Term
|
Definition
|
|
Term
What is RV?
What is ERV?
What is Vt? |
|
Definition
Residual volume: The volume of gas remaining in the lungs after maximal exhalation.
Expiratory reserve volume: The maximal volume of gas exhaled from the end of expiratory level.
Tidal volume: the volume of gas inhaled during quiet breathing. |
|
|
Term
What is VC?
What is FRC?
What is TLC? |
|
Definition
Vital capacity: the maximum volume of gas exhaled from the point of maximum inspiration.
Functional residual capacity: the volume of gas remaining in the lungs at end-expiration; the sum of RV and ERV.
Total lung capacity: the sum of all volume compartments; the volume of gas in the lungs after maximal inspiration. |
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Term
| What is the difference between a volume and a capacity? |
|
Definition
| A capacity is the sum of two or more volumes. |
|
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Term
What is FEV1?
When is it low?
When is it high? |
|
Definition
Forced Expiratory Volume 1: The volume of air you can expire in the first second from TLC.
Low is a sign a is a sign of narrowed airways (obstructive).
(relatively) High FEV1 is a sign of increased elasticity (restrictive). |
|
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Term
What is a typical TLC?
What is a typical FRC?
What is a typical RV?
What is a typical FEV1/FVC? |
|
Definition
|
|
Term
What is Dalton's law?
What is barometric pressure?
Po2? |
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Definition
The idea that the total pressure in a system is the sum of the partial pressures of all of the gasses in the system.
Pb = 760 mmHg
Po2 = 160 mmHg |
|
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Term
What do we use fractional concentrations for?
What is the equation?
What is Fo2? |
|
Definition
They replace partial pressures. They are useful because they don't vary with barometric pressure.
Fg=Pg/(Pb-Ph2o). Key - DRY room air.
Fo2 = 0.209 |
|
|
Term
| Why is the partial pressure the body sees less than the partial pressure in the atmosphere? |
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Definition
| You have to add the partial pressure of H2O in the body - this displaces the other gasses (total still has to be Pb), so you end up diluting them. |
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Term
What is equalized between gas and liquid phases, or two liquids?
What isn't equalized? |
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Definition
The partial pressure of the gas is equalized between the different states.
The concentration will change depending on the solubility. |
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Term
What is Henry's Law?
What does the solubility coefficient vary with? |
|
Definition
Cg = K * Pg
Cg = the concentration of the gas dissolved in a solution.
K = the solubility constant.
Pg = the partial pressure of the gas.
K varies with the specific gas, the specific solvent, and the temperature. |
|
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Term
| How does Henry's Law apply to oxygen content in the blood? |
|
Definition
| In the blood most of the oxygen binds to hemoglobin so it doesn't affect the partial pressure. This allows for a high partial pressure gradient to be maintained aiding oxygen uptake. |
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Term
| What does a normal inspiratory curve look like? |
|
Definition
| It is symmetric and shaped like a U. If it's flat, that often means they aren't trying hard enough or there's a disease. |
|
|
Term
| Why is a normal expiratory curve asymmetric? |
|
Definition
| It is due to decreasing tension as the lung decompresses. At first it's really stretched and helps push everything out, but that decreases as it collapses. |
|
|
Term
|
Definition
Forced vital capacity: The volume of air that can be forced out of the lung after full inspiration.
FEV1/FVC is an important measure of lung function. |
|
|
Term
What is BTPS?
What is STPD?
What is ATPS? |
|
Definition
Body temp, ambient pressure, saturated w/water vapor.
Standard temp (0/273), standard pressure (760 mmHg), dry.
Ambient temp, ambient pressure, saturated w/water vapor. |
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|
Term
What embryologic structure does the lung come from?
When does budding occur? |
|
Definition
| It comes from the ventral foregut diverticulum. Forgut outpouching into mesoderm and starts branching. Budding occurs in week 4. |
|
|
Term
| What are the 5 phases of development of the lung? |
|
Definition
1. Embryonic
2. Pseudoglandular
3. Canalicular
4. Saccular
5. Alveolar |
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|
Term
| What happens during the embryonic stage of lung development? When does it occur? |
|
Definition
| 3-6 weeks. Right and left primary bronchial buds form. Lobar and segmental bronchi form. Mesenchyme drives the differentiation. |
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|
Term
| What happens during the pseudoglandular stage of lung development? When does it occur? |
|
Definition
| 6-16 weeks. Distal airways form (branching to the terminal bronchioles). Cartilage, smooth muscle, and vessels form (mesenchyme laying the foundation). |
|
|
Term
| What happens during the canalicular stage of lung development? When does it occur? |
|
Definition
| 16-26 weeks. Branching to the level of the alveolar ducts and acinar tubules. Epithelial cells differentiate into secretory or lining cells. Capillaries surround acinar tubules to form gas exchange region. |
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|
Term
| What happens during the saccular stage of lung development? When does it occur? |
|
Definition
| 26-36 weeks. Lung acini continue to grow, epithelial cells differentiate into type I (surface area for exchange) and type II cells (surfactant). |
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|
Term
| What happens during the alveolar stage of lung development? When does it occur? |
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Definition
| From birth to adolescence. Continued development of alveoli. Keep gaining lung tissue. |
|
|
Term
| What drives lung development? |
|
Definition
| Epithelial/mesenchymal interactions. |
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|
Term
What is the function of type I pneumocytes?
What is the function of type II pneumocytes?
What is the function of clara cells? |
|
Definition
Type I: Increase surface area for gas transport. They are thin squamous cells and line 97% of alveolar surfaces.
Type II: Cuboidal cells that produce surfactant. They are the progenitors. They proliferate in lung injury.
Clara: Non-ciliated columnar cells with secretory granules (secrete a component of surfactant). They degrade toxins, and act as reserve cells. |
|
|
Term
| What is surfactant made of and what is its purpose? |
|
Definition
| It is 80% pospholipids, 12% neutral lipids, and 8% protein. It lines the alveoli reducing alveolar surface tension and prevent collapse. |
|
|
Term
| What is surfactant made of and what is its purpose? |
|
Definition
| It is 80% pospholipids, 12% neutral lipids, and 8% protein. It lines the alveoli reducing alveolar surface tension and prevent collapse. |
|
|
Term
| How is the lung divided anatomically? |
|
Definition
| Primary bronchus (2), secondary bronchus (lobe), tertiary bronchus (segmental - 10R, 9L), terminal bronchiole (lobules), pulmonary acinus (respiratory bronchioles, alveolar ducts, terminal alveoli). |
|
|
Term
| How are bronchi different from bronchioles? |
|
Definition
Bronchi have glands and cartilage. They are lined by pseudostratified ciliated columnar epithelium.
Bronchioles have circumferential smooth muscle. They are lined by columnar ciliated epithelium. |
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|
Term
| What is the smallest anatomic unit of the lung? |
|
Definition
| Pulmonary lobule. They are bounded by interlobular septa. Each lobule contains 20-30 acini. |
|
|
Term
| Which layer of the basement membrane is thickened in Asthma? What cells are over-expressed in asthmatics? |
|
Definition
| The lamina reticularis. Asthmatics also have goblet cell metaplasia and smooth muscle hyperplasia. |
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|
Term
What is the functional unit of the lung?
What are pores of Kohn? |
|
Definition
The functional unit of the lung is an acinus. It includes the respiratory bronchiole, the alveolar ducts, and the alveolar sacs.
Pores of Kohn are direct communications between adjacent alveoli. Involved in collateral ventilation. |
|
|
Term
What is Lambert's Canal?
What is Lambertosis? |
|
Definition
It is direct communication between non-respiratory bronchioles and alveoli. Provides collateral ventilation.
Lambertosis: Bronchiolarization (epithelium can start covering the alveoli) - seen in scarring of the airways and other lung diseases. |
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|
Term
Why do the lungs not often infarct?
Describe the bronchovascular bundle. |
|
Definition
They have two blood supplies. Bronchial and pulmonary.
In the bronchovascular bundle, the diameter of the lumen should be roughly the same for both. |
|
|
Term
| What are the components of the pleura? |
|
Definition
Visceral: supplied by bronchial arteries
Parietal: supplied by systemic circulation
Lymphatic system
Nerves (hence plueritis)
Mesothelial cells (single layer lining of the basal lamina) |
|
|
Term
| What are the features of obstructive lung disease? |
|
Definition
| It is usually disease which produces decreased airflow in the large and small airways. It is associated with increased lung volumes (trapping), and decreased elastic recoil. |
|
|
Term
| What are the 3 main categories of obstructive lung disease? |
|
Definition
1. COPD (smokers): includes chronic bronchitis, and emphysema. Irreversible.
2. Asthma
3. Bronchiectasis |
|
|
Term
| What are the characteristics of emphysema? |
|
Definition
1. It is smoking related (90+% of the time)
2. Leads to enlargement of alveolar spaces due to parenchymal destruction.
3. Loss of connective tissue (tethering) leads to airway collapse during expiration.
4. Pathology: a) Large overinflated lungs; b) enlarged alveolar spaces w/floating septae. |
|
|
Term
| What is the pathogenesis of emphysema? |
|
Definition
| It is due to protease/antiprotease imbalance. Proteases are produced by inflammatory cells (neutrophil elastase). Smoking attracts more inflammatory cells. Normally these proteases are inactivated by alpha 1 antitrypsin produced in the liver, but it can be inhibited in smoking (99%) or genetically defective (1% - Recessive, associated w/liver disease). |
|
|
Term
| What are the 2 variants of emphysema you see histologically? |
|
Definition
1. Centriacinar: Expansion of the respiratory bronchiole. Associated with smoking.
2. Panacinar: Expansion of the alveolus and alveolar duct. Related to A1AT deficiency. |
|
|
Term
| What are the characteristics of chronic bronchitis? |
|
Definition
| Smoking related. Disease of larger airways. Will have chronic airway inflammation, and mucus gland hypertrophy (due to irritation from smoking). Predisposes to infection. |
|
|
Term
How do you diagnose chronic bronchitis?
What is the Reid index? |
|
Definition
It is a clinical diagnosis. Productive cough for most days in 3 consecutive months for 2 consecutive years.
Reid index: ratio of mucus gland size to distance from epithelium to cartilage. (>0.4 consistent w/chronic bronchitis). |
|
|
Term
What is Bronchiectasis?
What causes it? |
|
Definition
| it is an obstructive disease caused by irreversible dilation of the airways. It is caused by a vicious cycle of obstruction, infection, and bronchial wall destruction. Common in cystic fibrosis (thick secretions), Kartagener's syndrome (ciliary dismotility), repeated infections. Clinically presents w/ a productive cough and foul smelling sputum. |
|
|
Term
| What are the 3 key things to remember about Asthma? |
|
Definition
1. It is a reversible episodic obstruction.
2. It is due to airway hyperreactivity.
3. Chronic inflammation is present. |
|
|
Term
| What are the 3 types of Asthma? |
|
Definition
1. Atopic asthma: related to a type 1 (IgE) hypersensitivity reaction (systemic reaction to an allergen).
2. Non-asthma: triggered by environmental irritants and infection (not an IgE reaction), e.g. exercise, cold air, etc.
3. Aspirin related asthma: Samter's triad - asthma, aspirin allergy, nasal polyps. |
|
|
Term
What happens early after exposure to a trigger in asthma?
Late? |
|
Definition
Early: Smooth muscle contraction around airways, mucus secretion, submucosal edema (airway hyperreactivity). This is mediated by leukotrienes, prostaglandins, histamine, etc.
Late: Inflammatory cell recruitment (eosinophils, Th2 leukocytes) |
|
|
Term
| What airway changes can occur in chronic asthma? |
|
Definition
| Long standing asthma can cause airway remodeling including smooth muscle cell hyperplasia, mucus gland hyperplasia, and epithelial damage. |
|
|
Term
| What are histopathologic findings in asthma? |
|
Definition
| Basement membrane thickening (non-specific), mucus plugging (casts), Curschmann's spirals, and Charcot-Leyden crystals. |
|
|
Term
What are Charcot-Leyden crystals?
What are Curschmann's spirals? |
|
Definition
C-L: They are structures formed from the products of eosinophil degranulation.
Curschmann's: Corkscrews forming in the mucus. Don't know why. Has something to do with a quality of the mucus in these patients. |
|
|
Term
| What is Respiratory Distress Syndrome (RDS)? |
|
Definition
| It is due to inadequate surfactant production, which leads to stiff lungs. Ground-glass CXR. It can lead to bronchopulmonary dysplasia if lung abnormalities develop. |
|
|
Term
What is Bronchopulmonary Dysplasia (BPD)?
How is severity measured? |
|
Definition
Aka Chronic Lung Disease of Infancy. Long term lung abnormalities resulting from RDS. Diagnosed if on O2 at 28 days. Re-assess at 36 week post-menstrual age if born <32 weeks. Re-assess at 56 days old if born >32 weeks.
Mild: room air, Moderate: <30% O2, Severe: >30% O2. |
|
|
Term
What factors lead to a higher risk of BPD?
What factors lead to a lower risk? |
|
Definition
Higher: Lower GA, lower birth weight, infections (maternal or neonate), positive pressure ventilation, oxygen toxicity.
