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Inflammation & Repair
INTRODUCTION
Q. I.I. What is inflammation ? Describe the salient features of inflammation and its main types. A property of living organism is self-defence. Aiming at selfdefence the human body (as any other living creature) reacts sharply to any stimulus received by it. The reactions of the body to the normal or noninjurious stimuli constitute, with other activities of the body, the physiologic process. The reaction of the body to injurious stimuli (trauma) is of the following types : 1. Vascular reaction termed inflammation. 2. Phagocytosis. 3. Entrapment by specialised cells (haemocytes) and subsequent ingestion. 4. Neutralization by cellular hypertrophy. Of these inflammation occurs only in vertebrates; in lower animals without vascular system, the reaction to trauma is of later three types. Thus inflammation may be defined as response of the vascular tissue to trauma. Inflammation is not a disease which enters from outside; it is rather a mechanism developed by body itself-a tool to fight an outside attack.

Cardinal signs of Inflammation
The cardinal signs of inflammation described by Cornelius Celsus in the first century A.D. are : 1. Rubor i.e. redness. 2. Tumor i.e. swelling. 3. Calor i.e. heat. 4. Dolor i.e pain. (In so many centuries only one sign has been added i.e.) 5. Loss of function.

Advantages of Inflammation and Repair
1. Limitation of infection 2. Healing of wounds 3. Normalisation of injured tissue.

Disadvantages of Inflammation and Repair

1. Development of crippling diseases e.g. rheumatoid arthritis. 2. Life-threating sensitivity reactions. 3. Fatal glomerular disease. 4. Disfiguring scars. 5. Joint stiffness. 6. Scar tissue hampers vital functions.

Causes of Inflammation
Inanimate Mechanical Foreign body Injury Necrosed tissue Physical Heat or cold Electric burn Radiation Chemical Acids Alkalis Other irritants Animate Bacteria Parasites Protozoa Helminths Fungi

Types of Inflammation and Repair
The response of the tissue to trauma depends upon the nature and amount of trauma. The response may be immediate and brief when trauma is extremely mild. The inflammation caused subsides before it becomes noticeable (latent

inflammation). To certain types of trauma the tissue may react sharply by undergoing severe changes. Such form of response is acute inflammation. The tissue changes occuring in acute inflammation may subside partly or completely after trauma is overcome. Often the type of trauma is such that is continues to elicit the response over prolonged period in subsidised form. The resultant inflammation is called the chronic inflammation. A' chronic inflammation may be the aftermath of acute inflammation ; in that case exacerbations may render the inflammation acute periodically. Alternatively chronic inflammation may originate as an independent entity without being preceded by acute form. The salient features of acute inflammation and chronic inflammation are enumerated below :

Acute Inflammation
I. Stereotypical response to all forms of injury irrespective of the type of causative agent. Causes of Inflammation Inanimate Animate Mechanical Physical Chemical Bacteria Parasites Fungi Foreign Injury Necrosed Acids Alkalis other Protozoa Helminths Body tissue irritants Heat or cold Electric burn Radiation 2. Relatively short duration, ranging from a few minutes to 1-2 days. 3. Exudation of fluid and plasma protein (oedema). 4. Emigration of leucocytes, mainly polymorphs.

Chronic Inflammation
1. Less uniform 2. Generally of longer duration 3. Presence of lymphocytes and macrophages. 4. Proliferation of small blood vessels and fibroblasts.

ACUTE INFLAMMATION
Q,. 1.2. What are the varieties of acute inflammation ? Describe vascular phenomena in acute inflammation.

Varieties of Acute Inflammation
1. Catarrhal inflammation (i) Affects mucous membranes, acini and ducts of glands, mainly of upper respiratory tract, large intestine, and urinary tract. (ii) Mucus secretion is abundant. (iii) Desquamation of surface epithelium. (iv) Discharge initially mucoid, later mucopurulent. Examples : Bronchitis, gastritis, colitis. 2. Serous inflammation (i) Affects mostly serous cavities viz. pleura, peritoneum, pericardium ; may occur anywhere. (ii) Exudate is fluid and composed mainly or serum. Example : Bristles of burnt skin.

3. Croupous or fibrinous inflammation (i) Affects serous membranes e.g. pleura, pericardium, peritoneum, joints, meninges. (ii) May occur in epithelial surfaces e.g. alimentary canal, urinary tract, gall bladder, lungs. (iii) Exudate more concentrated with excess of plasma, protein, mainly fibrinogen. Examples : Dysentery, lobar pneumonia (early stage). 4. Haemorrhagic Inflammation (i) Caused by increased fragility of blood vessels and capillaries as in leukaemia, anaemia, various forms of purpuras. (ii) Inflammation attended with extravasation of red blood cells. Examples : "Black" small pox, measles, diphtheria. 5. Purulent inflammation (i) Digestive softening of the tissues with formation of pus. (ii) Pus is semifluid, yellow or greenish-yellow material, opaque creamy and granular. (iii) Odour may be offensive if gas forming organisms e.g. Esch. coli are associated. Example: Abscesses. 6. Necrotic inflammation. Inflammation accompanied by necrosis e.g. oriental sore. 7. Pseudomembranous inflammation Formation of a false membrance composed of necrosed epithelium and fibrin. Examples: Diphtheria, dysentery.

Vascular phenomena
Vascular phenomena constitute the local manifestations of acute inflammation. These have three main components: 1. Dilatation of blood vessels. 2. Emigration of leucocytes. 3. Escape of blood plasma.

1. Dilatation of blood vessels
(i) Often preceded by a brief vasoconstriction. (ii) Most marked in arteries, less in veins, and least in capillaries. (iii) Transitory acceleration of blood stream followed by slowing. (iv) Increased vascularity results in redness and heat. (v) There may be complete stasis of local circulation, the condition being termed as sludging of the red blood corpuscles. This results in death of the part. (vi) Pavementing of the leucocytes. The leucocytes, which normally flow intermingled with the red cells, occupy the outer, plasma tic zone. Thus the inner wall of the vein becomes paved by an unbroken line of leucocytes. (vii) The lining cells of the vascular endothelium be come enlarged and

(iii) The fluid contained in inflammatory oedema is termed inflammatory exudate. 3. Vascular Phenomena 2.3). 1.1. In such a part. the inflamation is said to be haemorrhagic. (see Q. when these are numerous. 2. project into the lumen and exhibit arnoeboid movement. 1. the leucocytes flow out. the individual elements of the vessel wall lose their sharpness. Chemotaxis. (ii) This results in swelling of the tissue (inflammatory oedema). (ii) Through such vessel wall. the normal constrictor impulses are cut off and inflammation develops much more rapidly. Mechanism of Vascular Phenomena 1. The emigration of leucocytes is controlled by the phenomenon of . (iii) A number of erythrocytes also flow out . They assume a rounded form. The vascular changes. the capillaries permit a greater emigration of leucocytes and a greater transudation of lymph through their walls. Nervous impulses.proliferate. Emigration of leucocytes (i) The ground substance of the swollen endothelium becomes loosened . Fig. When nerve to a part is divided. Escape of blood plasma (i) Blood plasma accompanies the leucocytes through the damaged vessel wall. both dilatation and exudation are influenced by nervous impulses.

lymphocytes are much less active presumably because of smaller quantity of cytoplasm. 4. histamine and a permeability factor. 2. 5. (ii) Acid proteases. Polymorphs are most active. The chemical mediators may be divided into the following groups. (ii) Kallikrein. (ii) Fibrin degradation products. (Negative chemotaxis changed to positive one). 3. (b) Complement system (i) C3 fragment. 2. Two factors exist in the globulins of normal serum-one enhances the capillary permeability whereas the other inhibits this process. Permeability globulin precursor is activated by liberation of serotonin (5-Ht) and histamine in damaged tissue cells. The evidences of chemical mediation are: 1. Prostaglandins. Globulin factor. (iii) Neutral proteases. A soluble globulin factor has a powerful effect on the vessel wall. from cells. (i) Some substances such as quinine. (iii) Leucocytes show differential response to chemotaxis. Inflammatory reaction to different types of injurious stimuli has a fairly uniform pattern. (c) Coagulation-fibrinolytic system (i) Fibrinopeptides. (ii) Extremely virulent bacteria cease to have any chemotactic power . they just paralyse the leucocytes. Both positive and negative chemotaxis are recognised. Neutrophil products (i) Cationic proteins. (ii) Serotonin. Lymphocyte factors. Chemical mediators The tissue response to injury is believed to be mediated through chemical substances of varied nature originating from plasnia. (ii) C5 fragment. alcohol. and lactic acid repel the leucocytes but dilute solutions of the same chemicals attract the leucocytes. or from damaged tissue. Inflammation develops in tissues devoid of nerve supply. Plasma proteases (a) Kinin system (i) Bradykinin. 3. Vasoactive amines (i) Histamine. There is degranulation of mast cells which are thought to be a source of heparin. The products of parasites attract mainly the eosinophils.chemotaxis. I. .

Eosinophils 1. having devoured such bacteria. Pass through the tissue spaces by the their remarkable amoeboid movement but cannot swin through a fluid. as degeneration proceeds. the cytoplasm becomes granular the outline indistinct and the nucleus eventually disappears. 5. 2.6. they digest them by means of an enzyme which dissolves the bacterial bodies. (ii) Endogenous pyrogen. Eosinophils 3. Lymphocytes and plasma cells. Large number of neutrophils are killed by bacterial toxins . 3. Discuss the role played by the cellular exudate in the process of inflammation. Describe the formation of inflammatory exn-date and discuss its significance. they release a proteolytic enzyme which dissolves the dead tissue and thus hastens the process of recovery. Define inflammatory exudate and name its various components. 7. Q. 8. Many of the cells which survive reenter the circulation. (iii) Substance P. Cellular elements of Exudate 1. Chief constituent of pus. 6. Neutrophils 1. Active agents in acute inflammation particulaly when the causative organisms are pyogenic bacteria. Other mediators. Collect in great number around the dilated vessel. 5. Basophils and mast cells. Q. Form first line of defence of the body against the pyogenic bacteria . 1. (i) Show reacting substance (SRS-A). 1. 1.3. In a fresh exudate the cell outline is sharp and the nucleus distinct . Q.6. the vessels may he packed with these leucocytes. In section of inflammed tissue. 9.4. INFLAMMATORY EXUDATE Q. 4. Appear early in the inflammatory exudate and may disappear. 2. Neutropbils. . 6. Giant cells. Discuss the role it plays in limiting infections. 1. Describe in detail the cellular elements of the inflammatory exudate. on disintegration. Monocytes and macrophages.5. 4.

2. Eosinophils on breaking down release histamine with resulting increase in capillary permeability and outpouring of more antibodies with neutralisation of antigen. (ii) Lymph nodes in Hodgkin's disease. 5. . Eosinophilia in allergic reaction may be produced by antibodies rather than antigen as it rises in convalescence with rise in antibody titre. Cellular elements of exudate. Basophils are of haematogenous and mast cells of tissue origin.2. Cellular elentents of the inflammatory exudate. 7. 2. A marked eosinophlia is characteristic of many parasitic infestations. 1. 2. Eosinophilia may be a reaction against a foreign protein in both the above instances. 4. Basophils and Mast Cells 1. 6. the bronchial mucosa is often crowded with eosinophils. Fig. Fig. -A marked eosinophilia is sometimes seen in : (i) Subacute or chronic appendicitis. In bronchial asthma. 3. The two types of cells have similar function in hypersensitivity reactions mediated by immunoglobulin lgE.

syphilis. (iii) Miscellaneous. histamine. drugs and trauma. They release heparin. (b) Glioblastoma multiforme. Plasma cells develop from lymphocytes by synthesizing an increased amount of RNA and gamma-globulin in their cytoplasm. They are large cells and have one or several nuclei but these are never . they fuse together and form multinucleated giant cells. antigen. Degranulation of basophils and mast cells. (iv) Release of substances causing leucocytosis and fever (viz prostaglandins. The giant cells are of three types : (i) Tumour giant cells. (iii) Release of chemotactic and permeability factors which may prolong inflammation. (c) Rhabdomyosarcoma and (d) Primary carcinoma of liver. in response to antigenantibody complexes. Macrophages involved in inflammation are derived from monocytes and have the following properties : (i) Phagocytosis and digestion of invading organisms or foreign particles. 3. (ii) Release of potent enzymes which degrade connective tissue. Lymphocytes and plasma cells are a prominent source of globulin antibodies. 5.3. peripheral blood. 2. and serotonin. Immunoglobulin IgE binds selectively to the surface of these cells. triggered by : interaction of immunoglobulin (antibody) with specific. Lymphocytes and Plasma Cells I. also called reticuloendothelial system (RES). endogenous pyrogen). 4. 2. Tumour giant cells are seen in: (a) Osteogenic sarcoma. These are found in the bone marrow. (v) Release of factors which aid in healing. (vi) Secretion of antibacterial. (ii) Foreign body giant cells. other granulomous diseases. Giant Cells When the individual macrophages are unable to deal with particles to be removed. Monocytes and Macrophages 1. antiviral substances and such other proteins. and tissues with function of intracellular digestion . Appear late during the chronic phase of inflammation and are particularly prominent in tuberculosis. viral and rickettsial infections. Monocytesandmacro-phages belong to mononudear phagocyte system (MPS). in connective tissue these are termed histiocytes. results in release of histamine and other mediators. 3.

