RS PATH lssn 3.pptx

Pathology

1. VI. PULMONARY TUBERCULOSIS (PTB) PTB is a lung infxn caused by mycobacterium tubercle bacilli – a non-spore forming bacteria with mycolic acid in its cell wall. The bacilli are resistant to decolorisation with acid or alcohol.

2. Cont. Types of mycobacteria: Mycobact complex Myco tuberculosis Myco bovis Myco Africanum Opportunistic mycobacteria Myco . kansasii Myco . Xenopi

3. Cont. Myco . Mais complex Myco Aviam Myco intracellulare Myco scrofulaceum Myco leprae Myco ulcerans Myco malmonse Myco fortuitum Myco chelonei Myco haemophilum Myco genavense

4. Cont. Epidemiology: Tuberculosis affects > 2.5 million people globally and about a third of the world’s population has latent TB. About 80% of those affected are in sub-Saharan Africa. There are about 8-10m new cases with about 1.7m deaths per year.

5. Cont. PTB is re-emerging due to: Emergency of HIV/AIDS Social deprivation, poverty, civil unrest. Increasing population of elderly pple Ineffective control programmes Population increase - overcrowding.

6. Cont. Pathogenesis : Myco Tuberculosis is spread by droplet inhalation (aerosolized droplets nuclei) from other infected patients. Small particles (1-5 um) enter the periphery of the lungs and are engulfed by macrophages. In response to antigens presentation, CD4+ T- lymphocytes produce cytokines; interferon gamma etc that drives the recruitment of monocytes and directs the formation of granulomas limiting replications and spread.

7. Cont. The formation of granulomas leads to primary lesion in the lungs ( Ghon focus). The combination of a 1 lesion and regional LN involvement is termed ‘ Ghon complex’. If the bacilli spreads – direct, lymphatic or haematogenous b4 immunity is established, secondary foci is established in other organs – LN, serous membranes, meninges, bones, liver, kidney.

8. Cont. These foci resolves once immunity is established. In most cases, infxn of a healthy person is subclinical and mediated only by a cell-mediated, delayed type hypersentivity to tuberculin. If the organisms cannot be contained, primary progressive disease ensures.

9. Cont. Primary TB basically affects the hilar lymph nodes and refers to infxn of a previously uninfected ( tuberlin negative) persons. Post primary TB - presents with ill-defined opacity in one of the upper lobes of the lungs. PTB is the most frequent form of post 1 TB and CXR – consolidation, collapse or cavitation . A caseous LN may drain into an adjoining bronchus – tuberculous pneumonia.

10. Cont. The possibilities following TB infxn are: Body clears the infections Latent TB 1 TB Reactivation About 5-10% of patients get active TB.

11. Cont. Factors that increase the risk of TB : Age – children more than the elderly than young adults Close contacts of patients with smear + ve PTB Overcrowding –prisons, collective dormitories Chest infections < 1year previously treated Chest radiographic evidence of self-healed TB

12. Cont. Immunosuppresion –HIV, infiximab , high dose corticosteroids, cytotoxic agents. Malignancies – lymphomas, leukemias DM ( esp type 1) CRF Silicosis Deficiency of vit D&A

13. Cont. Clinical features of PTB Constitutional symptoms Fatigue.gen. lassitude Wt loss Anorexia Persistent fever Night sweats

14. Cont. Pulmonary symptoms - Cough, initially dry, later productive with haemoptysis NB: Up to 5% of cases are diagnosed at autopsy. Signs Wasting due to persistent fever and wt loss. Low grade fever. May be pale Finger clubbing

15. Cont. R/S Reduced air entry in a specific lobe Dullness on percussion Bronchial breathing due to consolidation Amphoric breath sounds Localized wheeze esp. in endo bronchial TB

16. Cont. Extra – pulmonary TB: Accounts for about 20% of cases in HIV negative pts and is more common in HIV positive pts. The most common sites affected are: LN – Lymphadenitis TB Bones – TB bone Serous membranes – Tuberculous pericarditis, TB peritoneum, TB of the gut etc. GUT – Renal TB, prostatitis . Brain – TBM Disseminated TB – Milliary TB NB: The most serious forms are disseminated TB and TBM.

