Haematology and oncology: USMLE Step 1 video lessons
Blood, haemostasis, anaemia, haematological malignancy and tumour biology.
Microcytic and macrocytic anaemia, hepcidin, haemolysis, G6PD deficiency, spherocytosis and sickle cell disease, then platelets, the coagulation cascade, bleeding disorders, anticoagulants, HIT, DIC and the thrombotic microangiopathies, the leukaemias, and oncogenes versus tumour suppressor genes.
5:37Microcytic anaemia: four causes, four iron fingerprints
In microcytic anaemia, small red cells look alike under the microscope, but each cause breaks a different step of haemoglobin making. The iron studies, the red cell count and HbA₂ show which step failed.
5:34Hepcidin: why iron falls in inflammation
Hepcidin is the liver hormone that locks iron inside cells. It explains why serum iron drops in inflammation without any bleeding, and how ferritin and iron-binding capacity tell it apart from iron deficiency.
5:23B12 vs folate deficiency: MMA, homocysteine and the nerves
How to tell B12 deficiency from folate deficiency using methylmalonic acid, homocysteine and the nervous system, and why folic acid alone can fix the blood while the nerves worsen.
5:27Intravascular vs extravascular haemolysis: site and labs
Both kinds of haemolysis destroy red cells too early. The site of destruction, and what haptoglobin, LDH, bilirubin and urine show, tells them apart.
5:36G6PD deficiency vs hereditary spherocytosis, by mechanism
Both cause haemolysis with jaundice, but one is an antioxidant enzyme failure and the other a membrane scaffold failure. The smear, the timing and the antiglobulin test sort them.
5:26Sickle cell disease pathophysiology: HbS to vaso-occlusion
How one amino acid change makes haemoglobin S polymerise when deoxygenated, what promotes sickling, and how the polymer causes haemolysis, vaso-occlusion and functional asplenia.
5:53Primary haemostasis: platelet adhesion, activation and aggregation
Primary haemostasis is the platelet plug, built in three steps. Learn where each antiplatelet drug acts and why aspirin's effect outlasts the tablet.
5:21Coagulation cascade: PT vs aPTT, pathway by pathway
PT and aPTT each test part of the coagulation cascade. Learn which factors sit behind each test, so a long result points to a pathway and not just to a bleeding risk.
5:32Von Willebrand disease vs haemophilia: the labs that separate them
Both conditions can give a long PTT, so the PTT alone cannot separate them. The bleeding pattern, the bleeding time and the factor levels can.
5:34Anticoagulants: target, monitoring test and reversal agent
Every anticoagulant in this lesson ends up blocking thrombin or factor Xa. Learn each drug's mechanism and the monitoring test and reversal agent follow from it.
5:29Heparin-induced thrombocytopenia: why a low count clots
In heparin-induced thrombocytopenia (HIT), an antibody against PF4–heparin complexes lowers the platelet count and, at the same time, drives thrombin generation, so the danger is thrombosis, not bleeding.
5:33DIC vs TTP vs HUS: mechanism and the PT/PTT
DIC vs TTP vs HUS: schistocytes and a low platelet count can appear in all three. What separates disseminated intravascular coagulation, TTP and HUS is what forms the clot, and that decides the labs.
5:44AML vs ALL vs CML vs CLL: leukemia classification made simple
Sort the four main leukemias by lineage, maturity and age, and learn why a high white cell count can be the milder disease and a low one the emergency.
5:17Oncogenes vs tumour suppressor genes: one hit or two
Oncogenes switch on with a single gain-of-function hit. Tumour suppressor genes classically must lose both copies. Knudson's two-hit hypothesis explains why the same gene can cause early or late tumours.