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By: Roohollah R. Sharifi, MD, FACS
- Professor of Urology and Surgery, University of Illinois at Chicago College of Medicine
- Section Chief of Urology, Jesse Brown Veterans Administration Hospital, Chicago, Illinois
Impaired absorption Intestinal short circuits Tropical sprue medications xr purchase 16 mg betahistine with amex, celiac disease Anticonvulsants symptoms you may be pregnant buy betahistine 16 mg low cost, sulfasalazine medicine qid discount 16 mg betahistine with amex, other drugs Congenital malabsorption C. Unexplained disorders Pyridoxine-responsive megaloblastic anemia Thiamine-responsive megaloblastic anemia Some cases of myelodysplastic syndrome Some cases of acute myelogenous leukemia will develop in about 1. The incidence of folate deficiency and drug-related megaloblastic anemia is less well established. Through its association with alcoholism, folate deficiency is far from a rare condition. Cobalamin functions as an essential cofactor for only two enzymes in human cells, methionine synthase and L-methylmalonyl coenzyme A (CoA) mutase. Methionine synthase catalyzes the recycling of homocysteine to methionine; this reaction requires 5-methylcobalamin as a coenzyme (see. Methionine, an essential amino acid for protein synthesis, also serves in the form of S-adenosylmethionine as the major methyl donor in numerous important enzymatic reactions. Thus cobalamin deficiency results in secondary intracellular deficiency of all forms of folate except 5-methyltetrahydrofolate. As a result, the activities of all of the enzymes using folate to transfer one-carbon moieties, including thymidylate synthase, are impaired. This concept of "methylfolate trapping" explains why cobalamin deficiency and folate deficiency produce indistinguishable hematologic abnormalities and why the hematologic abnormalities seen in cobalamin deficiency can be completely reversed by pharmacologic amounts of folic acid. This concept also explains why the hematologic abnormalities caused by folate deficiency respond only slightly, if at all to large amounts of cobalamin. A wide variety of neuropsychiatric abnormalities are seen in cobalamin deficiency and appear to be due to an undefined defect involving myelin synthesis. Because these abnormalities are not seen in folate deficiency, it has been tempting to ascribe them to deficient activity of the second cobalamin-dependent enzyme, L-methylmalonyl-CoA mutase, which is unrelated to any folate-dependent enzyme or pathway. Abnormal odd-carbon and branched-chain fatty acids are formed when the mutase is impaired. Genetic defects in which the synthesis of both adenosylcobalamin and methylcobalamin is impaired do lead Figure 163-2 Reactions involved in the metabolism of D- and L-methylmalonyl coenzyme A(CoA). The stomach is also the site of synthesis of intrinsic factor, which binds free cobalamin with high affinity and plays an essential role in cobalamin absorption. R protein binds cobalamin with a higher affinity than does intrinsic factor, particularly at an acid pH. Thus under normal conditions of gastric acidity, dietary cobalamin enters the duodenum bound to R protein. Additional cobalamin bound to R protein enters the duodenum after secretion into bile by the liver (the only significant route by which cobalamin is lost from the body). Cobalamin is not stored intracellularly; the entire intracellular vitamin is bound to the aforementioned two enzymes, which are present in greater amounts than is cobalamin. A large number of acquired and genetic diseases affect the pathway of cobalamin absorption and transport and result in cobalamin deficiency. The secretion of biliary cobalamin ranges from 5 to 10 mug/day, and approximately 90% is reabsorbed by strict vegetarians and other normal individuals. Achlorhydria and the loss of pepsin secretion are common in elderly subjects (>50% of individuals older than 70 years) and in those with partial gastrectomy. The same time span of 10 to 15 years is required for these subjects to acquire clinical signs of cobalamin deficiency as for those who have deficient diets. A complete lack of intrinsic factor occurs in individuals who have undergone total gastrectomy or who have pernicious anemia; these individuals have idiopathic and essentially complete atrophy of the gastric mucosa in association with autoantibodies to parietal cells and intrinsic factor. Cobalamin malabsorption occurs commonly in severe pancreatic exocrine insufficiency because of an inability to degrade R protein-cobalamin complexes in the jejunum. Clinically evident cobalamin deficiency rarely occurs, however, probably because oral therapy with pancreatic extract is usually instituted in these patients during the 3 to 5 years necessary for the signs of cobalamin deficiency to develop. In congenital R-protein deficiency, the total serum cobalamin level is very low, but no hematologic abnormalities are present because R proteins do not transport cobalamin to rapidly dividing cells, such as those in the bone marrow. Normal individuals have approximately 5000 to 20,000 mug of folate in body stores. The amount of dietary folate has increased approximately 100 mug/day in the United States because of the recent mandatory fortification of all grain products that was implemented to reduce the incidence of neural tube defects.
