8年制病理学英文课件（2版）：09呼吸系统

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1、Department of PathologyChina Medical UniversityWang Enhua9.1 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 leukocyte

2、s.Acute suppurative tracheobronchitis.There is a significant 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 l

3、ymphomonocytic and leukocytic infiltration of the submucosa accompanied by overproduction of mucous secretions.Bronchiolitis obliterans is characterized by polypoid masses of organizing inflammatory exudates and granulation tissue extending from alveoli into bronchiolesbroadly defined:any infection

4、in the lunghistologic spectrum-vary from a fibrinopurulent alveolar exudate acute bacterial pneumonia bronchopneumonia lobar pneumonia mononuclear interstitinal infiltrates viral/atypical pneumonias granulomas/cavitation chronic pneumonias9.1.3 Pneumonialan acute bacterial infection of a large porti

5、on of a lobe or of an entire lobefibrinous inflammationSymptoms:abrupt onset,high fever,shaking chills,pleuritic chest pain,a productive mucopurulent cough(“rusty”sputum)Etiology pathogens：streptococcus-pneumoniae,pneumobacillus inducing factors:cold,excessive tired,anethesia Pathogenesis bacteria-a

6、lveoli-proliferate,capillary dilate,serious 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,red,boggy LM alveolar wall:cap.dilate,congestion al

7、veolar space:proteinaceous edema fluid,few neutrophils,RBC,and numerous bacteria congestion stage（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,packe

8、d with fibrin nets which stream from one 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 a

9、long with the continued accumulation of fibrin Lobar pneumonia(gray hepatization).The upper lobe is uniformly consolidated.Lobar pneumonia(gray hepatization).（4）resolution stage:1 week the resorption of exudate and enzymatic digestion of inflammatory debris,with preservation of the underlying alveol

10、ar wall architecture Gross softening,volume LM WBC fibrin absorbedLobar pneumonia (resolution stage)exudates within the alveoli are enzymatically digested and either resorbed or expectorated,leaving the basic architecture intact.Complication(1)pulmonary carnification：hypoexudation of neutrophils-pro

11、teinase defficiency/over-exudation of fibrin-organization of the intra-alveolar exudate convert areas of the lung into solid fibrous tissue(2)empyemia-suppurative material accumulate in the pleural cavity(3)abscess formation-tissue destruction and necrosis(4)septicemia or pyemia-bacteremic dissemati

12、on(5)infectious shockLobar pneumonia（carnification）lclinic:infants,the aged,illness(much more prevalent at the extremes of age)l patchy distribution,a purulent inflammation that centered bronchiolesEtiology and pathogenesisPathogens:staphylococci,pneumococci,streptococci,influenzae haemophilusInduce

13、 factors:cold,heart failureInfection ways:respiratory tract,bloodgrosspatchy consolidation through one lobe,more often multilobar and frequently bilateral and basal0.5-1cm,gray-red to yellow,slightly elevated,poorly delimited at the marginsSevere:confluent bronchopneumoniaPathological changesLobular

14、 pneumonia(Scattered foci of consolidation are centered on bronchi and bronchioles)Foci of inflammatory consolidation are distributed in patches through one or several lobes,in severe cases the foci may confluent,producing the appearance of a lobar consolidation(1)a suppurative,neutrophil-rich exuda

15、tes centered the bronchi,bronchioles,adjacent alveolar spaces(2)walls of bronchioles and alveoli:congestion,edema(3)surrounding:hyperemic edematous compensative emphysema(4)the abscesses are marked by necrosis of the underlying architecture LMlobular pneumonia(A suppurative,neutrophil-rich exudates

16、fills the bronchi,bronchioles,and adjacent alveolar spaces)lobular pneumonia（1 1）respiratory failure （2 2）heart failure（3）pyemia（4）abscess （5）bronchiectasiscomplicationpathogens Most common:influenza virus A/BLess common:parainfluenza,respiratory syncytial virus(especially in infants and children)Ad

17、enovirus common in army recruitsMycoplasmal pneumonia common among children and young adultsOthers:measles,chickenbox 2.Viral pneumoniaMuch depends on the resistance of the host,range from mild to severeClinically,more serious lower respiratory tract infection is favored by infancy,old age,malnutris

18、hment,alcoholism,immunosuppressionpathologic changesgross:the affected areas are congested,volume slightly enlarge,subcrepitantLM:interstitial pneumonia the inflammation confined within the walls of the alveoli the septa are widened and edematous a mononuclear inflammatory infiltrate of lymphocytes,

19、histocytes,plasma cells alveolar spaces are remarkably free of cellular exudate viral containerhyaline membrane full-blown diffuse alveolar damageInterstitial pneumonia.The alveolar septa are widened and edematous and infiltrated with mononuclear cells.viral inclusion body is round or oval shape,ery

