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By: O. Marcus, M.B. B.CH. B.A.O., M.B.B.Ch., Ph.D.

Program Director, University of Illinois at Urbana-Champaign Carle Illinois College of Medicine

Genetic Disorders Associated with Hypokalemia these disorders hiv infection rates dc cheap 200 mg monuvir mastercard, mentioned earlier antiviral yiyecekler buy monuvir 200 mg fast delivery, are characterized by either excess mineralocorticoid production/activity or abnormal renal potassium excretion independent of mineralocorticoid activity hiv infection rate russia buy monuvir with paypal. Disorders associated with increased aldosterone production include glucocorticoid-remediable aldosteronism and congenital adrenal hyperplasia. Although cell-shift hypokalemia and decreases in total body potassium do occur as isolated problems, they frequently occur simultaneously. Decreases in total body potassium potentiate the effects 54 Chapter 3 the Patient with Hypokalemia or Hyperkalemia of drugs and hormones to shift potassium into cells. For example, small changes in potassium during insulin therapy may not cause hypokalemia if total body potassium is normal, but in the setting of total body potassium depletion. The manifestations of hypokalemia are mainly cardiac and neuromuscular Table 3-1). The most dramatic neuromuscular symptoms are paresis, paralysis, and respiratory failure. Potassium depletion causes supraventricular and ventricular arrhythmias, especially in patients on digitalis therapy. Although severe hypokalemia is more likely to cause complications, even minimal decreases in serum or total body potassium can be arrhythmogenic in patients with underlying heart disease or who are receiving digitalis therapy. The treatment of hypokalemia depends on the underlying cause, the degree of potassium depletion, and the risk of potassium depletion to the patient. In general, hypokalemia secondary to cell shift is managed by treating the underlying conditions. For example, hypokalemia in the setting of catecholamine increases, as in chest pain syndromes, is managed with appropriate treatments for the pain. However, when cell-shift hypokalemia is associated with life-threatening conditions such as paresis, paralysis, or hypokalemia in the setting of myocardial infarction, the administration of potassium is indicated. With potassium depletion, replacement therapy depends on the estimated degree of decreases in total body potassium. For example, decreases in total body potassium accompanied by a fall in serum potassium from 3. Decreases in serum potassium from 3 to 2 mEq/L are associated with 200- to 400-mEq additional decreases in total body potassium. Potassium can be administered intravenously, but in limited quantities (10 mEq/hour into a peripheral vein; 15 to 20 mEq/hour into a central vein). Larger potassium requirements can only be accomplished by oral therapy or with dialysis. Spurious hyperkalemia is caused by red blood cell hemolysis in vitro, ischemic blood draws, extreme thrombocytosis (greater than 1 million mL), or leukocytosis (greater than 50,000 mL). Hyperkalemia caused by cell shifts of potassium occurs acutely and results from decreased potassium transfer into cells (with decreases in insulin or -adrenergic blocker therapy), increased potassium movement from cells to the extracellular space (with metabolic acidosis), hypertonicity (with hyperglycemia or the administration of mannitol), exercise, muscle breakdown (with rhabdomyolysis), or drug intoxications from digitalis or succinylcholine. Hyperkalemia with less severe decreases in renal function is also associated with reductions in the distal nephron flow rate or low serum aldosterone levels as, for example, with hyporenin hypoaldosteronism. Hyperkalemia also occurs when drugs that block activation of the mineralocorticoid receptor (spironolactone, eplerenone) or inhibit the rate-limiting step in aldosterone synthesis (heparin) are administered. As 70% of renin production is prostaglandin dependent, blocking the latter indirectly results in hyporeninemia. Clinical studies also suggest that older adults are at increased risk for hyperkalemia. Although no clear explanation exists for this observation, it may be related to an age-associated decline in aldosterone synthesis or possibly a decline in tubular sensitivity to its action. The causes of hyperkalemia in this setting are distinguished on the basis of plasma or urinary aldosterone levels. Decreases in aldosterone occur in the setting of normal, increased, or decreased plasma renin activity. Decreased plasma renin activity (hyporeninemic hypoaldosteronism) tends to occur in older adults and is associated with a number of renal diseases, including diabetes, interstitial nephritis. Finally, increases in serum potassium can be associated with normal to high levels of aldosterone and end-organ resistance to aldosterone. Aldosterone resistance is caused by drugs (such as potassium-sparing diuretics, 58 Chapter 3 the Patient with Hypokalemia or Hyperkalemia Table 3-2.

