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General Pathology 2
Introduction to pathology
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variantcharacterised ofthisby typenon-specific of chronicinflammatory cell infiltration e g. chronic osteomyelitis, lung abscess. A inflammatory response is chronic suppurative inflammation in which infiltration by polymorphs and abscess formation are additionalfeatures e. actinomycosis. 2. Chronic granulomatousinflammation. Itis characterised by formation of granulomas e. tuberculosis, leprosy, syphilis, actinomycosis, sarcoidosis etc.
REPAIR
REPAIRRepair is the replacement of injured tissue by fibrous tissue. Twoprocesses are involved in repair:
- Granulation tissue formation; and 2. Contraction ofwounds. Repair response takes place by participationof mesenchymal cells (consisting of connective tissue stem cells, fibrocytes and histiocytes), endothelial cells, macrophages, platelets, and theparenchymal cells of the injured organ. Granulation Tissue Formation The term granulation tissue derives itsname from slightly granular and pink appearance of thetissue. Each granule corresponds histologically to proliferation of new small blood vessels which are slightly lifted on the surface by thin covering of fibroblasts and young collagen. Thefollowing3phases are observed intheformation of granulation tissue(Fig. 6):
1 OF INFLAMMATION. Following trauma, blood clots at the site of injury. There is acute inflammatory response with exudation of plasma, neutrophils andsome monocytes within 24 hours. 2. PHASE OF CLEARANCE. Combination of proteolytic enzymes liberated from neutrophils, autolytic enzymesfrom dead tissues cells, and phagocytic activity of macrophages clear off the necrotic tissue, debris andredblood cells
- PHASE OF INGROWTHOF GRANULATION TISSUE. Thisphaseconsists of 2mainprocesses:
angiogenesis or neovascularisation, and fibrogenesis. i) Angiogenesis (neovascularisation). Formation of newblood vessels at thesite of injurytakes place byproliferation of endothelial cells from the margins of severed bloodvessels. Initially,theproliferated endothelial cells are solidbuds but within afew hours develop a lumen and start carrying bloodii) Fibrogenesis. Thenewlyformed bloodvessels are present in anamorphousgroundsubstance or matrix. The new fibroblasts originate from fibrocytes as well as by mitoticdivision of fibroblasts. Someof these fibroblasts have combination of morphologic and functional characteristics of smooth musclecells(myofibroblasts). Collagen fibrils begintoappear by about 6th day. As maturation proceeds, more and more ofcollagen is formed while thenumberof active fibroblasts and new bloodvesselsdecreases. This results in formation of inactive looking scar known as cicatrisation.
Contraction of Wounds The wound starts contracting after 2-3 days and the process is completed by the 14th day. During this period, thewound is reducedbyapproximately 80% ofits original size. Contracted wound results in rapid healing since lesser surface area of the injured tissue hasto bereplaced order
to explain the mechanism of wound contraction, a number of factors have been proposed. These are as under:1. Dehydration as aresultofremovalof fluid bydrying ofwound wasfirst suggestedbut without being substantiated. 2. Contraction stage when of the collagen collagen was content thought ofto granulation be responsible tissue for is contraction very small. but3. wound contraction proceeds at a
contain morpDimembrathose cells Fibrils cells surrounding contractionscovery hologicahave demonstrates of present actin-myosin ne fibroblastsinfoldings of and decreasesthemyofibroblasts lin as desmosomes mechanism the well immunofluorescentandof cytoplasm similar as thenuclearsmoothfunctionalsize to appearing of which of that membrane woundof muscle thethese characteristics found are defect. in contraction not cells. cells active in likeseen non-striated resemble The Their in granulationin withsmooth evidences of ordinary migration These modified anti- smooth those muscle muscle cells in fibroblasts. tissueseen into support fibroblasts havecells. cells in the hassmooth features v) wound iii) of resolvedvi) These this antibodies. Cytoplasm or Drug myofibroblastsmuscle concept intermediate area cells response the and have controversycells iv) are their theseNuclei basementof bothii) betweengranulationasactiveThese modifiedunder:of thesecellsi)
tissue issimilarto that ofsmooth muscle.
WOUNDHEALING
WOUND HEALING
Healing described of above. skinwounds Wound provides healing acan classical beaccomplished exampleof in combination one of the followingof regeneration two ways:and repairHealing by first
intention (primary union) Healing by second intention (secondary union).of a wound which has the following
Healing characteristics: by First i) Intention clean and (Primary uninfected; Union] li) surgically This is defined incised; as ii) healing without much loss of cells andtissue; and
- iv) Initial edges hof aemorrhage are approximatedImmediately after by surgicalinjury, the suturesspace between the approximated surfaces of incised wound is filled with blood whichthen clots and seals the wound against dehydration and
Granulation tissue. Main bulk of secondary healing is by granulations. Granulation tissue is formed by proliferation of fibroblasts and neovascularisation from the adjoining viable elements.
Wound contraction. Contraction of wound is an important feature of secondary healing, not seen in primary healing. Due to the action of myofibroblasts present in granulation tissue, the wound contracts to one-third to onefourth of its original size.
Presence of infection. Bacterial contamination of an open wound delays the process of healing due to release of bacterial toxins that provoke necrosis, suppuration and thrombosis. Surgical removal of dead and necrosed tissue, debridement, helps in preventing the bacterial infection of open wounds.