Whenever acute interstitial nephritis is suspected medications are administered to cheap 16mg betahistine fast delivery, it has been suggested that a Hansel stain rather than a Wright stain of the urine sediment be made because it detects eosinophils more easily medicine omeprazole order betahistine 16 mg fast delivery. The 24-hour excretion of urea nitrogen is useful because it will be less than nitrogen intake medications quit smoking quality betahistine 16 mg. It is not wise to accept this guideline because the 1- to 2-mg/dL/day rise is based on results obtained from Vietnam war patients who had varying degrees of kidney damage. The maximal rate of rise in serum creatinine can then be calculated as creatinine production divided by total body water ([0. Hyperphosphatemia, hypocalcemia, hyperuricemia, and anemia usually develop after several days-or more rapidly in patients with rhabdomyolysis or hemolysis. In fact, dosages of all drugs should be adjusted according to guidelines for renal failure; plasma drug levels should be monitored because the guidelines provide only average dosing recommendations. For hypovolemic, hypotensive patients in the pre-renal classification, blood pressure should be restored by discontinuing the use of antihypertensive drugs and administering blood (if bleeding or anemia is present) or isotonic saline to expand the extracellular volume. If doubt exists about the adequacy of the plasma volume, an intravenous challenge of isotonic saline (250 to 500 mL) is warranted. If urine flow does increase to exceed 20 to 30 mL/hour, furosemide can be used to achieve fluid balance. Infusion of low doses (1 to 3 mug/kg/minute) of dopamine has become popular because it can cause renal vasodilatation, but dopamine does not hasten the recovery of renal function and may cause cardiac arrhythmias. If urine flow increases within hours of beginning dopamine, furosemide, or both, use of the drugs can be continued. If not, dopamine or furosemide administration should not be continued to prevent complications. Indwelling urinary catheters should be avoided in uncomplicated cases; intermittent catheterization using sterile technique usually suffices even in oliguric obtunded patients and reduces the risk of infection. The simplest and most accurate estimate of fluid balance is a compulsive daily weight measurement; fluid intake and output records are more cumbersome and less accurate. In febrile patients this limit can be increased as long as weight does not increase. If weight increases, sodium should be restricted, but as long as the serum sodium concentration is normal, water restriction is unnecessary. In patients who cannot eat, an intravenous infusion of essential amino acids and glucose may be necessary. On the other hand, this approach entails considerable fluid intake and may lead to the need for dialysis. However, none of these measures removes excess potassium, and dialysis is usually required. Renal tubular injury from ischemia or toxins is usually reversible; recovery to nearly normal renal function seems to be more likely in non-oliguric than in oliguric patients. Patients should be given intravenous saline before receiving iodinated radiocontrast material and before surgical procedures, especially patients with poor kidney function or those in whom renal blood flow will be interrupted. Pre-treatment with allopurinol can decrease uric acid production when leukemia or massive tumors are being treated. The initial hemodynamic influence of ischemia in the kidney reduces the pressure required for glomerular filtration and predisposes the tubular cells to ischemic damage. These modalities of treatment, dialysis and transplantation, are discussed in Chapters 105. Chronic hemodialysis is equivalent, for example, to only about 10 to 15% of normal renal function. Patients with progressive renal disease, including but not limited to patients with diabetes mellitus, must be regarded as "vasculopaths" and cardiovascular risk factors sought and treated vigorously. In the United States, about 220,000 patients are presently undergoing dialysis and another 80,000 are living with a functioning renal transplant. There is now good evidence that essential hypertension is caused by renal genetic mechanisms and that the propensity for the development of renal disease in response to renal injury may also, and separately, be partly genetically determined.
