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252 Cards in this Set
- Front
- Back
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What may be demonstrated when the CXR has one lung clearly defined and the other side of the chest abnormally clear?
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Pneumothorax
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What is Consolidation?
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Consolidation - solidification; the process of becoming or the condition of being solid, as when the lung becomes firm as air spaces are filled with exudate in pneumonia
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What is Atelectasis?
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Atelectasis - incomplete expansion of a lung or portion of a lung
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What is Emphysema?
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Emphysema - defined as a pathological accumulation of air in tissues or organs.
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What is Pneumothorax?
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Pneumothorax - an accumulation of air or gas in the pleural space
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What is Pleural Effusion?
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Pleural Effusion - an abnormal accumulation of fluid between the layers of the membrane that lines the lungs and chest cavity (pleural space)
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What is Bronchiectasis?
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Bronchiectasis - chronic dilatation of the bronchi marked by fetid breath and paroxysmal coughing, with the expectoration of mucopurulent matter
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What is Empyema?
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Empyema - pus filling the pleural space.
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What is Pulmonary Parenchyma?
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Pulmonary Parenchyma - The functional portions of the lung tissue
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What are the two kinds of pleural effusions?
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Transudate - low protein fluid (usually from CHF)
Exudate - high protein fluid, caused by malignancy, infection, sarcoidosis, asbestosis, etc. |
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What is pulmonary edema?
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Pulmonary edema - refers to fluid that has accumulated in the lung interstitium due to an imbalance between the hydrostatic and oncotic forces within the pulmonary capillaries and surrounding tissues.
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What is a common cardiogenic cause of pulmonary edema?
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Congestive Heart Failure
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What are examples of noncardiogenic causes of pulmonary edema?
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Noncardiogenic refers to pulmonary edema resulting from direct damage to the lung, including hematogenous injury (sepsis, IV drugs, pancreatitis) or direct injury (smoke inhalation, trauma, ARDS), etc.
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What two components contribute most to the pathogenesis of noncardiogenic pulmonary edema?
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Elevated Intravascular Pressure (implies cardiogenic influence)
Pulmonary capillary leak |
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What areas of the lungs contribute to acute shortness of breath (hours to days)? What diseases may be present?
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Suggests involvement of the airways (asthma), pulmonary parenchyma (bacterial pneumonia, acute pulmonary edema), pleural space (pneumothorax), or pulmonary vasculature (pulmonary embolus).
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What areas of the lungs contribute to subacute shortness of breath (days to weeks)? What diseases may be present?
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Preexisting Airway Disease (COPD, asthma)
Indolent Parenchymal Infection (TB, P. carinii) Inflammatory process (Wegener's granulomatosis) Neuromuscular disease (Guillan-Barre) Pleural disease (pleural effusion from cancer) Heart disease (CHF) |
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What problems are implicated by chronic shortness of breath?
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COPD
Chronic Interstitial Lung DIsease Chronic Heart Disease |
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How does a symptom of a "cough" aid in diagnosis? What may it suggest?
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Nonspecific cough not too helpful
A cough productive of sputum suggests airway disease - asthma, chronic bronchitis, bronchiectasis |
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How does "hemoptysis" as a symptom aid in diagnosis? What may it suggest?
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Relatively uncommon symptom, signals disease of the airways, pulmonary parenchyma, or vasculature.
Airways: acute/chronic bronchitis, bronchiectasis, CF, bronchogenic carcinoma Parenchymal: pneumona, lung abscess, TB, Goodpasteure's syndrome Vasculature: Pulmonary embolus, CHF, etc. |
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What does "chest pain" (symptom) suggest about the diagnosis?
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If caused by respiratory disease, usually originates from involvement of the parietal pleura.
Some common associated presentations: respiratory motion causing pleuritic pain, often with a history of preceding viral URI, though may also occur with pneumonia, inflammatory process, or neoplasm |
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What are the most common respiratory problems associated with smoking and/or second hand smoke?
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Neoplasm, COPD
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What are some occupational substances that may contribute to a respiratory problem?
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Asbestos, Silicosis, various allergans
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What are some comorbidities of respiratory problems?
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Rheumatic disease, AIDS risk, heart disease
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What are some characteristics of non-cardiogenic respiratory dyspnea?
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Problems with gas exchange, controller (pregnancy, metabolic acidosis), pump (asthma, COPD, kyphoscoliosis)
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What are some characteristics of cardiogenic respiratory dyspnea? Particularly with relation to low, normal, and high cardiac output.
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Low output - suggests CHF, MI, constrictive pericarditis
Normal ouptut - deconditioning, obesity, diastolic dysfunction High output - Anemia, hyperthyroidism, arteriovenous shunt |
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What is associated with auscultation findings of "crackles"?
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Associated with interstitial lung disease, or filling of alveoli with liquid
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What is associated with auscultation findings of "wheezes"?
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Tend to be more prominent during expiration
Associated with bronchospasm, airway edema or collapse, intraluminal obstruction |
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What is associated with auscultation findings of "ronchi"?
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Low-pitched, vibratory sounds produced by free liquid in the airway lumen.
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What is associated with auscultation findings of a "pleural friction rub"?
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A gritty sound produced by the inflamed pleural surfaces rubbing together during respiration.
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what's the fate of the blood vessels traveling through the fourth arch?
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fourth aortic arches
on left side, aortic arch on right side, right subclavian artery |
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In a graph of Tissue pO2 vs %Hb saturation, what does a shift to the left indicate?
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Less O2 is delivered
Hb more saturated Increases pH May also be from decreased 2,3 BPG Hypoventilation |
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In a graph of Tissue pO2 vs %Hb saturation, what does a shift to the right indicate?
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More O2 is delivered
Hb less saturated Decreased pH Higher CO2 in the system Increased in 2,3 BPG |
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What are some causes of Hypoxia?
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Anemia, respiratory factors (V/Q mismatch, hypoventilation), High-Altitude, Right-to-Left Extrapulmonary Shunting, CO intoxication
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What is Ventilation/Perfusion Mismatch? (V/Q mismatch)
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High V/Q mismatch - presence of ventilation but lack of perfusion (eg pulmonary embolism)
Low V/Q mismatch - presence of perfusion but absence of ventilation (eg consolidations, atelectasis) |
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What is an example of Right-to-Left Extrapulmonary Shunting?
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Tetralogy of Fallot, Transposition of the Great Arteries
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List the 4 main influences on ventilation control?