Candidal yeast infections often infect skin folds and present with peeling and satellite pustules antiviral blog purchase monuvir 200mg amex. Diagnosis Although the clinical presentation is often enough to make the diagnosis hiv infection and treatment buy 200mg monuvir with mastercard, a Gram stain and culture from the most eroded or purulent area can be helpful in defining the causative pathogen hiv infection chart generic 200 mg monuvir visa. However, the results of these cultures need to be interpreted 158 12 Bacterial Infections with the understanding that typical colonizing organisms, especially S. Although a rapid Strep test may be positive in streptococcal perianal dermatitis, this test has not been approved for use on non-posterior pharyngeal specimens. Potassium hydroxide scrapings and fungal cultures can help diagnose yeast infections. Course, management, treatment, and prognosis Intertrigo is worsened by skin occlusion, so allowing the area to aerate is important. For premature or immunosuppressed infants, or for multifocal and/or complicated infections, systemic therapy may be necessary. A similar approach, as described above for impetigo, should be employed when choosing an oral or parenteral therapeutic agent for intertrigo. A Gram stain and culture of the affected area should be taken before initiating empiric systemic antibiotics. Noninfectious pustulosis such as erythema toxicum neonatorum and transient neonatal pustular melanosis are addressed elsewhere in this book but typically are differentiated by their clinical presentation, including time course and superficial nature. Cutaneous findings Folliculitis presents as discrete, dome-shaped pustules with an erythematous base located at the ostia of the pilosebaceous canals. Occasionally, a lesion may extend to involve deeper tissues and form an abscess. Rarely, the local infection can progress to a systemic illness that is evident by fever onset and an ill-appearing child. A moist environment, maceration, poor hygiene, application of an occlusive emollient, and drainage from adjacent wounds and abscesses can be provoking factors. It is found in circulating water, and the bacteria become trapped under the clothing, leading to infection. Differential diagnosis Benign pustulosis of infancy is often on the differential of staphylococcal pustulosis in the neonate. Erythema toxicum neonatorum tends to be more transient and have a splotchy patch of erythema around fragile superficial pustules and the pustule contents contain eosinophils. Transient neonatal pustular melanosis is typically present at birth and the pustules rupture easily and are gone within hours to days; the pustules contain neutrophils similar to bacterial folliculitis but a Gram stain should be negative (although Gram stains have a significant false-negative rate in bacterial infection). Candida species, Pityrosporum ovale, and Malassezia furfur are all yeast pathogens capable of causing follicular papules and/or pustules. Identification of these fungal organisms can be made by potassium hydroxide examination of lesion scrapings or by skin biopsy. Several other conditions may mimic folliculitis, including miliaria, eosinophilic pustular folliculitis, acne neonatorum, tinea corporis, congenital cutaneous candidiasis, scabies, and erythema toxicum neonatorum. Course, management, treatment, and prognosis An attempt should be made to identify and eliminate predisposing factors. Localized uncomplicated folliculitis may be managed by removing causative factors, antiseptic cleansing. Similar to impetigo and intertrigo, bacterial Gram stain and culture can be extremely useful to guide appropriate therapy. Recurrent episodes should warrant investigation into asymptomatic nasal carriage of S. It is important for the clinician to be able to differentiate colonization from infection to determine if antibiotics are necessary. Cutaneous findings Erosions and ulcerations that are secondarily infected can present with a myriad of symptoms that include purulent drainage, crusting, erythema expanding from the wound, pain, and acute worsening that cannot be explained by the primary process. Green discharge or discoloration on dressings may be a marker of Pseudomonas infection.