The subdeltoid is the largest of the bursae around the shoulder (see Chapter 303); it is located between the deltoid muscle and the shoulder capsule and extends under the acromion symptoms diagnosis order betahistine 16 mg with amex. Acute inflammation of this or nearby bursae and tendons may be exceedingly painful symptoms 6 weeks pregnant order betahistine 16mg otc, resulting in restricted shoulder movement and tenderness over the rotator cuff treatment naive generic betahistine 16 mg overnight delivery. Intrabursal injection of lidocaine is diagnostic and often curative; however, recurrences are common. Pain is often perceived to be in the lateral aspect of the thigh and the low back and is aggravated by abducting the affected leg and by lying on the affected side. Tendinous lesions include tenosynovitis, a lesion of the gliding surfaces of a tendon and its sheath; tendinitis, painful scarring within a tendon; and trigger lesions, which are localized enlargements of the tendon that engage a constricted part of the sheath (as in "trigger finger"). Flexor digital tenosynovitis may cause pain in the metacarpophalangeal or proximal interphalangeal joints. The symptoms of carpal tunnel syndrome are paresthesias and pain in the palmar side of the first three fingers and at times the radial half of the fourth finger; the pain may radiate proximally to the shoulder, creating confusion with a cervical disk syndrome. Physical findings include sensory loss, weakness on abduction and opposition of the thumb, and atrophy of the thenar eminence. There is tender, most often unilateral, swelling at one or more costosternal junctions. The most common of these are probably synovial chondromas, which develop as cartilaginous synovial plaques that sometimes calcify. Radiographs reveal multiple opacities if ossification has occurred; arthroscopy may be useful for both diagnosis and treatment, which is surgical. Uncommonly, two or more joints are involved; similar lesions occur in tendons and bursae. These tumors are usually discovered as deep swellings within a tendon sheath, a bursa, or a joint capsule. A few have been described with extensive osteoid and bone formation, simulating the radiographic appearance of benign lesions. Chondrosarcomas and fibrosarcomas are other malignancies arising within or near joints, and intrasynovial myeloma and lymphoma are rare causes of a swollen or painful joint. They are often provoked by increasing ambient temperatures, although a few persons experience attacks only with febrile illnesses. To avoid attacks, some persons maintain environmental temperatures at levels that are uncomfortably low for themselves, as well as others. The feet appear normal between attacks, except in those persons who habitually walk barefoot because their attacks are provoked by wearing shoes. Some clinicians use the terms erythromelalgia and erythermalgia for the symptom-complex, which they classify into primary erythromelalgia, erythromelalgia associated with thrombocythemia, and secondary erythromelalgia associated with a potpourri of unrelated medications and disorders. In one paradigmatic kindred, the disorder is autosomal dominant, and it has afflicted 29 members. Most often beginning between ages 2 and 8, it has been responsible for severe adjustment problems in youth, engendered in part by an inability to sit comfortably in a heated classroom or to participate in physical activities. In essential thrombocythemia, erythromelalgia has been noted with platelet counts as low as 400-500 Ч 109 /L. Erythromelalgia disappears for 3 or 4 days after a single dose of aspirin, which is the duration of its inhibition of platelet aggregation; and studies by van Genderen and associates confirm that the erythromelalgia is caused by intravascular activation and aggregation of platelets, leading to endothelial cell damage. Other reported associations with erythromelalgia include diabetes mellitus, pregnancy, neurologic disorders, and gout and connective tissue diseases. In the absence of thrombocythemia, aspirin is ineffective for treating or preventing erythromelalgia. Although there is no proven treatment, examples of those agents for which effectiveness has been claimed for non-thrombocythemic erythromelalgia 1561 include intravenous nitroprusside, cyproheptadine, and, counterintuitively, capsaicin ointment. Erythromelalgia was the most common complication, occurring in 7 of the 13, of whom 7 were males. In the end stages the pathologic lesion is simply that of scar tissue, so by the time that this process causes clinical manifestations, little evidence of the initial inflammatory reaction may remain. As a general rule, the process tends to originate in the midline, around the great vessels, and to then spread laterally. Pulmonary and myocardial fibrosis syndromes have not generally been seen as being related to multifocal fibrosclerosis, although pleural fibrosis along with retroperitoneal fibrosis can be seen with ergotamine use.
