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This test should not be performed in children or during pregnancy because of whole body radiation order ventolin with amex. This test is dangerous in elderly patients and those with heart failure as there always remains a potential risk of inducing transient hyperthyroidism buy ventolin 100 mcg visa. Considerable suppression in thyroid uptake is noted in the range of 50 to 80 per cent by this amount of exogenous hormone cheap 100 mcg ventolin amex. In patients who are on antithyroid drug treatment for thyrotoxicosis, this test may be used as an indicator of remission of the disease. A return to normal suppressibility in treated patients usually indicates remission. It is not useful to scan all enlarged glands, but it is helpful to scan the thyroid when (i) a solitary nodule is palpated, (ii) in case of suspected retrosternal goitre or (iii) ectopic thyroid tissue. Only histological examination can reveal whether it is a carcinoma or one of other causes of nonfunctioning nodules such as a cyst, colloid-filled adenoma or a focal area of autoimmune thyroiditis. If a nodule is autonomous most of the isotopes will accumulate in the nodule and the rest of the gland will show little activity. But if the nodules are functioning but not autonomous, both the nodules and the rest of the gland will take up the isotopes. Metastasis can be demonstrated by scanning the whole body of the patient but there should be no functional thyroid tissue as the thyroid cancer cannot compete with the normal thyroid tissue in the uptake of iodine. In case of malignant thyroid, the bones (especially the skull) if suspected to be secondarily involved should be X- rayed for evidence of metastasis. X-ray after barium swallow may indicate whether there is any pressure effect on the oesophagus or not. Selective angiography can also differentiate between a functioning and non-functioning thyroid nodule. The term "goitre" denotes here any enlargement of thyroid gland irrespective of its pathology. There is uniform enlargement of the thyroid gland and it feels comparatively soft. At the time of puberty when the metabolic demands are high and in pregnancy when there is too much stress, this goitre may develop physiologically. This goitre usually subsides by itself (natural involution) or with iodine therapy. In endemic areas this goitre appears early between 20 and 30 years, whereas in sporadic areas it appears late between 30 and 40 years. Sudden enlargement with pain is complained of when there is haemorrhage into the inactive nodules. In long standing multinodular goitres most of the nodules gradually become inactive and myxoedema may ensue by the time she reaches 60 or 70 years of age. On examination the gland assumes asymmetrical shape and its surface becomes smooth and nodular. Consistency of the nodules vary from soft to hard (nodules which are tense with haemorrhage). A solitary nodule may be present anywhere in the thyroid gland, though its common site being the junction of the isthmus and one lateral lobe. In general, in case of nodular goitres the patient seeks medical advice for disfigurement, dyspnoea (from pressure on the trachea) or toxic symptoms (see secondary toxic goitre). Complications such as haemorrhage, calcification, secondary thyrotoxicosis and carcinoma may develop especially in the nodular type. Sudden haemorrhage into the goitre may cause dyspnoea, demanding immediate tracheostomy. The disease is characterized by five features : (1) exophthalmos; (2) some enlargement of the thyroid gland; (3) loss of weight inspite of good Fig. In a protruded tongue, which is a manifestation of addition to these/ there ma be thirst and primary toxic goitre (and not of secondary toxic j • t, j y t it J -rU , ,. Thyroid gland is enlarged, firm or soft, a bruit may be present mostly near the upper pole. It must be remembered that the brunt of attack falls on the cardiovascular system. The patient complains of precordial pain and exhaustion, later on auricular fibrillation and heart failure may set in. The most diagnostic feature is the presence of engorged veins over the upper part of the chest. X-ray pictures will show soft tissue shadow in the superior mediastinum or calcification. The diagnosis is suggested by the hard feel and indistinct outline of the thyroid swelling. It gradually infiltrates into the neighbouring structures such as the trachea, oesophagus, recurrent laryngeal nerve, infrahyoid muscles etc. The carotid sheath may be surrounded by the growth so that its pulsation cannot be felt at the back of the swelling. Metastasis in bone may be the first symptom with pathological fracture or pulsating bone tumour. Common presenting symptom is relatively slow growing painless lump in the neck for more than a year. This spreads by lymphatic channel in the early phase, so enlargement of regional lymph nodes is early. Presenting symptoms are similar to those of papillary carcinoma, but the age of the patient is more and there may be pain in the bones due to metastasis. The lump is slightly tender, hard, irregular and the margins are diffused due to infiltration. Dyspnoea, pain in the ear, hoarseness of voice are the complaints due to infiltration of surrounding structures. Thyroid may not move up during deglutition due to fixity to the surrounding structures. Though lymph nodes are almost always enlarged and hard, yet such enlargement may be obscured by the primary mass.