It contains numerous nuclei. The foreign body giant cell is larger than an ordinary cell and may be of enormous size. seldom large and are scattered through the cytoplasm. Foreign body giant cells are seen in. 4. 3. the intermediate stages are the phenomenon of stagnation. etc. in certain conditions e. Dilutes the irritant. 4. are regular in size. 2. exudation and diapedesis of red corpuscles.g. 5. Formation of Inflammatory Exudate I. Increased permeability or porosity of the capillary endo-thelium caused by damage results in increased flow as well as increased protein content of the lymph. The nuclei. sometimes as many as 50-100. Lowers the concentration of toxins e. tuberculosis the nuclei may be arranged around the periphery (Langerhan's giant cells).g. The third group 'miscellaneous' include the giant cells of mesodermal origin e.g. Aschoff cells of rheumatic nodule. Bactericidal effect on some species. 2. Another member is the Reed-Strenberg cell of Hodgkin's disease. whether connective tissue or epithelial in nature. plasma also escapes and adds to protein content of exudate. Makes bacteria susceptible to phagocytosis by leucocytes. Their nuclei are always hyperchromatic and may vary considerably in size and shape. The extreme result of damage is necrosis of capillary walls and thrombosis within. However. RESOLUTION . (c) Leprosy and (d) Actinomycosis. Role of Exudate 1. With the mechanical escape of red corpuscles. (a) Tuberculosis. May inhibit growth of some bacteria. leucocidin. These giant cells are not derived from the macrophages but from tumour cells. The exudation is thus a result of damage to the capillary endothelium. The presence of abundant leucocytes in the tissues may lead to local production of lactic acid by anaerobic glycolysis and this in turn further increases capillary permeability. The tumour giant cells are formed by division of the nucleus while cytoplasm of the cell fails to divide.numerous. Tumour giant cells are found in neoplasms only and are absent in inflammation. 3. Initial increase in permeability results from local release of histamine. (b) Syphilis. 5.

Fig. After destruction of the organisms. Connective tissue cells which have become swollen and separated in an inflammed part become attached again to fibres or form new fibres. within a macro-phage. With the absorption of the fluid content of the air vesicles. 4. The most striking example is met with in acute lobar pneumonia where all the phenomena described above are well observed. If fibrin is abundant or dense.7. by a process of organisation. Resolution is the process of retrogression of various phenomena occuring in inflammation. but those damaged and also extravasated red cells are either taken up by phagocytes or are carried by lymph to the lymph nodes where they are similarly dealt with. Resolution of Inflammation . a gradual softening and digestion of fibrin in the air vesicles follows and in this the leucocytes are chiefly concerned. As the irritant is removed from the tissue or its effect otherwise encountered. sometimes several polymorphonuclear leucocytes are seen. The exudate. The phagocytosed leucocytes are gradually digested and disappear. The phagocytes are macrophages developing from both monocytes and cells of tissue origin (histiocytes). the stagnation passes off and blood flow is restored though a certain amount of vasodilation often persists for some time. What is resolution of Inflammation ? Discuss the process of resolution in an acutely inflammed tissue. 2. Fig. 1. 6. 3. Healthy leucocytes may pass back through the endothelium of the venules to the blood stream. In resolution there is tendency to restoration of normal blood flow and absorption of exudate. there is marked diminution of inflammatory cells.3. The defects in the endothelial lining may be completely restored by the surviving cells. if fluid. 8. where they undergo intracellular digestion. 5. its absorption is effected only after ingrowth of fibroblasts and capillaries i. these again become air containing and part returns . 1. 3.Q. 1. The degenerated leucocytes and red cells are taken up by lymphatics to the bronchial lymph nodes. Resolution of Inflammation. Damaged red corpuscles are also taken up by these phagocytes and destroyed. lymphocytes become relatively increased in number. 7. As a sequel to phagocytosis by nongranular cells.e. ultimately' those left are almost exclusively of nongranular type. This is the common result in the case of a fibrinous exudate on serous membrane. is absorbed chiefly by lymphatics and fibrin is digested by leucocytes and thereafter absorbed.

Proliferation of fibroblasts. What are the causes of chronic inflammation ? Discuss its histological characters and effects. Some of the liquefied exudate is expectorated but the amount may not be large and in every case major part of the exudate is absorbed. Pathogenesis Chronic inflammation in various organs may occur in three ways: 1. as in rheumatoid arthritis. (ii) Treponema pallidum. . - CHRONIC INFLAMMATION Q. 2. gets changed into a much larger cell. Chronic inflammation may develop as a primary entity without a preceding attack of acute inflammation. 3.practically to normal. on reaching the extracellular tissue. Particulate irritants (i) Silica dust. Emigration of mononuclear cells is an important component of chronic inflammation. 3. tuberculosis. 2. Proliferation of blood vessels. Chronic inflammation is the response of body tissues to the persistent traumatic stimuli. There may be repeated attacks of acute inflammation with healing phase in between as in cholecystitis and pyelonephritis. 3. (ii) Vegetable cells (iii) Lime salts. It may follow an episode of acute inflammation where the inciting stimulus persists in the body. 2. 1. . Mild poison in solution .Lead. chronic bronchitis. Pathology The characteristic features of chronic inflammation are : 1. the macrophage. Infective organisms (i) Mycobacterium tuberculosis. (iv) Pigments. Macrophages accumulate in large numbers in three ways. Causes 1.8. Infiltration of mononuclear cells. The monocyte.

There is sometimes a considerable formation of new blood vessels and the interstitial tissue may appear reddish as is often seen in cirrhosis of liver and kidney. When degenetrative changes are going on in the neighbourhood. the macrophages may contain droplets of fat and other lipid material. (ii) Stenosis of small intestine in regional ileitis. Tubercle follicles are also very chharacteristic of sarcoidosis and are frequently induced in the tissue by foreign bodies. Also the Treponema pallidum commonly induces a diffuse chronic inflammatory response. . The tubercle follice is characteristic of lesion due to Mycobacterium tuberculosis. they are not always specific. in chronic pyelonephritis. and occasionally eosinophilis and poly-morphonclear leucocytes. Continuous inflow of monocytes from circulation maintained by chemotactic factors. The various types of chronic inflammatory lesions have some relatively distinguishing features in the structure. In the later stages or where the process has been of very slow nature throughtout. the chief change is a thickening of collagenous fibres whilst cells and vascularity are relatively scanty. 2. the cells being spindle shaped and connective tissue fibres delicate and scanty e. Cells filled with globules of myelin fat (foamy cells) are common being especially abundant in the granulomatous lesions of actinomycosis. Uneven affection of interstitial tissue results in coarse granularity of the surface e. Prolonged survival and immobilization of macrophages within the site of inflammation. (i) Stenosis of mitral valve and chronic endocarditis. however. but at times in older lesions.1.g. but this organism may at times produce a quite different and much more acute exudative lesions in the meninges or pleura.g. Replacement of specialised connective tissue by more resistant connective tissue cells e. Contraction of newly formed tissue leads to narrowing of orifices and tubes e. 4. Another characteristic of chronic inflammation is the overgrowth of interstitial connective tissue which in earlier stages may be comparatively cellular. The other cells encountered in chronic inflammation are plasma cells. lymphocytes. When the irritant is of particulate nature or a substance difficult for absorption. 2. foreign body giant cells are often a predominant feature. Effects of Chronic Inflammation 1.g. 3. 3. Local proliferation of macrophages by mitotic division. Loss of parenchymal cells of the organ. a markedly follicular character may be seen and an erroneous diagnosis of tuberculosis may then be made.g. in congenital syphilitic cirrhosis of the liver. The vascularity of the new tissue also varies greatly. in liver cirrhosis.

Gradual destruction and disappearance of the tissue elements. Digestion and liquefaction of the tissue is chiefly due to proteolytic enzymes produced by leucocytes. Liver abscess Subsequent fate . There is thus. an actual destruction of tissue and a return to normal is no longer possible. however numerous. The special cells of the part become necrosed. or confined space. as there is no evidence that leucocytes. Although the pyococci are most frequently concerned. will attack normal tissues. etc. The accumulation of leucocytes still goes on and the tissue gradually becomes replaced by pus. Two chief changes occur inside the tissues viz. of the tissue by leucocytes follows damage or actual necrosis due to bacterial toxin. break down into granular material and melt away. 4. A portion of dead tissue or solugh then forms and may persist for considerable times. Liver abscess. organ. In dense tissues. 1. Certain pyogenic organisms have a digestive action on proteins but others e. Fig. in which remains of the dead tissue are present. Formation of Abscess Abscesses are usually produced by the deep seeding of pyogenic bacteria into a tissue. suppuration may be produced by a great variety of organisms.g. in pleurisy. Digestive softening Fig.ABSCESS An abscess is a localised collection of pus caused by suppuration burried in a tissue. The progressive emigration of leucocytes is due to a continued supply of chemotactic substances from the bacteria. capillaries. the essential point being that they should be able to persist in the tissue and produce their effects. 2. complete suppurative softening may fail owing to the density of the tissue. while the supporting connective tissue fibrils. strepto-cocci and pneumococci have no such property.4. A progressive emigration of polymorphs which come to pack the tissue. The fibrin is to a large extent digested and disappears and this is closely analogous to the action of leucocytes in removing fibrin in the process of resolution of inflammation as seen in pneumonia.g. are digested and disappear. 1. Digestive action by the leucocytes is seen also when suppuration is preceded by much exudation of fibrin e.

Vitamin K. Then it. at the periphery of an art abscess. Nutrition. Vitamin C. the pus may be absorbed and a smaller scar results. the process is impaired due to comparatively less blood supply. however.9. Age. The abscess is then said to "point". 1. a reactive proliferation of the connective tissue cells with new formation of blood vessels forms a zone of granulation tissue around it. be too abundant for this to occur. 3.When suppuration ceases to spread. It is necessary for the formation of intercellular substance and maturation of collagen of connective tissue. 4. HEALING AND REPAIR Q. When an abscess forms near a free surface as in subcutaneous tissue. the tension of the contents causes the suppuration to extend in the direction of surface so that the overylying skin is involved. Mention the factors that may modify the course of healing. 2. The pus may. It may ultimately discharge its contents spontaneously. A. The outer part of it becomes denser and a definite wall to the abscess is formed (pyogenic membrane). deficiency with hypoprothrombi-naemia and a bleeding tendency may interfere with normal wound healing by the formation of haematomas and serum collection. Healing is quickest in children. Healing Factors affectin wound healing . As the age advances. lime salts may be deposited. Vitamin K. Describe the process of healing in a clean incised wound. Serious protein deficiency with hypoproteinaemia and oedema predisposes to prolonged and complicated wound healing. If the abscess is of small size. General factors 1. . These in turn predispose to wound separation and wound infections. particularly the protein intake is of utmost importance. The nutritional state of the patient. becomes thickened and changed into granular debris. In this debris.

6. 3. interferes with the healing process. Bacterial infection. 6. 4. Dehydration may be associated with delayed wound healing. Devitalised tissue from mechanical or chemical trauma predisposes to bacterial infection thus delaying the process' of healing. Haematomas and serum collections.Healing in a Clean Incised Wound 5. 2. Desiccation of the tissues. thus predisposing to local wound infection. either invasive or uninvasive.1 . Fluid and electrolyte balance. . It is necessary for optimum wound healing.Table 1. Foreign bodies. Their deficiency lowers the rate of phagocytosis and bacterial digestion. D and B-complex. 5. Vitamin A. Ischaemia. Wounds also heal poorly in presence of a water-salt overload and oedema. B. Local factors: I.