Lower: Antenatal steroids, surfactant therapy, nutritional support, ventilator management. |
|
|
Term
| What are the 3 main types of congenital lung malformations? |
|
Definition
1. Airway abnormalities
2. Parenchymal abnormalities
3. Vascular abnormalities |
|
|
Term
What is Laryngomalacia?
How does it present?
How is it diagnosed and treated? |
|
Definition
| It is an airway abnormality caused by an omega shaped epiglottis, short aryepiglottic folds, and/or prolapsed arytenoids. Presents w/stridor. Diagnosed w/bronchoscopy. Treatment: supportive (check for aspiration/reflux), unless severe then surgery. |
|
|
Term
What is Tracheo-bronchomalacia?
How does it present?
How is it diagnosed and treated? |
|
Definition
It is an airway abnormality of unknown cause (likely alterations in structural support) leading to smushed airways.
Presents as noisy breathing. Diagnosed w/expert opinion and bronchoscopy. Treatment: supportive, surgical if severe. |
|
|
Term
What is Tracheoesophageal fistula?
How does it present?
How is it diagnosed and treated? |
|
Definition
| It is an airway abnormality in which the esophagus doesn't completely separate from the laryngotracheal tube. Presents with drooling (can't swallow secretions), chocking w/feeding in first 24 hrs of life. Diagnose by inability to pass a gastric tube & radiography. Treatment: surgical. |
|
|
Term
What is Pulmonary sequestration?
What are the 3 types? |
|
Definition
| It is a type of parenchymal abnormality, in which there is normal non-functioning lung tissue that is not connected to the bronchial tree. It receives its blood supply from the systemic circulation. 3 types: Intralobar, extralobar, bronchopulmonary foregut malformation (GI tract). 3:1 Intralobar to extralobar. |
|
|
Term
How does pulmonary sequestration occur?
What defines intralobar vs. extralobar? |
|
Definition
| Congenital. Intralobar can be acquired from bronchial obstruction, pneumonia, parasitization of the pulmonary arteries. Intralobar occurs where the extra tissues is completely covered by normal lung. Drain via pulmonary veins. Extralobar is an accessory lung separated from the functioning lung, but covered with visceral pleura. 80% Usually in the lower left lobe. 80% males. Drain to systemic venous drainage. |
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|
Term
| What is Congenital pulmonary airway malformation (CPAM)? |
|
Definition
| Used to be Congenital cystic adenomatoid malformation. It is a heterogenious group of congenital lung masses caused by extensive overgrowth of the primary broncioles. 25-30% of all lung malformations. Most common in lower lobes. |
|
|
Term
How does the Stocker classification of CPAM work?
What do you need to be careful of when diagnosing CPAM? |
|
Definition
It is a classification from 0 (worst) to 4 that is dependent on the size of the masses and their origin.
When diagnosing beware of congenital diphragmatic hernia, which can look similar on CXR. |
|
|
Term
What is Congenital Lobar Emphysema?
What causes it?
Types (based on histology)? |
|
Definition
It is an overinflation or distension of one or more pulmonary lobes. Caused by intrinsic (weak) or extrinsic (mass) bronchial narrowing leads to trapping. Most commonly affects LUL.
Types: Hypoalveolar, Polyalveolar. |
|
|
Term
What does "Rings & Slings" refer to?
How does it present?
How is it diagnosed and treated?
What are the types? |
|
Definition
| It refers to vascular abnormalities in the development of the aortic arch which lead to compression of the esophagus and trachea. Presents with difficulty swallowing, stridor, respiratory distress, recurrent pneumonia, or apnea. Diagnosed with barium swallow, treated w/surgery. Types: Sling (aberrant left pulmonary/right subclavian artery), Ring (double arch). |
|
|
Term
What are Pulmonary arteriovenous malformations?
How does it present?
How is it diagnosed and treated? |
|
Definition
| They are abnormal connections between arteries and veins. Present w/pulmonary hemorrhage or hemoptysis or hypoxia (no gas exchange). Diagnosed with CXR or angiography. Treat with embolization. Can present as pediatrics or adult. |
|
|
Term
| What is hereditary hemorrhagic telangectasis (HHT)? |
|
Definition
| It is associated with pulmonary arteriovenous malformations. It is a genetic disorder that leads to telangectasias (red flecks) of the nose, mouth and hands. |
|
|
Term
What are the muscles of inspiration?
What are the muscles of expiration? |
|
Definition
Inspiration: diaphragm. If needed: scalenes, sternocleidomastoid, external intercostals.
Expiration: passive. If needed: rectus abdominous, obliques, transversus abdominous, internal intercostals. |
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|
Term
What is transpulmonary pressure?
What is transthoracic pressure?
What is transrespiratory pressure? |
|
Definition
Transpulmonary (lung) pressure is the pressure acting to inflate the lungs. Ptp = PA - Pip.
Transthoracic pressure is the pressure acting to comtract teh chest wall. Ptt = Pip - Pb.
Transrespiratory pressure is the whole gradient that leads to breathing; alveolar pressure - barometric pressure. |
|
|
Term
| Describe intrapleural pressure. |
|
Definition
| Intrapleural pressure is the pressure in the pleural fluid. It is a measure of the battle between lung elastic recoil, and chest wall stiffness. It drops when the battle between lung and chest wall increases. Think of a bubble in that space. Usually Pip is < Pb (pulling the lung out and the chest wall in). |
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|
Term
| What happens to the lung in a pneumothorax? What happens to the chest wall? Which side should you put the tube in? |
|
Definition
| The lung will collapse (elastic recoil dominates), while the chest wall will expand. If you're treating someone, put the tube in the side of their chest that looks large. |
|
|
Term
What is compliance?
What is the inverse of compliance? |
|
Definition
Compliance is ΔV/ΔP. That means it is the slope of the pressure volume curve. More compliant = stretchier.
Elastance is the inverse of compliance. More elastic = stiffer (higher recoil). |
|
|
Term
What conditions decrease compliance?
What conditions increase compliance? |
|
Definition
Decrease: Respiratory distress syndrome (no surfactant), edema, atelectasis (alveolar collapse), fibrosis.
Increase: Age, emphysema, increasing body size (due to increase in lung volume). |
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|
Term
What is the Law of LaPlace?
Why does the small bubble collapse? |
|
Definition
P = 2T/R. P = pressure, T = surface tension, R = radius.
Key takeaway: pressure increases as radius decreases.
This is due to geometry; as smaller radius → more inward force from neighboring molecules → greater pressure. Also tension is constant in a liquid as more molecules are added to the surface. This is in contrast with tissue where tension increases as radius increases. |
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|
Term
| What are 3 takeaways from surface tension with respect to the lung? |
|
Definition
1. Surface tension provides much of the elastic recoil force of the lung (and counteracts first breath)
2. Small alveoli will have a tendency to collapse
3. Surface forces tend to pull interstitial fluid into the alveolus |
|
|
Term
|
Definition
| It is the different relationship between pressure and volume during inflation compared to that during deflation. It is due to the interplay between surface tension and surfactant. |
|
|
Term
| What are the 4 effects of surfactant? |
|
Definition
1. Reduces surface tension (and thus work of breathing)
2. Preserves alveolar integrity (preventing collapse or emptying of small alveoli into large)
3. Reduces transudation (edema) in the lung.
4. Causes surface tension to vary with surface area (hysteresis) |
|
|
Term
What is surfactant?
About when is it functional in a humans? |
|
Definition
It is a lipoprotein complex (30% protein, 70% phospholipid - mostly dipalmitoylphosphatidylcholine).
It starts to be produced around 24-26 weeks. Weeks 30-34 the infant has enough to be functional. |
|
|
Term
| How does surfactant work? |
|
Definition
| It's amphipathic nature helps reduce the tension between water and air. On expiration it is compressed to form a virtual surface solid, decreasing surface tension to near 0. This prevents collapse of alveoli. On inspiration it has to fill in the gaps with fluid, so more surface tension is present. This difference explains hysteresis. |
|
|
Term
How do you sum the compliance of the chest and the lung?
What does this equation imply? |
|
Definition
1/Cr = 1/Cc + 1/Cl. Cr = total respiratory compliance, Cc = chest compliance, Cl = lung compliance.
This means that total compliance will be less than the individual compliances (blowing up two balloons inside each other). |
|
|
Term
What happens to FRC and Pip with a stuff chest wall?
With a stuff lung? |
|
Definition
Chest: Pip decrease (bigger battle). FRC increases (chest winning).
Lung: Pip decreases (bigger battle). FRC decreases (lung winning). |
|
|
Term
| How does regional ventilation in the lung work? |
|
Definition
| Intrapleural pressure is lower (larger magnitude) in the apices of the lung due to gravity pulling the lung down (think slinky). Since the alveoli are more stretched at the top, they are less compliant. At FRC the same ΔP leads to a larger ΔV at the base, so that's where most ventilation occurs (opposite occurs at RV). Blood flow is higher at the lower zone as well due to gravity. |
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|
Term
How does V=IR relate to airflow?
What happens to PA as resistance increases? |
|
Definition
Flow = (Pb-PA)/Resistance.
For a given rate of flow, if R↑, then PA↓. As PA drops, the lungs become harder to expand (stiffer) and Pip drops.
Asthma ↑ R, while COPD ↓P gradient (less recoil). |
|
|
Term
| Why doesn't intrapleural pressure follow a straight line during inspiration and expiration? |
|
Definition
| It would if we were only dealing with elastic recoil. However, airway resistance requires extra force to generate flow. |
|
|
Term
| What area of the lung has the lowest aggregate cross sectional area? |
|
Definition
| The segmental bronchi. This is the area we are most concerned about collapsing. |
|
|
Term
What do we learn from the Bernouli equation?
What affects velocity? |
|
Definition
It tells us that as velocity increases, pressure drops.
Velocity = Flow/Cross-sectional Area. The smaller the cross sectional area (segmental bronchi) the higher the velocity. This is where you'll have the least pressure. |
|
|
Term
| What are the 3 cases we care about with the Starling Resistor? |
|
Definition
1. Pe>Pi>Po - tube collapses
2. Pi>Pe>Po - tube flutters open and closed (flow will stabilize but with increased resistance and lower flow)
3. Pi>Po>Pe - continuous flow
Pe = external pressure (Pip), Pi = inflow (PA), Po = outflow |
|
|
Term
| What helps to reduce airway collapse due to Bernouli's Law? |
|
Definition
| Tethering. The connective tissue between the airways and the lungs hold the airways open when the lungs are expanded. At reduced lung volumes, there is more susceptibility for collapse. |
|
|
Term
| What causes the effort independent (flow limited) part of the expiratory curve? |
|
Definition
| Dynamic compression of the airways. The more you increase pressure, the more you compress the airways. This means increased effort can't affect flows. The narrowed airway can cause turbulent flow: wheezing. The biggest problem occurs at lower lung volumes. |
|
|
Term
| What does a concave expiratory curve indicate in spirometry? |
|
Definition
| It means the flow is dropping faster than it should. This is likely due to decreased elastic recoil (emphysema), or increased resistance (asthma). |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| What do you notice about restrictive lung disease in spirometry? |
|
Definition
| It has a low vital capacity, with a high FEV1. This is due to stiff lungs and lower compliance. Quick exhalation, but incomplete inhalation→ ↑ FEV1/FVC; ↓ TLC, FRC, FVC. |
|
|
Term
| What are the 3 main tests you use to measure lung function? |
|
Definition
1. Spirometry. This gives you Vol vs. time curves.
2. Gas dilution. This will help you find the true lung volume.
3. Diffusing capacity. Use CO to see how well gas is taken up by the blood. |
|
|
Term
Which diseases will lead to increased diffusing capacity?
Which will lead to decreased diffusing capacity? |
|
Definition
Increased: Polycythemia, Alveolar hemorrhage.
Decreased: Anemia, Pulmonary vascular disease, Pulmonary fibrosis, Emphysema. |
|
|
Term
|
Definition
V=Pel/R
Pel = Elastic recoil pressure (this drops in Emphysema)
R = Resistance
V = Flow |
|
|
Term
What is pulmonary ventilation?
What is alveolar ventilation? |
|
Definition
It is the amount of air expired in a minute. Ve = Vt * f
Ve = minute ventilation, Vt = tidal volume, f = frequency (RR)
It is the minute ventilation - dead space ventilation. VA = f * (Vt - Vd). Note: VA increases more with ↑ Vt than ↑ f. |
|
|
Term
| What is anatomic dead space? |
|
Definition
| Those airways where gas exchange can not occur (~1st 16 generations); the volume of the conducting airways, Vd, is about 1/3 of normal Vt. |
|
|
Term
| What is alveolar dead space? |
|
Definition
| It is ventilation not participating in gas exchange. It is generally due to alveoli ventilating without sufficient blood supply (apex of the lung). It could also be excess ventilation beyond what is required for oxygenation. |
|
|
Term
| What is physiologic dead space? |
|
Definition
| It is anatomic dead space + alveolar dead space. I.e. all parts of the lungs that are not participating in gas exchange. |
|
|
Term
| What is the respiratory quotient (RQ)? |
|
Definition
| Aka Respiratory exchange ratio (R). RQ = Vco2/Vo2 where Vco2 = CO2 production (basal 200 ml/min); Vo2 = oxygen consumption (basal 250 ml/min.). These numbers are set by metabolism. |
|
|
Term
What happens to the respiratory exchange ratio (R) with a diet of Carbohydrates? Fats? Protein?
