Pathology Flashcards
UIP: characteristics and diseases
IPF, c.t. disorders, asbestosis, chronic HP
Geographic Heterogeneity
Temporal Heterogeneity (Fibroelastic Foci - bluer, looser, hypercellular, younger)
More severe in subpleural regions
NSIP: characteristics and diseases
idiopathic NSIP, autoimmune (RA, Scleroderma)
Temporally and Geographically UNIFORM fibrosis
Uniformly thickened alveolar septate with fibrotic collagen
Sarcoidosis (pathology)
Extrapulmonary involvement common (eye, skin, spleen)
Well-formed non-necrotizing, non-inflammatory granulomas (compact naked granulomas), typically along bronchovascular structures
Must first rule out infectious etiologies with stains/cultures
Hypersensitivity Pneumonitis (acute vs. chronic)
acute sx: fever, cough, dyspnea
chronic sx: progressive respiratory failure
acute: poorly-formed non-necrotizing granulomas w/ LOTS lymphocytes, plasma cells, giant cells, typically around airways
chronic: UIP
Honeycomb Lung (diseases, pathology)
end-stage form of fibrosis in restrictive lung disease (assoc w/ UIP)
gross: fibrosis and cystic dilated spaces, dense fibrosis and loss of normal lung architecture
histo: cystic spaces lined with columnar bronchial epithelial cells (not pneumocytes)
COPD (emphysema vs. chronic bronchitis)
Emphysema: softer and more compressible, large overinflated lung; large alveolar spaces w/o inflammation, free-floating septate
can be centriacinar (smoking - resp bronchiole), distal acinar (alveolus/duct), or panacinar (A1AT gene deficiency, whole thing)
CB: chronic airway inflammation (high density inflammatory cells in submucosal glands), mucous gland hypertrophy (Reid Index > 0.4 [mucus gland size:epi to cartilage])
Bronchiectasis (what is it, path)
Not a disease, but a process of airway dilatation that complicates other diseases
Gross: large airspaces in periphery
Histo: airways > blood vessel, airway irregular shape and loss of normal wall, accumulations in airway (mucus, inflammatory cells)
Asthma (path: acute v. chronic)
acute: eosinophils (Charcot Leyden Crystals), mucus plugging, churchman spiral (abnormal mucus production)
chronic: basement membrane thickening, smooth muscle hyperplasia, airway fibrosis
Acute Lung Injury (Etiology, Path)
E: Infection, Physical Injury, Inhaled Irritants, Chemical/Drug Injury
Path: DAD - intraalveolar dense pink/eosinophilic hyaline membrane, increased inflammatory cells, interalveolar exudate (necrotic cells, fibrin, other plasma proteins)
Bacterial Pneumonia (Path)
- Patchy (bronchopneumonia) or diffuse (lobar pna)
- parenchyma is firm, congested, consolidated (hepatization due to exudate/edema)
- Numerous sheets of NEUTROPHILS and hyaline membranes in alveolar spaces
Viral Pneumonia (Path)
- LYMPHOID infiltrate w/in alveolar septate/interstitium (nothing in alveolar spaces)
- may see viral inclusions in CMV (large purple balls in cells); or glassy chromatin in herpes (multinucleated macrophages, chromatin margination)
Chronic Granulomatous Infections (Etiologies, Path)
E: Mycobacterial (TB) and fungal (histo, blasto, cocci)
P: 1. Granuloma + Inflammation (+/- necrotic core: multinucleated giant cell or granular eosinophilic+basophilic cell debris in center)
2. Staining: Silver GMS stain: fungi (black)
Acid Fast Bacilli (AFB): mycobacteria (red)
Adenocarcinoma (Type, Path)
Most common form of NSCLC
Esp in NON-Smokers
Peripheral Tumors
1. Gland formation (single layer of columnar epithelium)
2. Mucin Production (pale blue intracellular)
3. Immunoreactive for TTF1 (antibodies against tumor cell - look brown)
Tx: mLc testing for driver mutations key for precision therapy
Squamous Cell Carcinoma (type, path)
2nd most common form NSCLC, esp in SMOKERS
Large Central Tumors
1. Keratinization (abundant dense pink - intra and extracellular)
2. Intracellular Bridges
3. TTF1 Negative
Large Cell Carcinoma (type, path)
Wastebasket category
No evidence of squamous or glandular differentiation
Poorly differentiated tumors, no specific features
