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PATHOLOGY
BASIC INTRODUCTION TO PATHOLOGY OF COMMON LUNG DISEASES
DISEASES
FOR
UNDERGRADUATE DENTAL STUDENTS AND NURSES
RE...
Lecture outline
Introduction to
o Bronchial asthma
o Chronic bronchitis and Emphysema
o Bronchiectasis.
o Pneumonia
o Tube...
RESPIRATORY TRACT
Background information
RESPIRATORY TRACT
Background information
Function of lungs….
Gas exchange (O2, CO2)
■ Can only occur in alveoli that
are b...
RESPIRATORY TRACT
Background information
BRONCHIAL ASTHMA
BRONCHIAL ASTHMA (BA)
• Most common chronic respiratory disease in children.
More common in children than adults
• Is a ch...
Complications of Bronchial Asthma
 Superimposed infection
 Chronic bronchitis or Emphysema
 Status asthmaticus:
•most s...
CHRONIC
BRONCHITIS
Chronic Bronchitis
 Common among cigarette smokers and urban dwellers, age 40 to 65
 Definition  persistent productive ...
EMPHYSEMA
Emphysema
 Is abnormal permanent enlargement of the
airspaces distal to the terminal bronchioles
accompanied by destructi...
■ Normal ■ Emphysema
Morphology: The lungs are pale, voluminous. Histology thinning
and destruction of alveolar walls cre...
Centriacinar (centrilobular) emphysema
■ Occur in heavy smoker in association with chronic bronchitis
■ The central or pro...
Panacinar (panlobular) emphysema
 Cause: occurs in 1-anti-trypsin deficiency.
 Uniform injury: Acini are uniformly
enla...
Distal acinar (paraseptal) emphysema
■ The proximal portion of the acinus is
normal but the distal part is dominantly
invo...
Pathogenesis of Emphysema
 Normally there is a balance between protease and anti protease
activity.
 An imbalance betwee...
Emphysema: Morphology
■ The lungs are pale, voluminous.
■ Histologically: thinning and destruction of alveolar walls
creat...
BRONCHIECTASIS
Bronchiectasis
 is chronic necrotizing inflammation and destruction of the bronchi and bronchioles  leading to
abnormal ...
Normal
■ Airways are dilated airways up to four times of normal.
Bronchiectasis
Morphology of Bronchiectasis
■ Usually affects lower lobes bilaterally.
■ Dilated airways up to four times of normal.
■ Ac...
PNEUMONIA
Pneumonia
 Pneumonia is defined as any infection of lung parenchyma
 Portal of entry for most pneumonia is
 Inhalation ...
CLASSIFICATION OF PNEUMONIA
1. Bronchopneumonia:
■ occur in two extremes of life.
■ multiple small patches of
inflammation...
Stages of pneumonia
There are 4 stages:
I. Congestion: lung is heavy, boggy and red. The alveoli are filled with fluid and...
Red hepatization
Opportunistic pneumonias
• Infections that affect immunosuppressed patients (AIDS, cancer patients and
transplant recipien...
TUBERCULOSIS
TUBERCULOSIS
■ TB is a communicable granulomatous disease caused mainly by Mycobacterium
tuberculosis hominis (Koch bacill...
TUBERCULOSIS
Reservoir of infection:
• humans with active tuberculosis.
Increased risk:
• poverty, crowding, malnutrition,...
Cavitatory TB lung
Cavitatory tuberculosis with intracavitary
hemorrhage. Extensive necrosis with
cavitation, usually occu...
Langhans Giant Cell
Caseous Necrosis
Epithelioid Macrophage
Lymphocytic Rim
Diagnosis of TB
Ziehl-Neelsen stain shows red acid-fast
staining M. tuberculi.
Tubercle bacilli are acid fast:
 Character...
LUNG TUMORS
Lung Tumors
■ Most lung tumors are malignant.
■ Lungs are frequently the site of metastases.
■ Primary lung cancer is a co...
Examples of Primary Lung Tumors
MALIGNANT EPITHELIAL TUMORS /BRONCHOGENIC CARCINOMA:
I. Non-Small Cell Lung Carcinoma
a) S...
BRONCHOGENIC CARCINOMA
Bronchogenic carcinoma is a malignant neoplasm
of the lung arising from the epithelium of the lung....
SO: It is important to differentiated between the Non-small cell and small cell because treatment is different:
• Non- Sma...
