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General Pathology 4
Introduction to pathology
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HAEMORRHAGE
internally Haemorrhage into is the the serous escape cavities of blood (e. from haemothorax, a blood vessel. haemoperitoneum, The bleeding may haemopericardium), occur externally, oror into a hollow viscus. Extravasationofblood into the tissues with resultant swelling is known ashaematoma. Large extravasations of blood into the skin and mucous membranes are called ecchymoses. Purpuras are small areas of haemorrhages (upto 1cm) intothe skin and mucous membrane, whereas petechiae are minute pinhead-sized haemorrhages. Microscopic escape of erythrocytes into loose tissues may occur followingETIOLOGY,marked The blood congestion loss mayand be is largeknown and as suddendiapedesis.(acute), or small repeated bleeds may occur over a
period 1 of time tothe (chronic). vessel wall The e. variouspenetrating causes ofwound haemorrhage in the heart are as or undergreat vessels, during labour etc. 2. Spontaneous haemorrhage e.g of ananeurysm, septicaemia, bleedingdiathesis (such as purpura), acute leukaemias, pernicious anaemia, scurvy,
Inflammatory lesions of the vessel wall e. bleeding from chronic peptic ulcer, typhoid ulcers, blood vessels traversing a tuberculous cavity in the lung, syphilitic involvement of the aorta, polyarteritis
nodosa.
Neoplastic invasion e. haemorrhage following vascular invasion in carcinoma of the tongue
Vascular diseases e. atherosclerosis
Elevated pressure within the vessels e. cerebral andretinal haemorrhage in systemic hypertension, severe haemorrhagefrom varicose veins due to high pressure in the veins of legs or oesophagus. EFFECTS The effects of blood loss depend upon 3 main factors: the amount of blood loss; the speed of blood loss; and the site of haemorrhage. The loss up to 20% of blood volume suddenly or slowly generally has little clinical effects because of compensatory mechanisms. Asudden loss of 33% of blood volume may cause death, while loss of up to 50% of blood volume over a period of 24 hours may not be necessarily fatal. However, chronic blood loss generally produces iron deficiency anaemia, whereas acute haemorrhage may lead to serious immediate consequences such as hypovolaemic shock.
TUBERCULOSIS
CAUSATIVE ORGANISM. Tubercle bacillus or Koch's bacillus (named after discovery of the organism by Robert Koch in 1882) called Mycobacterium tuberculosis causes tuberculosis in the lungs and other tissues of the human body. The organism is a strict aerobe and thrives best in tissues with high oxygen tension such as in the apex of the lung.
MODE OF TRANSMISSION. Human beings acquire infection with tubercle bacilli by one of the following routes: 1. Inhalation of organisms present in fresh cough droplets or in dried sputum from an open case of pulmonary tuberculosis 2. Ingestion of the organisms leads to development of tonsillar or intestinal tuberculosis. This mode of infection of human tuberclebacilli is from self-swallowing of infected sputum ofanopen case of pulmonary tuberculosis, or ingestion of bovine tubercle bacilli frommilk of diseased
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Transplacental cows. 3. Inoculation routeof resultsthe organismsin developmentinto the of skin congenital may rarely tuberculosis occur fromin infected foetus from postmorteminfected mothertissue.
and is a rare mode of transmission.
SPREAD OFTUBERCULOSIS. The disease spreads in the body by various routes: 1. Local spread. This takes place by macrophages carrying the bacilli into the surrounding tissues. 2. Lymphatic spread. Tuberculosis is primarily an infection of lymphoid tissues. The bacilli may pass into lymphoid follicles of pharynx, bronchi,intestines or regional lymph nodes resulting in regional tuberculous lymphadenitis which is typical of childhood infections. Primary complex is primary focus with lymphangitis and lymphadenitis. 3. Haematogenous spread. This occurs either as a result of tuberculous bacillaemia because of the drainage of lymphatics into the venous system or due to caseous material escaping through ulcerated wall of a vein. This produces millet seed-sized lesions in different organs of the body like lungs, liver, kidneys, bones and other tissues and is known as miliary tuberculosis. 4. By the natural passages. Infection may spread from: i) lung lesions into pleura (tuberculous pleurisv); iil transbronchial >pread intotheadjacent lungsegments;iil) tuberculous salpingitis into peritoneal cavity(tuberculous peritonitis]; iv) infected sputum into larynx (tuberculous laryngitis); v) swallowing of infected sputum (ileocaecal tuberculosis]; and vi) renal lesions into ureter and down to trigone of bladder.
HYPERSENSITIVITY AND IMMUNITY IN TUBERCULOSIS. 1. In the primary infection, intradermal injection of tubercle bacilli into the skin of a healthy guinea pig evokes no visible reaction for 10-14 days. After this period, a nodule develops at the inoculation site which subsequently ulcerates and heals poorly as the guinea pig, unlike human beings, does not possess any natural resistance. The regional lymph nodes
an TUBERCULOUS individual with CASEOUS high degree PNEUMONIA. of hypersensitivity The caseous may spread material to from rest of a case the lung of secondary producing tuberculosis caseous in
pneumonia.
MILIARY TUBERCULOSIS. by entry of tuberculosis, of infection This is lymphohaematogenous sites The into spread pulmonary may vein occur spread to systemic of tuberculous organs and bone or isolated infection or marrow) isolated organ. from orintoorganprimaryThe focus spread or is later different either stages extra-pulmonary producing kidney, brain disseminated lesion in the development (e. liver, of miliary spleen, lesions within the lung (Fig. 6). The miliary pulmonary are millet artery seed- sized restricting (1 mm diameter), yellowish, firm areas without grossly visible caseation lesions necrosis.