17. Cont. Investigations: 1. CXR – Hilar LN enlargement -Segmental atelectasis -Calcified 1 focus ( Ghon focus) - Ranke focus – 1 calcified forms + hilar LN - Pneumonia infiltrates - Fibrocavitary dz -‘Millet seed’ distribution - Atypical features in HIV and PTB infxns

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20. Cont. 2. Sputum for AAFB esp. if CXR is suggestive 3. Bronchial washings for those not able to produce sputum 4. Broncho -alveolar lavage 5. Susceptibility studies on sputum – Nucleic acid amplification test (NAAT)

21. Cont. 6. Biopsy from pleura, LN, bone for ZN stain, culture 7. PCR – Differentiates myco . Tb from other myco . Organisms 8. Blood cultures 9. FBC, ESR, CRP 10. CT scan of chest esp. in early TB 11. Special tests - Heaf test - Tuberculin test - Mantoux test - indicated in those at risk and in screening for latency infxns

22. Cont. Interpretation : Above 5mm – significant in drug abusers, pts at risk or those with h/o prior Rx and have fibrosis Above 10mm – significant in: Pple from Asia and Africa HIV neg. individuals or drug abusers Pple with low SES Chronic debilitating illnesses e.g DM, CKI, Silicosis exposure, Leukaemia , Lymphomas, pts on corticosteroids

23. Cont. False positives occur with non TB mycobacterium False neg occur in: Concurrent infxns – measles etc Malnutrition Malignant dzs Immunosuppressive drugs Sarcoidosis CKI -Measuring of interferon gamma – Th 1 – Quantiferon gamma assay which aims to know whether pt is at risk of active TB.

24. Cont. VII. Lung abscess Def . A lung abscess is a localized suppurative infxn of the lung leading to necrosis and cavitation . Commonly follows aspiration pneumonia. It may be: 1 – 60% 2 – 40%

25. Cont. Risk factors : Aspiration ( Oropharyngeal /Gastric) –alcoholism is the most common predisposing factor Penetrating chest injury Inadequately treated pneumonia, necrotizing pneumonia Chronic respiratory sepsis -Sinusitis - Tonsillitis -Dental infxn

26. Cont. Bronchial obstruction - Carcinoma esp.pry. carcinoma of lung - Intramural FB Septicemia, septic emboli, Rt heart endocarditis, IV drug use Vasculitis – Wegenersgranulomatosis Subphrenic or hepatic abscess Pulmonary infarct

27. Cont. Causes 1.Bacterial Anaerobic bacteria; streptococcus, Bacteroides ,, Fusobacteria Aerobic bacteria; Staph aureus , Klebsiella, Haemophillus influenza, Pseudomonas, Nocardia , Esch . Coli 2. Fungi 3. Parasites; Lung flukes esp. ParagonimusWestermania , Entamoebahistolytica

28. Cont. Pathogenesis: Pyogenic lung abscess usually occurs as a result of aspiration of septic debris during a period when the cough reflex is suppressed. The most direct route for the airway embolus to travel is into the Rt main bronchus. The most common sites of lodgement of septic emboli and development of lung abscesses are the superior division of the Rt lower lobe and the posterior segment of the Rt upper lobe.

29. Cont. Following the development of severe pneumonitis in response to the embolus, liquefaction may occur. As the liquefied necrotic material empties through the bronchus, a necrotic cavity containing air is formed.

30. Cont. Clinically, lung abscesses present as indolent conditions in pts with predilection for aspiration. An area of dense pneumonic consolidation precedes the appearance of the xtic cavitary lesion. Multiple abscesses may form multiple cavities.

