Medicine Hack

The colour of a bruise changes with time and is due to the disintegration of the red blood cells. There is hemolysis and breakdown of the hemoglobin into the pigments hemosiderin, hematoidin and bilirubin by the action of enzymes and histiocytes.  A fresh bruise is red in colour. This is due to oxy-hemoglobin. Within 1 day, the colour changes to blue i.e. deoxy-hemoglobin. In 2-4 days, the colour becomes brown i.e. hemosiderin. It then becomes green in about 5-7 days. This green colour is due to hematoidin. Then the bruise becomes yellow in 7-10 days which is because of bilirubin. The colour then fades and the skin regains its normal colour in around 15 days. This is because the pigments have been removed by the phagocytes. Thus the colour change is red,blue,brown,green and yellow.  An exception to this is a subconjunctival hemorrhage which changes colour from red to yellow directly. This is because the hemoglobin is being constantly kept oxygenated by the air during degradation.

Virchow's triad refers to the 3 primary influences for thrombus formation and it includes: 1) Endothelial injury 2) Stasis, turbulence or abnormal blood flow 3) Blood hypercoagulability. Endothelial injury Physical loss of endothelium leads to exposure of subendothelial extra-cellular matrix, adhesion of platelets, release of tissue factor, and local depletion of PGI 2 and plasminogen activators. Abnormal blood flow Turbulence can cause endothelial injury which is in itself a major influence for thrombosis. Apart from that abnormal blood flow can: 1) Disrupt laminar flow and bring platelets into contact with the endothelium 2) Prevent dilution of activated clotting factors by fresh-flowing blood 3) Retard the inflow of clotting factor inhibitors and permit the buildup of thrombi 4) Promote endothelial cell activation, resulting in local thrombosis, leukocyte adhesion, etc.  Hypercoagulability It can be primarily due to a genetic disorder and secondarily due to some acqui

It is also called as Gustilo-Anderson classification. It is a well established system to establish the severity of the open fracture. e.g. if you are on night duty and you have to phone the orthopedic surgeon regarding a case, you just have to tell which type it is according to the Gustilo's classification, instead of describing the fracture in details. The classification goes as follows: Typ e I - Puncture wound < 1 cm, minimal contamination, low energy and simple fracture Type II - Laceration > 1 cm; moderate soft tissue damage with adequate bone coverage Type IIIA - Extensive soft tissue damage, often associated with high energy trauma, massive contamination but adequate bone coverage Type IIIB - Extensive soft tissue damage with periosteal stripping and bone exposure, flap coverage is usually required Type IIIC - Arterial injury associated and requiring repair

Bennett's fracture is an unstable intra articular fracture of the base of the first metacarpal bone.  It extends into the carpometacarpal (CMC) joint and is  the most common type of fracture of the thumb. It is nearly always accompanied by some degree of subluxation or frank dislocation of the carpometacarpal joint and this subluxation/dislocation makes the fracture unstable. The mechanism of injury is that when an axial force is applied against a partially flexed metacarpal, there is a resulting fracture of the base of that metacarpal and usually associated with subluxation/dislocation.  This fracture is common in cases of fall on thumb usually from bicycles and punching to a hard object. If intraarticular fractures (such as the Bennett's fractures) are allowed to heal in a displaced position, significant post-traumatic osteoarthritis of the base of the thumb can occur.

Type I – A transverse fracture through the growth plate ( incidence is about 6-7%) Type II – A fracture through the growth plate + metaphysis and sparing the epiphysis (incidence is about 70-75% ) Type III – A fracture through growth plate + epiphysis, sparing the metaphysis (7- 8% incidence) Type IV – A fracture through all three elements growth plate + metaphysis + epiphysis (8-10% incidence) Type V – A compression fracture of the growth plate

The table above shows how chronic kidney diseases are classified. Risk factors include hypertension, diabetes mellitus, autoimmune disease, older age, African ancestry, a family history of renal disease, a previous episode of acute renal failure, and the presence of proteinuria, abnormal urinary sediment, or structural abnormalities of the urinary tract. Stage 0 Not commonly included in many classifications but in this stage there is no kidney damage evident but patients have one or more risk factors mentioned above. Stage 1 Kidney damage is there demonstrated by persistent proteinuria, abnormal urine sediment, abnormal blood and urine chemistry, abnormal imaging studies but GFR i.e kidney function will be normal. Stage 2 Kidney damage is there and slight decrease in kidney funtion. Stage 3-5 The older term chronic renal failure corresponds to these stages. It is characterized by a progressive, significant and irreversible kidney damage with a GFR < 60 for 3 month

A simple mnemonic to remember how the carpal bones are arranged is: " S he  L ooks  T oo  P retty;  T ry  T o  C atch  H er" S caphoid L unate T riquetrum P isiform T rapezium T rapezoid C apitate H amate Last reviewed on: 1 September 2015