Zaman: Lung Pathology 2 & 3 (COPD, RPD) Flashcards
COPD patients tend to _________ air, retain _______, and develop respiratory _______________,
trap; CO2; acidosis
RPD patients tend to have an increased effort to breathe with ____________, reduced ____________ diffusing capacity, and respiratory _____________ due to hyperventilation.
dyspnea; oxygen; alkalosis
COPD patients are more prone to get respiratory ____________ while RPD patients are more prone towards respiratory ______________.
acidosis; alkalosis.
List clinical features of emphysema.
- Pulmonary HTN
- RIGHT heart failure
- PINK PUFFERS = compensated COPD/non-hypoxic
- BLUE BLOATERS = COPD iwth hypoxia (tends to be seen in severe BRONCHITIS and severe hypoxia)
- death d/t severe acidosis and coma
- pneumothorax
- patients are more predisposed to infection
What is the requirement for the diagnosis of CHRONIC bronchitis?
Persistent cough with sputum production for 3 months in 2 consecutive years. (years are consecutive, months are not).
What is the common etiology of choronic bronchitis?
Tobacco and environment
List the pathological findings of chronic bronchitis.
- increase in thickness of bronchial mucinous glands relative to the thickness of the bronchial wall (i.e. gland is 50% of the wall)
- usually emphysema is present to some degree
Is asthma a restrictive or obstructive disorder?
OBSTRUCTIVE. (like COPD)
Definition of asthma?
- REVERSIBLE bronchoconstriction commonly d/t allergic stimuli, leading to a restriction in peak expiratory flow measured on spirometry (FEV1)
- airway markers of inflammation correlate with bronchial hyper-responsiveness (type 1 hypersensitivity)
- TX w. inhaled corticosteroids (not oral) reduces symptoms AND diminishes airway-hyperresponsiveness. Antibiotics are not effective.
List the pathogenesis of airway inflammation in asthma.
HARD:
- hyper-responsiveness
- airflow limitation
- respiratory symptoms
- disease chronicity
List the pathogenesis of airwau wall remodeling in asthma.
- Collagen deposition under BM
- Mucus gland hyperplasia
- Smooth muscle hypertrophy
- Vascular proliferation
- Elastic fibers lost
List the clinical features of asthma.
- inflammation causes:
- recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particulaly at night or in the morning.
- increase in bronchial hyper-responsiveness to a variety of stimuli (i.e. viral infection)
- widespread but variable airflow obstruction (reversible)
- sub-BM fibrosis in some patients contributes to persisten abnormalities in lung function (if no treatment with corticosteroids)
What are the features of restrictive lung disease (RLD)?
- lung filling/total lung capacity is decreaed
- elasiticty is increased
- no obstruction, air trapping, CO2 retention, or acidosis as seen in COPD
- VELOCITY of airflow may be increased
What is the most common acute pulmonary RLD?
ARDS (Adult Respiratory Distress Syndrome)
What is the AKA that pathologists use for ARDS?
DAD: Diffuse Alveolar Damage
Describe the three phases of DIffuse Alveolar Damage (DAD)
Exudative Stage:
- initial injury that involves all layers of the alveolar wall (epithelial, interstitial, and endothelial)
- edema pools in the interstitium; capillaries leak plasma proteins leading to HYALINE membranes made of fibrin
Proliferative Stage:
- Metaplasia: Type 1 pneumocytes are replaced by Type 2.
- Fibroblasts proliferate -> fibrous tissue seen in 10-15 days
Organizing or Resolving Stage: (FIBROUS PLUGS/MASSON BODIES)
- more fibrous tissue is made; alveolar spaces enlarge
- prominent cyctic spaces (honeycomb lung)
Pics: Hyaline Membrane disease as seen in stage 1 of DAD (exudative stage)
Hyaline Membrane Disease: Histology
What is the clinical presentation and prognosis of UIP?
- smoker with dyspnea, >50yo with a gradually deteriorating clinical course (so pt has COPD and iwll now develop a restrictive disease)
- Lesions are worse at base of lungs and periphery, under the pleura
- Bi-basilar reticular abnormalities with minimal ground-glass opacities
- UIP is the “usual” pattern of IDL and is the most common of these disorders
- UIP and NSIP are very similar but NSIP has a much better outcome as improvement of UIP is rare and survival is approx 3y
What are the histological features of UIP?
- patchy geographical distribution and heterogeneity (temporal)
What is non-specific interstitial pneumonia (NSIP)? How is it different from UIP?
NSIP: a diffuse lung pattern with varying proportions of interstitial inflammation & fibrosis that appeared to be occuring over a single time span
VS UIP: NSIP has a better prognosis; pattern is diffuse whereas in UIP, pattern is patchy
What are the BAL (bronchiole alveolar lavage) findings in COP (cytogenic organizing pneumonia)?
BAL findings in COP:
- increases in lymphocytes (20-40%), neutrophils (5-10%), and eosinphils (5-25%). level of lymphocytes is higher than eosinophils
- “mixed pattern” of cellularity if characteristic but not diagnostic
- Tx: glucocorticoids and/or macrolides
What is the pathology of sarcoidosis?
Activated T-lymphocyte is the eliciting cell:
- lymphocytes dominate in inflammatory exudates
- t-cells release mediators with attract macrophages which then form the granulomas
- in order to aid in dx, can have pulmonary lavage fluids tested: BAL>ILD
RDS in the newborn is due to failure of the immature lung to make ________________, resulting in _____________.
surfactant; collapse.
Endothelial cells leak plasma proteins and hyaline membranes form.