31. Clinical features: Usually gradual in onset Swinging fevers Cough; purulent foul smelling sputum, haemoptysis. Night sweats Pleuritic chest pain Lethargy/ malaise Cachexic , wt loss May have finger clubbing Localized dullness Bronchial breath sounds/ crackles

32. Cont. Diagnosis : 1. Clinical 2. CXR – Unilateral consolidation with cavitating shadow. - Air fluid level 3. Laboratory investigations - Blood tests; FBC ( Hb , WBC, ESR, CRP) 4.Bronchoscopy 5.CT scan

33. Cont. Complications Septicemia Brain abscess Emphysema Bronchiectasis

34. Cont. DISORDERS OF PLEURA 1. PLEURAL EFFUSION Def : Excessive accumulation of serous fluid in the pleural space. Epidemiology- pleural effusion affects more than 1.5 million people in the USA and probably more people in sub-Sahara Africa. Classification Transudative Exudative

35. Cont. Causes – grouped according to type of effusion Transudative causes Cardiovascular causes- CCF, pericardial disease, myocardial infarction, SVC obstruction Hypoalbuminemia –cirrhosis/ liver failure, nephrotic syndrome, malnutrition. Intra- abdo: Fluid- peritoneal dialysis, ascites.

36. Cont. Exudative causes Infections- pneumonia, PTB, fungal, viral or parasitic infection. Neoplasm- mesothelioma , metastatic lesions- ca breast, lymphomas. Trauma to the chest- haemothorax , chylothorax , post cardiac injury.

37. Cont. Pulmonary infarction. GIT diseases- oesophageal perforation, post-abdo surgery, pancreatic disease. Collagen (vascular) diseases- Rh . Arthritis, SLE, wegeners granulomatosis .

38. Cont. Others Drug induced- nitrofurantoin , bromocriptine , amiodarone. Uremia Radiation therapy Meig’s syndrome Lymphedema (yellow nail syndrome) NB: Most common causes Pneumonia, PTB, pulmonary infarction, malignant diseases, CCF, sub-diaphragmatic disorders (sub- phrenic abscess, pancreatitis).

39. Cont. Pathology Pleural fluid usually accumulates when there is an imbalance between pleural fluid formation and pleural fluid absorption. Excess fluid can be from parietal pleura, interstitial space of lung or the peritoneal cavity or when there is decreased removal by the lymphatics.

40. Cont. A transudative pleural effusion occurs when systemic factors that influence the formation and absorption are altered (increases in vascular hydrostatic pressures or decrease in plasma oncotic pressures.) An exudative pleural effusion occurs when local factors that influence the formation and absorption of pleural fluid are altered such as increases in vascular permeability from trauma, abnormal communication between pleural space and peritoneal space lung parenchyma.

41. Cont. Clinical presentation May be asymptomatic Symptoms Breathlessness; Severity depends on size and rate of accumulation. Chest pain; classically sharp and exacerbated by coughing or deep breathing.

42. Cont. Signs Tachypnea , there may be features of the underlying disorder; Cachexia, finger clubbing RD, +asymmetrical chest, deviated trachea towards normal side in unilateral effusions. Decreased chest expansion on the affected side, stony dullness, decreased vocal fremitus ; decreased breath sounds or absent breath sounds. There may be aegophony (bronchial breathing and bleating vocal resonance) at the superior edge of effusion due to lung compression.

43. Cont. Investigations To confirm diagnosis To determine cause. Investigations 1. CXR – Erect PA –elevation of hemidiaphragm , curved shadow at base of lung -blunted costophrenic angle and ascending towards axilla -Lat. decubitus -demonstrate free flowing fluid, for estimating vol. and R/o sub- pulmonic effusion.

44. Cont. 2. Diagnostic aspiration/ thoracocentesis Pleural fluid Naked eye exam/gross- clear, yellow chyle , blood, pus, milky,brown . Biochemical studies- protein, glucose, LDH, PH, amylase Microbiological studies- Gm stain, c/s, AAFB, fungal cultures. Cytology- neutrophils, lymphocytes, mesothelial cells, lupus erythematosus cells. Immunological studies- Rh factor, antinuclear antibodies, complement levels. Pleural fluid Hct .→ blood stained effusion.