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Arterial pH, pCO2, pO2
Brainstem tissue pH |
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What are some effectors of ventilation control?
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Respiratory musculature
Intercostal muscles Diaphragm Abdominal muscles Accessory muscles |
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What are some sensors of ventilation control?
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Medullary receptors for PaCO2 and H+
Carotid bodies - PaO2, H+ Lungs (stretch, irritant) Upper airway Aortic/Carotid sinuses (baroreceptors) |
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What complication may arise from pregnancy (principally the hormone progesterone), with regards to respiratory problems?
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Pregnancy-induced dyspnea may result, it is a controller problem (as opposed to a gas exchange or pump problem)
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When a CXR reveals a large, localized mass in a lung, what may be included in the DDx?
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Primary/metastatic neoplasm
Localized infection (bacterial, fungal...) Pneumonia Wegener's granulomatosis Rheumatoid nodule Vascular malformation Radiation pneumonitis (other rare conditions) |
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What is a "button" lesion in a CXR?
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May indicate lung cancer - not very good to see in a CXR
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What may be on the DDx for a CXR with thicker cottony look to the lungs and fluid accumulation?
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Pulmonary edema
ARDS Diffuse alveolar hemorrhage Infection (Pneumocystis, viral or bacterial pneumonia) Sarcoidosis |
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What may be in the DDx for a CXR revealing thickened, larger nodular alveoli?
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Idiopathic pulmonary fibrosis
Sarcoidosis Pneumoconiosis Infection Other uncommon causes *Enlarged hilar lymph nodes also associated with this, particularly sarcoidosis* |
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What condition is indicated by a "wall of bleb", vertical heart, lower set diaphragm, hyper lucent lung fields, and increased AP diameter?
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Emphysema/COPD - the "wall of bleb" shows the edge of a large single membrane (as in, not broken up into small alveoli) - lung cavity is expanded due to loss of gas exchange surfaces.
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What is the use of a sputum analysis? What can it tell you? How do you obtain a sputum sample?
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Sputum may be obtained via spontaneous expectoration or a respiratory technician (bronchoscopy)
An adequate sample contains alveolar macrophages, inflammatory cells - inadequate is mostly squamous epithelial cells from upper airways (contaminated with normal flora) Lab processes: Gram stain, culture, special stains (fungi, mycobacteria), viral culture Cytology for assessment of malignant cells |
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How is a bronchoscopy useful for diagnosing a respiratory problem?
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It will help obtain an adequate sputum sample, with which one can narrow down the cause of the problem.
Can also collect washings, tissue samples |
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When does one perform an ABG?
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Usually reserved for cases in the hospital requiring the most immediate assessment of pH, pCO2, HCO3 - and to fine tune respiratory intervention, and refocus the DDx.
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When should lung function be assessed (Spirometry)?
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To detect pulmonary disease - history of dyspnea, wheezing, chronic cough, orthopnea, chest pain; chest wall abnormality, cyanosis, decreased breath sounds, clubbing; Abnormal ABG, CXR
To assess severity or progression of disease - COPD, CF, interstitial lung disease, sarcoidosis To do risk stratification of patients for surgery - thoracic surgery, organ transplantation To evaluate disability - police and firefighters, insurance, social security |
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What kind of cyanosis and pathologies may be indicated by clubbing?
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Central cyanosis, possibly from lung disease, and could be the result from congenital heart disease causing right-to-left shunting.
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What are three main layers of the normal conducting airway?
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Cilated pseudostratified respiratory epithelium
Seromucinous gland Cartilage |
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In a patient with bronchitis, how would their seromucinous glands appear?
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The seromucinous glands would be enlarged, producing excess amounts of mucus
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Where are neuroendocrine cells located in the airways?
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The normal bronchial epithelium (ciliated, pseudostratified)
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What are neuroendocrine cells?
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They are the source of the most malignant lung cancer: small cell carcinoma of the lungs. Triggered by smoking.
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How would one differentiate a pulmonary artery and the bronchus on a slide of normal lung parenchyma?
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The bronchus has a darker ring, made up of a layer of the nuclei of the pseudostratified cells.
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What are some cells that may be seen in the bronchiolus?
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Macrophage with ingested carbon
Goblet cells Clara cells Ciliated respiratory epithelial cells |
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What are some cells that may be seen in the alveolar septa?
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The alveolar septa is lined by type 1 pneumocytes and contain a thin-walled capillary. There may be occasional alveolar macrophages.
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What is a heart failure cell?
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Cells (macrophages) in the lung parenchyma which contain unusually high amounts of hemosiderin.
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Describe the appearance of a normal pulmonary vein (close up).
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Thin alveolar septa with a normal, thin-walled pulmonary vein which receives blood from smaller veins.
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What are three major ways of damaging pulmonary capillaries which result in leakage and dilation of the vessels?
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Epithelial Damage - irritant gases, near drowning
Endothelial Damage - ARDS, endotoxemia, fat embolism Hydrostatic Edema - congestive heart failure, mitral stenosis |
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What are some gross characteristics of lungs with pulmonary edema?
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Heavy, wet, airless lung tissue - the septal lines are visible (where the vessels are) - the veins are full of fluid and blood.
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How would acute pulmonary edema and congestion appear microscopically?
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There is edema with no PMNs, engorged capillaries
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What are some gross characteristics of lungs with chronic congestion or multiple episodes of acute congestion?
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Brown, indurated lungs - brown due to the hemosiderin-containing macrophages.
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What are some microscopic characteristics of lungs with chronic congestion?
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The lungs are fibrotic, and alveoli contain many hemosiderin containing macrophages.
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What is a saddle embolus?
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A saddle embolus blocks both the right and left paths of a branching vessel, high mortality.
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What are lines of Zahn? What do they indicate?
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Lines of Zahn are layers of fibrin, RBCs, and platelets which are put down as the thrombus forms - indicates a pulmonary thromboembolus.
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How does a fresh hemorrhagic infarct contrast with an organizing infarct with pleural reaction?
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A fresh hemorrhagic infarct has a dark necrotic region, cone shaped, typical of a pulmonary infarct.
An organizing infarct with pulmonary reaction results in organized pleural exudate and fibrosis, causing adhesions. There may be a fibrotic border and thickened pleura. |
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What is a plexiform lesion?
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In plexogenic angiography, the parent muscular artery shows medial and intimal thickening. The plexiform lesion develops at a branch point (arrow) probably as a result of shear stress. Damage results in transmural destruction that is repaired by granulation tissue (=plexiform lesion).
