Respiratory II Flashcards
Chronic Obstructive pulmonary disease is charcterized by?
1) Decreased (↓) FEV [Forced Expiratory Volume]
2) ** Decreased FVC** [Forced Vital Capacity]
3) Decreased FEV : FVC ratio
*The “opposite” of Restrictive Pulmonary Disease
Group of diseases causing chronic Obstructive Pulmonary disease (COPD)
1) Emphysema
2) Chronic Bronchitis
3) Bronchial Asthma
Types of Asthma
1) Extrinsic (immune):
–> Mediated by type I hypersensitivity response
(IgE binding to mast cells)
–> Begin in childhood
–> Patients with a family history of allergy
2) Intrinsic (non-immune):
–> Association with chronic bronchitis, and exerciseor cold-induced asthma
–> Begin in adult life
–> NO history of allergy
Histopathologic findings:
Smooth muscle hypertrophy of the bronchi
Hyperplasia of bronchial submucosal glands and
goblet cells
Thickening and hyalinisation of basement membranes
Proliferation of eosinophils
Airways plugged by viscid mucous containing
Curschmann spirals (whorl-like accumulations of epithelial cells) and Charcot-Leyden crystals
(crystaloids of eosinophil-derived proteins)
Are the features of what condition?
Bronchial Asthma
Clinical features of Asthma
1) Dyspnoea
2) Wheezing aspirtation (due to stenosis of the airways)
Complications of Bronchial Asthma
1) Superimposed infection
2) Chronic Bronchitis
3) Pulmonary Emphysema
4) Status asthmaticus:
* Prolonged bouts of asthma
* Lasts days
* Unresponsive to therapy
* Death
———————- :Persistent productive cough that
occurs during at least three consecutive months over
at least two consecutive years
Chronic Bronchitis
causes of Chronic Bronchitis
1) Cigarette smoking
2) Air-pollution
3) Infection
4) Genetic factors
Pathogenisis of Chronic Bronchitis
1) Causative agents (environmental irritants) : - Hypertrophy of mucous glands (trachea and main bronchi) +
-Increase in mucin-secreting goblet cells
–> Inflammation with infiltration of CD8+ lymphocytes, macrophages and neutrophils
2) airflow obstruction –> Small airway disease (goblet cell metaplasia, mucous plugging of the bronchiolar lumen,inflammation, bronchiolar wall fibrosis), Coexistent emphysema
Clinical features of Chronic Bronchitis
1) Prominent productive cough
2) Production of sputum
3) Development of COPD with outflow obstruction:
- Hypercapnia
- Hypoxaemia
- Cyanosis (“Blue bloaters”)
Complications of Chronic Bronchitis
1) Pulmonary Hypertension –> Cor pulmonale –>
Cardiac failure
2) Recurrent infections and Respiratory failure
Chronic Bronchitis is Charecterised by?
Cyanosis “BLUE BLOATERS”
Macroscopic features:
- Hyperaemic and swollen (by edema fluid) mucosal
lining of the larger airways
- Covering of the mucosa by a layer of mucinous or
muco-purulent secretions
are the features of what Condition?
Chronic Bronchitis
Microscopic findings:
* Hypertrophy of the mucous-secreting glands (Reid index: Ratio thickness of submucosal gland layer to thickness of the bronchial wall >0.4)
*** Mainly, mononuclear inflammatory cells, but
admixed with variable numbers of neutrophils **
Airway obstruction caused by:
- Goblet cell metaplasia
- Mucous plugging
- Inflammation
- Fibrosis
Are the features of what condition?
