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DISEASES OF THE ARTERIES AND VEINS: ARTERIAL SPASM – RAYNAUD’S PHENOMENON

July 28th, 2011

Spasm of the arteries is a rare cause of arterial blockage. Often it is associated with taking medications that provoke spasm, especially ergots (which are in some medications used to treat migraine headaches).Raynaud’s Phenomenon. Raynaud’s phenomenon is an exaggerated response to the normal reflex mechanism which causes blood vessels in the hands and feet to narrow (spasm) in the cold or with emotion. It affects 1 in 20 Americans to some degree, mostly women.If you experience Raynaud’s phenomenon, your fingers or toes (and in some people, ears and nose) turn chalky white when you are exposed to cold, and they also sting. Your skin may turn blue or bright red upon return to a warmer environment before normal color returns.*203\252\8*

DISEASES OF THE ARTERIES. ANEURYSM

July 17th, 2011

Who Is Affected by Aneurysm? Abdominal aortic aneurysm is most likely to occur in people older than 60 years, and it affects men more often than women.How Serious Is an Aneurysm?  The main risk of an abdominal aortic aneurysm is that, like a balloon that is blown up too far, it may rupture, and rupture results in life-threatening internal hemorrhage (bleeding). The larger the aneurysm gets, the more likely it is to rupture. Timely surgery prevents rupture.Surgery usually is warranted only  when the aorta (which normally has a diameter of less than 1 inch) enlarges to about 2 inches, because the likelihood of rupture increases at that point. A 2-inch-wide aneurysm has a 1 in 25 chance of rupturing within 1 year. An aneurysm that is 2 3/4 inches across a 1 in 5 chance of rupturing in the next year. Aneurysms usually grow about to 1/8 inch to 1/4per year, but this rate can be highly variable.Surgical correction often involves replacing a part of the diseased artery with a graft or tube made from synthetic materials.Berry Aneurysm. Important, but less common, types of aneurysm are not related to atherosclerosis. Berry aneurysms are bulges in the walls of arteries within the brain. As the name implies they appear like little berries attached to a blood vessel, usually at a point of branching. They usually do not cause symptoms unless they rupture, in which case they may cause stroke or coma or be fatal.*197\252\8*

SUPPORTIVE CARE OF CHILDREN WITH CANCER: PREVENTION AND TREATMENT OF URINARY TRACT TOXICITY (SUPPORTIVE CARE MEASURES TO AVOID/AMELIORATE TOXICITY