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What is characteristic of a fat embolism? What stain is used to visualize it?
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In a fat embolism, there are many fat globules - it can be stained with Oil Red O. It is most often a consequence of long bone fractures, since the marrow starts releasing cells which cause emboli.
May also be seen in soft tissue trauma, severe fatty liver, burn injuries. |
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What is an amniotic fluid embolism?
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A rare complication of pregnancy - seen at term during or shortly after labor - amniotic fluid may gain access to uterine veins, following a tear in the placental membrane. It then embolizes to the lungs.
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How does amniotic fluid embolism present clinically? What is the pathology?
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Clinically - acute dyspnea, cyanosis, shock, sudden death
Pathology - fetal squames, lanugo hair, vernix, mucin emboli in small pulmonary arteries. |
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What percentage of pulmonary thromboembolisms are clinically silent?
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80%
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How many people with a previous pulmonary thromboembolism will have another one?
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30%
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What are some factors that contribute to secondary pulmonary hypertension?
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COPD, restrictive lung disease, recurrent pulmonary thromboemboli, heart disease, vasospasm, Crotalara spectabilis, adulterated olive oil, antiobesity drugs (aminorex, fenfluramine and phentermine)
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What is the proposed mechanism for the chemical factors that contribute to secondary pulmonary hypertension?
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It affects the activity or expression of serotonin transporters
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Describe the pathogenesis of secondary pulmonary hypertension?
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Endothelial dysfunction - from increased shear and mechanical injury, or biochemical injury by fibrin (in PE)
Pulmonary Vasoconstriction - from decreased prostacyclin and NO and increased release of endothelin Platelet adhesion and activation from decreased prostacyclin and NO Endothelial activation makes endothelial cells thrombogenic and promotes the persistence of fibrin Migration and replication of vascular smooth muscle cells and elaboration of extracellular matrix is induced by growth factors and cytokines. |
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What is the etiology and pathogenesis of primary pulmonary hypertension?
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There is an abnormality in the TNF-b signaling pathway - it is caused by inactivating germ line mutations in BMPR2 (bone morphogenic protein receptor 2 gene) and is found in 50% of familial cases and 26% of sporatic cases of primary pulmonary hypertension.
BMP-BMPR2 signaling is important for embryogenesis, apoptosis, and cell proliferation and differentiation. |
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What does BMPR2 signal?
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In healthy cells, BMPR2 signaling causes inhibition of proliferation and favors apoptosis in vascular smooth muscle cells, when stimulus is missing, vascular smooth muscle cells proliferate.
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What factors in addition to BMPR2 cause primary pulmonary hypertension?
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Modifier genes and environmental triggers
The three factors combine to effect pulmonary vascular thickening and occlusion |
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Is clubbing of the fingers associated with secondary or primary pulmonary hypertension?
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Primary pulmonary hypertension (lung associated)
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What is the clinical course of secondary pulmonary hypertension?
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No specific age of onset
Clinical features reflect the underlying disease Respiratory insufficiency, right heart failure, cor pulmonale, may also be sarcoidosis, lung fibrosis, hypertrophy |
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What is the clinical course of primary pulmonary hypertension?
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Patients are usually young women
Fatigue, dyspnea or syncope on exertion Chest pain Severe respiratory insufficiency with cyanosis Death from right sided heart failure within 2-5 years of Dx, grim prognosis without lung transplant. |
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What are some changes that occur histologically in pulmonary hypertension?
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Greater density of cells, increased pink stained infiltrates, more nucleated walls of the arteriolus
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What disease that afflicts dogs may also cause primary pulmonary hypertension? How does it present in humans?
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Dirofilariasis immitis (dog heartworm) blocks pulmonary arteries and causes pulmonary hypertension.
May present as a coin lesion in the lungs of humans. |
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What are three major vascular changes in primary pulmonary hypertension?
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Atheromatous streaks in large pulmonary arteries
Medial hypertrophy Plexiform lesions in severe pulmonary hypertension |
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What are diffuse alveolar hemorrhage syndromes? With what triad of symptoms do they present?
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Triad: Hemoptysis, Anemia, Diffuse Pulmonary Infiltrates
DAH syndromes: Goodpasture, Wegener, SLE, Leukocytoclastic vasculitis (aka microscopic polyangiitis, hypersensitivity angiitis), Churg-Strauss vasculitis |
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What may be present in a slide of a diffuse alveolar hemorrhage?
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Hemosiderin-laden macrophages, black dots from carbon, diffuse RBCs, thickened alveolar septa
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What are the gross and histological appearances of Goodpasture syndrome?
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Brownish-black lungs full of blood and hemosiderin.
DAH in Goodpasture syndrome is accompanied by linear immunofluorescence from immunoglobulin IgG, IgA, or IgM deposition. *90% of patients have antibodies against the non-collagenous domain of the a3 chain of type IV collagen* |
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How does DAH syndrome with SLE appear upon tissue examination? (electron microscope)
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DAH is associated with focal, electron dense deposits of alveolar-capillary basement membrane. At higher magnifications, there appear to be layered fingerprint-like patterns, accounting for a "lumpy-bumpy" discontinuous pattern seen via immunofluorescence.
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What are the clinical findings for Wegener Granulomatosis?
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>80% patients develop necrotizing granulomatous upper respiratory or pulmonary lesions manifested as chronic sinusitis, epistaxis, nasal perforation, cough, hemoptysis, chest pain, and possibly kidney involvement.
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How would Wegener Granulomatosis appear in a CXR?
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Multiple nodules will be visible, which may coalesce and cavitate
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What are the laboratory findings for Wegener Granulomatosis?
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Anti-neutrophil cytoplasmic antibodies (c-ANCA) in serum, target neutrophil granule proteins
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What are the morphological findings in the lung and kidney in Wegener Granulomatosis?
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Lungs - necrotizing granulomas in parenchyma, capillaritis, and necrotizing granulomas in vasculitis with or without fibrinoid necrosis in small and medium-sized vessels
Kidney - focal necrotizing crescent glomerulonephritis |
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For P-ANCA, is it cytoplasmic or perinuclear for IIF on ethanol-fixed PMNs? Formalin-fixed PMNs? In EIA, is it anti-MPO or anti-PR3?
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P-ANCA
IIF on ethanol-fixed PMN = perinuclear IIF on formalin-fixed PMN = cytoplasmic Anti-MPO |
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For C-ANCA, is it cytoplasmic or perinuclear for IIF on ethanol-fixed PMNs? Formalin-fixed PMNs? In EIA, is it anti-MPO or anti-PR3?
