing of fractures. It may occur where

there is unique mobility.there is unique mobility.

DysplasiaDysplasia Dissordered cellular death which accompanied with Dissordered cellular death which accompanied with

metaplasia & hyperplasia occurs most oftenly in epithelial metaplasia & hyperplasia occurs most oftenly in epithelial cells. It occurs at cellular proliferation & cytologic change. cells. It occurs at cellular proliferation & cytologic change. These changes include- These changes include-

1)Hyperplasia of epithelial cells1)Hyperplasia of epithelial cells2) Dissorderly arrangement of cellfrom basal to surface layer.2) Dissorderly arrangement of cellfrom basal to surface layer.3) Cellular & nuclear pleomorphism.3) Cellular & nuclear pleomorphism.4) Increase cellular pleomorphism.4) Increase cellular pleomorphism.5) Nuclear hyperchromatism 5) Nuclear hyperchromatism 6) Increase mitotic activities.6) Increase mitotic activities. Dysplastic changes occurs commonly in uterine cervix & Dysplastic changes occurs commonly in uterine cervix &

respiratory tract. Dysplasia occurs due to chronic irritation respiratory tract. Dysplasia occurs due to chronic irritation & prolong inflammation . On removal of stimulus changes & prolong inflammation . On removal of stimulus changes may disappear. It may progress into carcinoma.may disappear. It may progress into carcinoma.

DEGENERATIONDEGENERATION It is the term use to denote morphology of It is the term use to denote morphology of

irreversible cell injury.irreversible cell injury. There are following types of degeneration:There are following types of degeneration:1)1) Cellular degeneration. Cellular degeneration. 2)2) Hyline degeneration Hyline degeneration 3)3) Mucoid degeneration. Mucoid degeneration. 4)4) Fatty degeneration.Fatty degeneration.

Cellular degenerationCellular degeneration Causes – Bacterial toxins, burns, chemicals, high fever etc. it Causes – Bacterial toxins, burns, chemicals, high fever etc. it

results from impaired cellular volume- operative at 3 levels- results from impaired cellular volume- operative at 3 levels- 1)Plasma membrane 1)Plasma membrane 2)Sodium pump on plasma membrane 2)Sodium pump on plasma membrane 3)Supply of ATP. Grossly – organ such as kidney, liver & 3)Supply of ATP. Grossly – organ such as kidney, liver &

heart, muscle enlarge due to swelling, cut surface bulges heart, muscle enlarge due to swelling, cut surface bulges outward & slightly opaque. Microscopically – outward & slightly opaque. Microscopically –

1. Cells are swollen & microvasculature compressed. 1. Cells are swollen & microvasculature compressed. 2. Small clear vacuoles are seen those represent distended 2. Small clear vacuoles are seen those represent distended

cisternae of ER. cisternae of ER. 3. Ultra structural changes-3. Ultra structural changes- a) Dialatation of ERa) Dialatation of ER b) Detachment of polysoms from the surface of RER b) Detachment of polysoms from the surface of RER c) Mitochondrial swelling. c) Mitochondrial swelling.

Hyline DegenerationHyline Degeneration Descriptive histologic term for glassy homogenous Descriptive histologic term for glassy homogenous

eosinofilic appearance of material under eosinofilic appearance of material under hematoxyline & eosin stained section & does not hematoxyline & eosin stained section & does not refer to any specific substance. refer to any specific substance.

A.A. Intracellular hyline- mainly seen in epithelial cells Intracellular hyline- mainly seen in epithelial cells e.g. Hyline drpoplets in proximal epithelium cells in e.g. Hyline drpoplets in proximal epithelium cells in case of exessive reabsorption of plasma protein. case of exessive reabsorption of plasma protein. Nuclear or cytoplasmic hyaline inclusions seen in Nuclear or cytoplasmic hyaline inclusions seen in viral infection. viral infection.

B.B. Extra cellular hyline- seen in connective tissueExtra cellular hyline- seen in connective tissue e.g. Hyaline degeneration seen in leiomyomas of e.g. Hyaline degeneration seen in leiomyomas of

uterus. uterus. Hylinised old scar of fibrocollagenous tissue.Hylinised old scar of fibrocollagenous tissue.

