Lung Pathology Flashcards
Disease of lungs:
Disease of conducting Airway:
Bronchi: bronchiectasis, chronic bronchitis
Bronchioles: asthma, inflammation, fibrosis
Disease of resp bronchiole & alveolus: emphysema
Disease of alveoli & interstitium:
Alveoli: luminal filling (pulm edema, pneumonia, hemorrhage, adult RDS) or intersitital thickening (fibrosis & inflammation….interstitial pneumonia, sarcoidosis, hypersensitivity pneumonitis)
Bronchiectasis
Permanent dilitation of bronchi & bronchioles due to destruction of the elastic tissue & muscle
Lumen tends to fill with mucus plug including inflammatory cells
Lower lobes more common
Acute & chronic inlammation, fibrosis too
Associated with disease that impair clearing of mucus: CF, foreign body inpaction, chronic bronchitis w/repeated infection, immotile cilia
Can cause pneumonia distal to the bronchiectasis, bc it obstructs airway
Chronic bronchitis
Persistent cough with sputum production for 3 months in 2 consecutive years
Often due to smoking, often results in repeated infections
Airway epithelium is red, mucus plugging, fibrosis
Histologically:
- smooth muscle hypertrophies, bronchiole glands hyperplasia –> increased mucus secretion
- Goblet cell hyperplasia
- Thickening of basement membrane
- Squamous metaplasia & loss of cilia
Result: increased production of mucus, decreased clearance –> airway resistance/obstructive lung disease, but normal lung capacity (bc alveolar zones not affected)
Asthma
Inflammatory disorder of the airways –> airway hyperresponsiveness, airflow obsstruction, clinical symptoms
Often acute, usually reversible, can have allergic/non-allergic triggers
Thick wall, dripping mucus
It’s a clinical syndrome with these path correlates:
Asthma lung looks normal grossly (can see hyperinflation, mucous plugging) but most of the changes are microscropic
Radiographically, you can see depressed diaphragm, no heart shadow due to hyperinflation of lungs
Microscopic: thick basement membrane, inflammatory cells (eosinophils), edema, smooth muscle hypertrophy
Changes lead to increased lung capacity, increased work of breathing due to resistance (remodeling, mucus, inflammation, edema), more resistance during expiration
Bronchiolitis
Inflammation of the bronchioles i.e viral, allergic
Bronchiole fibrosis
Smoke inhalation, connective tissue disease, post lung transplant
Emphysema
Destruction of acinar walls (bronchiolar & alveolar wall)
Obstructive disease
Can be panacinar (damage to entire acinar unit from resp bronchiole to alveolar sac) or centriacinar (mostly around the respiratory bronchiole)
Grossly: you see dilated thin walled airspaces, loss of parenchyma
Microscopic: dilated alveoli, anthracotic pigment (related to cigarette smoke)
Note that recoil also decreases: lose radial traction on airways, airways collapse, worse on forced expiration
Panacinar v. Centriacenar Emphysema
Centriacinar: smoking, damage to resp bronchiole, upper lobes most affected
Panacinar: damage to entire acinar unit from resp bronchiole to alveolar sac, more sever at bases, more diffuse than CLE, alpha-1 antitrypsin deficiency
Hypothesis is that smoking causes an acquired alpha-1 antitrypsin deficiency
alpha-1 antitrypsin –> anti-elastase –> keeps balance on elastase; without it, neutrophil elastase is unchecked –> tissue destruction
Pulmonary edema
Due to increased pressure from left heart disease, can be non-cardio causes
Luminal filling of alveoli: seen grossly (heavy, wet, lung with light red frothy fluid), microcopic edema, more severe in lower lobes
Pneumonia
Inflammaton of the lung, often infectious
Paler color, firm region with pneumonia (acute)
Patchy: takes more time- days to weeks
Histologically: neutrophils filled with alveoli
Pulmonary hemorrhage
Filling of alveolar spaces wtih blood, fibrin
If repeated, you get iron deposition in lung
Groslly: filled with brighter red fluid bc it’s all blood
Histologically: see blood & fibrin, brown pigment if iron deposition
Causes: trauma, structural leisions, pulmonary vasculitis, immunologic
Adult respiratory distress syndrome
Acute alveolar injury with microvascular damage leading to edema and tissue injury
Many causes including pulmonary infection, shock, sepsis, pancreatitis, burns, toxic inhalations, radiation, near drowning
What are 2 causes of interstitial lung disease?
Fibrosis or inflammation
Mass lesions: 2 types
Benign: granulomatous disease; histologically: lots of inflammatory cells, can include necrosis
Malignant tumors: grossly shows sunken tissue
Pulmonary embolism
Obstruction of pulm artery usually by thrombus but can be fat, bone marrow, cancer, silicon injections
Most arise from deep venous thrombosis
Can occlude pulm artery at bifurcation or pulm artery branches
Results in infarct only 10% of the time due to dual lung circulation
Small emboli organize & recanalize; chronic PE can lead to pulm htn
Often results in sudden death
