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Dundee - Autopsy Pathology > 1: Lung > Flashcards

1: Lung Flashcards

1
Q

Summarise the impact of tobacco smoking on mortality and morbidity.

A
  • Smoking is the most readily preventable cause of death in humans
    • Second hand smoke can cause lung cancer in non-smokers
    • 1/3 tobacco deaths due to lung cancer
    • More than 4 million deaths annually
      ○ Cardiovascular disease
      ○ Various types of cancer
      ○ Chronic resp problems
    • Reduces overall survival through dose-dependent effects
    • Pack years = average number of cigarette packs smoked each day multiplied by number of years smoking
    • Tobaccos smoke contains mixture of 7000 chemicals - more than 60 have been identified as carcinogens
    • Nicotine strongly addictive
      ○ Binds to nicotinic acetylcholine receptors in brain
      ○ Stimulates release of catecholamines form sympathetic neurons
      ○ Increases heart rate and blood pressure
      Elevation in cardiac contractility and output
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2
Q

Are there health implications associated with occasional or low-level smoking?

A

Dose-dependent

Pack years = average number of cigarette packs smoked each day multiplied by number of years smoking

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3
Q

How rapidly do the health risks dissipate following cessation?

A
  • Cessation of smoking risk reduces
    ○ Within 5 years overall mortality and risk of death from cardiovascular disease decreases
    ○ Lung cancer mortality decreases by excess risk persists for 30 years
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4
Q

What diseases are associated with smoking?

A 
Lung cancer
Cancers of oesophagus, pancreas, bladder, kidney, cervix and bone marrow
Bronchitis
Empyema, chronic bronchitis and COPD
Exacerbates asthma 
Increased risk of pulmonary tuberculosis
Atherosclerosis
Harm to developing foetus
Diabetes
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5
Q

Smoking and lung cancer

A

○ Presence of carcinogens in smoke
○ Cytochrome P-450 phase 1 enzymes and phase II enzymes increase water solubility of carcinogens
○ Intermediates produced by CYPS are electrophilic and form DNA adducts that are repaired by error-prone mechanisms leading to potentially oncogenic mutations
○ Thousands of mutations produced by carcinogens
○ Risk of developing lung cancer linked to number of pack years
○ Increases with other carcinogenic influences
- 10 fold higher in asbestos workers and uranium miners for lung carcinomas
- Increased incidence of oral and laryngeal carcinomas with alcohol and smoking

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6
Q

Smoking and bronchitis

A

Agents in smoke have direct irritant effect on tracheobronchial mucosa, producing inflammation and increased mucus production

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7
Q

Smoking and atherosclerosis

A

○ Leading to myocardial infarction and stroke
○ Increased platelet aggregation, decreased myocardial oxygen supply with increased myocardial oxygen demand, decreased threshold for ventricular fibrillation

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8
Q

Smoking and developing foetus

A

○ Maternal smoking increases risk of spontaneous abortions and preterm birth
○ Results in intrauterine growth retardation
○ Birth weights of mothers who stopped smoking before pregnancy are normal

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9
Q

Definition of obstructive lung diseases

A
  • Characterised by increase in airflow resistance due to airway disease
    • May affect any level of the respiratory tract
    • FEV1/FVC ration < 0.7
    • Includes: COPD, asthma and bronchiectasis
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10
Q

Features of bronchiectasis

A 
○ Area affected: bronchi
		○ Caused by chronic inflammation
			§ Past severe/recurrent infections
			§ Obstruction or aspiration
			§ Cilia problems
			§ ABPA
		○ Pathological changes
			§ Airway dilation
			§ Scaring of proximal and medium sized bronchi > 2mm
		○ Mucus plug obstructs airflow
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11
Q

Features of emphysema

A 
○ Permanent enlargement of airspaces distal to terminal bronchiole with destruction of walls
		○ Decreases surface area available for gas exchange
		○ Area affected: Acini and alveoli
		○ Aetiology
			 - Tobacco smoke
			 - Air pollutants
			 - AAT deficiency
		○ Pathological changes
			 - Air space enlargement
			 - Alveolar wall destruction
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12
Q