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IIF on ethanol-fixed PMN = cytoplasmic
IIF on formalin-fixed PMN = cytoplasmic Anti-PR3 |
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For Wegener Granulomatosis, what signs may be seen on a CXR?
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Multiple cavitary lesions
Fluid in the cavity |
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What are some histological signs of Wegener Granulomatosis?
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RBC and proteinaceous exudate in the alveolar spaces
Increased PMNs and other inflammatory cells in the alveolar walls Iron stain will reveal many hemosiderin-filled macrophages ~2 days post-bleed Necrotizing granulomatous inflammation |
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What other names are there for Churg-Strauss Vasculitis?
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Allergic Granulomatosis
Angiitis |
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What are the clinical findings for Churg-Strauss Vasculitis?
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Patient Hx of allergic rhinitis, asthma
Infrequent renal involvement May manifest after oral steroid therapy for asthma has been discontinued |
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What are some laboratory findings for Churg-Strauss Vasculitis?
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High blood eosinophils
Positive P-ANCA (anti-neutrophil cytoplasmic antigen with perinuclear distribution directed against neutrophil primary granules, mainly MPOs) in 50% of patients |
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What are the general morphological findings for Churg-Strauss Vasculitis?
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Granulomatous inflammation, necrotizing vasculitis, eosinophils - affecting small vessels and perivascular tissues in the upper respiratory tract, lung (eosinophilic pneumonia), heart, spleen, GI-tract, skin, peripheral nerves
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What is the typical cause of death for a patient with Churg-Strauss Vasculitis?
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Coronary Arteritis
Myocarditis |
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What is characteristic of bronchoalveolar lavage fluid in a patient with Churg-Strauss Vasculitis, especially with lung involvement?
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Siderophages
Numerous Eosinophils Charcot-Leyden Crystal |
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What histological signs are present with Churg-Strauss allergic angiitis?
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Inflammation in the vascular wall
Necrotizing granulomas Multinucleated giant cells, eosinophils |
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What are two kinds of Large-Vessel Vasculitis (affecting Aorta, large branches to extremities, head and neck)? Briefly describe each.
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Takayasu - usually in younger patients - Gran. inf.
Giant Cell (temporal) Arteritis - Often involves temporal artery, patients over 50, associated with polymyalgia rheumatica. Gran. inf. |
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What are two kinds of Medium-Vessel Vasculitis (affecting main visceral arteries and their branches)? Briefly describe each.
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Polyarteritis nodosa (PAN) - Necrotizing inflammation, usually involves renal arteries but spares pulmonary vessels
Kawasaki - arteritis with mucocutaneous lymph node syndrome, usually in children, coronary artery involvement with aneurysm and/or thrombosis - also strawberry tongue, redness on mucus membranes |
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What are three kinds of Small-Vessel Vasculitis (affecting arterioles, venules, capillaries, small arteries)? Briefly describe each.
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Wegener - Gran. inf. involving respiratory tract, necrotizing vasculitis in small vessels, including glomerular vessels. Associated with PR3-ANCAs.
Churg-Strauss - Eosinophil-rich Gran. inf. involving the respiratory tract and necrotizing vasculitis of small vessels, associated with asthma and blood eosinophilia. Associated with MPO-ANCAs. Microscopic polyangiitis - necrotizing small-vessel vasculitis with few or no immune deposits, necrotizing arteritis of small/medium arteries, necrotizing glomerulonephritis and pulmonary capillaritis are common, associated with MPO-ANCAs. |
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Briefly describe Giant Cell (Temporal) Arteritis.
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Large vessel vasculitis.
Often involves temporal artery, patients over 50, associated with polymyalgia rheumatica. Granulomatous inflammation. |
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Briefly describe Takayasu disease.
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Large-Vessel Vasculitis
Usually affects patients younger than 50, characterized by granulomatous inflammation. |
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Briefly describe Polyarteritis nodosa.
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Medium-Vessel Vasculitis
Necrotizing inflammation, usually involves renal arteries but spares pulmonary vessels |
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Briefly describe Kawasaki disease.
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Medium-Vessel Vasculitis
Arteritis with mucocutaneous lymph node syndrome, usually in children, coronary artery involvement with aneurysm and/or thrombosis - also strawberry tongue, redness on mucus membranes. |
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Briefly describe Wegeners Granulomatosis.
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Small-Vessel Vasculitis
Granulomatous inflammation involving respiratory tract, necrotizing vasculitis in small vessels, including glomerular vessels. Associated with PR3-ANCAs. |
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Briefly describe Churg-Strauss vasculitis.
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Small-Vessel Vasculitis
Eosinophil-rich granulomatous inflammation involving the respiratory tract and necrotizing vasculitis of small vessels, associated with asthma and blood eosinophilia. Associated with MPO-ANCAs. |
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Briefly describe Microscopic polyangiitis.
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Small-Vessel Vasculitis
Necrotizing small-vessel vasculitis with few or no immune deposits, necrotizing arteritis of small/medium arteries, necrotizing glomerulonephritis and pulmonary capillaritis are common, associated with MPO-ANCAs. |
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What is Idiopathic Pulmonary Fibrosis (IPF)? Other names for it?
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Idiopathic Pulmonary Fibrosis (IPF) aka Usual Interstitial Pneumonia (UIP), Cryptogenic fibrosing alveolitis
Unknown etiology, insidious onset, characterized by diffuse interstitial fibrosis. Patchy recurring alveolitis, heals by fibrosis, lesions of different ages are present, immune mechanism suspected |
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What is the most common demographic (age, gender) that presents with IPF?
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Males > Females
60% of patients are 60+ years old |
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Describe the CXR of a patient with IPF.
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Reduced lung volume
Reticulo-nodular infiltrates - more prominent in lower lobes Larger heart |
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What lung condition(s) may be indicated by clubbing of the fingers?
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Chronic Lung Disease
Restrictive Lung Disease ~50% of patients with IPF develop clubbing, also patients with asbestosis |
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Describe the histology of the lungs in IPF.
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Atypical alveolar lining cells
Remodeling of the lung Interstitial Fibrosis (especially visualized with thrichrome stain, bluish color) Sparse mononuclear inflammatory infiltrates Irregular air spaces Honey comb lung (end stage) - also associated with cor pulmonale, pulmonary embolus |
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What is Cryptogenic Organizing Pneumonia (COP)? Any other names? Histological features?