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Ascending infection along the umbilical vein is a particularly serious complication hiv infection rate in ghana order discount monuvir online. Septic umbilical arteritis or suppurative thrombophlebitis of umbilical or portal veins boots anti viral monuvir 200 mg, portal vein thrombosis antiviral vitamins supplements cheap monuvir 200 mg without prescription, and liver abscesses may occur. Septic embolization from infected umbilical vessels (arteries or the vein) is uncommon, but may seed various organs, including the lungs, pancreas, kidneys, liver, brain, heart. As with all cutaneous infections, the results of Gram stain and culture must be interpreted along with clinical signs to determine true infection as cultures will likely yield colonizing organisms, even in the absence of infection. Differential diagnosis the serous secretions of funisitis/omphalitis must be distinguished from those of a vitelline duct remnant, umbilical papilloma, or urachal remnant. Inflammatory disorders, such as seborrheic dermatitis and psoriasis, can affect the umbilical region. Course, management, treatment, and prognosis As progression to severe sequelae is a major concern, patients should be initiated on parenteral broad-spectrum antibiotics directed against Gram-positive and Gram-negative organisms. In an infant who is ill-appearing, broadening coverage to include vancomycin, a higher generation cephalosporin and metronidazole may be warranted. Intravenous antibiotics should be continued until the erythema and drainage subside. Complications include evisceration, umbilical hernia, necrotizing fasciitis, cellulitis, peritonitis, superficial abscess, liver abscess and peritoneal adhesions. Patients should be monitored closely for signs of necrotizing fasciitis, which has a high mortality rate. A break in the skin resulting from trauma, surgery, or an underlying skin lesion predisposes to cellulitis. Cellulitis may be seen more commonly in patients predisposed to abnormal lymphatic drainage. The lateral margins tend to be indistinct because the process is deep in the skin. There is often some break in the skin that is a portal of entry for the bacteria, leading to infection. Extracutaneous findings Regional adenopathy and constitutional signs and symptoms of fever, chills, and malaise are common. Complications of cellulitis include bacteremia with additional sequelae such as osteomyelitis, septic arthritis, and thrombophlebitis. Additionally, Streptococcus pneumoniae, group G or C streptococci and Gramnegative agents, such as E. In premature newborns, or newborns with immunologic defects, a number of other bacterial or fungal organisms need to be considered. Pasteurella multocida is implicated in cellulitis that follows dog or cat bites, whereas human bites may become infected with Eikenella corrodens. Immunization against Haemophilus influenzae type B has significantly reduced the incidence of cellulitis due to this organism. Importantly, an aspirate taken from the point of maximum inflammation yields the causal organism more often than does a leading-edge aspirate, and thus this approach may be favored. Differential diagnosis Wells syndrome, insect bites, drug reactions, contact dermatitis, subcutaneous fat necrosis, and cold panniculitis may resemble cellulitis. Course, management, treatment, and prognosis Empiric therapy for cellulitis should be directed by the history of the illness, the location and character of the cellulitis, and the age and immune status of the patient. Cellulitis in the neonate should prompt a sepsis workup, followed by initiation of empiric therapy intravenously with a penicillinase-stable antistaphylococcal antibiotic such as cefazolin, oxacillin, or nafcillin, and an aminoglycoside such as gentamicin or a cephalosporin such as cefotaxime. Once the regional erythema, warmth, edema, and fever have decreased significantly, transition to an oral regimen for completion in the outpatient setting is reasonable, provided that other sites of infection. Cutaneous findings the orbital septum connects the orbital periosteum to the upper and lower eyelid structures. This tough fibrous band acts to prevent superficial infections from extending into the orbit and threatening vision. Periorbital cellulitis is a superficial infection that presents with redness, swelling, and tenderness of soft tissues anterior to the orbital septum. Orbital cellulitis can be associated with sinusitis or direct penetrating trauma to the orbital septum. Orbital cellulitis presents with eyelid erythema, edema, and conjunctival hyperemia, and is distinguished clinically from periorbital cellulitis by ocular involvement. Extracutaneous findings Periorbital cellulitis can be associated with bacteremia, particularly when Streptococcus pneumoniae is involved.