Squamous cell carcinoma
(SqCC)
■ strong association with smoking
■ Poor prognosis
■ SqCC arise in the central airways (cen...
adenocarcinomas
■ They do not have a clear link to
smoking history
■ They are classically peripheral tumors
arising from t...
Large Cell
Carcinoma
■ Frequency: 10%
■ strongly associated with smoking
■ usually located peripherally.
■ poor prognosis.
Small cell carcinomas
■ SCLC are a poorly differentiated highly malignant
neuroendocrine tumors arising from
neuroendocrin...
Carcinoid tumor
■ Carcinoid tumors of the lung are well differentiated
neuroendocrine tumor. They arise from the
neuroendo...
Etiology of bronchogenic carcinoma
1. Tobacco smoking: cigarette smoking is linked to squamous cell carcinoma and small ce...
Clinical features of bronchogenic carcinoma
 Can be silent or insidious lesions
 Respiratory symptoms e.g. Cough, expect...
Mesothelioma
■ Highly malignant tumor of mesothelial
cells lining the pleura
■ History of exposure to asbestos is
common.
...
Metastatic carcinoma of lung
■ Pulmonary Metastases are More
Common than Primary Lung Tumors
■ Typically multiple and circ...
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Pathology basic introduction to pathology of common lung diseases for undergraduate dental students and nurses sufia husain

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Intro to lung pathology for nurses and dental students

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Pathology basic introduction to pathology of common lung diseases for undergraduate dental students and nurses sufia husain

  1. 1. PATHOLOGY BASIC INTRODUCTION TO PATHOLOGY OF COMMON LUNG DISEASES DISEASES FOR UNDERGRADUATE DENTAL STUDENTS AND NURSES REFERENCE: ROBBINS BASIC PATHOLOGY, 9TH EDITION. Dr. Sufia Husain Pathology
  2. 2. Lecture outline Introduction to o Bronchial asthma o Chronic bronchitis and Emphysema o Bronchiectasis. o Pneumonia o Tuberculosis o Lung tumors
  3. 3. RESPIRATORY TRACT Background information
  4. 4. RESPIRATORY TRACT Background information Function of lungs…. Gas exchange (O2, CO2) ■ Can only occur in alveoli that are both ventilated and perfused
  5. 5. RESPIRATORY TRACT Background information
  6. 6. BRONCHIAL ASTHMA
  7. 7. BRONCHIAL ASTHMA (BA) • Most common chronic respiratory disease in children. More common in children than adults • Is a chronic episodic inflammatory obstructive lung disease characterized by hyper-reactive airways (patients have hyper-irritable airways which react to various stimuli). • Primarily targets the bronchi and terminal bronchioles • In it the airways go into bronchoconstriction/spasm. • It results in a triad of: 1. intermittent and reversible airway constriction 2. Edema, inflammation with eosinophils and excess mucus production 3. bronchial smooth muscle cell hypertrophy C/F of BA  In a classic asthmatic attack there is wheezing, dyspnea, cough.  Nocturnal cough
  8. 8. Complications of Bronchial Asthma  Superimposed infection  Chronic bronchitis or Emphysema  Status asthmaticus: •most severe form of asthma  severe acute respiratory distress •severe bronchoconstriction that does not respond easily to drugs. •serious and requires hospitalization and may  severe cyanosis and death. Extrinsic (atopic, allergic) Asthma 70% Intrinsic (non-atopic)Asthma 30% Allergic type 1 hypersensitivity reaction induced by exposure to extrinsic antigen/allergens e.g. food, pollen, dust, etc. Non- allergic. Usually family history present No personal history of allergy. No family history of allergy. Develop early in life Develops later in life Sometimes extrinsic and intrinsic can co-exist in the same
  9. 9. CHRONIC BRONCHITIS
  10. 10. Chronic Bronchitis  Common among cigarette smokers and urban dwellers, age 40 to 65  Definition  persistent productive cough (with sputum) for at least 3 consecutive months in at least 2 consecutive years  Can coexists with emphysema (Often, there are features of emphysema as well) Causative factor are: – Cigarette smoking and pollutants. – Infection – Genetic factors
  11. 11. EMPHYSEMA
  12. 12. Emphysema  Is abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls, without obvious fibrosis.  Tends to coexist with chronic bronchitis  Types of emphysema: – Centriacinar (centrilobular) : Occurs in heavy smoker in association with chronic bronchitis – Panacinar: there is Alpha 1 antitrypsin deficiency – Distal acinar /paraseptal – Irregular Clinical features: • Cough and wheezing. Respiratory acidosis • Abnormal pulmonary function tests
  13. 13. ■ Normal ■ Emphysema Morphology: The lungs are pale, voluminous. Histology thinning and destruction of alveolar walls creating large airspaces.