What is a normal value for R? |
|
Definition
Carbohydrates: R=1
Fats: R=0.71
Protein: R=0.83
Normal: R=0.8 |
|
|
Term
| What is the Alveolar gas equation? |
|
Definition
|
|
Term
| What is the normal PAO2? PACO2? |
|
Definition
PAO2 = 80-100 mmHg
PACO2 = 35-45 mmHg |
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Term
| Why is the alveolar ventilation equation important? |
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Definition
| It relates ventilation, metabolism, and blood gas composition. Key takeaway: As ventilation increases, PCO2 will drop if metabolism is held constant. In practice, a healthy person will maintain a normal PCO2 by increasing ventilation by the same fold as metabolism. |
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Term
What is the true definition of hyperventilation?
What is the true definition of hypoventilation? |
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Definition
Hyperventilation is greater ventilation than necessary to maintain a normal PCO2 (isocapnea). i.e. Hyperventilation = hypocapnia.
Hypoventilation is lower ventilation than necessary to maintain a normal PCO2. i.e. Hypoventilation = hypercapnia. |
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Term
What is it called when ventilation increases appropriately to match metabolism?
What about when it decreases appropriately? |
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Definition
Hyperpnea. E.g. Exercise hyperpnea.
Hypopnea. |
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Term
| What is Fick's law of diffusion? |
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Definition
Vg = A/t * D * ΔP
Vg: flow of a gas. A: Surface area. t: thickness of the diffusion barrier. D: diffusion coefficient. α solubility/(molec. wt.)^.5. (Dco2 is 20x Do2) |
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Term
| How long does a typical RBC stay in the pulmonary capillary? |
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Definition
| 0.75 sec. This is more than enough time for sufficient diffusion to occur in order to equilibrate gas partial pressures. |
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Term
| What is a Diffusion Limitation? |
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Definition
| It occurs when the diffusion pathway provides a barrier that limits gas transfer such that equilibrium is not achieved. The more soluble something is the more of it must be loaded on to equalize partial pressures, so it is more likely to be diffusion limited. CO is an example. |
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Term
| What is a Perfusion Limitation? |
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Definition
| In a perfusion limitation partial pressure equibrilation occurs rapidly. Increased perfusion is required to maintain a gradient. This tends to be the case with less soluble gasses, where not much transfer has to occur before partial pressures equalize. An example is N2O. |
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Term
| Is oxygen perfusion or diffusion limited? |
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Definition
| Under normal conditions O2 is perfusion limited (equilibration occurs 1/3 of the way down the capillary). However, increasing PAO2 (giving O2) can cause it to become diffusion limited. |
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Term
How do we calculate diffusing capacity of the lung?
Why do we need this number? |
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Definition
| DL = V/(PA - Pc). V: flow of gas. PA: Alveolar pressure. Pc: capillary pressure. Think of this as a capacitance. That means that 1/DL is the resistance to diffusion. |
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Term
What causes resistance to diffusion?
How do we account for them? |
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Definition
Diffusion is limited by 1) the physical diffusion through a barrier, and 2) chemical reactions (binding to Hb, etc.)
We account for them as resistances in series, so 1/DL = 1/Dm + 1/Dc |
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Term
How much Oxygen can one molecule of Hemoglobin hold?
What is O2 capacity of the blood? |
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Definition
Hemoglobin can hold 4 molecules of oxygen.
Hb + 4O2 = Hb(O2)4
Thanks to Hb, blood has an O2 capacity of 20.1 vol%. |
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Term
What is the Hb saturation at 100 mmHg of O2?
At 90 mmHg?
At 40 mmHg?
At 27 mmHg? |
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Definition
100 mmHg 98% saturation. Arterial blood.
90 mmHg 90% saturation. Clinical cutoff for arterial blood.
40 mmHg 75% saturation. Venous blood.
27 mmHg 50% saturation. This is the P50, an expression of affinity of Hb for O2. |
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Term
| What things increase P50 (i.e. decrease the affinity between Hb and O2)? |
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Definition
1. Increased temp. 2. Decreased pH or increased CO2 (Bohr effect). 3. Increased levels of 2,3-diphosphoglycerate (2,3 DPG). This is increased in chronic hypoxia.
We want O2 to fall off easier near muscle that will have higher temp, higher CO2, lower pH. |
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Term
| Why is the Hb O2 curve shaped the way it is? |
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Definition
Flat top: small changes in alveolar PO2 won't be a big deal.
Steep middle: Tissues can extract a lot of O2 with a small drop in PO2. |
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Term
| What are the 4 types of hypoxia? |
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Definition
1. Hypoxic hypoxia (low PaO2).
2. Anemic hypoxia (not enough Hb).
3. Circulatory hypoxia (not enough perfusion).
4. Histotoxic hypoxia (cyanide poisoning - O2 can't be used). |
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Term
| How is CO2 transported from the tissues? |
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Definition
| In 3 forms: 1) Dissolved in the blood 2) Bicarbonate 3) Carbamino compounds (mostly bound to Hb). The conversion to bicarb occurs in the RBC via carbonic anhydrase. Bicarb is transported out of the cell for Cl-. This pulls the reaction forward. |
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Term
What is the Bohr effect?
What is the Haldane effect? |
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Definition
B. effect: H+ displaces O2 from Hb. Drives O2 delivery at the tissues.
H. effect: Adding O2 displaces H+ form Hb. This in turn drives the release of CO2 from bicarb. Drives exchange at the lungs. |
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Term
| How much do each of the 3 forms of CO2 contribute to its transport and release? |
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Definition
Transport: Bicarb 90%, Carbamino 5%, Dissolved 5%
Release: Bicarb 60%, Carbamino 30%, Dissolved 10%.
This is due to the slow reaction speeds (bicarb), and the Bohr/Haldane effects (carbamino). |
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Term
| What does the CO2 saturation curve look like? |
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Definition
It is much more linear than the O2 curve. It has the 3 phases, and although it has a smaller partial pressure, content is ~ 2x O2 content (due to solubility).
Note: at a given pressure you have more CO2 in venous than arterial blood due to the Bohr/Haldane effects (more carbamino). |
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Term
| What is the A-a gradient and what does it tell us clinically? |
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Definition
| It is PAO2 - PaO2. Normal is 2.5 + (0.25)*age. Usually around 10 (up to 20 in an older person). It measures how efficient gas transport is. If there is a wide A-a gradient that is a sign of underlying lung disease. |
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Term
| How do you calculate an A-a gradient? What is normal? What does it tell you? |
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Definition
| PAO2 - PaO2. (Find PAO2 from the alveolar gas equation). Normal is between 10-15. It tells you about the efficiency of the lung. How well is it able to transfer an Alveolar pressure into an arterial pressure. If it is abnormal that means there is underlying lung disease. |
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Term
| What are the 3 categories of causes of hypoxemia? |
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Definition
| 1. Decreased A-a gradient (underlying lung disease). 2. ↓ Venous Saturation 3. Decreased PAO2. |
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Term
| What are the 3 things that cause a wide A-a gradient? |
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Definition
1. Shunt
2. ↓ V/Q
3. Diffusion |
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Term
| What are the 4 things that can cause a decrease in PAO2? |
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Definition
The key is the alveolar gas equation.
1. Altitude: drops Pb.
2. ↓ FiO2 (fire, etc.)
3. Hypoventilation: drops PaCO2.
4. R changes: not important. |
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Term
| What are the 8 things that cause hypoxemia? |
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Definition
| 1. Shunt 2. ↓ V/Q 3. Diffusion 4. ↓ Venous Saturation 5. ↓ Pb (altitude) 6. ↓ FiO2 7. Hypercapnia (hypoventilation) 8. R changes. |
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Term
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Definition
| It is blood flow from right heart to left heart having never been ventilated. |
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Term
What are conditions that cause shunts in the lung?
How well do shunts respond to oxygenation?
What determines if you can go home? |
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Definition
A blocked alveolus. Can fill with: Pus; Water; Blood; Atelectasis. Or there could be a L→R intracardiac shunt.
Shunts are refractory to oxygen. Not a lot of bang for your buck. Can calculated using a weighted average of the O2 sats.
The degree of shunting is the important measure. |
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Term
| What is the P/F ratio, and what is it used for? |
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Definition
| It is PaO2/FiO2. It is used in place of the A-a gradient when a patient is not on room air. A normal value is >450. |
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Term
| What is a low V/Q and what causes it? |
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Definition
| A low V/Q is a decreased ventilation to perfusion ratio. It can be caused by Asthma, COPD, (perfused but not well ventilated) or a Pulmonary Embolism (increase in flow to unblocked areas). Basically anything that doesn't put enough oxygen and blood next to each other. These patients respond well to oxygenation (in effect increasing V). |
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Term
| What is diffusion limitation and what causes it? |
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Definition
| It occurs when the oxygen cannot properly diffuse through the alveolus into the blood. This can be due to fibrosis (interstitial thickening) or emphysema (decreased area available for diffusion). |
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Term
| What lowers mixed venous O2 saturation (SvO2)? |
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Definition
*Decreased oxygen delivery: ↓ Cardiac Output; Anemia, ↓ PaO2.
Increased oxygen consumption (febrile, excessive movement).
Note: This will only matter if the lungs are already unhealthy. Otherwise you'll be able to overcome a decreased SvO2 quite easily. You can oxygenate it right back to normal. |
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Term
| What is the equation for O2 delivery to the tissues (DO2)? |
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Definition
DO2 = C.O. * [(1.34 * Hg * SaO2) + 0.003 * PaO2]
That is, cardiac output times arterial oxygen content. |
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Term
| Why does hypercapnia (hypoventilation) lead to hypoxemia? |
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Definition
| As PaCO2 rises, PAO2 falls, lowering PaO2. This is seen via the Alveolar gas equation. The key is to increase minute ventilation. |
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Term
| What kinds of things can cause hypoventilation? |
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Definition
1. Low lung compliance (fibrosis)
2. CNS depression (injury, etc)
3. Inadequate ventilator settings
4. Muscle paralysis/fatigue
5. High airway resistance (asthma)
By definition will by hypercapnic. |
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Term
| We all have a little bit of shunt. What causes that? |
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Definition
| Bronchial or thebesian circulations. Thebesian circulations are circulations in the heart that empty directly into the left ventricle. |
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Term
| How do you find O2 levels in a shunt? Can you average partial pressures, content, saturations or what? |
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Definition
| You use a weighted average of content (saturations work too). Partial pressures cannot be used since low content blood will pull the pressure down due to Hb scavenging. |
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Term
| Shunt leads to hypercapnia and hypoxemia. What does hyperventilation do to these levels? |
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Definition
| Hyperventilation can solve the hypercapnia, but not the hypoxemia. This is due to the fact that increasing alveolar ventilation can get rid of excess CO2, but it can't add much O2 content to the blood since the blood that's being ventilated is already almost saturated. That's why it is refractory to oxygen supplementation. |
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Term
| Why can't we take the overall V/Q to see if we have sufficient ventilation to perfusion? |
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Definition
| Because areas of high V/Q can't compensate for areas of low V/Q due to the oxygen Hb dissociation curve. Therefore mismatching in individual areas of the lung is what matters. |
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Term
| What causes V/Q maldistribution in the lung? |
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Definition
1. Gravitational forces: ventilation is higher in the lower parts of the lung, but flow is even more affected (gravity has a bigger effect on blood). V/Q ↓ as we go down the lung.
2. Local mechanical differences: Change in compliance in parts of the lung can lead to over-ventilation of some areas and under-ventialtion of others leading to V/Q mismatching.
3. Changes in flow: A pulmonary embolism will divert flow to areas of the lung, leading to V/Q mismatching.
5. Increase diffusion distance: Emphysema can lead to mismatching due to poor diffusion (V). |
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Term
| How does the lung compensate for V/Q mismatching? |
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Definition
1. Under conditions of alveolar hypoxia (low V/Q) pulmonary vasoconstriction occurs trying to shift Q to better ventilated areas of the lung (can be good, but bad if systemic).
2. Under conditions of hypocapnia (high V/Q) bronchoconstriction occurs trying to shift ventilation to better perfused regions of the lung (only used in extreme cases). |
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Term
| What do we call a V/Q of infinity? |
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Definition
| Dead space. Ventilated but not perfused. |
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Term
What is the dead space to tidal volume ratio?
What does it tell us?
What is a normal value? |
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Definition
Vd/Vt = (PaCO2 - PeCO2)/PaCO2.
It tells us how much of a tidal volume is wasted in dead space. A normal value is between 0.3 and 0.4. |
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Term
| What is the equation for PaCO2? |
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Definition
PaCO2 = R*T*VCO2/VA. This is a hard equation to conceptualize so in practice you can convert it to this:
PaCO2 = (VCO2*863)/Ve(1-Vd/Vt)
Where VCO2 is CO2 production (200 mL/min) |
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Term
| What is the most common cause of hypocapnia (respiratory alkalosis)? |
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Definition
| Increased Ve. This could be due to pain, anxiety, fever, sepsis, asthma, pneumonia, pulmonary edema, pulmonary embolism, aspirin intoxication, stimulant overdose, liver failure, pregnancy, metabolic acidosis, hyperthyroidism, psychosis, and other conditions. |
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Term
| What causes hypercapnia (respiratory acidosis)? |
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Definition
1. ↑ VCO2: fever, excess movement, over-feeding, etc.