The acute loss of 1 L of predominantly solute-free water treatment viral pneumonia 16mg betahistine amex, as in diabetes insipidus medications venlafaxine er 75mg buy 16mg betahistine with visa, reduces the blood volume by 2 medicine jokes cheap 16mg betahistine overnight delivery. Consequently, even modest signs and symptoms of volume contraction are amplified appreciably in patients with diminished myocardial reserve or reduced sympathetic nervous system function. A decrease in orthostatic diastolic blood pressure of 10 mm Hg is considered to be the most reliable indicator of significant volume depletion. A convenient way of achieving this goal is to administer 500 mL of normal saline over 1 to 3 hours. In patients with a normal cardiac reserve, the effect of a fluid challenge may be monitored safely by evaluating the pulse, blood pressure, and urine flow. Because volume contraction is associated with vasoconstriction, both in the venous and the arterial circuits, transient changes in the pulmonary capillary wedge 544 pressure may not accurately reflect volume status. The kidney initially responds to a decrease in effective circulating blood volume by reducing urine volume and sodium excretion. Severe degrees of volume contraction also reduce filtration rate and result in prerenal azotemia and a decrease in fractional excretion of sodium (see Chapter 100). The type of fluid, the route and rate of fluid administration, and the total amount of fluid to be given will vary with the particular circumstance. Because less than 10% of total body water is in the intravascular compartment, infusing 1 L of D5 W expands the intravascular volume by 75 to 100 mL, that is, by about 2%. This kind of fluid replacement is most helpful in burns, in which cutaneous protein losses are appreciable, and in circulatory collapse, in which rapid intravascular expansion is critical. In most other instances of volume contraction, using colloid-containing solutions is difficult to justify, since the half-life of infused albumin in ill patients is relatively short, only 4 to 6 hours, and the cost of colloid solutions such as iso-oncotic albumin is more than 50 times greater than that of an equal volume of crystalloid solution. There are also disorders in which inadequate arterial filling occurs in the absence of external fluid losses and which indeed are often associated with increased total body water. However, the signs and symptoms of these disorders mimic closely those that characterize true volume contraction. Table 102-3 lists three commonly encountered classes of derangements that may manifest clinically with tachycardia, acute hypotension, oliguria, azotemia, and a reduced fractional excretion of sodium. A profound collapse of cardiac output, due to acute myocardial infarction with pump failure (cardiogenic shock) or to acute pericardial tamponade, may clearly result in circulatory collapse. Circulatory collapse with its attendant signs and symptoms occurs when there is a sudden increase in the capacitance of the vascular bed, most notably in the venous part of the circulation. This kind of increase in ratio of vascular capacitance to vascular volume occurs most commonly in sepsis and cirrhosis with increased arteriovenous shunts and decreased systemic vascular resistance. Increased vascular capacitance also may be seen in circumstances in which peripheral vasodilators, particularly those having a postarteriolar locus of action, are administered injudiciously. It is, however, worth citing certain factors particularly germane to managing fluid therapy in such patients. Normal plasma albumin Acute pancreatitis Bowel infarction Rhabdomyolysis Non-cardiogenic pulmonary edema 545 might be mistaken for true cardiogenic shock. The combined findings of acute left ventricular infarction, systemic arterial hypotension, the absence of pulmonary edema on the chest radiography, a reduced pulmonary capillary wedge pressure, and an antecedent history of prolonged diuretic therapy, when taken together, indicate that improved systemic hemodynamics may be achieved by cautious attempts to expand volume while also measuring-serially-the cardiac output and the pulmonary capillary wedge pressure. This distinction is particularly difficult in individuals who have been in intensive care units for prolonged periods of time and in those at high risk for developing sepsis, such as cancer patients treated with potent chemotherapeutic agents. Both in true hypovolemia and in sepsis, the pulmonary capillary wedge pressure is reduced, but in septic circulatory collapse, the calculated systemic vascular resistance falls, because of peripheral vasodilation, whereas in true hypovolemia, peripheral vasoconstriction ordinarily raises the systemic vascular resistance. This therapy necessarily expands total body water, particularly in the vascular and interstitial compartments. Consequently, during recovery from the underlying disorder, care must be taken to avoid unnecessary expansion of the vascular bed and consequently the risk of volume-mediated cardiac decompensation. Volume expansion occurs whenever the rate of salt or water intake exceeds the rate of renal plus extrarenal losses; in chronic volume expansion, the external salt and water balance may be normal. First, the systemic venous pressure may be increased because of primary cardiac disorders, such as right-sided heart failure or constrictive pericarditis. Second, local elevations in pulmonary or systemic venous pressure may occur, as in left-sided heart failure, vena caval obstruction, or portal vein obstruction. Third, a reduction in plasma oncotic pressure, and consequently a net increase in the tendency for fluid to transudate from capillaries to interstitium, accounts plausibly for edema formation in the nephrotic syndrome.
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