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The peculiarity of the sodium in the bone is that only 45% of it is exchangable and takes place in the metabolic processes buy generic ventolin on line. Sodium exchanges in sweat ventolin 100mcg without prescription, its renal regulation and its normal intake and output have been discussed earlier purchase ventolin on line. Here we shall discuss about (i) sodium in bone and (ii) sodium conservancy following trauma. Loss of sodium from bone has been noticed in acute sodium depletion or with adrenal hypofunction. Similar shifts of sodium may occur in patients particularly after losses by diarrhoea or sweating, in diabetic acidosis or prolonged restriction of sodium intake. That the sodium is conserved after trauma is due to increased adrenocortical activity. Due to this it is not wise to administer large quantities of normal saline immediately after operation. The sodium level should be at least less than 130 mEq/L in extracellular fluid to be called hyponatraemia. Such hyponatraemia may also be seen in cases of secretion of antidiuretic hormone as in bronchial carcinoma. This is also noticed after operation when excessive quantities of glucose solution is administered. The students should remember the various electrolyte concentrations of different gastrointestinal secretions. Saliva contains 15 mEq/L of Na+ and 40 mEq/L of K+ and it is secreted about 1,500 ml/24 hours. Gastric secretion contains 50 mEq/L of Na+, 80 mEq/L of C1-, 10 mEq/L of K+ and it is secreted about 2,500 ml/24 hours. Intestinal secretion contains 140 mEq/L of Na+, 100 mEq/L of C1-, 25 mEq/L of bicarbonate and 10 mEq/L of K+ and its secretion is about 3,000 ml/24 hours. Biliary secretion contains 140 mEq/L of N+, 100 mEq/L of C1-, 30 mEq/L of bicarbonate and 5 mEq/L of K+. Pancreatic secretion contains 140 mEq/L of Na+, 70 mEq/L of C1-, 120 mEq/L of bicarbonate and 5 mEq/L of K+. These secretions can be compared with the electrolyte concentration of plasma which is about 140 mEq/L of Na+, 100 mEq/L of C1-, 25 mEq/L of bicarbonate, 5 mEq/L of K+ and 1. The tongue is dry, hard and reddish brown in colour, though the patient is usually not thirsty. Haemoconcentration may be noticed, but this may be masked by pre-existing anaemia. The sodium concentration will be low only when lost fluid is replaced with solutions containing less concentration of sodium. When there is severe loss of plasma volume, infusion of plasma or plasma substitute should be considered. Even a daily intake of sodium may increase total sodium content when renal excretion of sodium is delayed due to renal disease or altered by the administration of adrenal cortical hormones. The result of hypematraemia is over loading of the circulation, as excess sodium will increase osmotic pressure within the capillaries and will draw excess water into the circulation from the interstitial tissue. This may result in oedema of the dependent tissues and also oedema of the suture lines after abdominal operations. This may occur if there is loss of both water and sodium, but the loss of water is greater. Treatment of apparent hypematraemia should be according to the merit of the individual cases. Nearly 98% of the total content of the potassium in the body (130 gm) is in the cells or intracellular. Potassium is the predominant cation of intracellular fluid and accounts for 2/3rds of total active intracellular cations, the remainder being the magnesium. Normal Intake and output,— A healthy adult consumes about 2 to 3 gm of potassium each day and almost the same quantity is excreted in the urine everyday. The most striking difference between sodium and potassium is the way in which they are handled by the kidneys. Sodium is always under careful control and any excess of intake will be excreted in the urine and any deficiency of sodium will be tackled by renal conservation. Excess intake of potassium after absorption in the