July 5th, 2011

)A. Children with a single kidney or hydronephrosisAre ineligible to receive ifosfamide in rhabdomyosarcoma protocols. The use of ifosfamide is discouraged for all patients with a single kidney.Have greater nephrotoxicity with cisplatin than those without hydronephrosis, in spite of adjustment of doses for decreased GFR.B. Primary prevention of nephrotoxicity including adequate toincreased hydration, maintenance of normal intravascularfluid status, and avoidance of intravascular volume depletionAdequate intravascular hydration and diuresis can be enhanced by the use of 0.45% or 0.9% saline, mannitol, and diuretics.Use mannitol and diuretics to increase diuresis only after determining adequate intravascular hydration.Where possible, avoid:Nephrotoxic antimicrobials and other renal-toxic medications.The use of intravenous contrast dye for computed tomographic scanning during and after infusion of nephrotoxic chemotherapy.Prevention of bladder toxicityProvide hyperhydration to ensure increased urine output to dilute and decrease the bladder mucosal contact time of toxic oxazaphosphorine metabolites.Strongly encourage ample oral intake for the 12-24 hours preceding cyclophosphamide or ifosfamide infusion.Maintain a urine output of > 65 mL/m2/h for at least 18 hours after cyclophosphamide or ifosfamide therapy.4. Encourage the patient to void at least every 2 hours for the 24 hours after oxazaphosphorine treatment.E. Specific measures to prevent renal toxicity from renal-toxic drugs1. Hydrationa. Before infusion of high-dose methotrexate, moderate to high-dose cyclophosphamide, cisplatin, or ifosfamide, give hydration at 125 mL/m2/h (2x maintenance) for a minimum of 2 hours to increase urine output to > 100 mL/m2/h (> 3 mL/kg/h).b. Before the chemotherapy infusion, urine specific gravity should be < 1.010.c. The hydration fluid most frequently used is 596 dextrose /0.4596 NaCl + 10 mEq/L KCL.d. During infusion of these agents, in general, maintain hydration at > 125 mL/m2/h and urine output at >90 mL/m2/h.e. After the infusion of nephrotoxic chemotherapy (including high-dose melphalan), maintain urine output at 65-100 mL/m2/h (depending on agent and protocol) with oral/intravenous fluids to equal 90-125 mL/m2/h.f. Where needed to maintain isovolemic fluid balance (avoidance of over- and underhydration), diuresis can be forced (in the presence of adequate hydration) through the use of mannitol 6 g/m2 (200 mg/kg) in at least 25 mL of fluid over 15-60 minutes and/or furosemide 0.5-1 mg/kg push intravenous (IV).2. AlkalinizationBefore infusion of high-dose methotrexate, urine alkalinization of >pH 6.5 can be achieved with 40-60 rnEq NaHC03/L added to the intravenous hydration fluid.3. Uroprotectanta. Mesna has been used as a uroprotectant with high-dose cyclophosphamide and ifosfamide (oxazaphos-phorines). Mesna, which has a half-life of 90 minutes, binds the toxic oxazaphosphorine metabolite acrolein within the urinary collecting system to detoxify it. In adult patients, Mesna may not be more effective in preventing bladder toxicity than vigorous hydration.b. The dosage guidelines for Mesna vary. The majority of Children’s Cancer Group protocols recommend a total Mesna dose equivalent to the total ifosfamide dose(i.e., 1 mg of Mesna /l mg of ifosfamide) and a total Mesna dose of about 8056 of the total cyclophosphamide dose.c. Studies have shown that lower doses of Mesna may be uroprotective.4. Hypertonic salinea. The effectiveness of prevention of cisplatin nephrotoxicity by infusion in 3/6 saline is controversial.b. Prevention or diminution of nephrotoxicity associated with cisplatin is possible with hydration with normal saline, continuous infusion of cisplatin, and prophylactic supplementation with magnesium.5. Magnesiuma. During infusion of cisplatin, add mannitol in a dose of 15 g/nr (10-24 g/m2/L) and MgS04 in a dose of 20 mEq/L to the hydrating solution to prevent hypomagnesemia.b. Continue postchemotherapy hydration with 5% dextrose/0.45% NaCl + 20 mEq/L KC1 + 20 mEq/L MgS04 + mannitol 20 g/L.c. When chemotherapy includes cisplatin, routine magnesium supplementation with a minimum of 6 mEq/m2/day by mouth (PO) or IV is recommended.6. Continuous versus intermittent infusionFor cisplatin or ifosfamide, there are insufficient data to determine if continuous versus intermittent infusion or dosing by pharmacokinetic measurement of area under the curve can decrease their nephrotoxicity.Adjust the administered dose of chemotherapeutic agents according to the GFR.Limited total dose of agentMore than eight courses of ifosfamide (approximately 72 g/m2) are not recommended, as the incidence of serious nephrotoxic complications increases markedly when this dose is exceeded.Hematuria1. Microscopic hematuriaa. Transient microscopic hematuria (no more than 2 abnormal urinalyses on 2 separate days during a course of therapy); no modification of the oxazaphosphorine or Mesnab. Persistent microscopic hematuria (>2 abnormal urinalyses during a course of therapy)i. Do not modify the oxazaphosphorine dose.ii. Change the Mesna to a continuous infusion: 360 mg/m2 during oxazaphosphorine, followed by 120 mg/m2/h for 24 hours.2. Gross hematuriaEvaluate all episodes of gross hematuria by cystoscopy. Also consider further testing, such as urine culture, excretory urogram, and voiding cystogram, and perform as indicated.a. Transient gross hematuria during or after a course oftherapy (only one episode, which clears to less thangross hematuria)i. Do not modify the oxazaphosphorine dose.ii. Change the Mesna to a continuous infusion: 360 mg/m2 during oxazaphosphorine, followed by 120 mg/m2/h for 24 hours.b. Persistent gross hematuria after completion of a course of therapyi. Hold subsequent oxazaphosphorine until the urine shows less than gross hematuria.ii. Reinstitute oxazaphosphorine at full dose, with the Mesna changed to a continuous infusion: 360 mg/m2 during oxazaphosphorine, followed by 120 mg/m2/h for 24 hours after each dose of oxazaphosphorine.iii. If gross hematuria does not resolve to microscopic hematuria or less, withhold further oxazaphosphorine therapy.c. Persistent gross hematuria occurring during a course of oxazaphosphorinei. Interrupt the oxazaphosphorine.ii. Withhold further oxazaphosphorine until the next course of therapy.iii. If the gross hematuria resolves to microscopic hematuria or less, subsequent courses of oxazaphosphorine may be administered at full dose, with Mesna changed to a continuous infusion: 360 mg/m2 during oxazaphosphorine, followed by 120 mg/m2/h for 24 hours.d. Occurrence of a second episode of gross hematuria or persistence of microscopic hematuria on the continuous infusion regimeni. Continue the oxazaphosphorine when the urine shows less than gross hematuria.ii. Double the loading dose of Mesna to 720 mg/m2 and the subsequent hourly dose to 240 mg/m2/h.iii. Continue to give Mesna by continuous infusionfor 48 hours after the last dose of oxazaphosphorine.e. Persistent gross hematuria in the face of the “doubledose, continuous infusion” regimen Discontinue oxazaphosphorine.G. Renal tubular dysfunctionIf significant renal Fanconi syndrome (serum phosphate <3.5 mg/dL, potassium <3 mEq/L; 1+ glycosuria with serum glucose <150 mg/dL, bicarbonate <17 mEq/L, and ratio of urine protein/urine creatinine <0.2) develops while receiving ifosfamide, consider substituting cyclophosphamide.*36\168\2*

