When we eat iron, we generally get it in one of two forms: elemental iron or heme (from meat). In the intestine (proximal duodenum to be precise) the iron is either absorbed or actively transferred in. Iron is transported in the blood bound to transferrin and is stored in the liver bound to ferritin. This is why ferritin is measured when assessing iron stores.
Though most of the time you can make the diagnosis of iron deficiency anemia by assessing the patient’s history and CBC (microcytic anemia), you can also do an “iron study” that looks at the following:
Ferritin: indicator of iron stores, will be reduced in iron deficiency anemia
Serum iron (SI): decreased in iron deficiency anemia
Total iron binding capacity (TIBC): measures transferrin, this is elevated when iron is low
% saturation = SI/TIBC x 100, reduced in iron deficiency anemia
It’s good to keep the other causes of microcytic anemia in mind. To remember you can use the mnemonic TAILS
Anemia of chronic disease
*I realize that using “anemia” as the A is a little bit of a cop out in a mnemonic devoted to anemia, but I wasn’t the one who came up with it and TCILS just isn’t as easy to remember.
Neutrophils (70%): These are the big guys in infection. Generally when someone has an “elevated white count” it’s due to the neutrophils (unless there’s a lymphoma grumbling along). They are the major players in fighting off bacterial infection and the main component in pus.
Lymphocytes (20-60%): These are the B cells, T cells, and Natural Killer (NK) cells. When you’re looking at a blood smear, you can’t tell the difference between them.
T cells: cell-mediated immunity
B cells: humoral (antibody-mediated) immunity
Natural Killer cells: protect against viruses and tumours
Monocytes (3-8%): Mature into macrophages and mast cells, they play a major role in mounting an inflammatory reaction. Macrophages are the “professional antigen presenting cells“, displaying foreign peptides in Class II MHC.
Eosinophils (1-6%): fight against parasitic infections (back in the good old days), now they’re the bane of many people’s existence as they’re involved in asthma and allergies.
Basophils (0.1%): contain many base-loving (hence baso-phil) granules containing histamine
Each of these sections has a main function in adjusting the amount and kind of solutes in the urine. Different drugs and diuretics work at distinct areas, which is why some diuretics are potassium sparing while others (like Lasix/furosemide) are potassium wasting.
Red blood cells (fancily known a erythrocytes) are the simple, non-nucleated cells that transport oxygen in the body. This just outlines their development in the bone marrow (hint, they start off with a nucleus) and the major growth factor erythropoietin that stimulates their production.
By looking at the peripheral blood and bone marrow, you can work on sorting out where and what kind of disease process is going on. For example, if there are too many reticulocytes in the peripheral blood.
Looks for the presence of IgG and/or complement on the RBCs. This causes hemolysis and can be due to an autoimmune disease, transfusion reaction, etc.
Indirect antibody Test
This is used when cross-matching people for a blood transfusion. It tests patients for the presence of unexpected alloantibodies (anti-D, anti-E, anti-C, anti-Kell, anti-Duffy). This is just a screen, if it is positive, you can then test for specific antibodies and then only transfuse blood that is negative for those specific antigens.
* 19/06/2013 Please excuse the doodle for saying “agglutination” though it is testing by agglutinating, the “A” in DAT stands for antibody. Thanks Robina for pointing this out!
The types of hypersensitivities can get a little confusing, especially 2, 3, and 5.
Type 1: Plain old allergy (asthma, anaphylaxis, atopy) Type 2: Antibody-dependent, cytotoxic (think of autoimmune hemolytic anemia) Type 3: Immune complex disease (like a lot of the autoimmune conditions: rheumatoid, lupus) Type 4: Delayed/Cell-Mediated (mediated by T cells, T cells are slower to react than antibodies, so this reaction takes a couple days) Type 5: Receptor-mediated autoimmune disease (Graves, myasthenia gravis)
Liver enzymes can be elevated for a number of reasons, but the first step in an approach is to determine if the enzymes are in a hepatic pattern or cholestatic pattern. It is also very important to realize that Alk phos, GGT, ALP, and AST are liver enzymes, but they don’t give an indication of function; for that you need to look at INR and bilirubin.
It seems as though the clotting cascade is something you can study over and over again and it never sticks.
The important things to know are:
HEPARIN affects factor VIII in the INTRINSIC pathway and this is measured using PTT (partial thromboplastin time) WARFARIN affects the vitamin K dependent synthesis of some clotting factors (purple in the image), particularly factor VII in the EXTRINSIC pathway and this is measured using PT (prothombin time) or INR (International Normalized Ratio, which is derived from the PT)