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COP, aka Bronchiolitis Obliterans Organizing Pneumonia (BOOP)
Clinically - cough and dyspnea Histology - Polypoid plugs of connective tissue (fibroblasts) in alveoli and bronchioli, all the same age (unlike UIP/IPF which has older lesions as well as newer ones), no honey comb changes (usually) |
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Since COP is kind of a disease of exclusion, what other possibilities should be considered and ruled out before considering COP?
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Infection
Organizing DAD Bronchial Obstruction Aspiration Pneumonia Hypersensitivity Pneumonia Drug Reaction Toxic Gas Bone Marrow/Lung/Heart transplantation |
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List at least 5 types of granulomatous inflammation in the lungs.
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Tuberculosis
Fungal infections Sarcoidosis Wegener granulomatosis Churg-Strauss allergic angiitis and granulomatosis |
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What is Sarcoidosis?
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Sarcoidosis - an uncommon idiopathic systemic granulomatous disease.
Often affects the lung and causes respiratory insufficiency, lesions are non-caseating granulomas without identifiable organisms of any kind. Commonly distributed along the bronchovascular bundle or adjacent to the pleura. Hilar nodes usually affected. Sarcoidosis may "burn out" but leaves a scarred, fibrotic lung. |
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What is the epidemiology for Sarcoidosis?
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Patients are often younger than 40 years old
Danes, Swedes, and African Americans have a higher incidence Higher prevalence in non-smokers? |
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What is the proposed etiology/pathogenesis? What cells may be involved?
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Disordered immune regulation in genetically predisposed individuals exposed to environmental agents
Cell-mediated response to an unidentified antigen is proposed: Oligo-clonal expansion of T-cell subsets Intra-alveolar and interstitial accumulation of CD4+ T-cells BAL: CD4/CD8 > 2.5; CD3/CD4 < 0.31 TNF is released from activated alveolar macrophages TNF-level in BAL is a marker of disease activity Systemic immunological abnormalities: Anergy to common skin test antigens (Candida or PPD) due to pulmonary recruitment of CD4+ T-cells Polyclonal hypergammaglobulinemia |
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What organs are commonly affected in Sarcoidosis?
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Lungs
Lymph nodes Spleen Liver Bone Marrow Skin Eye: Iritis or iridocyclitis Salivary glands: Mikulicz syndrome (combined uveoparotid involvement) Muscle |
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What is Acute Restrictive Lung Disease?
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Clinically acute respiratory distress syndrome (ARDS)
Morphologically diffuse alveolar damage (DAD) It is the most common cause of non-cardiogenic pulmonary edema. A continuum of progressive respiratory failure, occurs in several clinical settings, associated with direct injury to the lung or indirect injury from a systemic process. |
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What is the most common cause of non-cardiogenic pulmonary edema?
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Acute Restrictive Lung Disease
ARDS, DAD |
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About how many people are affected by ARDS, DAD each year? What is the mortality rate?
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~150,000 people per year
60% mortality rate |
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What are the clinical features of ARDS, DAD?
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Patient usually already hospitalized, from trauma or underlying medical problem
Acute onset of dyspnea and tachypnea Ventilation-perfusion mismatch Cyanosis due to decreased arterial oxygen pressure (hypoxemia) Development of bilateral diffuse pulmonary infiltrates (ground-glass X-Ray) Absence of clinical evidence of primary left-sided failure |
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What is the etiology of ARDS/DAD (many)?
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Diffuse pulmonary infection (viral, mycoplasmal, pneumocystis, miliary TB)
Aspiration of gastric contents Sepsis Severe trauma with shock, head injuries, near drowning, fractures with fat embolism, severe burns Direct injury to the lungs, pulmonary contusions, radiation Drug overdose - heroin, methadone, acetylsalicylic acid, barbiturates Inhaled irritants and gases - smoke, oxygen, chlorine Chemicals - Paraquat Hematologic conditions - multiple transfusions, DIC Metabolic disturbances - pancreatitis, uremia Reperfusion after cardiopulmonary bypass Hypersensitivity reactions - organic solvents, drugs |
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What is the underlying mechanism of ARDS/DAD?
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An imbalance of pro-inflammatory and anti-inflammatory mediators
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In ARDS/DAD what happens to the alveolar capillary walls?
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Diffuse damage to alveolar capillary walls - increased vascular permeability, alveolar flooding
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In ARDS/DAD, what is the effect of Type I and II pneumocyte injury?
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loss of surfactant
loss of diffusion capacity (hypoxemia), collapse of alveoli (ventilation-perfusion mismatch) increased vascular permeability sequestration of neutrophils release of inflammatory cytokines alveolar flooding |
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What inflammatory cytokines are released in ARDS/DAD?
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IL-8 synthesis by pulmonary macrophages, IL-1, TNF
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What fibrogenic cytokines are released in ARDS/DAD?
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Macrophage-derived transforming growth factor beta (TGF-b)
Platelet-derived growth factor (PDGF) |
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True or False - Hyaline membrane formation is seen in DAD/ARDS?
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True
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In DAD/ARDS, what is the effect of releasing proteases, oxidants, platelet activating factor (PAF), leukotrienes, macrophage inhibitory factor (MIF)?
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Active tissue damage
Accumulation of edema fluid Inactivation of surfactant Maintenance of the inflammatory cascade |
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True or False - neutrophils are absent in DAD/ARDS?
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False
Neutrophil sequestration and activation occurs |
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What kind of chest x-ray feature is characteristic of DAD/ARDS?
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BIlateral fluffy ground-glass infiltrates
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What is occurring during the exudative stage of ARDS/DAD?
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Hyaline membranes line the alveoli
Damaged type I and II pneumocytes are sloughing off Plasma proteins leak into alveoli and form hyaline membranes *May occur post-chemotherapy/myeloid leukemia* |
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What is happening in the proliferative stage of ARDS/DAD?
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Started about 9 days after beginning of symptoms
No normal lung parenchyma is present Alveolar walls are diffusely widened Grossly - the lungs are dark red Beginning organization of plugs and fibroblasts inside the alveoli, obliterate the alveoli Beginning fibrosis, prominent type II cell hyperplasia - they replace the damaged type I cells |
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In what stage of ARDS/DAD does lung consolidation occur?
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The proliferative/organizing stage
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Describe the gross appearance of the lungs in the FIBROTIC stage of DAD/ARDS?
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Dense, airless, heavy "carnified" meaty lungs
Dense yellow areas may also be present |
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How does ARDS/DAD progress pathologically?
