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类型呼吸系统病理1(英文版)课件.pptx

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    呼吸系统 病理 英文 课件
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    1、Basic PATHOLOGYRespiratory DiseasesReview ofthe architecture of the respiratory systemPULMONARY DUCTAlveolusBronchusBronchiolesAcute bronchitisPULMONARY ACINUSRespiratory bronchioles Alveolar ductAlveolar cystEmphysemaChronic bronchitisAsthmaBronchiectasis Bronchiolar pneumoniaLobular pneumoniaSquam

    2、ous cell carcinomaAdenocarcinomaBronchioloalveolar carcinomaPulmonary tuberculosisPneumoniaPneumonia can be very broadly Defined as any infection in the lung.Pathologically,it may be defined as any inflammation of lung.Classification of pneumonia1.Etiological classification:bacterial pneumonia viral

    3、 pneumonia fungal pneumonia etc.2.Anatomical classification:lobar pneumonia lobular pneumonia interstitial pneumonia.Clinically,etiological classification is more beneficial to the treatment;but the etiological classification usually can not be made readily.The anatomical classification may give a g

    4、reat help to the etiological diagnosis sometimes.90%:caused by Streptococcus pneumoniae(pneumococcus);interstitial pneumonia are caused by virus or mycoplasm.Bacterial PneumoniaLobar pneumoniaDef.In lobar pneumonia the contiguous air spaces of part or all of a lobe are homogenously filled with an ex

    5、udates that can be visualized on radiographs as a lobar or segmental consolidation and is thus sometimes referred to as “air space”pneumonia.The disease which is often seen in previously healthy young adults has a sudden onset and is accompanied by chills,fever,cough with pink-foam sputa and chest-a

    6、che.Etiology and pathogenesis90%S.pneumonia enter the lungs via the airwaysOccasionally other organisms(Klebsiella pneumoniae,staphylococci,streptococci,Haemophilus influenzae).Lobar pneumonia is initiated in periphery acinus,from there the exudative fluid containing etiologic agent flows into the a

    7、djacent air passage to infect adjacent lobules until a segment or entire lobe is infected.MorphologyFor purposes of description,it is convenient to divide the process into four phases:(1)Congestion(2)Red hepatizatio(consolidation)(3)Gray hepatization(4)Resolution1.Congestion stage(1st-2nd days)The a

    8、ffected lobe is heavy,red and boggy.A frothy blood-stained fluid canbe squeezed from the cut surface.Histologically,there is vascular congestion with proteinaceous fluid,scattered neutrophils,and many bacteria in the alveoli.Clinically,the onset is sudden with fever and rigors.2.Red hepatization sta

    9、ge(2nd-4th day)Liver-like in consistencySeptal capillaries are congested markedlyAlveolar spaces are packed with many red cells,and several neutrophils,fibrin.The pleura usually demonstrates a fibrinous or fibrinopurulent exudates.3.Gray hepatization stage(4th 8th day)More solid in consistencyPleura

    10、l surface is covered with a confluent fibrinous exudates.The cut surface is dry and granular but of a grayish-white color.Histologically,congestion of septal capillaries lightens.The fibrinous exudate persists within the alveoli and a fibrin net forms.There are many neutrophils but is relatively dep

    11、leted of red cells in the alveoli.4.Resolution stage(8th-9th day)With the elimination of bacteria,the inflammation subsides.Since there is no tissue destruction the lung return to normal apart from the pleura.X光肺叶密度增光肺叶密度增高高肺叶实变肺叶实变Complications:1.Carnification:Organization of intraalveolar fibrinou

    12、s exudates instead of resorption may convert areas of the lung into solid fibroustissue.2.Tissue destruction and necrosis may lead to abscess formation.3.Suppurative material may accumulate in the pleural cavity,producing purulent pleurisy and empyema.4.Septicemia or pyemia:Bacteremic dissemination

    13、may lead to meningitis,arthritis,or infective endocarditis.5.Infective shock:Failure of terminal circulation and appearance of toxic symptoms.BronchopneumoniaConception:Defined as an acute purulent inflammation characterized by diffuse patchy pneumonic consolidation often with bronchiolitis inits ce

    14、nter.It is a threat chiefly to the vulnerable infants,the aged,and those suffering from chronic debilitating illness or immuno-suppression.Children:Whooping cough and measles are important antecedentsAdult:influenza,chronic bronchitis,alcoholism,malnutrition,and carcinomatosis are all predisposing c

