HY lecture notes:
Asthma (outpatient) –> albuterol (short-acting beta-2 agonist; SABA) inhaler for immediate Mx –> if insufficient, start low-dose ICS (inhaled corticosteroid) preventer –> if insufficient, maximize dose of ICS preventer –> if insufficient, add salmeterol inhaler (long-acting beta-2 agonist; LABA); in other words:
- 1) SABA; then
- 2) low-dose ICS; then
- 3) maximize dose ICS; then
- 4) LABA.
That initial order is universal. Then you need to know last resort is oral corticosteroids, however they are most effective.
In other words:
12M has ongoing wheezing episodes + is on albuterol inhaler; next best step? –> add low-dose ICS.
12M has ongoing wheezing episodes + is on albuterol inhaler; what’s most likely to decrease recurrence –> oral corticosteroids –> student says “wtf? I thought you said ICS was what we do next and that oral steroids are last resort.” Yeah, you’re right, but they’re still most effective at decreasing recurrence. This isn’t something I’m romanticizing; this distinction is assessed on the FM NBME forms.
After the LABA and before the oral steroids, any number of agents can be given in any order – i.e., nedocromil or cromolyn sodium, zileuton, montelukast, zafirlukast.
MOA of nedocromil and cromolyn sodium –> mast cell stabilizers.
MOA of zileuton –> lipoxygenase inhibitor (enzyme that makes leukotrienes from arachidonic acid).
MOA of the -lukasts –> leukotriene LTC, D, and E4 inhibitors. LTB4 receptor agonism is unrelated and induces neutrophilic chemotaxis (LTB4, IL-8, kallikrein, platelet-activating factor, C5a, bacterial proteins).
16M goes snowboarding all day + takes pain reliever for sore muscles afterward + next day develops wheezing out on the slopes again; what’s going on? –> took aspirin + this is Samter triad (now cumbersomely known as aspirin-exacerbated respiratory disease [AERD]) –> triad of aspirin-induced asthma + aspirin hypersensitivity + nasal polyps). Just to be clear, other NSAIDs can precipitate Samter triad, but the literature + USMLE will make it explicitly about aspirin.
16M takes aspirin + gets wheezing; what are we likely to see on physical exam? –> answer on USMLE = nasal polyps.
“Wait I don’t understand. Why would aspirin cause asthma?” –> arachidonic acid can be shunted down either the cyclooxygenase or lipoxygenase pathways; if you knock out COX irreversibly by giving aspirin (or reversibly with another NSAID), more arachidonic acid will be shunted down the lipoxygenase pathway –> more leukotrienes –> more bronchoconstriction.
Kid has Hx of AERD; physician considers agent to decrease his recurrence of Sx –> zileuton, or -lukasts (both are correct; and only one will be listed).
Kid has Hx of AERD; what agent is most likely to decrease his recurrence of Sx –> oral steroids (sounds wrong, but once again, you need to know oral steroids are most effective for preventing asthma, period; this is exceedingly HY, especially on family medicine forms). We simply don’t want to give them because of their nasty side-effects (Cushing syndrome).
Any weird asthma Txs? –> omalizumab –> monoclonal antibody against IgE –> used for intractable, severe asthma unresponsive to oral steroids + in patients who have eosinophilia + high IgE levels (I asked a pulmonologist about this drug years ago when I was in MS3 and he said he was managing 1000 patients with asthma and just three were on omalizumab).
Acute asthma Mx (emergencies) –> most important piece of info straight-up is: USMLE wants you to know that inhaled corticosteroids (ICS) have no role in acute asthma management. First thing we do is give oxygen (any USMLE Q that shows depressed O2 sats, answer is always O2) + nebulized albuterol (face mask with mist); IV steroids are then administered. The Mx algorithm is more complicated, but that is what you need for the USMLE.
Acid-base disturbance in asthma? –> respiratory alkalosis –> low O2, low CO2, high pH, normal bicarb.
“Wait, why the low CO2? Aren’t you not able to breathe?” –> low CO2 is due to high respiratory rate; even if your bronchioles are constricted + filled with secretions, CO2 can diffuse really quickly; in contrast, O2 diffuses slowly and requires healthy airways; that’s why with a high RR, O2 and CO2 are both low (O2 can’t get in, but CO2 can still get out); 19 times out of 20 on the USMLE, if your respiratory rate is high, CO2 is low.
Dry cough in winter + eczema in summer + seasonal allergies in winter; what is the cough? –> cough-variant asthma (1/3 of asthmatics only have cough).
Young African American woman + dry cough + normal CXR –> asthma (activation of mast cells), not sarcoidosis.
Young African American woman + dry cough + nodularity on CXR –> sarcoidosis (non-caseating granulomas).
Electrolyte disturbance in sarcoid? –> hypercalcemia –> LOW PTH (suppressed) + high calcium. Phosphate can also be elevated because of the high vitamin D, but there is one Q on a newer CMS form where it’s normal.
Hypercalcemia in sarcoid, why? –> epithelioid (activated) macrophages produce 1-alpha hydroxylase, thereby activating vitamin D3.
Fecal calcium level in sarcoidosis? –> decreased –> activated D3 increases small bowel absorption –> this is asked on NBME.
Tx for sarcoid? –> steroids.
COPD management? –> similar to asthma, except muscarinic receptor antagonists (e.g., ipratropium) inhalers can be used, often mixed with albuterol or steroid. The literature does not give a very concrete step-wise Mx for COPD because it’s variable depending on patient risk factors. USMLE wants you to know that smoking cessation is always the first answer for decreasing severity of someone’s COPD.
If they ask how to best decrease mortality in COPD, if smoking cessation isn’t listed, choose home oxygen therapy as the answer. Apart from smoking cessation, home oxygen therapy is the only treatment for COPD shown to decrease mortality.
If the 2CK-level Q is quantitative and they ask you when to commence home oxygen therapy; answer? –> when patient’s pO2 on room air at rest is <55 mmHg (<88% saturation).
If you get a patient with COPD who’s already quit smoking and they ask for next best step + don’t list arterial oxygen values, choose pulmonary rehabilitation over home oxygen therapy. This is on one of the NBMEs.
Patient with exacerbation of COPD (i.e., acute shortness of breath + decompensation + has Hx of COPD), apart from ABCs, USMLE wants you to know that we give antibiotics, even when patient is afebrile. This is because most exacerbations of COPD are due to infection.
Acid-base disturbance in acute exacerbation of COPD? –> “acute respiratory acidosis + chronic respiratory acidosis”; aka acute on chronic respiratory acidosis. You will see the RR is 28, pCO2 is 80 mm Hg (super high), bicarb 32-34 mEq/L; O2 50 mm Hg; and then your thought is, “wait, but if the RR is high, why is the pCO2 high, not low?” –> Because in COPD, the alveolar surface area for gas exchange is actually obliterated because of the emphysema, so even though the RR is high (which would normally cause respiratory alkalosis in patients with, e.g., asthma, PE), the CO2 is still high in exacerbation of COPD. You’ll be able to infer that it’s chronic respiratory acidosis as well because the bicarb will be elevated; ordinarily bicarb is unchanged in acute respiratory disturbances because it takes 12-24 hours to change. When bicarb is high, it means you either have metabolic alkalosis or chronic respiratory acidosis; in the case of COPD, it will clearly be the latter.