  14. 14. Centriacinar (centrilobular) emphysema ■ Occur in heavy smoker in association with chronic bronchitis ■ The central or proximal parts of the acini are affected, while distal alveoli are spared
  15. 15. Panacinar (panlobular) emphysema  Cause: occurs in 1-anti-trypsin deficiency.  Uniform injury: Acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli.
  16. 16. Distal acinar (paraseptal) emphysema ■ The proximal portion of the acinus is normal but the distal part is dominantly involved. ■ Sometimes forming multiple cyst-like structures with spontaneous pneumothorax.
  17. 17. Pathogenesis of Emphysema  Normally there is a balance between protease and anti protease activity.  An imbalance between protease and antiprotease activity in the lung  emphysema.  Protease (e.g. elastase) is proteolytic enzymes that damages alveolar elastic tissue. It is produced by neutrophils and macrophages.  Smokers have increase in the numbers of alveolar macrophages and neutrophils  imbalance.  Note: Alpha 1 antitrypsin is an anti-protease. It is normally present in the serum, in tissue fluids and in macrophages. Deficiency  panacinar emphysema.
  18. 18. Emphysema: Morphology ■ The lungs are pale, voluminous. ■ Histologically: thinning and destruction of alveolar walls creating large airspaces. Clinical features: • Cough and wheezing. Respiratory acidosis • Weight loss. • Pulmonary function tests reveal reduced FEV1.
  19. 19. BRONCHIECTASIS
  20. 20. Bronchiectasis  is chronic necrotizing inflammation and destruction of the bronchi and bronchioles  leading to abnormal permanent dilation of these airways.  most often involves the lower lobes of both lungs.  characterized by • fever and cough • production of purulent foul smelling sputum, • and recurrent pulmonary infection that may lead to lung abscess.
  21. 21. Normal ■ Airways are dilated airways up to four times of normal. Bronchiectasis
  22. 22. Morphology of Bronchiectasis ■ Usually affects lower lobes bilaterally. ■ Dilated airways up to four times of normal. ■ Acute and chronic inflammation (neutrophils, lymphocytes, histiocytes and plasma cells) ■ Necrosis and ulceration in the wall of the bronchi and bronchioles and fibrosis.
  23. 23. PNEUMONIA
  24. 24. Pneumonia  Pneumonia is defined as any infection of lung parenchyma  Portal of entry for most pneumonia is  Inhalation of air droplets  Aspiration of infected secretions or objects  Hematogenous spread. Pneumonia can be acute or chronic Histology: variable, can be: acute fibrinopurulent alveolar exudate chronic interstitial inflammation  granulomatous inflammation
  25. 25. CLASSIFICATION OF PNEUMONIA 1. Bronchopneumonia: ■ occur in two extremes of life. ■ multiple small patches of inflammation centered around bronchioles. 2. Lobar pneumonia: • acute infection of a large portion of a lobe or entire lobe (widespread fibrinosupurative consolidation). - Note: overlap of the two patterns often occur
  26. 26. Stages of pneumonia There are 4 stages: I. Congestion: lung is heavy, boggy and red. The alveoli are filled with fluid and bacteria. II. Red hepatization: the lung is firm/solid, red and alveoli are filled with neutrophils, rbcs (congestion) and fibrin. III. Gray hepatization: the red cells are reduced but neutrophils and fibrin (fibrinopurulent/suppurative exudate) are still present. The lung is still firm/solid but grey. IV. Resolution (hepatization = solidification = liver like consistency)
  27. 27. Red hepatization
  28. 28. Opportunistic pneumonias • Infections that affect immunosuppressed patients (AIDS, cancer patients and transplant recipients) Causative organisms: • Cytomegalovirus • Pneumocystis jiroveci (formerly P. carinii) • Mycobacterium avium-intracellulare • Invasive aspergillosis • Invasive candidiasis • "Usual" bacterial, viral, and fungal organisms Pneumocystis carinii Aspergillus Cytomegalovirus  Methods of diagnosis are:  identify the organism in bronchoalveolar lavage fluids or in a transbronchial biopsy specimen.  Culture  PCR-based assays.