Q. serious discharge from the vessels may be considerable. but often little vascularisation is necessary. These cells in the form of fibroblasts. Healing process in an infected wound is by granulation tissue and is termed secondary union. When bleeding has been arrested and the margins have been fixed in apposition. the process of healing is simple and rapid. In addition to the fixed cells of the part (fibroblasts and vas cular endothelium). as far as possible. migrate into the thin layer of coagulum. these are mainly poly-morphonuclear leucocytes which migrate from the new capillaries in response to irritation. It involves the invasion and replacement of dying and dead tissue by immature mesenchyme . They serve to keep the surface free from . the adjacent surfaces are glued together with a thin layer of coagulum. Such a wound is said to heal by primary union.called granulation tissue. Such a surface is highly vascular and bleeds very readily. The process of healing is summarised on page 19. Improper examination. It consists of two parts : 1. In such a case the emigration of leucocytes contirnues for a longer time and formation of fibroblasts and new capillaries is likewise of longer duration and more abundant resulting in a more distinct line of fibrous tissue than in the case of simple aseptic healing. Within a short time the connective tissue cells become swollen and divide by mitosis. so that the youngest tissue is always at the surface. The process commences at the base and works to the surface. but ordinarily this is scanty and only a few leucocytes emigrate from the vessels into the clot. If the wound surface has been irritated or if the wound has been a large one. Capillary bands accompany the fibroblasts.7. Replacement or reconstruction of the original tissue. 1. The fibroblasts from adjacent sides become intermingled . In the early stages. Removal of inflammatory material and necrotic debris which may be much or little. At the end of 5-6 days the process is practically completed and only a narrow band of young connective tissue remains to mark the line of incision. wandering cells also form an important element of granulation tissue. Healing in a clean incised wound In a simple incised wound such as is made in aseptic surgery. which undergoes absorption by the action of these cells and of leucocytes. they arrange themselves at right angles to the line of wound and produce the collagen fibrils which bring about the permanent union. There is a slight degree of congestion of the superficial vessels with some liberation of plasma which coagulates.10. At the same time the epithelial cells grow over the line of incision from the two sides and restore the continuity of epithelial covering. 2. Describe the process of healing in an infected wound.

All these cells possess osteogenic function i. the osteoblasts have branching processes from which delicate fibrils pass in all directions. the epithelium begins to cover the surface and true healing is said to have commenced. Enumerate the causes of delayed union. In this newly formed tissue the young bone cells. In the superficial layers the fibroblasts run at right angle to the surface and therefore parallel to the vessels. Bleeding soon ceases and coagulation of the effused blood occurs. whereas in deeper parts of the wound where the process is older they are arranged parallel with the surface.e. Repair of Fracture When a bone undergoes a simple fracture. There is exudation from them which leads to a swelling of the tissues at the site. It presents so powerful a barrier that septicaemia cannot occur once an intact wall of granulation tissue has been formed. eventually all the fibroblasts and the fibres which they produce run in this direction. The periosteum is usually torn through and separated from the bone to a varying extent in the neighbourhood of the breach. or in filling the gap by connective tissue when the original tissue has no power of regeneration. in liver and kidney parenchyma. What is repair ? Describe in detail the process of repair in a fractured bone. The process of repair may result in regeneration of normal tissue e. are osteoblasts. The proliferation takes place in cells of the endosteum and of the deep or cambium layers of the periosteum as well as in cells derived from the bone especially from the Haversion canals. The term repair refers to the process of restoration to a normal stage after injury. Q. Till the leucocytes have overcome the infection. In the later stages and in deeper layers. When the surface is covered by epithelium the process of de-vascularisation begins. the young bone cells and the fibrils are seen to become enclosed in a . The granulation tissue grows in maturity from below upwards. Soon there follows reaction on the part of the vessels. The process of repair begins by proliferation of cells and . the wandering cells are mainly macrophages and lymphocytes.11.g. 1. formation of new blood vessels. On account of its cellularity a granulating surface has a remarkable power of resisting bacterial infection. The new vessels gradually disappear and the scar which is first red becomes white and bloodless.infection. The direction depends largely upon the pull which is exerted on them. there is necessarily tearing of blood vessels and of soft tissues and a varying amount of haemorrhage occurs between the broken ends. In the process of bone formation. The new blood vessels accompanied by the cells grow out from the pre-existing blood vessels and make their way into the clot which gradually becomes replaced by a cellular and vascular tissue.

suppuration may in this way. The newly formed bone has a somewhat spongy character. be kept up for an indefinite period of time. There is an advancing line of ordinary granulation tissue behind which granulation goes on and ultimately any space occupied by pus may be obliterated and the process of bone formation may be completed. Loss of fracture haematoma. Poor reduction. the newly formed bone is not only more abundant but is arranged and moulded in a striking way. which forms the permanent union . so in the case of compound fracture there may be considerable and irregular formation of new bone. When a sequestrum is present. Just as in soft tissues.somewhat homogeneous matrix forming trabeculae of osteoid tissue which become osseous (bony) tissue by deposit of lime salts. 5. Infection. the pus being discharged from the sinus which leads down to the dead bone. islets of young cartilage may also develop especially when there has been much movement. pus forms around it . this is known as the definitive callus. Causes of delayed union 1. 4. When abone has been united in a wrong position. according to the muscular requirements. 7. Ischaemia. Parts of the callus are penetrated and resorbed by the new blood vessels surrounded by osteoblasts and these cells then lay down bone by lamellar apposition in the form of Haversian systems. it becomes a nidus for organismal growth. 2. While the newly formed tissue is mainly a vascular osteoid and osseous tissue. Improper immobilisation. The callus is sometimes artificially divided into an internal callus in the medullary cavity. It is then known as provisional callus. The repair of the compound fracture proceeds in a similar way but entry of organisms may cause suppuration and may interfere with formation of callus sometimes leading to resorption of callus already formed. The next stage is one of strengthening the union and adapting the configuration of the bone to the functional requirements. This process goes on till a more compact type of bone is produced. . The external callus is to a great extent absorbed so that if there has been a proper apposition. an intermediate callus between the ends of the bone. Pro-visional callus is formed rapidly and serves to bring about early union. 3. Destruction of fragments. Interposition of soft tissue. When there is exit for pus the healing takes place very much as in a granulating fracture would. The amount of callus varies very much in different cases and is least abundant in case of simple fractures. and an external callus outside. 6. and it coroes to enclose and unite the ends of the fractured bone. the configuration of the bone is largely restored. where long continued suppuration produces much overgrowth of fibrous tissue.

Lipoidal degeneration. Mucoid degeneration. Water is ab-sorbed into the cells which become swollen. Commonly affected organs are kidney. (iv) Malnutrition. Types ofdegenerations 1. (iii) Chemical poisons. The cells are swollen. . 4.9. Cyto plasm shows albuminous granules soluble in Fig. Kidney-Cloudy swelling. Fatty change (degeneration and infiltration)..--------------------------------------------------------------------------------------------------------------------------------------------------------- 2. 1. As. Hyaline degeneration.2. Fig. 5.Nutritional Disturbances DEGENERATIONS Q.1 Describe briefly the various types of degene-rations occuring in the tissues. (ii) Bacterial infections. Hg.Cloudy swelling Cloudy swelling results from disturbance in protein and water metabolism resulting in increased intracellular colloidal osmotic pres-sure. 3. 2. The organ is slightly enlar-ged and looks pale. Mitochondria are damaged. Cloudy swelling. Cloudy swelling It is the commonest form of degeneration caused by : (i) Acute fevers. Glycogen infilteration. Kidney . The cut surface is hazy. Hydropic degeneration. acetic acid. liver adrenals and heart. 6. 7.1. e. 2.g.

The organ becomes greasy and yellowish. infaras. The cellular hyaline is seen in : . Microscopic examination reveals small vacuoles representing fat globules dissolved away during staining process. The common organs are liver. It is commonly found in liver. 5.). it is called muCoid degeneration. dermoid cyst. When this process is exaggerated with excessive secretion of mucus associated with degeneration of the cells. (iv) Reticulum of lymph nodes (in chronic inflammation). There may be individual cells or fat cysts. Hyaline degeneration It is a non-specific degeneration affecting mainly the collagenous connective tissue and fibrous tissue-in the walls of the blood vessels (connective tissue hyaline. Tissue with such cells is said to have developed lipoidal degeneration. Mucous granules appear to be produced by mitochondria. (iii) Stroma of tumor . Fatty degeneration and infiltration (Fat.2. 4. kidney and heart. then moving to the Golgi apparatus. bydro-cele fluid etc. cholesterol becomes visible as needle shaped crystals. diethylene glycol and carbon tetrachloride. It also occurs due to anoxia in chronic venous congestion. Granules are absent in the cytoplasm. Thus it is degeneration of mucous membranes.ty change) Fatty degeneration is caused by poisons which may be bacterial or chemical. Lipoidal degeneration In the cells undergoing autolysis. Fatty infiltration is caused by overload of fat and lack of lipotropic factors. (ii) Chronic nephritis . It is present in (i) Vascular hypertension . Macoid degencration Mucus is a loose combination of protein with mucopolysaccharides of high molecular weight. Hydropic degeneration Very large amount of water is retained by the cells resulting in marked swelling. The nucleus is pushed to the periphery and becomes elongated and narrow. Cytoplasm is vacuolated or reticulated. atheroma. Connective tissue hyaline appears as a homogeneous swelling of collagen and the walls of the vessels in arteriosclerosis. The other form is cellular hyaline. 6. old haemorhages. Cholesterol crystals may be present in caseous tissue. Hydropic degeneration of liver is caused by poisoning due to chloroform. degenerating goitres. where they are changed into mucin granu-es. 3.

Causes of fatty degeneration 1. (i) Chemical : (a) Phosphorus. What arc the causes of fatty degeneration? How does it differ from fatty Infiltration ? Discuss the change occuring in any organ during fatty degeneration. (ii) Bacterial toxins : (a) Typhoid. Thus the two conditions are collectively termed fatty change. Macroscopic appearance : (i) Enlarged. (b) Collections of desquamated cells as in chronic nephritis. (iii) Greasy to touch. Neurogenic. (ii) Nucleus pushed to the periphery. 2. (ii) Pancreas (in amyloidosis). However. (iv) Soft.2. (b) Smallpox. (b) Arsenic. FATTY DEGENERATION Q. synonymous with fatty infilteration. Accumulation of fat in degenerated or damaged cells is termed fatty degeneration. (iv) Old infarcts of lungs. (iii) Prostate. 3. 2. (a) Tumours. What do you understand by Amyloidosis ? Describe the methods of demonstrating it in the laboratory. (c) Yellow fever. In stead. Poisons. AMYLOIDOSIS Q.(i) Renal tubules (in amyloidosis). Diminished oxidation (i) Severe anaemia (a) Pernicious anaemia (b) Post-haemorrhage anaemia (ii) Arteriosclerosis (iii) Imperfect nourishment. Fatty Liver. (d) Diphtheria. the differentiation is an obsolete one and now it is believed that fat seen in fatty degeneration is in fact also the infilterated fat. pathological adiposity. It is differentiated from the term fatty infiltration in which fat accumulates in obviously normal cells. Wallerian degeneration.2.3. is the term used for an increase in fat in the' tissues which normally store fat. (ii) Yellowish in colour. (c) Carbon tetrachloride. . Microscopic appearance: (i) Liver cells represented by large fat globules.

but chronic suppura-tive osteomyelitis is often a cause. in the sinusoids of the lobules. Van-Gieson's stain gives khaki colour. Methyl violet and cresyl violet give a metachromatic reaction.involving the basement membrane. (ii) Primary. In the liver. Amyloid is demonstrated by its staining reactions. Periodic acid-Schiff gives an intense positive red reaction 5. amyloid may be found lying under the epithelial cells of tubule. With ultraviolet light. hepatic cirrhosis and rheumatoid arthritis.5. Amyloid is a glyepprotein. amyloid in most cases affects primarily small arteries and veins of Glisson's capsule. It is likely to be most. kidneys. Methods of demonstration. 3. elastic and firm. the carbohydate part being a sulphated polysaccharide and the protein part being globulin. Still later it extends out through the pulp of the spleen. Amyloidosis a type of cellular degeneration in which there is a deposition of amyloid in the tissue. particularly chronic suppuration. 4.. 2. In the kidneys. It may also be secondary to nonsuppurative tuberculosis. however. Iodine solution produces a dark brown colour when poured over the cut surface of an organ. As it becomes more extensive. the amyloid is found first in the media of the central arteriole of the follicles. amyloidosis is secondary to other disease. 2. 2. liver and adrenals but may also be present in other organs. leprosy. extensive. The following methods are employed : 1. 6. Congo-red produces a brilliant pink colour. the amyloid material staining rose red whilst the surroun-didg tissue is coloured blue-the most reliable reaction. tumour. spleen. In the spleen. particularly in the middle parts of the lobule. to lesser extent. syphilis. the central and peripheral parts of the lobule also are affected. usually along the walls of the splenic sinuses. amyloid gives a specific bright yellow fluorescence.Q. In advanced cases. Secondary amyloidosis affects principally the parenchymatous organs viz. Grossly the kidneys are enlarged but may be shrunken in the chronic cases owing to the associated fibrosis. Here it appears immediately outside the endothelium of sinusoids. Vsually this is the result of chronic tuberculosis of lungs. 2. in the interlobular arterioles of the cortex. What are its effects ? Q. Localised. A cut surface looks waxy and transluscent. bones and joints. Describe the lesions in primary generalised amyloidosis. Grossly the organ is large. Generalised Secondary Amyloidosis Most frequently. Name the various cellular degencrations. Describe the various types of amyloidosis. the change is seen first in the capillary loops of the glomerular tufts. Generalised: (i) Secondary.' chronic nephritis. Types of Amyloidosis 1. It is also likely to be found in the walls of the arteriae rectae of the pyramids and. As the condition advances the pressure atrophy of the liver cells .4. Subsequently it appears in the follicles as a network made up of very coarse fibres which finally collect to form a solid mass of amyloid.

