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Showing posts from July, 2011

Bruise - colour changes with time

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

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

Gustilo open fracture classification

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

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.

The Salter-Harris classification of epiphyseal injuries

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

Stages of Chronic Kidney Diseases

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

Carpal bones arrangement - anatomy and mnemonic

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

Best insulin regimen

We have 2 classic regimens that have been used on a large scale. 1) Multiple component insulin regimen Here, usually a basal insulin level is maintained by a long acting insulin like glargine insulin (lantus) injected at night. Then short acting insulin analogues are injected just after breakfast, lunch and supper. In total the patient has to do 4 injections per day. 2) Twice a day pre-mixed insulin This is more commonly used. It consists of twice daily injected mixture of an intermediate acting insulin like NPH insulin and a short acting insulin or regular insulin in a ratio of 70:30. 2/3rd of the total insulin requirement is given in the morning and the remaining 1/3rd at night. The total number of injections is 2 per day. For the patients' convenience, the second regimen seems better as he/she has to do only 2 injections but the first regimen i.e multiple component insulin regime is actually the better of the two. Studies have recently shown that a better HbA1c goal i

Bronchial asthma - Definition of well controlled B.A

Bronchial asthma is considered to be well controlled if the patient experiences cough, shortness of breath and wheezing less than 3 times/week during the day, less than 3 times/month of night time awakenings and no asthma related interference with normal activity. Recently it has been found that only 1/3rd of asthma patients can be categorized as being into the well controlled group.

Chronic gastritis/peptic ulcer - pathogenesis

Peptic ulcers are created by an imbalance between the gastroduodenal mucosal defenses and the damaging forces that overcome such defenses. It is very well depicted above. H.pylori does not invade the tissues but it causes intense local inflammation. It has flagella that allows it to move in the viscous mucous. Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in the gastric mucous, thus weakening the first line of mucosal defense. It also produces urease that breaks down endogenous urea to form ammonia. This causes the pH to increase locally. The H.pylori also has adhesins that make it bind to the cells and finally they elaborate toxins that cause further damage like metaplasia. NSAIDs and aspirin are inhibitors of cyclooxygenase (COX). Thus they prevent the synthesis of prostaglandins. The latter is responsible for the promotion of mucin synthesis and vasodilation. In the absence of prostaglandins, the mucinous layer is depleted and the decreas

The plantar reflex - Babinski's sign

The plantar response is an important test to identify an upper motor neuron lesion.  PROCEDURE  To elicit it, the muscles of the lower limbs must be relaxed. The outer edge of the sole of the foot is stimulated by firmly scratching a blunt object like a key or a stick along it from the heel towards the little toe. This is what  Joseph Babinski did in the year 1896. He described the 'great toe sign' that year and then in 1903 the 'toe abduction or fan sign'. Nowadays, a final medial movement across the sole of the metatarsus is also done. i.e. we start at the heel to the little toe and finally arcing to the big toe. The final arcing movement is absent in the original Babinski plantar response test. Babinski sign refers to a combination of 'the great toe sign' and the 'fan sign'.  SIGNIFICANCE  The normal response is plantar flexion of the toes (down going) and they are drawn together. More precisely, there is flexion of the big toe and addu

Hypokalemia - Potassium replacement calculation

 DEFINITION  Hypokalemia is defined as a serum potassium level of less than 3.5 mmol/L. Normal level= 3.5-5.5 mmol/L. It is encountered in >20% of patients. Patients are usually asymptomatic but severe arrhythmias and rhabdomyolysis can occur. Non-specific complaints include easy fatiguability and skeletal muscle weakness. The preferred method of replacement is via the oral route but at times this is not possible. The article below will give you an idea about how to calculate the amount of KCl to be given I.V. 1) Potassium deficit in mmol is calculated as given below: K deficit  (mmol) = (K normal lower limit  - K measured ) x kg body weight x 0.4 2) Daily potassium requirement is around 1 mmol/Kg body weight. 3) 13.4 mmol of potassium found in 1 g KCl . ( molecular weight KCl = 39.1 + 35.5 = 74.6) Suppose we get an asymptomatic patient of  70 Kg with a serum potassium level of 3.0 mmol/L and he is on nil by mouth but having an adequate diuresis, w

Hypokalemia - ECG changes

The ECG changes in hypokalemia is mainly due to a delayed ventricular repolarisation. The changes normally do not correlate well with the plasma concentration. Early changes include flattening or inversion of the T wave, a prominent U wave, ST-segment depression k/a thumbprint-like ST depression, and a prolonged QU interval but the QT interval will be normal. Severe K + depletion may result in a prolonged PR interval, decreased voltage and widening of the QRS complex, and an increased risk of ventricular arrhythmias, especially in patients with myocardial ischemia or left ventricular hypertrophy. The QT interval may be normal or lengthened.