2. ↓ Ve: Due to ↓ neuromuscular strength (nervous system trauma, CNS depression, disease, etc.) or due to ↑ load (Restrictive/obstructive lung disease, chest wall deformity)
3. ↑ Vd/Vt: Anything that ↑ Vd (PE, emphysema, etc.) or ↓ Vt (shallow breathing, bad ventilator settings, etc.) |
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Term
How much O2 should you give to someone with COPD?
Why? |
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Definition
| You should titrate it to get them to 90% sat. if the patient shows signs of CO2 ↑. This is because their CO2 will ↑ as you give them more oxygen causing problems. This is probably due to oxygen increasing dead space due to its broncho-dilator effects. |
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Term
Where does control of breathing come from?
What two things are required for breathing? |
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Definition
| Breathing is controlled by the central nervous system. Breathing requires an internal oscillator (to pace breathing) and a pattern generator (to turn that signal into breaths). |
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Term
| What are the two types of sensory feedback receptors used in respiration? What are the different types of each? |
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Definition
1. Pulmonary mechanoreceptors: Slowly adapting pulmonary stretch receptors (PSR), Rapidly adapting pulmonary stretch receptors (RSR), C-fibers.
2. Chemoreceptors: Peripheral chemoreceptors (Carotid bodies, aortic bodies), central chemoreceptors (CNS). |
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Term
Describe the PSR.
What occurs when it is activated? |
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Definition
| It is a myelinated fiber located in airway smooth muscle. It is activated by lung inflation and bronchoconstriction. When activated it causes: The Breuer-Hering reflex (facilitates expiration), abdominal muscle activation (prolongs expiration when volumes remain high - obstruction), bronchodialtion (negative feedback) |
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Term
| What is the Breuer-Hering inspiratory terminating reflex? |
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Definition
| It is a reflex from the PSR to facilitate expiration. When they are stretched to a high Vt it terminates inspiration and initiates expiration. It also prolongs expiration (slows breathing). |
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Term
Describe the RSR.
What occurs when it is activated? |
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Definition
| Smaller myelinated fibers located between epithelial cells. Stimulated by irritants and rapid large inflation. Activation causes airway protective reflexes: cough/sneeze, tachypnea, bronchoconstriction (filtering). |
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Term
Describe the C-fibers.
What occurs when they are activated? |
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Definition
| Small unmyelinated fibers close to the alveoli (stimulated by edema) or within airway epithelium (stimulated by irritants). They elicit airway protective reflexes (rapid shallow breathing pattern). May contribute to dyspnea. They can be activated by left heart failure, interstitial lung disease, pneumonia, PE. |
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Term
What are the two types of peripheral chemoreceptors that are important in control of breathing?
What stimulates them and what is their effect? |
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Definition
| Carotid and aortic bodies are the two peripheral chemoreceptors. They are stimulated by ↓ PaO2, ↑ PaCO2, and ↓ pH. Since they are stimulated by PaO2 they aren't directly activated in anemia. Activation leads to ventilatory responses (↑). |
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Term
| Describe central chemoreceptors and their role in control of breathing. |
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Definition
| Located on the ventrolateral surface of the medulla (retrotrapezoid nucleus). They respond to ↑ PaCO2 and ↓ pH (not ↓ PaO2). H+ is measured indirectly since it doesn't cross the BBB. When stimulated they lead to a large (↑) ventilatory response . |
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Term
| How does ↑ CO2 affect ventilation? |
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Definition
| In vivo there is a linear relationship between CO2 and minute ventilation. Every 2mmHg increase in PaCO2 leads to a doubling of Ve. PaCO2 is the most potent respiratory stimulus. In chronic hypercapnia the chemoreceptor can in effect "reset", leading to decreased respiratory drive at the same levels. |
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Term
| How do PaCO2 and PaO2 levels interact? |
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Definition
| A change in one augments the body's ventilatory response to changes in the other. |
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Term
| What is Cheyne-stokes breathing? |
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Definition
| It occurs in sleep apnea. Decreased C.O. leads to a delay between change in PACO2 and detection by chemoreceptors leading to decreased sensitivity of central chemoreceptors. |
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Term
| What are the 3 main areas where respiratory neurons are concentrated? |
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Definition
1. Dorsal Respiratory Group (DRG): Processes respiratory afferent input.
2. Ventral Respiratory Column (VRC): a) Retrotrapezoid nucleus (central chemoreceptor) b) PreBotzinger Complex (Inspiratory rhythm generator, can generate rhythm by itself)
3. Pontine Respiratory Group (PRG): Coordination w/other systems and higher brain function. |
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Term
| What are the different types of sleep apnea? |
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Definition
1. Obstructive Sleep Apnea (OSA): a) Apnea - cesation of breathing that lasts >10 sec. b) Hypopnea - shallow breathing Vt<1/2 normal. Usually associated w/desaturation.
2. Central Sleep Apnea: failure of the CNS to initiate breath. |
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Term
| What causes sleep apnea (6 factors)? |
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Definition
| 1. Anatomy 2. Physics 3. Genetics 4. Neural Control (even in OSA) 5. Hormonal Control (testosterone) 6. Muscle Control (may fatigue early) |
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Term
What is the Venturi effect?
What is the Bernoulli principle? |
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Definition
Venturi effect: airflow velocity increases in a narrow passage.
Bernoulli principle: Faster moving fluid lowers pressure, creating a vacuum around the edges of flow. |
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Term
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Definition
| It is a sleep study. Includes EEG, EOG (EYE), EKG, Leg movement, Respiratory flow - nasal/ oral sensor, O2 saturation, Abdomen and Thoracic strain gauges. |
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Term
| What kind of complaints will people with OSA present with? |
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Definition
| Daytime fatigue/sleepiness, Morning headache, vivid dreams, insomnia, hyperactivity, memory and learning impairments, snoring, unrefreshing sleep. |
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Term
| What is the STOP questionnaire? |
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Definition
| It is a test for sleep apnea. 1. Snoring 2. Tired 3. Observed 4. Blood Pressure. 2+ positives = high risk for OSA. |
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Term
| What are risk factors for OSA? |
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Definition
| 1. BMI 30+ 2. >17 in. neck 3. Crowded pharynx 4. Alcohol 5. Supine sleep 6. Smoking 7. Nasal congestion 8. Post-menapause 9. Hypothyroidism. |
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Term
| What are the outcomes of sleep apnea? |
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Definition
| 1. Cardiovascular (HTN) 2. Cognitive 3. Inflammatory (Asthma improves w/management) 4. Metabolic 5. Cancer 6. Quality of Life. |
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Term
|
Definition
1. Lifestyle: Positional therapy.
2. Dental: Jaw positioning device.
3. Surgical: Lots of options. Tracheostomy, gastric bypass, etc.
4. Positive Airway Pressure: Push everything open. Great results, but adherence is difficult at times. |
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Term
What is a normal pH/PaCO2 (Bicarb) profile?
How do changes in PaCO2 and pH relate? |
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Definition
7.40/40 (24).
For every 10 mmHg change in PaCO2 you should have a 0.08 change in pH in the opposite direction. |
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Term
| How do you identify respiratory acid-base changes vs. metabolic ones? |
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Definition
Respiratory: pH and PaCO2 will move in opposite directions.
Metabolic: pH and PaCO2 will move in the same direction. |
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Term
| How do you identify compensate from acute respiratory acid-base changes? |
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Definition
Acute will have the 10 mmHg : 0.08 pH ratio.
Compensated will not follow that ratio. Full compensation takes 3 days. |
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Term
| How do you know if the body is compensating properly for a metabolic acid-base change? |
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Definition
| The last two digits of the pH should be close to the PaCO2. If it is, there is proper compensation. If not, there is a problem. |
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Term
How do you calculate an Anion Gap?
What is a normal measurement? |
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Definition
| The anion gap comes from the electrolyte panel. AG = Na - (Cl + HCO3). Normal is 12 meq/L +/- 2. Higher than this indicates metabolic acidosis. |
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Term
What should you look for if you have an increased anion gap (AG)?
What does MUD PILES stand for? |
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Definition
This indicates an acid add-on state: MUD PILES
Methanol: Antifreeze metabolizes to Formic Acid
Uremia: will have ↑ BUN and creatinine
Diabetic Ketoacidosis: also starvation/intoxication
Propylene Glycol: Antifreeze/drugs
Iron Overdose, INH (isoniazid)
Lactic Acidosis: Circulatory shcok
Ethylene Glycol: Antifreeze
Salicylic Acid: Aspirin |
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Term
What do we look for in metabolic acidosis with a normal anion gap (AG)?
What does USED CARS stand for? |
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Definition
This indicates a bicarb wasting state: USED CARS
Uretero-enterostomy: Poop bag
Saline
Endocrinopathy: Shock, Addison's, etc.
Diarrhea
Carbonic anhydrase inhibitors (acetazolamide)
Alimentation: Bad mixture - ammonium chloride.
Renal Tubular Acidosis
Spironolactone |
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Term
What are the two types of Metabolic alkalosis?
What could cause each? |
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Definition
1. Chloride responsive: This is usually due to vomiting & volume depletion (low Cl from vomiting HCl). NaHCO3 is being resorbed to restore volume at the expense of alkalosis
2. Chloride unresponsive: This is due to too much aldosterone. This causes a Na/H exchange and H+ secretion. Hypokalemia will also lead to H+ secretion due to H/K exchange. |
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Term
What is delta-delta analysis?
How is it done?
How is it interpreted? |
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Definition
| It is used with elevated AG to see if the tradeoff ratio between bicarb and acid is appropriate. The increase in AG should match the decrease in bicarb. If the bicarb is low: Metabolic acidosis (bicarb wasting). If the bicarb is high: Metabolic alkalosis (bicarb excess - pancreatitis, etc.) |
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Term
| What are the 4 T's of the anterior & superior mediastinum? |
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Definition
1. Thymoma (and thymic cyst)
2. T-cell rich lymphoma: T cell- ALL and Hodgkin's disease (Ree-Sternberg cells surrounded by reactive T lymph)
3. Teratoma (and other germ cell tumors)
4. Thyroid and Parathyroid: Carcinoid - 35% functional, poor prognosis, salt and pepper histology. |
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Term
| What are common conditions of the mediastinum in order of frequency? Describe them. |
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Definition
1. Peripheral nerve sheath tumors: Schwannoma - benign, Antoni A&B. Neurofibroma (NF-1), wound rope. Ganglioneuroma - asymptomatic/diarrhea.
2. Thymoma: 1/3 symptomatic. 30-50% associated w/Myesthenia Gravis. More epithelial cells to lymphocytes = bad prognosis. Degree of encapsulation matters for staging.
3. Cysts: Thymic - unilocular (congenital), multilocular (adult)
4. Lymphoma: Hodgkin's (Young females - Reid-Sternberg cell: looks at you); T-cell (males - ALL, bad prognosis), B-cell (females - good prognosis).
5. Germ cell tumors: Teratoma - adolescents; Germinoma - males teens-30s, good prognosis |
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Term
| Do symptoms matter in mediastinal growths? |
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Definition
| Yes. 90% of asymptomatic ones are benign. 50% of symptomatic ones are malignant. Overall 25-40% are malignant. |
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Term
| What are the lymph node lesions of the anterior/middle mediastinum? |
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Definition
1. Chronic fibrosing mediastinitis: Chest pain, fever, hemoptysis, SVC syndrome. Infectious lymphadenitis; IgG type IV fibrosclerosing disease.
2. Infectious granulomas
3. Sarcoidosis: systemic, idiopathic. Peaks in 20/30s. Black and female are risks. Treat w/corticosteroids. |
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Term
| What is the classification of thymomas? |
|
Definition
Type A: Spindle cell. Good prognosis
Type AB: Mixed (spindle and epithelial cell). Good prognosis.
Type B1: Lymphocyte-rich, scattered epithelial cells. Good prognosis.
Type B2: Lymphocytes=epithelial cells. Fair prognosis.
Type B3 Epithelial-rich, scattered lymphocytes. Fair-poor prognosis.
Type C: Thymic carcinoma. Poor prognosis. |
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|
Term
What is pneumonia?
What are the two main categories of pneumonia that guide treatment? |
|
Definition
It is infection of the pulmonary parenchyma. There are many different types and causes.
Categories are: 1. Community-acquired pneumonia (CAP) and 2. Nosocomial pneumonia including Hospital-acquired (HAP), ventilator-associated (VAP), and healthcare associated (HCAP). |
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Term
| What is the incubation period of pneumonia typically? |
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Definition
| The typical incubation period is between 48-72 hours. This is the cutoff to define HAP vs CAP and VAP and HAP. HCAP is more about associations w/recent hospital/clinic visits, IV therapy, or nursing home/care facility. |
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Term
What are the 3 main causes of pneumonia?
