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  • 1. Pathology Slides
  • 2. Bronchiectasis
  • 3.
    • Bronchiectasis is a disease characterised by permanent dilatation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue.
    • Causes
      • CONGENITAL:Cystic fibrosis,Kartageners syndrome
      • POST-INFECTIOUS:as a complication of pneumonia
      • BRONCHIAL OBSTRUCTION:due to foreign body,tumor,mucus impaction
    • MORPHOLOGY
    • Affects lower lobes ,bilaterally
    • The bronchi and bronchioles are dilated upto 4 times the normal size
    • - Cylindrical or tube like
    • - Fusiform
    • - Saccular or sac like
    • - The bronchioles are markedly dilated and extend upto the pleural surface
    • HISTOLOGY
    • The walls of the bronchi and bronchiles show dense inflammation,with desquamation and ulceration of the wall.
    • Fibrosis of the wall in chronic cases
    • CLINICAL COURSE
    • Persistent cough, with foul smelling bloody sputum
    • Dyspnea
    • COMPLICATIONS
    • Cor pulmonale(Heart failure)
    • Lung abscess,metastatic abscess
    • Amyloidosis
  • 4. Chronic Lung Abscess
  • 5.
    • Localised area of suppurative necrosis in lung parenchyma
    • Causes
      • Primary - in normal lung due to aspiration
      • Secondary - diseased lung
      • Aspiration of infective material from teeth, sinuses, tonsil oral surgery, coma, anaesthesia
      • Aspiration of gastric contents
      • Complication of necrotising bact pneumonia eg: Staph. aureus, Strep.
      • Bronchial obstruction
      • Septic embolism – thrombophlebitis, infective endocarditis
      • Hematogenous spread
  • 6.
    • Infection in pulmonary infarct, amoebic abscess
    • Organisms
      • Anaerobic bacteria
      • Mixed infection
      • S aureus, Strep., Nocardia, gram negative organisms
    • Morphology
      • Location & number depend on cause
      • Aspiration: Single , Rt side, Post seg of upper lobe & apical seg of lower lobe
      • Pneumonia, bronchiectasis— multiple, basal, diffusely scattered
      • Hematogenous— Multiple, any region of lung
  • 7.
    • Exudate partially drained by rupture into airways
    • X-ray: air fluid levels.
    • Cavity contain exudate, air & necrosis
    • As abscess ages – forms fibrous wall around.
    • Clinical features
      • Similar to bronchiectasis
      • Lung abscess in older patients underlying Ca must be ruled out
    • Complications
      • Rupture into pleural cavity: B Pleural fistula, Empyema, Pneumothorax
      • Septic emboli— Meningitis, Brain abscess
      • Secondary amyloidosis
  • 8. Emphysema
  • 9.
    • Emphysema is characterised by abnormal permanent dilatation of air spaces distal to terminal brochioles, accompanied by destruction of their walls. (Overinflation)
    • Types
      • 1)Centriacinar
      • Central part of the acinus (respiratory bronchioles)is affected,while distal alveoli is spared.Upper lobes,particularly apical segments are involved
      • Cause:Cigarette smoking
      • 2)Panacinar
      • Entire acinus(from respiratory bronchiole to distal alveoli affected). Affects lower lobes
      • Cause: 1 antitrypsin deficiency
      • 3)Distal acinar (Paraseptal)
      • Distal acinus involved. Upper lobes affected commonly
      • Adjacent to areas of scarring or atelactasis
  • 10.
    • Causes:
      • IMBALANCE in Protease-Antiprotease Mechanism :  Protease(elastase) and decreased Anti protease (antielastase)
      • In genetic deficiency of 1 antitrypsin –unchecked action by elastase causing destruction of alveolar walls
    • Clinical signs
      • Cough
      • Wheezing
      • Dyspnoea,weight loss
      • Barrel chest
      • Resp acidosis,RHF,Collapse,
      • Pneumothorax
      • Hyperinflation
  • 11. Miliary TB
  • 12.
    • Extensive infection
    • Hematogenous spread
    • Low immunity
    • Pulmonary or Systemic types
  • 13. Lobar Pneumonia
  • 14.
    • Inflammation of entire or almost entire lobe of lung
    • Rare due to antibiotic treatment.
    • CAUSATIVE ORGANISM ~95% - Streptococcus pneumoniae
    • Four stages:
      • Congestion.
      • Red Hepatization.
      • Gray Hepatization.
      • Resolution.
  • 15.
    • 1)STAGE OF CONGESTION:
    • Lungs are heavy, boggy and red
    • Microscopically: Vascular congestion, scattered neutrophils and many bacteria
    • 2)STAGE OF RED HEPATIZATION:
    • Lungs appear like liver
    • Microscopy: Alveolar spaces packed with neutrophils, red cells and fibrin
    • 3)STAGE OF GREY HEPATIZATION:
    • Lungs are red, grey and firm
    • Microscopy: Fibrinous exudate persists, but red cells are depleted
    • 4)STAGE OF RESOLUTION:
    • Exudate is digested enzymatically, and is resorbed or coughed up
  • 16. Complications
    • Spread of infection to pleural cavity-EMPYEMA
    • Tissue destruction and necrosis-ABSCESS
    • Bacterial dissemination to other organs-meningitis, arthritis, infective endocarditis
    • Organisation-to form scar
  • 17. Clinical features
    • Acute onset
    • High fever, chills
    • Pleuritic chest pain
    • Sputum - frankly purulent with haemoptysis or rusty sputum
  • 18. Pneumonia in immunocompromised
    • Cytomegalovirus
    • Pneumocystis carinii
    • Mycobacterium avium intracellulare
    • Aspergillosis
    • Candidiasis
  • 19. Primary TB w/ cavitations
  • 20. Primary Tuberculosis
    • In Non-immunized individuals(Children)
    • Primary Tuberculosis:
      • Self Limited disease
      • Ghon complex or Primary complex.
