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555 Cards in this Set
- Front
- Back
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How does the respiratory system regulate acid base balance?
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By it's influence on CO2
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What non-respiratory functions does the respiratory system have?
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Acid-base balance
Vocalization Heat elimination Water loss Filtration and mucociliary transport. Immunological defense. Lipid synthesis - surfactant from type II alveolar cells. Angiotensin converting enzyme (ACE). Storage - histamine, prostaglandins, serotonin, leukotrienes. Removal- prostaglandins E1, E2, F2α, leukotrienes, bradykinin. |
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What are the normal partial pressures of gases in the various parts of the circulation?
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What is an Aa gradient?
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A small decline in PO2 between the alveolus and arterial blood.
A=Alveolar a=arterial |
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Why is there an Aa gradient?
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Anatomical shunts in the circulation where venous blood enters the arterial blood.
(bronchial circulation, thebesian veins etc.) Ventilation perfusion mismatches also account for it. Diffusion impairment in regions of the lungs can also raise the Aa gradient. |
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What is the conducting zone of the respiratory system?
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The conducting zone consists of all those parts that do not preform gas exchange and are thus repiratory deadspace.
The smallest structure in the conducting zone is the terminal bronchiole. Everything distal to it from the respiratory bronchiole down to the alveolar sac is part of the transit and respiratory zone Z and represents a MAJOR increase in cross sectional area for diffusion. |
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What are the standard lung volumes and capacities for a 70kg adult?
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What is tidal volume (Vt)?
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The air that you move during a quite normal respiratory cycle.
(~0.5L) |
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What is inspiratory reserve volume (IRV)?
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The volume of air taken in beyond the tidal volume in a forced inspiration.
(~2.5L) |
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What is inspiratory capacity (IC)?
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The sum of tidal volume and inspiratory reserve volume.
(~3L) |
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What is expiratory reserve volume (ERV)?
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The volume of air moved on forced expiration at the end of a normal expiration.
(~1.5L) |
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What is residual volume (RV)?
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The minimum amount of air left in the lung after a forced expiration.
(~1.5L) |
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What is functional residual capacity (FRC)?
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The sum of expiratory reserve volume (ERV) and residual volume (RV).
(~3L) |
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What is total lung capacity (TLC)?
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The sum of inspiratory capacity (IC) and functional residual capacity (FRC).
(~6L) |
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What is vital capcity?
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The sum of all the volumes but the residual volume. (IRV, Vt and ERV)
Typically about 4.5L. |
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Why do the inspiratory reserve volume and expiratory reserve volume change depending on position (supine vs.standing) ?
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The change of the position of the diaphragm.
On standing, the diaphragm is lower than in the supine position which means expiratory reserve volume is bigger and inspiratory reserve volume is smaller. (The diapragm has a longer way up to go on forced expiration and a shorter way to go on forced inspiration when we stand). |
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What is the dominant muscle of inspiration?
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The diaphragm. When it contracts it moves down and thus lowers the thoracic pressure and consequently the intrapleural pressure.
External intercostals also play a role. Inspiration is an ACTIVE process mediated by nerve impulses. |
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How does contraction of intercostal muscles function in breathing?
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When the external intercostals contract, the ribs are pulled upwards and forwards and they rotate on an axis joining the tubercule and head of the rib.
As a result both the lateral and anteroposterior diameters of the thorax increase and cause inspiration. The internal intercostals have the opposite effect. |
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How does expiration work?
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In normal quite breathing, expiration is passive.
Under high demand though, expiration becomes active and the primary muscles involved are the internal intercostals and abdominal muscles. |
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What produces the subatmospheric intrapleural pressure?
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The lung and the chest wall are like springs that oppose one another. When the lungs are expanded by the chest wall, this opposition creates a force which generates the negative intrapleural pressure.
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What is compliance?
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Change in volume/change in unit pressure.
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What do we mean when we say that lung compliance changes as a function of lung volume?
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The lung is lesss compliant when it is expanded than when it is not.
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What do we mean when we say that pressure volume relationships in the lungs have the property of hysteresis?
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The deflation curve is different from the inflation curve because of the presence of surface tension.
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What can change lung compliance?
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Increased compliance:
Emphysema Aging (loss of fibroelastic tissue) Decreased compliance: Fibrosis Fluid Obesity etc. |
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What is specific compliance?
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A measure of compliance normalized to lung volume. Mostly so that we can compare between individuals of different sizes.
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What is La place's law?
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The pressure in a bubble (P)=
(2xsurface tension)/radius of the surface P=2T/R |
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What keeps alveoli from collapsing and emptying into one another during an expiratory cycle?
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Surfactant
Lipid protein mixture: 85% lipid (mostly phophatidylcholine) 15% protein Surfactant is made by type II alveolar cell and modulates the effect of surface tension on the alveoli. Surfactant not only reduces surface tension (like detergent) but reduces it as a function of cross sectional area. (bigger effect in smaller alveoli). This normalizes the surface tension and keeps the small alveoli from collapsing into the large alveoli. |
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What are the main functions of surfactant?
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Helps stabilize the alveoli.
Reduces work of breathing. Helps keep alveoli dry by preventing surface tension from pulling fluid into the alveoli. |
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What transmural pressures affect respiration?
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What do we see on spirometry at FRC? (no air moving)
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The combined airways pressure curve is at zero.
ie. the tendency of the lung to collpase is balanced by the tendency of the chest wall to spring out. The Lung airways pressure curve is positive at FRC. The chest wall airways pressure curve is negative at FRC. |
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At about what volume does the chest wall stop contributing to lung expansion?
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~80% of vital capacity.
This is roughly the resting state of the chest wall. |
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Reductions in airway diameter necessitate...
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Increased work of breathing.
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Sympathetic stimulation tends to have what effect on the airways?
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Dilation.
Relaxation of smooth muscles |
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Parasympathetic stimulation tends to have what effect on the airways?
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Constriction.
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What region are most of the increases in resistance to breathing due to?
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The larger conducting zone rather than the respiratory zone which is highly interconnected (anastomotic).
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After a certain lung volume expiration flow becomes independant of....
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Effort.
No matter how hard a patient pushes on forceful expiration at some point the flow continues at the same rate. This happens because the pressure inside the airways falls below the intrapleural pressure and the airway collapses. |
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People with emphysema have more trouble with expiration rather than inspiration because..
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They have to use more active muscular effort to exhale.
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How maximal expiratory flow-volume curves appear in obstructive and restrictive disease?
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When does flow become independent of effort?
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When pressure within the airway becomes less than the intrapleural pressure surrounding the airway and it collapses.
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What is Dalton's law?
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The partial pressure of a gas in solution is equal to the pressure it would exert if it occupied the entire volume by itself.
PO2 in atmosphere = % 02 x barometric pressure PO2 = 21% x 760 mm Hg PO2 = 159 mmHg |
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What is alveolar ventilation?
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The volume of FRESH air introduced into the gas exchanging regions of the lungs per minute.
VA = f(TV - VD) Frequency times the difference between tidal volume and deadspace volume. |
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What is the initial change in alveolar gas tensions during inspiration?
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Initially, there is a small drop in pO2 and increase in pCO2 because of the air in the anatomical deadspace.
This is of course followed by a rise in pO2 and fall in pCO2. |
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How do we calculate minute volume?
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Minute Volume = Tv● f
(Tidal volume*frequency) |
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What is the equation for alveolar ventilation?
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Where K=0.863mmHg/L/ml
PaCO2=(VC02/VA)*K |
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What is the most simplified relationship illustrated by the alveolar gas equation?
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What the respiratory quotient R that is used in the alveolar gas equation?
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The ratio of the amount of carbon dioxide produced and the amount of oxygen consumed per unit time.
In normal people on a regular diet ~0.8 In people eating lots of carbs, closer to 1. High fat diet the number gets below 0.8. |
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In what region of the lung is pulmonary blood flow greatest?
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At the bottom of the lung.
Least flow at the apex. |
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What region of the lung has the greatest ventilation?
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At the bottom of the lung.
This is because the weight of the lung itself compresses alveoli somewhat which leads to smaller alveoli and thus greater compliance. |
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What region of the lung has the highest V/Q ratio?
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The apex.
This is because the blood flow declines less than the ventilation as we move up the lung. The lowest V/Q ratio is at the bottom of the lung. |
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What does a high V/Q ratio mean in terms of gas content?
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Higher pO2 and lower pCO2.
Low V/Q ratios mean the reverse, ie. lower pO2 and higher pCO2. |
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What does a healthy V/Q scan show?
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Good ventilation perfusion matching.
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What does an abnormal VQ scan show?
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Poor ventilation perfusion matching aka VQ mismatch.
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How does the lung regulate ventilation/perfusion matching?
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Localized hypoxic pulmonary vasoconstriction shunts blood to areas of high ventilation.
Shunting of ventilation to high perfusion areas also happens by constriction of airway smooth muscle in areas of poor perfusion. |
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Can a high VQ ratio compensate for a low oxygen in the blood produced by a low VQ ratio?
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Not entirely.
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How do we differentiate a true anatomical shunt from a V/Q mismatch?
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100% oxygen will cause a patient with a VQ mismatch to have a very high arterial pO2 but levels will not get as high in a true shunt.
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What are the charcteristics of the pulmonary circulation?
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High flow
Low resistance Low pressure This is in contrast to systemic circulation which is high flow, high pressure, high resistance. |
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Why is it that there is not a big rise in pulmonary arterial pressure with increased cardiac output?
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Pulmonary resistance decreases with increased cardiac output because additional "reserve" capillaries open up.
In addition, the pulmonary vessels have a vasodilator reserve which is used in response to increased cardiac output . |
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What neurohumoral factors vasoconstrict pulmonary vessels?
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Constrictors:
Hypoxia Sympathetic stimulation Seratonin NE Leukotrienes Thromoboxanes Dilators: Adenosine Ach NO |
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When in the respiratory cycle is there the lowest pulmonary vascular resistance?
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At FRC.
It goes up in either direction from this point because of the tendency of the alveoli to compress or stretch the blood vessels. |
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What forces are at play in the pathophysiology of pulmonary edema?
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Hydrostatic presure and alveolar surface tension.
vs. Colloid osmotic pressure and alveolar air pressure. Fluid that gets into the pulmonary interstitium is drained through lymph ducts into the vena cava. When the flow out of the vasculature exceeds the rate of lymph drainage, pulmonary edema occurs. (interstitial pulmonary edema) When the hydrostatic pressure in the interstitium get high enough it causes fluid to actually enter into the alveolar spaces. (alveolar edema) |
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What is Congenital Cystic Adenomatoid Malformation (CCAM)?
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aka Congenital Pulmonary Airway Malformation.
NOT neoplastic DISORGANIZED hamartomatous mass of lung tissue. Cystic changes vary with subtype. Structures resembling terminal bronchioles with polypoid growths of cuboidal epithelium and increased underlying stromal elastica, smooth muscle. Equal occurence in right and left lung but usually unilateral. Stillborn infants Newborn infants with respiratory distress Older children and adults (rare) 20 to 40% of resected congenital lung lesions. Can obstruct vena cava resulting in anasarca (stillborn) or cause RDS. Can shift mediastinum. Good prognosis with surgical resection. Predisposition to recurring infections if not resected. |
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What is the most common fatal hereditary disease in caucasians?
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Cystic fibrosis
1 in 3000 live births. chromosome 7 (7q31.2) Autosomal recessive Cystic Fibrosis Transmembrane Receptor defect (CFTR). Most commonly deletion of phenylalanine residue at amino acid 508 (F508) but many others possible. Salty sweat. Thick dehydrated mucous (Inspissated tenacious) hard to clear and predisposes to infections . Sometimes absent vas deferens. Widespread bronchiectasis involving all lobes (especially upper). |
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What is primary cillia dyskinesia?
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aka Immotile Cilia Syndrome
Kartagener’s Syndrome is a subset of primary ciliary dyskinesia (50%) which includes: Bronchiectasis Sinusitis Situs inversus Abnormal cilia can cause this: Absent/shortened dynein arms Absence of radial spokes Microtubular disarrangement or absence Ciliary disorientation |
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What is the predominant sputum organism in COPD patients?
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s.pneumonia
h.influenza Mucoid, apparent sputum |
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What is the predominant sputum organism in bronchiectesis patients?
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p.aeruginosa,
h.influenza Purulent sputum |
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What are the mechanisms of airflow limitation in COPD?
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Emphysema and chronic bronchitis
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What is the difference between centrilobular emphysema and panacinar (panlobular) emphysema?
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In centrilobular emphysema, dilation is primarily in respiratory bronchioles.
In panacinar (panlobular) emphysema, there is enlargment and destruction of airspaces, with uniform involvement of the acinus. |
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What is the leading cause of malignancy death in women?
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Lung cancer has displaced breast cancer.
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The chest moves out but the belly sucks in at the same time is a common finding in...
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COPD
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The chest moves in and abdomen moves out on inspiration. This is a common finding of...
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Upper airway obstruction.
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What is Wegener's granulomatosis?
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A lung vasculitis.
Typically affects: Upper airway Lower airway (lung) Kidney Can rarely be limited to lung only. Remission: 40% cytoplasmic anti-neutrophilic antibody positive (c-ANCA +)* Active Disease: 90% c-ANCA + c-ANCA+=antibodies to proteinase-3, a component of neutrophilic granules. Pathologic triad: Parenchymal necrosis (basophilic/ “dirty”) Vasculitis Granulomatous inflammation |
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What is necrotizing capillaritis?
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A collagen vascular disease of the lung.
Associated with: Systemic lupus erythematosis Wegener’s Granulomatosis (Caution) Henoch-Schonlein purpura Cryoglobulinemia Behcet’s disease Drug reactions (sulfonamides) Goodpasture’s syndrome Microscopic: Focal necrosis of alveolar septa. Neutrophilic infiltration. Numerous fragmented neutrophils. Capillary fibrin thrombi. Interstitial hemorrhage. |
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What is Churg-Strauss Syndrome?
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aka “Allergic Angiitis and Granulomatosis”
Asthma Systemic vasculitis Mononeuropathy or polyneuropathy Nonfixed lung infiltrate Paranasal sinus abnormalities Eosinophilia Elevated serum IgE (characteristic finding) p-ANCA + (NOT c-ANCA+ like wegeners granulomatosis) P-ANCA =antimyeloperoxidase antibodies Microscopic: Eosinophilic infiltrates Granulomatous infiltration Necrotizing vasculitis |
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What are the risk factors for pulmonary embolism?
