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26 Cards in this Set
- Front
- Back
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type I pneumocytes
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line the alveoli; squamous; thin for optimal gas diffusion
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type II pneumocytes: 2 functions
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1. secrete surfactant (diplamitoyl phosphatidylcoline) which decreases surface tension
2. precursors to type I and replace type I during injury |
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clara cells: 3 functions
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non ciliated.
1. secrete clara cell secretory protein (CCSP) which decreases neutrophil recruitment. 2. degrade toxins 3. secrete component of surfactant |
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Where does IVC perforate the diaphragm?
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T8
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Where do the esophagus and vagus trunk penetrate the diaphragm?
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T10
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Where does the aorta, thoracic duct, and azygous vein perforate the diaphragm?
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T12
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what is the formula for collapsing pressure?
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P = 2 (surface tension)/radius
Tendency to collapse on expiration as radius decreases. |
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what is the formula for physiologic dead space?
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Vd = tidal volume x (PaCO2 - PeCO2)/PaCO2
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methemoglobin
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oxidized hemoglobin (ferric, Fe3+) that does not bind O2 as readily but has high affinity for CN- and can be used in treatment for CN- poisoning.
Use nitrites to oxidize, Hb --> metHb, then thiosulfate to excrete it. *also prolonged dapsone use (like leprosy rx) can form this |
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carboxyhemoglobin
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form of Hb with CO in it instead of O2.
Causes decreased O2 binding affinity, and a left shift in O2-Hb curve. |
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alveolar gas equation
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PAO2 = PIO2 - (PACO2 / R)
PAO2 = 150 -(PACO2 / 0.8) |
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What would be the alveolar PO2 during:
- pulmonary embolism - airway obstruction |
- pulmonary embolism: increased because it doesn't lose the O2
- airway obstruction: decreased because the O2 that was in the alveoli gave up its O2 and there's nothing left. |
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V/Q = 0
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airway obstruction (shunt) no gas exchange
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pulmonary embolism
what is V/Q? |
V/Q is infinity - physiologic dead space
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How does bicarb know to turn in to CO2 at the lungs, so it can be exhaled?
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Haldane effect: The oxygenation of Hb causes dissociation of Hb from H.
The extra H shifts the equation to make more CO2 + H20 |
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If you see air in an alveoli which has a partial pressure of 150mmHg what is most likely the problem?
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normally alveolar O2 = 104mmHg, so this is very high. It must mean there is no blood to take the alveolar O2 aka pulmonary embolism (V/Q = infinity - physiologic dead space)
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3 steps in ARDS
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1. diffuse alveolar damage = gram neg sepsis, gastric aspiration, trauma
2. increased alveolar capillary permeability 3. protein rich leavage in tol alveol --> formation of alveolar hyaline membrane and damage to alveolar wall |
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affects upper lobes and has eggshell calcifications of hilar lymph nodes
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silicosis
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3 risk factors for neonatal respiratory distress syndrome
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prematurity
maternal diabetes C-section (less fetal glucocorticoids released) |
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what lung abnormality causes tracheal deviation toward lesion, which has deviation away from lesion?
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bronchial obstruction = absent breath sounds over affected area, tracheal dev toward lesion
tension pneumothorax = hyperresonant sounds, decreased breath sounds, tracheal deviation away from side of lesion |
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lung cancer that makes PTHrP
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squamous cell carcinoma
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lung cancer that makes ACTH, ADH, autoantibodies against Ca2+ channels
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small cell carcinoma
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lung cancer that can cause hypertophic osteoartrhopathy
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broncioalveolar adenocarcinoma
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2 main causes of lobar pneumonia
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Strep Pneumonia
Klebsiella *intra-alveolar exudate, may involve entire lung |
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4 causes of bronchopneumonia
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S aureus
H flu Klebsiella S pyogenes acute inflammatory infiltrates from bronchioes --> alveoli patchy distribution involving more than one lobe |
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4 causes of interstitial pneumonia
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Atypical pneumonia
viruses = rsv, adenovirus mycoplasma legionella chlamydia diffuse pathcy inflammation localized to interstitial areas at alveolar walls - doesn't fill alveoli, more indolent |
