Pulmonary I - Introduction, Normal & Vascular Diseases
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| The entire respiratory tract with the exception of true cords, epiglottis, and aryepiglottic folds are lined by what types of cells? | Pseudostratified columnar epithelium. Most are ciliated and some produce mucous (goblet cells). Basal cells also exist, which are thought to be precursor for cells of the lung
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| What are Kulchitsky cells found in the lungs? | Neuroendocrine cells that contain a variety of hormonally active polypeptides and vasoactive amines
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| Type of cell of the lung that makes up only 40% of the cells in the alveoli, but covers 95% of the alveolar surface. Mainly responsible for alveolar gas exchange. | Type I pneumocytes
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| Type of cell of the lung that makes up 60% of the cells in the alveoli. These cells produce surfactant and also important for response in lung injury. | Type II pneumocytes
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| Type of cell of the lung that are non-ciliated secretory cells | Clara cells
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| What is the dual supply of the lung productive against? | Ischemic injury
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| Describe the primary function of the pulmonary blood supply | Primary function is gas exchange. Low pressure system consisting of arterioles, capillaries, venules, and veins.
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| Describe the primary function of bronchial arteries | Originates off the aorta and follows the bronchial tree. Anastomoses distally with pulmonary circuit. Serves a nutritive function.
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| What are the mechanical and cellular defense mechanisms of the lung against environmental particles/insults | (1) Nasal clearance (2) Tracheobraonchial clearance (3) Alveolar clearance
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| When does the surfactant production begin during embryonic development? | Week 20-22
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| At what age are majority of alveoli develop? | Most alveoli develop after birth through 2 years.
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| Signs of Acute/Active Pulmonary Injury | (1) Inflammatory cells (2) Edema (3) Hyaline membranes (4) Fibroblastic changes (5) Myxoid fibrosis (6) Presence of regenerating cells
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| Signs of Chronic Pulmonary Injury | (1) Mature collagen (2) Hyperplastic smooth muscle (3) Metaplasia (4) Honeycomb changes grossly
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| Why are certain upper respiratory diseases much more significant in children than adults? | The diameter of airways in children are smaller than in adult, leading to a higher likelihood of functional obstruction of the airway
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| Describe the mechanism of atelectasis | (1) bronchial obstruction (2) external compression of lung parenchyma (3) intrinsic inability to expand the lung
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| A condition characterized as compressive accumulation of air in the pleural cavity resulting in collapse of the lung. Most commonly occurs spontaneously, but also occurs due to injury or disease. | Pneumothorax
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| Describe the mechanism of pulmonary edema | (1) Increase in hydrostatic pressure within capillaries (2) Decrease in oncotic pressure in capillaries (3) Increased permeability of capillary wall secondary to injury/inflammation
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| Most common origin of pulmonary emboli | Venous thrombosis of lower extremities occurring in the setting of venous stasis
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| Describe the pathophysiology of sudden death by massive pulmonary emboli. | The obstruction of the pulmonary artery leading to a (1) marked decrease in left ventricular filling (2) acute decrease in cardiac output (3) hypotension (4) hypoperfusion to heart and brain
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| What are the chances of developing a second pulmonary emboli without anticoagulation? | 30%
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| What are the clinical symptoms of pulmonary emboli? | (1) Dyspnea (80%) (2) Tachypnea (88%) (3) Pleuritic chest pain (62-80%) (4) Cyanosis
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| What percentage of pulmonary emboli results in infarction? | 15-20%
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| What percentage of pulmonary emboli results in infarction in the setting of congestive heart failure? | 90%
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| Etiology of cavitating pulmonary infarction | Infectious embolus
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| What are the clinical symptoms of pulmonary infarction? | (1) Dyspnea (2) Hemoptysis (3) Pleuritic chest pain (4) Cough (5) Fever
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| What is the most common cause of pulmonary hypertension? | Pulmonary venous congestion
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| What is the prognosis of Primary pulmonary hypertension? | Poor prognosis: death within 2-3 years of diagnosis in >50% of patients
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| What is the median age of Primary veno-occlusive disease? | Median age: 15 years
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| What are the symptoms of pulmonary hypertension? | (1) Fatigue (2) Dyspnea on exertion/rest (3) recurrent syncope (4) chest pain (4) cor pulmonale (5) sudden death
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| What are the histological findings in Grade I-III pulmonary hypertension? | (1) muscular hypertrophy (2) Fibrosis
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| What are the histological findings in Grade IV-VI pulmonary hypertension? | (1) plexiform lesions (2) arterial dilatation (3) Fibrinoid necrosis
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| A vasculitis characterized by (1) Necrotizing granulomatous lesion (2) necrotizing vasculitis | Wegener’s Granulomatosis
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| Most common lesion of the kidney in Wegener’s Granulomatosis | Necrotizing glomerulonephritis
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| Organs classically involved in Wegener’s Granulomatosis | (1) Upper respiratory tract (nose, nasal sinus, nasopharynx) (2) lungs (3) kidneys
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| Classic symptoms of Wegener’s Granulomatosis | (1) Nasal bleeding and/or purulent discharge (2) Hemoptysis (3) cough (4) Chest pain (5) fever
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| Diagnostic workup of Wegener’s Granulomatosis | (1) Biopsy (2) c-ANCA (+)
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| An autoimmune disease characterized by antibodies against pulmonary and renal basement membranes. 90% of patients are male with median age of 21 years. | Goodpasture’s Disease
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| Symptoms of Goodpasture’s Disease | (1) Hemoptysis (94%) (2) Dyspnea on exertion (3) Gross hematuria
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| Prognosis of Goodpasture’s Disease | Median survival is 3 months. 5% survive 3 years.
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| Pathophysiology of pulmonary hemorrhage secondary to Systemic Lupus Erythematosus | Intra-alveolar hemorrhage attributable to acute necrotizing vasculitis involving small blood vessels of the alveolar septae
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| Histological findings of SLE with pulmonary involvement | Granular staining for immunoglobulin and complement along the alveolar basement membranes
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| Idiopathic Pulmonary Hemosiderosis | Recurrent hemoptysis of unknown etiology. 80% of patients are <16 years of age. No sex predilection. No renal involvement.
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