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Treatment of COPD

enrollment in a pulmonary rehabilitation program -> exercise sessions (muscles become more efficient -> decrease buildup of lactic acid)

Bronchial asthma

reversible COPD

Chronic bronchitis, emphysema, bronchiectasis (less common)

irreversible COPD

Obstructive lung disease

normal or decreased FVC, TLC increased, FEV1 reduced -> FEV1: FVC ratio reduced (<75%)


morphological definition -> two main conditions causing COPD -> permanent enlargement and destruction of airspaces beyond terminal bronchioles (not just overinflation) -> symptoms = obstruction (takes a while to cause symptoms) -> elasticity lost (cannot recoil to expel air passively as normal) -> distinction between centroacinar and panacinar can be done only in early stages

Centriacinar (centrilobular)

seen mostly in smokers, smog filled city dwellers -> not uniform -> involves upper lobes -> damage is at respiratory bronchioles -> distal alveoli spared -> no gross changes

Panacinar (panlobular)

seen mostly in alpha1 antitrypsin deficiency -> takes over whole acinus -> uniform enlargement from respiratory bronchioles, alveolar ducts and alveoli -> involves lower lobes -> large, pale, voluminous lungs, cover the heart

Septal emphysema

rare variety (distal acinar), next to scars, may form bullae -> chances of pneumothorax (mediastinum shifted to opposite side)

Pathogenesis of emphysema

tobacco causes free radicals (can cause tissue damage directly) -> inactivation of antiproteases (functional a1 AT deficiency -> low anti-elastase); free radicals also release IL8, LTB4, TNF to bring neutrophils -> increase neutrophil elastase which either with functional or congenital deficiency of a1 AT deficiency -> causes tissue damage; increased macrophage, elastase and metalloproteinases also cause tissue damage (loss of tethering in alveoli)

ADAM33 (S1 polymorphism)

SNP in this gene predisposes you to COPD

Pi MM normal, Pi ZZ worst

congenital alpha1 antitrypsin deficiency (2% of emphysema) -> hepatocytes accumulate A1AT-> ground glass appearance in LIVER

Cigarette smoking

particles lodge at bifurcation of respiratory bronchioles -> engulfed by macrophages which release elastase -> not inhibited by A1AT and can digest the A1AT; also contains oxidants -> along with free O2 radicals released by PMNs inhibit A1AT

Clinical emphysema

symptoms appear late -> barrel chest, dyspnea, prolonged expiration -> X-ray has flat domes of diaphragm, hypertension (blood gases normal till late) -> pink puffers -> late stage hypoxia, respiratory acidosis -> usually patients are weak and skinny -> weight loss because of excessive puffing and panting due to hyperventilation -> hypoxia and Hypercapnia -> pulmonary vasoconstriction, compensatory Polycythemia (due to increased EPO) -> death by respiratory failure, acidosis, hypoxia, coma OR cor pulmonale

Other types of emphysema

congenital, compensatory (pneumonectomy), interstitial, bullous, obstructive overinflation (tumor, foreign body)

Mediastinal emphysema

air escapes in to the connective tissue of lung stroma, mediastinum and subcutaneous tissue -> sudden increase in intra-alveolar pressure -> violent cough, vomiting, whooping cough, trauma usually with some obstruction (mucous plug), tear in interstitium -> patient bloats like a balloon (including chest head and neck) -> crackling crepitations over chest wall -> recovers spontaneously after defect is sealed

Chronic bronchitis

cigarette smokers, persistent cough for at least 3 consecutive months in at least 2 consecutive years (clinical definition) -> types: simple, mucopurulent, asthmatic and obstructive

Pathogenesis of chronic bronchitis

irritation -> excess secretion by mucus glands -> hypertrophy of glands -> metaplastic goblet cells in surface epithelium, secondary bacterial infection (ciliary dysfunction) -> inflammation and fibrosis (CD8 cells) -> obstruction of small airways (bronchiolitis obliterans) -> superimposed emphysema

Pathology of chronic bronchitis

externally lungs appear normal -> large airways, hyperemia, edema, mucous secretion ->

Bronchitis in the bronchi

hypertrophy and hyperplasia of mucous glands -> increased goblet cells in surface epithelium -> squamous metaplasia

Reid index

ratio of glands to cartilage chronic bronchitis >.5 (normal is .4)

Chronic bronchitis in the bronchioles

goblet cell Metaplasia, inflammation, fibrosis (collapse in expiration), smooth muscle hyperplasia

Chronic bronchitis: clinical

eventually small airways obstruct -> low PO2, increased PCO2, cyanosis -> blue bloaters (edema due to heart failure), pulmonary hypertension, cor pulmonale -> prone to secondary infections