Chronic Bronchitis
cause of Emphysema
cigarette smoking
Types of Emphysema
- Centri-acinar (95% of cases)
- Pan-acinar
- Para-septal
- Irregular
Clinical features of Emphysema
1) “Pink puffer” vs. “Blue bloater” (Chronic Bronchitis)
2) ↑ Antero-posterior chest-diameter (“Barrel” chest)
3) ↑ Total vital capacity
4) Hypoxia
5) Cyanosis
6) Respiratory acidosis
cause of Emphysema
- Action of proteolytic enzymes (e.g. elastase) on the
alveolar wall
1) Elastase:
–> Induces destruction of elastin
–> Neutralised by the opposing action of alpha1-
antitrypsin
2) Cigarette smoking:
–> Attracts neutrophils and macrophages (sources of
elastase)
–> Inactivates alpha1-antitrypsin
pathogenisis of Emphysema
↑ in Neutrophil Elastase –> Tissue damage
*caused by tobacco
Complications of Emphysema
1) Chronic Bronchitis
2) Interstitial Emphysema: Tear in the airways
“Leakage” of air into the interstitial tissue of the chest
3) Rupture of a surface bleb (apical bulla) –> Pneumothorax
causes/patho of Interstital Emphysema
cause/Pathology: Coughing + bronchiolar obstruction
–> Sharply increased pressures within the alveolar sacs –> Alveolar tears –> Entrance of air into the lung’s stroma
Other Causes:
1) Wound of the chest –> Entrance of air within the lung substance
2) Fractured rib –> Puncture of the lung parenchyma
Entrance of air within the lung substance
Patho of Bronchiectasis
Destruction of the muscle and elastic tissue, resulting from or associated with chronic necrotising infections
pre-disposing factors of Bronchiectasis
[1) Post-infectious conditions (necrotising pneumonia: caused by bacteria, viruses and fungi)
2) Bronchial obstruction (e.g. tumour)
3) Cystic fibrosis
**4) Kartagener Syndrome **
5) Rheumatoid Arthritis
6) Systemic Lupus Erythematosus
7) inflammatory Bowel Disease
Macroscopic features:
* Dilated airways (4x normal size)
* Lumen of bronchi and bronchioles can be followed
up to the pleural surfaces
*Cut surface of the lung: Appearance of dilated
bronchi as cysts filled with muco-purulent secretions
Are the features of what condition?
Bronchiectasis
Localisation of Bronchiectasis
lower lobes, bilaterally (of the lungs); Most severe in the more distal bronchi and bronchioles
Microscopic findings:
* Intense acute and chronic inflammatory exudation,
within the walls of the bronchi and bronchioles
* Desquamation of the lining epithelium
* Extensive areas of necrotising ulceration
* Possible, pseudo-stratification of the columnar cells
or squamous metaplasia of the preserved epithelium
* Complete necrosis of the bronchial or bronchiolar
walls –> Lung abscess
* Fibrosis both of the bronchial and bronchiolar walls
and peri-bronchiolar –> Subtotal or total obliteration
of bronchiolar lumens
Are the features of what condition?
Bronchiectasis
Clinical features of Bronchiectasis
1) Severe, persistent cough
2) foul-smelling, sometimes bloody sputum
3) Haemoptysis (life-threatening)
4) Dyspnoea and orthopnoea (severe cases)
5) Obstructive respiratory insufficiency –> Marked
dyspnoea and cyanosis
6) Recurrent pulmonary infection –> Lung abscess
7) Less frequent complications: Cor pulmonale, brain
abscesses, amyloidosis
Clinical features of restrictive pulmonary disesae
1) Dyspnoea
2) Tachypnoea
3) End-inspiratory crackles
4) Eventually: Cyanosis, secondary lung hypertension,
right-sided heart failure with Cor pulmonale
Chest radiograph of restrictive pulmonary disease
Bilateral infiltrative lesions, in form of
- Small nodules
- Irregular lines
- Ground-glass shadows
Restrictive pulmonary disease is charcterised by>
- Reduced expansion of lung parenchyma and
- Reduction in total lung capacity
Types of A.fibrosing Restrictive pulmonary disease
a. Usual Interstitial Pneumonia (UIP)
b. Non-Specific Interstitial Pneumonia (NSIP)
c. Cryptogenic Organising Pneumonia
d. Pneumoconioses:
- Anthracosis
- Coal worker’s Pneumoconiosis
- Silicosis
- Asbestosis
e. Associated with Connective Tissue Diseases:
- Rheumatoid Arthritis
- Scleroderma
- Systemic Lupus Erythematosus
Epi of Usual interstital Pneumonia (UIP)
Most common and with worst prognosis
interstitial pneumonia
Pathogenisis of Usual interstitial Pneumonia (UIP)
Unknown agent triggers repeated cycles of epithelial activation/injury –> Release of cytokines –> Abnormal epithelial repair –> Exuberant myo-/fibroblastic proliferation –> “Fibroblastic foci” –> Proximal dilatation of the small airways
TGF-β1
–> Driver of the process
–> Fibrogenic properties
–> Released by type I alveolar epithelial cells
–> Transformation of fibroblasts into myofibroblasts
–> Deposition of collagen and other ECM molecules
Macroscopic features:
* Pleural surfaces of the lungs: Cobblestone
appearance, due to retraction of scars along the
interlobular septa
* Cut surface: Fibrosis (firm, rubbery white areas) of the lung parenchyma; Lower-lobe predominance
and a distinctive distribution in the sub-pleural
regions and along the interlobular septa
Are the features of what Condition?