Amyloid Spleen. Grossly. Elastic. 3. Amyloid deposited in : (i) Walls of the arteries in Malpighian bodies. heavy and firm. bronchi and nasal septum are sometime composed mainly of amyloid. It may or may not be preceded by degenerative changes. Endocrine glands : Pituitary. NECROSIS Q. Macroscopic appearance : 1. it is the rarest form. Heart : Amyloid is found in the subendothelial connective ' tissue of the endocardium of the right atrium. thyroid. Amyloid disease of the intestine is often attended by watery diarrhoea. ' 5. adrenals.becomes more and more marked and amyloid from adjacent sinusoids may fuse to form a solid mass of considerable size.I. A slice looks waxy and transluscent. the liver is enlarged. Generalised Primary Amyloidosis This idiopathic type of amyloidosis is rare and is characterised by the amyloid deposition. A cut surface looks waxy transluscent. (iii) Reticulum of the pulp. Firm. probably as a direct effect of suppuration on adjacent tissue elements. The amyloid is deposited between the muscle fibres. Enlarged. 3. 7. When it is preceded . 4. because of limitation of nutrition. whereas the nutritional changes are best seen in the kidneys. Define necrosis. thereby leading to cloudy swelling. G. However. Skeletal muscles. : The tongue is enlarged and voluminous (macro-glossia). in mesodermal tissues viz. The amount of amyloid may be so great as to substantially limit the internal callibre of the affected vessels.2. Urinary system : Ureters and bladder. the disease may not lead to any detectable effect on the function of an organ. Localised Amyloidosis Localised amyloid deposits are observed in the Vicinity of abscesses and the lymph nodes draining them. Mention inbrief. probably due to increased permeability though this is not certain. Not withstanding the presence of a considerable amount of amyloid. 4. I. (ii) Connective tissue of the venous sinuses. Respiratory tract : Larynx and lungs. The intestines are affected particularly in the muscular coat. Skin.T. 6. when they still form part of the living body. often massive. Effect of Amyloidosis The amyloid deposit may cause injury to cells because it accumulates in amount sufficient to produce pressure upon surrounding cells leading to atrophy of these cells. 2.6. causes and types of necrosis. 2. Cellular atrophy is best seen in the liver. Small connective tissue growths in the larynx. fatty degeneration and atrophy or necrosis. Microscopic appearance. By necrosis is meant death of a cell or group of cells. It may occasionally be found in the capillaries or the myocardium of the ventricular walls. but occasionally amyloid may be found sharply defined in the capillary loops of the villi.

It occurs in the organs exposed to atmosphere directly or indirectly e. Caseation is the characteristic necrotic change of tuberculosis and syphilis. (3) Cassation Necrosis. 5. It is the commonest form and is seen in the infarcts of the spleen and kidney. but at the margin of the infarcted area there is a gradual process of absorption owing to the action of the proteolytic enzymes in the leucocytes brought about by the circulating blood. *lnitials remembered by the word 'RESTED' 4. strong acids. It frequent gets calcified. Lipase acts upon the surface of the omentum and the pancreas with the production of small opaque white areas of fat necrosis. It occurs in the central nervous system. The change probably. (1) Coagulation Necrosis. This isseeninaninfarct caused by blockage of a vessel by a blood clot which produces immediate local anoxia. Diabetes-Due to narrowing of arteries. 2. All the cellular detail is lost. Embolism-Due to blockage of arteries. (4) Fat Necrosis. in some way.by degenerative changes. all the details of structure are wiped out. inflammation is produced . lung. Both the cells and the stroma are involved. The part becomes dry. It may also result from trauma.g. Fat necrosis occurs in acute pancreatitis. 6. homogeneous opaque. Types of necrosis. Thromboangitis obliterans (Buerger's disease). Ergot poisoning 3. Excessive heat. What is gangrene ? Describe its causes and types in detail. . ischaemia and followed by putrefaction. cervix etc. Raynaud's disease due to spasmodic narrowing of the arterioles 2. with the production of a dry. the term 'necrobiosis' is applied. Even if the loss of blood supply is incomplete the cells may be killed. (3) Physical irritants. (2) Bacterial toxins. excessive cold. Causes. (2) Liquefaction Necrosis. In the course of time calcification may occur. radiation. and the fluid material is absorbed leaving a cyst like space. Old age (Senile)-due to narrowing of arteries by arteriosclerosis. The coagulated material may remain unchanged for long periods of time. There is COagulation of the cytoplasm by intracellular enzymes. (4) Chemical irritants. The necrosed areas becomes softened and liquefied. Causes of gangrene? The part may be killed by putrefactive bacteria (primary gangrene) or death of part may be produced by some other cause e. GANGRENE Q.7. the result is necrosis. Caustics. Perhaps some of the surrounding lymph may be absorbed and coagulated in the same way. depends upon the high lipid content of the nervous tissue. Primary gangrene is produced by Clostridium welchii and fusiform bacillus. Caseous material has a high fat content. If the toxin is weak. What is gangrene ? Gangrene is death of a part accompanied by putrefaction of the tissue by saprophytic bacteria.. The causes of secondary gangrene are as follows* : 1. bowel.g. In this type. (1) Loss of blood supply. mouth. if it is strong. trauma. skin. cheesy granular material which is completely amorphous.

the neighbouring muscles remaining unaffected. Dry gangrene . Dry gangrene Dry gangrene occurs where there is little fluid in the tissues owing to vaporisation or a good venous drainage. lack of vaporisation.Types of gangrene I. Deficient intake of vitamin B-complex especially of nicotinic acid. II. Secondary gangrene: 1. etc. pulseless and there is no collateral circulation. The organism has practically no power of breaking down proteins.. predisposes to the condition. affects a muscle throughout its length. Noma. Gas gangrene The affection is common in the wounds inflicted in wars or in street accidents. confined to the extremities and is caused by the gradual narrowing of the lumen of an artery by arteriosclerosis so that the tissues have a time to dry out. In the early stages there is no pus formation and very little emigration of leucocytes. having been killed by the Clostridium welchii are invaded by putrefactive organisms and true gangrene results. There is. 2. with or without a slight injury. The infection is predisposed by damaged muscle and by foreign bodies in the wound as the necessary anaerobic conditions are then more easily established. The affected muscles become swollen and pinkish and are crepitant owing to the formation of gas bubbles by the fermentive action of the Clostridium welchii on the muscle sugar. Later the tissues. Moist gangrene develops also when there is sudden obstruction of an artery as the part has no . thus. The part is cold. therefore. It is. The part contains so little blood that invading bacteria grow with difficulty in the dead tissue and spread of the gangrene is slow. there is abundant fluid in the part due to venous obstruction. Noma It is gangrenous condition which occassionally occurs in poorly nourished children especially after some debilitating infection. the dead tissue then undergos putrefaction. At this level. a condition which favours the growth of putrefying bacteria.. Gas gangrene. shrivelled and dark. a disintegration and breaking up of tissue beyond what is seen in simple necrosis. Moist gangrene In this type. a line of separation is formed between the living and dead tissue and finally brings about complete separation The microscopic picture is one of complete necrosis. It begins in one of the toes. 2. Primary gangrene : 1. It begins on gum margin and spreads to the cheek where an inflammatory patch of dusky red appearance forms and then becomes darker in colour and ultimately gangrenous. owing to the spread of the organisms within the sarcolemmal sheath. The original necrosis is caused by a characteristic fusiform bacillus. The infecting organisms are anaerobic clostridia of which Clostridium welchii is the most common and important member. Moist gangrene. The part becomes dry. but in addition there is usually a blurring and sludging of outline. The gangrene extends slowly upwards until it reached a point where the circulation is sufficient to keep the part alive. a rapidly spreading oedema followed by necrosis which..

The part becomes foul smelling. so that blebs of fluid form under the skin and bubbles of gas give an emphysematous crackling when the part is palpated. the overgrowth of connective tissue becomes very marked. the kidneys and heart to lesser degree whilst the central nervous system is only slightly affected In the great majority of cases of wasting disease. There is liquefaction of the tissues and sometimes gas formation. its functional activity is stopped and it undergoes atrophy. however. The functional parenchymatous elements of the tissue then undergo atrophy and sometimes there is also a concomitant overgrowth of the connective tissue. Similarly tubules of the kidney undergo atrophy when their glomeruli are thrown out of action. The classical example in the bowel is the gangrene of the strangulated hernia. Owing to the abundant moisture. the blood supply diminishes. atrophy is seen is cases of starvation. anaemia and weakness. The muscles around a joint which has been fixed for some time . It may also develop in naturally moist external organs e. When the muscle cells of arterial wall are atrophied.. Accordingly it is likely that atrophy depends on diminished metabolism. the condition being called fibroid atrophy. such as malignant growth of the alimentary tract. the liver and spleen are markedly affected. when the reduction is not so severe as to cause fiecrosis.8. emaciation depends chiefly upon utilisation of fat of the adipose tissue but there is also a great wasting of the tissues. pancreas has its duct obstructed. (iii) Interference with nerve supply. when veins as Well as arteries are occluded. Diminished Functional Activity Diminution in the ketabolic process leads to anabolism below the normal and thus to diminution in size of the cells. The term cachexia is often applied to a condition of wasting.time to become dried up.g. When a part is under-functioning. The tissue becomes rotten and putrid. a toxic element is concerned in production of the wasting. there is rapid growth of putrefactive bacteria. The absorption of toxic products causes profound toxaemia and finally death. 2. (ii) Diminished functionl activity. chronic tuberculosis or suppuration. Defective Nutrition This may be produced locally by arterial disease interfering with blood supply to a part. (iv) Continuous pressure. The various organs may thus diminish in weight. This is probably compensatory since it gives support and minimises dilatation. Various degenerations may thus come to be associated with atrophy and secondary anaemia is present. The local spread is rapid and there is no attempt at forming the line of demarcation. What is 'atrophy'? Give an account of the causes. This disuse atrophy is seen when a gland e. This is often well seen in the heart wall and in the kidneys where small atrophic depressions result from narrowing of the lumina of the small arteries. lung) or in the extremities. The term 'atrophy' refers to the acquired wasting or diminution in size of a cell or of the essential tissue of an organ. General. vulva. .g. It occurs in the internal organs (bowel. Causes of Atrophy (i) Defective nutrition. and it might be supposed that this is the cause of atrophy. ATROPHY Q. the latter condition being absent or little marked in case of pure starvation. etc.

