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Insulin - action on peripheral cells

Insulin binds to receptor on target sites. These sites have an intrinsic tyrosine kinase activity that lead to receptor autophosphorylation and recruitment of intracellular signalling molecules. The latter result in widespread metabolic and mitogenic effects of insulin as shown in the diagram above. Another effect is the activation of phosphatidylinositol 3 kinase that fastens the translocation of GLUT-4 containing vesicles to the cell surface. This is important to allow uptake of glucose by skeletal and fat cells. When insulin action ceases, the transporter-containing patches of membrane are endocytosed and the vesicles are ready for the next exposure to insulin. On the other hand, in the liver, this is not the mechanism of glucose uptake. Instead, it induces glucokinase, and this increases the phosphorylation of glucose, so that the intracellular free glucose concentration stays low, facilitating the entry of glucose into the cell by diffusion. Insulin-sensitive tissues l

Insulin secretion - local regulation

The diagram shows a beta cell of the islet of pancreas and will explain how local factors regulate secretion of insulin from it. Glucose enters the cell via the GLUT-2 transporter. Inside the cell there is metabolism with the generation of ATP. This causes the ATP-sensitive K+ channel to close, as shown in A. Closure of this channel leads to cell membrane depolarization. This in turn allows calcium ions to enter the cell via another calcium channel, shown in B. Increased intracellular calcium activates calcium dependent phospholipid protein kinase. This leads to exocytosis of insulin granules.

Macewen's sign / cracked pot sound

The sign was described by Sir William Macewen. The test is performed by percussing on the skull of the patient and a cracked pot sound can be heard to the naked ears of the examiner brought closed to the skull. This sound can be heard even better if percussion is done on one side while a stethoscope is placed on the other side. A positive test is indicative of separated sutures. As long as the anterior fontanel is open i.e. up to 18 months, the test will be positive. In pathological cases, it is due to a raised intracranial  tension due to hydrocephalus or an abscess.

Mittelschmerz's syndrome

Definition: It refers to pain at the time of ovulation. It is not that frequently encountered. Clinical features: Patient will complain of pain in either the suprapubic region or right/left iliac fossa. It usually starts around the mid cycle. The pain does not shift and is not associated with nausea or vomiting. It is there for less than 12 hours. Patient may have slight vaginal bleeding or leucorrhea. Relief of pain occurs spontaneously. Severity varies from patients and usually range from 3 to 5 on a scale of 10. Mechanism: The most probable causes are: 1) increased tension of the growing Graafian follicle just prior to rupture, 2) irritation of the peritoneum by the released follicular fluid following ovulation. Treatment: Non opiod analgesics and assurance do good in this condition. In difficult cases, we may look into a possibility to render the cycle anovular with contraceptive pills.


Definition: It is strictly defined as an excessive normal vaginal discharge and it should fulfill the following criteria: 1) the excess secretion is evident from persistent moistness of the vulva or staining of the undergarments, 2) it is non-purulent, 3) since it is non-irritant, it never causes pruritus. Mechanism: Normal vaginal secretion depends on the estrogen level. So a rise in the level of estrogen eventually causes increased secretion. This rise is seen during puberty, around ovulation and pregnancy. Some cervical causes of leucorrhea include erosions, chronic cervicitis, polyp and ectropion. Treatment: 1) Local hygiene is very important. 2) Use of cotton undergarments is recommended. 3) Anxiety of the patient must be relieved through counselling. 4) Treat the possible cause of the leucorrhea.

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