Usual Interstitial Pneumonia (UIP) (of Restrictive pulmonary disease)
Microscopic findings:
* Patchy interstitial fibrosis, variable in intensity and age of the lesion
* Coexistence of early (exuberant fibroblastic proliferation) and late lesions (more collagenous and less cellular foci)
* Dense fibrosis –> Destruction of alveolar architecture and formation of cystic spaces, lined by hyperplastic type II pneumocytes or bronchiolar epithelium (honeycomb fibrosis)
*Mild to moderate mixed inflammatory infiltrates
* Intimal fibrosis + Medial thickening (lung hypertension)
Are the features of what condition?
Usual Interstitial Pneumonia (UIP)
Causes of Non-Specific Interstitial Pneumonia (NSIP):
Secondary to a variety of aetiologic factors
(e.g. infection, collagen vascular disease,
hypersensitivity pneumonitis, drug reaction)
Pathological findings:
* Distinction in two patterns:
1) Cellular: Mild to moderate chronic interstitial
inflammation (mainly lymphocytes, few plasma cells) in a uniform or patchy distribution
2) Fibrosing: Diffuse or patchy interstitial fibrosis
Are the pahtological features of what type of restrictive pulmonary disease?
Non-Specific Interstitial Pneumonia (NSIP)
Clinical features of Non-Specific Interstitial Pneumonia (NSIP)
1) Dyspnoea
2) Cough
Prognosis of Non-Specific Interstitial Pneumonia (NSIP)
- Better than for UIP (5 year survival > 80%)
- Patients with cellular pattern (younger) better outcome than those with the fibrosing pattern (older)
Cryptogenic Organising Pneumonia (COP) is aka?
Bronchiolitis Obliterans Organising
Pneumonia (BOOP)
Microscopic findings:
- Polypoid plugs of loose organising connective tissue(“Masson bodies”) within alveolar ducts, alveoli and bronchioles
- The connective tissue is all of the same age
- Normal underlying lung architecture
- NO interstitial fibrosis or honey-comb lung
Are the features of what disease?
Bronchiolitis Obliterans Organising
Pneumonia (BOOP) [aka Cryptogenic Organising Pneumonia (COP)]
Clinical features of Cryptogenic Organising Pneumonia (COP)
1) Cough
2) Dyspnoea
Chest X-ray findings of Cryptogenic Organising Pneumonia
Sub-pleural or peri-bronchial patchy
areas of airspace consolidation
Treatment of Cryptogenic Organising Pneumonia
Oral administration of steroids for ≥6 months
The 4 Types of Pneumoconiosis
1) Anthracosis
2) Coal worker’s Pneumoconiosis
3) Silicosis
4) Asbestosis
Inhalation of inorganic dust particles (coal dust, silica, asbestos and beryllium) –> Interstitial fibrosis
Causes of what type of condition?
Pneumoconioses
note:
* Coal dust –> Least fibrogenic
* Silica, asbestos and beryllium –> Very fibrogenic
Pathogenisis of Pneumoconioses
Development of pneumoconiosis depends on following factors:
1) The amount of dust retained in the lung and airways
2) The ** size and shape, thus the resilience (elastic capacity) of the particles
3) Theparticle’s solubility**and physicochemical reactivity
4) The possible additional effects of other irritants
(e.g. concomitant tobacco smoking)
Etiology of Anthracosis
Inhalation of carbon dust
Usually asymptomatic
Macroscopic-/Microscopic findings:
- Irregular black patches, within lung tissue
- Carbon carrying macrophages (“dust cells”)
Are the features of what condition
Anthracosis (Type of Pneumoconioses)
Epi of Coal worker’s Pnumocpniosis
Inhalation of coal dust (contains both carbon and silica)
Simple va Complicated caol Workers’ Pneumoconiosis
1) Simple Coal Workers’ Pneumoconiosis:
Coal macules (<1cm; result of ingestion of coal dust
by macrophages) around the bronchioles of upper
lobes and upper portions of lower lobes
2) Complicated Coal Workers’ Pneumoconiosis (progressive massive fibrosis)
- Fibrotic nodules filled with necrotic black fluid
- Results in: Bronchiectasis, pulmonary hypertension,
Cor pulmonale, Caplan Syndrome (Rheumatoid
arthritis + Pneumoconiosis), death from respiratory
or right-sided heart failure
Causes of Silicosis Pneumoconioses
Exposure to free silica dust
patho of Silicosis Pneumoconioses
Ingestion of silica dust by alveolar macrophages –> Damage of macrophages –> Release of lysosomal enzymes and chemical mediators (e.g.
