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Cardiothoracic pathology Dr Amanda Hilton HistopathologySpecialtyRegistrar,Leeds Teaching HospitalsIntroduction  Lung  Chest wall  Heart  Vascular  Mediastinum  Benign entities  Malignancies  Staging  Prognostic factors  Gross  Micro  Clinical Lung nodules Malignant Benign  Granuloma  Carcinoma  In-situ  Sarcoid  Primary vs metastasis  Tuberculosis  Lymphoma  Aspiration  Sarcoma  Fungal  Infection  Hamartoma  Aspergilloma  PE  Vasculitis  Congenitaldefect Adenocarcinoma Non-Smallcell Squamouscell carcinoma Lung cancer Large cell carcinoma Others eg mucoepidermoid SmallcellLung cancer Neuroendocrine (Small cell carcinoma) Squamouscell carcinomaAdenocarcinoma  Peripheral  Commonestlung cancer in non- smokers  Multifocal- REMEMBER METS  Wedge, lobectomy(wholevspartial), pneumonectomy,navigational Bx, pleural fluid  Invasionbeyond visceralpleura into chest wallcavity/parietalpleura  TTF-1, NapsinA  PD-L1, EGFR, ALK, ROS1, RET, MET, NTRK, KRAS (BRAF)Arise from pneumocytes A common adenocarcinoma scenario • ?Resection status • ?Seeding OP FINDINGSON REQUESTFORM EVG stain - elastinDysplasia  Cellsremainin theirplace and do not invade  Can be interchangeablewith “in-situ”  Lung adenocarcinomain-situ<3cm  “Lepidic”Adenocarcinoma buzz words  Glandular/acinar  Columnar  Vacuolation  Papillary  Micropapillary  Cribriform  Lepidic  MucinousMucinous adenocarcinoma of the lung  More likelyto spread intrapulmonary  Immunoprofileunhelpful  Important to rule out metastasis CLINICALLYImmunostaining  Antibody against membranous/cytoplasmic/nuclear protein  Immunohistochemistry  Immunocytochemistry  Performed on formalin-fixed paraffin embedded tissue  Identifying cells of origin  Prognosis and treatment eg Her2 Breast CaSquamous cell carcinoma  Central  Bronchial brushings/washings/biopsy, lobectomy, pneumonectomy  Obstructive symptoms  Carina involvement  Smoking  Immunostains - CK5, CK14, p40, p63  Molecular - PD-L1, RET, MET, KRAS, NTRK Metaplasia  Mature tissue changes to different mature tissue type  Physiological  Adaptive to stressorsNormal trachea/bronchusMetaplasia Dysplasia CarcinomaSquamous cell carcinoma buzz words  Keratin/keratinizing  Intercellular bridges Pulmonary neuroendocrine tumours Few mitosesical carcinoid No necrosis •Atypical carcinoid Focal necrosis •Neuroendocrinecarcinoma Mitoses++ Necrosis++all/largecell) Small cell carcinoma  Central  Smokers  Paraneoplasticsyndromes– Carcinoid,Cushing, SIADH  Late presentation,metastases  Surgery option for T1-2a/N0/M0 dx  CD56, chromogranin, synaptophysin, TTF-1  Not eligiblefor immunotherapy no moleculars  Ki-67  Considersecondary spreadSmall cell carcinoma buzz words  Scant cytoplasm  Nuclearmoulding  Smearartefact  Salt and pepper chromatinSTAGING Tumour size PLUS Extent of invasion TNM 8Staging lung cancer Staging lung cancer •Atelectasis/obstructive pneumonitis extendingto hilum •Invasionbeyondvisceral pleura pT2 •Involvesmainbronchus (adeno) •Intrapulmonarymets insame lobe pT3 •Invasionof egparietalpleura/chestwall/pericardium •Intrapulmonarymets indifferentlobe of ipsilaterallung •Invasionof egdiaphragm/mediastinum/heart/trachea pT4 •Stations 10-14 pN1 •Stations 1-9 pN2 •Mets incontralaterallung pM1a •Malignanteffusion PROGNOSTIC FACTORS  Margin status  Number of nodal metastases  Grade  Lymphovascular invasionMargin status  R0 = Completeresection  R1 = Microscopic margin positive  R2 = Macroscopic margin positive  Rx = Unable to confirm definitively Tumour grade/differentiation  Resemblanceto tissueof origin  Well-differentiated/low-grade = similarto tissueof origin  Poorly-differentiated/high-grade = No resemblanceto tissueof origin  Sarcomatoid  Obstructivelung disorder COPD  SMOKING  Alpha-1 antitrypsindeficiency  Centrilobularemphysema  Bullae/spontaneouspneumothorax Restrictive vs Obstructive Obstructive Restrictive  EXhaling  INhaling  Reduced FEV1/FVC  Normal FEV1/FVC  Reduced FEV1 and FVC  COPD, asthma, bronchiectasis  Sarcoidosis,pulmonary fibrosis,neuromuscular disorders,posturalA word on O2 sats… Moving onto…Granuloma Aggregates of phagocytic macrophages/histiocytesDifferential for granulomatous lung disease/lymphadenopathy  