Features of asthma

A 
○ Group of conditions with airways inflammation and hyperplasia
		○ Reversible obstruction
		○ Area affected: bronchi
		○ Aetiology
			§ Immunological or undefined cause
		○ Pathological changes
			§ Smooth muscle hyperplasia
			§ Excess mucus
			§ Inflammation
Reversible obstruction
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13
Q

Patterns of emphysema

A
  • Centriacinar
    ○ Most common pattern
    ○ Occurs mainly in heavy smokers
    ○ Affected area: central or proximal parts of acini - distal alveoli spared
    ○ Lesions more common in upper lobes of lungs, particularly apical segments
  • Panacinar
    ○ Associated with alpha 1-antitrypsin deficiency
    ○ Entire acinus uniformly enlarged
    ○ Tends to affect the lower lobes of the lungs
  • Paraseptal/distal acinar
    ○ Associated with smoking
    ○ Distal portion of acinus affected with proximal portion spared
    ○ Tends to affect lung tissue on periphery of lobules near interlobular septae
    ○ Enlarged distal portion can rupture -> pneumothorax
  • Irregular
    • Acinus is irregularly enlarged
    • Most cases occurs in small foci and not clinically significant
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14
Q

What are the mechanisms that contribute to alveolar damage in emphysema?

A
  • Inflammation
    ○ Noxious particles damages respiratory epithelium and causes inflammation
    ○ Inflammatory mediators released
    ○ Inflammatory cells recruited - mainly neutrophils
    • Protease-antiprotease imbalance
      ○ Elastase
      ○ Proteases released by inflammatory cells - decreased in smokers
      ○ AAT deficiency
    • Oxidative stress
    • Infection
      ○ Acutely exacerbate existing emphysema
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15
Q

What are the macroscopic and histological features of emphysema?

A
  • Macroscopic
    ○ Large airspaces on cut surfaces
    ○ Anthracosis - black pigmentation in lungs due to smoke pollution
    ○ Bulla - large airspaces seen in advanced disease
    • Histological
      ○ Loss of alveolar wall
      ○ Abnormally large airspaces
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16
Q

Pathogenesis of chronic bronchitis

A

nflammation
§ Triggered by noxious inhaled particles
§ Will lead to scarring and thickening of airway walls
§ Smoking will also interfere with ciliary action -> reduced mucus clearance
○ Mucus hypersecretion
§ Earliest features - enlargement of submucosal glands
§ Driven by inflammation
○ Acquired CFTR dysfunction
§ Caused by smoking
§ Caused by dehydrated mucus which exacerbates severity
○ Infection

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17
Q

Morphology of chronic bronchitis

A

○ Gross
§ Swelling and oedema of mucous membranes
§ Excessive mucus / purulent secretions
○ Microscopic
§ Chronic inflammation of airways - lymphocytes and macrophages
§ Thickening of bronchiole wall - smooth muscle hypertrophy
§ Goblet cell hyperplasia in small airways
§ Enlargement of mucus secreting glands in trachea and bronchi

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18
Q

What are the morphological features of status asthmaticus?

A
  • An acute exacerbation of asthma that remains unresponsive to initial treatment with bronchodilators
    • Macroscopic
      ○ Lungs are overinflated and contain small areas of atelectasis
      ○ Occlusion of bronchi and bronchioles by thick mucus plugs - often contain shed epithelium
    • Microscopic
      ○ Thickened basement membrane
      ○ Increase in size of submucosal glands
      ○ Increased goblet cell count
      ○ Bronchial wall smooth muscle hypertrophy
      ○ Airway wall oedema
      ○ Eosinophilic infiltration
      ○ Sputum/bronchoalveolar lavage samples
      § Curschmann spirals - casts of smaller bronchi made of mucus plugs
      § Charcot-Leyden crystals - made from protein galectin-10 derived from eosinophils
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19
Q

