《病理学》教学课件：10 结核

1、Tuberculosis（结核）,病理系：刘颖 Mail: liu_,Introduction,A chronic infectious disease Mycobacterium Tuberculosis Pulmonary TB is the most common type. involve all organs (rare in thyroid, pancreas and myocardium) Characteristic changes: tuberculous granuloma+caseous necrosis,Epidemiology,History Worldwide 1.

2、7 billion infected 8-10 million new cases 3 million deaths China 0.55 billion infected 0.13 million deaths,Predisposing factors social factors: poverty, crowding, aging chronic debilitating disease: diabetes mellitus, hodgkin disease, pulmonary silicosis, alcoholism, et al immunity deficiency: HIV,E

3、tiology,Robert Koch 24th, March Pathogen species: M. hominis ( 人型） M. bovine (牛型） M. avium (鸟型） M. piscium (鱼型) M. murium (鼠型),human,HIV infected host,Pathogenicity Lipid: mycolic acid（分枝菌酸） cord factor（索状因子） Wax D（蜡质D） phospholipid（磷脂） mycosides（分枝菌糖苷脂） Protein：结核菌素 Glycogen,Etiology,transmission,R

4、espiratory tract (pulmonary T.B) : inhale the airborne organisms expose to contaminated secretions Digestive tract (intestinal T.B): drinking infected milk Skin injury: Congenital BCG : non pathogenic, living T.B ,undergoing 230 passages,13yrs）,Pathogenesis,infection disease Only a small fraction of

5、 those who contract an infection develop active disease.,Pathogenesis,Koch phenomenon: cell mediated immunity (CMI) accompanied with delayed tissue hypersensitivity (DTH),PPD test,PPD test false-negative false-positive,Pathogenesis,CMI and DTH are different immunoreactions Different antigens Differe

6、nt T cell subtypes The amount of organisms or antigen and Th1/Th2 excursion Different CKs Different methods to kill organisms,Pathological changes,Exudation dominant changes: happened in early stage of infection or deterioration of Dis. Predisposing factors: suppressed immunity, plenty of mycobacter

7、ium T.B high virulence and strong DTH changes: serous inflammation, serous-fibrinous inflammation location: pleura, meninges, peritoneum,Pathological changes,Exudation dominant changes: development: unstable absorbed without any changes change into proliferation dominant or necrosis dominant changes

8、 easy to find organisms,Proliferation dominant change (Tubercle formation, granuloma) Predisposing conditions: strong immunity few mycobacterium low virulence,Pathological changes,Proliferation dominant change (Tubercle formation, granuloma) Changes: Epithelioid cells Langhans giant cells Lymphocyte

9、s difficult to find organisms,Pathological changes,Necrosis dominant change Predisposing factors: weakened immunity, severe hypersensitivity large amount of mycobacterium T.B. high virulence Changes: caseous necrosis （干酪样坏死) Gross: granular, cheesy appearance( rich in lipid) LM: acidophilia granular

10、 materials without structure,Pathological changes,Necrosis dominant change easy to find organisms Development: Exist for long timing bomb The amount of mycobacterium will increase sharply when the disease deteriorate Fibrosis,Pathological changes,Pathological changes,exudation changes,granuloma lesi

11、on,caseous necrosis,Consequence,Healing exudative lesion: absorption proliferative lesion: fibrosis no organisms necrotic lesion: fibrosis and calcification (calcification foci may harbor viable bacilli for years),Deterioration 1. lesion enlarges, the disease progresses granulomaexudation change exu

12、dation caseous necrosis caseous necrosis foci enlarge (infiltrative progressive stage),Consequence,Deterioration 2. Cavitation and Dissemination caseous materials liquefy nature canal cavities formation in original sites mycobacterium disseminate to multiple sites open T.B lymphatic canal blood vess

13、el (disseminated stage),Consequence,Pulmonary Tuberculosis,Primary pulmonary T.B. Secondary pulmonary T.B.,Previously unexposed Most in children, aged or immunosuppressd persons (HIV) Exogenous organism Pathological change: Ghon Complex （原发复合征) 1-1.5-cm area of gray-white inflammatory consolidation

14、(lower part of upper lobe or upper part of lower lobe) Tuberculous lymphatitis Regional node involvement, often with caseate,Primary Pulmonary Tuberculosis,Ghon Complex,Chief implications: 1. It induces hypersensitivity and increased resistance 95% control 2. The foci of scarring may harbor viable b

15、acilli for years nidus for reactivation,Primary Pulmonary Tuberculosis,Primary Pulmonary Tuberculosis,Deterioration and Dissemination,C. bronchial spreading: uncommon in children.,A. blood circulation. acute miliary T.B. subacute or chronic miliary T.B. secondary or extrapulmonary T.B. (lie down),Ac

16、ute Miliary T.B.,Secondary Pulmonary T.B.,Previously infected Adult type Pathogenesis 95% endogenous seeding,Some special points,1. Location: apex of lobe low arterial blood pressure, less M , less ventilation, high O2 pressure 2. Changes: caseous necrosis - proliferation focus localization less lym

17、phatic and vascular spreading more bronchial dissemination 3. Long course of disease, complex changes,Pathological changes,Focal lesion: (局灶型） 1. location: 24 cm beneath apex of lobe 2. pathological changes: less than 2cm in diameter single or multiple focuses proliferation dominant caseous necrosis