Mucoid DegenerationMucoid Degeneration Mucine is normally produced by epithelial cells of Mucine is normally produced by epithelial cells of

mucus membrane & mucous glands as well as by mucus membrane & mucous glands as well as by some connective tissues like umbilical cord.some connective tissues like umbilical cord.

1) Disturbances in epithelial mucin 1) Disturbances in epithelial mucin e.g. catarrhal inflammation of mucous membrane. e.g. catarrhal inflammation of mucous membrane.

Cystic fibrosis of pancreas. Cystic fibrosis of pancreas. 2) Connective tissue mucin disturbances 2) Connective tissue mucin disturbances e.g. Myxomatous change in dermis in myoedema. e.g. Myxomatous change in dermis in myoedema.

Myxoid change in synovium of ganglion on the wrist.Myxoid change in synovium of ganglion on the wrist.

Fatty DegenerationFatty Degeneration Intracellular accumulation of neutral fat within parechymal Intracellular accumulation of neutral fat within parechymal

cells. It occurs especially in liver but may occur in nonfatty cells. It occurs especially in liver but may occur in nonfatty tissue like heart, skeletal muscles, kidneys & other.tissue like heart, skeletal muscles, kidneys & other.

Fatty liver – Accumulation of fat in liver.Fatty liver – Accumulation of fat in liver. Etilogy –Etilogy – 1)Alcohol consumption 1)Alcohol consumption 2)Starvatoin 2)Starvatoin 3)Malnutrition etc.3)Malnutrition etc. Pathologic changes- Pathologic changes- Enlarge with tense glistering capsule & rounded margines cut Enlarge with tense glistering capsule & rounded margines cut

surface is pale yellow to yellow &greesy to touch.surface is pale yellow to yellow &greesy to touch. Microscopically –Microscopically – Vacuoles are initially small & present around nucleus. But Vacuoles are initially small & present around nucleus. But

with progression becomes layer pushing the nucleus to with progression becomes layer pushing the nucleus to periphery.periphery.

HEALINGHEALING It is final stage of tresponse to tissue injury. The capacity of tissue of It is final stage of tresponse to tissue injury. The capacity of tissue of

regeneration depends upon its proliferative ability, on the type & on the regeneration depends upon its proliferative ability, on the type & on the sevearity of damage. sevearity of damage.

3 broad groups of cell are considered in the cell cycle. 3 broad groups of cell are considered in the cell cycle. 1)Labile cells- Normally continues turnover 1)Labile cells- Normally continues turnover e.g. covering epithelium & bone marrow.e.g. covering epithelium & bone marrow. Changes of regeneration are excellent. Changes of regeneration are excellent. 2)permanent cells- Not capable to proliferation 2)permanent cells- Not capable to proliferation e.g. neuron in adult.e.g. neuron in adult. Healing by scaring (no regeneration). Healing by scaring (no regeneration). 3)Stable cells- Normally little little proliferation but remain capable of more 3)Stable cells- Normally little little proliferation but remain capable of more

rapid cell division of following injuryrapid cell division of following injury e.g. liver, renal tubular epithelium. e.g. liver, renal tubular epithelium. Changes of regeneration are good. Regeneration involves 2 processes Changes of regeneration are good. Regeneration involves 2 processes

a)proliferation of surviving cells to replace the lost tissue. a)proliferation of surviving cells to replace the lost tissue. b)migration of surviving cells into the vacant space. b)migration of surviving cells into the vacant space. The factors which control the healing & repair are complex. They include The factors which control the healing & repair are complex. They include

variety of growth factors. variety of growth factors. e.g. epidermal growth factor in case of speciallised cell regeneration. e.g. epidermal growth factor in case of speciallised cell regeneration.

Transforming GFbeta incase of fibroblast. Vascular GF in case of new Transforming GFbeta incase of fibroblast. Vascular GF in case of new capillary formation.capillary formation.

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