病理学英文教学课件：ch7 Diseases of Respiratory System

1、Etiological factor DiseaseGenetic 1-antitrypsin deficiency Some asthma Environmental Smoking Lung cancer Chronic bronchitis and emphysema Susceptibility to infectionAir pollution Chronic bronchitis Susceptibility to infectionOccupation Silicosis AsbestosisInfection Influenza Bacterial pneumonias7.1

2、Infection of respiratory tract Acute tracherobronchitis Acute bronchiolitis PneumoniaAcute catarrhal tracheobronchitis. The inflammatory exudate on the mucosal surface is chiefly a stringy, basophilic mucus only scantily mixed with leukocytes.Acute suppurative tracheobronchitis. There is a significa

3、nt element of leukocytic infiltration.Acute ulcerative tracheobronchitis. The inflammatory reaction is more intense, with necrosis of the mucosa in areas, it constitutes an ulcerative form.The bronchioli mucosa is hyperemia and swelling with a lymphomonocytic and leukocytic infiltration of the submu

4、cosa accompanied by overproduction of mucous secretions. Bronchiolitis obliterans is characterized by polypoid masses of organizing inflammatory exudates and granulation tissue extending from alveoli into bronchiolesPneumoniaBacteria pneumonia1. Lobar pneumoniaan acute bacterial infection of a large

5、 portion of a lobe or of an entire lobefibrinous inflammationSymptoms include a cough, fever and production of “rusty” sputum Etiology pathogens： streptococcus-pneumonia, pneumobacillus inducing factors: cold, excessive tired, anethesia Pathogenesis bacteria alveoli proliferate , capillary dilate, s

6、erious exudates kohns pores spreading entire lobe Pathologic changes （1）congestion stage：1st-2nd days the outpouring of a protein-rich exudate into alveolar spaces and rapid proliferation of bacteria. gross heavy, boggy, red LM alveolar wall: cap. dilate congestion alveolar space: proteinaceous edem

7、a fluid, few neutrophils, RBC , and numerous bacteria （2）red hepatization: 3rd-4th days grosslthe lobe distinctly red, firm, and airless with a liver-like consistencylan overlying fibrinous or fibrinosuppurative pleuritis LM alveolar space: a flock of RBC, packed with fibrin nets which stream from o

8、ne alveolus through the pores of kohn into adjacent alveoli, neutrophils （3）gray hepatization: 5th 6th day gross gray-brown and solid, liver like consistency LMl the alveolar capillaries appear compressed l alveolar spaces: progressive disintegration of neutrophils along with the continued accumulat

9、ion of fibrin （4）resolution stage: 1 week the resorption of exudate and enzymatic digestion of inflammatory debris, with preservation of the underlying alveolar wall architecture Gross softening, volume LM WBC fibrin absorbedcongestion stage Lobar pneumonia (red hepatization)red hepatizationLobar pn

10、eumonia (red hepatization)Lobar pneumonia(gray hepatization) Lobar pneumonia (gray hepatization)Lobar pneumoniaLobar pneumonia (gray hepatization)Complication(1) pulmonary carnification：hypoexudation of neutrophils proteinase defficiency/ overexudation of fibrin exudate can not be absorbed completel

11、y and organised brown-solid fibrous tissue（2）empyemia（3）abscess formation（4）septicemia or pyemia（5）infectious shockLobar pneumonia（carnification）2. Lobular pneumonia ( Bronchopneumonia ) lclinic: infants, the aged, illnessl patchy distribution, a purulent inflammation that centered bronchiolesEtiolo

12、gy and pathogenesisPathogens: staphylococci, pneumococci, streptococci, influenzae haemophilusInduce factors: cold, heart failureInfection ways: respiratory tract, bloodgrosspathy consolidation through one lobe, more often multilobar and frequently bilateral and basal0.5-1cm,gray-red to yellow, poor

13、ly delimited at the marginsSevere: confluent bronchopneumoniaPathological changesLobular pneumonia (Scattered foci of consolidation are centered on bronchi and bronchioles) (1) a suppurative, neutrophil-rich exudates centered the bronchi, bronchioles, adjacent alveolar spaces(2) walls of bronchioles

14、 and alveoli: congestion,edema(3)surrounding: alveolarspace: proteinaceous edema, compensative emphysema(4)the abscesses are marked by necrosis of the underlying architecture LMlobular pneumonia (A suppurative, neutrophil-rich exudates fills the bronchi, bronchioles, and adjacent alveolar spaces) （1

