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Respiratory > Lung Pathology > Flashcards

Lung Pathology Flashcards

1
Q

Acute vs chronic pattern of lung injury

A

Acute
• Inflammation (neutrophils)
• Edema/Pleural effusion
• Acute lung injury (ARDS/DAD = Diffuse alveolar damage)
• Pulmonary hemorrhage (infarct/vasculitis)

Chronic
• Inflammation (lymphocytes/macrophages)
• Fibrosis
• Emphysema

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2
Q

Describe the different types of pulmonary inflammation

A

Acute
• Polys
• Infection (bacterial)
Pattern of infection:
• Bronchopneumonia = patchy, distributed around airway
• Lobar pneumonia = diffuse
Also from infarct, abscess, DAD, any necrosis
Pulmonary abscess
o Localized suppurative process
o Walled off
o Oral anaerobes (60%), Staph, Gram-negative
o From aspiration, septic embolus, traumatic

Chronic
• Lymphocytes
• Infection (viral or chronic)
• Also from any chronic lung disease

Granulomatous
•	See macrophages/giant cells and lymphocytes
Two types: (both appear similar) 
•	Foreign body granulomas
•	Immune granulomas

Eosinophilic
• Infection (parasitic)
• Also from asthma, allergy, Eosinophilic syndromes

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3
Q

Causes of granulomas in lungs

A 
TB infection
Fungal infection
Sarcoid
Foreign body
Wegeners Granulomatosis
Hypersensitivity pneumonitis
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4
Q

Fungal pneumonia

A 
Causes:
Histoplasma capsulatum:
-round to oval small yeast (2-5 microns)
-darkly staining foci
-narrow based budding

Coccidioides immitis:

  • thick-walled, non-budding spherules (20-60 microns)
  • often filled with small endospores

Blastomyces dermatitidis:

  • round to oval large yeast (5-15 microns)
  • Broad based budding

Aspergillis:

  • 45 degree (acute) angle branching
  • septated hyphae

Mucor:

  • 90 degree (right) angle branching
  • non-septated hyphae

So when see pulmonary granulomas in specimen
o Perform Acid-Fast and Fungal (GMS –Silver) stains
o Rules out mycobacterial and fungal infections

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5
Q

Granulomas from TB

A

caseating granulomas (necrosis)

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6
Q

Granulomas from sarcoid

A

o “Naked” bland granulomas (well-defined)
o Non-caseating
o Not associated with acute inflammation, necrosis, foreign material or demonstrable infectious agents
o See prominent hilar lymphadenopathy

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7
Q

Foreign body granulomas

A

o Has foreign material

o From IVDA/aspiration

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8
Q

Granulomas from Hypersensitivity pneumonitis

A

o Immune response to inhaled antigen
o Loose granuloma (not sarcoid)
o Without necrosis (not TB)
o No foreign material (not foreign body)
o Negative on AFB/GMS stain
o Suggests Type IV hypersensitivity reaction
o Also complement and Ig in vessels (Type III)

Other types:
• Farmer’s lung: thermophilic actinomyces in hay
• Pigeon Breeders Lung (Bird Fancier’s disease)
• Humidifier (or air-conditioner) lung = bacteria

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9
Q

Emphysema

A
  • Irreversible enlargement of airspaces distal to terminal bronchioles
  • Destruction of alveolar walls without obvious fibrosis
  • Apical and subpleural bullae (“blebs”)

Types:
Centriacinar (centrilobular)
o Affects respiratory bronchioles (proximal acinus)
o Smoking
Panacinar (panlobular)
o Affects entire acinus (RB, AD, alveolus)
o Alpha-1-antitrypsin
BOTH: protease (elastin) and antiprotease (alpha-1-antitrypsin imbalance

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10
Q

Chronic bronchitis

A
  • Persistent cough with sputum production for at least 3 months in at least 2 consecutive years, in absence of any other identifiable cause
  • Mucus gland hyperplasia
  • Chronic inflammation
  • Mucinous metaplasia of epithelium
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11
Q

Asthma

A
  • Pulmonary hyperplasia
  • Mucus plugs with eosinophils
  • Sub-basement membrane thickened (type I and II collagen under type IV)
  • Curschmann spirals (whorls of shed epithelium in mucus plugs) and Charlot-Leyden crystals (derived from eosinophils)
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12
Q

Bronchiectasis

A

• Permanent dilation of bronchi/bronchioles
• Destruction of muscle and elastic tissue
Associated with chronic necrotizing infection:
• Hereditary: CF, Kartageners (mucus/cilia)
• Infectious: necrotizing (TB, Staph, Aspergillus)
• Obstruction: tumor, foreign body

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13
Q

Pulmonary eosinophilia (IL-5)

A

Asthma, allergies, and parasites (secondary)

Loffler Syndrome = simple pulmonary eosinophilia
• Transient pulmonary lesions, peripheral (blood) eosinophilia, benign course

Acute eosinophilic pneumonia with respiratory failure
• Rapid onset acute illness of unknown cause
• Fever, dyspnea, hypoxemic repiratory failure
• BAL > 25% eosinophils
• Chest x-ray = diffuse infiltrates
• Prompt response to corticosteroids

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14
Q

Primary Ciliary Dyskinesia

A
  • Autosomal recessive defect in dynein arms in cilia
  • Retention of secretions → infection → bronchiectasis

Half of patients have Kartageners Syndrome:
• Triad: bronchiectasis, sinusitis, situs inversus
• Males = infertility

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15
Q

Cystic Fibrosis

A

CF in lungs = abnormal transport of Chloride and sodium
o Results in thickened viscous airway secretions
o Chronic infections
o Progressive respiratory failure

