Medicine Hack

Introduction: Homocysteine is a sulphur containing amino acid that is produced during the conversion of methionine to cysteine. Hyperhomocysteinemia results when there is an abnormality in the homocysteine metabolism. It is an independent risk factor for stroke, MI, peripheral arterial disease and venous thrombotic disease. Even mild to moderate hyperhomocysteinemia is a significant risk factor for vascular disease. Pathophysiology: The amino acid homocysteine is normally metabolized via the transsulfuration pathway by the enzyme cystathionine-β-synthase (CBS), which requires vitamin B6 as co-factor and via the remethylation pathway by the enzymes methylenetetrahydrofolate reductase (MTHFR), which is folate dependent and methionine synthase, which requires vitamin B12 as co-factor. 1 - Methylenetetrahydrofolate reductase 2 - Methionine synthase Hyperhomocysteinemia can be either: 1) Inherited or 2) Acquired. Inherited Inherited severe hyperhomocyste

As soon as a diagnosis of VTE / PE is strongly suspected, anticoagulant therapy should be started unless there are contraindications. Parenteral drugs like unfractionated heparin (standard heparin) and low molecular weight heparin (lovenox) are started and therapy shifted to a long term stable vitamin K antagonist like warfarin. Unfractionated heparin The anticoagulant action is by binding to and accelerating the activity of antithrombin III. This inactivates thrombin, factor IXa and Xa and thus prevents further clot formation. The classical regimen for the dosage is a loading dose of 5000 - 10000 units followed by a continuous infusion of 1000 - 1500 units/hour. Unfortunately we all do not have the same weight. So, a more appropriate dosage is a loading dose of 80 units/kg and a continuous infusion of 18 units/kg/hr. The aim is to achieve a target activated partial thromboplastin time (aPTT) aka partial thromboplastin time with kaolin (PTTK) of 2-3 times the normal laboratory val

This is a slide at 50X magnification of a beta thalassemia patient. This is also a type of microcytic hypochromic  anemia as shown in the slide. The red blood cells have a diameter smaller than that of the nucleus of the lymphocyte. They are also bizarre shaped. Target cells aka codocytes or mexican hat cells are predominantly seen. They are characterised by a dark centre followed by a white ring and then a second rim of dark region.

It is a typical peripheral blood smear for an iron deficiency anemia patient showing microcytic hypochromic red blood cells at magnification 50X. In normal conditions, the size (diameter) of an RBC should roughly correspond to that of the nucleus of a lymphocyte. In this slide, it is smaller. The numerous small dots refer to platelets and they are found in a larger number (thrombocytosis), a finding commonly seen in iron deficiency anemia. Differential diagnosis includes: 1) anemia of chronic disorders, 2) thalassemia, 3) sideroblastic anemia.

Under certain specific stimuli, pluripotent stem cells form CFU-E i.e Colony Forming Units - Erythrocytes. These cause production of cells that are the first to belong to the RBC series, proerythroblast . The next generation is called basophilic erythroblast because it stains with basic dyes.  As the genesis continues, hemoglobin concentration increases while the nucleus condenses to a very small size. The remnant of the nucleus is either absorbed or extruded out of the cell. Endoplasmic reticulum is also absorbed. The cell is now called a reticulocyte .  The reticulocyte has some basophilic remnants of Golgi apparatus, mitochondria and other organelles. During this reticulocyte stage, the cells pass from the bone marrow into the blood capillaries by diapedesis i.e squeezing through the pores of the capillary membrane. The remaining basophilic material in the reticulocyte normally disappears within 1 to 2 days, and the cell is then a mature erythrocyte .