15、 1）respiratory failure （2 2）heart failure （3）pyemia （4）abscess （5）bronchiectasiscomplicationpathogens: influenza virus pathologic changes gross: volume slightly enlarge,edema LM: interstitial pneumonia, viral container hyaline membraneViral penumoniainterstitial pneumonia. The alveolar septa are wid

16、ened and edematous and infiltrated with mononuclear cells.viral inclusion body is round or oval shape, erythrocyte-like in size, eosinophilic cytoplasmic or nuclear A group of conditions that share a major symptom dyspnea and are accompanied by chronic or recurrent obstruction to airflow within the

17、lungpersistant cough with sputum production at least 3 months in at least 2 connective yearsEtiology1. Infection virus：influenzae virus, adenovirus bacteria:2. Physical chemical factors （1）smoking （2）air pollution （3）cold（4）others: neuroendocrine, nutrition Pathological changeslinjury/ repair of res

18、piratory epithelium cilia epithelium injured: adhere, detachment, degeneration, squamous metaplasialHyperplasia and hypertrophy of the mucous cells and an increased proportion of mucous to serous cells, mucosa and submucosa inflammationlasthematic type: SMC increase, stenosis, calcification Chronic

19、bronchitis (degeneration, necrosis of the bronchial epithelium with loss of ciliated cells) Mucous glandular metaplasiaClinical pathologic correlationlCough and sputum production lExertional dyspnea and cyanosis lMost patients have a mixture of chronic bronchitis and emphysema lcor pulmonale or resp

20、iratory failure A condition of the lung characterized by abnormal permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls, and without obvious fibrosis. Etiology and pathogenesis 1. obstructive ventilatent dysfunction of bronchiioles: narro

21、wing of bronchioles 2. 1-antitypsin defficiency 3. smokingELASTASEELASTICDAMAGEEMPHYSEMA 1-ANTITRYPSIN DEFICIENCY SMOKING ANTIELASTASE1-antitrypsinTypes 1. Alveolar emphysema（1）centriacinar：respiratory bronchiole dilate（2）panacinar：alveolar duct,alveolus dilate（3）periacinarAlveolar emphysema. The lu

22、ng shows large, irregular air spaces and a markedly reduced number of alveolar walls. Alveolar emphysema (The lung shows large, irregular air spaces and a markedly reduced number of alveolar walls )2.interstitial emphysema3.others: paracicatrical emphysema bullae lung emphysema senile emphysema comp

23、ensatory emphysema interstitial emphysemaPathologic changesgross：voluminous with round margin, pale/gray-white, softLM：labnormal enlargement of alveolilalveolar wall: capillary lessldestruction of septal wall CPCCPC（1 1）pulmonary dysfunction:insidious onset of dyspnea（2）barrel-shaped chest-enlarged

24、lungs, depressed diaphragms, and an increased posteroanterior diameter （3）cor pulmonary（4）pneumathoraxbronchial asthmaa chronic lung disease characterized by periodic episodes of air-flow obstruction and increased responsiveness of the airways to a variety of stimuli. lthe airways are filled with th

25、ick, tenacious, adherent mucous plugs (strips of epithelium and many eosinophils). needle-like Charcot-Leyden crystals (eosinophil membrane protein)/ whorls of shed epithelium-the Curschmann spirals. lBronchial submucosal mucous glands are hyperplastic.lthe epithelial basement membrane appears thick

26、enedlThe submucosa is edematous and contains a mixed inflammatory infiltrate.lalso hyperplasia of bronchial smooth muscle.a chronic infection of the bronchi and bronchioles leading to or associated with abnormal dilation of these airways.Etiology and pathogenesis1. Infective destruction of bronchi2.

