Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
333 Cards in this Set
- Front
- Back
|
What are common causes of intrinsic and extrinsic asthma? What immune cell moderate each?
|
* Intrinsic: aspirin, infections, cold, stress, exercise. IL-4 & IL-5 stimulate IgE synthesis and mast cell and eosinophil growth and activation
* Extrinsic: Type I hypersensitivity. CD4+ Th2 cells |
|
|
Explain what happens during the early and late phases of an asthma exacerbation
|
Early: 30-60 min. Degradation of mucosal lining and epithelium. Allergen activates Th2 APC and releases cytokines (IL-4, IL-13, IL-5) which causes smooth muscle spasm, IgE isotype switching (allowing for mast cell degranulation), and eosinophil proliferation( leukotriene release). Result is bronchoconstriction, edema, and mucus secretion
* Late phase: 4-8 hours. Epithelial cells and macrophages produce TGF-ß increasing myofibroblast proliferation, smooth muscle hypertrophy, and secretory gland hyperplasia |
|
|
What are the two underlying pathologies of COPD?
|
* Emphysema: Acinar level. Permanent enlargement of airspaces resulting from fibrotic destruction within alveolar walls
* Chronic bronchitis: Bronchial level. Persistent increased bronchial mucus secretion with a productive cough |
|
|
The imbalance of what two enzymes is responsible for COPD?
|
Alpha-1 antitypsin is responsible for inhibiting elastase release from neutrophils.
|
|
|
Is emphysema an obstructive or restrictive disease? Inspiratory or expiratory?
|
Emphysema is a expiratory obstructive disease. The degradation of elastic tissue in the lung parenchyma reduces radial traction on the respiratory bronchioles and alveoli which collapse during expiration
|
|
|
Explain the pathophysiology of COPD
|
Chronic inflammation (cigarette smoke/pollution) triggers epithelial cells & macrophages to recruit neutrophils which degranulate releasing proteases (elastase, cathepsin, matrix metalloproteinase). These proteases overwhelm the protease inhibitor (a1-AT) causing emphysema (alveolar wall destruction leading to hyperinflation and air trapping) and chronic bronchitis (submucosal gland hyperplasia and mucus hypersecretion).
|
|
|
What is the criteria used to diagnose COPD?
|
Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines.
* A: FEV1≥50%, Minimal symptoms, Few exacerbations * B: FEV1≥50%, Severe symptoms, Few exacerbations * C: FEV1<50%, Minimal symptoms, 2≤ exacerbations * D: FEV1<50%, Severe symptoms, 2≤ exacerbations |
|
|
Hyperinflation in COPD leads to a change in which lung volume?
|
Air trapping leading to hyperinflation of the lungs increases the lung's residual volume
|
|
|
What are the treatment recommendations for COPD?
|
* A: Short-acting bronchodilator (albuterol) as needed
* B: Daily long-acting bronchodilator (formoterol/salmeterol)+ SA bronchodilator * C: Daily inhaled corticosteroid (budesonide, fluticasone)/LA bronchodilator (symbicort, advair, spiriva) + SA bronchodilator * D: PDE4i + ICS + LA/SA bronchodilator |
|
|
What two things have been shown to increase survival in COPD patients?
|
Smoking cessation and O2 (if hypoxemic)
|
|
|
Can you diagnose an obstructive disease with spirometry? Restrictive?
|
Spirometric indices (FEV1/FVC) define obstructive diseases, but can only suggest a restrictive disease
|
|
|
Will FEV1 be decreased in obstructive disease? Restrictive? How about FVC? FEV1/FVC?
|
In obstructive disease, FEV1, FVC, and FEV1/FVC will all be decreased. In restrictive disease, FEV1 and FVC will both be decreased, but the FEV1/FVC ratio can be normal or even high
|
|
|
What are some intra and extrapulmonary causes of reduced total lung capacity?
|
* Intrapulmonary: pneumonectomy, collapsed lung, consolidation, edema, fibrosis
* Extrapulmonary: pleural disease, rib cage abnormality, respiratory muscle weakness, gross abdominal distention, severe obesity |
|
|
What are some intra and extrapulmonary causes of increased residual volume?
|
Intrapulmonary: Generalized airway obstruction, pulmonary vascular congestion, mitral stenosis
Extrapulmonary: Expiratory muscle weakness (spinal injury, myopathy) |
|
|
Will intrapulmonary lesions cause inspiratory or expiratory obstructions? Extrapulmonary? Why?
|
Intrapulmonary lesions will cause expiratory flow obstructions as the intrathoracic pressure increases during expiration.
Extrapulmonary lesions will cause inspiratory obstructions as inspiration increases tracheal pressure |
|
|
What does DLCO test and how do [hemoglobin], [carboxyhemoglobin], and PiO2 affect the DLCO?
|
Diffusing capacity of the lung for CO. Measures the rate of CO uptake into the blood and estimates driving pressure for CO from alveoli to capillary blood. An increase in hemoglobin concentration increases the DLCO. A increase in carboxyhemoglobin or PiO2 decreases the DLCO.
|
|
|
What are some common conditions with low DLCO? High DLCO?
|
* Low DLCO: Obstructive (emphysema, cystic fibrosis, bronchiolitis) and Restrictive (diffuse parenchymal lung disease, pneumonitis, alveolitis)
* High DLCO: asthma, obesity, intrapulmonary hemorrhage |
|
|
How are maximal respiratory pressures measured?
|
Maximal inspiratory and expiratory pressures are measured by the patient trying to inhale or forcing an exhale through a blocked mouthpiece
|
|
|
What is the ideal particle size for airway deposition?
|
0.5-5µm is the optimal size for clinical benefit. Larger than 5µm and the particle will likely be swallowed and systemically absorbed. Smaller than 0.5µm and the particle will likely pass through the terminal bronchioles and be systemically absorbed through the alveoli
|
|
|
How does the delivery of medication differ between CFC, HFA, and DPI inhalers?
|
CFC and HFA inhalers are dose-dependent and the propellant administers the drug to the site of action. DP inhalers utilize the patient's inspiratory flow to deliver the "unit dose" of the drug
|
|
|
What is the mechanism of ß-receptor agonists?
|
ß-agonists interact with G-coupled receptors on bronchial smooth muscle cells and trigger smooth muscle relaxation (bronchodilation)
|
|
|
How does the chemical structure of albuterol differ from salmeterol and formoterol and how does that difference affect it's action.
|
Albuterol is a ß-agonist with a short side chain, making it less hydrophobic and less likely to stay in the lipid bilayer, this gives it a quick onset. Formoterol has a medium side chain and sameterol has a long side chain. This increases their hydrophobicity and affinity for the lipid membrane, slowing their onset of action and increasing the duration
|
|
|
What is the mechanism of action of budesonide, beclomethasone, fluticasone, and ciclesonide?
|
Inhaled corticosteroids. They passively diffuse across the lipid membrane, bind and activate their glucocorticoid receptor which dimerizes, travels to the nucleus and acts a transcription factor for increased anti-inflammatory elements
|
|
|
Which two inhaled corticosteroids use a prodrug characteristic to decrease oropharyngeal side effects?
|
Budesonide and Ciclesonide
|
|
|
How does adding a LABA to an ICS affect it's mechanism?
|
They complement each other. ß-agonists can prime steroid receptors so it takes less steroid for activation. Also, the ß-agonist primed steroid receptor will increase ß-receptor synthesis in addition to anti-inflammatory elements
|
|
|
What is the mechanism of action for Zileuton and how does it differ from Montelukast & Zafirlukast?
|
Leukotriene modifiers. They all disrupt the arachidonic acid pathway. Zileuton inhibits 5-lipoxygenase from metabolizing leukotrienes. Montelukast & Zafirlukast are leukotriene D4 receptor antagonists
|
|
|
What affects do leukotrienes have in asthma?
|
They increase permeability of blood vessels, increase mucus secretion and decrease it's transport, trigger smooth muscle contraction and proliferation, and recruit eosinophils which leads to epithelial cell damage
|
|
|
What is the mechanism of action of tiotropium and ipratropium?
|
They are muscarinic antagonists, decreasing vagal tone. They relax bronchial smooth muscle, reducing bronchospasm and mucus secretion. Good for COPD.
