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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.

ECG waves, their meaning and normal duration.

1) P wave - atrial depolarisation, < 120 ms 2) PR segment - end of P wave till beginning of QRS complex i.e. time taken between atrial and ventricular activation. 3) PR interval - onset of P wave till onset of QRS complex, 120-200 ms 4) QRS complex - ventricular depolarisation, <110 ms 5) T wave - ventricular repolarisation 6) U wave - repolarisation of Purkinje fibres 7) QT interval - beginning of QRS complex till end of T wave