Complications of Wound Healing
During the course of healing, following complications may occur: 1. Infection of wound due to entry of bacteria delays the healing. 2. Implantation (epidermal) cyst formation may occur due to persistence of epithelial cells in the wound after healing. 3. Pigmentation. Healed wounds may at times have rust-like colour due to staining with haemosiderin. Some coloured particulate material left in the wound may persist and impart colour to the healed wound. 4. Deficient scar formation. This may occur due to inadequate formation of granulation tissue.
Factors Influencing Healing Two types of factors influence the wound healing: those acting locally, and
Those acting in general.
A LOCAL FACTORS:
Infection is the most important factor acting locally which delays the process of healing
Poor blood supply to wound slows healing e .g. injuries to face heal quickly due to rich blood supply while injury to leg with varicose ulcers having poor blood supply heals slowly. 3. Foreign bodies including sutures interfere with healing and cause intense inflammatory reaction and infection. 4. Movement delays wound healing. 5. Exposure to jonising radiation delays granulation tissue formation. 6. Exposure to ultraviolet light facilitates healing. 7. Type, size and location of injury determines whether healing takes place by resolution or organisation.
B. SYSTEMIC FACTORS: 1. Age, Wound healing is rapid in young and somewhat slow in aged and debilitated people due to poor blood supply to the injured area in the latter. 2. Nutrition. Deficiency of constituents like protein, vitamin C (scurvy) and zinc delays the wound healing. 3. Systemic infection delays wound healing. 4. Administration of glucocorticoids has anti-inflammatory effect. 5. Uncontrolled diabetics are more prone to develop infections and hence delay in healing. 6. Haematologic abnormalities like defect of neutrophil functions (chemotaxis and phagocytosis), and neutropenia and bleeding disorders slow the process of wound healing.
Fracture Healing Healing of fracture by callus formation depends upon some clinical considerations whether the fracture is; traumatic (in previously normal bone), or pathological (in previously diseased
Bone); complete or incomplete like green-stick fracture; and simple (closed), comminuted (splintering of bone), or compound (communicating to skin surface). However, basic events in healing of any type of fracture are similar and resemble healing of skin wound to some extent.
Primaryunion of fractures occurs in a few special situations when the ends of fracture are approximated as is done by application of compression clamps. In these cases, bony union takes place with formation of medullary callus without periosteal callus formation.
The patient can be made ambulatory early but there is more extensive bone necrosis and slow healing. Secondary union is the more commonprocess of fracture healing. Though it is a continuous process, secondary bone union isdescribed under the following 3 headings: i) Procallus formation ii) Osseous callus formation iii) Remodelling.
I. PROCALLUS FORMATION. Steps involved in the formation of procallus are as follows: 1. Haematoma forms due to bleeding from torn blood vessels, filling the area surrounding the fracture meshwork is formed by blood and fibrin clot which acts as framework for subsequent granulation tissue formation.
Local inflammatory response occurs at the site of injury with exudation of fibrin, polymorphs and macrophages
Ingrowth of granulation tissue begins with neovascularisation and proliferation of mesenchymal cells fromperiosteum and endosteum. A soft tissue callus is thus formed which joins the ends of fractured bone without much strength
APOPTOSIS IN BIOLOGIC PROCESSES
Apoptosis is responsible for mediatingcell deathinawidevariety of physiologicand pathologic processes as under: Physiologic Processes: 1. Organisedcell destruction in sculpting of tissues during
and tissues on withdrawal of stimuli e g. prostatic atrophy after orchiectomy, atrophy of kidney or
GANGRENE
Gangrene is a form of necrosis of tissue with superadded putrefaction. The type of necrosis is usually coagulativegangrenousdue toischaemia(e.g,gangreneoflimb).Ontheotherhand,
main types bacteria inflammation gangreneforms of gangrene, resulting isof theor are: gangrene-dry necrotising samein gangrenous necrosis massive buttheinflammation undergoes tissue wayand appendicitis, wet, thenecrosis. twoliquefaction and ischaracterised area gangrenous Thus, variant produced,the by form the end-result stomatitis by isof action different wet gangrene of of (noma, putrefactive necrotising inflammation Theexamplescancrum called inflammation bacteria provokedoforis). gangrene, necrotisingThere byvirulentandare In all
Dry example Gangrene is the This dry gangrene form of gangrene in the toesbegins and in feet the of distal an old part patient of a limb dueto due arteriosclerosis. to ischaemia. The Other typicalcauses
of dry gangrene foot include thromboangitis obliterans (Buerger's disease), Raynaud's disease, trauma, ergot poisoning. It is usually initiated in one of the toes which is farthest from the blood supply.
containing so little blood that even the invading bacteria find it hard to grow in the necrosed tissue. The gangrene spreads slowly upwards until it reaches a point where the blood supply is adequate tokeep the tissue viable. A line of separation is formed at this point between the gangrenous part and the viable part
Wet Gangrene Wet gangrene occurs in naturally moist tissues and organs such as the mouth, bowel, lung, cervix, vulvaetc foot isanother example of wet gangrene due to high sugar content in the necrosedtissue which favoursgrowth of bacteria sores occurring in a bed-riddenpatient due to pressure on sites like the sacrum, buttocks and heels are the other important clinical conditions included
in wet gangrene. Wet gangrene usually develops rapidly due to blockage ofvenous, and less commonly. arterial blood flow from thrombosis or embolism. The affected part is stuffed with blood which favours the rapid growth of putrefactive bacteria. The toxic products formed by bacteria are absorbed causing profound systemic manifestations of septicaemia, and finally death. The spreadingwetgangrene generally lacks clear-cut line of demarcation and may spread to peritoneal cavity causing peritonitis.
General Pathology 2
Course: Introduction to pathology
University: Rajiv Gandhi University of Health Sciences
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