What is the pathogenesis of pneumonia? |
|
Definition
1. Aspiration (most common): macro or micro, upper airway flora (S. pneumoniae, etc). 2. Inhalation: aerosol (Tb) 3. Hematogenous spread (fairly rare): endocardiits (S. areas).
Organism load/virulence overwhelms host defenses, leading to the accumulation of organisms, inflammatory cells, and fluid in the interstitium and alveolar spaces. |
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Term
| What are some risk factors for pneumonia? |
|
Definition
1. Impaired consciousness
2. Impaired cough reflex
3. Alveolar macrophage dysfunction (related to alcohol)
10% of people on a ventilator and ~1% of hospitalized pts. |
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|
Term
| What are the 4 different patterns of pneumonia? |
|
Definition
1. Lobar pneumonia: alveolar spaces are socked up
2. Bronchopneumonia: inflammation centered around airways
3. Interstitial pneumonia: very diffuse. More viral.
4. Lung abscess: PMNs, fibrin, necrotic debris.
Note: these are not super helpful in diagnosing the etiology. |
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|
Term
| What is a pleural empyema? |
|
Definition
| It is a collection of pus in the pleural space. |
|
|
Term
| What are the usual suspects of CAP? |
|
Definition
| S. pneumoniae, H. influenzae, M. pneumoniae, C. pneumoniae, L. pneumophila, Oral anaerobes. Also influenza and RSV. The usual therapy will treat all of these bacteria. |
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|
Term
| What are less common organisms you should look for in pneumonia that doesn't respond to the typical therapy? |
|
Definition
Viruses, Tb, atypical mycobacteria, nocardia spp. fungi. Rarely: Actinomyces, Chlamydophila psittici, C. burnetti, F. tularensis, hantavirus pulmonary syndrome.
Also remember biological warfare agents (B. anthracis, Y. pestis). |
|
|
Term
| What is the typical presentation for someone with pneumonia? How do you diagnose it? |
|
Definition
Presentation: cough (dry or productive), dyspnea, and fever.
Exam: dullness, bronchial sounds, egophony, crackles.
The key is a CXR. Cultures aren't overly helpful. If vital signs are normal (temp) the probability of pneumonia is low. |
|
|
Term
| What are the usual suspects for Nosocomial pneumonia? |
|
Definition
| S. areaus, Klebsiella pneumoniae, E. Coli, Enterobacter spp, P. aeruginosa, Acinetobacter baumanii. |
|
|
Term
What characteristics do you see in nosocomial pneumonia?
What is the differential? |
|
Definition
1. New or progressive pulmonary infiltrates 2. Purulent tracheobronchial secretions 3. Fever 4. Leukocytosis
DD: Fluid overload, atelectasis, pulmonary hemorrhage, pulmonary embolism, malignancy. |
|
|
Term
How do you treat CAP?
How do you treat Nosocomial Pneumonia? |
|
Definition
CAP: Respiratory fluroquinolone (_floxacin) or β-lactam+macrolide.
Nosocomial: Base on judgement and knowledge of what's going around. Early onset: limited spectrum ABs. Late onset: broad spectrum ABs for MDR pathogens. |
|
|
Term
What are the outcomes of pneumonia?
How do you prevent it? |
|
Definition
15% mortality for hospitalized CAP. 20-30% attributable mortality for nosocomial.
Prevention: influenza and pneumococcal vaccines. |
|
|
Term
What are the endemic fungal causes of pneumonia?
What fungal pneumonias are associated w/immunosuppression? |
|
Definition
Endemic (dimorphic from soil): 1. Histoplasmosis 2. Blastomycosis 3. Coccidioidomycosis
Immuno: 1. Aspergillosis 2. Penumocystosis. |
|
|
Term
| What factors go into the diagnosis of a fungal infection? |
|
Definition
| They are never a lab contaminant so if you have it you can be sure. However, they are slow growing, and you have to order a fungal culture. Some new techniques are decreasing reliance on cultures (antigen assay - not specific for individual fungi, but you treat the same so not a big deal). |
|
|
Term
Where is Histoplasmosis found?
What is it associated with?
What does it look like clinically? |
|
Definition
| Ohio and Mississippi River Valleys. Associated w/ birds and bats. Causes granulomas (caseating or non-caseating). A Ghon complex and pulmonary calcifications are common in healed histoplasmosis. Complications include mediastinal lymphadenitis & fibrosis and disseminated infection. |
|
|
Term
| How do you treat the endemic fungal pneumonias? |
|
Definition
| Most of the time you don't treat. If symptoms are severe, you treat with Itraconazole, or Amphotericin B. |
|
|
Term
Where is Blastomycosis found?
What is it associated with?
What does it look like clinically? |
|
Definition
| Found in Mississippi/Ohio river basins + Great Lakes. Associated w/soil exposure. Key finding: lots of PMNs. Similar to pyogenic bacteria, Tb, other fungal infections, and malignancy. Has a tendency to go to skin and bone. |
|
|
Term
| How will Histoplasmosis look? Blastomycosis? Coccidioidomycosis? Aspergillosis? |
|
Definition
Histo: small narrow budding yeast.
Blasto: Broad based budding yeast. If you see purulence + granulomas it should be the first thing you think of.
Cocc: Large spherule w/endospores.
Asper: septate hypae w/acute angle branching. |
|
|
Term
Where is Coccidioidomycosis found?
What is it associated with?
What does it look like clinically? |
|
Definition
| Aka valley fever, it is found in the southwest U.S. Can cause pulmonary nodules that look like malignancy, chronic fibrotic pneumonia, or disseminated disease (skin, bone, joints, meninges). Can use serological or antibody testing to diagnose. |
|
|
Term
What is Aspergillosis?
What does it look like clinically?
How do you diagnose and treat it? |
|
Definition
| It is ubiquitous. Risk - Neutropenia. Infection progresses across tissue planes and invades blood vessels (possibly leading to infarction). Can involve sinues, CNS, heart, & skin. Diagnose: CT. Nodules, "Halo sign" nodule w/ground glass around it. Treat: Voraconazole, neutrophil recovery. |
|
|
Term
What is Pneumocystis Pneumonia?
What does it look like clinically?
How do you diagnose and treat it? |
|
Definition
| Aka PCP. Found worldwide. Person to person transmission (unlike others). AIDS era disease. Presents w/progressive exertional dyspnea, fever, dry cough, chest discomfort. Diagnosis: diffuse symmetrical infiltrates. Immunofluorescence. Treat: Trimethoprim-sulfamethoxazole +/- corticosteroids. |
|
|
Term
| List common respiratory tract viruses by location. |
|
Definition
Nasopharynx: Rhinovirus (most common respiratory viral infection by far), Coronavirus (next most common), Coxsackie virus
Oropharynx: EBV, Adenovirus, Enteroviruses
Conjunctiva: Adenovirus, Herpesviruses
Layrnx-trachea: Parainfluenza viruses
Bronchi: Influenza viruses, Measles virus
Bronchioles: RSV |
|
|
Term
| How does influenza (orthomixovirus) work? |
|
Definition
| -ssRNA. HA binds to sialic acid and is endocytosed into the cell. If HA was activated by tryptase clara it will be triggered by low pH (thanks to the M2 channel protein), releasing it's DNA. NA plays a role in release of newly made virus. |
|
|
Term
What is genetic drift?
What is genetic shift? |
|
Definition
Drift: Changes in a genome through random mutations.
Shift: Changes in a genome due to reassortment with another virus. Animals (pigs) are a site of reassortment for type A - the cause of pandemics. |
|
|
Term
What do Amantadine and rimantadine do?
What about oseltamivir and Zanamivir? |
|
Definition
A&R block the M2 channel protein to prevent activation of the virus.
O&Z block NA activity so the virus has trouble leaving the infected cell. |
|
|
Term
| How does coronavirus work? |
|
Definition
| It is a +ssRNA, acting as an mRNA. Proteins on the surface give it a crown-like appearance. It is a cause of the common cold. SARS is also a corona virus (huge mortality). |
|
|
Term
| What are some paramyxoviruses? |
|
Definition
| -ssRNA. Paramyxovirus: parainfluenzavirus (kids), mumps (worse in adults, parotid glands). Pneumovirus: RSV (kids - working on vaccine). Morbillivirus: Measles (very infectious. Dry cough, sore throat, conjunctivitis). Little genetic variation, so vaccines are easily made. |
|
|
Term
| What are some picornaviruses? |
|
Definition
| +ssRNA. Polio, coxsackieviruses (usually NBD, but can have severe side effects), rhinovirus (most common cause of colds - 105 serotypes), enterovirus. Make a single polyprotein that is then cleaved. |
|
|
Term
| Describe Adenoviruses: what do they look like? How do they work? What do they cause? |
|
Definition
| Non-capsulated dsDNA virus w/a long glycoprotein fiber (IV) which interacts w/MHC 1 and is important in its phagocytosis. Common cause of colds, but can also cause a variety of clinical syndromes including respiratory diseases, and conjunctivitis. |
|
|
Term
| What are some other respiratory viruses? |
|
Definition
| Reovirus, Hantavirus (deer mouse 4 corners), Human Metapneumovirus, Human Bocavirus. |
|
|
Term
| What are the major causes of shunts? |
|
Definition
| Pus (pneumonia), water (cardiogenic - transudate, non-cardiogenic - exudate), blood (diffusion capacity will sky), atelectasis (pulls medistinum). |
|
|
Term
| What is the Starling equation? |
|
Definition
Qe = K[(Pmv - Pis) - σ(πmv - πis)]
Qe - flow into the interstitium. K - permeability factor for water. Pmv - Microvascular hydrostatic pressure. Pis - Interstitial hydrostatic pressure. σ - reflection coefficient (protein permeability) - normal = 0.7 (not very permeable). πmv - microvascular oncotic pressure. πis - interstitial oncotic pressure. |
|
|
Term
What would cause in increase in the pressure gradient?
What would cause an increase in the oncotic gradient?
What changes K?
What changes σ? |
|
Definition
Pressure: CHF, ARDS, hanging, thoracentesis.
Oncotic: Hypoalbunemia (due to malnutrition, liver disease, malnutrition)
K: Increases with increased permeability
σ: Decreases from 0.9 to 0.0 (proteins flow freely) during injury. |
|
|
Term
| Why do we have a pleural space? |
|
Definition
| It acts as a reservoir of fluid so it doesn't enter the alveoli. Also putting fluid there raises Pis, so it helps prevent pulmonary edema. |
|
|
Term
How is pulmonary edema cleared?
What is the driving force in its formation? |
|
Definition
It is cleared by a Na-K ATPase pump. Passive diffusion into the space, active clearance.
Pmv is the driving force in all pulmonary edema formation. |
|
|
Term
| What is Acute Respiratory Distress Syndrome (ARDS)? |
|
Definition
| Severe acute lung injury with diffuse alveolar damage, increased microvascular permeability (ARDS is all about σ), and noncardiogenic pulmonary edema. Acute refractory hypoxemia (aka: acute hypoxemic respiratory failure) - shunt, that isn't due to the heart. Acute lung injury (ALI) is mild ARDS. |
|
|
Term
What can lead to the development of ARDS?
What do we call it when we can't find a cause? |
|
Definition
Aspiration, penumonia, sepsis, blood transfusion, pancreatitis, trauma, among many others.
If we can't identify the cause we call it acute interstitial pneumonia (AIP). |
|
|
Term
| How is the degree of ARDS determined? |
|
Definition
P/F (PaO2/FiO2) Ratio. P/F < 300 → ARDS.
P/F = 200-300 → ALI.
P/F = 100-200 → moderate ARDS.
P/F < 100 → severe ARDS. |
|
|
Term
| What are the 7 mechanisms of ARDS injury? |
|
Definition
1. Activation of inflammatory mediators - damage to capillary and alveolar endothelium.
2. Increased permeability (σ↓)
3. Influx of protein-rich fluid and inflammatory cell to airspaces.
4. Abnormalities of coagulation system.
5. Abnormalities in production, composition and function of surfactant. → alveolar collapse, gas exchange abnormalities.
6. Ventilator-induced lung injury (VILI). Key: lower Vt.
7. Potential for aberrant repair/fibrosis. |
|
|
Term
| What is the diffuse alveolar damage (DAD) we see in ARDS? |
|
Definition
| The most classic finding is hyaline membrane formation. Inflammatory cells, ROS, cellular debris, coagulation, etc. You can actually end up with a fibrotic condition after recovering from ARDS. |
|
|
Term
What does TB look like on a CXR?
How many people are infected with it? |
|
Definition
The classic presentation is a cavitary lesion on the apical posterior upper lobe.
