Summary: Episode 82: Sample the Gold Standard USMLE Audio Reviews in this episode – decide for yourself if you like this Pharmacology of Asthma sample from a professional audiobook. If you do, we have an entire collection for every USMLE and medical school you take!<br> Listen to the podcast here…<br> I. A-a gradient – know how to calculate:<br> Alveolar O2 and arterial pO2 are never the same. The difference between the two is called alveolar arterial gradient.<br> [ad#300×250]<br> Reasons for it: (1) Ventilation and perfusion are not evenly matched in the lungs. When standing up the ventilation is better than perfusion in the apex, whereas perfusion is better than ventilation at lower lobes. This explains why almost all pulmonary infarctions are in the lower lobes – perfusion is greater there. Also, this explains why reactivation TB is in the apex – TB is a strict aerobe and needs as more O2, and there is more ventilation in the upper lobes (higher O2 content). Normally, alveolar O2 is 100 and the arterial pO2 is 95. So, normally, the gradient is 5 mmHg. As you get older, the gradient expands, but not that much. Most people use their upper limit of normal – in other words, have a very very high specificity of 30 mmHg. If you have an A-a gradient of 30 mmHg or higher there is a problem. It is very high specificity (aka PPV – truly have something wrong). The concept is easy – you would expect the gradient btwn the alveolar O2 and the arterial O2 to be greater if you have primary lung dz. What will do this? Ventilation defects (produces hypoxemia, and therefore prolongs the gradient – dropping the PO2 and subtracting, and therefore a greater difference btwn the two), perfusion defect (ie pul embolus), and diffusion defect. But the depression of the medullary resp center by barbiturates does not cause a difference in A-a gradient. So, prolonged A-a gradient tells you the hypoxemia is due to a problem in the lungs (vent perfusion/diffusion defect). A normal A-a gradient tells you that something outside the lungs that is causing hypoxemia (resp acidosis – in resp acidosis, PO2 will go down). Causes of resp acidosis: pulmonary probs (COPD), depression of resp center (obstruct upper airway from epiglottitis, larygiotracheobronchitis, café coronary (paralyzed muscles of resp), Guillain Barre syndrome, amyotrophic lateral sclerosis, and paralysis of diaphragm. These all produce resp acidosis and hypoxemia, but the A-a gradient will be NORMAL). So, prolonged A-a gradient, something is wrong with the lungs. If A-a gradient is normal, there is something OUTSIDE of the lungs that is causing a resp problem. Few things must always be calculated: anion gap (with electrolytes) and A-a gradient for blood gases – all you need to do is calc alveolar O2. We can calculate the A-a gradient = 0.21 x 713 = 150 (0.21 is the atmospheric O2; and 760 minus the water vapor=713). So, 150 minus the pCO2 (given in the blood gas) divided by 0.8 (resp quotient). So, normal pCO2 = 40, and 40/.8=50 and 150-50 = 100; so, now that I have calc the alveolar O2, just subtract the measured arterial pO2 and you have the A-a gradient. This is very simple and gives a lot of info when working up hypoxemia.<br> II. Upper Respiratory Disease:<br> A. Nasal Polyps:<br> 3 diff types of nasal polyps – MC is an allergic polyp. Never think of a polyp in the nose of kid that is allergic as an allergic polyp. Allergic polyps develop in adults after a long term allergies such as allergic rhinitis – Example: 5 y/o child with nasal polyp and resp defects, what is the first step in management? Sweat test – b/c if you have a polyp in the nose of the kid, you have cystic fibrosis; it’s not an allergic polyp.<br> B. Triad Asthma – take an aspirin or NSAID, have nasal polyps and of course have asthma. They don’t tell you the pt took aspirin and that the pt has a polyp. The aspirin or NSAID is the answer but this is how they will ask the question: 35 y/o woman wi...
