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If this state continues for a long period of time or till death purchase rumalaya 60pills visa medicine 013, the patient can be termed a Coma-patient order 60pills rumalaya visa treatment degenerative disc disease. The fear psychosis that has been created by this word is not really justified as coma is not always so dangerous, but at the same time it is not to be taken too lightly either. It is more common now, due to high blood pressure caused by the modern day lifestyle, habits and stress, diabetes, and road accidents etc. Diseases related to blood circulation of the brain : Thrombosis (clotting of blood in the vessels), Embolism, Hemorrhage, and Sub-arachnoid Hemorrhage. Brain Tumor: Cancerous tumors (primary or secondary) like Glioma or Metastasis, simple tumors like meningioma. In all these tumors, symptoms like headaches, vertigo, convulsions, vomiting, and paralysis of one or both the sides are seen. Oxygen deficiency, fluctuation in the blood sugar level, liver diseases, kidney diseases, respiratory disorders etc. Hormonal Imbalance: Imbalance in the hormones of thyroid, parathyroid, adrenal, pituitary glands can also lead to coma. Poison: Organophospherous poisoning or heavy metals like arsenic or lead used for murder or suicide, overdose of sleeping pills, can also lead to coma. Psychogenic Coma: (the patient is not actually in coma) The treatment of coma should be done systematically. Usually, the patient is thoroughly examined and his/her history, pulse, temperature, respiration are noted. Before a coma patient is considered brain dead, the brain death has to be ascertained very carefully and the rules and regulations made specifically for this purpose are to be followed before declaring it. In this situation, the brain never regains consciousness, so such a patient can donate his/her kidney and other parts to save the life of another patient before his/her heart stops functioning. Immediate treatment is initiated to normalise important functions like respiration, blood circulation, blood pressure. If the cause is unknown, immediate glucose, vitamin B1 and injection Nalorphine are administered as the first line of treatment: 4. If there is dehydration, intravenous administration of fluids is done; if there is an acid base imbalance, an intensive treatment is given. If the coma is due to the defect of any organ, its treatment is given or if the problem is due to diabetes or thyroid disorder, its immediate treatment is commenced. Brain tumor, paralysis and brain hemorrhage caused by accident, are included in the structural causes, where the brain is attacked directly. Whereas in the metabolic coma, abnormality is first observed in other parts of the body rather than the brain. The growing numbers of paralytic and coma patients can be controlled only if blood pressure, diabetes, obesity etc. Along with the right treatment proper nourishment and care, love and prayers can also give miraculous results. The will-power of the patient, which remains strong even in the unconscious state and the doctor’s loving care can also help the patient recover faster. After remaining in a comatose state, for a considerable period when the patients recover, some may lose their speech or memory. This may be a case of Epilepsy: You would have noticed people attending to such persons in a very funny manner for observing curiously without helping the person correctly. This chapter deals with the problem: its causes, its correct approach and the myths associated with it. Epilepsy is a disease of the brain in which excessive electrical impulses are produced in the brain for a short period of time resulting in tremors or seizures. One in every hundred persons suffers from epilepsy and thus over l o million people in our country are afflicted with this disease. According to a survey, 4 out of every 100 persons h ave suffered from a convulsion at least once in his lifetime e. Grandmal epilepsy or seizure of the entire body: In this type of epilepsy, loss of consciousness, screaming, frothing from the mouth, tremors, tongue biting may occur and sometimes urine and stool are also passed unconsciously. After regaining consciousness, the patient remains in a semiconscious state for some time or goes to sleep He may be paralyzed temporarily.