  29. 29. TUBERCULOSIS
  30. 30. TUBERCULOSIS ■ TB is a communicable granulomatous disease caused mainly by Mycobacterium tuberculosis hominis (Koch bacillus) and occasionally by Mycobacterium tuberculosis bovis. ■ Primarily affects the lungs but other organs can also be infected. ■ Reservoir of infection is humans with active tuberculosis. ■ Characteristic lesion: epitheloid granuloma with central caseous necrosis. ■ Mycobacterium tuberculi are non-motile rod-shaped aerobic acid fast bacilli.
  31. 31. TUBERCULOSIS Reservoir of infection: • humans with active tuberculosis. Increased risk: • poverty, crowding, malnutrition, chronic debilitating illness, elderly, people with AIDS, immunosuppression etc. Route of transmission • M. tuberculosis generally enters lung by inhalation (by inhaling infected aerosols from the cough of a person with active cavitatory TB). • M. bovis generally enters by drinking unpasturized infected cow's milk  oropharyngeal & intestinal TB. Clinical features • Malaise, anorexia, weight loss, fever (low grade evening rise of temperature) with chills and night sweats. • Cough with sputum, hemoptysis etc. • Extrapulmonary manifestations of tuberculosis depend on the organ system involved. • Localized secondary tuberculosis may be asymptomatic.
  32. 32. Cavitatory TB lung Cavitatory tuberculosis with intracavitary hemorrhage. Extensive necrosis with cavitation, usually occurring in the upper lung lobe .
  33. 33. Langhans Giant Cell Caseous Necrosis Epithelioid Macrophage Lymphocytic Rim
  34. 34. Diagnosis of TB Ziehl-Neelsen stain shows red acid-fast staining M. tuberculi. Tubercle bacilli are acid fast:  Characteristically the bacilli stain red/pink with Ziehl-Neelsen acid-fast stain and the glow with fluorescent dye auramine O.  TB culture of the sputum or tissue is still the most sensitive and specific, albeit slowest, way to make the diagnosis. Culture is the gold standard  PCR testing allows for rapid diagnosis.
  35. 35. LUNG TUMORS
  36. 36. Lung Tumors ■ Most lung tumors are malignant. ■ Lungs are frequently the site of metastases. ■ Primary lung cancer is a common disease BUT metastatic tumors are more common than the primary tumors. ■ The most common benign lesions are hamartomas.
  37. 37. Examples of Primary Lung Tumors MALIGNANT EPITHELIAL TUMORS /BRONCHOGENIC CARCINOMA: I. Non-Small Cell Lung Carcinoma a) Squamous cell carcinoma: Strong association with smoking, poor prognosis, usually central (perihilar) in location, can be well/ moderate/ poorly differentiated b) Adenocarcinoma: do not have a clear link to smoking history, usually peripheral in location, sometimes associated with pulmonary scars (scar carcinoma) c) Large cell carcinoma: uncommon, strongly associated with smoking, very poor prognosis. II. Small cell lung carcinoma: poorly differentiated highly malignant, aggressive neuroendocrine tumors. Poor prognosis. Strongly associated with cigarette smoking. Central (perihilar), can be associated with paraneoplastic syndrome. Microscopy  small round blue cells. III. Combine patterns IV. Carcinoid tumor: well differentiated neuroendocrine tumor; not related to cigarette smoking. Tumor cells produce serotonin and bradykinin  carcinoid syndrome (flushing, wheezing, diarrhea etc.), can also produce ectopic ACTH  Cushing syndrome. Low malignancy, good prognosis (often resectable & curable). MALIGNANT MESOTHELIAL TUMOR: malignant mesothelioma OTHERS Miscellaneous malignant tumor e.g. Carcinosarcoma, Pulmonary blastoma, Melanoma, Lymphoma etc
  38. 38. BRONCHOGENIC CARCINOMA Bronchogenic carcinoma is a malignant neoplasm of the lung arising from the epithelium of the lung. Most patients are 50-80 years. For therapeutic purposes, bronchogenic carcinoma are classified into: 1. Non- Small cell lung carcinoma (NSCC) 2. Small cell lung carcinoma (SCC) Important to differentiated between the 2 because treatment are different. For NSCC therapy: •Surgical - the best chance for curing. •Radiation – to control local disease. •Chemotherapy – not effective. SCC therapy •Chemotherapy - very effective, small cell carcinomas are highly responsive to chemotherapy
  39. 39. SO: It is important to differentiated between the Non-small cell and small cell because treatment is different: • Non- Small cell lung carcinoma (NSCC)  surgery • Small cell lung carcinoma (SCC)  chemotherapy is very effective
  40. 40. Squamous cell carcinoma (SqCC) ■ strong association with smoking ■ Poor prognosis ■ SqCC arise in the central airways (centrally located). So they appears as a hilar mass. ■ Tumor cells secrete a parathyroid hormone (PTH)- like peptide  hypercalcemia. ■ Histologically they are graded according to degree of squamous differentiation: • well-differentiated SqCC • moderately differentiated SqCC • poorly differentiated SqCC
  41. 41. adenocarcinomas ■ They do not have a clear link to smoking history ■ They are classically peripheral tumors arising from the peripheral airways and alveoli. ■ The hallmark of adenocarcinomas is the tendency to form glands that may or may not produce mucin. ■ Peripheral adenocarcinomas are sometimes associated with pulmonary scars (from a previous pulmonary inflammation/infection) and therefore is also referred to as scar carcinoma.