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Hypercoagulable states:
Malignancies Recent surgery Oral contraceptive use Prostate cancer, pancreatic cancer or just cancer in general. Immobility including hip fracture. Indwelling central venous lines. Right atrial thrombus from arrythmia. Obesity |
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What is Primary Pulmonary Hypertension (PPH)?
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Raised pulmonary artery pressure in the absence of underlying causes like heart disease, chronic thromboembolic disease or underlying pulmonary disorder.
M : F ratio = 1 : 2 Most commonly presents: Females in 3rd decade of life Males in 4th decade of life No ethnic predisposition Familial: Autosomal dominant Penetrance of 10-20% Genetic anticipation (earlier age of onset with successive generations) |
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What are the risk factors for sporadic pulmonary hypertension?
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Female
Drugs/Toxins: Aminorex (appetite suppressant) Fenfluramine Dexfenfluramine Toxic rapeseed oil Amphetamines L-tryptophan Diseases: HIV Portal hypertension Collagen vascular diseases Eisenmenger syndrome |
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What is the earliest sign of pulmonary hypertension?
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Medial hypertrophy and muscularization of arterioles.
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When do we see plexiform lesions in pulmonary hypertension?
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Late
Severe pulmonary hypertension. NOT mild PH |
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What are the key clinical characteristics of diffuse alveolar damage as in ARDS?
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ACUTE onset of dyspnea
Diffuse pulmonary infiltrates Rapid respiratory failure. multiple causes possible. |
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What is the idiopathic variant of diffuse alveolar damage?
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Known as Acute Interstitial Pneumonia (AIP)
Hamman-Rich Syndrome |
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What are the two stages in which diffuse alveolar damage occurs?
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Exudative stage (acute):
Interstitial edema Type I pneumocyte sloughing !!Hyaline membranes!! Organizing stage (proliferative): !!Proliferating type II pneumocytes!! Interstitial fibroblasts (focal airspace organization) |
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The classic radiographic finding of the exudative stage in diffuse alveolar damage is...
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patchy bilateral areas of ground-glass attenuation and consolidation.
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The classic radiographic finding of the organizing stage in diffuse alveolar damage is...
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Areas of consolidation in dependent lung regions and extensive areas of ground-glass attenuation with little normal parenchyma.
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What is Cryptogenic Organizing Pneumonia (COP) aka Bronchiolitis Obliterans Organizing Pneumonia (BOOP)?
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Subacute onset:
Cough Dyspnea Fever Multiple PATCHY airspace opacities on CXR. Usually bilateral. Minimal or lack of interstitial connective tissue/fibroblasts. Lack of hyaline membranes. Intraluminal plug of immature (loose bluish) connective tissue filling alveolar duct; lung architecture is preserved. Favorable course with corticosteroids. |
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In a large pleural effusion (or hemothorax) the trachea is shifted...
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Away from the side of effusion.
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In atelectasis, the trachea is shifted....
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Towards the side of the atelectasis.
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What dose of radiation is required to produce a deterministic effect?
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>0.5 Gy [50 rad]
Lymphocytes are most radiosensitive cells < 1 gray (100 rad) Severity increases with dose and can include skin erythema, cataracts and sterility. |
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What is the annual background radiation exposure in america?
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300 millirem
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Which chedst imaging study has the highest radiation exposure?
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chest CT (478mrem) is much higher than CXR (6mrem).
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What do we mean when we say that low dose radiation (<0.5 Gy [50 rad]) that produces a stochastic effect?
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Stochastic means random or probabilistic.
Refers to the carcinogenesis and genetic damage or radiation. Severity is independent of dose Dose only effects probability of occurrence Existence of any threshold is controversial. Stochastic risk depend on gender and age of exposure. |
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X-rays are attenuated by...
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Metals
Water Fat Gas |
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A standard chest X-ray is...
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PA (film in front of the chest) and lateral.
PA is better for visualizing the heart because it is further from the beam (very anterior in the chest). |
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For a left lateral film the side closest to the film is....
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Left chest.
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How do we tell left from right ribs on left lateral film?
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The left ribs will be larger.
The left hemidiaphragm will dissappear where it meets the heart while the right will typically not. |
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What should be the width of a normal cardiac slihouette?
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0.6 of the total diameter.
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What contrast medium is typically used with CT?
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Iodine.
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What radiographic tool is used for V/Q scans?
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Gamma camera.
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What is a PET scan?
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Fluorine-18-fluorodeoxyglucose (F18-FDG)
most commonly used PET radioisotope Demonstrates increased uptake/localization in some infectious and neoplastic processes. Poor spatial resolution (6-8mm limits) Commonly combined with a CT scanner to facilitate localization of pathology. |
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What is responsible for the difference in the rate of diffusion of CO2 compared to oxygen?
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Solubility.
Molecular weights are pretty similar but CO2 is significantly (~20x) more soluble. PO2 is thus usually affected first because it diffuses more slowly. |
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According to ficks law...
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Diffusion across a membrane is directly related to surface area and inversely proportional to membrane thickness.
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What is the limiting factor in transfer of oxygen into the blood?
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It is perfusion limited.
If everything else is normal, increase in cardiac output is the only way to do it. |
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What is the limiting factor in transfer of carbon monoxide into the blood?
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Diffusion limited
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What is the limiting factor in transfer of carbon dioxide into the blood?
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Perfusion limited
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Diffusing capacity is given by...
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D=VCO/pCO
(measured with carbon monoxide) |
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Where does the oxygen association curve start to flatten?
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~80mmHg
At about 100mmHg saturation does not increase much. |
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Where does the oxygen association curve start to get steeper?
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~40mmHg
Below 40mmHg Saturation starts to drop dramatically. (unload oxygen easily). |
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What is P50?
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The pO2 at which Hb is 50% saturated.
Usually about 27-30mmHg. |
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Increases in H+, pCO2, Temp and 2,3 BPG all shift the O2 dissociation curve to the....
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Right.
This means reduced oxygen binding affinity of Hb. |
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How do we calculate O2 capacity?
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Hbx1.34 ml O2/g Hb
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How do we calculate O2 content?
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O2 capacityX %Sat + dissolved O2
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How do we calculate %saturation?
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O2 bound to Hb/O2 capacity x100
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What are the PO2 and %Sat in anemia?
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Normal
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What are the pO2, %Sat and O2 capacitance in Carbon monoxide poisoning?
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Normal pO2
Normal capacitance %Sat supressed. |
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The vast majority of CO2 in the blood is carried as...
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Bicarbonate.
Made by carbonic anhydrase in RBC and diffuses out while chloride diffuses in. |
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We can carry more CO2 in the blood under conditions of....
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Low oxyhemoglobin %Sat.
This helps CO2 carriage as O2 is removed at the level of the tissues. |
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What are two good summary statements of the Bohr effect?
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We can carry more oxygen in the blood when the CO2 is low.
We can get rid of oxygen easier when CO2 is high. |
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What are the two primary organs responsible for regulating acid base balance?
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Lungs
Organs |
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What is the henderson hasslebach equation as it pertains to the blood?
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pH=pK+Log{HCO3-/(0.03*pCO2)}
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What are normal arterial blood gas numbers?
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pH: 7.38-7.42 7.40
PO2: 90-110 100 PCO2:35-45 40 HCO3: 23-29 24 |
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Acidosis is a pH <....
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7.4
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A chest with an anteroposteriorly increased diameter suggests....
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Obstructive lung disease.
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What happens to the clavicles in chronic hyperinflation? (emphysema)
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the lateral aspects go up.
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What happens to the distance between the sternal angle and the larynx in chronic hyperinflation? (emphysema)
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It is reduced.
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Clubbing of nails (non hereditary) is associated with....
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Lung cancer
Idiopathic pulmonary fibrosis Asbestosis |
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What is the primary location of the inspiratory center is the brain?
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Along the floor of the fourth ventricle in the medulla.
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What happens if we sever both the entire pons and the vagi?
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Apnusence
Prolonged inspirations seperated by brief periods of expiration. |
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The site of respiration rythmicity is located in....
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The medulla.
Can be influenced by voluntary control (breath holding hyperventilation etc.) |
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How does a cough happen?
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Receptors in the larynx and trachea stimulated by noxious stimuli, cold or mechanical irritation send afferents via the vagus to central centers which then stimulate a cough.
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What sort of effect does stimulation of stretch receptors in the chest wall and lungs have on breathing?
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Turns off inspiratory neurons and allows for expiration.
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Why do patients with pulmonary edema cough?
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J receptors stretch and cause coughing.
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What are the characteristics of the blood brain barrier in termsof acid base control?
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Relatively impermeable to H+ and HCO3-.
Highly permeable to CO2 though. CSF has low protein content (not good buffer). |
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What is the main responsiveness difference between the central chemoreceptors in the medulla (4th ventricle) and the peripheral chemoreceptors in the carotid and aortic sites?
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Central chemoreceptors only respond to pH and pCO2.
NOT pO2. |
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What do we mean when we say there is a synergistic interaction between pO2 responsiveness and pCO2 responsiveness?
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A more pronounced increase in ventilation happens when we increase pCO2 in the presence of low pO2 than in the presence of normal or high pO2.
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Why is hypoxic drive important in COPD?
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Chronic high pCO2 desensitizes the hypercarbic drive.
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How does progesterone affect respiration?
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It acts directly on central respiratory centers in the medulla.
As progesterone goes up, ventilation increases and pCO2 consequently decreases. Towards the end of pregnancy mom's blood gas looks like a respiratory alkalosis but this is normal. Progesterone also decreases sleep apnea and disordered breathing. |
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What is cheyne-stokes respiration?
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Disordered breathing spurts in terms of depth seperated by periods of no repiratory efforts.
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What is biot's breathing?
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Very deep repiratory effort spurts seperated by periods of no activity.
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What is Kussmauls breathing?
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Very deep inspiratory and expiratory efforts at a slow rate.
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Where does perfusion/perfusion matching have to occur?
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The placenta.
Maternal blood in the intervillus space has to match fetal blood in the fetal side of the placenta. |
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In a fetus how does right heart output compare to left heart output?
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Righ heart output is always greater (~65-70% of total ventricular output)
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How do we quantify dyspnea?
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Threshold discrimination (e.g. walking on flat surface or incline, etc)
Scaling techniques (e.g. Borg Scale) Validated questionnaires (British Medical Research Council Questionnaire; Pulmonary Functional Status and Dyspnea Questionnaire) |
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Why is diaphragm paralysis associated with open heart surgery?
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Icing of the heart on the pump.
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What is platypnea?
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Dyspnea in the upright position
Liver disease- may be associate with orthodeoxia |
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What is Trepopnea?
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Dyspnea on either right or left decubitus positions.
Pleural effusion, airway obstruction |
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What is the most common cause for seeking medical attention?
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Cough
Second most common reason for a general medical examination. |
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How long does a cough have to last to be considered chronic?
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3 weeks.
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Brassy cough is associated with...
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Major upper airways.
Croupy- laryngeal Barking- laryngeal |
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Frothy cough secretions are associated with...
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broncheoalveolar carcinoma
Pink foamy secretions- congestive heart failure. |
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Rust or prune-juice colored cough secretions are associated with...
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Pneumococcal pneumonia
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What is considered massive hemoptysis?
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>200 ml per 24 hours
Differentiate from hematemesis and epistaxis |
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What are the characteristics of pleurisy pain?
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Localized but may radiate (e.g. diaphragm pleurisy radiating to ipsilateral shoulder or neck)
Sharp, catch, burning Worsened with deep breath or cough or sneeze or position changes. Acute- pneumothorax, pulmonary embolism, pneumococcal pneumonia |
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What are the charcteristics of neuritis or radiculitis pain?
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Knifelike; like electric shock
Worse with deep breathing, cough, sneeze, straining |
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What is costochondritis?
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Inflammation of rib joints, cartilages.
Tietze’s syndrome- redness, swelling and soreness of costochondral junction. Point tenderness on palpation. |
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What fungal lung infections are associated with various U.S geographic locations?
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Southwest- Coccidiomycosis,
Southeast- Blastomycosis, Ohio river basin-Histoplasmosis |
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What infection is associated with marijuana smoking?
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Aspergillosis.
The marijuana is often not well dried. |
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What lung injury is associated with crack-cocaine use?
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Airway burns.
Very high heat in crack pipes. |
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What are the main pathological breathing patterns?
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Tachypnea- rapid shallow breathing
Kussmaul’s- rapid deep breathing (air hunger) Cheyne-Stokes- rhythmic crescendo-decrescendo with periods of apnea Biot’s- irregular breaths with periods of apnea Snoring with paradoxic movements of chest wall. Accessory muscle use . |
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What information does tactile fremitus give us?
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Increase (consolidation) Decrease (pleural fluid)
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What is a sibilant rhonchus?
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A wheeze.
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A crepitation is...
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A fine crackle
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A coarse rale is the same thing as a...
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Coarse cracle
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Bronchial breath sounds heard in the periphery suggests...
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Consolidation
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What is a mediastinal crunch?
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Pneumo-mediastinum
Synchronous with cardiac cycle (instead of respiratory cycle) |
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What is a pleural friction rub?
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Pleura rubbing caused by thickened pleura.
Inflammatory, malignancy. Leathery, creaking quality. Both inspiration and expiration. Possible even with pleural effusion. |
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Erythema nodosum is associated with..
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Sarcoidosis
(uveitis also common in sarcoidosis but can occur with ankylosing spondylitis) Coccidiodomycosis Histoplasmosis |
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Erythema multifome is associated with...
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Bacterial pneumonia especially Mycoplasma Pneumoniae.
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Palpable purpura are associated with...
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Vasculitis
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Keratoconjunctivitis Sicca is associated with...
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Sjogrens syndrome.
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Proptosis is associated with...
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Wegeners Granulomatosis
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Heliotrope rash is associated with...
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Dermatomyositis
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Lupus vulgaris is associated with...
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TB
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Adenoma sebaceum is associated with...
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Tuberous sclerosis.
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Sinus inversus,Sinusitis and bronchiectasis is the triad associated with...
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Cartageners syndrome.
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Loss of alveoli, blebs in the upper areas of the lungs and loss of alveolar septal walls is associated with...