* Tiotropium: long-acting * Ipratropium: short-acting |
|
|
What is the mechanism of action of theophylline?
|
Methylanthine. Phosphodiesterase inhibitor causing bronchodilation
|
|
|
What is the mechanism of action of nedocromil and cromolyn?
|
They are mast cell stabilizers. Were used for exercise-induced asthma. No longer used.
|
|
|
What is the mechanism of action of omalixumab?
|
It is an IgE immunomodulator. It is a monoclonal antibody that binds free IgE, reducing the IgE bound to mast cells, decreasing the mast cell's response to an allergen
|
|
|
What is the gender and racial breakdown of asthma in the US?
|
Males get asthma when they are younger but women tend to remain asthmatic. Puerto Ricans and non-hispanic Blacks have the highest prevalence. Blacks have the highest mortality rate
|
|
|
What is the temporal pattern of airway obstruction in asthma?
|
Episodic and reversible, responding to a variety of stimuli
|
|
|
What are the main effector cells in allergic asthma?
|
Eosinophils and mast cells. Triggered by Th2 pathobiology
|
|
|
What is the main effector cell in nonallergic asthma?
|
Neutrophils, triggered by Th1 of Th17, cause airway remodeling
|
|
|
What are the 3 classic asthma symptoms?
|
Episodic. Cough (at night, in cold, paroxysmal), wheezing (chest tightness, noisy breathing), breathlessness (intermittent, after exertion, at night)
|
|
|
What are the 4 classes of asthma severity and what step should each class be started at when initiating treatment?
|
* Intermittent: ≤2 days/wk, normal lung function in between exacerbations. Step 1 (SABA)
* Mild Persistent: >2 days/wk, minor function interference, >2 exacerbations/yr. Step 2 (low-dose ICS) * Moderate Persistent: Daily, functional limitations, decreased lung function, >2 exacerbations/yr. Step 3 (med-dose ICS or low-ICS/LABA) * Severe Persistent: Multiple times daily, extremely functionally limited, >2 exacerbations/yr. Step 4+ (med-dose ICS+LABA) |
|
|
What are the guidelines for changing asthma treatment based on therapeutic control?
|
* Well controlled: Maintain and consider stepping down
* Not well controlled: Step up 1 step and reevaluate * Very poorly controlled: Consider short course of oral corticosteroid. Step up 1-2 steps |
|
|
What is pulmonary hypoplasia and what are some of its causes?
|
Incomplete of defective development of lung, causing fewer acinar units. Causes include thoracic constriction or compression, intrathoracic lesions, or diaphragmatic hernia,
|
|
|
What are the 3 common congenital abnormality syndromes associated with tracheoesophageal fistulas?
|
VATER: vertebral, anus (inperforate), tracheoesophageal, renal
VACTER: vertebral, anus (inperforate), cardiac, tracheoesophageal, renal * VACTERL: vertebral, anus (inperforate), cardiac, tracheoesophageal, renal, limb (radial agenesis) |
|
|
Do pulmonary sequestrations receive systemic or pulmonary circulation?
|
Pulmonary sequestrations receive systemic arterial supply
|
|
|
What are the different etiologies of extra and intralobar pulmonary sequestrations?
|
* Extralobar: congenital lesion sequesters lung tissue outside visceral pleura
* Intralobar: lesion acquired after 20 year sequesters lung tissue inside visceral pleura |
|
|
What is the epidemiology of extralobar pulmonary sequestrations?
|
Male predominace. Associated with pulmonary hypoplasia, diaphragmatic hernia, cardiovascular malformations, pectus excavatum
|
|
|
How do you differentiate CPAM from extralobar pulmonary sequestrations?
|
Extralobar pulmonary sequestrations will be surrounded by its own visceral pleura, Congenital Pulmonary Airway Malformation (CPAM) will not.
|
|
|
What histologic changes are seen in intralobar pulmonary sequestrations?
|
Chronic infection, lymphoid hyperplasia, foamy macrophages, and fibrosis
|
|
|
What is CPAM, how is it characterized, and what is its gross appearance?
|
* Congenital Pulmonary Airway Malformation is a hamartomatous (maldeveloped) mass of disorganized lung tissue.
* It's characterized based on where in the tracheobronchial tree it occurs (0: trachea - 4: alveoli). * Spongy mass of abnormal tissue comprised of small, enclosed cysts and adjacent darker atelectatic tissue * Dilated bronchiole-like structures surrounded by alveoli-like structures |
|
|
What is bronchiectasis and what are some diaseases it's associated with?
|
Dilation of bronchi/bronchioles due to destruction of elastic tissue and muscle. Associated with cystic fibrosis, Kartagener syndrome, obstructions, fungal infections, some autoimmune disorders
|
|
|
What is the genetic mutation in cystic fibrosis and how does it lead to the disease pathology?
|
Cystic fibrosis is caused by an autosomal recessive deletion of a phenylalanine residue at amino acid 508 on chromosome 7, leading to a mutated cystic fibrosis transmembrane receptor. This mutation affects a Cl- transporter that normally allows for the transport of Cl- out of the cell allowing for a sodium-water-chlorine balance. This mutated Cl- transporter causes a Cl- backup within the cell, causing an influx of Na+ and H20 into the cell dehydrating the mucus in the airway. This dehydrated mucus leads to mucus plugs and widespread bronchiectasis, especially in the upper lobes
|
|
|
What are some common pulmonary complications from cystic fibrosis?
|
Atelectasis, pneumothorax, hemoptysis, acute and chronic respiratory failure, cor pulmonale
|
|
|
What is the pathology of primary ciliary dyskinesia and what is a common subset syndrome?
|
Absent or shortened dynein arms of the cilia lead to absence of radial spokes and microtubular disarrangement or absence. These abnormalities lead to absent, scattered, and uncoordinated ciliary movement. A subset of primary ciliary dyskinesia, seen in 50% of cases is Kartagener's syndrome (bronchiectasis, sinusitis, and situs inversus)
|
|
|
What is the Reid index used to classify and how is it measured?
|
The Reid index is used to quantify the submucosal gland hypertrophy seen in chronic bronchitis. It measures the thickness of the submucosal wall to the submucosal glands as a ratio. Normal ratio is ~0.4
|
|
|
Is a1-AT deficiency associated with centrilobular or panacinar emphysema?
|
a1-AT deficiency is associated with panacinar emphysema
|
|
|
Do blebs arise from the lung parenchyma or visceral pleura?
|
Blebs arise from visceral pleura
|
|
|
Do bullae arise from the lung parenchyma or visceral pleura?
|
Bullae arise from lung parenchyma
|
|
|
What is the general function of the conducting portion of the respiratory system vs. the respiratory portion of the respiratory system?
|
The conducting portion warms, moisturizes, and filters the air, serving as a protective and conditioning barrier. The respiratory portion is responsible for gas exchange.
|
|
|
What is the structure of the respiratory mucosa?
|
* Pseudostratified columnar epithelium: goblet cells, ciliated cells, basal cells, neuroendocrine cells, and brush cells
* Lamina propria: thin-walled venous sinuses that adjust air to body temperature via heat exchange * Submucosa: mucous and serous glands that humidify air and aid in filtering |
|
|
What sections of the respiratory system have a different type of epithelial layer?
|
The oropharynx, the laryngopharynx, and the vocal folds are exposed to high speed airflow and/or physical abrasion and therefore are covered in stratified squamous epithelium
|
|
|
What are the general changes in epithelial and sub-epithelial components of the airway as you progress towards the alveoli?
|
There are decreases in mucus-producing components, epithelial height, and subepithelial connective tissue
|
|
|
What is the last level of the respiratory system where gland and cilia are present?
|
The bronchi
|
|
|
What are the definitions of primary and secondary pulmonary lobules and a pulmonary acinus?
|
* 1˚ pulmonary lobule is the volume distal to one respiratory bronchiole
* Pulmonary acinus is the volume distal to one terminal bronchiole * 2˚ pulmonary lobules are the smallest unit bound by the connective tissue of an interlobular septum |
|
|
How do the mucosal epithelium and goblet cells change in the bronchioles?
|
* The mucosa changes from pseudostratified columnar to simple cuboidal epithelium
* Goblet cells disappear, replaced by Clara cells, which secrete a surfactant-like substance |
|
|
What are the roles of type I and type II pneumocytes?
|
Type I: Simple squamous cells that permit gas exchange
Type II: Epithelial cells responsible for producing surfactant, preventing alveolar collapse and surface adherence |
|
|
What is the name of the physical opening allowing for the communication of adjacent alveoli?
|
Pores of Kohn
|
|
|
Name the three blood vessels associated with the respiratory system and describe their path and what they look like
|
* Bronchial arteries: afferent, small vessels that travel with the bronchial tree and are within the wall of the bronchus
* Pulmonary arteries: afferent, large, thick-walled vessels that travel with the bronchial tree * Pulmonary veins: efferent, large, thin-walled vessels that are located in the margins of lobules, then follow larger bronchi |
|
|
What are dust cells?
|
Lymphocytes and macrophages that exist in the airway and fight contamination by microorganisms and ingest excess surfactant.
|
|
|
What type of immune cells do Th1 cells activate? Th2? Th17?
|
* Th1: B-cells
* Th2: B-cells, mast cells, eosinophils * Th17: Neutrophils |
|
|
Is hypersensitivity pneumonitis Th1-related or Th2-related? Granulomatous or not?
|
Hypersensitivity pneumonitis is a Th1-related inflammatory condition
|
|
|
Is chronic obstructive pulmonary disorder Th1-related or Th2-related? Granulomatous or not?
|
Chronic obstructive pulmonary disorder is a Th1-related inflammatory condition
|
|
|
Are sarcoidosis and berylliosis Th1-related or Th2-related? Granulomatous or not?
|
Sarcoidosis and berylliosis are Granulomatous Th1-related inflammatory condition
|
|
|
Is allergic rhinitis Th1-related or Th2-related? Granulomatous or not?
|
Allergic rhinitis is a Th2-related inflammatory condition
|
|
|
Is asthma Th1-related or Th2-related? Granulomatous or not?
|
Asthma is a Th2-related inflammatory condition
|
|
|
Is allergic bronchopulmonary aspergillosis Th1-related or Th2-related? Granulomatous or not?
|
Allergic bronchopulmonary aspergillosis is a Th2-related inflammatory condition
|
|
|
Is Churg-Strauss Th1-related or Th2-related? Granulomatous or not?
|
Churg-Strauss is a Granulomatous Th2-related inflammatory condition
|
|
|
What are the characteristics of Allergic Rhinitis?