What are the types of pigmentation occuring in the tissue ? Describe each type with suitable examples. there is active absorption of tissue by cellular activity. is seen in myxoedema due to thyroid deficiency. There occurs marked atrophy of the structures of skin. Wallerian degeneration takes place. in which the myelin breaks down into fatty globules . Even bone may undergo atrophy from pressure but in this instance. hair follicles. PIGMENTATION Q. sweat glands.g. 2. A striking example of true atrophy in the adult. the motor nerves. • Types of Pigmentation 1. Haeroatogenous pigmentation : (i) Malarial pigmentation : (ii) Haemochromatosis (iii) Biliary pigmentation. cysts. There is not only a simple wasting but also more active degenerative changes in the nerve fibres and muscles.with the Nerve Supply This form of atrophy is seen where there is any destructive lesion of the lower motor neurones or their axons. and sebaceous glands. By inhalation: . Thus the pressure atrophy may be produced by simple tumours. This bones of the limb may become thin and light.9. 3. Continuous Pressure The continuous pressure acts mainly by interfering with the blood supply and also the functions of a tissue. in cases of infantile paralysis.. Melanin pigmentation: (i) Addison's disease (ii) Chloasma (iii) Vitiligo (iv) Irregular pigmentation of skin : (a) Chronic arsenical poisoning I (b) Bronzed diabetes (c) Familial multiple polyposis (v) Melanosis coli (vi) Ochronosis. In the former. Interference. This type is often called neuropathic atrophy. Sometimes marked atrophy occurs also in the bones from the same cause e. Exogenous pigmentation 1. Endogenous pigmentation 1.undergo marked atrophy and the bones may also be affected.2. II. fatty degeneration also occurs followed by absorption of the sarcous substance and increase of the interstitial connective tissue. Deficiency of the Endocrine Glands The effects of endocrine deficiency are seen mainly when it occurs at an early period of life. so that the full development of the body is interfered with and thus hypoplasia results. etc. This is especially seen in the deficiency of thyroid and of the anterior lobe of the pituitary. Atrophic pigmentation: (i) Brown atrophy (ii) Fuscous degeneration.. however. i. whilst in the latter.e. osteoclasts being concerned in the process.

There may also be pigmentary deposit on the inner surface of the checks on a line corresponding to the junction of the teeth. (iv) Chronic arsenic poisoning. The resulting pigments may be deposited in the tissues around some local destruction. or in certain organs where there has been a process of . conjugated with glucuronic acid is excreted in the bile. may become of deeper tint under the influence of oestrogenic and melanocyte stimulating hormone. pigmented patches occur on the skin of the face. Melanin pigmentation occurs in the following conditions. the position of the deposit being apparently determined by irritation. the nipples.(i) Anthracosis (ii) Silicosis. Normally the breakdown of haemoglobin begins with opening of the porphyin ring system. Endogenoas Pigmentation 1. especially in the parts exposed to light and in those normally pigmented. haemoglobin is broken down in similar manner and many cells have the power to effect the change. e. Following destruction of the adrenal cortex there occurs a general increase in pigmentation.g. and pigmented parts. (i) Addison's disease. They are related to the aromatic compounds. (v) Neurofibromatosis. Melanin Pignientation. It is a condition sometimes due to ovarian disorder and sometimes related to pregnancy. The residual biliverdin pigment is then reduced to bilirubin which is absorbed and carried by the plasma *a-globulin to the liver where it is dissociated and the pigment. The only cells in the skin which are dopa-positive in vivo are the dendritic cells which lie extended between the basal cells of the epidermis. These cells are the only true melanoblasts and after elaborating the pigment in the form of fine granules they transfer it by means of their processes into the basal epidermal cells and also into certain phagocytic cells in the dermis which may thus become heavily pigmented with coarse pigment granules. and on the sides of the tongue. that following a haemorrhage. tyrosine. (iii) Leucoderma (vitiligo) may be attended by increase in pigment in the intervening parts. They are formed intracellularly from colourless precursors.. (vi) Bronzed diabetes. melanogens. In the affected areas the dendri-tic cells are of abnormal structure and have lost their capacity to oxidize 'dopa' to form pigments. (vii) Peutz syndrome. The melanins are iron-free sulphur containing pigment varying in colour from pale yellow to deep brown. (ii) Chloasma. 2. by the metabolic activities of the cells and are very stable substances resistant to acids and many other reagents. e. These cells are 'dopa-positive'. By ingestion : (i) Argyria (ii) Chronic lead poisoning. On treating sections of the skin with dihydroxyphenylalanine (dopa) certain cells in the epidermis oxidize this subsiance by means of an enzyme like tyrosinase and become blackened in consequence. Iron is carried away attached to the plasma *bglobulin transferrin (siderophyllin) for preferential reutilization in blood-formation. Hacmatogenoas pigmentation.g.. 2. but soluble in strong alkalis. In pathological states. phenylalanine and tryptophan and may be formed from such substances by oxidation.

thyroid etc. It is found both in the free condition and within cells. the change being known as fuscous degeneration. etc. in purpuric diseases. In the heart muscle the pigment accumulates in the central parts of the cells at the poles of the nucleus. 'so that in the lower parts hyaline cylinders of brownish-green colour may be present. The pigments usually deposited are haematoidin (iron-free) and haemosiderin (iron-containing). In the last situation a considerable amount of pigment is met with in senile insanity and allied conditions. Haematoidin is formed mainly from large accumlations of blood . The degree . 3. usually with enlargement. Accumulation of haemosiderin in organs. the term. and in wasting diseases this accumulation of pigment is more marked. or visceral siderosis occurs in malignant malaria and where there has been much haemorrhage into the tissues. cinnabar and various organic substances. Exogenous Pigmentation 1. and is taken up by phagocytes and deposited in the organs. It appears to be an inherited abnormality of iron metabolism leading to excessive absorption.g. but the accumulation becomes excessive in those whose occupation exposes them to an atmosphere rich in dust. where it remains practically unchanged for many years. haematin. Similar pigments may occur in the liver cells. In the liver it is always accompanied by a somewhat fine cirrhosis. most prominently in the central parts of the lobules. but the haemosiderin may occur in even greater concentration in the lymph nodes in upper part of the abdomen. Haemochromatosis. haemorrhagic infarct. Portions of the pigmented cells are broken off and form granular collections In the tubules. thus the rhombic crystals are often met with in the sites of old cerebral haemorrhages. By inhalation. This term is applied to a condition in .general blood destruction. The malarial parasites within the red corpuscles produce from the haemoglobin a dark-brown pigment. The reabsorbed bile pigment is excreted by the kidneys. It occurs in the skin especially around the sweat glands. The lungs may be infiltrated in this way by foreign particles of various kinds-coal. gastric glands. . brown atrophy is applied. Biliary pigmentation. especially in the central parts of the lobules. and these on passing downwards become condensed. heart muscles. e. iron. also in the pancreas. nonstriped muscle. The bile pigment retained in the liver cells is deposited in the form of small greenish brown granules. When haemorrhage occurs into the tissues the red cells become haemolysed and their haemoglobin is broken down by tissue enzymes and by the action of phagocytes.. without anaemia or other evidence of increased blood destruction. This occurs especially in jaundice. in the cells of the testis and the nerve cells of the brain cortex. In the later years of life a fine brownish-yellow pigment tends to appear in the heart muscle. Malarial pigmentation. A certain amount of coal-dust and stone dust enters and accumulates in the lungs of all individuals living in urban co'nditions. etc.and pathological results may follow. and a finely granular deposit occurs in the cells of the convoluted tubules. in thrombi. It become free when the corpuscles are broken down. and when this is associated with wasting of the muscle. The largest amount is present in the liver. which accumulates within the intracorpuscular parasites. the coloration of skin and other tissues is usually due to reabsorption of bile pigments from the liver after conjugation with glucuronic acid.which there is an extensive deposit of haemosiderin in the organs and tissues. in the form of very minute granules. Atrophic Pigmentation. stone. especially the spleen and liver.

S on it around the teeth produces the characteristic blue line on the gums. Large collections of carbon particles may provoke little or no overgrowth of connective tissue. The common example is argyria. Some particles are carried also by the lymph stream to the regional lymph nodes and then are conveyed by phagocytes into the lymphoid tissues. In the former case. anthracosis. in the skin. whereas this is very marked in the case of certain kinds of stone-dust. Tattooing.). The calcium is either removed from the bones or not laid down there. Pathological Calcification Pathological calcification may occur in normal tissue as a result of blood being flooded with calcium or it may represent the deposition of calcium in tissue which is injured. Dystrophic calcification. but deposited in other tissues. There is a tendency for any dying or dead tissue. By ingestion. . (vii) Lithopedion (calcified foetus from a tubal pregnancy). 2. (viii) Renal convoluted tubules in mercuric chloride poisoning. etc. mesoblast can only produce mesoblast. (v) Phleboliths. ultramarine. is much more common. the more important being : (i) Caseous tuberculous areas free from viable tubercle bacilli. are taken up by histioeytes and lodge in small spaces or clefts in the connective tissue of the cutis. (vi) Degenerating uterine fibroids. dystrophic calcification. degenerating or dead. osteomalacia.. in which calcium is laid down in dying or dead tissue irrespective of blood calcium level. 3. etc. fine particles such as India ink. Both phosphate and carbonate are deposited in practically the same proportion as is found in the bone. more particularly the kidneys. liver and kidneys. introduced through the epidermis. (iii) Arteriosclerosis-Monckeberg's sclerosis. it is known as melastatic calcification and in the latter. In chronic lead poisoning an albuminate is produced in a similar way and the action of H. the condition ofsilicosis resulting. connective tissue metaplasia and endothelial metaplasia. metaplasia may be epithelial metaplasia. which results from the ingestion of silver preparations for long periods. Several examples of pathological calcification are often seen. accessible to the body fluids to become calcified. In tattooing. Metaplasia Metaplasia is the transformation of one type of tissue into another type.of irritation resulting depends on the nature of the particles. Thus depending upon the type of tissue involved. (iv) Healed endocarditis and pericarditis. cinnabar. general carcinomato-sis of bone and multiple myeloma. These are present especially in the wall of the intestine. Metaplasia is best seen in the closely related connective tissues as when cartilage is converted into bone. Necrosis and hyaline changes are the two chief antecedents of calcification. Metastatic calcification may be induced by repeated injections of parathyroid hormone or it may occur in decalcifying diseases of bone such as osteoporosis of forced immobility (poliomyelitis. Silver forms an albuminate which is carried in the plasma to various tissues and when it undergoes reduction. This process has define limits. An epiblastic tissue can only produce another epiblastic tissue. many minute brownish-grey nodules are formed.

Fibrous tissue.Circulatory Disturbances OEDEMA Q.common.). from gall stones. 2. Define the term 'Oedema'. cartilage or bone. When free. 3. ossification of the laryn-geal and tracheal cartilages is . When water collects in the tissues. columnar or even stratified. Common forms of Oedema I.2.. Collection of oedema fluid in the peritoneal cavity. Discuss the factors concerned in the development of oedema in the following conditions : (a) Acute nephritis. The commonest change is that of cartilage into a bone. if may be in free or combined form. 3. In place of being flattened it may become cubical.tion of fluid in the tissue spaces and serous cavities. As a result of continued irritation. Discuss in detail the various factors involved in the formation of oedema. kidney. This accumula-tion may be local or general.1. The term "Oedema" may be defined as an abnormal accumula. The more highly specialised glandular epithelia (liver. Collection of oedema fluid in the pleural cavity. In myositis ossificans. cartilage and bone are all closely related and one may become changed into another. Anasarca. Ascites.True epithelial metaplasia occurs in response to call for altered unction or at least the result of altered environment. Q. It may be encountered in the edges of a wound in the abdominal wall. the colu-mar epithelium of the gall bladder may also become squamous. myxomatous tissue. it lies between these elements and can be moved from one place to another. the columnar epithelium is changed into a stratified squamous form better suited to withstand friction. The cubical and columnar cells may surround spaces so as to give glandular appearance. 3. giving examples. 4. Connective tissue metaplasia is of common occurence. This is certainly not due to altered function but may be connected with the altered environment. (b) Nephrotic syndrome. Transudate is protein-poor noninflammatory oedema fluid as occurs in heart failure and kidney disease. etc. When combined. Exudate is the protein-rich inflammatory oedema fluid. If the prolapsed uterus becomes everted. Severe and generalised oedema causing diffuse swelling of all tissues and organs in the body) particularly noticeable in the subcutaneous tissues. Bone may be formed in the walls of degenerated arteries or in an eye which is destroyed and functionless. Hydrothorax. it is united with the protoplasm of the tissue elements. Endothelial metaplasia is observed when serosal endothelium as that lining the pleura or peritoneum is irritated. Pericardial effusion (hydropericardium). e. . appear to be incapable of true metaplasia. --------------------------------------------------------------------------------------------------------------------------------- 3.g. bone is formed in the voluntary muscles and may replace them to a large extent. Collection of oedema fluid in the pericardial sac. The cells of an osteogenic sarcoma of bone may form fibrous tissue. In old age.