intestine is transported to the cells by the extracellular fluid. The rapid uptake of this absorbed potassium by the cells prevents any increase in the concentration of the potassium in the extracellular fluid. When there is excessive metabolism in the body, endogenous protein is used as source of energy, both potassium and nitrogen are mobilised. With the shift of potassium into the extracellular fluid, concentration of potassium rises. But usually this is dealt with by the kidneys which excrete the potassium in the urine sufficiently fast to maintain the concentration of the potassium in the extracellular fluid within the normal limits. During starvation and after injury protein is catabolized and large quantities of potassium are released. In patients with anuria the accumulation of potassium occurs in the extracellular fluid and raises its concentration to a toxic level. The daily output of potassium in the urine is closely related to the dietary intake. This loss is highest during the first day following trauma, but this duration depends directly with the degree of trauma and tissue damage. The students must remember that in the immediate postoperative period there is excessive loss of potassium, but the sodium is conserved. If nasogastric aspiration is continued for a long time with fluid replacement by intravenous isotonic saline solution there is chance of potassium depletion. The patient lies in bed with the head drooping down on one shoulder and the jaw and cheeks hanging slack. Potassium depletion causes diminished motility of the intestinal musculature, which results in the accumulation of intestinal secretions. This in turn stimulates further secretion and more potassium is thereby lost into the lumen of the intestine. This causes ileus and abdominal distension which are common features of potassium deficiency in the postoperative period.

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The initial goal is <100– 110 beats/min buy ventolin 100mcg mastercard, although slower rates are sometimes recommended for severely ill patients generic 100 mcg ventolin mastercard. Beta blockers generic ventolin 100 mcg with visa, calcium channel blockers, and digoxin are the drugs most commonly used for rate control. These agents do not convert atrial fibrillation to sinus rhythm and should not be used for that purpose. Digoxin, because of the inotropic effects, is the drug of choice in patients with coexisting systolic heart failure. Factors that should guide drug selection include the patient’s medical condition and the presence of concomitant heart failure. The following drugs are recommended for their demonstrated efficacy in rate control at rest and during exercise: atenolol, metoprolol, verapamil, and diltiazem. Therefore, anticoagulation is beneficial for many patients despite its risk of bleeding. It is used to determine whether treatment is required with anticoagulation or antiplatelet therapy. If the patient is hemodynamically unstable, then immediate synchronized cardioversion is indicated (synchronized cardioversion). Avoid digoxin, beta blockers, and calcium-channel blockers, as they can inhibit conduction in the normal conduction pathway, increasing aberrant conduction. That could increase the likelihood of developing ventricular or supraventricular tachycardia. Independent and asynchronous atrial and ventricular contractions produce the following signs. Variation in systolic blood pressure, as measured peripherally Variation in intensity of the heart sounds Intermittent cannon A waves in jugular venous pulses caused by the simultaneous contraction of the atrium and ventricles Extra heart sounds Because of asynchronous activation of the right and left ventricles, the first and second sounds are widely split. Cardiac pacing or isoproterenol infusion may suppress episodes of tachycardia, useful for emergency treatments. Because it has a long half-life (>50 days), drug interactions