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Type I cells die as a result of diffuse alveolar damage DAD
Intra-alveolar edema follows, then formation of hyaline membrane with proteinaceous exudate and cell debris In the acute phase, the lungs are markedly congested and heavy Type II cells multiply to line the alveolar surface Interstitial inflammation is characteristic The lesion may heal completely or progress to interstitial fibrosis |
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Compare the healing of lung lesions in viral vs bacterial pneumonia.
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Uncomplicated bacterial pneumonia - complete resolution is the usual outcome, because the alveolar wall is not damaged
Severe viral pneumonia may result in fibrosis |
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What general process may lead to interstitial fibrosis and remodeling of the lung?
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Significant or continuous injury to the alveolar wall for whatever reason may lead to interstitial fibrosis and remodeling
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How does alveolitis play a role in restrictive lung diseases?
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Alveolitis is the primary problem in restrictive lung diseases regardless of specific cause or interstitial disease
If it is mild or self-limiting, healing may be complete, but if it is severe or even ongoing low-grade alveolitis, there will be fibrosis |
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What is the role of pulmonary macrophages in the development of pulmonary fibrosis?
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Chemoattractants from the activated macrophages activate and recruit PMNs (IL-8, LTB4).
Oxidants and proteases from macrophages and PMNs injure type I pneumocytes and degrade lung scleroproteins. |
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How do type II pneumocytes behave with regard to the lung tissue and macrophages in the development of pulmonary fibrosis?
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Type II pneumocytes proliferate, repair the epithelium
They secrete chemotactic and growth factors that attract more macrophages to alveoli and stimulate fibroblast growth (PDGF, TGF-b) |
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What are some chronic interstitial lung diseases that cause fibrosis?
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Pneumoconioses
Collagen vascular diseases and associated lung diseases Drug reactions Radiation pneumonitis Idiopathic pulmonary fibrosis - aka cryptogenic fibrosing alveolitis - histologic pattern of UIP and exclusion of all other causes are required for IPF Cryptogenic organizing pneumonia (COP) aka bronchiolitis obliterans organizing pneumonia (BOOP) Non-specific interstitial pneumonia |
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What are some categories of chronic interstitial lung disease which have granulomatous inflammation?
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Sarcoidosis
Hypersensitivity Pneumonitis |
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What are some eosinophilic chronic interstitial lung diseases?
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Eosinophilic pneumonia
Loffler syndrome Chronic eosinophilic pneumonia Tropical eosinophilia Secondary eosinophilia due to parasitic, fungal, and bacterial infections Asthma Drug allergies |
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What are some occupational and environmental exposure-caused chronic interstitial lung diseases?
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Asbestosis
Silicosis Coal Worker's Pneumoconiosis Hypersensitivity Pneumonitis |
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What are some Post DAD Immunologic Lung Diseases?
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Sarcoidosis
Collagen Vascular Diseases Wegener Granulomatosis Goodpasture syndrome Allograft rejection |
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What is the gross morphology of lungs in patients with rheumatoid arthritis and associated pulmonary fibrosis?
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Nodular surface, evidence of fibrosis
Honeycomb lung - visible when sliced |
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What is Pneumoconiosis? How is it caused?
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These are diseases induced by inorganic and organic particulates and chemical fumes and vapors
Development depends on... The amount of dust retained in the airways and lung parenchyma The size and shape of particles - most dangerous ones are 1-5micrometers, since they can reach the terminal airways and alveoli Particulate solubility and physiochemical reactivity Additional effects of other irritants, such as tobacco smoke |
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What are some mineral dusts associated with lung disease?
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Coal dust
Silica Asbestos Beryllium Iron Oxide Barium Sulfate |
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What are some organic dusts that induce hypersensitivity pneumonitis?
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Moldy hay, bagasse, bird droppings
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What are some organic dusts that induce asthma?
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Cotton
Flax Hemp Red Cedar Dust |
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What are some chemical fumes and vapors that are associated with lung disease?
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Nitrous oxide
Sulfur dioxide Ammonia Benzene Insecticides |
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How would anthracosis appear histologically?
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There is chronic congestion
Pigment in the macrophages within the bronchial wall, and in the peribronchovascular lymphatics due to inhalation of carbon particles (smoker) There is LACK of fibrosis |
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How would silicosis appear histologically?
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There are silicotic nodules - eosinophilic, nearly acellular, fibrotic
Thickened pleura Up to 5 mm palpable gray-white nodules and star shaped scars in the apical portion of the lung May be fibrinoid necrosis Bi-refringent crystalline material and carbon in the fibroblasts and macrophages |
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How would mixed dust pneumoconiosis appear grossly?
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Caused by Anthracosilicosis, Bullous emphysema
There are gray, black silicotic lesions |
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What is a gross feature(s) of anthracosilicosis?
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Silicotic granuloma - grey/black
Anthracosilicotic nodules, fibrotic |
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What is a histological feature of recreational silicosis in an IV drug user?
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Perivascular granuloma with a perivascular silica nodule
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How does asbestos in the lung develop into asbestosis?
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The asbestos fibers develop into asbestos bodies
Asbestos bodies are club-shaped and are coated with iron, as well as surrounded by macrophages attempting to phagocytose the fiber. Also known as a Ferruginous Body - not necessarily indicative of asbestosis, however |
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What may be visible in a CXR of a patient with asbestosis?
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Pleural plaques - calcified
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What kinds of inflammatory cells and lymphocytes are present in hypersensitivity pneumonitis in BAL?
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Increased number of mast cells, lymphocytes
Few macrophages Minimal increase in eosinophils 29% CD4 T cells, vs 83% CD8 T cells |
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How do the granulomas appear in hypersensitivity pneumonitis?
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Poorly formed
Multinucleated giant cells |
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Describe the gross appearance of "bird fancier's lung"
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Lung parenchyma is stiff and compact
Severe pulmonary fibrosis The pleural surface is nodular |
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What are some histological characteristics of Welder's Lung?
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Hemorrhages
Pigment deposits - carbon and iron from welding smoke and fumes Focal interstitial accumulations of siderophages, silicoanthrocotic pigment, moderate fibrosis TB test is negative, due to T cell sequestration |
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What is fibrin?
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the insoluble protein formed from fibrinogen by the proteolytic action of thrombin during normal clotting of blood; it forms the essential portion of the blood clot.
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What is fibrosis?
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the formation of fibrous tissue, as in repair or replacement of parenchymatous elements.