Clinical Features and Diagnosis of Tuberculosis depending upon the location, extent and type
of features The lesions. clinical are However, manifestations as under: in 1. secondary Referable in tuberculosis pulmonary to lungs-such may tuberculosis be variable as productive which cough, is the common may apical be with type, changes haemoptysis,the like usual pleuralclinical
in and untreatedcases of
tuberculosis effusion,aspleural fever,effusion, nightnodularity,may sweats,dyspnoea, develop andfatigue, miliary systemic orthopnoea lossor diffuse ofsecondary weight etc. infiltrates Chest and i) amyloidosis appetite. X-ray the Mantoux may lung Long-standing show parenchyma. skin typical test. ii) ERR), 2. Positive Systemiciv) Chest sputum features-suchX-rayfor AFB
The diagnosis is made by the following tests:
(on smear orculture). iii) Completehaemogram (lymphocytesis and raised
(characteristic hilar nodules and other parenchymal changes). v) Fine needle aspiration cytology of an
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LEPROSY Leprosy or Hansen's disease (after discovery of the causative organism by Hansen in 1874), was
first described in ancient Indian text going back to 6th Century BC, is a chronic non-fatal infectious disease affecting mainly the cooler parts of the body such as the skin, mouth, respiratory tract, eyes, peripheral nerves, superficial lymph nodes and testis. Though the earliest and main involvement in leprosy is of the skin and nerves but in bacteraemia from endothelial colonisation or by bacilli filtered from blood by reticuloendothelial system, other organs such as the liver, spleen, bone marrow and regional lymph nodes are also involved. Advanced cases may develop secondary amyloidosis and renal disease, both of which are of immunologic origin.
Causative Organism The disease is caused by Mycobacterium leprae which closely resembles
Mycobacterium tuberculosis but is less acid-fast. The organisms in tissues appear as compact rounded masses (globi) or are arranged in parallel fashion like cigarettes-inpack. M. leprae can be demonstrated in tissue sections, in split skin smears by splitting the skin, scrapings from cut edges of dermis, and in nasal smears by the following techniques: 1. Acid-fast (Ziehl-Neelsen) staining. The staining procedure is similar as for demonstration of M. tuberculosis but can be decolourised by lower concentration (5%) of sulphuric acid (less acid-fast) (Fig. 6). 2. Fite-Faraco staining procedure is a modification of Z. procedure and is considered better for more adequate staining of tissue sections. 3. Gomor methenamine silver (GMS) staining can also be employed. 4. Molecular methods by PCR. 5. IgM antibodies to PGL-1 antigen seen in 95% cases of lepromatous leprosy but only in 60% cases of tuberculoid leprosy
Mode of Transmission Leprosy is a slow communicable disease and the incubation period between first exposure and appearance of signs of disease varies from 2 to 20 years (average about 3 years). The infectivity may be from the following sources: 1. Direct contact with untreated leprosy patients who
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shed numerous bacilli from damaged skin, nasal secretions, mucous membrane of mouth and hair follicles. Materno-foetaltransmission acrossthe placenta. 3. Transmission from milk of leprosy patient toinfant
- ClinicalFeatures i) The macules, skin The lesions two papules, 2. main which in ii) Tuberculoid LL The forms are are nodules lesions generally hypopigmented of leprosy leprosy: are or diffuse hypoaesthetic symmetrical, show i) The infiltrates. and distinctiveskin erythematous multiple, lesions or The clinical nodular slightly macules. features: but lesions hypopigmented the 1. may sensory There Lepromatouscoalesce single is disturbancea anddistinctor to as givea
- leonine is erythematous not as facies distinct appearance. as in TT. anaesthetic in TT occur as ii) either few asymmetrical lesions sensory impairment.
- Anti-leprosy vaccines is quite have long, been the developed efficacy of and such are vaccines undergoing will be human known trials after but a since number the of incubationyears. period of leprosy
- CausativeOrganism T. pallidum is a coiled spiral filament 10 um long that moves actively in fresh preparations. The organism cannot be stained by the usual methods and can be demonstrated in the exudates and tissues by: 1, dark ground illumination(DGI) infresh preparation; 2 antibody technique; 3, silver impregnation techniques; and 4. PCR as a research method. The organism has not been cultivated in any culture media but experimental infection can be produced in rabbits and chimpanzees. The organism is rapidly destroyed by cold, heat, and antiseptics.
- Immunology T. pallidum does not produce any endotoxin or exotoxin. The pathogenesis of the lesions appears to be due to host immune response. There are two types of serological tests for syphilis treponemal and non-treponemal. A. Treponemal serological tests: These tests measure antibody to T. pallidum antigen andare as under: i) Fluorescent treponemal antibody-absorbed (FTA-ABS) test. a) Agglutinin assays e .g. microhaemagglutination assayfor T. pallidum(MHA-TP), andSerodia TP-PAwhich is more sensitive) T. pallidum passive haemagglutination(TPHA) test. Non-treponemalserological tests. These tests measure non-specific reaginic antibodies lgM and lgG immunoglobulins directed against cardiolipin-lecithin-cholesterol complex and are more commonly used. These tests are as under: () Reiter protein complement fixation (RPCF) test:test of choicefor rapid diagnosis. ii) VenerealDisease Research Laboratory (VDRL) test: Wassermann described a complement fixing antibody against antigen of human syphilitic tissue.
- Mode ofTransmission Syphilitic infectioncan be transmitted by the following routes: 1. Sexual intercourse resulting in lesions on glans penis, vulva, vagina and cervix. 2. Intimate person-to- person contact with lesions on lips, tongue or fingers. 3. Transfusion of infected blood. 4. Materno-foetal transmission in congenital syphilis if the mother is infected.
- STAGES OF SYPHILLIS
General Pathology 4
Course: Introduction to pathology
University: Rajiv Gandhi University of Health Sciences
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