cytokines) –> Stimulation of fibrogenesis
Macro-/ Microscopic findings:
Silicotic nodules: Concentric layers of collagen with or without central cavitation
Silicosis
Cause of Asbestosis Pneumoconioses
Inhalation of asbestos fibers
Patho of Asbestosis Pneumoconiosis
Uptake of asbestos fibers by macrophages –> Release of fibroblast-stimulating growth factors –> Diffuse interstitial fibrosis (lower lobes)
Histopathologic findings:
- Ferruginous bodies: Fibers coated by iron and
protein; Yellow-brown, rod-shaped bodies,
with clubbed ends (Prussian blue [+])
- Hyalinised fibro-calcific plaques of the parietal
pleura
Are the features of what condition?
Abestosis Pneumoconioses
Connective tissue diseases associated with Fibrosing Restrictive pulmonary disesae
1) Rheumatoid Arthritis
2) Scleroderma
3) Systemic Lupus Erythematosus
Pathogenesis of Sarcoidosis
CD4Th cells interact with unknown airborne Ags (e.g. mold or mildew, pesticides) –> Release
of cytokines –> Formation of non-caseating granulomas
Immunologic phenomena of Sarcoidosis
- Reduced sensitivity and often anergy to skin test Ags
(Tuberculin test [-]) - Polyclonal hyperglobulinaemia
Radiological and Labratory findings of Sarcoidosis
1) Radiologic findings:
- Bilateral hilar lymphadenopathy
- Interstitial lung disease (diffuse reticular densities)
2) Laboratory findings:
- Hypercalcaemia and hypercalciuria
- Hypergammaglobulinaemia
- Increased activity of serum Angiotensin-Converting
Enzyme
Clinical features of Sarcoidosis
1) Interstitial lung disease
2) Enlarged hilar lymph nodes
3) Anterior uveitis
4) Erythema nodosum of the skin
5) Polyarthritis
Macro-/Microscopic findings:
- Granulomas located in the interstitium, and
mediastinal and hilar nodes
- Granulomas containing multinucleated giant cells
- Schaumann bodies and “asteroid” bodies
Are the features of what condition?
Sarcoidosis
Histopathologic picture:
- Patchy mononuclear cell infiltrates in the
pulmonary interstitium (typical peri-bronchiolar accentuation)
- Mainly lymphocytes, but also plasma cells and
epithelioid cells; In acute forms: Also neutrophils
- Interstitial non-caseating granulomas, in peribronchiolar location
- Chronic cases: Diffuse interstitial fibrosis
Are the histopathological feature of what condition?
Hypersensitivity Pneumonitis
Characteristic condition of Hypersensitivity Pneumonitis
Farmer’s lung –> casued by moldy hay
Describe the features of the First exposure , Second exposure and chronic phase of farmer’s lung caused by hypersensitivity Pneumonitis
- First exposure: Development of IgG Abs
- Second exposure: Binding of Abs to inhaled
allergens –> Formation of immune complexes
(Type III hypersensitivity reaction)
*Chronic: Granulomatous inflammation (Type IV
hypersensitivity reaction)
Immunological findings of Hypersensitive Pneumonitis
1) Bronchio-alveolar lavage specimens: ↑ numbers of T lymphocytes, of both CD4+ and CD8+ phenotype
2) Presence of specific precipitating Abs in patients’ serum, and Complement and Igs within the vessel walls (Type III hypersensitivity reaction).