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What are the normal values for an arterial blood gas measurement (ABG)? pH, pCO2, HCO3-, pO2, SaO2?
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pH - 7.35-7.45
pCO2 - 35-45 mmHg HCO3- - 22-26 mmHg pO2 - 80-105 mmHg SaO2 - 94-100% |
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Is HCO3- calculated directly or indirectly?
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HCO3- is calculated from the Henderson-Hasselbalch equation - pCO2 and pH are measured directly
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What two blood tests are necessary to diagnose an acid-base disorder?
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Arterial Blood Gas
Serum Electrolytes |
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What values in the serum electrolyte panel and an ABG should be roughly the same?
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Calculated HCO3- from ABG should be within 3 mmol of the CO2 value from the serum electrolyte panel
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What are the four basic serum electrolytes?
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Na+
Cl- K+ CO2 |
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Why should serum CO2 and calculated HCO3- be roughly the same?
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Because of the dissociation characteristics of carbonic acid at body pH, dissolved CO2 is almost exclusively in the form of bicarbonate
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What is the Henderson-Hasselbalch equation for blood CO2 and pH?
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pH = 6.1 + log (HCO3- / (pCO2 x 0.03) )
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What is the primary disorder when pH is above the normal range? Below the normal range?
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Higher pH = Alkalemia
Lower pH = Acidemia |
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What is the primary disorder when pCO2 is above the normal range? Below the normal range?
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High pCO2 = Respiratory Acidosis
Low pCO2 = Respiratory Alkalosis |
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What is the primary disorder when HCO3- is above the normal range? Below the normal range?
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High HCO3- = Metabolic Alkalosis
Low HCO3- = Metabolic Acidosis |
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What kind of compensation exists if the pCO2 is abnormal?
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Respiratory Compensation
(in response to a primary metabolic process) |
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What kind of compensation exists if the HCO3- levels are abnormal?
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Metabolic Compensation
(in response to a primary respiratory abnormality) |
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What is the rule of thumb for recognizing primary acid-base disorders?
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Rule 1 - look at the pH - compensation mechanisms cannot return it entirely to normal, so whichever side of 7.4 it is on, indicates the type of shift and disorder.
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How does one differentiate between acute and chronic respiratory alkalemia or acidemia?
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In acute respiratory alkalemia/acidemia, the kidneys have not yet started compensating and HCO3- is still within normal limits
In chronic respiratory acidemia/alkalemia, the HCO3- is abnormally high or low because kidneys have begun compensating |
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What organ regulates the metabolic component of the arterial acid-base balance?
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The kidneys
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What organ regulates the pCO2 component in the arterial acid-base balance?
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The lungs - pulmonary ventilation
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What are some causes for respiratory alkalosis?
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Anxiety
Hypoxia Lung disease CNS disease Drugs - salicylates, catecholamines, progesterone Pregnancy Sepsis Hepatic Encephalopathy Mechanical Ventilation |
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What are some causes for acute respiratory acidosis?
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CNS depression - drugs, CNS event
Severe pneumonia, pulmonary edema Impaired lung motion - pneumothorax Thoracic injury - flail chest Acute airway obstruction Neuromuscular disorder Ventilator dysfunction |
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What are some causes for chronic respiratory acidosis?
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Chronic lung disease - obstructive or restrictive
Chronic neuromuscular disorders Chronic respiratory center depression - central hypoventilation |
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What are four major reasons to assess lung function?
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To detect pulmonary disease
To assess severity or progression of disease To do risk stratification of patients for surgery To evaluate disability |
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When would one suspect pulmonary disease?
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History of dyspnea, wheezing, chronic cough, orthopnea, chest pain
Evidence of chest wall abnormality, cyanosis, decreased breath sounds, clubbing Abnormal blood gas or chest imaging |
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What are some lung diseases for which a lung function test is useful for assessing severity or progression?
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COPD
Cystic fibrosis Interstitial lung disease Sarcoidosis |
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What is spirometry?
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Spirometry measures the volume of air exhaled or inhaled as a function of time.
It is a dynamic test of how fast the lung volume changes during forced breathing maneuvers |
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How is a spirometry test performed?
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The values are obtained by a patient forcefully expelling air from a point of maximal inspiration to a point of maximal expiration
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What general information about pulmonary functions can be determined by a spirometry test?
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It can determine whether pulmonary functions are normal, restricted, or obstructed
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What is Diffusing Capacity (DLCO)?
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Performed in a respiratory lab
The measurement of gas transfer function of the lungs, or the patient's ability to absorb alveolar gases |
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How is a Diffusing Capacity (DLCO) test performed?
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Patient inhales a known volume of gas (usually containing He, CO, O2, N2), and holds breath for 10 seconds. The patient exhales and the sample is collected.
The exhaled helium concentration is used to calculate the single-breath estimate of total lung capacity, and the initial alveolar concentration of carbon monoxide |
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How is Diffusing Capacity (DLCO) calculated?
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DLCO is calculated from total volume of the lung, breath-hold time, and the initial and final alveolar concentrations of carbon monoxide. Low DLCO requires measurement of hemoglobin concentration.
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What may be indicated by a decreased DLCO?
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COPD, anemia, lung resection
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What may be indicated by an increased DLCO?
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Anything that can increase pulmonary blood volumes, such as polycythemia, left-right cardiac shunt, etc.
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What is a maximal respiratory pressure test?
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In some diseases, it is very useful to test respiratory muscle strength
The maximum static mouth pressure made against an occluded airway is the most widely used and simple way of gauging respiratory muscle strength. |
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When is Oximetry performed and why?
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Pulse oximetry can be used at rest, during and after exercise - determines if desaturation occurs
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What is a cardiopulmonary exercise test (CPX)?
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This is used when exertional dyspnea is a symptom
The patient does a graded exercise to the point of exhaustion or other end point. May also determine if deconditioning is present. |
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What is measured in a CPX?
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Cardiac, ventilatory, and gas exchange responses are measured.
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Where are lung volumes and capacities tested?
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Lung volumes and capacities can only be measured in a pulmonary lab, usually tests are ordered by pulmonologists.
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What is FRC?
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Functional Reserve Capacity
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How is FRC measured?
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FRC is measured with gas diffusion techniques, like closed-circuit helium dilution or open-circuit nitrogen washout. Body plethysmography may also be used.
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What is body plethysmography?
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A patient is placed in a sitting position in a closed box with a known volume and pants with an open glottis against a closed shutter to produce changes in box pressure.