Asthma phenotypes

A

Atopic
Non-atopic
Drug-induced
Occupational

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20
Q

Key features of atopic asthma

A 
○ IgE mediated
		○ Family hx of atopy
		○ Early onset 
		○ Common triggers
			§ Pollen 
			§ Dust
			§ Animal dander
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21
Q

Key features of non-atopic asthma

A 
○ Not allergy related - pathophysiology not entirely understood
		○ Later onset
		○ Triggers
			§ Resp infections
			§ Inhaled pollutants - tobacco smoke
			§ Exposure to cold
			§ Exercise
			§ Stress
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22
Q

Key features of drug-induced asthma

A

○ Rare
○ Triggers
§ NSAIDs
§ Beta-blockers
§ Aspirin can trigger in patients with recurrent rhinitis and nasal polyps
○ Caused by drug inhibiting cyclooxygenase pathway of arachidonic acid metabolism -> low prostaglandin E2 levels
○ Prostaglandin E2 normally inhibits enzymes that generate proinflammatory mediators

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23
Q

Key features of occupational asthma

A

○ Type of allergy
○ Underlying immunological response varies
○ Triggered by
§ Fumes - plastics
§ Dusts - wood, cotton, latex glove dust
§ Gases
§ Others

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24
Q

Pathology of interstitial lung disease

A
  • Environmental factors causing epithelial injury and increased age and genetic mutation put epithelium at risk
    • Persistent epithelial injury and activation
    • Innate and adaptive immune response and pro-fibrogenic factor release
    • Activation of fibroblasts
    • Proliferation and collagen production
    • Fibrosis and remodelling of pulmonary interstitium
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25
Q

Key features of idiopathic pulmonary fibrosis

A

Interstitial lung disease of unknown cause

- Usual interstitial pneumonia on histology or radiology
- M>F
- Age of onset 60-70 years

- Site
	○ Bibasal subpleural distribution
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26
Q

Key features of Non-specific interstitial pneumonia

A
  • ILD and NSIP pattern on histology
    • Less common
    • F>M
    • Age of onset 40-50 years
    • Site
      ○ Bibasal with immediate subpleural sparing
27
Q

Key features of Cryptogenic organising pneumonia

A

LD + granulation tissue plugs within alveolar ducts and small airway histology
- Rare
- M=F
- Age of onset 50-60 years
- Site
○ Subpleural or peribroncial distribution

28
Q

What is pneumoconiosis

A

Non-neoplastic lung reaction to inhalation of mineral dusts encountered in workplace

29
Q

Pathogenic factors of pneumoconiosis

A

○ Dust retention - determined by dust concentration, duration of exposure, effectiveness of clearance mechanism
○ Particle size - most dangerous 1 to 5 micrometre
○ Particle solubility and cytotoxicity - highly soluble more likely to produce rapid-onset lung injury
○ Particle uptake by epithelial cells or egress across epithelial linings
○ Activation of inflammasome
○ Tobacco smoking
- Main agents
○ Asbestosis
○ Coal worker’s pneumoconiosis
○ Silicosis

30
Q

Diseases associated with asbestos exposure

A
  • Asbestosis
    • Pleural plaques
    • Caplan syndrome
    • Mesothelioma
    • Carcinoma of the lung, larynx, stomach, colon
31
Q

Pathogenesis of pulmonary asbestos-related diseases

A

○ Smoking enhances effect of asbestos by interfering with mucociliary clearance of fibres
○ Inhalation of dust particles
○ Phagocytosed by macrophages
○ Asbestos fibres activate inflammasome
○ Stimulate release of proinflammatory factors and fibrogenic mediators
○ Fibroblast activation, direct injury and persistent inflammation
○ Fibrosis and remodelling of pulmonary interstitium

32
Q

Morphological features of asbestosis

A 
- Macroscopic
		○ Irregular fibrotic changes in subpleural region of lower lobes
		○ Fibrous thickening of pleura
	- Microscopic
		○ Interstitial fibrosis
Golden-brown ferruginous asbesto
33
Q

Morphological features of coal-workers pneumoconiosis

A
  • Small discrete black lesions
    • Coal macules and nodules
    • Multiple large blackened scars
    • Black pigment from coal and fibrotic response histologically
34
Q

Morphological features of silicosis

A
  • Scarring contracts upper lobe into small dark mass

Several coalescent collagenous silicotic nodules histologically

35
Q

What are the main local pulmonary defence mechanisms against infection?