20、throcyte-like in size,eosinophilic cytoplasmic or nuclearClinical coursepExtremely variedpOnset:acute,nonspecific febrile illnesspFever,headache,malaise,cough with minimal sputumpChest radiography:transient,ill defined patches,mainly in the lower lobespphysical findings:minimal and indistinguishable

21、 from bronchopneumonia pIdentifying the causative agent is difficultpRising titers of specific antibodiespMycoplasmal and chalymydia pneumonia-erythromycinpPrognosis is goodPathogen:SARS associated cornonavirusLM:diffuse alveolar damage in varying phages of organization pneumocystis A group of condi

22、tions that share a major symptom dyspnea and are accompanied by chronic or recurrent obstruction to airflow within the lungA persistent productive cough for at least 3 consecutive months in at least 2 consecutive yearsEtiology1.Infection virus/bacteria2.Physical chemical factors（1）smoking （2）air pol

23、lution （3）cold（4）others:neuroendocrine,nutrition PathogenesisHypersecretion of mucus beginning in the large airwaysIrritants-hypersecretion of the bronchial mucous glands-hypertrophy of mucous glands-metaplastic formation of mucin-secreting goblet cells in the surface epithelium of bronchi.Pathologi

24、cal changesGrosspthe mucosal lining of the larger airways is hyperemic and swollen by edema fluid,covered by a layer of mucinous or mucopurulent secretionspthe smaller bronchi and bronchioles filled with similar secretions LMpinjury/repair of respiratory epithelium cilia epithelium injured:adhere,de

25、tachment,degeneration,squamous metaplasiaphyperplasia and hypertrophy of the mucous cells and an increased proportion of mucous to serous cellspmucosa and submucosa inflammationpasthematic type:SMC increase,stenosis,calcificationChronic bronchitis(degeneration,necrosis of the bronchial epithelium wi

26、th loss of ciliated cells)Mucous glandular metaplasiaClinical coursepCough and sputum production pHypercapnia,hypoxemia,and cyanosis pMost patients have a mixture of chronic bronchitis and emphysema pcor pulmonale or respiratory failure A condition of the lung characterized by abnormal permanent enl

27、argement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls.Etiology and pathogenesis 1.obstructive ventilate dysfunction of bronchioles:narrowing of bronchioles 2.the protease-antiprotease imbalance:1-antitypsin deficiency 3.smoking Types 1.Alveolar emphys

28、ema（1）centriacinarprespiratory bronchiole dilatepthe central or proximal parts of the acini,the distal alveoli are sparedptoth emphysematous and normal airspaces exist within the same acinus and lobulepCommon and sever in the upper lobes pmost commonly in cigarette smoking people（2）panacinarpthe aci

29、ni are uniformly enlarged from the respiratory bronchiole to the terminal blind alveolip common in the lower lung zonespoccurs in the a1-antitrypsin deficiency（3）periacinar:distal acinar(paraseptal)pstriking adjacent to the pleura,along the lobular connective tissue septa,the margin of the lobulesAl

30、veolar emphysema.Pale,voluminous.Alveolar emphysema(marked enlargement of airspaces,with thinning and destruction of alveolar septa.)2.interstitial emphysema3.others:paracicatrical emphysemabullae lung emphysemasenile emphysemacompensatory emphysema Pathologic changesgross：voluminous with round marg

31、in,pale/gray-white,softLM：pthinning and destruction of alveolar wallspabnormal enlargement of alveoli-alveolar losspalveolar capillaries diminishedpdestruction of septal wall CPCCPC(1)pulmonary dysfunction:insidious-progressive dyspnea and hyperventilation(2)barrel-chested-enlarged lungs,depressed d

32、iaphragms,and an increased posteroanterior diameter(3)cor pulmonary(4)pneumothorax(5)pulmonary function test:FEV1/FVC reduced(forced expiratory volume at 1 sec./forced vital capacity)Death from emphysemapPulmonary failure with respiratory acidosis,hypoxia,and comapRight-sided heart failure(cor pulmo

33、nale)9.2.3 bronchial asthmaa chronic lung disease characterized by periodic episodes of air-flow obstruction and increased responsiveness of the airways to a variety of stimuli.Clinically,severe dyspnea with wheezing;the chief difficulty lies in expirationGrosspThe lung are overdistendedpMost striki

34、ng-occlusion of bronchi and bronchioles by thick,tenacious mucus plugs.pthe airways are filled with thick,tenacious,adherent mucous plugs(strips of epithelium and many eosinophils).pedema,hyperemia,an inflammation in the bronchial walls,with prominent eosinophils.pa thickened basement membranephyper