3) Presence of non-caseating granulomas –> Type IV reaction
Categories of Pulmonary Eosinophilia
- Acute Eosinophilic Pneumonia with respiratory failure
- Simple Pulmonary Eosinophilia (Loeffler Syndrome)
- Tropical Eosinophilia
- Secondary Eosinophilia
- Idiopathic Chronic Eosinophilic Pneumonia
CM of Acute Eosinophilic Pneumonia with respiratory failure
Rapid onset of fever, dyspnoea, hypoxia
chest X-ray/ Labratory test of Acute Eosinophilic Pneumonia with respiratory failure
X-RAY: diffuse pulmonary infiltrates
Labratory test: Broncho-alveolar lavage: >25% eosinophils
Causes of Loeffler Syndrom (simple Pulmonary eosinophilia)
- Unidentifiable aetiologic agent in up to 1/3 of patients
- Parasitic infections (especially Ascaris lumbricoides)
- Drugs (aspirin, penicillin)
–> Self-limiting condition; Resolution of the lung opacities
within a month
Causes of Tropical Eoisnophilia
infection with
microfilariae and helminthic parasites
Secondary Eosinophilia is associated with?
1) Asthma
2) Drug allergies
3) Certain forms of vasculitis
Clinical features of Idiopathic Chronic Eosinophilic Pneumonia
High fever, night sweats and dyspnoea
Eosinophilic Granuloms is aka?
Unisystem Langerhans Cell Histiocytosis
Clinical features of Eosinophilic Granuloma
i. Bone pain,
ii. Pathologic fractures
Radiological findings of Eosinophilic Granuloma
Unifocal lytic lesions in skull, ribs
and femur
Histopathology:
- Localised proliferation of histiocytic cells (similar to
Langerhans cells of the skin)
- Characteristic cytoplasmic inclusions (“Birbeck
granules”; tennis racket appearance)
- Presence of monocytes-macrophages, lymphocytes
and eosinophils
Are the features of what condition?
Eosinophilic Granuloma
Smoking related Restrictive Pulmonary lung disease
Desquamative Interstitial Pneumonia (DIP)
Epi of Desquamative Interstitial Pneumonia (DIP)
- Smokers in their 30s or 40s
- Association with respiratory bronchiolitis-interstitial
lung disease
Histopathologic picture:
- Alveolar spaces, filled with macrophages
- Preservation of alveolar architecture
- Minimal fibrosis
Are the features of what condition?
Desquamative Interstitial Pneumonia (DIP)
Clinical features of Pneumonia
1) Chills and fever
2) Productive cough
3) Blood-tinged or rusty sputum
4) Pleuritic pain
5) Hypoxia with shortness of breath
6) Cyanosis (sometimes)
7) Neutrophilic leukocytosis (if bacterial cause)
cause of Lober Pneumonia
Streptococcus pneumoniae
Macro-/Microscopic picture:
-Intra-alveolar exudate (involving an entire lobe
of lung) –> Consolidation
Macroscopic featurs of what type of Pneumonia?
Lobar Pneumonia
stages of Lobar Pneumonia
1) Congestion
2) Red Hepatisation
3) Gray Hepatisation
4) Yellow Hepatisation
5) Resolution
cause of Broncho-Pneumonia
1) Staphylococcus aureus,
2) Haemophilus influenzae,
3) Klebsiella pneumoniae,
4) Streptococcus pyogenes
Macro-/Microscopic picture:
- Extension of acute inflammatory exudate
from the bronchioles into the adjacent alveoli
- Patchy distribution, involving one or more
lobes
Are the features of what type of Pneumonia
Broncho-Pneumonia
Causes of interstital Pneumonia
Viruses, Mycoplasma pneumoniae
Macro-/Microscopic picture:
- Involvement of more than one lobes
- Diffuse, patchy inflammation localised to
interstitial areas of the alveolar walls
Are the features of what type of Pneumonia?
Interstitial Pneumonia
Epi of Mycoplasma Pneumoniae Pneumonia
Most common interstitial pneumonia
* Children and young adults
* Possible occurrence in epidemics
Clinical features of Mycoplasma pneumoniae Pneumonia
1) Insidious onset
2) Mild, self-limited course
Macro-/Microscopic findings:
- Inflammatory reaction limited to the interstitium
- NO exudate in the alveolar spaces
- Intra-alveolar hyaline membranes
Are the features of what type of Pneumonia?
