Every anemia from HEM02 (Anemia I), HEM03 (Anemia II), HEM05 (RBC Case Review) and HEM06 (RBC Lab) on one page: where each one sits by size and marrow response, which mechanism family it belongs to, and how the anemias connect to, mimic, cause or protect against each other.
Rows are size (MCV). Columns are the marrow's answer (reticulocytes): low means a production problem, high means destruction or loss. Dashed chips appear in more than one box, and those crossovers are what exams like to test. Select any anemia to see its essentials and everything it connects to; connected anemias light up on the map.
Think of RBC mass as water in a bathtub. The faucet is the marrow (production), the drain is destruction (hemolysis), and the leak is blood loss. Every anemia fits one of the three, and the thalassemias sit on two at once. Select an anemia to reveal what is missing or broken, how that becomes anemia, and its flowchart from the lecture notes. Select a group question to reveal the group summary.
The same routine runs through all four lectures: history, then MCV × corrected retics and the other cell lines, then targeted labs, then smear or marrow. Each step has the matching flowcharts from the lecture notes.
Pick a kind of relationship. Use Focus on to see only the links for one anemia. Select any anemia name to jump to it on the map.
Each card shows the answer a question wants you to jump to. Decide why it's wrong, then reveal the catch.
| Topic | In-house | Boards / standard | On the exam |
|---|---|---|---|
| Microcytosis cutoff | MCV <70 fL (HEM02) | MCV <80 fL (also used in HEM06) | Match the lecture the question comes from |
| Normal marrow erythroblasts | "About 0–2%" (HEM06) | Erythroid precursors ≈20–30% (M:E ≈3:1) | 0–2% on in-house items; standard value for boards. 0–2% is the normal blood retic range |
| Normal neutrophil lobes | 3–4 (HEM06 megaloblastic station) | 3–5; hypersegmented = ≥6 lobes (or >5% with 5) | Six or more lobes is hypersegmented either way |
| Human Plasmodium species | Four (HEM06) | Four classic + P. knowlesi as a fifth | Answer "four" in-house |
Filtered by the lecture highlight above.
| Anemia | Lectures | MCV | Retics | Family | Clinches it |
|---|
Answer before you open each one.
Combined B12 + iron deficiency. Large (B12) and small (iron) cells average to a normal MCV; the high RDW and dimorphic smear give it away.
LDH ↑ and haptoglobin ↓ with low retics and normal bilirubin = ineffective erythropoiesis (megaloblasts dying in marrow), not hemolysis. Treat with parenteral B12 (neuro signs) + IV iron.
Hb electrophoresis → ↑ HbA2 (β-thal minor). Mentzer 64/6.0 ≈ 10.7 (<13). Stop the iron (overload risk) and offer genetic counseling: two carriers have a 25% chance of a child with β-thal major.
Parvovirus B19 aplastic crisis. The virus infects erythroid precursors and stops production. Any chronic hemolytic anemia (HS, sickle cell) depends on a high retic output, so a short shutdown crashes the Hb. Treat with transfusion.
G6PD level: primaquine is an oxidant (the "oxidize" arm of drug hemolysis) and causes bite cells and Heinz bodies in G6PD deficiency. Primaquine is given for vivax/ovale hypnozoites. Sickle cell trait and G6PD deficiency both protect against P. falciparum.
Valve hemolysis → iron deficiency. Chronic intravascular hemolysis spills Hb into the urine (hemoglobinuria, hemosiderinuria), so iron is lost. A destruction anemia becomes a production anemia.
Secondary hemochromatosis (transfusions + ↑ gut absorption from ineffective erythropoiesis): the opposite of iron deficiency. Cardiac iron → CHF, the main cause of death. Treat with chelation (deferoxamine, deferasirox, deferiprone).
Autoimmune disease can cause warm AIHA (IgG autoantibody, DAT +, high retics; first patient, SLE) or anemia of chronic disease (IL-6 → hepcidin → iron trapped; low retics; second patient, RA). The retic count splits them.
Black pigment (calcium bilirubinate) gallstones from chronic hemolysis: heme → excess unconjugated bilirubin. Distractors: cholesterol stones (↑ cholesterol:bile acid ratio) and brown stones (infection, β-glucuronidase).