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Extravascular Versus intravascular hemolysis There are two general sites in which hemolysis may take place (Table 17 purchase 60pills rumalaya with mastercard medications and mothers milk 2014. In intravascular hemolysis discount 60pills rumalaya amex medicine expiration dates, which is uncommon, red blood cells are destroyed directly within the circulatory system. Extravascular hemolysis is more common than intravascular hemolysis and involves the destruction of red blood cells within mononuclear- phagocytic cells, often in the spleen. They are usually inherited, and generally (but not always) the abnormality is observable in the peripheral blood smear. Extracorpuscular defects refer to problems in the environment of the red blood cell, not in the red blood cell itself (Table 17. Extracorpuscular hemolysis is usually acquired and is often but not always discernible in the form of morphologic abnormalities in the peripheral blood smear. Welchii *Intravascular hemolysis*Intravascular hemolysis Laboratory findings • The major criteria for the laboratory diagnosis of hemolytic anemia are reticulocytosis and an increase in serum level of unconjugated bilirubin. For example, many spherocytes suggest hereditary spherocytosis or immunohemolytic anemia and sickle cells suggest one of the sick cell syndromes. In the majority of cases hematocrit levels are normal or near normal with minimal hemolysis; greater than 25 percent (often 75%) of red cells are elliptocytes. It should be noted that some elliptical cells also occur in thalassemia, iron deficiency, myelophthisic anemias, sickle cell disease, and megaloblastic anemia. Erythrocyte enzyme deficiencies Hereditary hemolytic anemia has been associated with 284 Hematology at least ten red cell enzyme deficiencies. Rather than producing acute hemolysis in association with drug ingestion, it causes a chronic congenital nonspherocytic hemolytic anemia. Pyrimidine-5’-nucleotidase deficiency A chronic hemolytic anemia inherited as an autosomal recessive and characterized by large numbers of erythrocytes with basophilic stippling is due to deficiency in an enzyme, Pyrimidine-5’-nucleotidase, which dephosphorylates the ribonucleotides of cytidine and uridine. Generally the term hemoglobinopathy is used to signify a structurally abnormal hemoglobin with at least one amino acid substitution. Structural abnormalities may cause premature red cell destruction; easily denatured hemoglobins; hemoglobins with abnormal oxygen affinity; altered hemoglobin solubility; and, in a few instances, reduced globin synthesis. Hemoglobin S By far the most important hemoglobinopathies are those related to the presence of sickle hemoglobin (HbS). Sickle hemoglobin results form replacement 287 Hematology of the sixth amino acid form the N-terminal end of the β- chain, glutamic acid, by valine. Hemoglobin C syndromes Hemoglobin C (HbC) is probably the second most common hemoglobinopathy (2-3% gene frequency in black populations). HbC is caused by substitution of lysine for glutamic acid in the sixth position form the N- terminal end of the β-hemoglobin chain (same location as the substitution in HbS). A variety of acquired clinical conditions result in shortened survival of previously normal red cells. These include immune-mediated destruction, red cell fragmentation disorders, acquired membrane defects, splenic effects, and the results of infections and environmental toxins. Immunohemolytic anemia 288 Hematology Immunohemolytic anemias are the result of the binding of antibody, complement, or antibody plus complement to red cells. Antibodies formed against erythrocyte antigens may be either warm (active at 37oC) or cold (active at room temperature and below). In some cases, these antibodies activate a series of proteins, referred to collectively as complement; in others, the red cells are coated with antibody alone. As a result of complement activation by hemolytic antibodies, intravascular red cell lysis and release of hemoglobin may occur. Immunohemolytic anemias fall into one of three major categories: autoimmune, in which the patient makes an autoantibody against his or her own red cells; alloimmune, where the patient’s antibody is directed against foreign red cells; and drug-induced, where a drug-dependent or related antibody is responsible for hemolysis (Table 17. The red cells are usually coated with IgG alone, IgG and complement or complement alone, but a minority of cases show IgA or IgM coating alone or combined with IgG antibody. Part of the coated membrane is lost so the cell becomes 290 Hematology progressively more spherical to maintain the same volume and is ultimately prematurely destroyed, usually predominantly in the spleen. The disease may occur at any age in either sex and presents as a hemolytic anemia of varying severity. Laboratory findings The hematological and biochemical finding are typical of a hemolytic anemia with spherocytosis prominent in the peripheral blood. The hallmark of autoimmune hemolytic anemia is the presence of antibody or complement, or both, on the patient’s own red cells. In these syndromes the autoantibody, whether monoclonal (as in the idiopathic cold hemeagglutinin syndrome or associated with 291 Hematology lymphoprolifertative disorders) or polyclonal (as following infection, e.