are possible for weeks after discontinuation. In medium doses, they increase arteriolar dilatation and subsequently decrease afterload and preload. In high doses, they increase coronary artery dilatation and subsequently increase oxygen supply. Side effects of nitrates include orthostatic hypotension, reflex tachycardia, throbbing headache, and blushing—all caused by vasodilation. There must be a window-free period of >8 hours with nitrate therapy to reduce the incidence of tachyphylaxis. Nonselective beta blockers may mask hypoglycemic symptoms in insulin- dependent diabetics. Beta blockers can cause fatigue/insomnia, mental depression, lipid abnormalities, hallucinations, Raynaud phenomenon, bronchoconstriction, mask signs/symptoms of insulin-induced hypoglycemia, and sexual dysfunction. Nebivolol is a unique beta blocker; it is a beta-1 specific blocker that increases nitric oxide and thus does not cause erectile dysfunction. They may be harmful in the postinfarction period, especially if the patient has left ventricular failure. Four general types of shock syndromes are recognized: distributive, cardiogenic, hypovolemic, and obstructive. Physiologic Characteristics of Various Forms of Shock In shock, cardiac output varies, increasing in the hyperdynamic state of distributive shock (and sometimes in hypovolemic shock depending on how much volume has been lost), but is always decreasing in cardiogenic shock. Maximize arterial oxygen saturation Circulatory support with normal saline or blood is used early. Hypotensive patients who do not respond to saline or blood will need pressor support: dopamine, vasopressin, or epinephrine in distributive shock, and dobutamine in cardiogenic shock. Hypotensive patients with septic shock who do not respond promptly to saline should be given a single dose of hydrocortisone, since adrenal insufficiency is common in severely ill patients. It is most commonly a result of iron deficiency, anemia of chronic disease, thalassemia, sideroblastosis, or lead poisoning. It can be caused by an early form of the conditions described, as well as most forms of hemolysis and aplastic anemia. The symptoms of anemia tend to be based on the severity of the anemia rather than the specific etiology. Eventually, confusion and altered mental status may develop as oxygen delivery to the brain decreases. Death from anemia is most often caused by decreased oxygen delivery to the heart and resulting myocardial ischemia. A healthy young patient may have no symptoms at all with hematocrit 27–29%, whereas an older patient with heart disease may develop dyspnea or anginal symptoms with the same hematocrit. A healthy young patient can have transfusion withheld until hematocrit is in the low 20%. An older patient with coronary artery disease will need to be maintained when hematocrit >30%. If there is even a modest increase in blood loss—occult blood in the stool, heavier menstrual flow, or increased demand such as in pregnancy— the body is poorly equipped to increase its level of absorption to exceed 3–4 mg per day. Other etiologies are increased urinary loss of blood, malabsorption, hemolysis, and poor oral intake. As hematocrit lowers to 25%, tachycardia, palpitations, dyspnea on exertion, and pallor develop. Older patients and those with coronary artery disease may become dyspneic at higher levels of hematocrit. More severe anemia results in lightheadedness, confusion, syncope, and chest pain. A systolic ejection murmur (“flow” murmur) may develop in any patient with moderately severe anemia. These symptoms are not specific for iron deficiency anemia and may develop with any form of anemia provided it is sufficiently severe. Symptoms specific to iron deficiency are rare and cannot be relied upon to determine the diagnosis: brittle nails, spoon-shaped nails, glossitis, and pica. Iron deficiency anemia as a specific diagnosis is determined by laboratory findings, not symptoms.