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Emphysema
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What are the subcategories of diffuse alveolar hemmorage?
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Gooodpastures syndrome:
M:F = 9:1 Young adults Lung and kidney thing. Antibody-mediated immune reaction to basement membranes (IgG) in both lung and kidney. (HLA DRw15, DQw6) Linear IgG immunofluoresence staining. Idiopathic Pulmonary Hemosiderosis: M:F = 1:1 Mostly adolescents and children. No renal involvement. Unknown mechanism. Coarse granules of hemosiderin fill alveolar spaces; many contained within macrophages. Wegener’s Granulomatosis, Necrotizing Capillaritis, and Churg-Strauss may also cause acute hemorrhage !! |
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What is Pulmonary Alveolar Proteinosis?
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Impaired clearance of alveolar surfactant by alveolar macrophages.
IgG antibodies against GM-CSF. Mostly ages 30-50. |
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What are the non-caseating Granulomatous Lung Diseases?
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Sarcoidosis
Hypersensitivity Pneumonitis (HP) |
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What is the epidemiology of sarcoidosis?
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Young adults 20-40 (most common)
Slight female predominance >> in African-Americans (US) >> Irish and Scandinavians (outside US) Asymptomatic (most common presentation) |
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How do we diagnose sarcoidosis?
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Clinical and radiologic findings.
Interstitial noncaseating granulomas in a lymphatic and bronchovascular distribution. Exclude other granulomatous disease. Heightened/exaggerated helper T-cell type 1 (Th1) immune response to unidentified antigen (self or foreign) at sites of disease. No specific lab test. Serum level of angiotensin converting enzyme (ACE) elevated (2/3 of patients) 24-hour urine calcium excretion frequently increased |
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What are the typical CXR findings of sarcoidosis?
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Marked, symmetric, bilateral hilar and mediastinal lymphadenopathy.
Mild reticulonodular interstitial infiltrate in the perihilar regions. |
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What is a granuloma?
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A collection of histiocytes.
(not necessarily multinucleated giant cells) |
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Which disease has "well-formed" non-caseating granulomas with a nodular cluster of epithelioid cells and giant cells?
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Sarcoidosis
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What are the complications of sarcoidosis?
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Interstitial fibrosis with honeycombing in advanced stages.
Cavitation/cystic changes. Aspergillomas. |
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How do we treat sarcoidosis?
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Almost 50 percent spontaneously remit but 5-10% mortality makes decision hard.
Corticosteroids or cytotoxic drugs. Radiation. |
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Hypersensitivity pneumonitis is also known as...
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Extrinsic Allergic Alveolitis
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What causes hypersensitivity pneumonitis?
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Immunologic reaction to inhaled organic antigens or, rarely simple chemicals.
Farmer's lung Bird Fancier's lung Humidifier lung Air conditioner lung Maple bark strippers lung Malt workers lung |
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What are the clinical characteristics of hypersensitivity pneumonitis?
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Symptoms may develop hours, weeks or months after exposure.
History of allergic disease uncommon. |
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What sort of immune reaction is hypersensitivity pneumonitis?
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Combination of Immune complex–mediated (type III) and T cell–mediated, delayed (type IV) hypersensitivity reactions.
Precipitating immunoglobulin (IgG) antibodies against offending agent in serum in most cases. |
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What are the pathological findings of hypersensitivity pneumonitis?
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Chronic interstitial inflammation with peribronchiolar accentuation.
Bronchiolocentric cellular interstitial pneumonia. In some patients (2/3): Nonnecrotizing poorly formed granulomas in peribronchiolar interstitium. or Foci of BOOP/COP Cryptostroma corticale in Maple bark stripper's disease. |
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How do we treat hypersensitivity pneumonitis?
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!!removal of offending antigen!!
Corticosteroids. Irreversible once dense fibrosis develops with honeycomb changes Majority near total recovery of lung function. May take several years after the inciting exposure ceases. Bird fanciers have a worse prognosis than farmers with HP. |
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What is usual interstitial pneumonia?
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aka.
Chronic interstitial pneumonitis Cryptogenic fibrosing alveolitis !!Idiopathic pulmonary fibrosis!! Insidious onset of dyspnea with chronic, progressive downhill course. Males >> Females (50-70) Cigarette smoking 1.6- to 2.3-fold excess risk. Long-term exposure to metal dust or wood dust independent risk factor. Thought to be intrinsic abnormality of tissue repair. (has to do with TGF beta 1 which negatively regulates telomerase). Influences Calveolin-1, an endogenous inhibitor of pulmonary fibrosis. |
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What are the clinical characteristics of UIP (usual interstitial pneumonia)?
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Most tachypneic, with rapid shallow breaths, increased work of breathing
Bibasilar late inspiratory fine crackles ("velcro" rales) Clubbing, Pulmonary hypertension and cyanosis are late manifestations. Reduced compliance. All volumes reduced. Hypoxemia. Respiratory alkalosis. Increased Aa gradient Low pO2 Low %Sat |
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What are the key histological charcteristics of UIP (usual interstitial pneumonia)?
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Patchy lung involvement which is spatially and temporally heterogeneous.
Most prominent in subpleural and peripheral lobular regions (not usually bronchocentric). Dense fibrosis with remodeling of lung architecture. Frequent “honeycomb” fibrosis. Mild/moderate interstitial inflammation. |
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What is the prognosis of UIP?
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It is a death sentence.
Hence a diagnosis of exclusion. |
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What are the pathologic features of UIP?
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Early:
firm lungs, pulmonary edema, hyaline membranes, mononuclear infiltration, type II pneumocyte hyperplasia Later: fibrous tissue, fibrogenic foci (areas of active disease), thickened alveolar septa (solid and normal lung), hyperplastic smooth muscle, microcysts, loss of alveolar capillaries End stage: spaces lined by cuboidal/columnar epithelium separated by fibrosis and forming honeycomb lung (particularly in the superior portion of lobes); also lymphoid hyperplasia, thickening of intima and media of pulmonary arteries. |
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What type of biopsy is needed to diagnose UIP?
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Requires open wedge biopsy!
Transbronchial biopsy inadequate! |
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What types of diagnoses are attainable by transbronchial biopsy?
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Malignancy, infections, sarcoidosis, hypersensitivity pneumonitis, cryptogenic organizing pneumonia, eosinophilic pneumonia, or Langerhans' cell histiocytosis.
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What percentage of UIP patients have lung carcinoma?
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13 to 31% of patients
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How do we treat UIP?
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Steroids
20% improve somewhat. Median survival from diagnosis 3 years Worse prognostic factors: Eosinophilia Increased fibroblastic foci |
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What is NSIP (non-specific interstitial pneumonia)?
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Average duration of illness prior to diagnosis
8 to 18 months. Younger than UIP (46-57) Correlated with smoking. Cause is unknown. Either cellular or fibrosing pattern. Pattern similar to UIP. Small portion antinuclear antigen (ANA) and/or rheumatoid factor positive. Ground glass opacity mainly in the lower lobes. |
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What is the most distinguishing charcteristic between UIP and NSIP?
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NSIP is temporally uniform and not patchy.
Unlike UIP, architecture is preserved and there is no increase in dense fibrosis. |
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How do we treat NSIP?
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Spontaneous remissions do not occur.
Expected disease progression and shortened survival times (if untreated) Very corticosteroid-responsive. |
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What is desquamative interstitial pneumonia?
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~90% of patients smokers
Clinically similar to UIP M:F 2:1 Fourth to fifth decade of life. Rare cases in children. Predominance of intra-alveolar macrophages. No scarring fibrosis causing remodeling of the lung architecture (unlike UIP) Focal DIP-like reactions can be seen around mass lesions, such as infarcts or tumors. Tx: Smoking cessation and steroids. |
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What are the five main clinical pulmonary function tests?
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1. Spirometry and flow-volume curve
2. Static lung volumes 3. Carbon monoxide transfer 4. Maximal mouth pressures 5. Arterial blood gas analysis |
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What is FEV1?
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FORCED EXPIRED VOLUME IN ONE SECOND.
The maximal volume of air exhaled in the first second of a forced expiration from a position of full inspiration, expressed in liters at BTPS. |
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What is FVC?
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FORCED (or FAST) VITAL CAPACITY
the maximal volume of air exhaled with maximally forced effort from a maximal inspiration, i.e. vital capacity performed with a maximally forced expiratory effort, expressed in liters at body temperature and ambient pressure saturated with water vapor (BTPS). |
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What is the utility of F-V curves?
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Assess FVC manuever
effort. Assess for possible central airway obstruction. |
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What is an obstructive pattern on spirometry?
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Reduced FEV1/FVC ratio
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What pattern on spirometry suggests restrictive lung disease?
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Close to normal FEV1/FVC ratio but reduced vital capacity.
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How do we define lower limit of normal (LLN)?
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mean predicted or reference value minus 1.64 X SEE
SEE=standard deviation |
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What do pulmonary function testing reference equations take into account?
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Gender
Height Age (Ethnicity) eg. FVC = 0.491H - 0.0255A -3.590 |
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90% confidence interval for spirometric values will produce
statistical error of.... |
5% misclassification in a population.
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What is the algorithm for assesing pulmonary function testing?
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Pulmonary function tests for COPD can be classified as very severe when FEV1 as percentage of the predicted value is less than...
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~30-35%
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What percentage change in PFT's do we expect to see with bronchodilators in an asthmatic?
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FVC at least increase of 12% and 200ml absolute change
FEV1 at least increase of 12% and 200ml COPD will typically not have this magnitude of change. |
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How do we measure residual volume?
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Helium dilution
Nitrogen washout Body plethysmography Chest x-ray measurements Spirometry alone cannot measure residual volume (RV) or any volume that includes it like functional residual capacity (FRC) or total lung capacity (TLC). |
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How is total lung capacity (TLC) calculated?
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T.L.C. = R.V. + I.V.C
or T.L.C. = F.R.C. + I.C Low TLC occurs in restrictive lung disease. |
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How do we calculate residual volume (RV)?
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R.V. = F.R.C. – E.R.V
or R.V. = T.L.C. – I.V.C RV tends to rise in severe obstructive lung disease. |
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How do the volumes on PFT change with the various types of pulmonary disease?
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What is the diffusing capacity of the lung for carbon monoxide (DLCO) [aka transfer factor of the lung for carbon monoxide (TLCO)] used for?
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To evaluate gas transfer from the distal air spaces into the pulmonary capillaries.
Known very low concentrations CO are inspired. The rate of CO disappearance is calculated from the ratio of the CO concentrations of the inspired and expired gas and then expressed as a function of the driving pressure. DLCO =V CO / (PACO - PcCO) V CO is the uptake of CO in ml of CO at STPD conditions per minute. PACO is the average partial pressure of CO in alveoli. PcCO is the average partial pressure of CO in the pulmonary capillary plasma. DLCO units = ml / min / mmHg |
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What does a low DLCO mean?
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LOW DLCO WITH OBSTRUCTION
Emphysema Cystic fibrosis Bronchiolitis LOW DLCO WITH RESTRICTION Diffuse parenchymal lung disease Pneumonitis/alveolitis OTHER Carboxyhemoglobulinemia. Altitude. Anemia. Pulmonary embolism. Pulmonary arterial hypertension. |
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What does a high DLCO mean?
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Asthma
Obesity Intrapulmonary hemorrhage |
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What percentage of predicted value DLCO signify what degree of gas transfer problems?
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Mild >60% and ,LLN
Moderate 40–60% Severe <40% |
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What are normal maximun inspiratory and expiratory pressures for men and women? (MIP and MEP)
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adult men:
-100 cmH2O and +170 cmH2O adult women: -70 cmH2O and +110 cmH2O |
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Which one of the following can cause an increased DLCO?
a. Pulmonary fibrosis b. Emphysema c. Pulmonary embolism d. Asthma e. Lung resection surgery |
Asthma
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Which one of the following is most suggestive of an obstructive disorder?
a. FEV1/FVC ratio of < 0.70 or 70% ( i.e. below LLN) b. FVC < 70% of predicted c. TLC < 70% of predicted d. DLCO < 70% of predicted e. Maximal inspiratory pressure < 70% predicted. |
FEV1/FVC ratio of < 0.70 or 70% ( i.e. below LLN)
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Which one of the following suggests air trapping in chronic obstructive pulmonary disease?
a. Increased RV/TLC ratio b. Decreased TLC c. Decreased DLCO d. Decreased RV e. Increased maximal inspiratory pressure |
Increased RV/TLC ratio
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What are the risk factors for COPD?
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Smoking.
Occupational / environmental exposure (coal dust, silica). Air pollution. Poor nutrition. Childhood respiratory infections. Preexisting BHR (bronchial hyperresponsiveness) Alpha-1 antitrypsin deficiency (rare) |
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Twitchy airways in asthma are caused by...
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Eosinophils (IgE)
Chronic bronchitis and emphysema inflammatory reactions caused by toboacco smoke are mediated primarily from neutrophils. |
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What are the main pathophysiological changes of COPD at the level of the alveolus?
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Decreased lumen size
Increased mucous Increased goblet cells Wrinkling of alveolus Airway wall thickening Disrupted alveolar attachment Lymphoid follicles (severe) |
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What immune cells are involved in the inflammatory process of COPD?
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Neutrophils
Macrophages, T-lymphocytes (specifically CD8+) Eosinophils (not as much as asthma but present) |
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Do the inflammatory changes of COPD persist after smoking cessation?
|
Yes
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What sort of mucocilliary dysfunction is seen in COPD?
|
Destroyed cilia
Loss of beat frequency |
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What spirometry results confirm COPD?
|
FEV1/FVC < 0.70
AND Postbronchodilator FEV1 < 80% predicted Elevated TLC : Think hyperexpansion Elevated RV: Think air trapping Decreased DLCO: Think emphysema |
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What are the GOLD criteria stages of COPD?
|
Mild COPD:
FEV1/FVC < 0.70 FEV1 ≥ 80% predicted Moderate COPD: FEV1/FVC < 0.70 50% ≤ FEV1 < 80% predicted Severe COPD: FEV1/FVC < 0.70 30% ≤ FEV1 < 50% predicted Very severe COPD: FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted with chronic respiratory failure |
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What is a normal age related decline in FEV1?
|
25-30 mL / yr from age 25
In smokers: Average 45-60 mL/yr 20% experience 150-200 mL/yr "Some smokers may not experience a decline" |
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What prophylaxis is recommended for COPD patients?
|
Long term anticholinergic bronchodilator.