A
  • Huge surface area - ~60 m2 = ¼ tennis court = 30 x skin surface area
    • Nose hairs
    • Lymphoid tissue; tonsils and adenoids – Waldeyer’s ring
    • Cilia + mucous => mucociliary escalator
    • Alveolar macrophages
    • Coughs and sneezes
    • Impaired defence mechanisms
      ○ Smoking!
      § Impairs cilia and alveolar macrophages but ↑mucous
      ○ Alveolar macrophages impaired by alcohol, anoxia
      ○ Cough lost with drugs, neuromuscular disorders, coma -> aspiration
      ○ Pulmonary congestion, pulmonary oedema
      ○ Systemic; chronic disease, immunosuppressive drugs, genetic conditions, splenectomy
36
Q

How is pneumonia classified?

A
  • Community-acquired cute pneumonia
    • Health care-associated pneumonia
    • Hospital-acquired pneumonia
    • Aspiration pneumonia
    • Chronic pneumonia
    • Necrotising pneumonia and lung abscess
37
Q

Causative organisms for CAP

A 
○ Streptococcus pneumoniae
		○ Haemophilus influenzae 
		○ Staphylococcus aureus
		○ Others 
		○ Moraxella 
		○ Klebsiella 
		○ Pseudomonas
38
Q

Risk factors for CAP

A

○ Age
○ COPD – confers 2-4x risk
○ Cigarette smoke – esp. pneumococcal pneumonia
○ Alcohol intake
○ Proton pump inhibitors
○ Contact with children
○ Chronic disease – a risk for HAP and mortality

39
Q

Morphology of CAP

A

○ Lobular
§ Consolidation of large part of lobe
§ Tends to be caused by Streptococcus pneumoniae; 4 classical stages;
§ Congestion
□ Red and boggy lung -> acute inflammation
§ Red hepatisation
□ Movement of cells/fluid from vascular compartment -> alveolar space.
□ Liver-like consistency/appearance
§ Grey hepatisation
□ Red cells disintegrate
§ Resolution
□ Clean up: enzymes, macrophages, resorption, coughing, scarring
○ Bronchopneumonia
§ Patchy consolidation
§ Commoner than lobar pneumonia
§ Focal areas of consolidation that tend to be basal due to gravity
§ Several lobes/both lungs can be affected at once – consolidated areas can group together to form lobar pneumonia
§ Lesions are granular, discoloured (red/yellow) and poorly demarcated from normal tissue

40
Q

Define healthcare-associated pneumonia

A

○ Recent hospitalisation of ≥2/7, nursing/care home, regular contact with hospital (e.g. dialysis), recent IV Abx therapy, chemotherapy, wound care
○ (MR)SA, Pseudomonas aeruginosa, Streptococcus pneumoniae

41
Q

Define hospital acquired pneumonia

A

○ Acute LRTI at least 48 hours post-admission
○ NB acute LRTI at least 48 hours after endotracheal intubation = ventilator-associated pneumonia
○ MRSA, pseudomonas, Enterobacteriaceae (Klebsiella, E. coli)

42
Q

How is lung abscess defined?

A
  • Local suppurative process causing necrosis of lung tissue
    • Variety of causes;
      ○ Aspiration -> pneumonia -> abscess
      § Alcohol, coma, dysphagia etc.
      ○ Pneumonia esp. in immunosuppression
      ○ Septic embolism e.g. bacterial endocarditis
      ○ Post-obstructive pneumonia
      ○ Trauma including surgery
      ○ Direct extension, haematogenous spread
      ○ Primary cryptogenic lung abscesses
43
Q

Common causative organisms of lung abscess

A

○ s.aureus
○ Gram negative organism
○ Mixed infections often occur because of inhalation of foreign material
○ Bacteroides

