Pathoma Respiratory Part II Flashcards
Group of diseases characterized by airway obstruction + air trapping; decreased FVC, FEV1, FEV1/FVC ratio; increased TLC, RV, FRC
Obstructive lung dz:
- chronic bronchitis
- emphysema
- asthma
- bronchiectasis
Chronic productive cough (due to excessive mucus production) lasting at last 3 months over at least two years; characterized by hypertrophy of bronchial mucinous glands (goblet cells); leads to increased thickness of mucus glands relative to bronchial wall thickness (Reid index > 50%; normal
Chronic bronchitis
- Productive cough
- Cyanosis (“blue bloaters”) - mucus plugs trap CO2 –> increased PaCO2 + decreased PaO2
- Increased risk of infection and cor pulmonale
Chronic bronchitis
Highly associated with SMOKING –> pollutants –> irritation and inflammation –> mucinous gland hypertrophy + hyperplasia
Chronic bronchitis
Destruction of alveolar airs sacs –> loss o f elastic recoil and collapse of airways during exhalation; due to imbalance of proteases and antiproteases
Emphysema
Smoking –> inflammation + protease-mediated damage
CENTRIACINAR emphysema in UPPER lobe
Inflammation in the lungs normally leads to
release of proteases by neutrophils and macrophages
Alpha-1-antitrypsin normally …
neutralizes proteases
Lack of anti-protease leaves the air sacs vulnerable to protease-mediated damage; mutated protein accumulates in the ER of hepatocytes (pink, PAS+ globules on biopsy_–> cirrhosis; due to PiZ mutation
Alpha-1-antitrypsin deficiency –> PANACINAR emphysema in LOWER lobes
- Dyspnea + cough with minimal sputum
- Prolonged expiration w/ pursed lips (“pink puffers”)
- Weight loss
- Increased AP diameter of chest (“barrel chest”)
- Hypoxemia due to destruction of capillaries in the alveolar sac and cor pulmonale are late complications
Emphysema
Type I HS –> reversible AW bronchoconstriction
Atopic asthma
Allergens –> TH2 –> IL4 + IL5 + IL10
Re-exposure –> IgE mediated activation of mast cells –> release of preformed histamine granules + LTC4, LTD4, LTE4 –> bronchoconstriction, inflammation and edema
Asthma (early phase reaction)
Mediates class switch to IgE
IL-4
Attracts eosinophils
IL-5
Stimulates TH2 cells and inhibits TH1
IL-10
Asthma: Allergens –> TH2 –> ?
IL4, IL5, IL10
Inflammation, especially MAJOR BASIC PROTEIN derived from eosinophils, damages cells and perpetuates bronchoconstriction
Late-phase reaction
Curschmann spirals (spiral-shaped mucus plugs) Charcot-Leyden crystals (eosinophil-derived)
Asthma
Besides allergens, what else can provoke asthma
- Exercise
- Viral infxn
- Aspirin (NASAL POLYPS)
- Occupational exposures
Permanent dilatation of bronchioles and bronchioles and bronchi; loss of airway tone results in air trapping; due to necrotizing inflammation with damage to airway walls.
Bronchiectasis
Causes of bronchiectasis include:
- CF
- Kartagener syndrome
- Tumor or foregoing body
- Necrotizing inflection
- Allergic bronchopulmonary aspergillosis (ABPA)
What is Kartagener syndrome?
Inherited defect of the dynein arm, which is necessary for ciliary movement –> sinus, infertility (poor motility of sperm), + situs inversus
Cough, dyspnea, foul-smelling sputum –> hypoxemia w/ cor pulmonale + secondary amyloidosis
Bronchiectasis
Characterized by restrictive filling of the lungs; decreased TLC, FEV1, FVC; increased FEV1: FVC ratio; most commonly due to interstitial diseases of the lung; may also arise with chest wall abnormalities (obesity)
Restrictive pulmonary dz