Pneumovax Fluvax Bone densitometry for osteoperosis in: Females (post-menopausal) Smokers Steroid users Every 2 years for screening |
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What are the main pharmacological interventions for COPD?
|
Bronchodilators
Steroids Theophylline. |
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How much of an increase in arterial pO2 can we get from increasing ventilation on room air?
|
~10mm tops
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What is the most common defect in the CFTR gene which causes cystic fibrosis?
|
Delta F-508
Homozygous or heterozygous. Material is synthesized but there is a blockage in processing on the way to the surface. |
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What are the major classes of functional CFTR mutations that can lead to cystic fibrosis?
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What is physically the problem in cystic fibrosis?
|
Chloride cannot efflux from the cell into the airway lumen and normal liquification of the mucocilliary mechanism does not occur.
This results in chronic obstruction, infection and bronchiectasis. The damage eventually becomes irreversible. |
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How do we image CF lungs?
|
High resolution CT (HRCT) is more sensitive than conventional chest x-rays in detecting structural lung damage in individuals with CF.
Structural lung damage precedes the deterioration of lung function. |
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What are the most common presentations of cystic fibrosis patients?
|
Respiratory Symptoms – 35.5%
Failure to thrive/malnutrition–23.2% Steatorrhea/abnormal stools–16.1% Meconium ileus – 14.5% Neonatal screening – 21.6% Family history – 13.4% Nasal polyps – 5.8% |
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What are the "respiratory symptoms" most commonly seen in cystic fibrosis children?
|
Chronic cough.
Recurrent pneumonia. Staphylococcal pneumonia. Pseudomonas aeruginosa in sputum cultures. Nasal polyposis. Upper lobe bronchiectasis. Sinusitis. Digital clubbing. |
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What type of inheritance pattern is Cystic Fibrosis associated with?
|
Autosomal recessive
(1 in 4 disease, 1 in 2 carrier) |
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What GI symptoms are most commonly seen in cystic fibrosis children?
|
Meconium ileus
(15% of CF newborns) Pancreatic insufficiency. Rectal prolapse. Biliary cirrhosis. Distal intestinal obstruction syndrome. Hypoproteinemic edema. Recurrent pancreatitis. |
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By what mechanism does hepatobilliary dysfunction occur in cystic fibrosis?
|
Billiary fibrosis
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How is cystic fibrosis diagnosed?
|
Positive sweat test (pilocarpine iontophoresis):
>60 meq/l Cl (40-60 is a gray zone) Genetic analysis compatible with CF. A negative genetic analysis does not rule out CF. Newborn screening. |
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How is newborn screening done?
|
Immunoreactive trypsinogen followed by another immunoreactive trypsinogen test on those that are positive.
or Immunoreactive trypsinogen followed by DNA test. |
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How does gender affect survival curves in cystic fibrosis?
|
After adolescence, females have a poorer outcome and are thus evaluated for lung transplant earlier.
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What are the main modalities of the current treatment of CF?
|
Augment clearance
Antibacterial therapy Reduce inflammation Replace damaged lungs |
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What lung organisms are CF patients susceptible to?
|
Varies with age.
Young kids: S. Aureus P. Aeuriginosa Older kids: P. Aeuriginosa S. Aureus |
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What are the two main approaches to cystic fibrosis antibiotic therapy?
|
-Intermittent use of systemic antibiotics.
-Intermittent and chronic use of inhaled antibiotics. Infection and the accompanying inflammation is the cause of lung damage. Once infection is established it can be controlled but not eradicated. Intermittent flare-ups of infection occur (pulmonary exacerbation). They are treated with discrete courses of antibiotic therapy. |
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What signs and symptoms suggest a pulmonary exacerbation in a cystic fibrosis patient?
|
Increased cough.
Change in sputum production. Hemoptysis. Change in appetite or weight. Change in activity. Exercise intolerance. Fever is uncommon Increased respiratory rate Change in chest sounds (increased crackles) Accessory respiratory muscle use. Decreased weight. Change in spirometry. Changes in chest radiograph. |
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How does rhDNAse, dornase alfa improve clearance in cystic fibrosis patients?
|
Neutrophil-released DNA increases viscoelasticity and adhesiveness of CF sputum.
Dornase alfa breaks down extracellular DNA which liquifies the secretions, improving clearability. |
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How do bronchodilators help cystic fibrosis patients?
|
Reverse bronchospasm and also increase ciliary beat frequency.
Works consistently in ~25% of patients. Some may exhibit decreased pulmonary function with bronchodilators Common but controversial. |
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What anti inflammatory agents have been evaluated for CF?
|
Systemic steroids:
Side effects outweigh benefits Ibuprofen: Shown to be helpful in high doses, potential side-effects limit use Azithromycin: This macrolide antibiotic is useful in low doses as an immuno-modulator. |
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What complications are associated with cystic fibrosis?
|
Hemoptysis
(from bronchial circulation) Pneumothorax (Blebs rupture into the pleural space) Allergic Bronchopulmonary Aspergillosis. Cor Pulmonale Chronic Respiratory Insufficiency |
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What anatomic boundary seperates upper respiratory infections from lower respiratory infections?
|
The larynx.
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What are the natural defense mechanisms of the upper respiratory tract?
|
Microflora
Mucociliary barrier/clearance mechanisms Secretory IgA Cough/gag reflexes; sneeze mechanism |
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What are the natural defense mechanisms of the lower respiratory tract?
|
Mucous layer/mucociliary clearance
Alveolar macrophages/circulating phagocytes Immunoglobulins/complement Glottic closure & cough reflexes |
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If they are to successfully produce disease, organisms deposited in the the respiratory tree must first...
|
Compete with normal microflora for mucosal binding sites.
Avoid expulsion from the RT by mucociliary clearance mechanisms & cough/sneeze reflexes Evade local host defenses in the form of phagocytes & immunoglobulins. |
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What times of year do we expect to see various upper respiratory infections?
|
HSV: Sporadic
Coxsackie and ECHO: Summer+Fall Influenzae, Adenovirus, Rhinoviruses and Coronaviruses: Late fall to early spring. Parainfluenza: Fall+winter RSV: Spring |
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What is the common cold?
|
Most cases of the common cold are caused by rhinoviruses & coronaviruses, occur during the winter, & are characterized by nasal obstruction & drainage.
Illness typically lasts ~7d & is managed symptomatically with decongestants. |
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What % of pharyngitis cases is bacterial (S. pyogenes, Group A beta hemolytic strep)?
|
15-30%
|
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What are some of the features of viral pharyngitis?
|
Conjunctivitis
Coryza Cough Diarrhea |
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What are some of the features of group A strep pharyngitis?
|
Sudden onset
Fever (T>101) Headache N/V & abd pain Discrete exudate Tender ant cerv LAD Pt 5-15 yo Winter or early spring H/O exposure |
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What is the Centor score for group A strep pharyngitis?
|
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What are the clinical predictors of acute bacterial sinusitis?
(usually S.Pneumo or H.Flu) |
“Double sickening”
Unilateral pain Pain above or below the eyes on leaning forward Maxillary toothache Purulent rhinorrhea by hx Purulent secretions in the nasal cavity on exam Poor response to nasal decongestants 0-1=No Rx; 2-3=XR; 4 or more=ATB Rx Rx: initiallly should be with “1st tier” ATBs such as amoxicillin or TSX in most cases. |
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What are the various types of lower respiratory tract infection?
|
Bronchiolitis
Bronchitis Pneumonia Lung abscess Pleural empyema |
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Why are we highly selective about giving antibiotics when we diagnose bronchitis?
|
In the normal host, bronchitis is primarily a viral infection that occurs during the winter months, is not associated with significant leukocytosis or CXR abnormalities, and resolves spontaneously without ATBs.
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What are the clinical characteristics of pneumonia?
|
Fever
Dyspnea Cough with production of purulent sputum Infiltrates on CXR |
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In what sense are Pneumonias one of the most common “serious” infections encountered in the US?
|
Mortality rate ranging from 10% for CAP to up to 90% for VAP.
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What are the etiological differences between community acquired and hospital acquired pneumonia?
|
Community-acquired pneumonia is most often due to selected typical and atypical bacteria (eg, S. pneumoniae, M. pneumoniae, Chlamydophila pneumoniae) or viruses.
Healthcare-associated or hospital-acquired pneumonia is typically caused by S. aureus and GNRs such as Pseudomonas. |
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Certain underlying clinical conditions lead us towards suspecting particular etiologies for pneumonia. What are these conditions?
|
Post-influenza:
S. pneumoniae, S. aureus, H. influenzae Altered consciousness/ esophageal dysmotility: Oral flora (aerobes/anaerobes) Alcoholism: Oral flora, S.pneumoniae, S.aureus, Klebsiella Chronic lung disease: S. pneumoniae, H.influenzae (nontypable) Cystic fibrosis: P. aeruginosa, S. aureus, Stenotrophomonas |
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How does the immune status of a patient help us identify the organism causing a pneumonia?
|
Hypogammaglobulinemia is susceptible to encapsulated organisms:
Streptococcus pneumoniae Haemophilus influenzae, type B Complement defects: Streptococcus pneumoniae H. influenzae, type B (encapsulated) Depressed cell-mediated immunity susceptible to intracellular pathogens: Typical and atypical mycobacteria Fungi (crypto, endemic mycoses) Viruses (cytomegalovirus, varicella-zoster virus, HSV, measles virus) Pneumocystis jirovecii Toxoplasma gondii Decrease in the number of fully functional granulocytes susceptible to pyogenic extracellulars and fungi later in the course: Oral bacterial flora Enterobacteriaceae Pseudomonas aeruginosa Aspergillus species |
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|
How can the acuity of the pneumonia help us identify the organism?
|
More acute process tends to be:
Pyogenic extracellular bacteria. Sub-acute to chronic tends to be: Intracellular bacteria or viruses, |
|
|
Which organisms generally produce "typical pneumonia" symptoms?
|
Streptococcus pneumoniae
Klebsiella pneumoniae Haemophilus influenzae Moraxella catarrahalis [Legionella pneumophila] |
|
|
Which organisms tend to produce "atypical pneumonia" symptoms?
|
Mycoplasma pneumoniae
Chlamydophila pneumoniae Chlamydophila psittaci Coxiella burnetii Legionella pneumophila Non-pneumophila Legionella species Viruses |
|
|
What is a typical pneumonia?
|
“Typical” pneumonias are sudden in onset and characterized by high spiking fevers, severe rigors, cough productive of purulent sputum, leukocytosis (WBC count >15,000), and lobar infiltrates on CXR. The prototypical causative pathogen would be S. pneumoniae.
The converse is true for pneumonias due to “atypical” pathogens. |
|
|
It is seldom possible to reach a specific etiologic diagnosis of pneumonia by x-ray alone! Nevertheless, generalizations about radiographic patterns & pathogens are that...
|
Lobar consolidation =Pyogenic extracellular bacteria (S. pneumo, GNRs)
Interstitial infiltrates=Viruses, Mycoplasma Cavitation without air-fluid level= TBC, fungi Consolidation + pleural effusion= S. pneumo, Staph, GNRs, anaerobes. |
|
|
Confirmation of the cause of pneumonia is achieved in about what % of patients?
|
<50% of pts; the most useful diagnostic tests are sputum & blood cultures and selected antigen screens on urine.
|
|
|
What T-cell pathways do eosinophillic type allergic responses (IgE) go through?
|
Th2 process
Production of non-IgE antibodies such as IgG is driven mostly by Th1 cells. Neutrophilic disorders tend to go through Th17. |
|
|
What is allergic rhinitis?
|
IgE-mediated inflammatory reaction of the nasal membranes.
Triggered after allergen exposure. Constellation of symptoms such as itching, sneezing, rhinorrhea, and nasal congestion. Often occurs simultaneously with or precedes asthma. |
|
|
What is the etiology of chronic rhinitis?
|
Allergic
Non-allergic "mixed" rhinitis: allergic plus non-allergic component (34%) |
|
|
What do we mean when we say an allergen is enzymatically active?
|
It has innate proteolytic activity and thus innate activities that elicit aberrant immune responses.
Enhances access to dendritic cells by cleaving tight junctions in the airway epithelium. Activates protease-activated receptors, eliciting thymic stromal lymphopoietin (TSLP), chemokine, and cytokine release by epithelium. |
|
|
How do dust mites elicit allergic responses?
|
Main house dust mite allergen, Der p 2, has structural and functional homology with MD-2, the lipopolysaccharide-binding component of TLR-4.
By mimicking MD-2, Der p 2 can facilitate TLR4 signaling and airway TH2-type inflammation. |
|
|
How do pollens elicit allergic responses?
|
Majority of pollens have NADPH oxidase activity3, increase levels of reactive oxygen species in airway epithelium, cause low grade inflammation.
|
|
|
How do chitins (from HDM, cockroaches) elicit allergic responses?
|
indirectly upregulate epithelial chemokine release through induction of acidic mammalian chitinase by airway epithelia and pulmonary macrophages.
Inflammation ensues. |
|
|
What are the similarities between allergic rhinitis and asthma?
|
T lymphocytes, Th2 cytokines, mast cells, eosinophils
Eosinophils in nose actually correlate well with eosinophilic infiltration in bronchi. NOSE has more involvement with BASOPHILS though. |
|
|
What is the major etiological difference between acute sinusitis and chronic sinusitis?
|
Acute sinusitis usually due to infection
but not necessarily bacterial. Chronic sinusitis often NOT infection |
|
|
How does sinusitis occur?
|
Ostial obstruction
Mucous impaction Purulent drainage Decreased O2 levels Anaerobic environment Bacterial growth favored Most common cause is viral. Bacterial: S. pneumoniae (25-50% PCN resistant) H. influenza M. catarrhalis Nosocomial: Gram neg enterics Gram pos cocci |
|
|
How do we treat acute sinusitis?
|
Antibiotics (after 7-10 days)
Adjunctive agents for symptomatic relief |
|
|
What is allergic fungal sinusitis?
|
Occurs in immunocompetent patients.