. This is an important factor in the production of local but not general oedema. Milroy's disease or hereditory oedema is also probably lymphatic in origin. 2. chylous ascites and chylothorax in thoracic duct obstruction. Under normal conditions.hat a vicious cycle is formed.Mechanism of Oedema Five factors are involved in formation and promotion of oedema. The colloid osmotic pressure. Marked ascites. But when the vessels are damaged e. As the fluid increases. protein is almost completely prevented from passing out from the blood into the tissues. 3. Increased Capillary Permeability. The osmotic pressure of albumin is about four times that of globulin. as in malignant disease of the peritoneum may lead to generalised oedema (anasarca) owing to severe blood protein loss. water readily passes out through the capillary wall. Thus when there is reversal of albumin-globulin ratio (3: 1) as in subacute glomerulonephritis and nephrotic syndrome. Increased capillary premeability. for it lowers the colloid osmotic pressure of the" blood and raises that of the tissues. Increased hydrostatic pressure of the blood. Lymphatic Obstruction. Under normal conditions. A fall of plasma proteins below five percent will cause oedema. when the fluid is rich in protein content. The pressure in the capillaries depends upon the venous blood pressure and not upon the arterial pressure. so that obstruction to outflow through these channels will cause local oedema.. Diminished colloid osmotic pressure of the plasma proteins. As a result. water passes out from the vessels into the tissues and hence oedema develops. the lymphatic obstruction becomes more marked. Salt retention. In cardiac failure. swelling of the legs. Although the capillary endothelium is completely permeable to water and crystalloids.etc. anoxia. 5. in elephantiasis. scrotum.g. 1. Examples of lymphatic oedema are swelling of the arm in breast cancer. Thus long continued anaemia is apt to be associated with oedema. When the level of plasma proteins become low resulting in decreased osmotic pressure. oedema sets in. oedema will result. Much of the intercellular fluid in the tissues escapes by way of the lymphatics. so t. to the presence of tumour cells within the lumen or filariasis. the outward passage of colloids is closely related to the condition of the vessel wall. etc. the colloid osmotic pressure of the plasma proteins hold the water inside the blood vessels and prevents it from passing into the tissues. The pressure in the capillaries is the force which overcomes the colloid osmotic pressure of plasma and enables the normal passages of nutritive material into the tissues. The stretching and dilatation of the capillaries also renders them more permeable. The escape of proteins is of the greatest importance in the production of oedema. 4. they become readily permeable to proteins as seen in inflammatory oedema. by toxins. and the increased capillary pressure leads to oedema. Decreased Colloid Osmotic Pressure of the Plasma Proteins. . The oedema which follows thrombosis of the main vein of a limb is largely due an increase in the capillary blood pressure. therefore depends partly on the total amount of plasma proteins and-partly on their relative proportion. If it is increased. the venous pressure rises markedly. Pressure from outside may be due to a tumour or to collection of fluid. Increased Hydrostatic Pressure of the blood. Lymphatic obstruction. The obstruction may be due to inflammation.

3. Acute Nephritis. Hyperaldosteronism. Liver Cirrhosis. In nephrotic syndrome. Once oedema is established and the chlorides pass into the tissues with water. further contributing to increased hydrostatic pressure. The consequent diminished cardiac output induces : 1. however it is not the chief cause. 2. because diuresis may occur in nephrotic syndrome without any rise in the albumin content of the plasma. 3. It has been shown experimentally that if there is no sodium in the diet. oliguria due to glomerular damage. Hypoalbuminaemia cannot be the only cause of oedema. This diuresis may be due to an increase in plasma volume. The factors involved include. A further fall in the albumin figure is compensated by a rise in globulin. Nephrotic Syndrome. and hence fluid passes from the blood into the tissue spaces. Sodium Retention. the plasma proteins may be low without the production of oedema. The oedema in acute nephritis cannot' be due to protein loss in the urine since the plasma proteins are normal and the oedema fluid is rich in protein. It is a secondary factor as it does not cause the production of oedema but it aggravates and continues the already existing oedema. In renal oedema the withdrawal of salt from food is often followed by rapid disappearance of the oedema and a corresponding increase in the flow of urine. The protein content of the plasma in nephrotic syndrome does not usually fall below 4 G percent. The colloid osmotic pressure is lowered by loss of protein in the urine. content. Liver cirrhosis often produces generalized oedema. Generalised Oedema in Clinical States Congestive Heart Failure. 2. In congestive heart failure. 2. This is of great importance. Reduction in Plasma Volume. The normal colloid osmotic pressure is 40-50 cm. It is probable that the cutaneous capillaries are simultaneously damaged with those of the kidneys. owing to the smaller size of its molecule. Increased hydrostatic pressure due to development of arteriovenous shunts in the scarred liver tissue (portal hypertension).Chloride Retention. Deranged renal baemodynamics. All these factors promote salt and water retention. and hypo-volaemia. The protein lost from the plasma is albumin rather than globulin. The following factors are probably concerned with the production of oedema : 1. A second factor which may be partially responsible for the fall of the albumin content of the plasma is failure to synthesize new protein from the aminoacids. and increased reabsorp-tion of sodium and water from the renal tubules. more water is retained by the tissues because of increased osmotic pressure. Sodium retention due to increase of vascular bed. . in nephrotic syndrome it is 5-20 cm. Increased adrenergic stimuli. The capillary permeability does not appear to be increased in nephrotic syndrome as the oedema fluid and the ascites fluid content is low. A further factor is congestive heart failure with riss in capillary blood pressure. particularly excessive accumulation of oedema fluid in the peritoneal cavity (ascites). of water . oedema results primarily from increased hydrostatic pressure due to venous stasis. of water. Hypoproteinaemia. The factors predisposing to oedema are: 1.

Allergic or immunologic reaction (c) Lymphatic obstruction. Causes of Oedema A. Diminished renal perfusion 2. Injury .3. Malnutrition 2. It occurs in inflammatory allergic conditions e. (b) Increased tubular sodium reabsorption 1. Nephrotic syndrome 4. The increased permeability in allergic conditions is due to release of histamine from mast cells induced by antigen-antibody reaction. Increased venous pressure 1. B. Sodium retention (a) Excessive salt intake. 1. 3. Inflammation 2. Hay fever 4. Inflammation 2. Urticaria 3. Compression of wins eg. Liver cirrhosis. In occurs in : 1. (b) Leaky vascular endothelium 1. Increased renin-angiotension-aldosterone secretion Localized Oedema in Clinical States Impaired Venous Drainage. Lymphatic Obstruction. C.g. Protein losing gastroenteropathy. Trauma 4. Diminished effective osmotic pressure (a) Hypoproteinaemia 1. Neurohumoral excess or deficit. Incompetent venous valves e. by tumours. enlarged organs. 2. It elevates the capillary hydrostatic pressure thus causing localized oedema. Prolonged periods of sitting in normal persons.g. Congestive heart failure 2. Arteriolar dilatation 1. in deep veins of legs. Heat 3. Burns 3. Increased Vascular Permeability. Toxins 4. Angioneurotic oedema. Thrombosis e. tight garments. surgical dressings or plaster casts. 1. D. Loss of plasma osmotic pressure due to lack of synthesis of senim albumin resulting from hepatocellular damage. 4.g. in varicose veins. Cirrhosis 3. Anaphylaxis 2. Thrombophlebitis 3.

(ii) Thrombophlebitis. Describe the mechanism of formation of intra-vascular thrombus. 4. 2. Common in the (a) Coronary arteries.g. (b) Cerebral artery.(i) Traumatic (ii) Surgical (iii) Inflammatory (iv) Radiation. (b) Interference with respiration. What is thrombosis? Clotting of the blood inside a vessel during life is termed thrombosis. Describe the different varieties and their ultimate fate. It occurs in cavernous sinus infections of the face and in pelvic veins in puerperal sepsis. I.4. Causes of thrombosis There are three factors described as Virchow's triad. The thrombosis may be divided into two groups : (i) Venous thrombosis : associated with (a) General circulatory failure. Arteries. Congenital malformation or absence of lymphatics (Mil roy's disease). (b) Malaria. Types of thrombosis ? Thrombosis is classified according to its site : 1. (d) Femoral arteries. (b) Left ventricle. THROMBOSIS Q. 3. 2. There may be painful swelling of an entire limb developing after delivery. Parasitic infestations e. (c) Trauma Common site is the deep veins of calf muscles. Slowing of the blood stream More common in veins due to slow blood flow commonly seen as post-operative complication in patients with an ageing heart muscle Common in conge¯tive heart failure . (b) Simple thrombophlebitis-associated with inflammatory reaction in the vein wall without any evident bacterial infection. 3. (a) Septic thrombophlebitis is secondary to infection and inflammation of the vein wall (phlebitis). What is thrombosis? Describe its effects and sequelae. Heart. Veins. 3. Found in (a) Valves. filariasis. 3. It may be septic or simple.3. Thrombosis is essentially a platelet deposition. The veins are the commonest site of thrombosis. Q. (c) Aorta. (c) Left auricle. Capillaries. Occurs in (a) Sickle-cell anaemia.

Post-thrombotic ulceration. the thrombus is mainly formed by the progressive deposition of platelets. Infarction of the myocardium. as in an artery or over heart valve.especially when combined with confinement to bed. it is clinically silent. In the heart. the first occurence is deposition of platelets which become agglutinated and fused together. Fibrinolysis. Around the platelet masses thromboplastin diffuses and leads to coagulation in the interspaces. 4. 2. Embolism. as in a vein the deposition of platelets leads to the formation of trabeculae or laminae which grow out from the vessel wall and to the surface of which the leucocytes adhere. Mechanism of thrombosis. but if at the same time the damaged part is projected inwards. If a vessel wall is merely damaged. 5. the type of vessel involved and the degree of occlusion : 1. Restoration of the vascular channel after thrombotic occlusion may occur . Gangrene of the bowel. 3. In the process of thrombosis generally. Normally platelets flow in the central portion of the stream. (ii) Rapid production of platelets-after operation.. Changes in the blood (i) Increased stickiness of platelets. Effects of thrombosis. Finally when the Formation of a thrombus. periarteritis nodosa or disseminated lupus. Oedema of a limb. Changes in the vessel wait Injury to the intima may occur in the arteries. the platclets are brought into contact with its surface to which they adhere. Occurs in the lower extremities due to local venous hypertension following canalization. The following effects pay be produced depending on the site of the thrombus. of the deep venous system. If it is less rapid. Due to thrombosis of the mesenteric artery or vein or to arterial embolism. -after childbirth. 3. heaping themselves up and in this way starting a thrombus. The veins are liable to injury by trauma. -after injury. Gangrene of a limb. the smooth intima may be roughened by atheroma which also narrows the lumen and retards the stream. It may become necrotic as a result of malignant hypertension. 2. If this is rapid. the valves are injured by inflammation so that thrombi are deposited on the surface. The subsequent structure of the thrombus depends mainly on the rate of blood flow. (iii) Increased viscosity of the blood-In polycythaemia. 6. retina. the veins or the heart. is formed with relative rapidity and is mainly the result of ordinary coagulation. In the arteries. thrombosis may not occur. Occurs when venous thrombosis is complicated by perivenous lymphangitis. due to arterial thrombosis. As the stream becomes slow. When a pure thrombosis is completely successful in its function. Caused by thrombosis of a main artery or occulsion by embolism from a thrombus in the heart or aorta. When complicated by clotting it may or may not become clinically manifest. they flow in the peripheral portion. by pressure and by infection. Ultimate Fate (Sequelae) of Thrombosis 1. etc.

