Respiratory Pathology Flashcards
1
Q
Asbestosis
A
- history of progressive dyspnea over many years
- right-sided, intractable chest pain and weight loss.
- Mining, milling, fabrication, and installation and removal of insulation
- asbestos bodies: fibers coated w/ ferratin (ferruginous bodies)
- Fibrosis of the lungs, especially the lower lobes
- associated visceral pleural fibrosis - “parenchymal asbestosis”
- white fibrous (hyaline) plaques on the chest wall and diaphragm
- parietal pleural plaques
- Collagen in basket- weave pattern.
- variable alveolar septal, peribronchiolar, and perivascular interstitial pulmonary fibrosis.
- presence of asbestos bodies and interstitial pulmonary fibrosis are needed to establish a diagnosis
- Associated w/ Mesothelioma, Carcinoma of the lung, larynx, stomach, colon
- two distinct geometric forms of asbestos:
1. serpentine: most common
2. amphibole: most pathogenic - synergy b/t smoking & developing lung carcinoma in asbestos
- Caplan syndrome: combo of RA & pneumoconiosis
- CXR: honeycomb pattern of irregular opacities
2
Q
Squamous cell carcinoma:
A
- production of keratin, dyskeratoic cells, or “keratin pearls”
- intercellular bridges (prickle cells or desmosomes)
- nests of malignant squamous cells
- Central location
- Hilar mass w/ cavitation
- Clearly linked to smoking
- Paraneoplastic syndrome: PTH release causes hypercalcemia
3
Q
Adenocarcinoma
A
- Tumor cells exhibit varying degrees of glandular differentiation.
- Sometimes mucin is secreted into the lumen of these glands or found as intracellular droplets.
- identified by mucin stains (PAS & mucicarmine stains).
- Glandular differentiation allows us to classify this tumor
- Scar carcinoma
- Less clearly related to smoking
- Multiple densities on xray mimics pneumonia
4
Q
Small Cell Carcinoma
A
- Central location
- Undifferentiated tumor
- Tumor cells are small with absent or scanty cytoplasm.
- Nuclei follow adjacent nuclei: nuclear molding
- EM and immunohistochemical studies may show neuroendocrine differentiation
- No gland or keratin formation.
- Most aggressive
- Least likely to be cured by surgery
- Usually already metastatic at diagnosis
- Paraneoplastic syndrome: ectopic ACTH or ADH
- Increased in smokers
5
Q
Large Cell Carcinoma
A
- Peripheral location
- Undifferentiated tumor
- May show features of squamous cell or adenocarcinoma
6
Q
HIV associated Respiratory Infections
A
- Cytomegalovirus: intranuclear and intracytoplasmic inclusions visible on H&E.
- CMV infected cells w/ both nuclear and cytoplasmic inclusions.
- Special immunohistochemical stains may be needed to confirm
- Patterns of injury range from minimal reaction with CMV cells present, to necrotic nodules, to diffuse interstitial pneumonia
- HIV infection predisposes to Pneumocystis jiroveci (carinii) pneumonia
- Intra-alveolar foamy exudate highly suggestive of Pneumocystis
- Gomori methenamine silver stain needed to ID organisms.
7
Q
Asthma
A
-chronic inflammatory disorder of the airways
-recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and/or in the early morning.
-Type 1 hypersensitivity response
*IgE binds mast cells
-Adult type: exercise/cold induced
-associated w/ widespread but variable bronchoconstriction and airflow limitation
-partly reversible, either spontaneously or with treatment.
-increased airway responsiveness to a variety of stimuli,
-episodic bronchoconstriction
-inflammation of the bronchial walls & smooth m. hypertrophy
-increased mucus secretion from goblet cells
-Eosinophil proliferation
-Intrabronchial mucus plugs w/ whorl like accumulations of epithelial cells (Curshmann spirals)
-mucin admixed with numerous inflammatory cells.
-Subepithelial fibrosis & mucosal inflammation
-submucosal glandular and smooth muscle hyperplasia
-
8
Q
Aspergillosis
A
- Colonizing: growth of the fungus in pulmonary cavities
- minimal or no invasion of the tissues.