Hypersensitivity response to saprophytic fungi such as Aspergillus that colonize the sinuses. More prevalent in certain geographic areas Often associated with nasal polyps and asthma. CT or MRI evidence of sinusitis “allergic mucin” (dark green or black, “peanut butter”consistency, w/ few hyphae & Charcot-Leyden crystals) Positive skin test to fungus Increase in total serum IgE Tx: Surgical exenteration Steroid therapy |
|
|
What are the four types of hypersensitivity reactions?
|
|
|
|
What are the anti-nuclear antibody (ANA) lung diseases?
|
Systemic Lupus Erythematosus
Scleroderma Sjogren’s disease Rheumatoid arthritis |
|
|
What are the anti-neutrophilic antibody (ANCA) lung diseases?
|
Microscopic polyangitis
Churg-Strauss Wegener’s Granulomatosis |
|
|
What disease is an anti-basement membrane antibody disease of the lung?
|
Goodpasture's syndrome
|
|
|
What disease is an anti-receptor or mediator antibody disease of the lung?
|
Pulmonary Alveolar Proteinosis
|
|
|
Type 1 hypersensitivity is often seen in allergic rhinitis or allergic asthma. Goodpastures for example is a type II hypersensitivity, how does this work?
|
An antigen in the extracellular or cellular matrix of the lung creates activation of complement and Fc receptor mediated recruitment/activation of inflammatory cells after deposition of antibodies.
This leads to tissue injury. Anti-glomerular basement membrane antibodies (anti-GBM Ab) are found in the serum during active Goodpasture's. Pulmonary hemorrhage with or without hemoptysis. Diffuse alveolar infiltrates on CXR, anemia and glomerulonephritis. M > F, most patients are young adults. Therapy includes plasmapheresis (plasma exchange to remove the anti-GBM Ab), high dose corticosteroids and cyclophosphamide. !!Linear staining!!. |
|
|
How do type III hypersensitivity lung diseases like SLE work?
|
Immune complexes deposit in the tissue, complement get's activated and release of granules from neutrophils (reactive oxygen species) causes tissue destruction and vasculitis.
SLE: Pleurisy, coughing, dyspnea abnormal pulmonary function tests abnormal chest x-rays may be detected in asymptomatic patients Pulmonary abnormalities do not correlate with antibody titers or complement Pleural effusion often small to absent Acute pneumonitis/pneumonia uncommon Chronic pneumonitis (<10%) Shrinking lung |
|
|
What are the cell mediated immune lung diseases?
|
Idiopathic Pneumonia Syndromes-IPF
Hypersensitivity Pneumonitis Sarcoidosis |
|
|
What is the pathogenesis of hypersensitivity pneumonitis?
|
Immune mediated inflammation involving alveolar walls and terminal airways, from organic dusts & other agents in susceptible host.
Increased CD8+ lymphs on BAL.. Restrictive NOT obstructive pattern on PFTs. Eosinophilia is NOT a feature. If CXR shows pleural involvement, hilar adenopathy, calcification, consider other diagnoses (e.g. sarcoid which has increased CD4+ lymphs) Lung biopsy: granuloma formation with an increased number of lymphocytes, particularly T suppressor cells. Avoidance of exposure is the best treatment, steroids. |
|
|
What is Allergic Bronchopulmonary Aspergillosis (ABPA) ?
|
Both antibody and cell mediated mechanisms.
Associated with asthma Not hypersensitivity pneumonitis! Findings: asthma, fleeting pulmonary infiltrates (may be asymptomatic), total serum IgE, specific IgE and IgG for Aspergillus, precipitins to Aspergillus, Asp in sputum, !!!eosinophilia!!!! Stages: I-acute, II-remission, III-reexacerbation, IV-corticosteroid-dependent, V-fibrosis. Management: slow taper prednisone, follow total serum IgE levels - if doubled, check CXR for asymptomatic infiltrates. |
|
|
What is the ideal sized particle for delivering medication topically to the lung base?
|
> 5 microns:
No clinical benefit Systemic absorption if swallowed 2-5 microns: Optimal size for clinical benefit < 2 microns: Clinical benefit uncertain. Systemic absorption |
|
|
What has replaced CFC's as a propellant gas for inhalers?
|
HFA
|
|
|
Why is there an FDA box warning on long acting beta agonist bronchodilators?
|
Increased risk of death in a subset of asthmatics who were on these drugs alone (SMART study).
|
|
|
What is the chemical difference between short acting and long acting beta agonist bronchodilators?
|
The side chain.
Binding site remains the same. Salbutamol has a longer side chain than albuterol for example. Formoterol is somewhere in the middle. The longer the side chain the more lipophillic the molecule. Lipophillic molecules have a lower onset but last longer. |
|
|
What do inhaled corticosteroids bind to?
|
Glucocorticoid Receptors.
This causes dissociation of the heat shock protein (hsp90). GR then travels to the nucleus and binds to DNA through glucocorticoid response elements (GRE). |
|
|
What is the problem with the inhaled corticosteroid beclomethasone?
|
It has an active metabolite.
|
|
|
What is unique about the inhaled corticosteroid fluticasone?
|
Very high receptor binding affinity.
|
|
|
Which inhaled corticosteroid is approved for pregnancy?
|
Budesonide.
Highly fat soluble and gets bound up in an inactive ester formation.(Budesonide-21-fatty acid ester) Not a lot of side effects but not the most potent drug either. |
|
|
What is unique about the inhaled corticosteroid ciclesonide?
|
Prodrug.
Activated by airway esterases. Minimized oropharyngeal side effects. |
|
|
What are the advantages of combination inhalers like Fluticasone/salmeterol or Budesonide/formoterol ?
|
Ideal marriage of two drug classes with complementary actions in one inhaler.
Able to use less steroid. Strengths and Weaknesses of combination drugs are those of the individual components. |
|
|
How do leukotriene modifier drugs for asthma work?
|
Oral medications
Mechanism of action involves disruption of the arachidonic acid pathway important in inflammatory cells. Two main classes of modifiers (LTMs): 5-lipoxygenase inhibitors Leukotriene (LTD4) receptor antagonists. |
|
|
What is Omalizumab?
|
Anti-IgE
Reduces activation of MAST cells. Recombinant humanized IgG First to market of the biologicals. |
|
|
What are the anticholinergic bronchodilators?
|
Quaternary Ammonium Compounds which are poorly absorbed:
Ipratropium (short-acting) Tiotropium (long-acting) Inhibit the M3 (muscarinic) receptor and reduce bronchospasm and mucus secretion. Used most often in COPD.Reduce bronchospasm AND secretions. FDA Boxed Warning: Increased risk of cardiovascular events. |
|
|
How do methylxanthine bronchodilators like theophylline work?
|
Old drugs.Hardly used anymore.
Bronchodilation by inhibiting phosphodiesterases via adenosine receptors. Very narrow therapeutic index with SEVERE toxicity requiring dialysis. |
|
|
What are MAST cell stabilizers?
|
Nedocromil
Cromolyn Both inhaled medications by DPI. Not used much anymore Were used for exercise induced asthma and in children as “steroid-sparing” anti-inflammatory drugs Weak drugs. Very safe. |
|
|
What is the best inhaled corticosteroid?
|
The best ICS are potent, highly active just in the lung and metabolized fast once outside the lung.
|
|
|
What is the epidemiology of asthma?
|
Higher in children (boys more than girls, opposite in adults)
Higher in blacks High in puerto ricans |
|
|
How does acute inflammation is asthma occur?
|
Allergen induces degranulation of mast cells and causes release of Histamine, Tryptase, Prostaglandins, Cysteinyl Leukotrienes and IL-4, IL-5
IL-4, IL-5 and GM-CSF cause Th2 CD4+ T-to attract eosinophils which release more leukotrienes ECP and MBP. Neutrophils are also involved in severe asthma. |
|
|
What happens in airways remodeling in asthmatics?
|
Subepithelial thickening.
|
|
|
What physiological tests are commonly done on asthmatics?
|
Spirometry to assess airflow obstruction.
(Patients can follow Peak Flows at home) Methacholine bronchoprovocation to induce wheezing. Exercise challenge while breathing dry air to induce wheezing. |
|
|
What is the most common symptom of asthma?
|
Cough
|
|
|
What physical signs are common in acute asthma exacerbation?
|
Tachypnea
Pulsus Paradoxus (fall in BP with inspiration) Use of accessory muscles to breathe Markedly prolonged expiration with wheezing. No air movement, “silent” chest |
|
|
What are the "steps" of asthma that help us determine treatment?
|
Step 1: Mild intermittent
Occasional symptoms. No daily medication Step 2: Mild persistent Monthly symptoms Low-dose ICS Step 3:Moderate persistent Weekly symptoms Low-to-medium dose ICS + LABA Step 4: Severe persistent Daily symptoms High-dose ICS + LABA AND, if needed, corticosteroid tablets long term. |
|
|
What biomarkers are under development that are thought will provide a better guide for steroid dosing?
|
Sputum eosinophils and exhaled nitric oxide.
|
|
|
What is the best imaging technique for interstitial lung disease?
|
Chest CT
Lung Function tests including arterial blood gas are most useful in measuring severity and estimating prognosis rather than making diagnoses. |
|
|
ILD which is rarely diagnosed without surgical biopsy can be associated with which connective tissue diseases?
|
Scleroderma
Mixed-connective tissue disease Rheumatoid arthritis Polymyositis Lupus (SLE) Sjogren’s Disease (Sicca syndrome) |
|
|
What are the main defects that occurs in interstitial lung disease?
|
An increase in the interstitial space between the alveolus and the capillary which impairs diffusion. (inflammation and fibrosis)
Reduction in volumes because of restriction. (RV, VC and TLC) Reduction in compliance. |
|
|
What are the classifications of idiopathic interstitial pneumoniae?
|
IPF/UIP
Non-specific interstitial pneumonia Desquamative interstitial pneumonia Respiratory bronchiolitis-associated interstitial lung disease Acute interstitial pneumonia Lymphocytic interstitial pneumonia Cryptogenic organizing pneumonia (COP/BOOP) |
|
|
Usual interstitial pneumonia (UIP) is also called....
|
Idiopathic Pulmonary Fibrosis (IPF)
|
|
|
What is thought to be the pathogenesis of pulmonary fibrosis?
|
Some sort of injury is incurred and some form of low grade abnormal abnormal remodeling and repair ensues.
Temporal and spatial heterogeneity. |
|
|
How is IPF diagnosed?
|
Gold Standard is Lung Biopsy
Diagnosis often made on clinical impression and imaging (HRCT). Biopsy especially indicated for younger patients that do not present with classic findings |
|
|
What is the five year survival for lung allograft transplant in IPF/UIP?
|
~60%
Lot's of exclusions though. |
|
|
What is non-specific interstitial fibrosis?
|
Dyspnea, cough
Bilateral infiltrates or consolidation without much honeycombing Occurs in association with hypersensitivity, resolving infection, collagen vascular disease. Prognosis better than UIP except for “fibrosing” NSIP. |
|
|
What are Desquamative Interstitial Pneumonitis and Respiratory Bronchiolitis Associated ILD (DIP/RBILD)?
|
Usually associated with cigarette smoking
Cough and dyspnea PFTs can show obstruction or restriction Does not improve if cigarette smoking continues |
|
|
What is Cryptogenic Organizing Pneumonia?
|
Formerly BOOP, Bronchiolitis Obliterans Organizing Pneumonia
Airspace organizing pneumonia occurs in response to infection or other inflammation Expected to respond to corticosteroids |
|
|
What is hypersensitivity pneumonitis?
|
Acute and Chronic forms
Acute: inhalation of antigen followed by malaise, fever, cough (mimics viral pneumonia) Chronic: presents like UIP, can lead to end-stage lung disease and death Causes: Thermophilic bacteria, molds, other bacteria, amoebi, insect products and chemicals Chronic: farmers, bird-fanciers |
|
|
Who do we do a methylcholine challenge on?
|
Asthma patients (normal PFT's)
|
|
|
What is PD20 in a methylcholine challenge study?
|
The pharmacological dose that produces 20% reduction in FEV1.
|
|
|
What is cardiopulmonary exercise testing?
|
A fancy stress test which includes the lungs.
Maximal stress test Measures the ability to perform work Takes into account all organ systems Relies on cohesive integration Can discriminate differential diagnosis and lead to a change in therapeutics. |
|
|
What do pulmonologists use electromagnetic navigation for?
|
Small peripheral lesions
Tattoo the lesion for thoracic resection Fiducials for gamma knife radiation |
|
|
What is the disadvantage of cryotherapy over laser and argon plasma in dealing with airway tumors?
|
It does not kill the blood supply. If the tumor is immediately removed, it will bleed.
Good for foreign body removal though because it will stick to to non-metallic objects. (hot dog in the airway) |
|
|
What is photodynamic therapy?
|
Ablation that involves using a radiosensitizer on the tumor.
Can sensitize skin too. Good for HPV airway dysplasia. |
|
|
How does bronchial thermoplasty in asthma?
|
It cooks the airway and reverses some of the smooth muscle remodeling.
|
|
|
What kind of emphysema do you get from smoking?
|
Centrolobular
|
|
|
How does endoscopic (bronchoscopic) lung volume reduction surgery work?
|
Valves are selectively placed that cut off a section of lung but still allow secretions out of it.
This reduces dead space. |
|
|
How do we define respiratory failure?
|
PaCO2>45 mmHg
PaO2 < 55 mmHg |
|
|
What is the difference between acidosis and acidemia? (or alkalosis and alkalemia)
|
Acidosis is a process.