    • Primary Progressive TB
      • 10% of adults, Immunosuppressed individuals
      • Common in malnourished children
      • Miliary TB and Meningitis.
  • 21. Ghon's complex
    • Primary tuberculosis is the pattern seen with initial infection with tuberculosis in children.
    • Specifically, the Ghon's complex is a combination of the Ghon's focus (area of initial infection by airborne bacillus) and a lymphatic lesion.
    • Reactivation, or secondary tuberculosis, is more typically seen in adults.
  • 22. Cavitary Tuberculosis
    • When soft, necrotic centre drains out leaving behind a cavity.
    • Cavitation is typical for large granulomas.
    • Cavitation is more common in the reactivation tuberculosis seen in upper lobes.
  • 23. Small cell carcinoma
  • 24.
    • Mutation seen in Small cell – high frequency of p53 & RB gene mutations
    • Highly malignant
    • Strongly associated with smoking
    • Grows & metastasizes rapidly
    • Paraneoplastic syndromes
  • 25.
    • Small cells, scant cytoplasm
    • Round nuclei, finely granular chromatin
    • Nuclear moulding +
    • Mitotic figures +, Necrosis ++
    • Cells fragile, fragmentation-Crush artifact
    • Neuroendocrine origin
  • 26. Clinical features
    • Local effect
    • cough, dyspnea, hemoptysis, chest pain, pleural effusion.
    • Pancoast Tumor
    • C 8 , T 1&2 nerves
    • Cervical Sympathetic nerves— Horner’s syndrome
    • Enophthalmos, ptosis, miosis, anhidrosis
  • 27. Heart w/ Aorta- Atherosclerosis
  • 28. RISK FACTORS
    • MAJOR
    • NON MODIFIABLE POTENTIALLY
    • CONTROLLABLE
    • Increasing age Hyperlipidemia
    • Male gender Hypertension
    • Family History Cigarette smoking
    • Genetic Diabetes
  • 29. Risk Factors
    • MINOR
    • Diet
    • Physical Inactivity
    • Obesity
    • Type A personality
    • Alcohol
  • 30.
    • High blood cholesterol
    • High blood pressure
    • Smoking
    • Obesity
    • Lack of physical activity
    Causes
  • 31. CLASSIFICATION OF ATHEROSCLEROTIC LESIONS American Heart Association Type I (Fatty dots) Type II (Fatty streak) Type III (Intermediate lesion) Type IV(Atheroma) Type V (Fibroatheroma) Type VI (Complicated lesion)
  • 32.
    • Fatty streaks
    • are the earliest lesion that can be recognised.
    • – are composed of lipid filled foam cells.
    • - multiple , yellow spots less than 1mm in diameter .
    • Can be seen in seen by the age of 1 year
  • 33. Atherosclerotic plaque
    • Appear white to whitish yellow ,measuring 0.3-1.5 cm in diameter ,patchy lesions along the vessel wall
    • may coalesce and form diffuse lesions
    • Abdominal aorta is the most involved, followed by coronary arteries
  • 34. Segment of Intestine
  • 35.
    • It’s a gangrenous red infarct caused by hemorrage
    • Reason why it is red is because the intestines have dual blood supply, the flow of blood from the unobstructed vessel into the necrotic zone is not enough to overcome necrosis
    • Any infarct is wedge shaped, the base is towards the periphery and apex the hilus
    • Microscopy
      • Coagulative necrosis
      • And if its chronic there is scar formation
    • Cause
      • Occultion of venous blood supply by tumor, strictures or loss of folds
  • 36. Causes
    • 99% - thrombotic or embolic occlusion of arteries
    • Local vasospasm
    • Compression of the vessel (eg. by tumour, edema)
    • Twisting of the vessels (eg. Testicular torsion or volvulus of bowel)
  • 37. RED INFARCT
  • 38. White infarct
  • 39. MORPHOLOGY OF INFARCTS
    • Wedge-shaped
    • Base is on the periphery
    • Apex towards the hilus, shows blockage of the vessel
    • Replaced by scar -depressed area on the surface
    • Microscopy
    • Ischemic coagulative necrosis
    • Liquefactive necrosis-in brain
    • Necrotic area is replaced by fibrous tissue – scar
  • 40. Section of Spleen
  • 41.
    • Multiple white infarct
    • Due to arterial occulsion with solid organs with end arterial blood supply
    • The solidity of the tissue limits the amount of hemorrage
    • What other organs
      • Kidney and heart
  • 42. Section of Lung
  • 43.
    • Normal lung appearance is honey combed
    • The apex is the site of occultion, the red infarct is caused because the lung has dual blood supply and it’s a loose tissue that allow blood to collect into the infarcted zone
    • Microscopy
      • Coagulative necrosis
      • And if its chronic there is scar formation
    • Cause
      • Occultion of venous blood supply by tumor, strictures or loss of folds
  • 44. Segment of Liver
  • 45.
    • Nutmeg appearance
    • Central regions of hepatic lobules are red brown
    • Macros