1/3 of the world's population is infected w/ TB. |
|
|
Term
| Describe Mycobacterium Tuberculosis. |
|
Definition
| It is an aerobic non-spore forming, non-motile bacillus. Humans are the only reservoir. It is lipid rich and slow growing (22-24hr. generation time vs. 20 min for e. coli), which my explain the difficulty the immune system has with it. |
|
|
Term
| What is the pathogenesis of TB? |
|
Definition
| Initial infection is in the midlung zone (greatest ventilation). Bacteria are ingested by macrophages, and carried to regional lymph nodes. Hematogenious spread is possible to lymph nodes, kidneys, epiphyses of long bones, vertebral bodies, meninges, and the apical posterior lungs. The immune response is cellular and tissue hypersensitivity (granuloma formation, tissue formation, skin reactivity) develops 3-9 weeks after infection. |
|
|
Term
|
Definition
| In some cases, antigen concentration in the primary complex (the Ghon complex) will be large enough that hypersensitivity will result in necrosis and calcifications seen on CXR. |
|
|
Term
| Describe the granulomas seen in TB. |
|
Definition
| They may or may not be caseating. Surrounded by T cells and macrophages. Bacteria are found in the necrotic center. 2 edged sword: prevents spread, but prevents clearance. Epithelioid cells (highly activated macrophages) and Langerhans giant cells (fused macrophages) are present. |
|
|
Term
|
Definition
Normally 30% of exposed people become infected, and of those only 10% will develop active disease in their lifetime.
For HIV 10% per year will develop active disease. |
|
|
Term
| What is the majority of TB seen clinically? |
|
Definition
| It is reactivation TB. Primary TB is only a problem in immunocompromised individuals (HIV, children, etc). Latent TB is a big issue, but often people are not treated. |
|
|
Term
How is the PPD test performed?
What is another option? |
|
Definition
This is also known as the Tuberculin skin test (TST). It takes advantage of the tissue hypersensitivity seen in TB. Place intradermally (raise a weal) and measure w/a ballpoint pen.
Interferon Gamma release assays are more specific, but more expensive. |
|
|
Term
What does TB look like clinically?
TB can present in 4 forms. What are they? |
|
Definition
Fever, night sweats, weight loss, dyspnea, hemoptysis.
Cough > 2 weeks. Exposure, or + TST. Upper lobe infiltrate, cavitary infiltrate, or hilar/paratracheal adenopathy on CXR.
You may see: 1. Primary TB. 2. Reactivation TB. 3. Extrapulmonary TB (chronic illness). 4. Miliary TB (all over). |
|
|
Term
| TB meningitis is rare, but what does it look like? |
|
Definition
| Abnormal CXR in 50%. If you see CSF that is lymphocytic or w/mixed pleocytosis, and has a high protein count, low glucose, and negative cultures, you should think TB. |
|
|
Term
| How do you diagnose TB histologically? |
|
Definition
| TB = acid fast bacillus. You can also see it via flurochrome staining. Culture takes a long time (broth is faster, but still 1-3 weeks). New Xpert MTB/RIF test is quite good and identifies rifampin resistance (key drug). |
|
|
Term
|
Definition
4 drugs for two months (Isoniazid, Rifampin, Ethambutol, Pyrazinamide) and 2 drugs for 4 more months (IR). Rifampin is key, it reduces duration from 18 to 6 months. Adherence is key! Directly observed therapy is standard of care.
Latent is treated slightly differently. I-9 mos. R-4 mos. |
|
|
Term
What is MDR TB?
What is XDR TB? |
|
Definition
Multi Drug resistant: IR resistance.
Extensively Drug resistant: Resistant to IR, fluroquinolones, + other 2nd line agent. |
|
|
Term
|
Definition
| It is a widely used TB vaccine. It protects against TB meningitis quite well, but is not effective for adult infection. Benefit only lasts 10-20 yrs and boosters are ineffective. |
|
|
Term
| What are Non-tuberculous Mycobacteria? |
|
Definition
| They are bacteria commonly found in the environment that infrequently cause pulmonary (chronic granulomatous pneumonia or bronchiectasis) or skin infections. They is no person to person transmission or latent infection. Grow best at colder temps. Can be a contaminant so ask: is it real? |
|
|
Term
| Who is infected with NTM? |
|
Definition
| Middle aged women, and people with underlying pulmonary disease/abnormalities are most often affected. |
|
|
Term
What are common causes of chronic brochopulmonary disease?
Disseminated infection?
Skin abscesses? |
|
Definition
Pulmonary: M. avium complex (MAC, aka. M. Avium intracellulare - MAI), M. kansasii, M. chelonae-abscessus.
Diseminated: MAC
Skin: M. marinum, M. chelonae-abscessus, M. fortuitum |
|
|
Term
| What are the criteria to diagnose NTM lung disease? |
|
Definition
Non-specific symptoms (cough, sputum, fatigue) so clinical:
1. Pulmonary symptoms, nodular or cavitary opacities on chest radiograph, or CT scan that shows multifocal bronchiectasis with multiple small nodules, AND
2. Exclusion of other diagnoses.
Micro: 1. >2 positive cultures OR 2. Positive lavage/wash results OR 3. Biopsy showing granulomatous inflammation and + culture. |
|
|
Term
| What does Mycobacterium avium complex (MAC) cause? |
|
Definition
| Pulmonary disease, disseminated disease, cervical lymphadenitis. Probably acquired by inhalation/ingestion. Treat: test sensitivities, multiple agents for 12-18 months; surgical resection. |
|
|
Term
| What does Mycobacterium kansasii cause? |
|
Definition
| It causes a pulmonary infection that mimics TB. Treat: test susceptibilities, multiple drugs (rifampin) for > 18 months. |
|
|
Term
| What causes cystic fibrosis? What populations are most affected? |
|
Definition
| Cystic fibrosis is an autosomal recessive disorder caused by a mutated Cystic Fibrosis transmembrane regulator (CFTR) gene. This is associated with defective ion transport in epithelial cells. Caucasians are most affected, but anyone can get it. |
|
|
Term
| What does the CFTR protein look like? |
|
Definition
| It is a cAMP regulated chloride channel with 3 main components: the transmembrane channel, a nucleotide binding component (ΔF508), and a regulatory component. The CFTR protein also regulates other channels (decreases activity of ENaC, affects bicarb movement, etc). |
|
|
Term
| What are the clinical manifestations of CF? |
|
Definition
Chronic sino-pulmonary infections → bronchiectasis, chronic sinusitus, nasal polyposis.
GI/nutritional abnormalities: pancreatic insufficiency, liver cirrhosis, bowel obstruction, etc.
Infertility: males especially (no vas deferens). |
|
|
Term
|
Definition
The "sweat test" is what has been used historically. Good sensitivity and specificity.
Nasal potential difference is more of a research test.
Genotyping allows screening for virtually all mutations. |
|
|
Term
| What are the different classes of CF mutations? |
|
Definition
Class I: X mutations. Premature stop, not transcribed.
Class II: Misfold - proteins can't leave the cell. Most common (ΔF508).
Class III: Abnormal regulation (can't open and close normally)
Class IV: Doesn't allow same movement as wild type.
Class V: A non-sequence mutation. Normal protein, small #s
Class VI: Increased protein turnover. |
|
|
Term
Can genotyping be used to predict CF severity?
Does CF affect the airways or the alveoli? |
|
Definition
It can predict the affect on the pancreas or infertility, but it can't predict lung disease, which is what matters in terms of morbidity and mortality.
CF is an airways disease. It blocks them causing other issues. |
|
|
Term
| What does CF look like on CT? |
|
Definition
| Bronchiectasis: big airways (should match size of adjoining pulmonary artery). Signet ring sign (looks like a big class ring). |
|
|
Term
What causes the respiratory tract symptoms in CF?
What are the two predominant organisms causing the chronic infection? |
|
Definition
| Altered airway secretions may impair innate immunity leading to chronic infection. This causes tissue damage which leads to an inflammation (trying to clear) which feeds back into the cycle of infection. Also, increased ENaC activity leads to a narrowed pericilliary fluid layer and dehydrated mucus. The two organisms are S. aureus, and P. aeruginosa. |
|
|
Term
How do you treat CF?
What's in the future? |
|
Definition
| You need to take a multi-disciplinary approach. Use mucolytics, oscillation devices, bronchodilators, anti-inflammatory agents, antibiotics. Also supplement pancreatic enzymes, vitamins, etc. New focus is on chemical chaperones, gene therapy, gentamycin (read through a premature stop). There is some promise. |
|
|
Term
| Describe the anatomy of the pleural space? |
|
Definition
| Normally it contains 3.5 ml of fluid. Connective tissue layer contains elastin and collagen. Mesothelium is the overlying layer. Lymphatics and nerves are only found in the parietal pleura (pleuritic chest pain: worry about effusion). |
|
|
Term
| What happens to pleural pressure at different lung volumes? |
|
Definition
| -5 cm H2O is average. At high volumes it is much more negative (-30 cm H2O), and at low volumes it is less negative (-1.5 cm H2O). |
|
|
Term
| What leads to transudates in the pleural space? |
|
Definition
| Alterations in starling forces across a normal membrane. Eg: Heart failure (↑ Pcap), atelectasis (↓ Pip), liver cirrhosis/nephrotic syndrome (↓ ∏cap), hypothyroidism, PE, urinothorax (check creatinine levels), Peritoneal dialysis (peritoneal fluid enters chest). |
|
|
Term
| What is the definition of pleural exudate? |
|
Definition
1. Pleural protein/serum protien > 0.5
2. Pleural LDH/serum LDH > 0.6
3. Plural LDH > 2/3 of normal serum LDH.
LDH (lactate dehydrogenase) is a sign of inflammation (leak). |
|
|
Term
What are the most common causes of pleural effusions in the US?
What is a loculated pleural effusion and what does it tell us? |
|
Definition
CHF, pneumonia, malignancy, PE, viral disease, cirrhosis, GI illness, CVD, TB.
It is an effusion that is not free flowing. This requires surgical debridement. |
|
|
Term
What direction will the trachea deviate in a pleural effusion?
A tension pneumothorax?
Massive atelectasis? |
|
Definition
In an effusion, the trachea will deviate away from the effusion. In a tension pneumothorax the trachea will also deviate away. These are both volume up conditions.
In massive atelectasis the trachea will deviate toward the collapse, since it is a volume down condition. |
|
|
Term
| What leads to exudates in the pleural space? |
|
Definition
Altered membrane permeability: pulmonary infection, pleural malignancy, PE, subdiphragmatic inflammation, collagen vascular diseases (lupus, rheumatoid, etc.), occupational or drug induced pleural diseases. Severe: esophogeal rupture, throacic duct rupture, bleeding. ER type issues. Decreased lymph clearance.
Note: This is just the beginning. A long list. |
|
|
Term
| What are the signs and symptoms of pleural effusion? |
|
Definition
| Asymptomatic. If symptoms: dyspnea, pleuritic chest pain, cough, rapid shallow breathing, dullness to percussion, decreased fremitus, tracheal deviation, decreased breath sounds, pleural rub. Little to no change in O2 or vital cap. |
|
|
Term
| What are the 3 types of parapneumonic (with pneumonia) effusions? |
|
Definition
1. Uncomplicated: Inflammation but no bugs.
2. Complicated: Very inflammatory, assume bugs, but can't confirm. Low glucose, low pH, high LDH.
3. Empyema: bugs in the pleural fluid. |
|
|
Term
What causes low pH effusions?
What causes low glucose effusions?
What causes high amylase effusions? |
|
Definition
Low pH: Malignancy, esophageal rupture, urinothorax
Low glucose: Complicated parapneumonic effusion, empyema, rheumatoid, TB, malignancy.
High amylase: Pancreatitis, esophogeal rupture, malignancy, other intrabdominal process. |
|
|
Term
| What will you see in a TB effusion? |
|
Definition
| Lymphocyte predominant (also in malignancy). < 5% mesothelial cells. Adenosine deaminase >47 (sensitive but not specific). Major reason for closed pleural biopsy. |
|
|
Term
| What are major causes of pneumothorax? |
|
Definition
1. Iatrogenic (health care - includes lung hyperinflation)
2. Traumatic
3. Bulbous disease - spontaneous (COPD, emphysema, sarcoidosis, LAM, eosinophilic granuloma).
4. Infection (PCP w/HIV) |
|
|
Term
| What will you see in a tension pneumothorax? |
|
Definition
| Clinically: Tracheal shift away, progressive dyspnea, tachycardia/hypotension (impaired venous return due to increased pressure), increased tympani. Imaging: Sulcus sign, depressed hemidiaphragm, mediastinal shift. |
|
|
Term
What is pneumoconiosis?
How do you find it? |
|
Definition
It is greek for lung dust. It is used to describe any lung disease associated with mineral dust exposure.
To find it you have to ask lots of questions. They come in with a cough and dyspnea. |
|
|
Term
|
Definition
| It is a chronic lung disease due to inhalation of silica (quartz). It is characterized by progressive parenchymal nodules and pulmonary fibrosis predominantly in the upper lung. The nodules It is the most prevalent of the pneumoconisoses. |
|
|
Term
What occupations is Silicosis associated with?
Anthracosis?
Asbestosis?
Berylliosis? |
|
Definition
Silicosis: Mining, quarrying, stonework, foundries, abrasive, ceramic, and sandblasting.
Anthracosis: Mining
Asbestosis: Mining, Industrial applications (brake lining, insulation, pipe-fitters/laggers, cement, ship building).
Berylliosis: high tech. industries (heat shield, X-ray, nuclear, fluorescent lights, etc.) |
|
|
Term
| What is the pathogenesis of the pneumoconioses? |
|
Definition
| Epithelial injury leads to inflammation that triggers a fibrotic response. Tregs, effector T cells and others release cytokines that cause myofibroblasts to lay down collagen. |
|
|
Term
How do you diagnose chronic Silicosis?