Acidemia is a condition. |
|
|
State the Henderson-Hasselbach equation for the body?
|
pH = 6.1 + log HCO3/ (0.03 PaCO2)
|
|
|
How do we calculate A-a gradient?
|
PAO2 = ( FiO2 * (760 - 47)) - (PaCO2 / 0.8)
A-a gradient = PAO2 - PaO2 >10 is an elevated A-a gradient |
|
|
How do we calculate delivered oxygen?
|
Delivery O2 = CO x [(Hgb x SaO2 x 1.36) + (PaO2 x 0.0031)]
|
|
|
In what range of physiological PO2's does oxygen saturation normally remain above ninety?
|
60 mmHg to 100 mmHg (>60mmHg)
|
|
|
What types of conditions are associated with widened A-a gradient?
|
(1) Ventilation-perfusion mismatch,
(2) Shunt (3) Diffusion limitation In the absence of underlying pulmonary disease, the hypoxemia accompanying alveolar hypoventilation is characterized by a normal alveolar-arterial oxygen gradient. |
|
|
Pink puffers are associated with..
|
Emphysema
|
|
|
Blue bloaters are associated with...
|
Chronic bronchitis.
|
|
|
What are acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)?
|
Acute Lung Injury (ALI):
Bilateral radiographic infiltrates (≥ 3 quadrants) Hypoxemia (PaO2/FiO2 < 300) Reduced lung compliance No evidence of left atrial hypertension Associated risk factor (sepsis, pneumonia, trauma, etc.) A.R.D.S. Same except P/F ratio < 200 |
|
|
What is the pathophysiology of ARDS?
|
Acute Phase
(Inflammation-Neutrophils): Endothelial/Epithelial Injury Pulmonary Edema Surfactant Deficiency Pulmonary Hypertension Fibroproliferative Phase (Fibrosis and Repair): Pulmonary Fibrosis Pulmonary Hypertension |
|
|
What are the etiologies of ARDS?
|
DIRECT (Starts in the lung):
Pneumonia Aspiration/Near Drowning Lung Contusion Toxic Inhalation Injury Reperfusion INDIRECT (starts elsewhere): Sepsis Syndrome (#1 cause) Severe Non-Thoracic Trauma/Burns Pancreatitis Transfusion/TRALI Fat Embolism Drugs |
|
|
Type 1 pneumocytes differentiate from...
|
Type 2 pneumocytes
|
|
|
When people die of ARDS, they generally die within the first...
|
2 weeks
If you survive by week 5-6 you have a 95% chance of survival. |
|
|
The damage that typically persists the longest after recovery from ARDS is...
|
Decreased DLCO
|
|
|
How do we treat ARDS?
|
!!Treat Underlying Etiology!!
Mortality is more related to cause of ARDS, NOT Respiratory Failure Anti-Inflammatory: Non Specific (steroids may exacerbate infection but used) Specific (anti-cytokine Ab’s, antioxidants, antiproteases,…) Supportive Care: Pulmonary Non-Pulmonary (GI/DVT prophylaxis, VAP prevention, line management, nutrition) |
|
|
What ventilation parameters are "lung protective" in ARDS?
|
Low volumes
Low pressures Tidal Volume = 6-8 ml/kg Plateau Pressure < 30 Permissive Hypercapnea Minimum FiO2 (< 60%) PEEP Overventilation can lead to increased inflammatory response and prolong the disease. |
|
|
What is the recommended fluid management strategy in ARDS?
|
Conservative.
Obviously the hypotension from sepsis has to be treated but after the pressure resolves, dryer is better for reducing ventilator time. |
|
|
Potential new therapies for ARDS include...
|
Prone Positioning
Inhaled Nitric Oxide Surfactant Replacement Therapy: Improve P/F ratio, NOT mortality or Vent Free Days ExtraCorporeal Oxygenation (ECMO) High Frequency/Oscillatory Ventilation |
|
|
What are the definitions of SIRS/Sepsis?
|
Systemic Inflammatory Response Syndrome (SIRS):
any systemic process with 2 or more of: hypo(< 36°C) or hyperthermia (>38°C) tachycardia (>90 bpm) tachypnea (>20 bpm) or PaCO2 <32 mmHg leukopenia (WBC < 4K) or leukocytosis (WBC >12K or bands >10%) Sepsis: SIRS caused by infection Severe Sepsis : Sepsis with organ dysfunction. Septic Shock: Shock secondary to sepsis that is refractory to fluid resuscitation. |
|
|
What is a recommended initial bolus of fluids for a sepsis patient?
|
Initial bolus of 20 cc/kg
The earlier the better. Target CVP = 8-12mmHg |
|
|
What is a SOFA score?
|
A score for multiple organ failure in sepsis.
The higher the score, the worse the prognosis. |
|
|
What % of patients with venous thrombosis suffer a PE?
|
~10%
~ 1% of all hospitalized pts have PE Contributes to 6% of all hospital deaths. 3rd most common cardiovascular cause of death (MI, CVA) Most deaths occur early – PREVENTION IS KEY!! Diagnosis of PE made in < 30% when contributes to death; < 10% if incidental. |
|
|
What Well's criteria for DVT score is considered high?
|
2 or more
|
|
|
What is the sensitivity and specificity of compression ultrasound for DVT?
|
In symptomatic patients both are excellent 90-95%.
In asymptomatic patients sensitivity only 50-80%. |
|
|
What is the best source of information on DVT prophylaxis?
|
ACCP Consensus Guidelines
|
|
|
What are the signs and symptoms of PE?
|
Sypmtoms:
Dyspnea Chest pain Cough Apprehension Hemoptyisis Signs: Tachycardia Tachypnea Fever Clinical DVT (30%) |
|
|
What is the gold standard for PE?
|
Pulmonary Arteriogram
Low morbidity and mortality Pulmonary Hypertension not a contraindication More expensive Fewer experienced radiologists |
|
|
What are the issues with using CT for diagnosing PE?
|
Accurate for segmental or larger PE.
Accuracy depends on interpreter. Significant contrast load on kidneys. Expensive but less than Pulm Agram. Can identify other pulmonary etiologies. Can be combined with CTV to increase yield of identifying VTE (DVT + PE) |
|
|
What are the pros and cons of using MRA for PE?
|
Pro:
Useful for patients with contrast allergy or renal insufficiency. Con: Less experience and data. Gadalinium can be toxic to soft tissues. Not bad IN EXPERIENCED HANDS. |
|
|
How does a V/Q scan work?
|
Radiolabeled Xenon inhaled for ventilation and radiolabeled Technetium for perfusion
Safe Not very specific Not very useful if pre-existing lung disease. |
|
|
How useful are D-dimers for diagnosing PE?
|
Not very.
Other diseases can cause elevated D-dimers and a negative does not rule out. |
|
|
What are the Wells criteria for PE?
|
|
|
|
How do we treat PE?
|
Anticoagulants
Thrombolytics in severe cases (large PE) to reduce severe acute pulmonary hypertension. |
|
|
Around normal values when we give oxygen but there is nor rise in PO2, it is because of...
|
Shunting.
|
|
|
What are the causes of hypoxemia due to impaired diffusion?
|
Altitude
Exercise (occasional) Pulmonary edema, cardiogenic or non-cardiogenic (ARDS-terminal stages) |
|
|
What are the causes of hypoxemia due to mild ventilation perfusion mismatching?
|
Asthma
COPD (bronchitis, emphysema) Interstitial lung disease. (Sarcoidosis, UIP etc.) Early alveolar filling. |
|
|
What are the causes of hypoxemia due to physiologic shunt?
|
Atelectasis
Airspace-filling processes (e.g., cardiogenic edema, pneumonia, ARDS, alveolar hemorrhage) Pulmonary embolism |
|
|
What is severe hypoxemia?
|
Caused by shunt
Usually acute, catastrophic High FI02 necessary, but (by definition) doesn’t resolve the problem. Positive airway pressure helpful by increasing lung volume (recruiting alveoli) CPAP (by mask) PEEP (by ventilator) |
|
|
What percentage of the pulmonary vascular bed needs to be occluded to see acute cor pulmonale?
|
~60-70%
|
|
|
What are the most common causes of hempotysis?
|
Pneumonia
Cancer Bronchiectesis |
|
|
What is the best radiographic view on CXR for left upper lobe collapse (atelectasis)?
|
Lateral.
Collpases anteriorly. Hardly discernible on AP. In contrast, the right upper lobe collapse is best seen on anterior view. Lower lobes collapse up against the spine. |
|
|
What is the difference between a nodule and a mass?
|
Mass >30mm
|
|
|
Typically masses or nodules in the lung that have fat in them are...
|
Hamartomas
|
|
|
What is the average thickness of the pleural space?
|
~10-20 microns
|
|
|
What normally maintains the volume of the pleural fluid?
|
Homeostatic balance between capillary filtration & lymphatic absorption.
|
|
|
The net force (+6) that creates the pleural fluid comes from which pleura?
|
The parietal pleura
|
|
|
What is the typical volume of a pleural effusion?
|
Usually 100 - 300 ml of fluid
Results from an imbalance between fluid formation and removal. |
|
|
By what mechanisms is a pleural effusion formed?
|
Increased interstitial fluid/hydrostatic pressure gradient or increased systemic venous pressure.
Decrease hydrostatic pressure in the pleural cavity. Decrease in systemic oncotic pressure. Increased permeability of the microvascular circulation/pleural surface (mostly visceral side unlike normal fluid production which is normally on the parietal side) Impaired lymphatic drainage Movement of fluid from the peritoneal space. Special conditions (bleeding into the space, extra-vascular: leakage of chyle into the space) Any combination of the above. |
|
|
What are the signs and symptoms of pleural effusion?
|
Determined by the underlying process causing the effusion.
Asymptomatic Inflammation of the pleura (pain, cough) Compromise of pulmonary mechanics (dyspnea) Interference with gas exchange (dyspnea/SOB) Decreased tactile fremitus & breath sounds Dullness to percussion Egophony or increased breath sounds at the superior border of the fluid collection Pleural rub Changes in the appearance of the hemithorax (Always compare to the contralateral hemithorax) Blunting of the costophrenic angle. Fluid meniscus on lateral view which moves on supination. |
|
|
What type of defect does a pleural effusion cause?
|
Restrictive
|
|
|
In what circumstances do we do a thoracocentesis despite the fact that the patient has CHF?
|
Fluid is unilateral or asymmetric
Chest pain is present Patient is febrile |
|
|
What are the three main causes of transudative pleural effusion?
|
CHF
Cirrhosis Nephrosis |
|
|
What are the two most common causes of exudative pleural effusion?
|
Infection (bacterial, mycobacterial) Malignancy (metastatic, mesothelioma)
|
|
|
What are Light's criteria for distinguishing an exudative vs. transudative pleural effusion?
|
Light’s Criteria for an Exudate:
(Protein pleural fluid) / (Protein serum) > 0.5 LDH* pleural fluid/ LDH serum > 0.6 LDH pleural fluid > 2/3 normal serum level (~170 U/L @ WFUBMC) Any one of the above is consistent with an exudative pleural effusion; all three increases the surety. Transudate - Albumin gradient > 1.2 g/dl (serum albumin minus pleural albumin) Especially helpful after diuresis. |
|
|
What percentage of diagnostic thoracocentesis is useful in determining the etiology of the pleural effusion?
|
60% - 80% of patients
Useful clinical information in 90% of patients when combined with History and Physical exam. |
|
|
How do we characterize the fluid we get back from thoracocentesis?
|
Putrid or Fetid odor - Empyema
Pleural Hct > 50% serum Hct= hemothorax (Malignancy, pulmonary Emboli, trauma) Turbid or milky: Empyema/pus Triglyceride >110 mg%=chylothorax (otherwise pseudochylothorax) Gram stain/cultures |
|
|
What information do we get from thoracocentesis aspirate cell counts?
|
PMN’s predominant:
Acute Process With infiltrates -- parapneumonic effusion (>10,000 WBC), pulmonary emboli, malignant Without infiltrates -- pulmonary emboli, viral infection, asbestos, GI, or acute Tb Mononuclear predominant: Chronic Process malignant disease, Tb, pulm. emboli, resolving viral infection. |
|
|
What information do we get from thoracocentesis aspirate LDH testing?
|
Helpful in assessing the degree and trend of pleural inflammation and can differentiate transudates from exudates.
|
|
|
What utility is there in doing a glucose test on thoracocentesis aspirates?
|
Pleural Fluid glucose < 60 mg/dl
implicates increased cell metabolism as can be seen with active inflammation. Tb, parapneumonic effusion, malignancy or connective tissue disorder (rheumatoid pleurisy) |
|
|
What does the Pleural Fluid Protein/Albumin ratio of a thoracocentesis aspirate tell us?
|
Marker of the membrane permeability
The higher the pleural fluid protein ratio and/or lower albumin gradient (serum minus pleural), the more leaky the membranes are. |
|
|
Malignant pleural effusions are most often...
|
bloody
May be sanguinous or serosanguinous though. |
|
|
What is a parapneumonic effusion?
|
effusion that is associated with an acute pneumonia; empyema is the name given for the progression to pus in the pleural space.
Charcteristics of the complication: Low pH (<7.1- 7.2) predicated if measured by BGA. Low glucose (<40 mg%) and/or high LDH (>1000 IU/L) Loculated (single or multiple) Positive gram stain/culture Pus (or high WBC; PMN predominant, >10000/cc) MAY NOT RESPOND TO ANTIBIOTICS ALONE AND MAY REQUIRE A DRAINAGE PROCEDURE. |
|
|
Patients with neutrophil defects such as early BMT, leukemia and certain types of chemotherapy are susceptible to...
|
S. Aureus
P. Aeuriginosa Aspergillus |
|
|
Patients with immunoglobulin defects such as those with multiple myeloma, chronic GVHD, HIV or CLL are susceptible to...
|
Encapsulated organisms
S.pneumoniae H. Influenza |
|
|
Patients with T-cell defects such as in advanced HIV, solid irgan transplant and late BMT are susceptible to...
|
Intracellulars
P. Carinii C. Neoformans Legionella Aspergillus M. TB CMV |
|
|
What is the highest yield diagnostic culture in HIV patients?
|
Bronchoscopic alveolar lavage.
|
|
|
Can High Res CT Avoid the Need for Bronchoscopy in diagnosing pneumonia?
|
No, except maybe with high index of suspicion for PCP when non-segmental ground-glass attenuation present.
|
|
|
What sort of immune deficiency is associated with the second most common immune disease, CVID (common variable immune deficiency)?
|
Immunoglobulin deficiency.
|
|
|
What clinical hints are there for PCP?
|
Epidemiology
Diffuse infiltrate on CXR Increased LDH Marked hypoxemia Relative risk: HIV w/CD4 < 200 SOT w/in 6 months Allo BMT, esp w/GvHD High dose steroids |
|
|
How doe we treat pneumocystis jiroveci pneumonia(PCP)?
|
Therapy:
Trimethoprim/ sulfamethoxazole Trimethoprim/dapsone clindamycin/primaquine pentamadine atovaquone Adjunctive steroids for: PaO2 < 70 Prevention: TMP/SMX dapsone inhaled pentamadine atovaquone Unusual presentations: pneumothorax; especially w/inhaled pentamidine dyspnea on exertion recurrent pneumonia with steroid tapers |
|
|
What are the more common fungal pneumonias?
|
Aspergillus spp.