|
Allergic rhinitis is characterized by nasal congestion, rhinorrhea, sneezing, itching of the nose and/or postnasal drainage
|
|
|
Which two cytokines are responsible for most of the symptoms in rhinitis?
|
* Histamines: Itching, sneezing, nasal congestion, stuffy nose, runny nose, postnasal drip
* Leukotrienes: Sneezing, nasal congestion, stuffy nose, runny nose, postnasal drip |
|
|
What are the main pharmacologic therapies for rhinitis?
|
Oral or nasal antihistamines, nasal corticosteroids, oral anti-leukotrienes, nasal anti-cholinergic (ipratropium), mast-cell stabilizers (cromolyn)
|
|
|
What usually causes the inflammation in acute and chronic sinusitis?
|
Acute sinusitis is usually caused by infection, but not always bacterial. Chronic sinusitis is usuall NOT caused by an infection
|
|
|
What cytokines are prevalent in nasal polyps in the context of sinusitis?
|
Polyp tissue will contain a predominance of Th2 cytokines (IL-5, IL-13), histamine, and eosinophils
|
|
|
Does allergic fungal sinusitis occur in the immunocompetent or immunocompromised host, what causes it, what is its diagnostic feature, and what treatment is indicated?
|
Allergic fungal sinusitis occurs in immunocompetent patients and is caused by a hypersensitivity response to saprophytic fungi like aspergillus. It is diagnosed with a positive fungal skin test or increased total serum IgE and is treated by surgical exenteration of the dark-green or black "allergic mucin"
|
|
|
What immune cells are responsible for hypersensitivity pneumonitis and what are some common triggers?
|
CD4+ Th1 and CD8+ lymphocytes cause alveolitis and result in non-caseating granulomas and pulmonary fibrosis. Irritants include fungi, bird droppings, hay, HVAC contamination, wood bark, grain vaporizers
|
|
|
What are the acute, subacute, and chronic presentations of hypersensitivity pneumonitis?
|
* Acute: Cough, fever, chills, malaise, dyspnea 6-8 hrs post inhalation, clears within a few days
* Sub-acute: Insidious, cough, dyspnea, hypoxemia * Chronic: Progressive cough and dyspnea |
|
|
Is hypersensitivity pneumonitis restrictive or obstructive?
|
Restrictive
|
|
|
What disease is known as asthma+ and what are some of its additional features?
|
Allergic Bronchopulmonary Aspergillosis. Asthma + pulmonary infiltrates (possibly leading to fibrosis), central bronchiectasis, increase total serum IgE, specific IgE and IgG for aspergillus, eosinophilia, aspergillus in sputum
|
|
|
What is the pathogenesis of Goodpasture's Syndrome, what are its common symptoms, and what is its treatment?
|
Goodpasture's is a young male predominant disease where anti-glomerular basement membrane antibodies (against the non-collagenous domain of alpha-3 chain of collagen type IV) attack the lungs and kidneys. It causes pulmonary hemorrhage ± hemoptysis and is treated with plasmapheresis, high dose corticosteroids, and cyclophosphamide
|
|
|
Name some of the major respiratory tree host defenses
|
* Upper tract: microflora binding site competition, mucociliary barrier/clearance mechanisms, secretory IgA, the cough/gag reflex and sneeze mechanisms
* Lower tract: Mucous layer and mucociliary clearing, alveolar macrophages and other circulating phagocytes, immunooglbulins and complement, glottic closure and cough reflexes |
|
|
Name some of the common ways pathogens enter the respiratory tract
|
* Upper airway: Inhalation or direct deposition
* Lower airway: Inhalation, aspiration, hematogenous spread, contiguous spread, direct penetration, reactivation of latent microbes |
|
|
Name 5 ways pathogens can evade respiratory tree defenses
|
They can optimize size, have intrinsic virulence, use a capsule, express IgA proteases, or have an increased affinity or ability to attach to the epithelial layer
|
|
|
Which viruses have a winter seasonal variance?
|
ChRIStmas. Coronavirus, RSV, Influenza, GABHS
|
|
|
Which viruses have a summer seasonal variance?
|
PEA. Enterovirus, adenovirus, parainfluenza virus
|
|
|
What is the etiology, presentation, and treatment for rhinitis?
|
Viral (rhino or coronavirus) infection in the young during the winter. Nasal discharge, sneezing, sore throat lasting ~7 days. Treat supportively, NO antibiotics
|
|
|
What is the etiology, presentation, diagnosis, and treatment for pharyngitis?
|
Winter viruses cause most pharyngitis, followed by GABHS. It presents as a fever, throat pain, pharyngeal erythema ± exudates, and cervical lymphadenopathy that is self-limiting. Use leukocytosis, Centor criteria, and rapid strep test to diagnose GABHS. Use penicillin only if GABHS, otherwise treat symptoms
|
|
|
What are the different clinical presentations of GABHS versus viral pharyngitis?
|
* GABHS: sudden onset, fever (>101˚), headache, nausea, vomiting, abdominal pain, discrete exudate, tender anterior cervical lymphadenopathy, younger (5-15), winter or early spring, exposure history
* Viral: Conjunctivitis, coryza, cough, hoarseness, oral ulcers, rash |
|
|
What is the etiology, presentation, diagnosis, and treatment for sinusitis?
|
"Double sickening" viral prodrome with subsequent S. pneumoniae or H. influenzae infection in adults during fall, winter, or spring. Facial pain, maxillary toothaches, fever, purulent nasal discharge. Treat supportively, if persistent 7-10 days, use amoxicillin
|
|
|
What is the etiology, presentation, diagnosis, and treatment for influenza?
|
Influenza A or B infections in fall, winter, or spring. Abrupt onset fevers, headache, myalgia, and malaise progressing to a dry cough and URI signs. Diagnose with PCR or direct antigens and treat with antiviral agents. NO aspirin for kids => Reye syndrome
|
|
|
What is the etiology, presentation, and treatment for acute bronchitis?
|
Acute inflammation of the bronchial mucosa. Mostly viral (rhino, flu, paraflu, adeno, RSV) in the fall, winter, spring. Productive cough, low grade fever, but a normal lung exam self-resolving in ≤3 wks. Treat symptomatically (humidifier, OTC pain relievers, cough suppressants)
|
|
|
What is the etiology, presentation, diagnosis, and treatment for pneumonia?
|
Microbial infection of the lung parenchyma. Fever, dyspnea with tachypnea, productive cough with purulent sputum. Infiltrates on CXR.
|
|
|
What are the common findings and diagnostics for a confirmed clinical diagnosis of pneumonia?
|
* Signs and symptoms: fever w/ dyspnea, cough, and purulent sputum, increased respiratory and heart rates, crackles
* Labs: Leukocytosis & confirmatory CXR |
|
|
What disease/pathogen should an exposure to cattle, goats, pigs, abattoir or veterinarian work lead you to?
|
Pneumonia from brucella
|
|
|
What disease/pathogen should an recent travel history to SE Asia, Australia, or Central or Southern America lead you to?
|
Pneumonia from Melioidosis
|
|
|
What disease/pathogen should an exposure to ground squirrels, prairie dogs, or rats specifically in the SW lead you to?
|
Pneumonia from the plague
|
|
|
What disease/pathogen should an exposure to birds (parakeets, parrots, turkeys) lead you to?
|
Pneumonia from Psittacosis
|
|
|
What disease/pathogen should an recent travel history to the San Joaquin Valley or the arid SW lead you to?
|
Pneumonia from Coccidioidomycosis
|
|
|
What disease/pathogen should an exposure to bat or bird droppings lead you to?
|
Pneumonia from histoplasmosis
|
|
|
What are the most common typical and atypical pathogens that cause CA or HA pneumonia?
|
* CA: S. pneumoniae, mycoplasma pneumoniae, chlamydophilia pneumoniae, or viruses
* HA: S. aureus or GNR (pseudomonas aeruginosa) |
|
|
What are pathogens of concern in the post-influenza patient?
|
S. pneumoniae, S. aureus, and H.influenzae
|
|
|
What are pathogens of concern in the altered consciousness/ esophageal dysmotility patient?
|
Oral flora (anaerobes)
|
|
|
What are pathogens of concern in the alcoholic patient?
|
Oral flora (anaerobes), S. pneumoniae, S. aureus, Klebsiella
|
|
|
What are pathogens of concern in the chronic lung disease patient?
|
S. pneumoniae, H. influenza
|
|
|
What are pathogens of concern in the cystic fibrosis patient?
|
P. aeruginosa, S. aureus, Stenotrophomonas
|
|
|
What are pathogens of concern in the patient with hypogammaglobulinemia?
|
Encapsulated bacteria. S. pneumoniae, H. influenza (B)
|
|
|
What are pathogens of concern in the patient depressed cell-mediated immunity?
|
Intracellular pathogens. Typical & atypical mycobacteria, fungi (crypto, endemic mycoses), viruses (CMV, VZV, HSV, measles), pneumocystis jirovecii, toxoplasma gondii
|
|
|
What are pathogens of concern in the patient with decreased fully functional granulocytes?
|
Pyogenic extracellular pathogens (early) and Filamentous fungi (late). Oral bacterial flora, enterobacteriacae, P. aeruginosa, aspergillus
|
|
|
What are pathogens of concern in the patient with complement defects?