- cavities usually result from preexisting TB, bronchiectasis, old infarcts, or abscesses.
- Proliferating masses of fungal hyphae
- fungus balls: brown masses mixed with mucus & cell debris
- The surrounding inflammatory reaction may be sparse
- there may be chronic inflammation and fibrosis.
- Invasive: Necrotizing pneumonia
- sharply delineated, rounded, gray foci w/ hemorrhagic borders
- target lesions
- Necrotizing pneumonia with hemorrhagic borders
- Allergic: Mucoid impaction in ectatic proximal bronchi & necrosis.
- Vasculitis with chronic eosinophilic pneumonia.
9
Q
Pneumonia
A
- Presents w/ chillis, fever, productive cough, rusty sputum, pleuritic pain, hypoxia, and SOB
- appear red initially (stage of red hepatization), then grayish-brown (stage of gray hepatization).
- Types: lobar, broncho, and interstitial
- Alveoli filled with polymorphonuclear cells.
- Fibrin strands in the alveolar spaces (fibrin looks like thin, filamentous, pink wisps).
- Congested capillaries in the alveolar walls.
- Depending on the causative organism, there may be necrosis of lung parenchyma with microabscesses.
- Causative agents: Strep pneumoniae, Staph aureus, strep pyogenes, Klebsiella pneumonia, H. influenzae, Legionella
10
Q
Tuberculosis
A
- common lesion is the “cheesy” caseous necrosis.
- coalescence of granulomas or tubercles to create a confluent area of caseous, coagulative necrosis.
- central area of necrosis is surrounded by the characteristic epithelioid histiocytes.
- Numerous Langhans type giant cells are seen at the periphery
- Primary - the parenchymal focus and draining lymph node will appear as focus of white caseation
- Secondary - the lesions are cavitary mostly confined to apices.
- causative bacilli should always be demonstrated by acid-fast stains to confirm the diagnosis.
11
Q
Sarcoidosis
A
- Noncaseating granulomas often in multiple organ systems
- Common pathological changes:
1. interstitial lung disease
2. Enlarged hilar lymph nodes
3. anterior uveitis
4. erethema nodosum or skin
5. Polyarthritis
12
Q
Emphysema
A
- Barrel chested from dilation of air spaces
- Destruction of lung tissue and dilatation of alveolar spaces
- Centrilobular: Dilation of respiratory bronchioles
- Most often localized to upper part or pulmonary lobes
- Panacinar: Dilation of entire acinus
- Associated with loss of elasticity and alpha1 antitrypsin deficiency
- Associated with smoking attracting neutrophils and macrophages that bring in elastase
13
Q
Pulmonary Hypertension
A
- Primary: unknown etiology and poor prognosis
- Absence of lung disease
- Secondary: Most commonly due to COPD
- Increased flow: Lt-RT shunt,
- Increased resistance: PE, hypoxia
- Increased viscosity
- Causes RT ventricular hypertrophy
1. Early changes in the pulmonary arteries: - medial hypertrophy of the medium-sized arteries
- muscularization of arterioles and intimal proliferation.
2. Irreversible disease is characterized by: - dilatation of the small arteries
- formation of plexiform and angiomatoid lesions
- ultimately, necrotizing arteritis.
14
Q
Acute Respiratory Distress Syndrome
A
- Produced by Diffuse alveolar damage
- Characterized by intra-alveolar hyaline membranes
- Interstitium thickened, congested & edematous
- small numbers of inflammatory cells.
- replicating Type II cells lining alveoli
- alveoli contain fibrinous exudate & hyaline membranes
- also mixture of macrophages and acute inflammatory cells.
- Phases of Diffuse alveolar damage
1. Exudative: < 7 days, edema, congestion, hemorrhage- type 1 pneumocyte necrosis & prominent hyaline membranes
- Proliferative: (1-3 weeks), consolidated and pale gray lungs
- type 2 pneumocyte proliferation, myofibroblast proliferation
- Fibrotic: > 3 weeks, spongy and cystic (honeycomb) lungs, significant fibrosis
- type 1 pneumocyte necrosis & prominent hyaline membranes
