pulmonary 3 Flashcards
What drugs can cause restrictive lung disease?
bleomycin, busulfan, amiodarone, methotrexate
Always check drug history!
Describe Sarcoidosis.
“A GRUELING DISEASE”
A= ACE & ca2+ increase; G= granulomas (non-caseating); R= Rheumatoid Arthritis; U= uveitis; E= erythema nodosum; L= lymphadenopathy; I= idiopathic; N= non-caseating granuloma; G= gammaglobulinemia; V= Vitamin D increase.
What is idiopathic pulmonary fibrosis?ADD PICTURE OF HONEYCOMB
Repeated cycles of lung injury & wound healing with increased collagen deposition, “honey-comb” lung appearance & digital clubbing.
Antibody for Goodpasture Syndrome? What organ does this condition affect?
Anti Glomerular-BM antibodies
Affects the lung & kidney (glomerulonephritis).
What is found on histology for Pulmonary Langerhans cell histiocytosis? Risk factor for this disease?
Langerhan’s-like cells on histology with Birbeck granules inside (tennis racket shaped granules)
Smoking.
What direction does the Flow-Volume Loop go for Obstructive diseases?
Left.
What direction does the Flow-Volume Loop go for Restrictive diseases?
Right.
Describe FEV1 & FVC for obstructive & restrictive diseases.
FEV1 & FVC are decreased for both. However, FEV1 is more dramatically reduced compared to FVC, resulting in a decreased FEV1/FVC ratio.
What is the pathogenesis for Hypersensitivity pneumonitis?
Mixed type III/IV hypersensitivity reaction to environmental antigen leading to dyspnea, cough, chest tightness, headache.
Often seen in farmers & those exposed to birds.
What is the overall title for pneumoconioses?
“Environmental lung disease”
Chronic, fibrotic lung disease due to inhalation of environmental dust.
What do coal worker’s pneumoconiosis, silicosis & asbestosis increase the risk for?
Cor pulmonale, cancer & Caplan syndrome (rheumatoid arthritis & pneumoconioses with intrapulmonary nodules).
How is asbestosis transmitted?
Shipbuilding, roofing, plumbing.
What lobes does Asbestosis affect?
Lower lobes.
What does having Asbestosis increase the risk of getting?
1) Bronchogenic carcinoma > risk of mesothelioma; 2) pleural effusions.
How is Beryllioses transmitted?
Exposure to beryllium in aerospace & manufacturing industries.
What is seen on histology in Beryllioses?
Granulomatous (non-caseating granulomas via cell-mediated immunity induction)
Looks like Sarcoidosis.
What lobes are affected in Beryllioses?
Upper.
What will be seen on chest X-ray in silicosis and anthracosis?
“Eggshell” calcification of hilar lymph nodes.
How is Coal worker’s pneumoconiosis transmitted?
Prolonged coal dust exposure leading to macrophages laden with carbon, inflammation & fibrosis.
What is Coal worker’s pneumoconiosis also known as?
Black lung disease.
What lobes are affected in Coal worker’s pneumoconiosis?
Upper.
What is Anthracosis?
Asymptomatic condition found in many urban dwellers exposed to sooty air.
How is Silicosis transmitted?
Foundries, sandblasting, mines.
Pathogenesis of Silicosis?
Macrophages respond to silica & release fibrogenic factors, leading to fibrosis.
What is thought that Silica disrupts & what does this potentially cause?
Disrupt phagolysosomes & impair macrophages, increasing susceptibility to TB.
What lobes are affected in Silicosis?
Upper.
What is the only pneumoconioses that affects the lower lobes?
Asbestosis.
What is the only pneumoconioses that does not increase the risk for getting cancer?
Coal worker’s pneumoconiosis.
What will be seen histologically in asbestosis?
Hemosiderin-laden asbestos (ferruginous) bodies are golden-brown rods resembling dumbbells, found in alveolar septum sputum sample, visualized using Prussian Blue stain.
Aside from noncaseating granulomas, what will be seen histologically in sarcoidosis?
“Asteroid bodies:” stellate inclusions within giant cells of the granulomas.
What will be seen on CXR in asbestosis?
“Ivory white” calcified, supradiaphragmatic & pleural plaques but NOT precancerous.
What is ARDS?
Clinical syndrome characterized by acute onset respiratory failure, bilateral lung opacities, decreased PaO2/FIO2, no evidence of HF/fluid overload.
What are the causes of ARDS?
“SPARTAS”
S= sepsis; P= pancreatitis; pneumonia; A= aspiration; R= uRemia; T= trauma; A= amniotic fluid embolism; S= shock.
What is the main risk factor for ARDS?
Alcoholism.
What is the pathogenesis of ARDS?
Endothelial damage leads to increased alveolar capillary permeability, protein-rich leakage into alveoli, diffuse alveolar damage & noncardiogenic pulmonary edema.
What does ARDS result in the formation of?
Intra-alveolar hyaline membranes.
What is the damage in ARDS due to?
Initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade & O2-derived free radicals.
Management of ARDS?
Mechanical ventilation with low tidal volumes, address underlying cause.
What is sleep apnea?
Repeated cessation of breathing lasting 10 seconds or longer during sleep leading to disrupted sleep and daytime somnolence.
What happens to the PaO2 during the day to a patient with sleep apnea?
Normal.
Complications of sleep apnea?
Nocturnal hypoxia leading to systemic/pulmonary hypertension, arrhythmias, sudden death.
What is obstructive sleep apnea?
Respiratory effort against airway obstruction.
What is associated with obstructive sleep apnea?
Obesity & loud snoring.
What is obstructive sleep apnea caused by?
Excess pharyngeal tissue in adults, adenotonsillar hypertrophy in kids.
Tx for obstructive sleep apnea?
Weight loss, CPAP, surgery, stimulation of CN XII.
Complications of obstructive sleep apnea?
Lungs become hypoxic leading to vasoconstriction of lung vessels & pulmonary HTN, which may turn to cor pulmonale, arrhythmias & sudden cardiac death.
What is Central Sleep apnea?
No respiratory effort due to CNS injury/toxicity, HF, opioids.
Who is central sleep apnea common in?
Pre-mature infants (tx with caffeine).
What is obesity hypoventilation syndrome?
Obesity (BMI greater than or equal to 30) leading to hypoventilation, decreased PaO2 & increased PaCO2 during sleep.
What is the normal pressure of the pulmonary artery?
10-14 mmHg.
What levels of pressure indicate pulmonary HTN, both at rest and during exercise?
Rest: >25 mmHg; Exercise: >35 mmHg.
What is the characterization of pulmonary HTN?
Arteriolosclerosis, medial hypertrophy, & intimal fibrosis of the pulmonary arteries.
What is the course of disease for pulmonary HTN?
Severe respiratory distress leading to cyanosis and RVH, eventually death from decompensated COR PULMONALE.