|
Encapsulated bacteria. S. pneumoniae, H. influenzae (B)
|
|
|
What are the differing clinical features between typical and atypical pneumonias?
|
* Typical (bacterial - S. pneumo, K. pneumo, H.flu, Moraxella): sudden onset of high, spiking fever, chills, tachycardia, tachypnea, pleuritic pain, purulent sputum, lobar or segmental consolidation, pleural effusions, and leukocytosis
* Atypical (viral, bacterial - M. pneumo, C. pneumo, C. psittaci, Coxiella, Legionella): gradual onset of low-grade fever, myalgias, scant sputum, and rare CXR consolidation |
|
|
What types of pathogens are associated with lobar consolidation on radiograph?
|
Pyogenic extracellular bacteria (S. pneumo, GNR)
|
|
|
What types of pathogens are associated with interstitial infiltrates on radiograph?
|
Viruses, mycoplasma
|
|
|
What types of pathogens are associated with cavitations without air-fluid level on radiograph?
|
TB, fungi
|
|
|
What types of pathogens are associated with consolidation and pleural effusion on radiograph?
|
S. pneumo, Staph, GNR, anaerobes
|
|
|
How should therapy be handled for pneumonias?
|
Initiate empiric therapy until etiology is identified, then de-escalate and direct towards that pathogen
|
|
|
What muscles are used for inspiration? What muscles can be recruited to help with inspiration? Expiration? Forced expiration?
|
* Inspiration: External intercostals, diaphragm are normally used for inspiration and the scalenes and sternocleidomastoid can be recruited.
* Expiration: Normal expiration is a passive process, but forced expiration used the internal intercostals and the abdominal muscles |
|
|
What lung volumes are altered when a patient lies down and why?
|
The inspiratory and expiratory reserve volumes change when the patient moves from standing to supine. When lying supine the diaphragm relaxes into a more superor position. This provides a larger contractile movement, allowing for an increased IRV. This decreases the ERV.
|
|
|
Explain hysteresis
|
Hysteresis is the difference in lung volume with inspiration and expiration at any given pressure. At any pressure the lung volume inspiration will be less than the volume during expiration. This change is caused by the extra energy required by inspiration to recruit and open alveoli.
|
|
|
How is alveolar pressure affected by size?
|
Alveolar pressure will increase as the radius decreases. P=2T/r. This means that small alveoli will push its air loads into larger alveoli
|
|
|
What is the physiologic effect of surfactant?
|
Surfactant, produced by type II pneumocytes, is made up of lipids and proteins and acts as a detergent, decreasing the alveolar surface tension. This decrease in alveolar surface tension is more pronounced in smaller alveoli
|
|
|
How do intrapleural and alveolar pressures change during inspiration and expiration?
|
Intrapleural pressure increases during inspiration as the lungs expand and decreases during expiration. As the lungs expand, the alveolar pressure decreases, drawing air into the alveoli, as the alveoli fill the intrapleural pressure begins normalizing the alveolar pressure back to zero. As the chest wall and lungs relax with expiration alveolar pressures increase, expelling air out.
|
|
|
Is expiration with emphysema effort dependent or independent? Why?
|
Emphysema expiration is effort dependent. This is due to the decreased elastic recoil of the lung parenchyma and common secretions, bronchospasm, or loss of airways
|
|
|
What are the physical exam and imaging findings in idiopathic pulmonary fibrosis?
|
Inspiratory crackles, basilar dullness, pleural rub. CT: Bibasilar subpleural interstitial reticulations, honeycombing
|
|
|
What are the PFT changes seen in IPF? (FEV, FVC, FEV/FVC, FRC, TLC, DLCO)
|
* Decreased FEV1 and FVC with a normal or increased FEV1/FVC
* Decreased FRC and TLC * Decreased DLCO |
|
|
What is the epidemiology, signs/symptoms, diagnostic standard, and therapeutic option for idiopathic pulmonary fibrosis?
|
IPF is more common in male smokers, aged 50-70. Presentation includes 2 year progression of dyspnea and cough, with velcro crackles on exam. Gold standard for diagnosis is a lung biopsy (VATS over BAL). The best therapeutic option (especially for younger, healthy patients) is a lung transplant
|
|
|
What is the presentation, imaging findings, and common associations for NSIP?
|
Non-specific Interstitial Pneumonia commonly presents as dyspnea and cough. CT shows bilateral infiltrates and consolidation without honeycombing. NSIP is associated with collagen vascular diseases, resolving infections, and hypersensitivity
|
|
|
What is the epidemiology, symptoms, and treatment for sarcoidosis?
|
Sarcoidosis occurs in 20-40 yo, African-American women. 1/3 are asymptomatic with only an abnormal CXR. For asymptomatic patients, observe and if they develop pulmonary or other organ involvement treat with corticosteroids, methotrexate, or infliximab
|
|
|
What is the offending agent and presentation in silicosis?
|
Silicosis is inhaled crystalline silica causing inflammation and fibrosis. Patients vary from being asymptomatic to having progressive massive fibrosis and respiratory failure
|
|
|
What are the two forms asbestos can take on and which are more like to lead to mesothelioma?
|
Serpentine fibers a long, pliable, curly fibers that are readily cleared by the lung. Amphibole (tremolite, amosite, or crocidolite) are short, straight, needle-like fibers that are durable, fibrogenic, and readily form asbestos bodies. Amphibole fibers lead to a greater risk of mesothelioma.
|
|
|
What are ferruginous bodies?
|
Ferruginous bodies are asbestos fibers that have been coated in iron-rich proteins (ferritin or hemosiderin) and phagocytized by macrophages
|
|
|
What is the latency period for a pleural effusions and pleural plaques caused by asbestos? For asbestosis? For mesothelioma?
|
Asbestos caused pleural effusions have a >10yr latency period. Pleural plaques have an average latency of 20 yrs. Asbestosis has an average latency of >20 yrs. Mesothelioma has an average latency of 30-40 yrs.
|
|
|
Do pleural plaques caused by asbestos exposure affect the visceral or parietal pleura?
|
Parietal pleura
|
|
|
What are the radiologic findings of asbestosis?
|
Fine reticular nodular markings in the lower lobes
|
|
|
Is asbestosis dose dependent? Mesothelioma?
|
Asbestosis is dose dependent, mesothelioma is not
|
|
|
What are the signs and symptoms and diagnostic standard for mesothelioma?
|
Mesothelioma presents with bloody pleural effusions, pleuritic chest pain, and dyspnea
|
|
|
A mesothelioma comorbidity adds how much of a risk of bronchogenic cancer to smokers?
|
100x
|
|
|
What is the clinical picture of reactive airways dysfunction syndrome?
|
Acute, high level exposure to an irritant causing respiratory symptoms with 24 hrs the persist and show reversible obstruction. No eosinophil infiltration or history of asthma
|
|
|
What occupation has the highest risk of silicosis, what is its presentation, and what are its imaging findings?
|
Sandblasters are at highest risk for inhaling silica dust. They present with dyspnea on exertion, productive cough, chest tightness, and wheezes. On CXR, they have large nodules in the upper lobes, calcification of hilar or mediastinal nodes, and can have lower lung bullae that lead to pneumothorax
|
|
|
What is an ILO score used to classify?
|
ILO scores classify scarring from asbestos. 0 - No scarring; 3 - severe scarring. Scores can increase based purely on smoking
|
|
|
What are the histologic changes and imaging findings seen in an acute bacterial pneumonia?
|
CXR will have lobar consolidation. Histologically, an abundance of neutrophils will infiltrate, initially causing necrosis and edema and can progress to diffuse alveolar damage or abscesses
|
|
|
How will DAD present and what are two clinical syndromes that diffuse alveolar damage can cause?
|
Diffuse alveolar damage will present as acute onset dyspnea, often severe enough for mechanical ventilation. Diffuse pulmonary infiltrates cause rapid respiratory failure with a mortality rate of 40-60%. If pathologic= Acute Lung Injury progressing to ARDS. If idiopathic= Idiopathic Pulmonary Fibrosis
|
|
|
How does acute epithelial and endothelial injury cause AIP or ALI/ARDS?
|
A lung toxin injures epithelial cells causing necrosis of type I pneumocytes and injures endothelial cell leading to leaky capillaries. These two injuries cause edema and hyaline membrane development. This process can organize and either resolve or cause fibrosis and alveolar collapse.
|
|
|
What are the histologic findings and pertinent negatives of diffuse alveolar damage (acute interstitial pneumonia)?
|
* Diffuse, temporally uniform distribution of alveolar septal thickening. Hyaline membranes (plasma proteins and nuclear debris) develop in the exudative phase.
* NO granulomas, abscess, or necrosis. NO infection or eosinophils |
|
|
What are the differences between the exudative and the organizing phases of diffuse alveolar damage?
|
The exudative stage of acute interstitial pneumonia is characterized by interstitial edema, type I pneumocyte sloughing, and hyaline membrane development. The organizing stage consists of type I pneumocyte proliferation, interstitial fibroblasts, and focal airspace organization
|
|
|
What are some common causes of a cryptogenic organizing pneumonia pattern?
|
Organizing pneumonia patterns can be caused by infections, collagen vascular diseases, drug reactions (amiodarone), neoplasms, or bone marrow transplants (part of GvHD)
|
|
|
What is the epidemiology, onset, and treatment for a cryptogenic organizing pneumonia?
|
OP usually occurs in the 5th or 6th decade of life and can present with a 2-3 month history. Cryptogenic Organizing Pneumonia is very responsive to corticosteroids.
|
|
|
What are the histologic findings and pertinent negatives of cryptogenic organizing pneumonia?
|
* Loose, watery, fibroblastic plugs with preservation of lung architecture in intervening areas. Temporally uniform, patchy, unilateral or bilateral intraluminal organizing fibrosis of the distal airways. There may be mild chronic interstitial inflammation.