TB/mycobacterial infection  Fungal infection  Sarcoid  Foreign body reaction inc aspiration  Vasculitis  Hypersensitivity pneumonitis(chronic)  Eosinophilicgranuloma (smoking)  Rheumatoid nodule Tuberculosis  Apical/cavitatinglesion  Nightsweats  Immunocompromised/from endemic country  Granuloma formation  Type 4 hypersensitivityreaction  AAFB  Bronchoalveolar lavage  NOT for excision/resection Type 4 (delayed) hypersensitivity reactions Cytotoxic T cells  Chronic(>3 days) Th1 cells  TB Type  Graft vs host 4  Contact dermatitis Th17 cells TissueTB and granulomas CLASSICALLY show central “caseaous” necrosis Ziehl-Neelsen stain Primary TB  Ghon focus – Parenchymalgranuloma  Ghon complex– Ghon focus+ Lymph node granuloma  Stable vsprogression  Langhan’s giant cell Secondary TB  Reactivated/reinfection  Irregularround nodules  Central necrosis→ Cavitatinglesion  Upper lobeMiliary/Tertiary TB  Multiplediffuse tiny granulomata  Extrapulmonary dissemination  Terminal Sarcoidosis  Idiopathic,Irish/Afro-Caribbean  SOB, cough, hypercalcaemia  Hilar lymph node and/or bronchial mucosal granuloma  Clinical diagnosis – Serum ACE  Asteroid body Aspergilloma  Aspergilluscolonisingpre-existing cavity  Opportunisticinfectionof  Immunocompromised patients  Lung disease  5-10µm branching septate hyphae  Haematogenousdissemination  Vascularinvasion  PAS/GrocottWegener’s granulomatosis Granulomatosis with polyangiitis Kidneys (glomerulonephritis) Necrotizing granulomatous vasculitis Upper Lower respiratory respiratory tract tract (sinusitis) (pneumonia)  Type 3 hypersensitivityreaction  Serum cANCA  Eosinophilrich Type 3 (immune complex) hypersensitivity reactions Antigen  Antigen + Antibody + Tissue = 3 Antibody Type 3  Immune complexes deposit in vessel walls Tissue  Vasculitis, renal, joints Mesothelial pathology Mesothelium Connectivetissue  Mesothelioma  Reactive fibrous changes/nodule  Spindlecell lesion  LymphoproliferativeMesothelioma  Older, M>>F  Asbestos exposure (occupational)  IHC - WT-1, calretinin,CK5  BAP1 tumoursuppressor gene  Diffuse >> localised  Epithelial,sarcomatoid,biphasicMesothelioma - Asbestos bodies in LUNG PARENCHYMA Perls (iron) stainMediastinal lesionsThymic lesions  Thymoma> thymiccarcinoma  >50 presentation  Asymptomatic  ObstructiveSx or MyaestheniagravisMediastinal germ cell lesions  Teratoma, seminoma,non-seminomatous germ cell tumour  Younger,↑ incidencepost puberty  Riskfactor – Kleinefeltersyndrome  Primary or secondary  Testicularexam/ultrasound Chest pain for surgeons  Aortic dissection  PE  Gastro-oesophageal disorder  Mesothelioma  Acute MI  LV aneurysm  Rupture papillary muscles of mitral valve  Infection  Empyema  Pregnant women – Dissection, MS, PE Thoracic aortic dissection  Young– Connectivetissuedisorders,aortitis(Takayasu, syphilis)  Older – Hypertension  Drugs, trauma, smoking  Tearing chest pain radiating between shoulderblades  Silent  Ischaemicstroke  BP discrepancy  High mortality Aortic dissection  Type A – Aortic root/ascending. Aortic root replacement  Type B – Descendingaorta, antihypertensives  Stable – imaging  Unstable – urgent surgeryMarfan’s Syndrome  Autosomal dominant  FBN1 mutation  Abnormal fibrillin  Aorta  Ligaments  Ciliary zonules  Aortic aneurysm → dissection  Mitral valveprolapse Pulmonary Embolism  Immobilityand hypercoagulablestates  Saddle - Rapid right sidedfailurefollowedquicklyby left  Smalleremboli– hypoxia, infarct  DOAC, warfarin, heparin, embolectomy,IVC filter Rheumatic heart disease  Present a few weeks after sore throat  Untreated Group A β-haemolyticstreptococcalinfection → antibodiesagainst streptococcus (Type 2 hypersensitivityreaction) 1. Pancarditis 2. Chorea 3. Subcutaneousnodules 4. Large joint polyarthritis 5. ErythemamarginartumRheumatic heart disease  Endocardium (Valves)mostaffected  Mitral > Aortic  Maincause of mitral stenosis→ AF  Heart failure,arrhythmia  Aschoff bodies – Necrosis/inflammation  Anitschkow cells – Macrophageswith “caterpillarnuclei” Type 2 (antibody mediated) hypersensitivity reactions  Acute rheumaticfever  Myaestheniagravis Antibody  Gravesdisease Type  Goodpasture 2 TissueThank you Questions? Referencesavailableon request