6. Firmly attached to vessel wall. the emboli may be : (1) Arterial. 1. the emboli may be :(1) Solid: (i) Detached thrombus. (3) Gas : Air. Essentially a conversion of fibrinogen into fibrin. Extravascular. In some instances. 3. Q. Fibrin threads and cellular components produce laminar lines ofZahn. What is thrombosis ? How does it differ from coagulation of blood ? What is thrombosis? (See Q. Weakly attached to vessel wall. Intravascular. What is embolism ? Partial or complete obstruction of some part of the cardi'o-vascular system by a foreign body transported by the blood stream if termed embolism. (ii) A mass of tumoni cells. 5. (4) Paradoxical: An embolus arising in the vein but obstructing an artery. It occurs in . 2. 4. Occurs in streaming blood. 2. 3. 4. 6. Differ dices from Coagnlation Thrombosis Coagulation 1. What is embolism ? What are the various types of emboli ? Describe the mode of their formation. Embolism common.6. (3) Lymphatic. 8. Thromboplastin not essential 3. Depending on the site.5. the young vessels that grow in from the vascular endothelium covering the thrombus anastomose and then enlarge to form new cannels by which the thrombus is said to be canalised. Depending on the physical state. 3. 7. Rubbery. The thrombus becomes permeated by young connective tissue cells and capillaries. (2) Venous. Occurs in stagnant blood. Essentially a platelet deposition. (ii) AmniotiC fluid. 7. Friable. Types of Emboli 1. Organisation. 5. 8. 3. 2. Venous thrombi may become infected with pyogenic organisms and may then undergo suppurative softening so that portions are carried away by the blood stream and give rise to abscesses in other parts of the body producing pyaemia. (iii) Parasites. non-laminated. (2) Liquid: (i) Fat gloubles. Infection. Homogeneous. Its substance becomes gradually absorbed and ultimately replaced by connective tissue. The fibrinolytic mechanism depends on the activation of plasminogen in the plasma and this may become very active when there has been large scale intravascular coagulation. EMBOLISM Q. Thromboplastin-an essential factor. 3. the latter growing in from the vasa vasorum and from the initial endothelium. Embolism rare.by a combination of fibrinolysis and shrinkage of the thrombus. 2.3).

Collateral circulation is usually inadequate. Kidney Infaret A cut surface shows wedge shaped area involving whole width of the cortex and some of the medulla. (a) The tumour cells may gain entrance in the blood stream and form an embolus in some distant capillaries. C. When collateral circulation is marked. The infaret is observed as an irregular area on the surface. What is an infarct ? t ' An infarct is an area of coagulation necrosis due to complete sudden loss of blood supply of an organ. Ligatures and contractures.. 3. In that case. the infaret is called 'red' haemorrhagic (e. 3. Ischaemia or local anaemia is the local diminution of blood supply due to obstruction of inflow of arterial blood. Air embolism.g. fluid embolism may occur during or immediately after labour. (i«) Tumour cell embolism may be formed in two ways. . .. If the cessation of blood supply is sudden and complete. (b) There may be growth of a tumour into a large vein and a portion of it may get detached. (ii) A venous thrombus commonly arises from pelvic veins. INFARCT Q. 1. 3. Ergot poisoning. heart and brain). What is an infarct ? Describe the pathology of infarction in kidney. Occurs in (i) Operation on neck. the result is infarction. Solid emboh. often slightly depressed . bowel and spleen). Causes of ischaemia A. (ii) Amniotic . (ii) Blood transfusions. Effects of ischaemia When the process of ischaemia is slow. Brain tissue is softened. carried by the blood and impacted in a vessel. What is ischaemia ? Enumerate its causes aad effects. Raynaud's disease. in kidney. 2. 1. Intravascular. Infaret is termed 'pale' when collateral circulation is minimal (e.8. Liquid embolism. (iii) Vaginal dousching. F'E 7. heart. Vascular.yet inadequate.congenital heart disease e. Mode of formation 1. Infarct of kidney. (i) Fat embolism occurs as a result of laceration of a vein surrounded by adipose tissue and its commonest cause is fracture of a long bone with laceration of the fatty marrow. lung and spleen. patent foramen ovale and septal defects. Tumours of surrounding structures 2. necrosis or gangrene. (i) An arterial thrombus may arise from left side of the heart or aorta. pale in colour and surrounded by a pink border. Fluid may enter through tears or during rupture of membranes through venous sinuses of the uterus. there is sufficient time for collateral circulation to develop. surrounded by a pink zone of hyperaemia. Extravascular. 2.g. in lung. Embolism. B. ISCHAEMIA Q. Microscopic examination reveals an area of coagulation necrosis surrounded by a zone of congestion. 2. the tissue changes are degenerative and atrophic with replacement fibre sis. laceration of a fatty liver and Caisson's disease.g. Endarteritis.7. Thrombosis. 3. 1.

3. (i) Dark and filled with blood and fluid. (v) Ischaemia and anoxia of the organs. the red cells disappear and decololisation takes place. (iv) Aortic aneurysm.I (i) Left atrial appendage in mitral stenosis. This material is produced by cortex of the kidney while the kidney loses the power to destroy it. 9. possibly due to the diversion of blood flow from the kidneys with consequent liberation of pressor substances but later the blood pressure falls. . The vasodepressor material is believed to be ferritin. 1. 3.A thin rim of uninvolved tissue separates the infaret from the capsule The emboli causing infaret of kidney may come from :. (ii) Fluid loss-Burns. I Infaret of Heart. -Anxiety states.5). (iv) Reduced arterial pressure.farct of spleen is red haemorr. crushing injuries to a limb. SHOCK Q. 2. 8. The lesions are those of anoxia and increased capillary permeability. Pathogenesis. The loss of capillary tone and increased capillary permeability have been attributed to the effects of anoxaemia leading to the liberation of vasodepressor material (VDM) from the liver and muscles.. bacterial toxins. (iii) Anoxia. In. (ii) Decreased venous return. are always pale for the haemoglobin is gradually removed. (v) Thrombosis of renal arteries and veins. They sequence of events in shock is believed to be : (i) Redaction in blood volume. Infaret of Spleen. (See Q.12). vomiting. Define shock. (ii) Paroxysmal tachycardia. owing to loss of tone in the capillaries throughout the body. 7.hagic. Kidney infaret).9. diarrhoea. Shock is the clinical manifestation of an inadequate volume of circulating blood accompained by physiological adjustment of the body to the progressive discrepancy between the capacity of the vascular system and the volume of blood to fill it. The shock may result from : I. Lungs . with result that blood accumulates in them and their permeability is increased so that plasma is lost into the tissues and the blood volume is further reduced. a vicious circle is thus established. I (ii) Mural thrombi from the left ventricle in myocardial in-farction. (vi) Reflex vasoconstriction. Increase in vasular bed. (See Q. Spleen Infaret. Acute circulatory failure : (i) Myocardial infarction. (ii) The capillaries are widely dilated. (ill') Alveoli show marked oedema. The infaret reaches the surface which is also involved. (i) Whole blood loss-Haemorrhage.. . Reduction of blood volume. Definition. (iii) Decreased cardiac output. The pressor substances causing initial hypertensive reaction are termed vaso-excitor material (VEM). Disenss its pathogenesis and poct-mortem appearance. (iii) Vegetations of bacterial endocarditis. Brought about by : (i) Neurogenic stimuli-Painful stimuli. Infaret of Lung. however. The vaso-excitor material and vasodepressor material are collectively termed humoral vasotropic factors. Post-mortena appearances. (iii) Cardiac temponade. Old infarcts. At first the blood pressure may be sustained (hypertensivereaction) or occasionally even raised. Fig. (ii) TOXins-Toxic metabolic products. (cf.

The pigment is haemosiderin.and red blood cells. The liver cells are degenerated and atrophic probably as a result of anoxia. Heart muscle :-Fatty degeneration. derived from the red blood cells Fig. 3. namely. The cut surface shows a mottled appearance of dark brown and light yellow areas (Nutmeg liver). but a pneumonic process may be added aa a result of terminal infection. These cells are known as heart failure cells.V. (ii) Pigment in the tubules. Microscopi. Cardiac. Describe the pathology of the liver and long in this condition. 5.3. tough and indurated. Changes in the liver Macroscopic. 9. (iii) Aortic valvular disease. Liver : (i) Fatty degeneration commencing in the cen-ral zone and extending to the capillaries. (ii) Mitral incompetence. 2. The liver becomes enlarged and tender. Changes in the lung Two forms are recognised. However. (ii) Foci of local necrosis in the cortex. 4. -(i) Mitral stenosis. The sinusoids at the centre of the lobule are distended with blood. (ii) Sinusoids dilated and engorged. it is a misnomer as the condition is not always associated with cardiac lesion. Describe the causes of chronic general venous congestion.C. (iv) Chronic myocardial failure. 1.Granulomata INTRODUCTION . -------------------------------------------------------------------------------------- 4. usually a terminal one. This condition has been called cardiac cirrhosis or cardiac sclerosis.2. the lung is filled with blood. brown in colour. In hypostatic congestion. the brown induration. Adrenals: (i) Cortex widened and bright yellow in colour. Causes. The lungs are voluminous. Pulmonary-(i) Emphysema.colly. Kidneys : (i) Severe tubular degeneration (Shock kidney). Microscopic. Lung-C. the alveolar vessels being widely distended and alveoli containing many red blood cells filled with yellow pigment. Brown induration is always associated with hypertension in the pulmonary circuit. (ii) Fibrosis. a chronic process and hypostatic congestion.10. whilst at the periphery the cells are normal or merely show fatty degeneration. the dependent part of the lung appears to be consolidated. CHRONIC VENOUS CONGESTION Q. In very chronic cases there may be collapse of the lobules and fibrous thickening of the walls of the central veins with extension of fibrous tissue into surrounding lobules. The air in the alveoli is replaced by plasma .

(i) Gramiloma inguinale. with viable bacilli in the sputum). like all macrophages.Q.4. reaching its maximum in women between 20-25 and 'n men . Infective granulomata: 1. (ii) Leprosy. Congenital infection through the placenta is rare. Spirochaetal.1. Thus the granuloma must be regarded as special example of inflammation a nd not as a tumour since the latter should have no co-relationship with the reaction to injury of limitation of infection. Infection is commonest under five years of age when it is likely to be rapidly progressive and fatal. Idiopathic. The lesion in granuloma is a small 1-2 mm collection of inflammatory cells. The characteristic cell is a modified macrophage (epithelioid cell) with abundant. (i) Sarcoidosis. Fungal (i) Actinomycosis. A granuloma is a variety of chronic inflammation characterised by lesions which tend to be strictly circumscribed and by cells of histiocytic rather than of haematogenous type. Infection with the human type is air-borne from patients "with pulmonary tuberclosis (i. In man it is mainly responsible for tuberculosis of lymph nodes and bones in children. Spread The tubercle bacillus re non-motile but it can be transported in the bodies of phagocytes.. Foreign body granulomata: (i) Lint granuloma. In the adult the discase in much more I chronic. Infection may occur through the alimentary tract by ingestion of infected milk especially in the rural population where proper boiling is not practised. are derived from blood monocytes. A number of epithelioid cells coalesce and fuse to form giant cells. (ii) Lymphopathia venerium. Etiology of Tuberculosis Tuberculosis is caused by the acid fast organism. 4. These are rich in endoplasmic reticulum. These are better adapted for extracellular secretion rather than phagocytosis. pale-pink cytoplasm. (v) Aspergillosis. Mycobac-terium tuberculosis. . 3. usually surrounded by a rim of lympbocytes. However. (iii) Lipogranuloma. Then it declines until late adolescene. (ii) Machiromycosis. are known to cause infection in human beings. principally modified macrophages. 4. (iv) Coccidiomycosis. (iii) Tularemia. Golgi apparatus. II. . Types of granulomata 1. 5. (iii) Blastomycosis. Epithelioid cells. Both types are equally pathogenic for man. The giant cells may be 40-50 n in diameter and may contain upto 50 nuclei. plasma cells and neutrophils. What is a granaloma and how docs it differ from a tumor ? Describe the various types of granniomata giving the histology of one of them. Two types. (ii) Berrylium granuloma. Bacterial (i) Tuberculosis. the epithelioid cells do not have marked phagocytic activity. Discuss the etiology and spread of tuberculosis. The bovine type bacillus is primarily a parasite of cattle. TUBERCULOSIS Q. Give the differences between lesions in childhood tuberculo* sis and adult tuberculosis. A granuloma is essentially a highly specific reaction of the reticuloendothelial system. between 40-50 years of age. In addition a granuloma may have fibroblasts.2. (i) Syphilis. 2.e. human and bovine. Viral. (ii) Yaws. vesicles and vacuoles.