Gross Pathology:
o	Mucus plugging
o	Bronchiectasis
o	Consolidation 
o	Green discoloration from pseudomonas infection

Histology:
o Dilated airways filled with mucous and pus (inflammation)

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16
Q

Idiopathic pulmonary fibrosis (IPF)

A

Histologic pattern = usual interstitial pneumonia (UIP)
o Repeated cycles of alveolar epithelial injury
o TGF-beta1 released from injured Type I alveolar epithelial cells → stimulates fibroblasts → fibrosis
o Temporal heterogeneity: key feature of UIP
• New/active fibrosis = “Fibroblastic foci”
• Old/collagenized dense fibrosis
o Progressive disease
• 3 year survival

17
Q

Asbetosis

A 
Two geometric forms:
Amphibole
•	Aerodynamic = travel deeper/more distally
•	Less soluble (lasts longer)
•	More pathogenic 
•	Fibrogenic 
•	Causes mesothelioma 
Serpentine 
•	Curly shaped (filtered out earlier)
•	Less pathogenic
•	More soluble 
•	Fibrogenic 
Complications:
Pleural plaques 
•	On diaphragm or chest wall
•	Most common manifestation of exposure
•	Dense fibrosis with dystrophic calcification 
Pleural effusions 
Pulmonary fibrosis
Malignancy Mesothelioma 
•	Pleural based tumor encasing lung 
•	Often grows along septae
•	Histology: TTF-1 marker to see if primary lung cancer 
Lung carcinoma

Histology
• Prussion blue (iron staining) → Ferruginous bodies

18
Q

Silicosis

A

o Most prevalent chronic occupational disease
• Sand blasters mine workers
• Crystalline silacon dioxide (silica)-quartz
o Nodular fibrosing pneumoconiosis
o “Eggshell” calcifications on x-ray (double rim)
o Fibrotic nodules may polarize under light
o Increased susceptibility to TB

19
Q

Pulmonary Thromboembolus

A
  • 95% from Deep vein thrombosis of legs
  • Large or saddle emboli lethal quickly
  • Non-perfused lung → Respiratory compromise
  • Hemodynamic compromise → acute cor pulmonale
  • Loss of pulmonary venous return → decreased CO
  • Electromechanical dissociated (rhythm on EKG, no pulses)

Histology = Lines of Zahn
• Layering effect due to thrombus forming in vessel with blood flow
• From alternating platelets, fibrin, and RBCs
• Allows identification of ante-mortem (true) thrombus vs. post-mortem clot

Smaller/peripheral emboli may infarct lung
o Cause pleuritic chest pain, hemoptysis, cough, dyspnea
o Wedge-shaped appearance
o In lungs = dual blood supply → red

20
Q

Pulmonary HT

A

Occurs when mean pulmonary BP reaches ¼ of systemic levels (normally is 1/8th of systemic)

Causes:
o Increased pulmonary blood flow/pressure
o Increased pulmonary vascular resistance
o Left heart resistance to blood flow (CHF)

Diseases:
o COPD/ILD = hypoxia and loss of capillaries
o Congenital (shunts) or acquired heart disease
o Recurrent small thromboemboli → obstruct → increased PVR
o CT disease (ex: systemic sclerosis)
o Obstructive sleep apnea (with obesity)
Familial
Primary pulmonary HT (common in 20-40 yr old females)
Bone morphogenetic protein receptor type 2 (BMPR2)
• Normally BMPR2 → decreased proliferation and increased apoptosis
• If lose/defective BMPR2 → increased smooth muscle cells in vessels → pulmonary HT

Morphologic changes in Pulmonary HT
o Atherosclerosis of pulmonary artery
• Normally not seen in pulmonary vessels due to low pressures
o Medial hypertrophy (smooth muscle proliferation)
o Plexiform lesion: in advanced and severe Pulmonary HT

21
Q

Pulmonary alveolar proteinosis (PAP)

A

o Like edema but acellular (only fluid), granular precipitate of surfactant

Acquired: (90%) anti-GM-CSF antibody (autoimmune)
• Decreased GM-CSF activity → reduced surfactant clearance → accumulation

Congenital: inherited GM-CSF or surfactant defects

Secondary: hematopoietic disease, malignancy

22
Q

Diffuse alveolar damage (DAD)

A

o What we see in lungs/the histologic manifestation of ALI and ARDS
o Hyaline membranes = histologic hallmark
• Line alveoli
• Fibrin-rich edema fluid mixed with cytoplasmic and lipid remnants of necrotic cells

23
Q

Pulmonary hemorrhage syndromes

A

Goodpasture syndrome
o Antibody against type IV collagen
o Basement membrane damage in lung and kidney
o Type II (Ab mediated) reaction
o Linear deposition of Ab along basement membrane
• Vs: SLE = granular pattern due to immune complex deposition in Type III reactions
o Most common cause of death = uremia
o Treat with plasmapheresis to remove antibody

Wegener granulomatosis
o Necrotizing granulomatous vasculitis
o Involves airways and kidneys
o Upper (sinus/pharynx) and lower (lungs) airways
o cANCA (anti-proteinase-3) in 95% patients
o Granulomas (necrotizing) and vasculitis
• Often infectious (fungal/TB/abscess) or neoplastic (necrotic tumor)
Histologically:
• Granulomatous inflammation with giant cells and vasculitis
• Need AFB/GNS stains (would be negative)
• Serum c-ANCA (anti-PR3) would be positive

Respiratory (18 decks)

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