45. Cont. 3. Blood tests FBC; Hb , neutrophils, WBC-T/D U/E serum protein ( ≥3g/dl in exudative), serum LDH   4. Ultrasonography - fluid vol. and distingiushes pl. fluid from pl. thickening. 5. Computed tomography- benign from malig . Pleural dz 6. Pleural biopsy – esp. suspected TB 7. Other- directed towards suspected cause.

46. Cont. 2. EMPYEMA Def : Presence of pus in the pleural space. Empyema may be loculated (involve whole space) or encysted (involved only part of pleural space) and is almost invariably unilateral. Empyema may be acute or chronic.

47. Cont. Causes May be secondary to Bacterial pneumonia - 40% leads to pl. effusion → empyema 15% PTB Others Infection of a haemothorax Rupture of sub- phrenic abscess or lung abscess.

48. Cont. Pathology - Thick, shaggy inflammatory exudate. The pus is usually under pressure → rupture into bronchus→ bronchopleural fistula and pyoneumothorax or track through chest wall → subcutaneous abscess or sinus. Delay in Rx → thickened, rigid visceral pleura. Clinical features Requires a high index of suspicion in patients with pulmonary infection

49. Cont. Symptoms Non specific systemic features Persistent or recurrent high fever despite administration of a suitable antibiotic. Rigors, sweating, malaise, weight loss Local features/ symptoms- Pleuritic chest pain, breathlessness, cough- productive of copious sputum if empyema ruptures into a bronchus Signs Patient is ill-looking , tachypnoenic Clinical signs of fluid in the pleural space.

50. Cont. Investigations 1. Radiological CXR – horizontal fluid level in pyopneumothorax . Ultrasound CT Scan R/O underlying lung parenchyma dz and patency of the major bronchi.

51. Cont. 2. Aspiration of pus Gross examination Bioch -P H <7.2, glucose decreased, LDH increased Microbiology Histology 3. Blood tests FBC, U/E, CRP

52. Cont. 3.PNEUMOTHORAX Def : Presence of air in the pleural space Classification and causes 1. Traumatic pneumothorax Follows chest injury, thoracic surgery or biopsy, transthoracic needle aspiration, thoracocentesis or central venous catheter.

53. Cont. 2. Spontaneous pneumothorax (SP) Primary sp mostly common in young males 15-30yrs, tall, thin and often smoking M:F 6:1 no evidence of overt lung disease. Follows rupture of apical pleural bleb or an emphysematous bullae Secondary sp –common in older people >40yrs. Follows an underlying lung disease- COPD, asthma, PTB, Pneumonia ,Lung abscess ,Ca lung ,cystic lung disease. Associated with highest mortality rate

54. Cont. Both types may be Closed type – mean pleural pressure is negative. Open type – mean pleural pressure is at atmospheric. Tension type – mean pleural pressure is positive through out cycle with mediastinal shift to opposite side. This is a medical emergency and commonly follows trauma, mech. Ventilation or resuscitative efforts.

55. Cont. Clinical features May be asymptomatic Symptoms Sudden onset unilateral chest pain and breathlessness. Those with asthma or COPD may present with sudden deterioration.

56. Cont. Signs Tachypnea (pain deflation reflex) Tachycardia, cyanosis, hypotension and deviated trachea to normal side in tension pneumothorax . Reduced chest expansion Resonant or hyper-resonant percussion note. Reduced or absent breath sounds on affected side. NB : Absent breaths sounds and resonant percussion note is diagnostic

57. Cont. Investigations CXR – sharply defined edge of deflated lung with complete translucency (no lung markings) between this and chest wall. Mediastinal displacement, R/O pleural effusion or pulmonary disease. CT scan – distinguishes bullae from pleural air.