HY lecture notes:
CML –> splenic enlargement; bloods show increased metamyelocytes + myelocytes. Seeing these two cell types in a question is essentially synonymous with CML. Let’s just say 19 times out of 20. Only time it won’t be CML is if they literally explicitly say “hey, the alkaline phosphatase activity is high” –> then you know it’s “leukemoid reaction,” not CML; LR is just a response to infection. In CML, LAP is low, not high.
AML –> myelocytes, myeloblasts, promyelocytes on CBC.
CML –> myelocytes, metamyelocytes, neutrophils on CBC.
Treatment for CML is imatinib –> bcr-abl tyrosine kinase inhibitor. Imatinib causes fluid retention (edema).
Student asks about which other drugs I’ve mentioned that cause fluid retention –> Dihydropyridine calcium channel blockers such as nifedipine are exceedingly HY for causing edema.
CLL –> smudge cells + warm autoimmune hemolytic anemia (IgG antibodies against RBCs)
AML –> Auer rods
ALL –> kids; Down syndrome
Before starting isotretinoin (high-dose vitamin A for acne), must do pregnancy test (beta-hCG). There is also a USMLE question floating around where they say they start a girl on OCPs due to starting isotretinoin, and they ask what else you should do, and the answer is “recommend barrier contraception.” Students will get this wrong because they say, “Wait, I don’t get it, why two methods?” We can debate it all we want, but it’s still on the NBME. This may have been on NBME 7 or 8 for 2CK.
Acne management:
- Topical retinoids first (i.e., topical tretinoin; NOT oral isotretinoin) ; cause photosensitivity (rash); also used for photoaging; mechanism is decreasing sebum production.
- Benzoyl peroxide used second; often coadministered with topic retinoids; mechanism is the killing of bacteria.
- Topical clindamycin
- Oral tetracycline; causes photosensitivity (blistering)
- Oral isotretinoin; must do beta-hCG in women; recommend barrier contraception even if on OCP; can cause elevations in LFTs; can cause dyslipidemia; main complaint is dry skin + peeling; takes several weeks to really start working but ultra-effective according to most patients; can be commenced earlier in patients with severe nodulocystic acne; works by diffusely shutting of sebum production
Student may ask, “USMLE is actually that pedantic about acne management?” My answer: 2CK will assume you know #1+2 are used first and that #5 is last resort for most patients, and that #1 and #4 cause photosensitivity; Step 1 wants you to know mechanisms of the drugs in terms of how they actually treat the acne (which I’ve written above).
African-American female in 20s-30s with dry cough:
Chest x-ray (CXR) normal: answer = asthma = “activation of mast cells.”
CXR: multiple nodular densities = bihilar lymphadenopathy = sarcoidosis = “non-caseating granulomas.”
About one-third of patients with asthma present with just a dry cough. This is really HY for the USMLE. This is known as cough-variant asthma.
For instance, person has dry cough in winter, allergies in spring, a bit of itchiness of antecubital fossae in summer –> atopy –> dry cough is actually asthma; doesn’t need they need Tx; but it’s the diagnosis. And the 2CK expects you to know that.
Wegener granulomatosis is now known as granulomatosis with polyangiitis (GWP). It’s not also known as; it’s formerly known as Wegener. Learn the new name. I had a student get an easy Wegener Q on the exam, and she said the answer was “polyangiitis.”
GWP causes hematuria + hemoptysis + “head-itis” (inflammation/pathology involving the head, such as mastoiditis, otitis, sinusitis, nasal septal perforation).
GWP is anti-PR3 (anti-proteinase 3; aka c-ANCA.
Churg-Strauss, now known as eosinophilic granulomatosis with polyangiitis (EGWP), is anti-MPO (anti-myeloperoxidase; aka p-ANCA). Microscopic polyangiitis (MP) is same antibodies as EGWP.
EGWP is asthma + eosinophilia + p-ANCA.
MP is hematuria + p-ANCA.
GWP is hematuria + hemoptysis + head finding + c-ANCA.
Goodpasture syndrome is hematuria + hemoptysis + anti-GBM antibodies (glomerular basement membrane).
Goodpasture is antibodies against the alpha-3 chains of type IV collagen. Causes linear immunofluorescence on renal biopsy.
Alport syndrome is mutations in type IV collagen, not antibodies. X-linked recessive (some sources say XD, but NBME 19 for Step 1 had XR as the answer). Presents as eye + ear problem in boy or man with red urine.