Results from reaction or super infection. Histology of Tuberculosis. a simple bacillaemia results leading to isolated lesions in almost any organ of the body. Haematogenous infection less common. The caseous centre becomes surrounded with a fibrous capsule. macroscopic or microscopic. Foci in the regional lymph nodes also become encapsulated and calcified but may harbour tubercle bacilli for many years. Spread by lymphatics results in transportation of the bacilli from the infected lymph spaces to the regional lymph nodes whence they disseminate widely in the lymphatic system. While ulceration of a caseous focus into a vein results in general miliary tuberculosis and the circulation is flooded with bacilli. usually single.The spread may occur by: (i) direct extension. In the '. Cavities usually chronic and walled up. Ultimately the bacilli are poured into the venous blood stream through the thoracic duct. Healing takes place by fibrosis and scarring. Thus the bacilli are carried into the lymph spaces of the surrounding tis'sue. Describe the gross and microscopic appearance of tuberculous inflammation-with special reference to fibro-caseous pulmonary tuberculosis. (i(r)) Glandular involvement usually predominates. (iii) blood stream. Spread occurs along the lymphatics so that regional lymph nodes are enlarged and caseous. The extension is effected by amoeboid movement of the phagocytes harbouring the bacilli. In these cases. seldom more than one cm in diameter. Calcification and sometimes ossification occur and the healed lesion is represented by a small scar or calcified nodule. ureters and vas deferens. A chain of tubercles can be traced from the primary lesion to the infected lymph nodes. however. The primary or Ghon lesion is a small caseous focus.3. former case. usually acute and necro-tic. tiny miliary tubercles. Spread by blood stream may occur either via the lymphatic-venous route or by ulceration of a caseous focus into a vein. (vi) Haematogenous infection is common.3). (v) Cavities. Spread along the natural passages may occur through the bronchi. are present in every organ of the body. (Described in Q. Gross appearance The gross appearance varies in primary infection and secondary infection. (iv) Parenchymal lesions usually perihilar. Parenchymal lesions usually apical. (H) Healing takes place by calcification or by complete removal of tuberculous tissue. The venous blood carries the bacilli to the lungs and sometimes to systemic circulation. (ii) lymphatics. by direct extension occurs from the primary site of lesion. Glandular involvement not common. when present. 4. Q. (iv) natural passages. Differences between Childhood and Adnit Tuberculofis Childhood Tuberculosis Adult Tuberculosis (i) Usually results from primary infection. 4. One . it is difficult to be certain that the bacilli have not been carried along the lymphatics in the submucosa.

Primary tubercle. Fibrocaseous ¯ Pulmonary Tuberculosis. (Described if' Q. the ultimate fate varies greatly and thus the tuberculous lesions come to present very different characters. their nuclei cease to stain and ultimately they become fused into a homogeneous or slightly granulan. Sometimes certain amount of fibrinous exudate is added to the necrotic material. structureless. they are rapidly ingested by phagocytes and a focus of reaction occurs resulting in the formation of what is known as atubercle follicle. material. reticulum fibres are numerous. The nuclei are often arranged at the periphery or in clumps while the central part of the cell may show signs of degeneration being granular or hyaline in appearance. they are then called epithelioid or endothe-lioid cells. These nodules may be nearly of the fame character and therefore of the same age due to extensive dissemination of the bacilli about the same time. the centre of focus consists of a collection of swollen macrophages whilst around them there is a \ zone of round cells chiefly lymphocytes.of the caseous nodes may open into a blood vessel and cause general miliary tuberculosis. The tubercle nodules in various organs present several partially fused tubercle follicles. epididymus. (iii) Tuberculous granulation tissue. results. When the tubercle bacilli gain entrance into the blood vessel through lymphatics or through ulcer-tion of a tubercular focus into a blood vessel. spindle shaped or irregular in form. (vi) Fibrotic lesions. In the outer zone of the follicle. The giant cells are formed from endotbelioid cells. The typical follicle may appear to contain a central giant cell surrounded by a zone of a epithelioid cells and those again by a zone of round cells. however the central cells become swollen Fig. Amongst the epithelioid cells of the tubercle are the giant cells. The appearance in the secondary infection depends on the dose of bacilli and the degree of resistance. 9. (ii) Caseous lesions. 10. suprarenals. with somewhat irregular outline and numerous oval or rounded nuclei resembling those of the epithelioid cells. miliary tuberculosis. Some examples are as follows : (i) Acute miliary tuberculosis. These are known as Langerhan's giant cells. . At a very early stage. The periphery is thus composed at first of the remains of the outermost ring of tubercles and around these connective tissue may form. some by amitotic division of the nuclei while the cytoplasm does not divide but si'mply increases in amount while others are formed by fusion of endothelioid cells. Whilst the initial reaction conforms generally to the description given above. etc.11). Very soon. Soon macrophages be come oval. If the resistance is not so good there may be rapid excavation. and lose their outline. If the dose is small and resistance high there will be complete healing or a quiet fibro-caesous lesion. The endothelioid cells are derived mainly from the tissue histio-cytes and also from nongranular leucocytes which emigrate from the blood to become incorporated in the follicle. the ultimate result is a necrotic centre surrounded by epithelioid cells and these again by small round cells. Microscopic appearance When a few tubercle bacilli gain a foothold in a tissue. with fairly' abundant protoplasm and a faintly staining nucleus. encapsulating the lesion. Large areas of caseation result by the fusion of individual tubercles with caseation in the centre. Large caseous masses are specially common in the lymph nodes and often occur in the kidneys.

2. In the testicle. there is dense accumulation of lymphocytes and plasma cells especially around the sm^ll vessels and fibroblasts multiply and lay down collagen fibrils. This is usually on the genitalia but it may be extragenital e. Describe the types of lesions enconntered in ' syphilis with a reference to congenital syphilis. If usually develops in form three to four weeks after infection but this latent period may be two to six \veeks. present several varieties of the lesions at the same time. Later it is caused by a marked degree of fibroplasia. In the. the . They affect deep as well as superficial structures and show a tendency to necrosis and destruction.e. In two or three months after infection.g.4. The one is gross and localised (the gumma). A few giant cells may be seen at the margin. It first takes the form of a hard nodule but the surface tends to become ulcerated and a 'hard sore' or chancere is formed from the surface of which enormous number of spirochacies are discharged. but they 'are symmetrical in distribution. mucous membranes and the central nervous system. The chancre is the earliest clinical manifestation but from the pathological standpoint the chancre is really a late affair. The primary lesion appears at the site of inoculation". gumma forms a hard mass which may be confused with tumour. primary.4. localised. The lesions may be macular. Gummata of skin. . The regional lymph nodes are enlarged. The common genitalia sites are the peais in the male and the cervix in the female. The subsidence of the secondary lesions is followed by another latent interval during which all is quiet. yellowish. there is a latent period. In a year or not for many years a third set of lesions appears. These are not infective. homogeneous mass of rubbery consistence composed of usual mononuclear cells. These are not symmetrical. Swelling of the epitrochlear or posterior cervical nodes are specially characteristic. Two main types of tertiary lesions may occur. Primary lesion. i. 1. 3. secondary lesions appear in the skin. The nodes all over the body are enlarged. The lesions of the skin are of great variety. The gumma is a necrotic. The cervical chancre is highly infective on account of the moist character of its surroundings and it is easily overlooked owing to its bidden nature and freedom from pain and discharge.SYPHILIS Q. Tertiary lesions. Secondary lymphadenitis is one of the earliest changes. Microscopically. They are polymorphous in type. These persist for a period of months and then disappear There is no destruction of the tissue at this stage so that no scars are left.. In the course of a few weeks. The lesions encountered in syphilis are described in three stages viz. the other is microscopic and diffuse. but three is not the same complete wiping out of structure as in tuberculous caseation. Destruction of the tissue is seldom marked but the surface epithelium is usually lo^t. tongue and nose may lead to extensive ulceration The liver may show one or several masses which heal with fibrosis so that deep scars are formed producing a peculiar lobed appearance known as 'Hepar lobatum. healing occur? which may or may not leave a scar. Gumma in the bone.centre of the lesion necrosis and caseation occcur with the formation of peculiar gummy material. The primary lesion is generally single but may be multiple. secondary and tertiary. hard and shotty but not painful ' or tender. on lips and fingers. Secondary lesion. After the appearance of primary lesion. papular or pustular. mouth. The hardness is due to dense cellular infiltration but does not appear during the first few days.

These may affect chiefly the meninges. Congenital Syphilis Syphilis may be transmitted from the father or mother but in all cases mother is infected though the infection may not be manifest. There may be involvement of the central nervous system similar to that seen in the acquired form. There is no primary lesion. Ths child may be born dead showing well marked evidence of syphilis. When the latter involve forehead and face together with loss of eye brows and eye lashes. It is firm and usually painless. The child may be born alive with external evidence of syphilis. widely spaced. When the child is born dead. palms of the hands and the soles of 'the feet. The nodules vary in size form microscopic to 2 cm. either discrete or fusing to form large conglomerate masses. Involvement of conjunctivae leads to blindness . anus. Syphilitic epiphysitis is the most diagnostic feature. The child is usually premature and undersized. The chief microscopic dhange is an interstitial round cell (infiltration of many of the internal organs combined with a varying degree of fibrosis. ace well defined. If the child is born alive the skin may show varied lesions described in the acquired form. swollen and often smooth and glistening. The spleen and often the liver are enlarged.Lepromatous. An interstitial keratitis develops at the time of puberty producing a ground-glass opacity in the cornea. Enlargement of spleen is very constant. angles of the mouth. 2. have a tense overlying epiderm. In the difiuse lesions.brain and other places may be confused with tumours of these. tissue destruction but no caseation..5. Common sites of lesion are the buttocks. as infection takes place through the placenta. Tuberculoid. the braita and the spinal cord. The large nodules. Nerve deafness is common. The skin may be macerated. These are small. Borderline or Dimorphic. the testicle. diameter. The child may appear healthy but lesion? develop after. hearing. In the thoracic aorta a frequent result is the development of an aneurysm of that vessel. Lepromatons Leprosy This form is manifested especially in the skin by diffuse involvement in which the skin becomes erythematous. 4. the face is described as leonine. the spirochaetes are widely distributed and set up a diffuse chronic inflammatory reaction which lymphocy-tes and plasma cells. 3. LEPROSY Q. 2. the appearance is usually chara-teristic. There are three possibilities : 1. Projecting nodules may develop. Describe the local and systemic changes in a case of leprosy. In the liver this produces a fine form of intercellular cirrhosis. peg-shaped and central incisors are notched : molars are pitted and honey-combed. The liver and the other organs show the changes already described. The principal sites are the thoracic aorta and. There are four types of lesions in leprosy : I . are firm somewhat elastic and . The most ^rious of all the late lesions are those of the central nerous system which may appear many years after the original infection. In the late type. smell and taste sensations are sometimes lost. organs.4. Indeterminate. The permanent teeth show the appearance known as "Hutchinson teeth". often in the skin. lesions develop over a period of years. 3.

----------------------------------------------------------------------------------------------- . Dimorphic Leprosy The histology is not characteristic. Situated in the cori-urn. Tnbercnioid Leprosy Tuberculoid lesions are tiny granulomas. Sometimes tuberculoid lesions. The bacteria may also be found in vascular endothelium. often near blood vessels. tuberculoid lesions undergo extensive necrosis with the formation of painless ulcers. the lepromatous or tuberculoid features may be prominent. Infiltration of lymphocytes may be noteworthy. Sometimes there is an ingrowth of connective tissue and the lesion becomes cicaterized. mononuclear cells. They show a slight buidging . they may extend deeply Microscopically. pale yellow or light grey in crosf section. In rare instances. As change" occur. especially around blood vessels. and the overlying epidermis is often atrophic. in polymor-phonocicar leucocytes and even in epithelium. large mononuclears. closely resemble the granulomas of sarcoidosis. Occasionally. They ar? present as small clusters of organisms termed 'Cigar pack' and as large masses. plasma cells and multinucleate giant cells of Langerhan's type. Indeterminate Leprosy The lesions are not distinctive histologically. The large mononuclears and giant cell are often foamy and contain the acid fast bacilli. These foam cells may also contain fat. Hyperaemia is prominent in the erythematous macules. The lesions are smaller than the usual leproma and also differ in that they contain few demonstrable bacteria. and occasional giant cells. Extracellular organisms are also found but these are originally intracellular. lepromas are made up largely of large mononuclear cells without foamy cytoplasm. especially in the lymph nodes and bones. made up of lymphocytes. the nodule is made up principally of large. When in the s^in they are in the upper corium. with an irregular intermingling of lymphocytes.cut with resistance. called lazarine leprosy.

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