* NO interstitial fibrosis, or hyaline membranes, granuloma, neutrophils, necrosis or abscesses. No vasculitis or prominent eosinophil infiltration. |
|
|
Is the Reid index normal in asthma? Chronic bronchitis?
|
The Reid index (submucosal wall thickness/submucosal glands~0.4) is normal in asthma. The Reid index is abnormal in chronic bronchitis
|
|
|
What are the histologic findings in asthma?
|
Peribronchiolocentric mononuclear inflammation with eosinophils. Mucus plugging with some upper lobe bronchiectasis.
|
|
|
What are Curschmann's spirals and Charcot-Leyden crystals and what disease are they associated with?
|
Asthma. Curschmann's spirals are desquamated epithelial cells. Charcot-Leyden crystals are produced by the breakdown of lysophospholipase, an enzyme synthesized by eosinophils
|
|
|
Name some eosinophilic pulmonary diseases
|
Th2-related inflammatory diseases. Eosinophilic pneumonia (Churg-Strauss), allergic bronchopulmonary aspergillosis, asthma, eosinophilic bronchitis
|
|
|
What are the clinical features of sarcoidosis?
|
Granulomatous Disease. Asymptomatic (most common). Dyspnea, nonproductive cough, nonspecific chest pain. Can affect be a multiorgan disease (lungs, lymphatics, liver, spleen, eyes...)
|
|
|
How is sarcoidosis diagnosed?
|
Clinically and radiographically. "Interstitial noncaseating granulomas in a lymphatic and bronchovascular distribution" Must rule out other granulomatous diseases (Berylliosis, Churg-Strauss)
|
|
|
What is the immunopathogenesis of Sarcoidosis?
|
Patients can have HLAs (HLA-A1 or HLA-B8) which are hyper-reactive to certain microbes (Mycobacteria, propionibacterium acnes, and rickettsia). These predispositions lead to T-cell expansion, macrophage activation, local cytokine level increases, and intra-alveolar and interstitial accumulation of CD4+ T-cells.
|
|
|
What kind of test are used for sarcoidosis?
|
Hyperglobulinemia (non-specific B-cell activation by helper T-cells) and increased TNF concentrations (released by activated alveolar macrophages
|
|
|
What are the imaging findings in sarcodosis?
|
Marked, symmetric, bilateral hilar and mediastinal lymphadenopathy with mild reticulonodular perihilar interstitial infiltrates. Small nodules located along pulmonary vessels and bronchi. Later stages have interstitial fibrosis, cavitary lesions, honeycombing, and apical subpleural cysts
|
|
|
What are the histologic findings and pertinent negatives in sarcoidosis?
|
Well-formed noncaseating granulomas distributed along lymphatics (bronchovascular bundles, pleura, septa). Schaumann bodies, asteroid bodies, calcium carbonate crystals, microcalcifications, hamazaki-wesenberg bodies. May be hyalinized.
* NO organisms (on culture or stain), exposures (beryllium, talc, or aluminum) |
|
|
How do you calculate pulmonary vascular resistance?
|
PVR(wood units)= (mean pulmonary artery pressure - LA pressure)/ cardiac output
|
|
|
What are the signs of pulmonary hypertension?
|
Cor pulmonale. Tricuspid murmur, right-sided gallop (S3/S4), RV (substernal) heave, JVD, peripheral edema (ascites)
|
|
|
What contrast Echocardiogram changes will result from pulmonary hypertension?
|
RA/RV hypertrophy, small LV, R-L or L-R shunt
|
|
|
The misregulation of what 3 proteins are responsible for pulmonary hypertension?
|
In pulmonary hypertension prostacyclin levels are reduced, endothelin levels are increased, and NOS is abnormally distributed. These breakdowns in control lead to proliferation of the intima of small pulmonary arteries at branch points, resulting in plexiform lesions. Intimal fibrosis causes muscular hypertrophy or hyperplasia
|
|
|
What is the treatment for pulmonary hypertension?
|
* In all patients treat their cor pulmonale symptoms (oxygen, diuretics, digoxin, cardiac exercise rehab)
* In pulmonary artery hypertension (WHO group 1), you can use prostacyclins, endothelin receptor antagonists, or phosphodiesterase inhibitors. * WHO Group 4 and some group 1: anti-coagulate |
|
|
How do you diagnose pulmonary artery hypertension (WHO group 1)?
|
Must have a right heart catheter performed
|
|
|
What are some diseases associated with anti-nuclear antibody?
|
Connective tissue diseases: SLE, scleroderma, sjogren's, RA
|
|
|
What are some diseases associated with ANCA?
|
* p-ANCA: Churg-Strauss, microscopic polyangitis
* c-ANCA: Granulomatosis with polyangitis |
|
|
What is the clinical triad associated with granulomatosis with polyangiitis?
|
C-Disease. Upper airway, lower airway, kidney. Cavities. Cyclophosphamide.
|
|
|
What is the epidemiology, presentation, and therapy for goodpastures' syndrome?
|
Young males. Pulmonary hemorrhage ± hemoptysis. Diffuse alveolar infiltrates, anemia, glomerulonephritis. Plasmapheresis, high dose corticosteroids, cyclophosphamide
|
|
|
What is the immunopathology of hypersensitivity pneumonitis?
|
Type III (Immune complex-mediated) and Type IV (delayed, T-cell mediated). Precipitating IgG antibodies against offending agent in serum
|
|
|
What are the histologic findings of hypersensitivity pneumonitis at it's three stages?
|
* Acute: Neutrophilic infiltration of alveoli and bronchioles (acute bronchioloits). Can have DAD pattern (temporally uniform, nonspecific, chronic interstitial pneumonia)
* Subacute: Lymphocytic interstitial pneumonitis, granulomas, organizing pneumonia, fibrosis * Chronic: TRIAD. Temporally uniform chronic interstitial inflammation with peribronchiolar accentuation, non-necrotizing poorly formed granulomas in peribronchiolar interstitum, foci of organizing pneumonia (intraluminal) |
|
|
What is the epidemiology and presentation of usual interstitial pneumonia?
|
Male smokers ages 50-70 presenting with insidious onset of dyspnea with chronic, progressive degradation
|
|
|
Dysregulation of what cytokine leads to usual interstitial pneumonia?
|
Up-regulation of TGF-ß1 leads to increased fibroblast to myofibroblast differentiation, increased deposition of collagen and ECM, which lead to pulmonary fibrosis.
|
|
|
What are some common findings in Usual Interstitial Pneumonia (IPF)?
|
Tachypnea, bibasilar, inspiratory velcro crackles. Clubbing, pulmonary hypertension, and cyanosis late
|
|
|
What are the pathologic features of early, late, and end stage usual interstitial pneumonia?
|
* Early: firm lungs, pulmonary edema, type II pneumocyte hyperplasia
* Late: Fibrous tissue, fibrogenic foci, thickened alveolar septa, hyperplastic smooth muscle, loss of alveolar capillaries * End stage: Cuboidal/columnar lined honeycomb spaces, lymphoid hyperplasia, intima and media thickening of pulmonary arteries |
|
|
What are the histologic features and pertinent negatives of usual interstitial pneumonia?
|
* Temporal heterogeneity. Established patchy, parenchymal fibrosis with subpleural/ paraseptal predominance. Fibroblastic foci with honeycombing.
* NO inorganic dust, granulomas, Langerhan's, other interstitial lung disease |
|
|
What are the epidemiologies and associations with nonspecific interstitial pneumonia?
|
* Slightly more common in women. Smokers. Associated with collagen vascular diseases (SLE, polymyositis, scleroderma, sjogren's, RA).
