HY lecture notes:
Pale RBCs –> think iron deficiency. In elderly, especially think per rectum blood loss.
Most common cause is diverticular bleed, but red flag is obviously colorectal cancer. Angiodysplasia is another important cause (tortuous superficial intraluminal colonic vessels).
Do colonoscopy to rule out CRC in elderly patient with fatigue, especially if fecal occult blood is positive.
DDx like ulcerative colitis are of course also possible, but diverticular bleed, CRC, and angiodysplasia are HY for elderly.
Angiodysplasia + aortic stenosis = Heyde syndrome.
Thalassemia has target cells classically. More likely in children (major) or younger adults (if minor).
Think demographics. For instance, USMLE Q likely won’t give you thalassemia in elderly patient, the same way they won’t give you diverticulitis in younger patient.
Red cell distribution width (RDW) is decreased in thalassemia and increased in iron deficiency. The USMLE likes that. The RBCs are uniformly small in thalassemia due to Hb production problem, whereas in iron deficiency you have a larger range of RBC size due to non-uniformity of how iron deficiency can affect bone marrow production.
Thalassemia Qs will classically give decreased serum iron (same as iron deficiency), but ferritin is normal in thalassemia. Both have microcytic anemia.
So microcytic anemia with low serum iron:
Ferritin normal + RDW low –> thalassemia
Ferritin low + RDW high –> iron deficiency
Thalassemia (notably alpha thalassemia trait; 1 out of 4 mutations) classically presents as a microcytic hypochromic anemia that doesn’t respond to iron supplementation. This is exceedingly HY, particularly for obgyn Qs. That is, pregnant woman has low iron scrutinized at first appointment; she’s started on standard pregnancy vitamins (include iron), then a few weeks later her ferritin is normal but iron is still low –> answer = do hemoglobin electrophoresis to diagnose thalassemia.
Increased HbA2 = alpha2, delta2 –> increased in thalassemia.
Same way in sarcoidosis Qs, you might get a large, rambling paragraph, with the last line saying, “oh and btw, there’s bihilar lymphadenopathy,” for thalassemia Qs, you might get a big vignette, with the last line saying “oh and btw, HbA2 is 6%” –> beta thalassemia.
CML is caused by t(9;22) translocation (Philadelphia chromosome; bcr-abl); treatment = imatinib, a tyrosine kinase inhibitor; imatinib causes fluid retention (peripheral edema).
Trastuzumab (Herceptin) used for ER/PR+ breast cancer. It’s cardiotoxic.
Tacrolimus (FK506 binder; decreases intracellular calcineurin) is an immunosuppressant; causes diabetes + nephropathy (increased BUN and Cr).
Ticlopidine (ADP2Y12 blocker); anti-platelet agent known to cause agranulocytosis (low neutrophils).
Ticagrelor also an ADP2Y12 blocker.
For aplastic anemia (can be caused by viral infection, eg Parvo B19) = defective bone marrow production = do bone marrow aspiration (sounds overly invasive but it’s the next best step USMLE wants).
Chemo-induced pancytopenia, if they want next best step to diagnose, answer also = do bone marrow aspiration.
SLE causes antibodies against hematologic cell lines. Classically thrombocytopenia. But can also cause antibodies against RBCs and WBCs. So for instance, if you have SLE vignette with all cell lines down, the answer is NOT aplastic anemia (i.e., bone marrow production problem is WRONG answer); the correct answer is “increased peripheral destruction” due to antibodies. Hard Q there.
Fanconi anemia is AR aplastic anemia seen in Ashkenazi Jewish population; causes aplastic/hypoplastic thumbs or radii (weird detail at first but pathognomonic).
Diamond-Blackfan anemia is pure-RBC aplasia that causes triphalyngeal thumbs. I can recall this Q from UWorld for Step 3 actually.
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