HY lecture notes:
Empiric Tx for community acquired pneumonia is usually azithromycin. Covers atypicals like Mycoplasma and also Strep pneumo.
Occasionally can use a fluoroquinoline instead of azithromycin, but 1) apparently hospitals are apprehensive about its use due to the fear of resistance, and 2) it’s only the answer if someone has been on other antibiotics the past three months. Even patients with COPD will usually just get azithro first-line.
Most common cause of pneumonia in HIV / immunocompromised is Strep pneumoniae, not Pneumocystis jirovecii (PJPneumonia).
It’s one of those tricky questions where questions where, for instance, they could give you someone with history of asbestos exposure, but the answer is still bronchogenic carcinoma, not mesothelioma, as the most likely lung cancer he or she will develop.
The USMLE won’t ask you, “What’s the most common cause of x?” That type of Q is more Qbank style.
For the exam, let’s say in an HIV patient with pneumonia, they expect you to know that Strep pneumo is lobar, whereas PJP is bilateral and ground-glass on CXR.
HIV patient + pneumonia:
Lobar –> Strep pneumo, not PJP
Bilateral ground-glass –> PJP
Mycoplasma is also bilateral, but the USMLE won’t make you guess PJP vs Mycoplasma based on merely having bilateral presentation. In this type of situation (i.e., when you have a bilateral pneumonia), do bronchoalveolar lavage (BAL) to diagnose. It’s basically injecting sterile fluid down into the lungs and then sucking it back up for analysis. Do silver staining of the fluid to look for yeast –> PJP.
Atypical pneumonia is also known as interstitial pneumonia. The word “interstitial” is really important. 9 out of 10 questions on atypical pneumonia will give you a bilateral pneumonia with interstitial infiltrates. I’ve seen one question where they said something along the lines of, “right lower lobe consolidation with interstitial markings,” and the answer was Mycoplasma. In other words, “interstitial” wins over “lobar” for pneumonia. Let me elaborate:
Pneumonia:
Right lower lobe consolidation with dullness to percussion –> Strep pneumo. Treat empirically with azithro.
Bilateral interstitial infiltrates in immunocompetent patient –> Mycoplasma. Give azithro.
Bilateral interstitial infiltrates in immunocompromised patient –> Mycoplasma or PJP. But the USMLE wants PJP. Do BAL to Dx, then Tx with TMP-SMX. If pt is already on PJP prophylaxis (also TMP-SMX), you know it can’t be PJP, so the assumption would be Mycoplasma –> give azithro.
Right lower lobe consolidation with interstitial markings –> “Interstitial” wins over the lobar picture –> Answer is Mycoplasma, not S. pneumo (1 out of 10 Qs –> HARD).
Normal Ca+ level is 8.4-10.2 mg/dL
Give normal saline first to treat hypercalcemia. If giving a med after, give a bisphosphonate (e.g, pamidronate).
For Step 3: Ca 10.2-12: fluids only; 12-14: add bisphosphonate only if symptomatic; 14+: add bisphosphonate regardless
Hypercalcemia can cause nephrogenic diabetes insipidus (weird but assessed).
Renal failure with high BUN (uremia) –> causes uremic platelet dysfunction –> NORMAL platelet count but increased bleeding time (normal range 2-7 minutes). Qualitative, not a quantitative platelet problem. They’ll give you epistaxis in someone with high BUN, normal platelet count, and low Hb –> answer is uremic platelet dysfunction (or “acquired platelet dysfunction”). Hb is low simply bc the pt has epistaxis.
High BUN can also cause neutrophil dysfunction, etc., but platelet dysfunction is highest yield.
Friction rub in the setting of high BUN –> uremic pericarditis (fibrinous). Answer on USMLE is immediate hemodialysis.
For pulmonary embolism, do heparin, THEN spiral CT.
If pregnant, do V/Q scan (ventilation/perfusion scan), NOT CT.
If the V/Q scan in pregnancy shows segmental defects (positive scan), and they ask you for the next best step in diagnosis, the answer is CT. You might say “wtf? I thought we don’t do CT in pregnant women.” It’s true. We don’t. But if they ask you for the next best step in Dx after V/Q scan, the answer is still CT.
You need to know the acid-base disturance in PE is respiratory alkalosis –> low O2, low CO2, high pH, normal bicarb. Bicarb is normal bc it doesn’t change so acutely – takes 12-14 hours to really move. High respiratory rate gets rid of CO2 despite lung pathology bc CO2 diffuses really fast, whereas O2 diffuses more slowly and requires healthy lung, so O2 is low.
Most common thing you see on an ECG in PE is sinus tachycardia. Don’t select S1Q3T3. It’s apparently a highly specific finding for PE, but not commonly seen.
So they might say: “Shortness of breath. HR 92. ECG shows no abnormalities.” But a HR of 92 + ECG that’s normal = sinus tachy right? Makes sense.
BPH is treated with alpha-1 blocker, e.g, terazosin, tamsulosin. 5-alpha-reductase inhibitors are also first-line (finasteride). Combination therapy is acceptable first-line over monotherapy and is superior / more effective.
For prostatic adenocarcinoma, give flutamide + leuprolide together. Flutamide blocks androgen receptors. Leuprolide agonizes GnRH receptors, but continuous administration desensitizes receptor, causing a decrease in LH and FSH after a couple days. In practice, both are administered at the same time. But if the USMLE forces you into a sequence, choose flutamide THEN leuprolide (i.e., block androgen receptors first). This is bc leuprolide will cause transient increase in LH and FSH, leading to higher T and DHT levels, before the desensitization.
Leflunomide is for rheumatoid arthritis. Don’t confuse that with leuprolide. Leflunomide is a dihydroorotate dehydrogenase inhibitor.
For RA, NSAIDs are used first-line for Sx relief in RA. Corticosteroids can be used for Sx only when starting a DMARD or when transitioning between different DMARDs. NSAIDs and steroids do not alter/slow disease trajectory.
DMARDs slow disease trajectory. Methotrexate is first-line.
Early RA: Methotrexate first. If insufficient, add leflunomide or sulfasalazine. OR, stop methotrexate and give anti-TNF-alpha drug monotherapy (i.e., infliximab, etanercept, adalimumab, golimumab, certolizumab).
Established RA: Methotrexate first. If insufficient, add anti-TNF-alpha agent.
USMLE won’t assess the high degree of specificity as per above, but you do need to know the info about NSAIDS and steroids being only for Sx, as well as that methotrexate is first, and that TNF-alpha the usual step-up after methotrexate.
Methotrexate causes pulmonary fibrosis. So does RA interestingly (rheumatoid lung). Both restrictive lung disease – might be hard to differentiate between whether the cause is RA or the methotrexate (probably both in most patients).
Methotrexate also causes hepatoxicity and mouth ulcers.
USMLE loves agranulocytosis (neutropenia) as a huge cause of mouth ulcers. Not sure why this happens mechanistically but is super HY and common.
Ganciclovir, ticlopidine, methimazole, propylthiouracil, clozapine also HY causes of neutropenia.
Carbamazepine and chloramphenicol can cause aplastic anemia (RBCs and platelets also down in addition to neutrophils).
Low neutrophils or mouth ulcers + fever = febrile neutropenia / neutropenic fever –> give immediate IV broad-spectrum antibiotics, such as pipericillin-tazobactam, or cefepime + vancomycin.