The prevalence of diabetes mellitus is reaching epidemic proportions 60pills rumalaya overnight delivery acute treatment, in large part because of obesity and sedentary life style in both adults and children The incidence and prevalence of diabetes mellitus in the general Ethiopian population are unknown order 60 pills rumalaya treatment mastitis. A population based study done near Gondar on 2381 individuals using glycosuria screening with blood glucose confirmation showed glucose intolerance in 12 only 0. Patient education, dietary management and exercise play a central role in managing diabetic patients in addition to pharmacologic therapy. Patient Education • It should be viewed as a continuing process with regular visits for reinforcement and not just a one-time affair. The majority of these individuals are obese, and weight loss is strongly encouraged and should remain an important goal • Food intake must be spread evenly throughout the waking hours and taken at regular times in relation to the insulin dose. Despite its benefits, exercise presents several challenges for individuals with diabetes mellitus because they lack the normal glucoregulatory mechanisms. If the insulin level is too low, the rise in catecholamines may increase the plasma glucose excessively, promote ketone body formation, and possibly lead to ketoacidosis. To avoid exercise-related hyper- or hypoglycemia, individuals with type 1 diabetes should • monitor blood glucose before, during, and after exercise • delay exercise if blood glucose is > 250 mg/dL, <100 mg/d), or if ketones are present • eat a meal 1 to 3 hours before exercise and take supplemental carbohydrate feedings at least every 30 min during vigorous or prolonged exercise • decrease insulin doses (based on previous experience) before exercise and inject insulin into a nonexercising area. Insulin formulations are available as U-100 (1ml of solution equivalent to 100 units) or U-40 (1ml of solution equivalent to 40units). It is very important that one designs and implements an insulin regimen that mimics physiologic insulin secretions. Twice daily administration of a short acting and intermediate acting insulin, given in combination before breakfast and the evening meal, is the simplest and most commonly used regimen. Therapy is initiated with one class of agent, depending on patient characteristics and a second agent is added if adequate glycemic control is not achieved. Many patients with type 2 diabetes mellitus have one or more of diabetes mellitus related complications at diagnosis. For the above reasons, it is recommended to screen those at risk of developing diabetes mellitus using fasting blood glucose. High risk individuals should be encouraged to • Maintain a normal body mass index • Engage in regular physical exercise The morbidity and mortality of diabetes mellitus related complications can be greatly reduced if detected and treated at an early stage. It is most commonly seen in patients with type 1 diabetes mellitus, but it can also be seen in type 2 diabetics especially during acute illness. Abdominal pain may be severe and sometimes may be mistaken for an acute abdominal condition like pancreatitis or ruptured viscous. Reduced insulin levels, in combination with elevations in catecholamines and growth hormone, lead to an increase in lipolysis and release of free fatty acids. Mortality is related more to the underlying or precipitating event, such as infection or myocardial infarction. Non-ketotic heperosmolar coma is characterized by marked hyperglycemia and loss of water up to 25% of body weight in severe cases. Incidence increases with attempts to achieve euglyemia with tight control of glucose concentrations Other causes in patients with diabetes include • Overdose of insulin or oral agents • ill timed administration of insulin or oral agents • administration of the wrong type of insulin • Missed or delayed meals or snacks • Uncompensated exercise • Alcohol consumption • Concomitant chronic renal failure • insulin clearance is reduced in patients with chronic renal failure Hypoglycemia can cause significant morbidity and can be lethal, if severe or prolonged. It should be considered in any patient who presents with confusion, altered level of consciousness, or seizures. The central nervous system can not synthesize glucose or store enough glycogen for more than a few minutes’ glucose supply. The brain cannot use free fatty acids as an energy source, and ketone bodies, which are generated late, are not useful in acute hypoglycemia. Autonomic signs and symptoms Result from increased autonomic nervous system activity They include • Palpitations • Tremor or shaking • Nervousness, Anxiety • Irritability • Sweating • Hunger • Nausea, vomiting • Tingling, Paresthesias • Tachycardia • Hypertension 28 Adrenergic symptoms are mediated by norepinephrine released from sympathetic postganglionic neurons and the release of epinephrine from the adrenal medullae. Neuroglycopenic signs and symptoms Neuroglycopenic symptoms are the direct result of central nervous system neuronal glucose deprivation. Signs and symptoms include • Confusion • Odd behavior • Inability to concentrate • Drowsiness • Visual disturbance • Tingling around the mouth • Convulsions • Focal neurologic deficits e. Blood should be drawn, whenever possible, before the administration of glucose to allow documentation of the plasma glucose level. Oral treatment with glucose tablets or glucose-containing fluids, candy, or food is appropriate if the patient is able and willing to take these. Intravenous glucose (25 g) should be given using a 50% solution followed by a constant infusion of 5 or 10% dextrose. If intravenous therapy is not practical, subcutaneous or intramuscular glucagon can be used, particularly in people with type 1 diabetes mellitus. Because it acts primarily by stimulating glycogenolysis, glucagon is ineffective in glycogen-depleted individuals (e.

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