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Showing posts from May, 2011

Income v/s calorie intake

It is a nice diagramatic representation of how the content of the diet of individuals varies with increase their income. This clearly causes an increase in the risk for cardiovascular diseases. As the income increases, there is a drastic increase in the intake of saturated animal fats and hydrogenated vegetable fats both of which contain atherogenic trans fatty acid. Simple carbohydrates are taken in more and vegetables are less eaten.

Life expectancy changes

Life expectancy in the United States has changed from 48.3 yr in 1900 to 78.4 yr in 2011. That of the United Kingdom from 46.4 yr to 78.0 yr. Both countries have passed through the age of pestilence and famine, the age of pandemics, the age of degenerative diseases to finally enter into the age of inactivity and obesity.

Clotting factors and their synonyms

Red blood cell formation

Under certain specific stimuli, pluripotent stem cells form CFU-E i.e Colony Forming Units - Erythrocytes. These cause production of cells that are the first to belong to the RBC series, proerythroblast . The next generation is called basophilic erythroblast because it stains with basic dyes.  As the genesis continues, hemoglobin concentration increases while the nucleus condenses to a very small size. The remnant of the nucleus is either absorbed or extruded out of the cell. Endoplasmic reticulum is also absorbed. The cell is now called a reticulocyte .  The reticulocyte has some basophilic remnants of Golgi apparatus, mitochondria and other organelles. During this reticulocyte stage, the cells pass from the bone marrow into the blood capillaries by diapedesis i.e squeezing through the pores of the capillary membrane. The remaining basophilic material in the reticulocyte normally disappears within 1 to 2 days, and the cell is then a mature erythrocyte .

Comparison between normal / uremic plasma and dialyzing fluid

Cardiac defects causing cyanosis

T ransposition of the great arteries T otal anomalous pulmonary venous return T runcus arteriosus T ricuspid atresia T etralogy of Fallot E bstein's anomaly E isenmenger physiology Critical pulmonary stenosis or atresia Functionally single ventricle Note there are 5 Ts and 2 Es.

Renin-angiotensin-aldosterone system

Angiotensinogen, the precursor of all angiotensin peptides, is synthesized by the liver. In the circulation it is cleaved by renin, an acid protease, which is secreted into the lumen of renal afferent arterioles by juxtaglomerular cells. Renin is synthesized as a large preprohormone called as preprorenin. It is then cleaved to prorenin and eventually to renin. Prorenin is also secreted by other organs like ovaries. But, conversion to renin is almost exclusively the job of the kidney. This has been seen after nephrectomies. The level of prorenin in the blood remains more or less the same while that of active renin falls to almost zero. Renin cleaves angiotensinogen, thereby forming angiotensin I. In turn, angiotensin I is cleaved by angiotensin-converting enzyme (ACE), an enzyme bound to the membrane of endothelial cells, to form angiotensin II. Much of the conversion occurs as blood passes through the lungs but it also occurs elsewhere in the other parts of the body too. In

Cockcroft-Gault formula

It is a formula used to get an estimated creatinine clearance. It goes as follows: Creatinine clearance : mL/min Age : years constant : 1.23 for males, 1.04 for females normal range: men : 90 - 140 mL/min women : 80 - 125 mL/min

Omalizumab - Anti-IgE Monoclonal Antibodies

It is a new approach to the treatment of asthma. It  is a recombin ant humanized gamma immunoglobulin (IgG)1 monoclonal antibody  that is targeted against the portion of IgE that binds to its receptors (FC -R1 and FC -R2 receptors) on mast cells and other inflammatory cells. It inhibits the binding of IgE to mast cells but does not activate IgE already bound to these cells and thus does not provoke mast cell degranulation. It may also inhibit IgE synthesis by B lymphocytes.    In addition, omalizumab causes down-regulation of IgE receptors on mast cells and basophils. Administration of omalizumab to asthmatic individuals for 10 weeks lowers plasma IgE to undetectable levels and significantly reduces the magnitude of both the early and the late bronchospastic responses to antigen challenge.  Repeated administration lessens asthma severity and reduces the corticosteroid requirement in patients with moderate to severe disease, especially those with a clear environment



Emphysema is defined as an abnormal, permanent dilatation of the airways distal to the terminal bronchioles due to a destruction in the walls. There are 4 types of emphysema: 1) centriacinar/centrilobular - seen in cigarette smokers 2) panacinar/panlobular - seen in α 1 -antitrypsin deficiency 3) distal acinar 4) irregular. Pathogenesis: Protease- antiprotease imbalance theory as shown in the picture above. On examination: Patient will be dyspneic, hyperventilating and have a prolonged expiration. The chest will be barrel shaped.

Microscopic structure of alveolar wall

From blood to air we have the following structures: 1) The capillary endothelium 2) A basement membrane and surrounding interstitial tissue  3) The pulmonary interstitium is most prominent in thicker portions of the alveolar septum. 4) Alveolar epithelium. The latter contains a continuous layer of two principal cell types: flattened, platelike type I pneumocytes covering 95% of the alveolar surface and rounded type II pneumocytes which produce pulmonary surfactant and are the main cell type involved in repair of alveolar epithelium in the wake of damage to type I pneumocytes.  The alveolar walls are not solid but are perforated by numerous pores of Kohn, which permit passage of bacteria and exudates between adjacent alveoli. Alveolar macrophages, mononuclear cells of phagocytic lineage, usually lie free within the alveolar space.