ADJUVANT ANALGESICS: ANTIDEPRESSANT

June 29th, 2011

SIndications-Antidepressants are indicated for the treatment of neuropathic pain and are more effective against the constant burning dysaesthetic type of pain. They are also useful for pain complicated by insomnia or depression.     Action-The analgesic effect is seen with doses lower than required for the treatment of depression (50-75 mg/d amitriptyline), occurs more quickly than the antidepressant effect (2-3 days) and has been documented in patients with no features of depression. The action is thought to relate to blocking the re-uptake of serotonin and noradrenaline in the central nervous system. Antidepressants can also aid analgesia by increasing night-time sedation, improving mood and relieving depression.     Drugs-For neuropathic pain, a tricyclic antidepressant (amitriptyline, imipramine or doxepin) should be used and may be superior to newer non-tricyclic antidepressants. Amitriptyline is started at a dose of 25-50 mg at night, increasing to 50-75 mg at night. If there is no benefit in one week the drug can be stopped. There is considerable individual variation in patients’ responses to different drugs, and a trial of a second antidepressant is sometimes successful.     Side effects-The side effects of these drugs (sedation, anticholinergic effects and postural hypotension) are usually mild when used in low dose for neuropathic pain.*62\55\2*

HIV INFECTION AND ITS EFFECTS ON THE BODY: PNEUMOCYSTIS CARINII PNEUMONIA

June 17th, 2011

Pneumocystis carinii pneumonia (PCP) is an infection of the lung (pneumonia) caused by a parasite called Pneumocystis carinii. The parasite appears to be in the lungs of almost everyone, presumably acquired sometime early in life. {Pneumocystis carinii is found almost exclusively in the lungs, but like most-facts in medicine, this is not an absolute, and pneu-mocystis infections have occasionally occurred in other parts of the body.) The parasite causes no problem unless the balance between the immune system and the microbial world is heavily tilted in favor of the microbe. As a result, physicians initially saw PCP mostly in malnourished children, in people with certain types of cancer, and in those who had received organ transplants. At present, over 95 percent of people with PCP have HIV infection.     The reason so many people with HIV infection get PCP is probably that the CD4 cell, which is infected by HIV, is also important in keeping Pneumocystis carinii in check. As the supply of CD4 cells decreases, Pneumocystis carinii is less constrained. In approximately 50 percent of the people with HIV infection, PCP is the first AIDS-defining diagnosis. This means that this infection is the first condition that meets the CDC’s criteria for AIDS; it also means that the loss of immune defenses is relatively severe. Without treatment, about 8t) percent of all people with AIDS will develop PCP at some time during the course of the disease.     PCP in people with AIDS evolves slowly. In fact, most people have had the symptoms for weeks before they seek medical attention. The disease can be serious, and at first approximately 25 percent of people with PCP died. The prognosis is better now because of earlier medical intervention and improved treatments.
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