* Cellular: 26-50 * Fibrosing: 30-71 |
|
|
What are the histologic features and pertinent negatives of CELLULAR and FIBROSING nonspecific interstitial pneumonia?
|
Diffuse involvement of affected parenchyma with mild to moderate chronic inflammation
CELLULAR * Preservation of alveolar architecture * NO interstitial fibrosis, dust, granulomas, eosinophils, organisms FIBROSING * Mild/moderate loss of alveolar architecture. Variable degree of interstitial fibrosis * NO dust, granulomas, Langerhan's cells, eosinophils, organisms, fibroblastic foci, honeycombing |
|
|
What is the epidemiology of desquamative interstitial pneumonia?
|
Male smokers, in the 4th to 5th decade of life. Children with surfactant deficiency or alveolar proteinosis.
|
|
|
What are some physical exam findings, diagnostic tools, and therapies for desquamative interstitial pneumonia?
|
Crackles and clubbing. Restrictive PFTs with reduced DLCO, hypoxemia on arterial blood gas. Bronchoalveolar lavage shows increased total cells with a predominance of macrophages. Smoking cessation is the only thing that works.
|
|
|
What are the histologic features and pertinent negatives of desquamative interstitial pneumonia?
|
* Uniform parenchymal involvement with marked accumulation of macrophages filled with brown pigment
* NO honeycomb, fibroblastic foci, eosinophils, dust, granulomas |
|
|
What are some mechanisms of shunt?
|
* Bronchial artery blood being collected by pulmonary veins after it perfuses the bronchi
* Coronary venous blood draining directly into the LV * Pulmonary arteriovenous fistula * Right-to-left shunt |
|
|
How does hypoxemia resulting from a shunt respond to added inspired O2?
|
It responds poorly because the alveoli are not seeing the increased PaO2, the increased O2 is being shunted.
|
|
|
What are the 4 general mechanisms of hypoxemia?
|
Hypoventilation, diffusion, shunt, V/Q mismatch
|
|
|
How do you calculate dead space?
|
Vd=Vt[(PACO2-PeCO2)/PACO2]
|
|
|
What is the alveolar gas equation?
|
Va=PIO2-(PACO2/R)
|
|
|
How do you calculate alveolar ventilation?
|
Va=VCO2/PCO2=f(Vt-Vd)
|
|
|
How do you calculate DLCO?
|
DLCO=VCO/PCO
|
|
|
How do you calculate O2 capacity?
|
O2 capacity=1.34*[Hb]
|
|
|
How do you calculate O2 saturation?
|
O2 saturation= (O2 bound to Hb/O2 capacity)*100
|
|
|
How do you calculate O2 content?
|
O2 concentration= (1.34[Hb]*O2 sat) + dissolved O2
|
|
|
Which direction does an increase in 2,3-DPG shift an oxyhemoglobin dissociation curve and why?
|
An increase in 2,3-DPG will shift an oxyhemoglobin dissociation curve to the right. 2,3-DPG binds and stabilizes the de-oxygenated form of Hb, promoting a higher amount of O2 unloading and delivery to the tissues
|
|
|
What enzyme is responsible for catalyzing the reaction from CO2 and H20 to carbonic acid (H2CO3)?
|
Carbonic anhydrase
|
|
|
What are the 4 general mechanisms of hypoxia?
|
* Hypoxic hypoxia: Pulmonary disease interferes with lungs ability to oxygenate blood
* Anemic hypoxia: Reduced ability to carry O2 (anemia or CO poisoning) * Circulatory hypoxia: Reduction of tissue blood flow (shock or obstruction) * Histotoxic hypoxia: Toxic substance interferes with tissue ability to utilize available O2 (cyanide poisoning) |
|
|
What lung disease leads to fine granular pigments? Coarse granular brown hemosiderin pigments?
|
Desquamative Interstitial Pneumonia and Respiratory Bronchiolitis has fine granular pigments. Idiopathic Pulmonary Hemosiderosis has coarse granular, brown pigment.
|
|
|
What is the treatment for desquamative interstitial pneumonia?
|
Smoking cessation. Corticosteroids.
|
|
|
What are the histologic findings and pertinent negatives in Respiratory Bronchiolitis?
|
* Bronchocentric macrophage accumulation with bronchiolar fibrosis and inflammation
* Diffuse acinar involvement, honeycombing, other airway damage |
|
|
Who should receive prophylactic anti-coagulation for a VTE?
|
Those at high risk of VTE and low risk of bleeding should receive LMWH, LDUH bid, LDUH tid, or fondaparinux. Those at high risk for VTE and bleeds should receive compression therapy
|
|
|
How is a Well score used?
|
Well score determines what kind of test should be used to diagnose a VTE.
* 0: <5%, low, D-dimer * 1-2: 17%, moderate, D-dimer or ultrasound * 3+: 53%, high, ultrasound |
|
|
What are the treatment differences for a provoked versus an unprovoked DVT?
|
* Provoked: Start warfarin on day 1 and continue for 3 months, bridge with LMWH or fondaparinux
* Unprovoked: Warfarin with LMWH or fondaparinux for at least 3 months |
|
|
How do you diagnose an acute pulmonary embolism?
|
Angiography ± CT
|
|
|
What is the definition of a massive pulmonary embolism?
|
Sustain hypotension for at least 15 minutes or requirement of inotropes, with signs and symptoms of shock (not caused by other etiologies - arrhythmia, sepsis) or persistent bradycardia
|
|
|
What is the treatment of chronic thromboembolic pulmonary hypertension?
|
Anticoagulation, lifelong warfarin, endarterectomy, treatment for pulmonary hypertension and cor pulmonale
|
|
|
How do ventilation, perfusion, and V/Q changes as you move up the lungs?
|
As you move up the lungs ventilation and perfusion both decrease, but V/Q increases
|
|
|
How does the V/Q, PO2, and PCO2 compare between alveoli experiencing shunt and alveoli in physiological dead spaces?
|
V/Q is decreased in shunt. This is caused by excess perfusion and the PCO2 will be increased. With dead space the V/Q will be increased. This is caused by excess ventilation and will result in an increased PO2
|
|
|
Is CO diffusion or perfusion limited? O2? N2O?
|
CO is diffusion limited. N2O is perfusion limited. O2 is normally perfusion limited, but in cases of pulmonary edema oxygen is diffusion limited
|
|
|
What are normal blood gas values for pH, PO2, PCO2, and HCO3?
|
pH = 7.4; PO2 = 100; PCO2 = 40; HCO3 = 24
|
|
|
In respiratory acidosis is PCO2 increased or decreased?
|
In respiratory acidosis PCO2 is increased
|
|
|
What are some causes of respiratory alkalosis and is PCO2 increased or decreased?
|
Increases in alveolar ventilation causes respiratory alkalosis: pneumonia, sepsis, pregnancy. PCO2 is decreased
|
|
|
In metabolic acidosis is HCO3 increased or decreased?
|
In metabolic acidosis HCO3 is decreased
|
|
|
In metabolic alkalosis is HCO3 increased or decreased?
|
In metabolic alkalosis HCO3 is increased
|
|
|
What are the general functions of the two portions of the pontine and medullary respiratory centers?
|
* Medullary respiratory center: ventral (forced expiration) and dorsal (inspiration)
* Pontine respiratory center: pneumotaxic (inhibits inspiration) and apneustic (prolongs inspiration) |
|
|
What chemical changes do the carotid and aortic bodies detect?
|
Changes in PO2 and [H+]. Significant falls in PO2 will close KO2 channel, releasing dopamine, and triggering increased ventilation via the medullary centers
|
|
|
What chemical changes do central chemoreceptors detect?
|
Central chemoreceptors detect small increases in PCO2 or [H+] and stimulate ventilation
|
|
|
How can pregnancy cause a respiratory alkalosis?
|
Progesterone levels increase as pregnancy progresses. Progesterone can induce an increase in respiratory rates. The increased alveolar ventilation drives the PCO2 down
|
|
|
What is the clinical definition of ALI/ARDS?
|
* Acute onset respiratory distress
* Decreased arterial oxygen pressure (hypoxia) * Decreased lung compliance * Diffuse pulmonary infiltrates on radiographs * No left-sided heart failure |
|
|
What are some causes of acute lung injury?
|
Infection, physical injury, inhaled irritants, chemical injury, hematologic, hypersensitivity
|
|
|
What is the general pathophysiology of acute lung injury?
|
Neutrophils migrate from capillaries into the airway where they activate alveolar macrophages, cause edema and endothelial necrosis. Hyaline membranes (edema fluid and necrotic tissue) form. In attempts to heal type II pneumocytes proliferate and granulation tissue forms leading to fibrotic thickening of the alveolar septa
|
|
|
What cytokine is responsible for causing fibroblast to proliferate and differentiate into myofibroblasts?
|
TGF-ß1
|
|
|
What are the three main mechanisms of atelectasis? Give examples
|
* Resorption: Mechanical obstruction and occlusion (foreign objects, mucus plugs, tumor growth, bronchiectasis)
* Compression: Accumulation of fluid, blood, or air in pleural cavity (pleural effusion, CHF, pneumothorax) * Contraction: Local or general fibrotic change |
|
|
What are the 3 physiologic implications of surfactant?
|
* Reduced work of breathing by reducing elastic recoil pressure of the lungs
* Protects against atelectasis by allowing surface forces to vary with alveolar surface area * Affects interstitial hydrostatic pressure |
|
|
What cellular and molecular changes occur as we age?
|
* More neutrophils, fewer macrophages
* Immune senescence: declining lymphocytic function, decreased IL-2, low cytotoxic T-cell and NK cell function, loss of self-recognition * Decreased compliance (elastic recoil pressure), FRC, DLCO, expiratory flow rate, PaO2. Increased A-a gradient. Unchanged TLC |
|
|
What are functional changes seen in older adults?
|
Decreased ventilatory response to hypoxia and hypercarbia. Comorbidities affect exertion level
|
|
|
What levels constitute hypercapnic respiratory failure? Hypoxic respiratory failure?
|
* Hypercapnic respiratory failure is PaCO2>45 mmHg
* Hypoxic respiratory failure is PO2<55 mmHg |
|
|
What are the two organ systems that regulate acid levels in the body and what molecules to they use?
|
Respiratory system uses PaCO2 levels to maintain ideal acid levels. The renal system adjust the HCO3 level to regulate acid levels
|
|
|
Does hypoxic respiratory failure from alveolar hypoventilation have a normal or widened A-a gradient?
|
Alveolar hypoventilation (respiratory muscle failure, neuromuscular disease) maintains a normal A-a gradient
|
|
|
How many branches are there in the conducting portion of the respiratory system?
