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.
This is the general way to approach an acid-base disturbance. They’re not really as bad as they seem at first. You just need to remember that CO2 is acidic and HCO3- is basic. So an increase in CO2 makes the body acidotic and an increase in HCO3- makes the body alkalotic.
It’s also good to remember to calculate the anion gap when doing these calculations.
AG = Na – (Cl- + HCO3-) it’s just the cations minus the anions. If this gap between the cations and anions is large, it means that the anions are stacking their team and have an extra anion helping out.
The classic mnemonic is MUDPILES
If the anion gap is big, it’s good to look at the ratio between the change in the gap and the change in the HCO3-.
Increase in AG < decrease in HCO3- = coexisting non-anion gap metabolic acidosis
Increase in AG > decrease in HCO3- = coexisting metabolic alkalosis
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!
Calcium homeostasis is largely controlled by the parathyroid glands (tucked away underneath the thyroid). I’ve included a little bit of the vitamin D synthesis pathway as well, though D3 (the form that is absorbed in the intestines) is also synthesized in the skin as long as you’re getting a little bit of sunlight.
Hyperparathyroidism: usually an adenoma
Malignancy: PTH-related peptide released by tumor (squamous cell, renal, breast, bladder)
Vitamin D excess: granulomas (sarcoidosis, TB, Wegener’s)
Increased bone turnover: hyperthyroidism, Paget’s
Familial hypocalcuric hypercalcemia: mutation in the calcium-sensing receptor in parathyroid and kidney
Hypoparathyroidism: sporadic, caused by thyroid surgery, Wilson’s, hypomagnesemia
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.
Insulin dosing has to be one of the most (seemingly) unnecessarily complicated dosings in medicine. Not only are there 4 ways to dose it (BID, QID with rapid, QID with fast, QID with extended-release) there are three different companies, all naming their insulins slightly differently. But how can you remember whether to give Humalog, Humulin N, Humulin R, NovoRapid, Novolin Toronto, NPH, Lantus, or some combination of the above?
This is a master illustration to help organize insulin dosing and amounts.
Total Daily Dose
0.3 – 0.6 units/kg Start low, titrate up
BID (conventional therapy)
2/3 : 1/3 rule
2/3 breakfast : 1/3 supper
2/3 long : 1/3 fast
QID (with either Rapid or Fast-acting and either long or extended)
Acute kidney injury can be caused by problems directly in the kidney, before the kidney or after the kidney. If you think about it that way, it’s much easier to develop a differentiate and establish a treatment.
The RIFLE criteria define the relative damage to the kidney and the outcome. RIF = Severity in terms of serum creatinine (sCr), glomerular filtration rate (GFR) and urine production. Though for simplicity I only included serum creatinine since that is most likely what you’ll be looking at on initial blood work. LE = Outcome variables (temporary or permanent)