  42. 42. Large Cell Carcinoma ■ Frequency: 10% ■ strongly associated with smoking ■ usually located peripherally. ■ poor prognosis.
  43. 43. Small cell carcinomas ■ SCLC are a poorly differentiated highly malignant neuroendocrine tumors arising from neuroendocrine cells. ■ Highly malignant and aggressive tumor, poor prognosis. ■ Strongly associated with cigarette smoking. ■ Centrally located perihilar mass. ■ Microscopically composed of small, round dark blue cells. ■ Chemotherapy responsive ■ It may be associated with paraneoplastic syndrome.
  44. 44. Carcinoid tumor ■ Carcinoid tumors of the lung are well differentiated neuroendocrine tumor. They arise from the neuroendocrine cells found in the bronchial epithelium. ■ These neoplasms account for 2% of all primary lung cancers and are not related to cigarette smoking. ■ Can be central or peripheral in location ■ Composed of uniform cuboidal cells that have regular round nuclei with few mitoses and little or no atypia. ■ Electron microscopy: dense-core neurosecretory granules. ■ Tumor cells produce serotonin and bradykinin leading to carcinoid syndrome (flushing, wheezing, diarrhea, and cardiac valvular lesions).Tumor cells can also produce ectopic ACTH leading to Cushing syndrome. ■ Can occur in patients with Multiple Endocrine Neoplasia (MEN-I) ■ Low malignancy, Often resectable and curable. ■ Spreads by direct extension into adjacent tissues
  45. 45. Etiology of bronchogenic carcinoma 1. Tobacco smoking: cigarette smoking is linked to squamous cell carcinoma and small cell carcinoma. The risk is 20 to 40 times greater among habitual heavy smokers. Passive smoking increases the risk to approximately twice than non-smokers. The nonsmoker who develops cancer of the lung usually  adenocarcinoma. 2. Radiation 3. Asbestos exposure  bronchogenic carcinoma and mesothelioma. 4. Industrial exposure to nickel and chromates, coal, mustard gas, arsenic, iron etc. 5. Air pollution: may play a role e.g. indoor air pollution by radon. 6. Scarring: sometimes old infarcts, wounds, scar (from a previous pulmonary inflammation/infection), granulomatous infections are associated with adenocarcinoma.
  46. 46. Clinical features of bronchogenic carcinoma  Can be silent or insidious lesions  Respiratory symptoms e.g. Cough, expectoration, hemoptysis, bronchial obstruction, lung collapse, bronchiectasis, pneumonia, chest pain, pleural effusion etc.  Hoarseness, chest pain, superior vena cava syndrome, pericardial or pleural effusion.  Paraneoplastic syndrome: are extrapulmonary, remote effects of tumors. About 10% of lung cancers develop paraneoplastic syndromes. In it the tumor cells produce various peptides/hormone  lead to metabolic and neuromuscular disturbances e.g. Carcinoid tumors and small cell carcinomas may secrete ectopic ACTH  Cushing's syndrome small cell carcinomas may secrete ADH  water retention and hyponatremia squamous cell carcinomas may secrete PTH like peptide  hypercalcemia. Etc.
  47. 47. Mesothelioma ■ Highly malignant tumor of mesothelial cells lining the pleura ■ History of exposure to asbestos is common. ■ Treatment is largely ineffective and prognosis  extremely poor
  48. 48. Metastatic carcinoma of lung ■ Pulmonary Metastases are More Common than Primary Lung Tumors ■ Typically multiple and circumscribed nodules. Radiologically  called cannon ball metastases. ■ The common primary sites are the breast, stomach, pancreas, and colon.

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