35、trophy and hyperplasia of the smooth muscle in the bronchial wallThe permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue,resulting from or associated with chronic necrotizing infectionsEtiology and pathogenesis1.Infective destruction of bro

36、nchi2.Congenital or hereditary condition p cartagener syndrome(sterility)p cystic fibrosisp immunodeficiency state Pathologic changesGross:bronchi and bronchioles dilate,inflammatory exudation with the walls of the bronchi and bronchioleLMppseudostratification of the columnar cellspnecrosis destroys

37、 the bronchial or bronchial wallsp fibrosis and peribronchiolar fibrosisBronchiectasis.Cut surface f lung shows transected,markedly distended peripheral bronchi.CPCpsevere persistent cough and expectoration of copious amounts of purulent sputum,fetid sputum or hemoptysispdyspneaphypoxemia,hypercapni

38、a,cor pulmonaleplung abscesspclubbing fingerspmetastatic brain abscesses and reactive amyloidosis 9.3.1 Pneumoconiosis inhalation and accumulation of harmful dust for a long time result in extensive fibrosis and injury in lung.Pathogenesis 5m silica particles can be inhaled into alveoli engulfed by

39、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 1.Silicosis-inhale of crystalline silica dioxide(silica)Pathologic changes 1.formation of silicotic

40、nodule 2.diffuse fibrosis in interstitial of lungGross:tiny,barely palpable,discrete,pale-to-blackened nodules in the upper zones of the lungsLM：1.Silicotic nodules（1）cellular silicotic nodules:macrophages engulf sio2（2）fibrous silicotic nodules:fibroblasts+fibrocytes+collogen fiber concentirc arran

41、gement（3）hyaline silicotic nodules:hyaline degeneration of fibrous silica nodules2.interstitial extensive fibrosisSilicosis.The silicotic nodule demonstrates concentrically arranged hyalinized collagen fibers surrouding an amorphous center.StagesStage located in hilar LN,without change in volume/har

42、dnessstage stage silica nodules below 1 cm(1/3 of the whole lung)stage stage weight hardness volume confluent,pleura thickenedComplications 1.tuberculosis 2.cor pulmonary 3.pulmonary infection 4.autopneumothorax9.4.1 acute respiratory distress syndrome9.4.2 neonatal respiratory distress syndrome con

43、stitutes right ventricular hypertrophy,dilation and potentially failure secondary to pulmonary hypertension caused by disorders of the lungs or pulmonary vasculature Etiology and pathogenesis1.COPD (1)hypoxia-induced pulmonary vascular spasm(2)loss of pulmonary capillary surface area from alveolar d

44、estruction resistance of lung circulation pressure of pulmonary A right heart hypertrophy/dilate2.Disorder affecting chest movement 3.Disease of pulmonary vessels:lessPathologic changes1.lesions of lungCOPDarteriole wall thicken(media and intima:collagenous,elastic fiber)/muscularization of arteriol

45、escapillary less2.heartthe right ventricular wall is hypertrophy,and papillary muscle thicken.CPC1.right heart failure:congestion,ascitis,and edema of lower extremities and palpitation.2.pulmonary encephalopathy.3.Other.9.6.1 nasopharyngeal carcinoma(NPC)Etiology:lInfection with EB viruslenvironment

46、 lheredity9.6 Respiratory tumorsMorphologyGross:nodular;cauliflower;infiltrative;ulcerative types.LM:squamous cell carcinoma(keratinizing;non-keratinizing)adenocarcinoma undifferentiated carcinomaNPCMorphology:glottic carcinoma-the most commonHistologically:squamous cell carcinoma the most commonEti

47、ology pSmoking-an impressive body of stastical,clinical,and experimental evidence incriminates cigarette smoking,among the major histologic subtypes of lung cancer,squamous and small cell carcinomas show the strongest association with tobacco exposurep Air pollutionpIndustrial hazards-radioactive or

48、es,asbestos workers,workers exposed to dusts containing arsenic,chromium,uranium,nickel,vinyl chloride,and mustard gaspMolecular genetics-a stepwise accumulation of genetic abnormalities that result in transformation of benign bronchial epithelium into neoplastic tissuePathologic changespBegin as sm

49、all mucosal lesions that are usually firm and gray-whitepForm intraluminal masses,invading the bronchial mucosapForm large bulky masses pushing into adjacent lung parenchymapSome large masses undergo cavitation caused by central necrosis or develop focal areas of hemorrhagepExtend to the pleura,inva

50、ding the pleura cavity and chest wall and spread to adjacent intrathoracic structurespLymphatic or hematogeneous metastasis 1.Types of gross p central type p peripheral type p diffuse typeLung cancer,centralized type.peripheral typeEarly stage pulmonary carcinoma:tumor mass 2cm,limited intrabronchi

