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Respiratory Pathology & Pathophysiology

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Respiratory Pathology & Pathophysiology Restrictive: Restrictive Overview Proliferative: organization & repair Physiology 1-3 weeks Can’t get air in, but can exhale normally gross: lungs are rigid, red, heavy normal FEV1/FVC histologically: hyperplastic type 2 cells ↓ TLC: hallmark is TLC < 80% of predicted cuboidal type II pneumocytes widen alveolar wall diffusing capacity often reduced w/parenchymal disease Acute (ARDS) vs. Chronic presentations Alveolar macrophage plays central role in chronic restrictive diseases: controls deposition of collagen/fibrosis not all chronic restrictive diseases are due to fibrosis (amyloid/malignancy) Fibrotic: end stage fibrosis Extra-Parenchymal (outside of lung) 3-4 weeks + Restrictive diseases lung now remodelled Etiology: gross: fibrosis/cysts Impaired muscle function histology: fibrotic microcysts represent ALS, MG, guillain-Barre, polio, etc…. progression of ring shaped alveolar duct fibrosis, alveolar walls widened by Chest wall disease collagen/scarring obesity, kyphoscoliosis, severe burns, etc…. “Other” etiology pneumothorax, pleural effusions, complete obstruction to major bronchus Physiology Whatever the etiology, lung parenchyma is normal The A-a gradient will be normal ARDS = DAD Prognosis Pathogenesis correlates with duration of injury, not nature of An acute problem! injury sysemic insult: sepsis, trauma, shock, DIC, etc 2/3 of survivors have abnormal pulmonary function afterwards injury (immune/cytokine) to alveolar capillaries: ↑ permeability eosinophilic edema fluid in alveoli hyaline membrane forms around alveoli gas exchange impaired Pathologic changes: 3 phases Exudative: edema & hemorrhage 4-7 days after onset of respiratory failure gross: focally hemorrhagic, airless, heavy lungs, solid histologically: Eosinophilic hyaline membranes, capillary congestion Hyaline membranes are da bomb made of fibrin, cellular debris, and leaked serum proteins Restrictive: ARDS & Pulmonary Edema Syndromes Clinical How does fluid get into the lungs? ARDS characterized by dyspnea, progressive Summary hypoxemia, bilateral radiographic lung infiltrates, and ↓ pulmonary compliance any abnormal Starling forces (except no known instance of primary increases in mortality rate approaches 50% π(pmv) = colloid perimicrovascular) ARDS is not a disease, but it is a resonse to injury MOST clinical cases of pulmonary edema are Infections due to ↑ permeability or ↑ capillary pressure sepsis cardiogenic: fluid in the lungs because of poor pneumona heart function Drugs non-cardiogenic: fluid in the lungs (usually) heroin due to lung vascular endothelium injury cocaine Specific: Hemodynamic EVLW = K[(PMV – PPMV) – σ(πMV – πPMV)] – LYMPH FLOW shock Variables Trauma EVLW = extravascular lung water content fat emboli K = measure of membrane leakiness to water lung contusion Pmv = capillary hydrostatic pressure massive blood transfusion Ppmv = interstitial hydrostatic pressure Inhaled toxins pmv = perimicrovascular oxygen!! free radical damage, can turn into DAD σ = measures vascular permeability to proteins smoke inhalation compared to water Misc πmv = osmotic pressure of capillary aspiration πpmv = osmotic pressure of interstitum pancreatitis ↑ K Æ ARDS ABG’s: ↓ σ Æ ARDS ARDS is said to exist when there is acute ↑ Pmv Æ CHF, volume overload, HTN, etc hypoxemic respiratory failure with large R Æ L ↓ Ppmv Æ (rare) upper airway obstruction, shunt reexpansion pulmonary edema R Æ L shunt defined as PaO2/FiO2 ratio of ≤ ↓ πmv Æ hypoalbuminemia, nephrotic 200 syndrome PaO2/FiO2 ratio: multiply % FiO2 by 7 Æ this is ↓ lymph flow Æ malignancy, trauma to what PaO2 should be thoracic duct Between 200 and 300: any lung injury Below 200: R Æ L Shunt Pathophysiology of ARDS See problem set for examples (i.e. Problem permeability pulmonary edema = ARDS set #3, case 1, problem 3) extends beyond Edema CXR: diffuse patchy infiltrates inflammation Æ cellular proliferation Æ fibrosis (pathologically called DAD) Cardiac Cath: ↓ or normal pulmonary capillary wedge pressure Hypoxemia this just proves that the L heart is normal blood perfuses liquid-filled alveoli, cannot equilibrate with air Treatment R Æ L shunt no role for systemic corticosteroids in early ARDS vessels lost ability to vasoconstrict, so shunting can’t be minimized: we don’t really vent: PEEP (positive end-expiratory pressure) know why but this can cause barotrauma: you can’t win Compliance Lungs become less compliant: restrictive defect Note: this “restriction” is theoretical because you don’t go around giving people with ARDS PFT’s Stiff lungs necessitate use of ↑ airway pressures on the vent this can cause barotrauma Restrictive: BOOP = BO = COP = UCP Histopathology: 3 stages, but hard to define Pathogenesis because stages