18、 in central and around fibrosis 3. development: healing by fibrosis or calcification few become infiltrative lesion,Pathological changes,Infiltrative lesion （浸润型）: 1. source: focal lesion 2. location: apex or subclavical area (subclavicular infiltration) 3. morphology: exudation dominant, caseous ne

19、crosis in central 4. clinical symptoms,Pathological changes,Infiltrative lesion （浸润型）: 5. development: healing by absorb, fibrosis，calcification disease progresses, acute cavitation may occur caseous pneumonia spontaneous pneumothorax tuberculous pyopneumothorax chronic fibro-cavitative type,Chronic

20、 fibro-cavitative lesion(慢性纤维空洞型) 1. source: infiltrative type with acute cavity 2. Characters: single or multiple chronic cavities three layers-inner: caseous necrotic materials mid: tuberculous granulation tissue outer: fibrous scar diverse foci fibrosis (cirrhotic pulmonary tuberculosis),Patholog

21、ical changes,Chronic fibro-cavitative lesion(慢性纤维空洞型) 3. clinical symptoms open T.B. (mycobacterium in sputum) emptysis, laryngeal T.B., Intestinal T.B., cor pulmonale 4. development healing : small cavity scar healing large cavity open healing,Pathological changes,Caseous Pneumonia(干酪样肺炎） 1. source

22、: infiltrative lesion bronchial spreading of acute or chronic cavity 2. modality: lobular or lobar caseous pneumonia acute cavity ( local liquefaction). LM: caseous necrosis with serous-fibrinous exudate 3. Poor prognosis (百日痨 or 奔马痨),Pathological changes,Tuberculoma（结核球) 1. source: fibrosis of case

23、ous necrosis in infiltrative type bronchia closure leads to caseous materials fill in the cavity combination of several tubercular 2. pathological changes: caseous lesion with fibrous capsule 2-5 cm in diameter 3. prognosis: stable deterioration,Pathological changes,Tuberculous pleuritis: wet and dr

24、y wet type - Exudative pleuritis： Most in young people Source: mycobacteria dissemination from primary focus or hilar lymphnods DTH induced by protein of mycobacteria in pleura Pathological changes: serous-fibrinous inflammation Clinical symptoms Prognosis: 1. absorb 2. rich in fibrin may cause adhe

25、sion of pleura,Pathological changes,dry type - proliferative pleuritis： T.B. focus beneath pleura extend to pleura Most in apex of lobe, local pleura adhesion and thickening Caseous pleuritis rare,Pathological changes,Secondary Pulmonary T.B.,Systemic symptoms response to T.B. “toxic” components Loc

26、al manifestations: cough hemoptysis chest pain lower respiratory function,CPC,malaise, weary, night sweat, low fever in the afternoon, hectic rosy cheeks, loss of appetite,Hematogenic tuberculosis,Result from Primary tuberculosis or Secondary tuberculosis,systemic military tuberculosis pulmonary mil

27、itary tuberculosis acute military tuberculosis subacute/chronic tuberculosis,Primary P T.B Secondary P T.B Infection previously uninfected previously infected Patient children adults Special CMI and DTH occur in the course preexist Pathological changes Ghon complex various changes, localized, cavity

28、 Original focus lower part of upper lobe apex of lobe upper part of lower lobe Dominant changes exudation, necrosis proliferation, necrosis Dissemination lymphatic and vascular bronchial Course of disease short, self-control long, fluctuant , clinical treatment,Comparison,Extrapulmonary Tuberculosis

29、,Involve all organs Reactivation of latent foci Pathological changes and character of organs are correlative,Intestinal Tuberculosis,Source of Mycobacterium primary: drinking infected milk secondary: swollen mycobacterium contained sputum Location : any segment of intestine most common at ileocecal

30、segment: 1. rich in lymph tissue, easy to invade 2. long time for food to stay in this segment,Ulcerative intestinal T.B. Tubercles in lymph tissue fused necrosis ulceration Features of ulcer: 1. long axis of the ulcer is vertical to long axis of intestine, because of the circular lymphatics of inte

31、stine 2. irregular margin of the ulcer (rat-bite-like), caseous base and tubercular granulation tissue beneath, fibrin exudate and miliary tubercles in serosa,Intestinal Tuberculosis,Ulcerative intestinal T.B. 3. Intestinal straitness after ulcer healing Fibrosis leads to a adhesion among serosa and

32、 adjacent tissues Hemorrhage and perforation are uncommon Clinical symptoms: chronic abdominal pain, intermittent diarrhea and constipation, tubucular toxic symptoms,Intestinal Ulcerative T.B.,Proliferative intestinal T.B. proliferative changes dominant, causing thickening of intestine, polyposis, l

33、eading to abdominal mass and/or ileus ,Intestinal T.B.,Mesentery T.B.,Tuberculous peritonitis,wet type peritoneal tubercle greenish yellow or hematic ascites,dry type peritoneal tubercle, fibrin exudation extensive adhesion and rubber-like consistency of abdomen,Intestinal Tuberculosis,Tubercular Me

34、ningitis,Source of infection: systemic dissemination via blood cerebral T.B. spread to meninges Changes: exudation dominant change The exudation consists of serum, fibrin, lymphocytes and M gelatinous appearance cerebral infarction or softening Organization of exudate adhesion disturbance of CSF cir

35、culation hydrocephalus,Renal Tuberculosis,Source of infection: systemic dissemination via blood Changes: begins from the border of cortex & medulla caseous foci enlarged and fused, cavity formed one kidney bladder contralateral kidney (fibrosis and contraction of bladder ) destructive kidney CPC: hematuria, pyuria