Cryptococcus neoformans Histoplasma capsulatum Coccidiodes immitis Rare: Zygomycetes (Mucor) Blastomyces dermatides (can present as ARDS) Pseudoallescheria boydii (Amphotericin B resistant) Candida spp. (Only consider a true pathogen if at risk for disseminated candidiasis) |
|
|
What are the classic radiological findings of aspergillis pneumonia?
|
Nodular infiltrates
Halo sign Air crescent sign |
|
|
What is the blood test for aspergillosis?
|
Serum Galactomannan Assay.
False positives may be more frequent in patients with mucositis and those on Piperacillin-tazobactam. |
|
|
How do we treat aspergillis pneumonia?
|
Voriconazole (better)
Amphotericin B Vori + Caspo may be even better but not tested. |
|
|
Owl's eye cells are associated with...
|
CMV infection.
|
|
|
What are the main causes of viral pneumonia in immunocompromised hosts?
|
Cytomegalovirus
particularly in allogeneic BMT patients Varicella Zoster or Herpes simplex usually as part of dissemination Community acquired: Respiratory Syncytial Virus (RSV) Influenza Parainfluenza |
|
|
Who is highest risk for CMV infection?
|
BMT
Lung transplant Other transplant. CMV is in itself immune suppressive so coinfection is common. |
|
|
Some of the less common cause of pneumonia in immunocompromised hosts?
|
Strongyloides stercoralis (hyperinfection syndrome)
Rhodococcus equii (look like TB infection) BOOP (unknown etiology) |
|
|
Which influenza strain contains M protein besides HA and NA?
|
Influenza A
|
|
|
Which influenza RNA viruses can infect humans ?
|
H1, H2,H3,H5
Swine: H1 and H3 Horse H3 and H7 Birds H1-H15 |
|
|
What is the major contributor molecule to pneumococcal pneumonia after influenza?
|
Neuroaminidase.
Oseltamivir and zanamavir are neuroaminidase inhibitors. CDC is recommending that neuraminidase inhibitors be used for treatment and Amantadine/rimantadine be used for chemoprophylaxis. !!!CDC now reports H1N1 strains of seasonal flu are resistant to oseltamavir!!! |
|
|
What is the only drug that currently works against seasonal influenza?
|
Zanamavir
|
|
|
Who has the highest burden of mortality from H1N1 pandemic?
|
Ages 25-49
|
|
|
If pneumococcal vaccine reduces the risk of invasive disease by ~70% and reduces hospital mortality due to IPD, why isn’t pneumococcal vaccine preventing more disease?
|
It does not last as long as people think.
The people who need it the most, the vaccine does not work best for. (immune senescence) |
|
|
How does race influence susceptibility to pneumococcus?
|
African-Americans have higher rates of invasive pneumococcal disease than whites at all ages.
|
|
|
When should we revaccinate with pneumovax?
|
Age > 65 years:
Recommended if > 5 years since first dose if: Immunocompromised CRF/Nephrotic Synd Transplant Recipient First dose before age 65 Age < 65 years: Recommended for the following situations: Age > 10 years, repeat if > 5 yrs and splenic dysfunction Age < 10 years, repeat if > 3 yrs and splenic dysfuction or immunocompromise The vaccine is safe regardless so better to err on side of caution. |
|
|
When is the ideal time to give seasonal flu vaccine?
|
Oct-Nov
|
|
|
How long does it typically take to enter REM sleep?
|
90-12 minutes
Much faster with narcolepsy. |
|
|
What normally happens to breathing parameters when we sleep?
|
Frequency Increases
Tidal Volume Decreases MV Decreases PCO2 Increases PaO2 Decreases |
|
|
What is the cardiac response to sleep?
|
NREM: Increases parasympathetic tone
Bradycardia 5-10% Cardiac Output Decreases Blood Pressure Decreases Arrhythmias: Sinus exit block, pauses, bradycardia, 1st degree AV block, Wenckebach. Gastric acid secretion is maximal 10pm and 2am. Swallowing frequency decreases during sleep. Hormonal Association (Leptin, GH). Thermal regulation is inhibited during REM. Shiver or sweat during NREM. |
|
|
REM behavior disorder is strongly associated with...
|
Parkinsons within five years.
These people don't paralyze themselves well with glycine during REM and this may be why they act out some of their dreams. |
|
|
What are some basic definitions of respiratory sleep disorders?
|
Apnea:
Cessation of breath for 10 seconds. Hypopnea: Flow reduction of 50% (or 4% desaturation) AHI: Number of events per hour UARS: Upper airway resistance syndrome RDI: Respiratory disturbance index RERA: Respiratory event related arousal. |
|
|
What are the different possible apneas?
|
Central No effort, no flow.
Obstructive Effort, no flow. Mixed Combination. |
|
|
What are the risk factors for sleep apnea?
|
Reduced airway size
Obesity (central), male Craniofacial features Retrognathia, Micrognathia, Macroglossia, etc Modified Mallampati scale works. Reduce Neuromuscular Output Gender Differences (male) Racial Differences |
|
|
What are the clinical manifestations of sleep apnea?
|
Restless Sleep 100%
Snoring 94% EDS 78% Cognitive impairment 58% Personality changes 48% Am cephalgia 36% Nocturia 30% (atrial natiuretic peptide-interesting) Insomnia 10% |
|
|
What are the sequelae of obstructive sleep apnea?
|
Hypertension and Cardiovascular Morbidity
Pulmonary hypertension CNS Renal Sudden Death |
|
|
How do we grade the severity of obstructive sleep apnea?
|
AHI (number of incidents)
Normal less than 5 per hour Mild 5 – 15 per hour Moderate 15-30 per hour Severe greater than 30 (Cardiovascular risk is high here) |
|
|
What are the consequences of untreated sleep apnea?
|
MI
Stroke Car accidents Glucose intolerance Impotence |
|
|
Does oxygen therapy work for obstructive sleep apnea?
|
No.
The problem is obstruction. O2 will prolong the apnea. CPAP and BIPAP treatment of choice. |
|
|
Is there good evidence that surgery works for obstructive sleep apnea?
|
No.
|
|
|
What test do we order if we suspect a PE?
|
CTA+CTV
|
|
|
What is a ferruginous body?
|
Coated asbestos fiber.
People have different abilities to coat asbestos fibers so this is NOT a quantitative measure. Must digest lung sample to determine degree of asbestosis. |
|
|
How long after exposure do we typically see asbestos related lung disease?
|
At least 10 years.
Longer the better therefore early jobs most important. |
|
|
How does asbestos lung pathology typically present?
|
Benign pleural effusions/plaque
Asbestosis Lung cancer. Mesothelioma. May develop > 10yrs after first exposure. May be benign or malignant. May be bloody. |
|
|
Bilateral pleural plaques usually mean...
|
Asbestos exposure.
Parietal pleura Posterior-lateral surface 6-9th ribs Usually bilateral Solitary abn. in 48% of workers 20 yr latency usual |
|
|
Asbestosis usually starts in what portion of the lung...
|
The bases and marches up.
Silicosis starts in the apex and marches down. Asbestosis look like a spider web and silicosis look like distinct nodules. |
|
|
What is the relationship between mesothelioma and asbestos exposure?
|
Risk NOT dose dependent.
|
|
|
What are the types of mesothelioma?
|
Epithelial
(most common, best survival, operable) Abdomen, pleura and occasional GU. Sarcomatous Desmoplastic |
|
|
What are the signs and symptoms of mesothelioma?
|
Bloody pleural effusion
Cytology rarely Dx (Bx usually required) Symptoms: Pleuritic CP 60% Dyspnea 35% Cough 15% Weight loss 5% |
|
|
Asbestos and smoking are related to bronchogenic lung cancer by...
|
Smoking 10 fold risk
Asbestos 5 fold risk Both ~50-100 fold risk |
|
|
What is occupational asthma?
|
"Variable airways narrowing causally related to exposure in the working environment to airborne dusts, gases, vapors or fumes"
Occupational exposures cause significant worsening in up to 15% of asthmatics. Estimated 2-5% of asthma cases in U.S. are de novo occupational asthma. |
|
|
What industries have major problems with occupational asthma?
|
Plastics industry 5%
Animal breeders/handlers 6% Bakers 10-30% Cotton workers (cardroom) 20-30% Metal refinery (platinum) 30-50% Western red cedar 5% |
|
|
How long does occupational asthma tend to develop?
|
Most de novo occupational asthma is thought to be caused by sensitization mechanisms which often involve IgE allergic antibody responses.
Typically, occupational asthma from sensitizers appears only after repeated exposures over months to years (latent period of sensitization); High molecular weight irritant takes longer. Most de novo occupational asthma is thought to be caused by sensitization mechanisms which often involve IgE allergic antibody responses. Typically, occupational asthma from sensitizers appears only after repeated exposures over months to years (latent period of sensitization); Most common are TDI (diisocyanates) metal salts and flour. |
|
|
What is Reactive Airways Dysfunction Syndrome (RADS)?
|
No previous history of asthma.
Acute, high level exposure to toxic/irritant agent. Respiratory symptoms within 24 hours of exposure. Persistent respiratory symptoms, non-specific bronchial hyperreactivity. Pulmonary functions normal or show reversible obstruction Obstruction less reversible than asthma. Eosinophilic infiltration not characteristic. |
|
|
What are some low molecular weight agents that cause occupational asthma?
|
Isocyanates (HDI, MDI, TDI, IPDI)
Woods (red cedar, exotic, sawmills) Glues (methacrylates, cyanoacrylates) Epoxies (anhydrides, amines...) Colophony Dyes |
|
|
What are some high molecular weight agents that cause occupational asthma?
|
Flour - cereals
Animals handlers Latex Psyllium Crab processing Antibiotics, enzymes |
|
|
How do we test for occupational asthma?
|
A positive challenge is usually defined by a sustained fall in FEV1 of ≥ 20%, as compared to the control mock day.
|
|
|
What are the classical findings of silicosis?
|
Shortness of breath on exertion
Cough/sputum production Chest tightness Wheezing Rounded (p, q, r) opacities approximately 1 mm in diameter Upper lung zones May coalesce or Calcify May have associated lower lung bullae that cause pneumothorax Egg-shell calcification of mediastinal, hilar nodes. |
|
|
What are silicosis patients at increased risk of...
|
High incidence of RF and ANA
High incidence of TB or m. Avium Caplan’s Syndrome |
|
|
What % of preventable causes of death are tobacco related?
|
~37.5%
1/3 of all tobacco users in this country will die prematurely from tobacco dependence losing an average of 14 years. |
|
|
How does smoking affect bones?
|
Smoking is an independent risk for osteoporosis and fracture.
|
|
|
How does buproprion work for smoking cessation?
|
Selectively inhibits reuptake of noradrenaline & dopamine.
Varenicline reduces cravings. |
|
|
What portions of the nasal cavity (external nares to internal nares) is not lined by respiratory mucosa?
|
The vestibule (unkeratinized stratified squamous epithelium) and olfactory region (olfactory mucosa).
|
|
|
Nasal respiratory mucosa (nasal cavity and paranasal sinuses) is made up primarily of...
|
Ciliated cells
Goblet cells Basal cells Also highly vascular (Venous sinuses) There are also occasional brush cells with microvilli thought to play a sensory role. |
|
|
What types of cells are the pharynx and larynx covered by?
|
Portions of the pharynx and larynx are lined by respiratory mucosa; the remainder is covered by stratified squamous epithelium.
Pharynx: Nasopharynx -respiratory epithelium Oropharynx - stratified squamous Laryngopharynx - stratified squamous |
|
|
The vocal folds are covered with...
|
Stratified squamous epithelium.
Reinke’s space (few lymphatic vessels) vocal ligament (fibroelastic) vocalis muscle (skeletal) The ventricular folds in contrast are covered with respiratory epithelium. |
|
|
What is the organization of the tracheal wall?
|
Mucosa (M):
pseudostratified columnar epithelium and cellular lamina propria Submucosa (SM) with mixed mucus and serous glands (G) Cartilaginous layer with c-shaped rings Adventitia (A) with connective tissue, blood and lymphatic vessels, and nerves Posteriorly cartilage is incomplete; trachealis muscle (T) joins the free ends. A few strands of longitudinal muscle (L) may be present behind the trachealis muscle. |
|
|
What cellular changes occur along the length of the trachea?
|
From upper to lower, see an increase in the relative proportion of ciliated cells
Parallel decrease in the relative proportion of goblet cells and basal cells Tracheal cillia move mucous in the opposite direction to nasal cillia. Both towards the pharynx. |
|
|
What changes occur progressively along the bronchial tree?
|
Along the bronchial tree:
decrease in cartilage, glands, goblet cells and height of epithelium; increase in smooth muscle and elastic tissue At level of bronchioles: glands and cartilage disappear (small amount of cartilage may appear at branch points) Along bronchioles: gradual transition from simple columnar epithelium (with very few goblet cells) to simple cuboidal epithelium (many cells with cilia) with a few Clara cells and no goblet cells to Clara cells with a few cuboidal cells. Narrowing lamina propria with less smooth muscle but continuing elastic fibers. |
|
|
What are clara cells?
|
Secreting cells. NOT mucous.
|
|
|
What does an intrapulmonary bronchus look like?
|
|
|
|
What are the components of the alveolar wall?
|
Type I pneumocytes:
(Dark cells) 35% cells, 95% surface area Type II pneumocytes: (cuboidal with dark centers) 65% cells, produce surfactant Endothelial cells of capillaries Macrophages |
|
|
What is the function of the Pores of Kohn ?
|
Permit communication between alveoli.
|
|
|
What constitutes the blood oxygen diffusion barrier?
|
the plasma
the endothelial cell plasma membrane and cytoplasm the fused basement membranes of the endothelial cell and type I pneumocyte the plasma membrane and cytoplasm of the type I pneumocyte a thin (virtually monomolecular) layer of surfactant. |
|
|
How does blood supply to the lung work?
|
For most of the lung there are two systems of afferent blood vessels, branches of the pulmonary and bronchial arteries, but only one set of efferent blood vessels, the pulmonary veins.