51、or infiltrated the bronchial wall and surrounding 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 classificationp squamous cell carcin

52、omap small cell carcinomap adenocarcinomap large cell carcinomap adeno-squamous carcinomap sarcomatoid carcinomap carcinoid tumorp salivary gland type carcinomaSquamous cell carcinomaHistologicallywell-differentiated squamous cell neoplasmas-showing kerati pearls and intracellular bridgesPoorly diff

53、erentiated neoplasms-having only minimal residual squamous cell featurepMore common in men than womenpTend to arise centrally in major bronchi and eventually spread to local hilar nodespDisseminate outside the thorax later than other histologic typespUndergo central necrosis,cavitationpOften precede

54、d for years by squamous metaplasia/dysplasia in the bronchial epitheliumcarcinoma in situpAtypical cells may be identified in cytologic smears of sputum or in bronchial lavage fluids or brushings,although asymptomatic and undetectable on radiographspA symptomatic stage,when a well-defined tumor mass

55、 begins to obstruct the lumen of a major bronchus-distal atelectasis and infection,invades the surrounding pulmonary substanceSmall cell carcinoma of the lung.Nests and cords of round to polygonal cell with scant cytoplasm,granular chromatin,and inconspicuous nucleoli.pPale gray,centrally located ma

56、sses with extension into the lung parencymapEarly involvement of the hilar and mediastinal nodespTumor cells with a round to fusiform shape,scant cytoplasm,and finely granular chromatinpMitotic figures are frequently seenpNecrosis is invariably present and may be extensivepTumor cells are markedly f

57、ragile and often show fragmentation and“crush artifact”in small biopsy specimenspIn cytologic specimens-nuclear molding resulting form close apposition of tumor cells that have scant cytoplasmpDerived from neuroendocrine cells of the lung,express a variety of neuroendocrine markers in addition to a

58、host of polypeptide hormones that result in paraneoplastic syndromesadenocarcinomaHistologicallyAssume a variety of forms most cases are mixed type.pacinar(gland forming)ppapillarypsolid types-requires demonstration of intracellular mucin production by special stains to establish its adenocarcinomat

59、ous lineageThe putative precursor of peripheral adenocarcinomas has been described as atypical adenomatous hyperplasis(AAH)pMay occur as central lesions,but usually more peripheral located,many arising in relation to peripheral lung scarspHave the weakest association with a previous history of smoki

60、ng among the four major subtypes of bronchogenic carcinomaspGrow slowly and form smaller masses than do other subtypespTend to metastasis widely at an early stageBronchioloalveolar carcinomas(BAC)-a subtype of adenocarcinomasInvolve the peripheral parts of the lung,either as a single nodule,or as mu

61、ltiple diffuse nodules that may coalesce to produce pneumonia-like consolidationThe key feature of BAC is their growth along preexisting structures and preservation of alveolar architectureBACLarge cell carcinomapConstitute a group of neoplasms that lack cytologic differentiation and probably repres

62、ent squamous cell or glandular neoplasms that are too undifferentiated to permit categorizationpHave a poor prognosis because of their tendency to spread to distant sites early in their coursepCells are large,usually anaplastic,and have large vesicular nuclei with prominent component of giant cells,

63、many of which are multinucleated(giant cell carcinoma),others are composed of spindle-shaped cells(spindle cell carcinoma);some have a mixture of both(spindle and giant cell carcinoma)Spread pathways 1.direct spread 2.metastasis plymphatic:carina-mediastinum-in the neck(scalene nodes)-clavicular reg

64、ion-distant metastasispsupraclavicular node(Vorchow node)is particularly characteristic phematogeneous:brain(20%),liver(30 to 50%),bone(20%),adrenal glands CPCp cough/weight loss/haemoptysispdyspnoea/chest pain/pericarditis or pleuritis with significant effusions/partial obstruction-focal emphysema;

65、total obstructionatelectasispinvasion of the superior vena cava can cause venous congestion,dusty head and arm edema,ultimately,circulatory compromisethe superior vena cava syndrome pParaneoplastic effects-due to ectopic hormones:ACTH and ADH(small cell lung carcinomas),PTH(squamous cell car.).carci

66、noid syndrome(5-HT/small cell lung cancer).Finger-clubbing and hypertrophic pulmonary osteoarthropathypApical lung cancers in the superior pulomary sulcus tend to invade the neural structures around the trachea,including the cervical sympathetic plexus,and produce a group of clinical findings that includes severe pain in the distribution of the ulnar nerve and Honer syndrome(enophthalmos,ptosis,miosis,and anhidrosis)on the same side as the lesion,such tumors are also referred to as Pancoast tumo