    15、onditions.Clinically,bronchopneumonia may appears as a complication of a disease.Hypostatic pneumoniaThe patient with pulmonary edema from cardiac failure or heavy uremia,et al,is particularly vulnerable,who are necessary to keep themselves in bed in prolonged time.Aspiration pneumoniaThe patient in

    16、 coma or apoplexy,heavyanesthesia and so on is particularly vulnerable.Almost any organism may cause bronchopneumonia,frequent offenders are staphylococci,streptococci,haemophilus influenza,proteus species etc.EtiologyFoci of inflammatory consolidation with a center of bronchiolitis are distributed

    17、in patches through one or several lobes,most frequently bilateral andbasal.MorphologyWell-developed lesions up to 3 or 4 cm (usually 0.5-1 cm)in diameter are slightly elevated,dry,granular,gray-red to yellow and demarcated distinctly.The lung substance immediately surrounding areas of consolidation

    18、is usually hyperemic and edematous,but the large intervening areas are generally normal.Histologically,the reaction consists of a suppurative exudates that fills the bronchi,bronchioles,and adjacent alveolar spaces.Hyperemia,edema and inflammatary infiltration can be seen in the walls of bronchioles

    19、.ComplicationThe same complication,as in lobar pneumonia.Viral pneumonia and mycoplasmal pneumoniaThey both belong to interstitial pneumoniaDef.an inflammatory process involving the interstitial tissue of the lungs.Etiology and pathogenesisThe common agents are viruses and mycoplasma.Attachment of t

    20、he organisms to the respiratory epithelium is followed by necrosis of the cells and an inflammatory response.Then,the inflammation extends to the interstitial tissue including peribronchial connective tissue and interalveolar septa.MorphologyMacroscopically:red-blue,congested,and subcrepitant.Becaus

    21、e much of the reaction is interstitial,little inflammatory exudates escapes on sectioning of the lung,although there may be slight oozing of red,frothy fluid.Histologically,the inflammatory process is largely confined within the walls of the alveoli.The septa are widened and edematous;they usually c

    22、ontain a mononuclear infiltrate of lymphocytes,histiocytes and occasionally plasmacells.In virus infection,inclusion bodies may be formed within cytoplasm or nucleus of the epithelial cells of bronchioles and alveoli.In severe cases alveolar damage with hyaline membranes may develop.A TRYChronic obs

    23、tructive pulmonary disease(COPD)chronic bronchitisemphysemabronchial asthmabronchiectasisChronicbronchitisDef.A persistent productive cough for at least three consecutive months in at least two consecutive years.Etiology and Pathogenesissmoking,air pollution(SO2,NO2)directly or throughneurohumoral p

    24、athwaysproliferation of bacteriahypersecretion of bronchial mucous glandhypertrophy of mucousgland,Goblet cell metaplasiaof bronchial epitheliumchronic bronchitisloss of ciliated epitheliumretention ofsecretionmicrobial infectionMorphologyGrosslymucosal lining of the larger airways is usually hypere

    25、mic and swollen by edemafluid;it is covered by a layer of mucinous or mucopurulent secretions.The smaller bronchi and bronchioles may also be filled with similarsecretions.3.病理变化病理变化部位部位主要特征主要特征 眼眼观观:早期早期 进展进展镜检镜检:(1)腺体肥大腺体肥大,分泌亢进分泌亢进后期腺体萎缩后期腺体萎缩,分泌耗竭分泌耗竭 (2)气管粘膜上皮细气管粘膜上皮细胞的损伤胞的损伤(3)支气管壁的病变支气管壁的病变Hi

    26、stologically:Hypertrophy of mucous gland and goblet cell metaplasia of bronchial wall.the diagnostic feature:enlargement of the mucus-secreting glands.Reid index:the ratio of the thickness of the submucosal gland layer to that of the bronchial wall.Normal:1:3Chronic bronchitis:usually exceeds 1:2.粘液

    27、腺肥大、增生粘液腺肥大、增生;浆液腺发生粘液化生。浆液腺发生粘液化生。粘液分粘液分 泌亢进泌亢进上皮鳞化上皮鳞化粘液腺粘液腺 增生肥大增生肥大Increased number of goblet cells in the lining epithelium with concomitant loss of ciliated epithelial cells.squamous metaplasia of lining epithelium followed by dysplastic changes.Mucosal and submucosal lining of bronchi are hyp