|
16 from trachea to terminal bronchioles
|
|
|
How do you measure how much oxygen is actually delivered to the tissues?
|
Oxygen delivery = 1.34*(%O2 sat)*[Hb]*cardiac output
|
|
|
What are the three different types of shunt?
|
Cardiac or great vessel, pulmonary vascular, or pulmonary parenchymal
|
|
|
What are the requirements for a diagnosis of an acute lung injury and how does it differ for acute respiratory distress syndrome?
|
Acute Lung Injury
* Bilateral radiographic infiltrates in ≥3 quadrants * Hypoxemia (PaO2/FiO2<300) * Reduced lung compliance * No left atrial hypertension * Associated risk factors (sepsis, pneumonia, trauma) Acute Respiratory Distress Syndrome has a P/F limit of 200 |
|
|
What are the two phases of ARDS?
|
* Acute: Injury, neutrophils, edema, macrophages
* Fibroproliferative: fibrosis, pulmonary hypertension |
|
|
What are two poor predictors of mortality for patients with ARDS?
|
Age and presence of sepsis
|
|
|
What are the ventilation and oxygenation guideline for ARDS?
|
Ventilate with a tidal volume of 6-8 ml/kg of predicted body weight. Oxygenate with PEEP with a minimum of 60% FiO2
|
|
|
What are the definitions of systemic inflammatory response syndrome, sepsis, severe sepsis, and septic shock?
|
* SIRS (2+): Hypo/hyperthemia, tachycardia, tachypnea, PaCO2<32, leukopenia or leukocytosis
* Sepsis: SIRS from infection * Severe sepsis: Sepsis with organ dysfunction * Septic shock: Shock, secondary to sepsis that is refractory to fluid resuscitation |
|
|
What are the variables and associated organ systems measured with a SOFA score?
|
* PaO2/FiO2 (Respiratory)
* Platelets (Hematalogic) * Bilirubin (Hepatic) * Hypotension (Cardiovascular) * Glascow Coma Scale (CNS) * Creatinine (Renal) |
|
|
What is the treatment for sepsis?
|
Early goal directed therapy: Close monitoring, fluids, vasopressors, transfusions, antibiotics, corticosteroids
|
|
|
What is the epidemiology, pathophysiology, and presentation of Goodpasture's Syndrome?
|
* Young adult male smokers
* HLA DRw15 or HLA DR4 predispose individuals to antibody-mediated immune reactions to basement membranes (noncollagenous domain of the a3 chain of collagen IV) in both the lung and kidney * Hemoptysis with acute/chronic hemorrhage, anemia, renal insuficiency, diffuse lung infiltrates |
|
|
What is the epidemiology, presentation, and treatment of Idiopathic Pulmonary Hemosiderosis?
|
Young adults present with insidious cough, hemoptysis, anemia, weight loss (NO renal). Responds to prednisone and/or azathioprine
|
|
|
What is seen histologically in idiopathic pulmonary hemosiderosis?
|
Hemorrhage. Macrophages in alveolar spaces filled with coarse granules of hemosiderin
|
|
|
What is the clinical triad, pathophyisiology, pathologic triad of granulomatosis with polyangiitis?
|
Wegner's Granulomatosis. C-disease. Upper/lower airways, kidney; sinuses. c-ANCA against proteinase-3. Parenchymal necrosis, vasculitis, granulomatous inflammation
|
|
|
What are the microscopic features of necrotizing capillaritis and what disease is it associated with?
|
Necrotizing capillaritis is focal neutrophilic necrosis of alveolar septa and capillary fibrin thrombi leading to interstitial hemorrhage. It is associated with collagen vascular diseases
|
|
|
What is the presentation and pathophysiology of Allergic Angiitis and Granulomatosis?
|
Churg-Strauss. Asthma (eosinophilia and elevated serum IgE), systemic vasculitis, mono/polyneuropathy, nonfixed lung infiltrates, paranasal sinus abnormalities. p-ANCA (myeloperoxidase) causing eosinophilic infiltrates, granulomatous infiltration, and necrotizing vasculitis
|
|
|
Do lines of Zahn suggest a pulmonary embolism that occur ante- or postmortem?
|
Lines of Zahn are seen in pulmonary emboli that occurred antemortem
|
|
|
What is the epidemiology, pathogenesis, morphologic changes, and treatment of primary pulmonary hypertension?
|
Females in their 30s, males in their 40s. Autosomal dominant mutation of bone morphogenetic protein receptor type II (BMPR2) dysregulates TGF-ß and BMP causing increases in endothelin, decreases in prostacyclins, and improper NO distribution leading to medial hypertrophy and muscularization of arterioles; severe pulmonary hypertension will have plexiform lesions. Treated with endothelin antagonists, synthetic prostacyclins, and phosphodiesterase inhibitors
|
|
|
What are some causes of abnormal pleural fluid collection?
|
Changes in the hydrostatic or oncotic pressure gradients. Increased interstitial fluid (hydrostatic pressure) or increased systemic venous pressure. Decreased hydrostatic pressure in pleural cavity or decreased systemic oncotic pressure
|
|
|
What are the physical exam findings accompanying pleural effusions?
|
Decreased tactile fremitus & breath sounds, dullness to percussion, increased breath sounds above fluid level, pleural rub, hemithorax appearance changes
|
|
|
What are the three main etiologies of transudative and exudative pleural effusions?
|
* Transudative: Congestive heart failure, nephrosis, cirrhosis
* Exudative: Infection. If bloody, malignancy |
|
|
What are Light's Criteria?
|
Exudate. 1/3=90%. 3/3=99%
* Protein (pleura)/ protein (serum ≥0.5 * LDH (pleura)/ LDH (serum) ≥0.6 * LDH (pleura) >2/3 normal serum levels Transudate. * Albumin gradient >1.2 (serum-pleura) |
|
|
How do you determine the etiology of a pleural effusion?
|
Thoracentesis. Gram stain and cultures
|
|
|
What processes does a pleural fluid glucose <60 suggest?
|
Pleural fluid glucose of greater than 60 implicates increased cell metabolism (active inflammation) and suggests TB, parapneumonic effusion, malignancy, or connective tissue disorders
|
|
|
What constitutes a parapneumonic effusion? What would make it complicated?
|
Parapneumonic effusions are effusions associated with an acute pneumonia.
Complicated parapneumonic effusions have low pH, low glucose and/or high LDH, loculated with a positive gram stain, and pus |
|
|
What are the three types of pleuritis and to what are infectious disease processes are they secondary to?
|
* Serofibrinous: Serum (pulmonary inflammation, collagen vascular diseases)
* Suppurative: Pus/empyema (pneumonia) * Hemorrhagic: Blood (tumor) |
|
|
What are the three types of pleuritis and to what are non-infectious disease processes are they secondary to?
|
* Hydrothorax: Transudate (CHF)
* Hemothorax: Blood (ruptured aortic aneurysm) * Chylothorax: Chyle (lymphatic obstruction) |
|
|
Do solitary fibrous tumors arise from visceral or parietal pleura?
|
Solitary fibrous tumors arise from visceral pleura
|
|
|
Describe the gross and histologic findings of solitary fibrous tumors
|
White, round, firm nodules. CD34+. Patternless pattern, haphazard arrangement of fibroblast-like cells in a background of collagen.
|
|
|
What are pleural plaques?
|
Hypocellular tissues rich in collagen that originates from the parietal pleura
|
|
|
What is the gross pathology of malignant mesothelioma?
|
Small nodules increasing in size until they coalesce and encase the lung. Invasive (chest wall/mediastinum, pericardium, contralateral pleura, peritoneum
|
|
|
Describe the histologic characteristics of epithelial and sarcomatoid mesothelioma
|
Epithelial has cells in a tubulopapillary arrangement that stain with cytokeratin AE1/AE3 and Calretinin. Sarcomatoid has a spindle-shaped oval cells
|
|
|
What constitutes a methacholine challenge that is positive for asthma?
|
If it requires less than 8 mg/mL of methacholine to elicit an FEV1 decrease of 20%, the test is positive for asthma
|
|
|
What are the diagnostic and therapeutic uses of bronchoscopy?
|
* Diagnostic: Persistent cough, hemoptysis, abnormal CXR, possible infection
* Therapeutic: Foreign body removal, stent placement, tumor debulking, bronchial thermoplasty |
|
|
What is the most common diagnosed cancer type for men and women?
|
Women is breast cancer, men is prostate cancer
|
|
|
What is the most common cancer related death for men and women?
|
Both men and women die more from cancer than from any other typeof cancer
|
|
|
When is lung cancer screening currently recommended?
|
Beginning at age 55 with a greater than 30 pk-yr history of smoking
|
|
|
What are common symptoms associated with lung cancers?
|
* Local: cough, wheezes, hemoptysis, dyspnea, stridor, obstructive pneumonitis, atelectasis, SVC syndrome, chest wall and pleuritic pain
* General: decreased appetite, weight loss, fatigue * Metastasis: bone pain, CNS symptoms |
|
|
What neoplastic syndromes are associated with small cell lung cancer?
|
ADH and ACTH secretion, gynecomastia, and Lambert-Eaton syndrome
|
|
|
What neoplastic syndromes are associated with large cell lung cancer?
|
Hypertrophic Pulmonary Osteoarthropathy
|
|
|
What neoplastic syndromes are associated with adenocarcinoma?