44
Q

Mechanisms of development of lung abscess

A

○ Aspiration
§ Aspiration causes pneumonia progresses to tissue necrosis and lung abscess
○ Antecedent primary lung infection
§ Post pneumonic abscess formations associated with S.aureus, K.pneumoniae and pneumococcus
§ Post-transplant or other immunosuppressed individuals at risk
○ Septic emboli
§ Arise from thrombophlebitis in any portion of systemic vascular system or vegetations of infective bacterial endocarditis of right side of lung
○ Neoplasia
Secondary infection common in bronchopulmonary segments obstructed by malignancy

45
Q

Aetiological factors associated with lung cancers

A
  • Tobacco smoking
    ○ Nearly linear correlation between frequency of lung cancer and pack-years of cigarette smoking
    ○ Lung cancer develops in 10-15% of smokers
    ○ Second hand smoking also increases risk
    • Industrial hazards
      ○ Asbestos, arsenic, chromium, uranium, nickel, vinyl chloride and mustard gas
      ○ High dose ionising radiation
    • Air pollution
      ○ Uncertain if alone increases the risk but likely adds to risk in those with other exposures
    • Genetic mutations
46
Q

Histological classification of lung cancers

A
  • Small cell carcinoma - 15%
    ○ High smoking association
    ○ Rapid growth rate and early metastasis
    • Non-small cell carcinoma
      ○ Adenocarcinoma - 50%
      § Low association with smoking
      § Intermediate growth and metastatic rate
      ○ Squamous cell carcinoma - 20%
      § High smoking association
      § Slow growth rate and late metastatic spread to hilar lymph nodes
      ○ Large cell carcinoma - 2%
      § High association with smoking
      § Rapid growth rate and early metastasis
    • Other - 13%
47
Q

Morphological features of adenocarcinoma

A
  • Glandular differentiation or mucin production by the tumour cells
    • Lesions small and peripherally located
    • Majority express TTF-1 or napsin A
    • Presence of EGFR and KRAS mutations
    • Categorised by histologic appearance – preinvasive lesion (atypical adenatomous hyperplasia and carcinoma in situ), minimally invasive and invasive
      ○ Invasive further categorised by histologic appearance
      § Acinar - malignant cells in the neoplastic tissue form acini and tubules
      § Lepidic – tumour cells forming along alveolar surface
      § Papillary -malignant cells of the tumour form complex papillary structures outward projections into lung tissue
      § Micropapillary - small, tight clusters of neoplastic cells resembling lymphatics or small papillary clusters,
      § Solid – no liquid or cyst areas
    • Often a mix of types, pure types rare
    • Genetic testing becoming more important due to advancement in targeted therapies
48
Q

Morphological features of squamous cell carcinomas - lung

A
  • Presence of keratinisation and/or intracellular bridges
    • Arise centrally from bronchi
    • Neoplastic tissue appears white and firm
    • Areas of focal haemorrhage or necrosis produce red or yellow-white mottling and softening
    • Often express p40 or p63
49
Q

Morphological features of small cell lung carcinomas

A

Cells grow in clusters than exhibit neither glandular or squamous origin

- Comprised of small cells with scant cytoplasm and ill-defined cell borders
- Dark stained nuclei with absent nucleoli
- Cells are round, oval or spindle shaped
- High mitotic count
- Necrosis is common and often extensive
- Often occurrence of neurosecretory granules
50
Q

Morphological features of large cell carcinomas

A
  • Undifferentiated malignant epithelial tumour
    • Expresses none of the markers associated with other types
    • Cells have large nuclei, prominent nucleoli and moderate amount of cytoplasm
51
Q

What are the local effects of lung tumour spread?

A
  • Partial obstruction -> focal emphysema
    • Total obstruction -> atelectasis
    • Impaired drainage -> suppurative or ulcerative bronchitis or bronchiectasis -> pulmonary abscess
    • Compression or invasion of SVC -> SVCO
    • Extension to pericardial or pleural spaces -> pericarditis or pleuritis
    • Apical lung cancers compress or invade nervous structures -> severe pain in distribution of ulnar nerve or Horner’s Syndrome
52
Q

What factors can lead to the accumulation of a pleural effusion?