What is the prognosis? |
|
Definition
| Microscopy: Birefringent crystals. Very well formed nodules. Small nodules on CXR (can be calcified). Symmetrical and bilateral in the upper lobes. Often hilar lymph nodes will show "eggshell" calcifications. PFTs show ↓ volumes, and ↓ DLco. Prognosis: no ↑ in morbidity & mortality unless progressive massive pulmonary fibrosis develops. |
|
|
Term
How do you diagnose acute Silicosis?
What is the treatment? |
|
Definition
| Alveolar proteinosis: poorly formed nodules & interstitial infiltrates. CXR: alveolar pattern (ground glass). CT: "Crazy paving" - ground glass + septal thickening. PFTs: ↓ volumes and DLco. Treat: no established treatment. Avoid more exposure. |
|
|
Term
| How does Coal Workers' Pneumoconiosis (aka black-lung, antracosilicosis, anthracosis) compare to silicosis? |
|
Definition
| Leads to black nodules, vs white nodules. Black lymph nodes. Carbon is much less fibrogenic than quartz, so greater exposure is required for disease development. Can lead to COPD w/out cigarette exposure. Often there are mixed dust exposures. |
|
|
Term
| What is Caplan's syndrome? |
|
Definition
| Caplan's syndrome is large nodules that cavitate. It occurs in the presence of pneumoconiosis and rheumatoid arthritis. |
|
|
Term
| How do you diagnose Coal Worker's Pneumoconiosis? |
|
Definition
| Clinical: asymptomatic; cough, SOB, cor pulmonale. CXR: same as silicosis. PFTs: ↓ volumes, ↓ DLco, mixed restrictive+obstructive. Silicosis will have bigger changes. Can lead to PMF (progressive massive fibrosis). No increased cancer risk unlike Silicosis. Treat: no established therapy. |
|
|
Term
| What are some unique findings in asbestos exposure? |
|
Definition
1. Benign asbestos pleural effusions.
2. Asbestos induced pleural plaques. Due to blockage of lymph drainage, leading to inflammation and plaque formation. Benign. 1+2 latency of ~20yrs.
3. Asbestosis (pulmonary fibrosis w/asbestos exposure).
4. Mesothelioma: long latency, no good screening test, bad prognosis. |
|
|
Term
| How do you diagnose Asbestosis? |
|
Definition
| Heavy exposure, right latency, CXR abnormalities. CT: like IPF, but w/plaques. PFTs: ↓ volumes and DLco. Progresses more slowly than IPF. Affects lower lobes. Required for the development of asbestos associated lung cancer. Synergy w/ smoking. |
|
|
Term
What are diseases associated w/Beryllium?
What other hard metals are associated w/lung disease? |
|
Definition
Acute Beryllium Disease: tracheobronchitis
Chronic Berylliosis: like sarcoid. Rx: avoid exposure, steroids.
Metals: Aluminum, Cadmium, Cobalt (giant cell), Iron (siderosis). |
|
|
Term
| What is the definition of Asthma? |
|
Definition
| Chronic airway inflammation that leads to variable & reversible obstruction. Recurrent episodes of wheezing, dyspnea, chest tightness, cough (esp. in AM). Airway hypersensitivity. |
|
|
Term
Who does Asthma affect?
What is Atopy? |
|
Definition
Children, boys, women, african-americans.
Atopy: propensity to launch an IgE response to allergens. Can be measured in blood. Includes: allergic rhinitis, asthma, hay fever, & eczema. |
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Term
| What is the mechanism of asthma? |
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Definition
| Allergens lead to Th-2 cell activation → IL-13, IL-4 → IgE → mast cells → histamines, leukotrienes, cytokines. This leads to bronchospasm, airway edema, & airflow obstruction. Also IL-5 leads to chemoatraction and prolonged survival of eosinophils. |
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Term
What are the histologic changes seen in Asthma?
What are the two elements to asthma treated clinically? |
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Definition
Hist: Goblet cell hyperplasia. Thickened BM. Cellular influx.
1. Chronic inflammation: Cell recruitment, epithelial damage, early structural changes - can lead to remodeling over time.
2. Acute response: Bronchoconstriciton, edema, secretions, cough. |
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Term
What is airway remodeling in Asthma?
What are known factors in the development of Asthma? |
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Definition
It is proliferation of smooth muscle & mucous. Increased matrix protein deposition. BM thickening. Angiogenesis.
Development: Dust mite, Cockroach, RSV, tobacco smoke. |
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Term
| How do you establish an asthma diagnosis? |
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Definition
1. Clinical history: atopy
2. Obstructive physiology which improves with bronchodilators.
3. Airway hyperreactivity w/bronchoprovocation.
A hallmark is variability in lung function. |
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Term
How do you differentiate between intermittent and persistent asthma?
What is the significance? |
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Definition
| Use the rule of 2's. Persistent is more than 2: days a week with symptoms, night awakenings a month, rescue inhaler use per week. Also minor limitation of daily activity, or 2+ exacerbations requiring oral corticosteroids. ANY of these indicates persistent asthma. Significance: give a controller med (inhaled steroids, +/- long acting beta agonist) in addition to a rescue inhaler. |
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Term
| What is the developmental pathway for squamous cell carcinoma (SCC)? |
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Definition
| Irritation (smoke) → squamous metaplasia → dysplasia → high grade dysplasia (aka carcinoma in situ - hasn't invaded BM) → invasive SCC. |
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Term
| What is the developmental pathway for adenocarcinoma (AdCa)? |
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Definition
| Smoke/mutation → Type 2 pneumocyte & clara cell hyperplasia → dysplasia (atypical adenomatous hyperplasia w/dyspastic hobnailed cells) → adenocarcinoma in situ (lepidic histology - along walls) → invasive AdCa |
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Term
| Which lung cancer is least associated with smoking? |
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Definition
| Adenocarcinoma. Also more common among women, and in Asia. |
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Term
Where do you find squamous cell carcinoma?
What are the histologic findings? |
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Definition
Central location - major bronchi. Paraneoplastic hypercalcemia (PTHrP production)
HIsto: keratin production, solid nesting pattern, intercellular bridges. |
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Term
Where do you find adenocarcinoma?
What are the histologic findings? |
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Definition
Found peripherally. Most common type of lung cancer.
Histology: glandular or acinar, papillary, solid patterns, lepidic in situ component.
When in situ (along septae)- ground glass appearance on radiology. |
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Term
What is large cell carcinoma?
What are the histologic findings? |
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Definition
It probably was adenocarcinoma or squamous cell carcinoma, but now you can't tell. Found peripherally or centrally.
Histo: Large cells, prominent nuclei (can be multinucleated). Looks like a mess. |
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Term
What is small cell carcinoma (aka Neuroendocrine Tumor)?
What are the histologic findings? |
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Definition
It is a high grade malignancy associated with paraneoplastic syndromes. Never a surgical disease.
Histo: small cells, little cytoplasm, granular chromatin, high mitotic rate - can look like lymphoma. |
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Term
What are the two genes for which we have molecular testing and treatment?
Which cancer are they a part of? |
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Definition
EGFR (KRAS part of downstream pathway). Activating mutation. Treat with tyrosine kinase inhibitors (TKIs) like Erlotinib. A KRAS mutation will make this treatment ineffective, as will certain EGFR mutations. Seen most in women, never smokers, & Asia.
EML4-ALK (fusion): Treat with an inhibitor (Crizotinib). Test w/ FISH. |
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Term
| What is a typical carcinoid tumor? |
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Definition
| It is a tumor that is not associated with smoking. Centrally located. Hemoptysis is a common presentation. Nests of neuroendocrine cells. Excellent prognosis. |
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Term
What % of lung cancer is caused by smoking?
What determines risk? |
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Definition
| 90% of lung cancer is caused by smoking. Risk is related to amount smoked, and age at initiation, among other things. ~15 year latency. Lung cancer is the deadliest of all cancers among both men and women. |
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Term
Why is lung cancer an attractive screening candidate?
How can we do it? |
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Definition
| 75% of the life of cancer is in the undetectable stage. We can identify those at high risk (smoking history). Most people present at advanced stages, where the prognosis is significantly worse. CT is best - 20% reduction in lung cancer mortality (7% reduction in all cause mortality). |
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Term
How do you treat the different stages of cancer?
What is their 5 year survival? |
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Definition
Stage I: Surgery. 5 yr 60-80%
Stage II: Surgery +/- chemo. 40-50%
Stage III: Some combo of surgery, chemo, radiation. 15-25%
Stage IV: Chemotherapy. 2% |
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Term
| What staging system is used in non-small cell lung cancer (NSCLC)? |
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Definition
| The TNM system is used. T is tumor size, N is related to the number and location of lymph node involvement, and M binary based on metastasis. |
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Term
| What are signs and symptoms of lung cancer? |
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Definition
| Cough, hemoptysis, bronchial obstruction, wheezing, pneumonic "coin" lesion on x-ray, or non-calcifed nodule on CT. |
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Term
| What is the SPHERE of lung cancer complications? |
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Definition
SVC syndrome: swelling of face due to obstruction of SVC
Pancoast tumor: Apex, nerve involvement (Horner).
Horner's syndrome: Cervical sympathetic involvement. Ptosis, miosis, anhidrosis.
Endocrine: paraneoplastic syndromes.
Recurrent laryngeal symptoms: hoarseness.
Effusions: pleural/pericardial. |
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Term
| What are some of the paraneoplastic syndromes seen in lung cancer? |
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Definition
Hormones produced: ADH, ACTH - Cushing's syndrome, Calcitonin hypercalcemia from PTHrP (parathyroid hormone related protein - seen in SqCC).
Lambert-Eaton Syndrome: Antibodies against voltage-gated Ca channel. Looks like Myesthenia Gravis.
Hypertrophic osteoarthropathy (clubbing). Seen in AdCa. |
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Term
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Definition
| It is a disease characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. It is #3 on the adult hit list. |
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Term
Who does COPD affect?
Why doesn't everyone get it? |
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Definition
| 40+ and 10+ pack year history. (both lower than they used to be). Starting to be more common in younger (40s) women. 40+ pack year history only 32% will get it. You need a two part hit: smoke exposure + some other factor (genetics, asthma, infection, etc.) |
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Term
What is the pathophysiology of COPD?
What cells drive everything? |
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Definition
| Imbalance between neutrophil elastase and anti-proteinases (Alpha-1 Anti-trypsin), and between oxidative stress and anti-oxidants. This is driven by macrophages, neutrophils, CD8s, and fibroblast activation (peribronchiolar fibrosis). Inflammation may drive co-morbid conditions/risk of cancer. |
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Term
| What are the 3 main elements of COPD? |
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Definition
1. Chronic bronchitis: Occurs in large airways. Goblet cell hyperplasia, squamous metaplasia, inflammation.
2. Small airway remodeling: Peribronchiolar fibrosis, lymphoid follicles, and disrupted tethering.
3. Emphysema: Permanent distal acinar enlargement, leading to breathlessness. Upper lobes affected. |
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Term
| What does Emphysema look like on diagnosis? |
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Definition
| Barrel chested, weight loss. Pink puffers. CXR: Decreased lung markings in the upper lobes. Flattened diaphragms, mediastinum pulled down (overinflation). CT shows holes in the parenchyma. PFTs: <70% FEV1/FVC that is non-reversible, ↓ DLco, ↑ volumes. |
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Term
| What will a patient with chronic bronchitis look like? |
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Definition
| They become hypoxemic sooner (V/Q mismatching), RV dysfunction. Blue blowers. Show the other COPD manifestations. |
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Term
| What predicts quality of life and mortality in COPD? |
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Definition
| FEV1 tracks quality of life, but there is a huge scatter. You can have people with the same FEV1 where one is in a wheelchair, and another is mowing their lawn. Lung hyperinflation, dyspnea, exercise capacity, and low BMI predict mortality. |
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Term
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Definition
Non-pharm: Smoking cessation (prevents progression), pollutant avoidance, vaccinations, nutrition, pulmonary rehab, O2 (if hypoxemic), surgical management.
Pharm: Rescue agent (albuterol), long acting bronchodilator, inhaled glucocorticosteroids. Add in that order. |
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Term
| What is Interstitial Lung Disease (ILD - aka Diffuse Parenchymal Lung Disease DPLD)? |
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Definition
| It is disease of the alveolar wall including the interstitium. May also involve the alveolar space and small airways. They are different diseases grouped due to similar clinical, radiologic, physiologic and pathologic features. |
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Term
| What is the proposed pathogenesis of ILD? |
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Definition
| Type I cells get damaged repeatedly. Type II cells produce inflammatory and proliferative mediators. Aberrant scar formation occurs (can occur independent of inflammation). The end stage is honeycomb lung (cyst formation and loss of gas exchange). |
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Term
| How do ILDs present clinically? |
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Definition
| Symptoms: Exertional dyspnea (usually insidious), cough (usually non-productive). Exam: Fine end-inspiratory crackles (velcro), clubbing (IPF). CXR: Interstitial pattern - reticular (lines), nodular (snowstorm), reticulonodular. Alveolar pattern - diffuse, patchy. CT: Reticular/nodular (tree-in-bud)/ground glass opacities, traction bronchiectasis, honeycomb cysts. |
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Term
| What will ILDs look like on PFTs? |
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Definition
| ↓ Volumes, normal or ↑ FEV1/FVC, ↓ compliance, ↓ DLco. Possible mixed restrictive and obstructive. ↑ A-a, ↓ PaO2. Exercise testing will show these changes earlier. |
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Term
| What are the main categories of ILD/DLPD? |
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Definition
1. ILD of known cause: pneumoconioses (mineral exposure), hypersensitivity pneumonitis (organic exposure), drugs, connective tissue disease (rheumatoid, etc).