    28、eremic and swollen.inflammatory infiltration(lymphocytes,plasmacytes,sometimes admixed with neutrophils).支气管粘膜慢性炎伴上皮鳞状化支气管粘膜慢性炎伴上皮鳞状化生生Complications1.Emphysema2.cor pulmonals3.Bronchiectasis4.Bronchopneumonia5.bronchogenic carcinoma of lungEmphysemaDef.characterized by abnormal permanent enlargement

    29、 of the air space distal to the terminal bronchiole accompanied by destruction of their walls.Etiology1.Alveolar wall destruction and airspace enlargement invokes excess protease or elastase activity unopposed by appropriate antiprotease regulationIncrease either the number of PMN and MP in the lung

    30、Increase release of protease from PMN and MP oxidants in cigarettesmoke and O-2radicals secreted byPMN&MP inhibit the active of 1-AT and decrease net anti-elastase activity in smokersDeficiencyPiMM/PiZZ(Chr14)EmphysemAntiprotease 1-antitrypsin inhibitionSmokingProtease:elastase collagenase1-antitryp

    31、sinDestruction of elastin and collagen of the lung2.Obstruction of the bronchioles.Air enter into the alveoli distal to the obstructed bronchiole through Kohns pore(interalveolar pore),and air is trapped during expiration because the pore is closed.Emphysema is ended.(四(四)病因与发病机理病因与发病机理(1)病因病因(2)发病的

    32、二个基本环节发病的二个基本环节细支气管阻塞和狭窄细支气管阻塞和狭窄小气道及肺泡支撑组织的破小气道及肺泡支撑组织的破坏坏Classification and MorphologyAlveolar emphysema:centriacinar emphysemapanacinar emphysema periacinar emphysemaInterstitial emphysema:Others:paracicatrical emphysemabullae lungsenile emphysema compensatory emphysemaDiagram of the fundamental

    33、unit of the lung centriarclinal and panacinar emphysema.MorphologyThe lesions of centriacinar emphysema are more common and severe in the upper lobes particularly in the apical segments.腺腺 泡泡 中中 央央 型型 肺肺 气气 肿肿Panacinar emphysema:pale,voluminous lungs全腺泡型肺气全腺泡型肺气肿肿Microscopic features:1.Thinning and

    34、destruction of alveolar walls.2.Adjacent alveoli become confluent,creating large air spaces.3.Capillaries in alveolar septa decreased.Terminal and respiratory bronchioles may be deformed because of the loss of septa.Bullous emphysema囊泡型肺气肿(大泡直囊泡型肺气肿(大泡直径径3cm)Conditions related to emphysema.There are

    35、 several conditions in which enlargement of air spaces is not accompanied by destruction;this is more correctly called overinflation.Compensatory emphysema Senile emphysemaInterstitial emphysema designates the entrance of air into the connective tissue of the lung,mediastinum and subcutaneous tissue

    36、.This may occur spontaneously with a sudden increase in intraalveolar pressure(as withvomiting or violent coughing)that cause a tear,with dissection of air into the interstitium.Complications:1.Cor pulmonale2.Pneumothorax3.Respiratory failureBronchiectasisDef.Permanent dilatation of bronchi and bron

    37、chiole due to destruction of the muscle and elastic supporting tissue.The characteristic symptom:cough and expectoration of copious amounts of purulent sputum.Etiology and pathogenesisBronchial obstruction (tumor,enlarged lymph node,foreign body)rise of intrabronchialpressure during respirationbronc

    38、hial dilatationloss of ciliated epitheliumcongenital orhereditory conditionsretention of secretioncoughinfectionWeakeningand loss ofelastic tissue,muscle andcartilage of bronchusMorphologyGrossly:usually affects the lower lobes bilaterally,particularly those air passages that are most vertical.The a

    39、irways may be dilated as much as 4 times their usually diameter and can be followed nearly to the pleural surfaces.(By contrast,in normal lungs the bronchioles cannot be followed by ordinary gross examination beyond a point 2 to 3 cm from the plural surface.)Patterns of dilatation:cysticcylindricalH

    40、istologically,there is an intense acute and chronic inflammatory exudates within the wall of the bronchi and bronchioles and desquamation of lining epithelium leaving extensive areas of ulcerated epithelium.there may be squamous metaplasia of the lining epithelium.In some instances,the necrosis dest

    41、roys the bronchial or bronchiolar walls and forms a lung abscess.When healing occurs,granulation tissue forms the base of ulcer.Clinicopathological correlation1.Postural coughing with large quantity of pus.2.hemoptysis due to erosion of the vessel in granulation tissue.Complications1.lung abscess2.Pyemia-metastatic abscesses3.Pulmonary fibrosis and cor pulmonale.

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