27、 Congenital or hereditary condition: cartagener syndromePathologic changesGross: bronchi and bronchioles dilate, inflammatory exudation with the walls of the bronchi and bronchiloeBronchiectasis. Cut surface f lung shows transected, markedly distended peripheral bronchi. LMlpseudostratification of t

28、he columnar cellslnecrosis destroys the bronchial or bronchial wallsl fibrosis and peribronchiolar fibrosisBronchiectasis 支气管扩张扭曲，管壁结构遭破坏（支支气管扩张扭曲，管壁结构遭破坏（支气管壁平滑肌及弹力纤维破坏），可见多量的肉芽组织。气管壁平滑肌及弹力纤维破坏），可见多量的肉芽组织。 CPClsevere persistent cough expectoration of foul smelling, bloody sputumldyspnea, orthopneal

29、a systemic febrile reaction 7.3.1 Pneumoconiosis inhalation and accumulation of harmful dust for a long time result in extensive fibrosis and injury in lung.Silicosis inhale a lot of crystalline silicon dioxide (silica) for a long time and caused the formation of silicotic nodules and diffuse inters

30、titial fibrosis in lung.Pathogenesis 5m silica particles can be inhaled into alveoli engulfed by macrophages destroy the stability of lysosome membrane release hydrolytic enzymes macrophages lyses IL/TNF/FN fibrosis; macrophages release sio2 accumulation of macrophages formation of silica nodules Pa

31、thologic changes 1. formation of silicotic nodule 2. diffuse fibrosis in interstitial of lungGross: round, 2-5 cm , clear border, gray-black, hard, sand-stone feeling. Nodules can influent with center necrosisLM：1. Silicotic nodules（1）cellular silicotic nodules: macrophages engulf sio2（2）fibrous sil

32、icotic nodules: fibroblasts+fibrocytes+collogen fiber concentirc arrangement （3）hyaline silicotic nodules: hyaline degeneration of fibrous silica nodules2. interstitial extensive fibrosisSilicosis. A silicotic nodule is composed of concentric whorls of dense, sparsely cellular collagen interspersed

33、with dust. StagesStage located in hilar LN, without change in volume/ hardnessstagestagesilica nodules below 1 cm ( 1/3 of the whole lung)stagestageweight hardness volume confluent, pleura thickenedComplications 1. tuberculosis 2. cor pulmonary 3. pulmonary infection 4. autopneumothorax constitutes

34、right ventricular hypertrophy, dilation and potentially failure secondary to pulmonary hypertension caused by disorders of the lungs or pulmonary vasculature Etiology and pathogenesis1. COPD BV lesshypoxemiapulmonary small artery spasmresistance of lung circulation pressure of pulmonary A right hear

35、t hypertrophy/dilate2. Disorder affecting chest movement 3. Disease of pulmonary vessels:less Pathologic changes1. lesions of lungCOPDarteriole wall thicken (media and intima: collagenous, elastic fiber)/ muscularization of arteriolescapillary less2. heartthe right ventricular wall is hypertrophy, a

36、nd the trabeculae acrneae, papillary muscle thicken. LMCPC1. right heart failure: congestion, ascitis, and edema of lower extremities and palpitation. 2. pulmonary encephalopathy. Coma7.6.1 Nasopharyngeal carcinomamalignant tumor originated from mucosa or glands Etiology 1. EB virus 2. Carciogenic a

37、gents 3. Inheritage factors 7.6 Respiratory tumors Pathologic changesgross：cauliflower/ nodular/ infiltrating mass/ ulcerated histology: squamous cell car.adenocarcinoma 7.6.2 Lung cancer ( bronchogenic carcinoma ) Etiology 1. Smoking 2. Air pollution 3. Industrial hazards 4. Molecular geneticsPatho

38、logic changes 1. Types of gross （1）central type （2）peripheral type （3）diffuse typeLung cancer, centralized type. The tumor grows within the lumen of the bronchus and invades the lung tissue. Early stage pulmonary carcinoma:tumor mass 2cm, limited intrabronchi or infiltrated the bronchial wall and su

39、rrounding tissue, no metastasis in LNOccult (concealed)carcinoama:cytologic smeares of sputum :tumor cells(+),clinic and X-ray(-),biopsy showed carcinoma in situ or early infiltrative carcinoma, no metastasis in LN 2. Histologic classification （1）squamous cell carcinoma （2）small cell carcinoma （3）ad

40、enocarcinoma （4）large cell carcinoma （5）adeno-squamous carcinoma （6）polymorphic sarcoid carcinoma Squamous cell car.Small cell carcinoma of the lung. The tumor consists of small oval to spindle-shaped cells with scant cytoplasm, finely granular nuclear chromatin. adenocarcinomaLarge cell car. Spread pathways 1. direct spread 2. metastasis （1）lymphatic: hilar lymph nodes - mediastinal, cervical, and para- aortic