2. Idiopathic interstitial pneumonias: IPF & other than IPF (Nonspecific interstitial pneumonia - NSIP)
3. Granulomatous: Sarcoidosis, TB, foreign body, etc.
4. Other: Pulmonary Langerhan's cell histeocytosis, LAM, pulmonary alveolar proteinosis, pulmonary vasculitides, etc. |
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Term
| What are the histologic features of UIP (IPF)? |
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Definition
| Evidence of fibrosis/architectural distortion with or without honeycombing in a sub-pleural/para-septal location, patchy fibrosis, fibroblastic foci. Possible inflammation. |
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Term
What is nonspecific intersitial pneumonia?
What are the two histologic types? |
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Definition
One of the idiopathic interstitial pneumonias. Associated with auto-immune, more common in women. May respond to steroids - better prognosis than IPF.
Types: Fibrotic (bad prognosis) and cellular (good prognosis). |
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Term
| How do you treat the Interstitial Lung Diseases? |
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Definition
1. Remove the offending agent (if present).
2. Steroids (effective for some - sarcoid)
3. Cytotoxic/immunosuppressive therapy
4. Antioxidants?
5. Immunomodulators/Antifibrotics (investigational)
Also: O2, vaccines, pulmonary rehab, transplant. |
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Term
| What is Lymphangioleiomyomatosis (LAM)? |
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Definition
| Abnormal proliferation of smooth muscle cells in the lungs, lymphatics and lymph nodes of the thorax and retroperitoneum. Affects women of reproductive age. |
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Term
What is Sarcoidosis?
How do you diagnose it? |
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Definition
Multisystem disease of unknown cause primarily affecting young and middle aged adults and African-Americans.
Presents w/: Cough, dyspnea, chest pain, often asymptomatic. Clinical/radiologic evidence of non-caseating granulomas (tree-in-bud) Most commonly affects upper/middle lobes. Also, ↓ cutaneous DTH (TST), ↑ Th1 response. PFTs don't correlate well w/pathology & prognosis. |
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Term
| What is the pathogenesis of sarcoidosis? |
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Definition
| Deposition of poorly soluble antigenic material initiates granuloma formation. T cell expansion occurs w/Th1 cytokines. TNF is released by Ts and macrophages. The antigenic material may be cleared (remission) or not (chronic) |
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Term
| What are some clinical manifestations of Sarcoidosis? |
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Definition
Constitutional symptoms: fever, malaise, fatigue, weight loss.
Skin involvement: erythema nodosum (red - tends to go away spontaneously), lupus pernio (nose/face - sign of chronic disease), hyperpigmented plaques.
Peripheral lymphadenopathy, eye involvement, rarely neuro/cardiac involvement. |
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Term
| What are the different stages of Sarcoidosis? |
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Definition
Stage 1: Bilateral hilar lymphadenopathy (BHL)
Stage 2: BHL + parenchymal infiltrate
Stage 3: Parenchymal infiltrate w/out BHL.
Stage 4: End stage fibrosis w/honeycomb lung.
Remission is quite likely in stage 1 & 2. |
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Term
| What is Lofgren's syndrome? |
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Definition
| It is sarcoidosis with fever, erethema nodosum, polyarthritis, BHL. It indicates a favorable prognosis. Pretty much anything else indicates a worse prognosis. |
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Term
How and when do you treat Sarcoidosis?
What are drawbacks to treatment?
2nd line agents? |
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Definition
Rx: Corticosteroids. Rx with severe/progressive symptoms, neuro/cardiac involvement, hypercalcemia, eye disease unresponsive to topic therapy. Drawbacks: side effects, relapse is common, unknown effect on natural Hx.
2nd line: Methotrexate (weak data), Infliximab, Adalimumab (good data, but expensive w/side effects). |
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Term
Who gets IPF? What are risk factors?
Where does it appear in the lung? |
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Definition
IPF is most common in older males. Risk factors include smoking, mineral dust, and organic dust.
IPF is primarily found in the base of the lung, sub-pleurally. |
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Term
What does IPF look like on radiology?
When do you need a biopsy? |
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Definition
CXR: Interstitial markings (reticular & nodular) in the lower lobes. Not sensitive, but pretty specific. CT: Subpleural basal predominance. Reticualr abnormality, honeycombing, traction bronchiectasis, no non-UIP findings.
If CT and clinical presentation fit: IPF. If unsure: biopsy (via VATS. Bronchoscopy won't provide enough tissue). |
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Term
What is the clinical course of IPF?
How do you treat IPF? |
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Definition
| Usually dead in 3 years. 3 phenotypes rapid to slow progression. Rx: AntiInflammatories (steroids) don't work. Anti-fibrotics show some promise. O2 supplementation, pulmonary rehab, palliative care, and Lung transplant. |
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Term
| What are pulmonary vasculitis syndromes? |
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Definition
| They are inflammation of the pulmonary vessels. Tend to be systemic disorders with extra-pulmonary manifestations. Respond to immunosuppresive therapy, but require long courses and relapses are common. Large, medium, and small (the important ones). |
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Term
| How are the small vessel vasculitides divided? |
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Definition
1. Pauci-immune: ANCA+ (Antineutrophil cytoplasmic autoantibodies): GPA (granulomatosis w/polyangiitis), MPA (microscopic angiitis), Churg-Strauss (EGPA - eosinophilc granulomatosis w/polyangiitis).
2. Immune complex disorders: anti-GBM, vasculitis associated with collagen vascular diseases (SLE). |
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Term
What is does large vessel vasculitis look like?
What are some examples?
Describe them. |
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Definition
Granulomatous inflammation of the aorta and its branches.
Eg: Giant cell arteritis (GCA or temporal arteritis): Carotid artery. Elderly females, headache, polymyalgia rheumatica, amaurosis fugax (blindness), elevated ESR (erythrocyte sedimentation rate).
Takayasu's arteritis: Aortic arch. Asian females <40. Pulseless disease, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances. Elevated ESR. |
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Term
What is the important medium-vessel vasculitis?
Describe it. |
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Definition
| Polyarteritis nodosa: Young adults, necrotising vasculitis associated with Hep B & C. Constitutional symptoms. Rare hemoptysis due to bronchial artery involvement. |
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Term
| What is the mechanism of ANCA-associated vasculitis? |
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Definition
| Autoantibodies appear to activating neutrophils which injure the endothelial cells. Weak associations w/silica, grain dust, heavy metals, S. aureus. |
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Term
What are the two types of ANCA?
What disease belong to which? |
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Definition
C-ANCA: Cytoplasmic immunofluorescence. Autoantibodies react with proteinase 3 (PR3-ANCA). GPA.
P-ANCA: Perinuclear immunofluorescence. Autoantibodies react with myeloperoxidase (MPO). MPA, EGPA. |
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Term
| Compare and contrast GPA with MPA. |
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Definition
Same: Pulmonary capillaritis. Can cause DAH. Similar clinical profile: White, 40s, necrotising glomerulonephritis.
GPA: Necrotising granulomas w/giant cells. Affects the respiratory tract - saddle nose. C-ANCA |
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Term
Describe Churg-Strauss (EGPA).
How do you treat it? |
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Definition
| Eosinophil rich granulomatous inflammation. May cause eosinophilic pneumonia and mononeuritis multiplex. P-ANCA+. Associated w/asthma and eosinophilia. Rarely causes DAH. Treat with steroids and immunosuppressants. |
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Term
What are the immune complex vasculitides?
Describe them. |
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Definition
1. Anti-GBM antibody disease (Goodpasture's if affecting kidneys and lungs): Damage to the lung (smoking) exposes the BM to attack. IgG deposits. Can cause DAH. Treat w/immunosuppressive therapy and/or plasma exchange.
2. Systemic Lupus Erythematosis: ANA+ Capillaritis w/immune complex deposition and DAH. Rx: systemic steroids, cyclophosphamide and possibly plasma exchange. Associated w/other lung problems including ILP, NSIP, pleuritis, PE, PH, acute pneumonitis, & "shrinking lung" |
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Term
| What are the 5 groupings of pulmonary hypertension? |
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Definition
1. Pulmonary arterial hypertension: Arterioles. ↑ Resistance. SM/endothelial proliferation. Middle aged women. Very rare.
2. PVH → left heart disease: Post capillary. Low resistance. Can lead to permanent remodeling. Most common.
3. Lung disease/hypoxia: Capillary bed. 2nd most common.
4. Chronic thromboembolic PH: Generally in larger arteries. 5. Other |
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Term
| How do you treat pulmonary hypertension? |
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Definition
1. Lots of treatments: Endothelin receptor antagonists, phosphodiesterase inhibitors, prostacyclins.
2. Treat HF. Pulmonary vasodilators could cause pulmonary edema due to hitting a dam.
3. Treat lung disease. Vasodilators could cause V/Q mismatching by sending flow to non-functional capillaries.
4. Treat w/thromboendarterectomy - bridge w/vasodilators. |
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Term
What are the symptoms of pulmonary hypertension?
Clinical signs?
How do you diagnose it? |
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Definition
| Progressive onset exertional dyspnea, fatigue, chest pain, (pre)syncope, Raynauds, and palpitations. Ortner's (hoarseness due to pressure on airway) is rare. Clinical: loud P2, tricuspid murmur, RV lift, & RV failure. Dx: R heart cath. |
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Term
| Define in words LR+ and LR-. |
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Definition
LR+: The probability of a positive test given disease/Probability of a positive test given no disease. Or True positive rate/False positive rate. Or sensitivity/(1-specificity).
LR-: The probability of a negative test result given disease/probability of a negative test result given no disease. Or False negative rate/True negative rate. Or (1-sensitivity)/specificity. |
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Term
What groups are at increased risk for pulmonary embolism?
What is the fatality rate of PE?
What percent of PEs come from the hospital? |
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Definition
1. Cancer 2. COPD 3. CHF 4. Age > 60
Untreated: 30% Treated: 10%
25% of PEs are from the hospital. |
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Term
| What is the mechanism of Cor pulmonale in PE? |
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Definition
| PE → ↑ PVR → RV overload → dilation, tricuspid regurg, edema, decreased coronary perfusion → ischemia & ↓ output. ↑ RV filling pressures → ↓ output → ↑ HR, but a ↓ in LV preload and overall a ↓ in CO → Hypotension. Give fluids. |
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Term
| What is the pathophysiology of hypoxemia in PE? |
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Definition
1. ↑ A-a gradient due to V/Q mismatching
2. ↑ PVR and pulmonary hypertension
3. Alveolar hyperventilation from ↓ O2 and irritant receptors.
4. ↑ Airway resistance due to bronchoconstriction.
5. ↓ Compliance due to edema, ↓ surfactant, & hemorrhage. |
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Term
|
Definition
1. Hypercoaguable: Genetics, birth control, cancer.
2. Stasis: Travel, obesity, pregnancy.
3. Trauma: Surgery, DVT.
Note: there is a synergistic effect between factors. |
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Term
What symptoms present with PE?
What signs are present with PE? |
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Definition
1. Chest pain (pleuritic), Dyspnea, apprehension, cough, hemoptysis, sweats, syncope.
2. RR>16, crackles, ↑ P2, tachycardia, fever, gallop, edema, murmur, diaphoresis, cyanosis. ECG: S1Q3T3 CXR: Small Pleural Effusion, atelectasis, Westermark's sign (large PA). |
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Term
| What is the Well's score? |
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Definition
Helps diagnose PE. DVT signs/symptoms - 3. PE > other Dx - 3. Tachycarida - 1.5. Immobilization - 1.5. Previous DVT/PE - .5. Hemoptysis- 1. Cancer - 1.
A score over 4 is likely. 4 or less is unlikely. |
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Term
|
Definition
If low suspcion: D-dimer. If high suspicion: Anticoagulate & go straight to CT. If allergy, V/Q scan. If indeterminate: Leg ultrasound. if + PE: test serum markers (TN/BNP) for risk.
Sometimes: echocardiography McConnel Sign: Akinesia mid free wall, but normal at apex. |
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Term
| How do you treat a pulmonary embolism? |
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Definition
| Prevention! Give fluids (↓BP) & O2. Anticoagulate (heparin most common, but other anticoagulants better - LMWH, fondoparinux). Give it early and avoid under-dosing. Start them on coumadin (or another anticoagulant). Thrombolyse if decompensating. Vena cava interruption (filter) indicated in high risk patients that can't have anticoagulants. |
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Term
| What suggests a genetic predisposition to a hypercoaguable state? |
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Definition
| FURY: Family history of PE/DVT or sudden death. Unrecognized PE/DVT risk factors in a patient w/one. Recurrent PE/DVT and Young age. |
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