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The right ventricular obstruction may be an infundibular stenosis or a valvular stenosis or a combination of the two discount ventolin 100mcg line. In this condition due to obstruction in the right ventricular outflow and presence of ventricular septal defect purchase ventolin 100 mcg amex, the venous blood entering thcright ventricle is shunted direcdy into the aorta to produce cyanosis buy ventolin in india. This condition also decreases pulmonary blood flow and thus limits and ability to absorb oxygen. Due to presence of large ventricular septal defect, right ventricular pressure can never exceed left ventricular pressure inspite of presence of pulmonary stenosis. Arterial oxygen saturation may come down to 30 to 35%, when the body can walk only a short distance. Very low saturations of 10 to 20% is also seen in rare cases when the infant is not only unable to walk, but also may lose consciousness due to cerebral anoxia. Chronic anoxia may produce compensatory polycythemia and eventually clubbing of the extremities. About l/3rd of patients are cyanotic at birth, these patients often do not survive infancy unless operation is performed quickly. Walking for short distances, interrupted by squatting, is a pathognomonic symptom of this condition. He created an anastomosis between the left subclavian artery and the left pulmonary artery. In fact the subclavian artery is divided at a distance from its origin and the cut proximal end of the subclavian artery is then anastomosed to the upper border of the left pulmonary artery which is already mobilised and doubly clampped for convenience of performing the anastomosis. A continuous thrill is felt over the anastomosis as soon as the clamps are released. A side-to-side anastomosis between the ascending aorta and the right pulmonary artery was advocated by Waterson. An anastomosis is made between the descending aorta and left pulmonary artery (Pott’s). Superior vena cava is sometimes anastomosed with the right pulmonary artery (Glenn). A high vertical ventriculotomy is performed which stops near the pulmonary annulus and is limited to the infundibular portion of the right ventricle. Through this incision the ventricular septal defect is closed with a Dacron patch. The pulmonary vulvular and infundibular obstruction is also widened with a patch graft of Dacron. Following closure of the ventriculotomy and removal of air from all cardiac chambers, extracorporeal circulation is stopped. Now the intracardiac pressure is measured to confirm that the right ventricular systolic pressure is reduced to less than 60 to 70% of that of the left ventricle. If right ventricular pressure is still elevated, more correction of the ventricular obstruction becomes necessary. While the risk is about 10% for smaller children, it is only 2 to 5% in older children. As a result venous blood is ejected through the aorta and the oxygenated blood returning from the lungs into the left atrium enters the left ventricle and is again pumped through the pulmonary artery to the lungs. This is obviously incompatible with life except for if a communication exists between the pulmonary and systemic circulations in the form of a patent ductus arteriosus, an atrial septal defect or a ventricular septal defect. One or more of these congenital anomalies must exist for the infant to survive even a few hours after birth. Transposition of the great vessels is often associated with other congenital abnormalities e. The children who survive beyond first 2 years of life, clubbing and polycythemia appear. Signs of congestive failure are always found with pulmonary congestion, cardiac enlargement and hepatomegaly. The simplest procedure is the Balloon Septostomy, in which the atrial septal defect already present is enlarged by passing a deflated balloon catheter through the defect into the left atrium, and after inflating the balloon it is forcefully pulled across the septum to enlarge the opening. This technique was first developed by Rashkind and it is almost always done at the time of cardiac catheterisation. If Balloon Septostomy is ineffective, atrial septal defect may be created by the Blalock-Hanlon technique. A portion of the atrial septum is excised and the two incisions are now anastomosed. This is achieved by switching over the aorta and pulmonary arteries with transposition of the abnormal coronary arteries. After the initial episode of rheumatic fever, symptoms of mitral stenosis may not appear for 10 years or more. It is suggested that scarring of the mitral valve due to rheumatic fever causes turbulent flow of blood which in tum causes more scarring and contraction over many years. Usually severe mitral stenosis takes about 20 to 30 years to develop after the last known bout of rheumatic fever. But in fact involvement of the mitral and aortic valves gives surgical importance to rheumatic fever. Endocarditis produces ulceration of the endocardium along the edges of the valve leaflets where they normally appose in systole. Tiny 1 to 2 mm nodules of fibrin and platelets accumulate and gradually progress to fusion of the leaflets at the commissures. The various stages from simple fusion of the commissures to grossly calcified and functionless valve are seen in different patients. Two other disabilities which appear with chronic mitral stenosis are atrial fibrillation and systemic embolisation. Arterial embolism is a serious consequence which may cause death by cerebral embolism in 20 to 25% of patients. The emboli evolve either due to stasis in the dilated left atrium or from the atrial appendages. When left atrial pressure exceeds 30 mm Hg, it produces significant transudation of fluid into the pulmonary capillaries, which causes pulmonary oedema and dyspnoea. The possible mechanism may be impaired blood flow through the coronary arteries or recurrent small emboli into the coronary arteries. The intensity of the murmur however does not correlate with the severity of the stenosis. A severe calcified and fibrosed valve may not produce audible murmur due to little mobility of the valve.