A 
- Transudate
		○ Occurs due to increased hydrostatic pressure or low plasma oncotic pressure
			§ CHF
			§ Cirrhosis
			§ Nephrotic syndrome
			§ PE
			§ Hypoalbuminemia
		○ Low in protein and LDH
	- Exudate
		○ Occurs due to inflammation and increased capillary permeability
			§ Pneumonia
			§ Cancer
			§ TB
			§ Viral infection
			§ PE
			§ Autoimmune
		○ Hight in protein and LDH
53
Q

What is mesothelioma?

A

Tumour of the pleural membranes

54
Q

Aetiology of mesothelioma

A
  • 90% cases related directly to asbestos exposure
    • Men age 60-80 years
    • Long latent period of 25-40 years
    • Typically presents in advanced stage
    • 50% of patients dying < 12 months following symptom onset with few surviving longer than 2 years
55
Q

Pathophysiology of mesothelioma

A
  • Tumour initiator and tumour promoter
    • Asbestos fibres generate free radicals near mesothelial cells in pleura which encourage mesothelial cell damage and proliferation
    • Macrophages secrete TNF-a prevents apoptosis and cell death
    • Mesothelial cells survive genetic damage
    • Rapid division of mesothelial cells
56
Q

Morphology of mesothelioma

A
  • Gross
    ○ Diffuse lesion arising from visceral or parietal pleura that spreads widely in the pleural space
    ○ Associated with extensive pleural effusion and direct invasion of thoracic structures
    ○ Lung becomes ensheathed by thick layer of soft, gelatinous, greyish pink tumour tissue
    • Microscopically
      ○ Epithelioid = 60-80%
      § Cuboidal, columnar or flattened cells forming tubular or papillary structures resembling adenocarcinoma
      § Strong positively for keratin proteins
      ○ Sarcomatoid = 10-12%
      § Resembles fibrosarcoma
      § Positive for keratin
      ○ Biphasic = 10-15%]
      § Mix of epithelioid and sarcomatoid patterns
57
Q

Clinical features of mesothelioma

A
  • Chest pain
    • Dyspnoea
    • Recurrent pleural effusions
    • Metastatic spread if lung invaded to hilar lymph nodes, liver and other distant organs
58
Q

Morphology of non-specific interstitial pneumonia

A 
○ Macroscopic
			§ Low volume and high weight
			§ Homogenous fibrosis of same age
		○ Microscopic
			§ Chronic interstitial inflammation
			§ Interstitial fibrosis of same age
		○ Radiologic
			§ Reticular opacities
			§ Immediate subpleural sparing
59
Q

Causes of non-specific interstitial pneumonia

A

○ Connective tissue disease
○ Hypersensitivity pneumonitis
○ Drug-induced injury
○ Infectious diseases

60
Q

Morphology of idiopathic pulmonary fibrosis

A 
○ Macroscopic
			§ Pleural surface: cobblestoned
			§ Cut surface: rubber white areas
		○ Microscopic
			§ Patchy interstitial fibrosis which varies in intensity and age
		○ Radiologic
			§ Honeycomb appearance
			§ Traction bronchiectasis
61
Q

Causes of idiopathic pulmonary fibrosis

A

○ Unknown

○ Several potential risk factors - environmental factors, genetics, age

62
Q

Causes of cryptogenic organising pneumonia

A

○ Connective tissue disease
○ Hypersensitive pneumonitis
○ Drug-induced injury
○ Infectious disease

63
Q

Morphology of cryptogenic organising pneumonia

A 
○ Macroscopic
			§ Normal lung volume
			§ Pale nodular consolidation
		○ Microscopic
			§ Chronic interstitial inflammation
			§ Masson bodies
		○ Radiology
			§ Patchy airspace consolidation
			§ Air bronchograms

Dundee - Autopsy Pathology (11 decks)

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