Pulmonary arteries follow bronchial tree Pulmonary veins located in lobules, then follow bronchi Bronchial arteries follow bronchial tree Bronchial veins evident only near hilus Intrapulmonary nerves follow bronchial tree Pulmonary vein – largest, thin-walled Pulmonary artery - large and thicker-walled Bronchial artery - small, within or closely associated with the wall of the bronchus |
|
|
Is there lymphatic drainage in the lung?
|
Lymphatic vessels are abundant, forming a superficial plexus in the pleura and a deep plexus that accompanies the blood vessels and bronchi.
Lymphatic vessels are NOT found in the alveoli; they begin at the level of the respiratory bronchioles. |
|
|
How is the lung innervated?
|
Autonomic and general viseral afferent Nerves form plexuses in the hilar region.
The intrapulmonary course largely follows the bronchial arterial system in its pattern of branching – mainly following the bronchial tree but also diverging to supply the walls of the pulmonary arteries and veins. Mediate reflex actions initiated from within and from outside the lung, as well as a poorly localized sense of pain. |
|
|
Which cancer causes the most deaths?
|
Lung cancer.
Incidence is not the highest but deaths are. |
|
|
Small cell lung cancer constitutes what % of lung cancers?
|
~20%
~80% NSCLC |
|
|
What is the clinical presentation of lung cancer?
|
Local symptoms:
cough dyspnea obstructive pneumonitis hemoptysis superior vena cava syndrome chest pain General Symptoms: weight loss fatigue Symptoms secondary to distant metastases. |
|
|
Hemoptysis is more common in which type of lung cancer?
|
Non-small-cell lung cancer
|
|
|
What physical signs are associated with lung cancer?
|
Clubbing
Horner's syndrome (Ptosis, Miosis, Anhidrosis) Pancoast tumor in the superior sulcus. Facial swelling, engorged chest veins. (SVC syndrome) Atelectasis/Pneumonia Pleural Effusions Pleuritic Pain Shortness of Breath Recurrent Nerve Palsy in the recurrent laryngeal and phrenic nerves. |
|
|
What sort of prognostic factor is an elevated white cell count in lung cancer?
|
Bad
|
|
|
What type of lung cancer is LDH a prognostic factor in?
|
Small cell.
Higher LDH=Bad |
|
|
Fouls smelling sputum is associated with which lung malignancy?
|
Squamous cell carcinoma.
Usually cavitary lesions. |
|
|
Inappropriate ADH secretion and ectopic ACTH production are the paraneoplastic syndromes most closely associated with...
|
Small cell lung cancer
|
|
|
Hypertrophic pulmonary osteoarthropathy is the paraneoplastic syndrome most closely associated with...
|
Large cell lung cancer
and Adenocarcinoma |
|
|
Non-metastatic hypercalcemia is the paraneoplastic syndrome most closely associated with...
|
Squamous cell carcinoma.
|
|
|
Lambert-Eaton syndrome is the paraneoplastic syndrome most closely associated with...
|
Small cell carcinoma
|
|
|
Gynecomastia is a paraneoplastic syndrome most closely associated with...
|
Small cell carcinoma
Can happen in large cell too though. |
|
|
How does lung cancer usually spread to lymph nodes?
|
Intrapulmonary
Peribronchial Hylar Mediastinal |
|
|
Where do we usually check for lung cancer metastases?
|
Lymph nodes
Liver Adrenals Bone Brain |
|
|
What are the prognostic factors for non-small cell lung cancer?
|
Age
Female > male (males worse) Physical strength - performance status Weight loss < 5% versus > 10% Stage (most important) Metastatic sites (number, location) |
|
|
How do we treat stages I and II NSCLC?
|
Surgical resection
Adjuvant chemotherapy for stage II |
|
|
How do we treat stage III NSCLC?
|
Combined modality treatment program including surgery, radiation, and chemotherapy
|
|
|
How do we treat stage IV NSCLC?
|
Palliative chemotherapy
Best supportive care |
|
|
What is small cell lung cancer?
|
Most tightly linked to smoking
Most aggressive lung cancer type Median Survival without treatment = 2-4 months More responsive to chemotherapy and radiation than NSCLC. |
|
|
What are the prognostic factors for small cell lung cancer?
|
Performance Status
Stage (Limited vs Extensive) LDH |
|
|
What stage is small cell lung cancer typically in at the time of diagnosis?
|
One third limited stage (stage I-III)
Two thirds extensive stage (stage IV) |
|
|
What role does surgery play in treating small cell lung cancer?
|
Only indicated for single pulmonary nodule without lymph node or distant metastasis.
Patients with surgically resected tumors benefit from adjuvant chemotherapy. |
|
|
How do we treat limited stage small cell lung cancer?
|
Chemotherapy concurrent with thoracic radiation therapy.
|
|
|
How do we treat extensive stage small cell lung cancer?
|
Chemotherapy
Radiation to special sites (i.e., brain metastases, painful bone metastases, spinal cord compression) Possible Prophylactic Cranial Irradiation if they do well. |
|
|
What are the overall survival rates for lung cancer?
|
1 year survival rate 41%
5 year survival rate 16% |
|
|
What % of heavy smokers develop lung cancer?
|
~11%
|
|
|
What is the characteristic of apical lung tumors?
|
Ulnar pain and ipsilateral Horner’s syndrome (Pancoast tumor).
|
|
|
What is the MOST common pattern of involvement in lung cancer?
|
Most arise near hilum
About 75% arise in first, second, or third order bronchi. Locally may result in: Intraluminal mass Peribronchial spread to carina or mediastinum Intraparenchymal mass Involvement of pleura |
|
|
What is the difference between grading and staging of lung cancer?
|
Grading:
how close to normal does it look? Incorporates “architecture” and nuclear atypia Staging: how far has it spread? For NSCLC use TNM. For SCLC use TNM; limited vs extensive. |
|
|
>95% of primary lung cancers are....
|
Carcinomas!!
Malignant neoplasms derived from epithelium. Carcinomas are classified based on the type of epithelium that they resemble (e.g., carcinomas that exhibit glandular architecture are adenocarcinomas) |
|
|
What are the male/female distributions of lung cancers from most to least common ?
|
Adenocarcinoma
(males 37%, females 46%) Squamous cell carcinoma (males 32%, females 25%) Small cell carcinoma (males 14%, females 18%) Large cell carcinoma (males 18%, females 10%) |
|
|
What is the definition of an adenocarcinoma?
|
A malignant epithelial tumor with glandular differentiation or mucin production showing acinar (glands), papillary (finger like projections), bronchioloalveolar or solid with mucin production growth patterns or a mixture of these patterns.
Seen more frequently in smokers but is the most common type of lung cancer in women and nonsmokers. Typically more peripheral Rarely cavitates Primarily spreads by lymphatic or hematogenous routes but may spread aerogenously (e.g., mucinous bronchioloalveolar carcinoma). |
|
|
What is bronchoalveolar carcinoma?
|
less than 3% of lung cancers
arise in region of terminal bronchioles/alveoli single or multiple nodules; may have a pneumonic appearance 5 year survival for localized resected BAC=100% neoplastic cells grow along alveolar septae !!!without evidence of stromal, vascular or pleural invasion!!! may or may not contain abundant mucin usually well-differentiated |
|
|
What is EGFR targeted therapy?
|
Epidermal growth factor receptor is a receptor tyrosine kinase (TK) of the ErbB family.
Tumors responding to EGFR tyrosine kinase inhibitors (gefitinib and erlotinib) contain somatic mutations of the EGFR TK domain Screening for common EGFR mutations in lung adenocarcinomas can be performed to predict which patients will respond to EGFR TKIs Response rates of 65-90% |
|
|
What tumors frequently have EGFR mutations?
|
Among adenocarcinomas, EGFR mutations are more prevalent in adenocarcinoma with bronchioloalveolar carcinoma features.
|
|
|
What mutation makes the use of EGFR tyrosine kinase inhibitors useless?
|
k-Ras
|
|
|
What is the definition of a squamous cell carcinoma?
|
A malignant epithelial tumor showing keratinization and/or intercellular bridges that arises from bronchial epithelium.
Closely related to smoking (>90%) Most common in men Paraneoplastic syndromes-especially associated with hypercalcemia Usually central (two thirds) but may be peripheral The type of lung cancer most likely to cavitate Tends to be locally aggressive Metastasizes to distant organs less frequently than adenocarcinoma. Stage for stage has a better survival than adenocarcinoma. Eosinophilic, hyaline cytoplasm Intercellular bridges Keratin pearls |
|
|
What is the danger to be aware of with Bevacizumab (Avastin)?
|
Bevacizumab (Avastin) is associated with a high risk of bleeding in squamous cell carcinoma of lung and has only been approved for “non-squamous” non-small cell carcinomas.
|
|
|
What is the definition of small cell carcinoma?
|
A malignant epithelial tumor consisting of small cells with scant cytoplasm, ill-defined cell borders, finely granular chromatin, and absent or inconspicuous nucleoli.
The cells are round oval or spindle-shaped. Nuclear molding is prominent. Necrosis is typically extensive and the mitotic count is high. Includes combined small cell carcinoma: small cell carcinoma combined with any of the histologic types of non-small cell carcinoma . Very closely correlated with smoking. Most often central. Highly aggressive. Rarely surgical candidates. Extensive lymphadenopathy. Salt and pepper cytoplasm. |
|
|
What is the definition of a large cell carcinoma?
|
An undifferentiated non-small cell carcinoma that lacks the cytologic and architectural features of small cell carcinoma and glandular or squamous differentiation.
Many are probably very poorly differentiated squamous cell carcinomas or adenocarcinomas. Often peripheral, but may be central. Tumor is often large, necrotic. Neuroendocrine variant stains positive for synaptophysin. |
|
|
How do we recognize an adenosquamous carcinoma?
|
The tumor exhibits glandular and squamous differentiation.
|
|
|
What is the definition of a carcinoid tumor?
|
Tumors characterized by growth patterns (organoid, trabecular, insular, palisading, ribbon, rosette-like arrangements) that suggest neuroendocrine differentiation. Tumor cells have uniform cytologic features with moderate eosinophilic, finely granular cytoplasm and nuclei with a finely granular chromatin pattern.
Typical carcinoid (uncommon): <2 mitotic figures per 2 mm2 and no necrosis Atypical carcinoid ≥2 mitotic figures per 2 mm2 and/or foci of necrosis |
|
|
What is the epidemiology of typical carcinoid tumors?
|
1-2% of lung tumors
Most patients less than 40 years old Not associated with smoking Distributed throughout lung, but often central, projecting into lumen; mucosa-covered Low rate of metastasis (10-15% regional nodal metastasis at presentation; eventually 5-10% with distant metastasis) 90-98% 5 year survival rate; 82-95% 10 year survival Cell nests; neoplastic cells with more cytoplasm than small cell carcinoma. Mitotic figures and necrosis are absent. |
|
|
What is the epidemiology of atypical carcinoid tumors?
|
More often peripheral than typical carcinoid tumor.
At presentation, 40-50% with regional nodal metastasis or beyond 5 year survival of about 61-73%; 10 year survival of approximately 35-59% |
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What are the four major types of neuroendocrine pulmonary tumors?
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Small cell carcinoma
Large cell neuroendocrine carcinoma Typical carcinoid tumor Atypical carcinoid tumor |
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What is a pulmonary hamartoma?
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Benign, non-neoplastic
Usually less than 3-4 cm Usually cartilagenous May simulate malignancy radiographically |
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What are the characteristics of metastases that end up in the lung?
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Lung is common site of metastasis
Typically metastases are multiple, bilateral, peripheral May show lymphangitic pattern of spread Occasionally solitary May be carcinomas, sarcomas, melanomas, etc |
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What are the disadvantages of sputum histology?
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Does not localize the lesion
Does not stage Not too good for peripheral lesions |
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What are two examples of PRIMARY pleural pathology?
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Primary intrapleural infections
Primary tumors (malignant mesothelioma) |
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What are some examples of the causes of pleural effusion?
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Increased hydrostatic pressure (CHF)
Decreased oncotic pressure (nephrotic syndrome) Increased vascular permeability (pneumonia) Increased intrapleural negative pressure (atelectasis) Decreased lymphatic drainage (tumor) |
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What kind of cells do we find in an empyema (Suppurative pleuritis)?
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Neutrophils
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What diseases commonly cause spontaneous pneumothorax?
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Emphysema
asthma TB |
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Is a solitary fibrous tumor in the pleura usually associated with asbestos?
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No.
Malignant transformation rare. origin: mesothelial vs submesothelial fibroblasts Gross: white, rounded, firm, several centimeters Histology: fibroblast-like cells in a background of collagen haphazard arrangement of cells (“patternless” pattern) CD34+ |
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What are asbestos related thoracic findings?
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Lung:
interstitial fibrosis carcinoma Pleura: pleural plaques malignant mesothelioma |
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What is the definition of malignant mesothelioma?
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A malignant tumor derived from the lining cells (that is, mesothelial cells) of a serous cavity.
Usually pleural but can be peritoneal or even pericardial. |
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How do we classify malignant mesothelioma?
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Epithelioid mesothelioma
Sarcomatoid mesothelioma (desmoplastic mesothelioma) Biphasic mesothelioma |
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How is the structure of asbestos fibers related to carcinogenicity?
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the types of asbestos with long thin fibers are more potent carcinogens
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What is the average survival for malignant mesothelioma?
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onset of symptoms=12-15 months
and from time of diagnosis=8-12 months longer times have been reported. |
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How does malignant mesothelioma typically progress?
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small nodules increase in size, eventually becoming confluent and encasing the lung
tumor may invade the chest wall/mediastinum tumor often spreads to pericardium, contralateral pleura and peritoneum may metastasize to mediastinal lymph nodes distant metastases may be present but are not usually clinically evident |
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Which is the most common type of malignant mesothelioma?
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Epithelial type (~50%)-tubules
Sarcomatoid type (~15%)-spindles Mixed type (~25%)-both |
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What is the TNM method of staging lung cancer?
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T - tumor characteristics
Size Proximity Nodal involvement Local or distant Metastatic |
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Hyponatremia is a paraneoplastic syndrome of...
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Small cell lung cancer.
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What are the radiographic characteristics of pulmonary malignancy?
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Diameter
Spiculation Upper lobe location Absence of calcification |
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What is the most common cause of hemoptysis?
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Bronchitis.
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An acute angle between a lesion and the chest wall suggests it started in ....
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The lung.
Obtuse suggests it started in the chest wall. |
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What type of immunity do steroids suppress?
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Cellular immunity
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