are so slow failed restoration after pneumonia Acute: seldom seen, indistinguishable from early DAD (edema, hyaline membranes), Pathology don’t worry about it patchy intraluminal polyps (= bronchiolitis Proliferative: interstitial/intraalveolar fibrosis obliterans) with central collection of macrophages, lymphocytes, and plasma cells. Fibrotic: can no longer recognize alveoli, architectural disorganization, collagen, polyps can block airway, causing an element of microcysts. obstruction Pathognomonic: focus of fibroblastic proliferation: manufactures collagen Clinical presentation 50-60 yo, M > F insidious onset: dry cough, gradual increase in dyspnea hypoxemia, ↓ PCO2 due to hyperventilation note: due to insidious course, patient may not seek medical attention until they have end- absence of honeycombing: unlike DAD, has no stage fibrosis microcystic change PE: rapid shallow respirations, fine end- Clinical inspiratory crackles (rales) over lower lobes, X-Ray: multiple nodular opacities digital clubbing Steroid responsive X-Ray: increased interstitial markings = “reticulonodular markings” UIP = IPF = Kiss of Death Not steroid responsive, transplant needed Pathogenesis PFTs: ↓ TLC, VC, RV; normal or ↑ FEV1/FVC. ↓ idiopathic, possibly immune corected DLCO Pathology ABGs: hypoxemia, low PaCO2 due to Gross: analogous to end-stage kidney hyperventilation small lungs, cirrhotic, hobnailed surfaces median survival: 5 years, W > M diffuse fibrosis with microcysts (looks just like rate of cancer is increased, as it is in other fibrotic DAD) lung dz microcysts peripherally distributed honeycombing (due to microcysts)/emphysema may be present Restrictive: HSP Sarcoid Pathogenesis Pathogenesis extrinsic allergic alveolities due to inhalation of multisystem granulomatous disease organic dusts cause is a mystery inflammation can result in parenchymal fibrosis Pathology Pathology initial lesion in lung is lymphocytic alveolitis key feature: incomplete non-caseating classic granuloma is non-caseating granulomas and inflammation involves wall of bronchioles diagnostic triad: can follow path of lymphatics 1) inflammation of bronchiole or around bronchiole (= bronchiolitis/peribronchiolotis) very little fibrinoid necrosis Clinical young adults: 20-40, hilar enlargement, expanded 2) chronic interstitial pneumonitis mediastinum biopsy to dx sarcoid vs. lymphoma but if skin lesions present, it’s sarcoid X-Ray: bilateral enlarged hilar lymph nodes, ↑ interstitial markings 3) baby (“incomplete”) granulomas = single multinucleated giant cell (at 5 oclock in picture) seen in 70% of biopsies NOTE that sarcoid has complete granulomas PFT: ↓ of lung volumes, ↓ diffusing capacity, hypoxemia, ↓ corrected DLCO can also be element of obstruction if granulomatous inflammation involves airways ABGs: hypoxemia, especially during exercise. Hypercapnia in advanced cases Active dz: treasted w/ steroids inactive disease: will regress or is already fibrotic Prognosis favorable: remove offending antigen Clinical: resolves on its own: 70% Responds to steroids responds to steroids: 25% presents with cough, fevers, dyspnea (especially gets worse, like IPF: 5% after Ag exposure) Obstructive: Overview of Obstruction/COPD if a smoker quits smoking, rate of decline in Important determinants of airway caliber: lung function returns to normal rate 1) material in lumen (BOOP) hypoxemia: pulmonary arterial vasoconstriction Æ rising pulmonary artery pressure 2) abnormally thick mucosa (chronic bronchitis) RV can fail Æ cor pulmonale 3) abnormal tethering of airways by parenchyma heart trouble due to the lung 4) smooth muscle contracted (asthma) bullous lesions can rupture Æ pneumothorax 5) ↑ pleural pressure (theoretical only) Treatment Pathophysiology: diffuse airway obstruction bronchodilators: β2 agonists ↓ FEV1/FVC ratio corticosteroids V/Q mismatch antibiotics in general, patients w/airway obstruction DO RESPOND to supplemental O2 Important: Home oxygen to prevent pulmonary hypertention ↑↑ work of breathing due to hypoxemia/dyspnea/work exceeding muscle NO Sedation (Atavan) capacity Less common diseases still called “COPD” COPD: A group of diseases with diffuse obstruction to bronchiectasis airflow in smaller airways especially during expiration. cystic fibrosis Most commonly, implies: Chronic bronchitis & α-1-antitrypsin deficiency Pulmonary Emphysema Bronchial Asthma Bronchial asthma also included Pathogenesis may progress to COPD, bronchiectasis, and paroxysmal widespread narrowing of small atelectasis conducting airways due to hypersensitivity of patients often have combination of these 3 diseases bronchial tree stimulus: could be allergic reversible, intermittent chronic inflammatory disease: cannot be cured, but can be controlled in most patients chiefly eosinophilic response note that these pink/blue nicknames have
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