Respiratory- pathology

drnieves's version from 2017-06-20 02:01


Question Answer
Hypersensitivity pneumonitisIII/IV to environmental ag Dyspnea, cough, chest tightness, headaches.
PneumoconiosesCoal workers' pneumoconiosis, silicosis, asbestosis
PneumoconiosesIncreased risk of cor pulmonale and Caplan syndrome
Caplan syndromeRA and pneumoconiosis with intrapulmonary nodules.
AsbestosisShipbuilding, roofing, plumbing.
AsbestosisSupradiaphragmatic and pleural plaques
AsbestosisBronchogenic carcinoma>malignant mesothelioma
AsbestosisLower lobes
AsbestosisFerruginous bodies. Golden brown fusiform rods resembling dumbbells in sputum
BerrylliosisAerospace and manufacturing industries
BerrylliosisGranulomatous. Upper lobes
Coal workers' pneumoconiosisCoal dust exposure. Black lung disease. Upper lobes
Coal workers' pneumoconiosisMacrophages with carbon produce inflammation and fibrosis
Anthracosisasx in many urban dwellers exposed to sooty air.
SilicosisSandblasting, mines. Fibrosis in uppe lobes
SilicosisIncreased risk of bronchogenic carcinoma and TB.
SilicosisEggshell calcification of hillier LN
Mainstem bronchus obstructionNo ventilation of lung leads to atelectasis and complete collapse. Opacification on CXR and mediastinum towards it.
Pleural effusionComplete hemithorax opacification. Tracheal deviation away.
Congestion phase24 hrs. Red, boggy lobe. Vascular dilatation and bacteria
Red hepatization2- 3 days Red, firm lobe (liver like). neutrophils, erythrocytes, fibrin.
Gray hepatization4-6 days. Gray firm lobe. RBCs disintegrate, neutrophils and fibrin.
ResolutionRestoration of normal tissue. Enzymatic digestion of exudate.
ElastaseProduced by neutrophils and macrophages
a1-anti-trypsininhibit neutrophil elastase
TIMPsinhibit macrophage elastase
Decrease in elastasepanacinar emphysema
ARDSAcute onset RF, bilateral lung opacities with decreased PO2/FiO2. Due to trauma, sepsis, pancreatitis, amniotic fluid embolism, shock, aspiration, uraemia.
ARDS physioDiffuse alveolar damage= increased in capillary permeability= leakage of protein and non cariogenic deem (normal PCWP). Intra alveolar hyaline membrane. Release of neutrophilic substances.
Mechanical ventilation with low TVARDS tx
Prolonged, substernal pain, ST elevation in 1, v3-v6Anterolateral L ventricle infarction.
LV infarction causesLV failure, cariogenic acute pulmonary oedema, pulmonary venous HTN, and transudate of plasma into the lung intertitium and alveoli.
x: x
Question Answer
Adenocarcinoma in situPeripheral. Non small cell. MC
Activating mutation in ALK, EGFR, KRAS. Clubbing.adenocarcinoma in situ.
Bronchioalveolar subtypehazy infiltrates similar to pneumonia. Good px Bronchorhea.
Glandular pattern, mucin +adenocarcinoma
Grows along septa. Thickening of alveolar wallBronchoalveolar subtype.

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