CO2 narcosis

in chronic bronchitis, persistent hypercapnia makes respiratory centers insensitive to PCO2 stimulus -> respiration is now driven by O2 -> if you administer O2 the drive is lost and they die of this

Bronchial asthma

sudden attacks of respiratory distress -> dyspnea, expiratory wheezing/Rhonchi, episodic, relieved spontaneously or by bronchodilators, thick sputum -> bronchial inflammation (important feature) precipitates the hyper reaction (hypersensitivity) of bronchial tree -> bronchiolar smooth muscle spasm -> intrinsic and extrinsic (final mechanism of damage similar -> distinction not relevant)

Intrinsic asthma

non-immune mechanism -> viral infection, cold, bronchitis in smokers, exercise induced, drug induced (aspirin)

Extrinsic (atopy)

type I hypersensitivity (exposure to an extrinsic antigen) -> childhood, familial (serum IgE is increased -> sensitivity to many antigens) -> raised eosinophils in blood -> older patients (serum IgE is normal)

Other types of asthma

allergic bronchopulmonary Aspergillosis, occupational asthma

Bronchial asthma

mechanism - increased TH2, decreased TH (absence of T-bet)


CD4 cells of TH2 subtype release IL-4,5, 13 -> favor synthesis of IgE, growth of mast cells and growth and activation of eosinophils

Genesis early phase

starts in 30-60 minutes of exposure and lasts up to 4-6 hours -> antigen + IgE on mast cells in mucosa -> release histamine, bradykinin, LT, PG, PAF -> bronchoconstriction, acute inflammation, thick mucus -> epithelial damage opens intercellular junctions -> Ag's get in, sensitize mast cells in submucosa -> aggravation of reaction, stimulation of submucosal vagal fibers leading to reflex smooth muscle contraction

Genesis late phase

starts after 4-6 hours -> eosinophils play the dominant role -> attracted by IL-5, PAF (mast cells), eotaxin (epithelial cells) -> amplify and sustain the reaction -> recruit PMNs, basophils, eosinophils, CD4 cells epithelial cells secrete endothelin and eotaxin -> lead to smooth muscle contraction

Eosinophils in the late phase

have granules like mast cells, contain eosinophil cationic protein and major basic protein which are toxic to epithelial cells -> they also produce LT (LTC4 and PAF activate mast cells) -> cytokines activate Myofibroblasts to lay down more collagen in the basement membrane


microenvironment of bronchial tree -> altered due to genetic mutations in metalloproteinases -> ADAM-33 -> this precedes the development of asthmatic attacks and may predispose to it

Effects of asthma

obstruction, more in expiration (wheeze) -> FEV1 < 30%, hyperventilation -> hypoxia, hypercapnia, respiratory acidosis

Asthma - lungs

occlusion of bronchi, bronchioles by thick tenacious mucus -> overinflated lungs

Asthma - micro

eosinophils, mucus plugs in lumen -> inflammation - eosinophils, mast cells, basophils, macrophages, CD4 lymphocytes, neutrophils -> edema -> thick basement membrane, patchy necrosis and shedding of epithelial cells -> hypertrophy of submucosal glands and increase in goblet cells in bronchial lining and hypertrophy of smooth muscle

Asthma - clinical

short acute attacks - expiratory dyspnea, Expiratory wheeze, dry cough -> thick stringy mucus, casts (Curschman's spirals; epithelial casts) -> Charcot Leyden crystals (crystalloids made up of eosinophilic membrane protein) in sputum -> status asthmaticus (severe, prolonged)

Asthma - management

acute attacks -> bronchodilators, steroid inhalers (anti-inflammatory), antihistamines, leukotriene blockers (Accolate); Prevention = desensitization


permanent, abnormal, irreversible dilation of bronchial tree proximal to terminal bronchioles -> result of chronic infection -> destruction, fibrosis, dilatation

Bronchiectasis - associated factors

obstruction (tumors, foreign bodies), congenital (CF, Kartagener's), post infectious states (necrotizing bronchopneumonia - TB, Staph, Pseudomonas, viruses - sequelae to measles, whooping cough), other (RA, SLE, IBD/inflammatory bowel disease)

Kartagener's syndrome

lack of ciliary activity, upper respiratory infections + sterility in males + Dextrocardia -> loss of cell motility during embryogenesis -> dynein arms (short, absent or smile), added/deleted central microtubules -> disoriented movement of cilia

Pathology of bronchiectasis

* localized or generalized -> cylindrical, fusiform or saccular -> bronchi reach up to pleura, walls inflamed, fibrosed, ulcerated, purulent, +/- lung abscess or amyloidosis


productive cough, large amount of foul sputum -> episodic fever, clubbing of fingers, pulmonary hypertension (cor pulmonale), amyloidosis

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