Mycoplasma
Epi of Viral Pneumonia
Most common types of pneumonia in childhood
Causes of Viral Pneumonia
1) Influenza viruses,
2) Adenoviruses,
3) Rhinovirus,
4) Expiratory Syncytial Virus,
5) Varicella Zoster Virus (Chickenpox and Shingles) or,
6) Rubeola (Measles)
*Rubeola virus –> Giant cell pneumonia (numerous
giant cells), complicated by tracheo-bronchitis
causative agent of Candidiasis
Candida albicans
Candida albicans is the most frequent casue of Human fungal infections.
These infections can manifest as:
1) Superficial lesions in healthy persons
2) Disseminated infections in immuno-compromised
patients
3) Pulmonary, renal and hepatic abscesses and vegetative endocarditis
4) Invasive form (Invasive Candidiasis) –> Blood-borne
dissemination
causative agent of Nocardiosis
Nocardia
Causative agent of Actinomycosis
Actinomyces israelii
Macro-/Microscopic features:
- Formation of abscess and sinus tract
- Exudate, with sulfur granules (yellow clusters of
the organism)
Are the features of what pulmonary infection?
Actinomycosis
Causative agent of Coccidioidomycosis
Coccidioides immitis
Causative agent of Cryptococcosis
Cryptococcus neoformans
Histopathology:
- Encapsulated organism
- India ink: Visualisation of the capsule in cerebral spinal fluid (zone of clearance or “halo” around the cells)
- Mucicarmine stain: Staining of polysaccharide cell wall in tissue
Are the features of what pulmonary infection?
Cryptococcosis
Causative agent of Histoplasmosis
Histoplasma capsulatum
Clinical feature of Rickettsial Pneumonias
Q- Fever
causative agent of Aspergillosis
Aspergillus fumigatus
patho of Aspergillosis
1) Aspergillus spores (2-3 μm) reach alveoli –>
Engulfment and killing of Aspergillus conidia by
alveolar macrophages –> Secretion of cytokines and chemokines (by macrophages), thus stimulating adaptive immune responses –> T lymphocytes confer protective immunity
Cause of Q-fever
inhalation of Coxiella burnetti
Ornithosis (Psittacosis) is caused by?
Chlamydia species
Pathogens causing Lung Abscess
I. Staphylococcus
II. Pseudomonas
III. Klebsiella
IV. Proteus, combined with anaerobes
Patho of Lung abscess
- Bronchial obstruction
-
Aspiration of gastric contents (due to loss of
consciousness; from alcohol or drug overdose,
neurologic disorders, general anesthesia) - Complication of bacterial pneumonia
Clinical features of lung abcess
1) Fever
2) Foul smelling purulent sputum
3) Fluid-filled cavity (X-ray)
causative agent of Tbc
Mycobacterium tuberculosis
cause of Pulmonary and non-pulmoary Tbc
- Pulmonary form: Inhalation of droplets with the organism
- Non-pulmonary form: Ingestion of infected milk
patho of Tbc
- Ingestion of organism by macrophages–>
Presentation of Ags to CD4 Th cells –> Proliferation of CD4 Th cells and secretion of cytokines - Attraction of lymphocytes and macrophages
- Macrophages either ingest and kill some of the
organisms or undergo alteration and form epithelioid
cells and Langhans multinucleated giant cells
Clinical picture of Primary Tbc
Asymptomatic; No clinically evident
disease
Primary Tbc is characterised by?
Initial infection, characterised by primary or Ghon complex (Peripheral sub-pleural parenchymal
lesion + Hilar lymph nodes)
Histopathology:
- Central caseous necrosis
- Langhans giant cells
Are the features of what lung infection ?
primary Tbc
Secondary Tbc is charcaterised by?
Activation of a prior Ghon complex, with spread to a
new pulmonary or extra-pulmonary site
Clinical featurs of secondary Tbc ?
1) Progressive disability
2) Fever
3) Haemoptysis
4) Bloody pleural effusion
5) Generalised wasting
Macroscopic picture:
Localised lesions: Apical or posterior segments of
the upper lobes
Involvement of hilar lymph nodes
Are teh features of what lung infection?
Secondary Tbc
Microscopic picture:
Liquefaction and expulsion of the caseous contents
Formation of cavitary lesions
Cavitation
Caseation
Scarring and calcification
Are the features of what lung infection
Secondary Tbc
note:
- Cavitation: Only in secondary Tbc
- Caseation: Both primary and secondary Tbc
what are the 3 types of Tuberculosis?
1) Primary
2) Secondary
3) Miliary