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The major regulator of serum phosphorus concentration is renal phosphate excretion hiv infection rates russia buy generic monuvir 200 mg. In kidney antiviral universal order monuvir with a visa, phosphate is reabsorbed primarily in the proximal tubule (80%) hiv infection brain purchase monuvir us, where it is cotransported with sodium across the luminal membrane. Most dietary phosphate is reabsorbed in the small intestine, but a component of unregulated secretion is present in colon (100 to 200 mg/day). The net effect is to increase plasma calcium concentration while keeping serum phosphorus concentration constant. As a result, renal excretion can no longer keep pace with dietary intake, and serum phosphorus concentration rises. A new steady state is eventually established, albeit at a higher serum phosphorus concentration. A sudden, massive phosphate load may result in an increase in serum phosphorus concentration. Phosphate either may be released from the intracellular space, as is the case in tumor lysis syndrome or rhabdomyolysis, or can be ingested and absorbed, as in vitamin D intoxication. Tumor lysis syndrome most commonly is seen with treatment of rapidly growing malignancies such as leukemias and lymphomas. It can occur after treatment of solid tumors such as small cell lung carcinoma, breast cancer, and neuroblastoma. Risk factors for tumor lysis syndrome in patients with solid tumors include pretreatment renal impairment, an increased lactate dehydrogenase level, and hyperuricemia. Increased lactate dehydrogenase levels and hyperuricemia are indicators of a large tumor burden. They can occur in hypoparathyroidism; in acromegaly, as a result of direct stimulation of insulin-like growth factor on phosphate transport; with bisphosphonates, through a direct effect on renal phosphate reabsorption; and in tumoral calcinosis. Tumoral calcinosis is an autosomal recessive disorder associated with hyperphosphatemia and soft tissue calcium deposition caused by mutations in three genes. Many of the signs and symptoms of an acute rise in serum phosphorus concentration are secondary to concomitant hypocalcemia (mechanism discussed earlier- page 93). Hyperphosphatemia can also cause hypocalcemia by decreasing 1-hydroxylase activity and calcitriol formation. Clinically unexplained, persistent hyperphosphatemia should raise the suspicion of pseudohyperphosphatemia, the most common cause of which is paraproteinemia. No consistent relationship of immunoglobulin 100 Chapter 5 the Patient with Disorders of Serum Calcium and Phosphorus type or subclass has been identified. This is a method-dependent artifact, and paraprotein interference may be a general problem in spectrophotometric assays. Treatment of hyperphosphatemia is aimed at reducing intestinal phosphate absorption. This is accomplished through the use of oral phosphate-binding drugs such as calcium carbonate, calcium acetate, sevelamer carbonate, lanthanum carbonate, and aluminum hydroxide. Aluminum hydroxide may be used in the short term, but chronic use in patients with kidney disease should be avoided because of the potential for aluminum toxicity. The non-calcium containing binders sevelamer and lanthanum carbonate are high in cost. Lanthanum carbonate is frequently associated with nausea and gastrointestinal upset. In patients with coexistent hypocalcemia, it is preferable to lower serum phosphorus below 6 mg/dL, if possible, before treating hypocalcemia to avoid the potential complication of metastatic calcification from calcium phosphate coprecipitation. Hypophosphatemia may result from redistribution of phosphorus from the extracellular to the intracellular space, a decrease in intestinal phosphate absorption, a decrease in renal phosphate reabsorption, or extrarenal losses from the gastrointestinal tract or through dialysis. Respiratory alkalosis causes a rise in intracellular pH that stimulates phosphofructokinase, the rate-limiting step in glycolysis. This results in severe hypophosphatemia with serum phosphorus concentrations of less than 0. Intracellular shifts are also seen with the treatment of diabetic ketoacidosis and in "hungry bone syndrome," which occurs after parathyroidectomy for secondary and tertiary hyperparathyroidism. In "hungry bone syndrome," serum calcium and phosphorus concentration fall dramatically in the postoperative period, although clinically, hypocalcemia is more of a management issue than hypophosphatemia.

 

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