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What is RV?
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Reserve volume - volume remaining after maximal expiration
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What is TLC?
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Total lung capacity - the volume of air in the lungs at maximal inflation
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What is VC?
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Vital capacity - the largest volume measured on complete exhalation after full inspiration
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What values are considered lung volumes?
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ERV - expiratory reserve volume
IRV - inspiratory reserve volume RV - residual volume VT - tidal volume |
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What values are considered lung capacities?
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FRC - functional residual capacity
IC - inspiratory capacity TLC - total lung capacity VC - vital capacity |
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What values can be used to calculate TLC?
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TLC = IRV + VT + FRC
= IC + FRC = IC + ERV + RV = RV + VC |
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What values can be used to calculate RV?
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RV = TLC - VC
= FRC - ERV = TLC - (ERV + IC) = TLC - (IRV + VT + ERV) |
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What are the most important spirometric values measured?
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FVC, FEV1, FEV1/FVC ratio
Measured in liters |
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What is FVC?
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Forced vital capacity - the total volume of air that can be exhaled during a maximal forced expiration effort (sometimes referred to as Vital Capacity, VC)
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What is FEV1?
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Forced expiratory volume in one second - the volume of air exhaled in the first second under force after a maximal inhalation
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What is the FEV1/FVC ratio?
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The percentage of the FVC expired in one second - usually expressed as a whole number rather than a decimal.
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What is FEV6?
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The forced expiratory volume in 6 seconds - normal lungs can empty more than 80% of their volume in 6 seconds or less.
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What percentage of lung volume can normally be expelled in or under 6 seconds?
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80%
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What is FEF25%-75%?
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Forced expiratory flow over the middle one half of the FVC - useful in determining small airways narrowing.
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What does MVV stand for?
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Maximal voluntary ventilation
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How does a volume-flow loop curve in a patient with obstructive airway disease compare to a normal patient? What about patients with restrictive lung disease?
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Normal lung disease - curve is triangular above X-axis and a semicircle below X-axis
Obstructive airway disease - the overall length of the curve has increased, there is a sharper peak above the X-axis with a long trail, then a stretched semicircle beneath the X-axis Restrictive lung disease - a shortened version of the normal curve, more closely resembles a tear drop or upside down ice cream cone |
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Describe what characterizes an obstructive lung disorder.
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It is characterized by a limitation of expiratory airflow, so that airways cannot empty as rapidly compared to normal.
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What are some examples of obstructive lung disorders?
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Asthma
COPD Bronchiectasis Cystic Fibrosis |
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Describe what characterizes a restrictive lung disorder?
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It is characterized by reduced lung volumes/decreased lung compliance.
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What are some examples of restrictive lung disorders?
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Interstitial fibrosis
Scoliosis Obesity Lung Resection Neuromuscular Diseases Cystic Fibrosis |
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What combination FEV1/FVC, FVC, and FEV1 values suggests normal lungs? An obstruction disorder? A restrictive disorder? A mixed disorder?
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Normal: FEV1/FVC > 70, FVC 80-120% of predicted, FEV1 80-120% of predicted
Obstruction: FEV1/FVC < 70, FVC 80-120% of predicted, FEV1 < 100% of predicted Restrictive: FEV1/FVC > 70, FVC < 80% of predicted, FEV1 < 80% of predicted Mixed: FEV1/FVC < 70, FVC < 80% of predicted, FEV1 < 80% of predicted |
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If FEV1/FVC is below normal range, does this suggest restrictive or obstructive disorders?
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Below normal FEV1/FVC suggests an obstructive disorder.
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What is more common, a restrictive lung disorder or an obstructive lung disorder?
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Obstructive lung disorders
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If a patient has a normal FEV1/FVC ratio but the FVC is low (<80%) what does this suggest?
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The patient most likely has a restrictive lung disorder.
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Describe spirometry used in conjunction with bronchodilators.
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First you obtain a pre-bronchodilator flow-volume loop
Then you administer a bronchodilator, like albuterol, and obtain the flow-volume loop after a minimum of 15 minutes. Calculate percent change (usually of FEV1) If change is 12% or greater and there is at least 200ml increase in expired volume, it is considered a reversible disorder |
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How does reversibility differentiate asthma and COPD?
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COPD shows a lack of reversibility
Asthma shows reversibility |
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What percent change must be observed in FEV1 pre and post-bronchodilator spirometry tests to qualify as reversibility? What about expired volume?
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12% or greater
Expired volume must increase by at least 200ml |
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What is Bronchoprovocation?
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Bronchoprovocation is a test to rule out asthma if it is still a possible diagnosis even after a normal spirometry test.
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How is Bronchoprovocation performed? What constitutes a positive test?
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A patient is given 5 increasing doses of methacholine (or histamine) to induce airway hyperreactivity, each dose followed by spirometry.
A positive test is a decline of 20% in FEV1 following the 5th dosage. |
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What may cause a patient to have a false positive from bronchoprovocation?
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Allergic rhinitis, recent URI, etc - correlate the results with patient history.
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What is a disruption of normal architecture by an acute necrotizing inflammatory process?
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Abscess
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What may cause resorption atelectasis?
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Blockage of an airway (ie to a lug lobe or segment)
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What is a characteristic of CXRs that are often missed?
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Rib lesions
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If an elderly patient presents with bimodal illness (felt ill a week or two ago, then got better, now returns with similar symptoms as before), what does it suggest about his illness?
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An elderly patient is unlikely to recover untreated from a bacterial or viral infection and then get worse again
It is more likely to be a chronic or other underlying condition which manifests periodically, such as a pulmonary embolism throwing clots here and there. |
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Where should the end of the endotracheal tube be?
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2-3 cm above the carina
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Which vessel is most at risk during pneumothorax?
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Vena cava - veins are thin walled, so mediastinal shift from air filling the pleural cavity will compress or damage them more easily.
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If a patient presents acute infection and DIC, how would you control the diffuse clotting?
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Anticoagulant therapy - prevents clots, and loss of clotting factors.
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In what phase is Coccidiomycosis infectious?
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Only when it is freely growing - so in cultures or the environment. It is not infectious when a person is infected.
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What ethnic and/or racial groups have a higher risk of dissemination in Coccidiomycosis?
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Hispanics, African Americans, and Filipinos
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What is a useful stain for visualizing fungi?
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Silver stains - good at visualizing the endospore.
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With what are mesotheliomas most often associated with?
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Asbestos
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