|
Hypertrophic Pulmonary Osteoarthropathy
|
|
|
What neoplastic syndromes are associated with squamous cell carcinoma?
|
Hypercalcemia
|
|
|
Where are the most common sites for lung cancer to metastasize?
|
Brain, bone, adrenals, liver, lymph nodes
|
|
|
What are some prognostic factors in lung cancer?
|
Age, physical strength, weight loss %, metastatic sites, and TNM stage
|
|
|
What is the treatment for NSCLC stages I and II?
|
Surgical resection. Stage II also gets adjuvant chemo
|
|
|
What is the treatment for NSCLC stages III?
|
Surgery, chemo, and radiation
|
|
|
What is the treatment for NSCLC stages IV?
|
Palliative chemotherapy and supportive care
|
|
|
What is the median survival of small cell lung cancer without treatment?
|
2-4 months
|
|
|
What are the prognostic factors for small cell lung cancer?
|
Female gender is good, performance status, stage (limited v. extensive), LDH
|
|
|
What fraction of small cell lung cancers are diagnosed in the limited stage? Extensive stage?
|
1/3 are diagnosed at the limited stage (I-III). 2/3 are diagnosed at the extensive stage (IV)
|
|
|
When is surgery indicated for smal cell lung cancer?
|
For a single pulmonary nodule without lymph node or distant metastasis. Give adjuvant chemotherapy.
|
|
|
What is the treatment for limited stage small cell lung cancer?
|
Chemotherapy and radiation
|
|
|
What is the treatment for extensive stage small cell lung cancer?
|
Chemotherapy and radiation if it will fit in one radiation field
|
|
|
What symptoms are associated with Pancoast tumors?
|
Apical tumor. Horner's syndrome and ulnar pain
|
|
|
In what kind of lung cancer do you see keratin pearls and intercellular bridges?
|
Squamous cell carcinoma
|
|
|
Which type of lung cancer is most likely to cavitate?
|
Squamous cell carcinoma
|
|
|
What are the histologic findings in small cell carcinoma?
|
Small, round, or oval cells with scant cytoplasm, ill-defined cell borders, fine granular "salt-and-pepper" chromatin, and absent nucleoi
|
|
|
Is large cell carcinoma more often centrally or peripherally located?
|
Large cell carcinoma is more often a large, necrotic tumor that is peripherally located
|
|
|
What immunoreactive stain is used for large cell neuroendocrine carcinoma?
|
Synaptophysin
|
|
|
Are adenocarcinomas centrally or peripherally located?
|
Adenocarcinomas are peripherally located
|
|
|
Are small cell lung cancers centrally or peripherally located?
|
Small cell lung cancers are centrally located
|
|
|
Are squamous cell carcinomas centrally or peripherally located?
|
Squamous cell carcinomas centrally located
|
|
|
EGFR mutations are most commonly associated with which type of lung cancer?
|
Adenocarcinoma. Allows for the tyrosine kinase inhibitors (gefitinib/erlotinib) to work
|
|
|
Are atypical adenomatous hyperplasia (proliferation of type II pneumocytes) and adenocarcinoma in situ invasive?
|
No
|
|
|
Is typical or atypical carcinoma more mitotic?
|
Atypical
|
|
|
What immunologic stain is used to suggest adenocarcinoma?
|
TTF1
|
|
|
What immunologic stain is used to suggest squamous cell carcinoma?
|
p63
|
|
|
What are some clinical and radiographic characteristics that favor malignancy with solitary pulmonary nodules?
|
* Clinical: age, smoking, history of cancer
* Radiographic: large diameter, spiculation, upper lobe location, absence of calcification |
|
|
What are the five A's?
|
Ask, advise, assess, assist, arrange
|
|
|
How do you clinically diagnose obstructive sleep apnea?
|
ISNORED. Insomnia, snoring, not breathing, obesity/older, restorative sleep, excessive daytime sleepiness, drugs
|
|
|
What are some commonly used health promotion measures to prevent respiratory disease
|
Smoking cessation/abstinence, influenza & pneumococcal vaccine, upright posture, oral care, hand-washing, anticoagulation/calf compression, early mobilization, sleep hygiene, weight loss, protective masks, avoid allergens and workplace exposures
|
|
|
What subtypes of hemagglutinin infect humans? Neuraminidase?
|
Hemagglutinin 1, 2, 3, 5, & 9. Neuraminidase 1 & 2.
|
|
|
What type of influenza contains M protein?
|
Type A
|
|
|
Does antigenic drift cause pandemics or epidemics?
|
Antigenic drift causes epidemics
|
|
|
Does antigenic shift cause pandemics or epidemics?
|
Antigenic shifts cause pandemics
|
|
|
What is responsible for antigenic drift?
|
Viral adaptation to the development of host antibodies
|
|
|
What is responsible for antigenic shift?
|
Recombination of H and or N subtypes caused by crossover between species
|
|
|
What age group is most at risk for influenza-related mortality?
|
Older adults
|
|
|
What are the most common pneumonia causing pathogens in the post-influenza patient?
|
S. pneumonia and then S. aureus
|
|
|
What are some pathophysiological responses to an influenza infection and what secondary complications can they promote?
|
* Destroyed physical barriers, NA mediated adherence augmentation, decreased mucociliary activity
* Pneumonia, empyema, abscesses, shock, sepsis |
|
|
What treatment is indicated for an influenza infection?
|
Oseltamivir (PO) or Zanamivir (INH) are neuraminidase inhibitors
|
|
|
What strains are included in the seasonal influenza vaccine?
|
2 strains of influenza A and 1 influenza B
|
|
|
What are the three types of inactivated influenza vaccines and what are the epidemiological indications of each?
|
* Regular TIV: all persons over 6 months
* High-dose TIV (FluZone): 4x normal dose, 65+ * Intradermal TIV: 40% less antigen, 18-64 |
|
|
What is the epidemiology of the live, attenuated intranasal influenza vaccine?
|
Healthy, not pregnant persons aged 2-49
|
|
|
Who should and shouldn't receive the influenza vaccine?
|
* Everyone over 6 months should be vaccinated
* Don't give if: allergic to eggs, previous allergic reaction, less than 6 months, current febrile illness, history of Guillain-Barré |
|
|
When should the public receive an influenza vaccine?
|
October-November
|
|
|
What is the clinical efficacy of giving Oseltamivir to treat influenza?
|
Reduces hospitalizations for LRI, shortens the duration of cough and allows patients to get back to work sooner
|
|
|
What are some groups at risk for invasive pneumococcal disease?
|
CHD, DMII, CLD, smokers, alcoholics, immunocompromised
|
|
|
What are the different indications for the pneumococcal polysaccharide v protein-conjugate vaccines?
|
* Polysaccharide (Pneumovax): adults over 65, 19-64 who smoke or have asthma, children ≥2 with high risk of disease
* Protein-conjugate (Prevnar13): children <5, immunocompromised adults |
|
|
What are the two vaccines fro bordatella pertussis?
|
DTaP and Tdap
|
|
|
What is the most effective strategy to improve immunization rates?
|
Have standing orders during office visits
|
|
|
What are the only things proven to increase survival in patients with COPD?
|
Smoking cessation and oxygen (if hypoxemic)
|
|
|
What are the two different pieces of the combination therapy for smoking cessation?
|
Behavior modification and pharmacotherapy
|
|
|
What are the 3 pieces of behavior therapy in smoking cessation?
|
Identify and avoid high risk situations, recognize cues and triggers, and substitue alternative or coping behaviors
|
|
|
What are the 3 most effective types of counseling for smoking cessation?
|
Practical withdrawal (dispose of paraphernalia, substitute behaviors, abstain from alcohol), intra-treatment social support, extra-treatment social support
|
|
|
What are the 7 first-line pharmacotherapies for smoking cessation?
|
Nicotine (Gum, patch, nasal spray, inhaler, lozenge), bupropion, varenicline
|
|
|
Which form of nicotine has the highest compliance and which do most prefer?
|
The patch has the highest compliance. More people like the inhaler.
|
|
|
What is the mechanism of action for varenicline?
|
Nicotine partial agonist. It limits craving and withdrawal symptoms and blocks rewards
|
|
|
What normally happens to respiratory rate, tidal volume, minute ventilation, PCO2, and PaO2 when we sleep?
|
Respiratory rate and PCO2 both increase. Tidal volume, minute ventilation, and PaO2 all decrease
|
|
|
Spindles and K-waves are present in which stage of sleep?
|
N2
|
|
|
What does AHI stand for?
|
Apnea-Hypopnea Index
5-15/hr=mild; 15-30/hr=moderate; 30+=severe |
|
|
What are some risk factors for obstructive sleep apnea?
|
Reduced airway size (central, male-patterned obesity), craniofacial features (retrognathia, macroglossia), reduced neuromuscular output
|
|
|
What is the Epworth Sleepiness Scale and how is it used?
|
Measures daytime sleepiness. 11≤ suggests OSA
|
|
|
What is a common comorbidity in obstructive sleep apnea?
|
Systemic HTN
|
|
|
What are some common medical and surgical therapies used to treat obstructive sleep apnea?
|
* Weight loss, sleep hygiene, oxygen therapy, CPAP, BIPAP, REM suppressing medications, stimulants
* Tracheostomy, uvulopalatopharyngoplasty, maxillary-mandibular-hyoid advancement, gastroplasty or Roux en Y |
