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Based on all of the available posttransplant morbidity and mortality data, it is imperative that posttransplant hypertension be identified and managed appropriately. 40 there are several mechanisms responsible for posttransplant hypertension including renal dysfunction, increased sensitivity to endothelin-1 and angiotensin, increased density of glucocorticoid receptors in the vascular smooth muscle, and decreased chapter 55  |  solid organ transplantation  855 table 55–7  recommended vaccinations pre- and posttransplant39 administration vaccine before sot after sot additional information hepatitis a hepatitis b x x     herpes zoster x   human papilloma virus influenza x   immunize as soon as possible during course of disease immunize as soon as possible during course of disease (before transplant, administer 40 mcg dose in a series of three to four doses) livea virus, administer ≥ 14 days before immunosuppressant agents are initiated (experts advise 1 month before) recommended for females aged 9–26, no recommendations for sot x x measles-rubella x   pneumococcal x x tetanus/diptheria x   varicella x   annual vaccination with inactivated intramuscular formulation recommended before and after sot livea virus, administer to patients who are seronegative, before transplant, or in women of childbearing age for prevention of congenital rubella syndrome 23-valent polysaccharide vaccine should be given once before transplant and boosters at 3 and 5 years after initial dose tdap booster indicated for < 65 years old (may be given ≤ 2 years after last tdap booster in sot patients) livea virus, administer to patients who are seronegative, before transplant tdap, tetanus, diphtheria, and pertussis. A all live vaccines are contraindicated post solid organ transplant (sot), as they can cause serious infection. Live vaccines. Bacillus calmette-guerin herpes zoster live intranasal attenuated influenza live oral typhoid measles-rubella vaccinia (smallpox) varicella production of vasodilatory prostaglandins. 40 however, one of the most easily recognized causes of posttransplant hypertension is the use of corticosteroids and cnis. Corticosteroids cause sodium and water retention, thus increasing blood pressure, whereas cnis reduce glomerular filtration rate and renal blood flow, increase systemic and intrarenal vascular resistance, promote sodium retention, reduce concentrations of systemic vasodilators (ie, prostacyclin, nitric oxide), and increase concentrations of thromboxanes. Compared with cyclosporine, tacrolimus displays significantly less severe hypertension, and patients taking tacrolimus require significantly fewer antihypertensive medications after transplant. 40 treatment controlling hypertension after transplant is essential in preventing cardiac morbidity and mortality and prolonging graft survival. The target blood pressure in transplant patient encounter part 3 identify your treatment goals for the patient in terms of antimicrobial prophylaxis. Create a plan for her antimicrobial prophylaxis, making sure to compare and contrast the pros and cons of the different agents in this patient. Recipients should be less than 130/80 mm hg. 40 this goal blood pressure may not be suitable for all patients. Note. National guidelines for treating hypertension in the general population are often followed, despite their lack of transplant recommendations. Refer to chapter 5, hypertension, for additional information. Lifestyle modifications to achieve a goal blood pressure, lifestyle modifications including diet, exercise, sodium restriction, and smoking cessation are recommended. 40 unfortunately, lifestyle modifications alone are often inadequate in high-risk populations, and antihypertensive medications are usually initiated early after transplant. 40 immunosuppressive regimen modification  because tacrolimus has shown the propensity to cause less severe hypertension compared to cyclosporine, conversion from cyclosporine-based immunosuppression to tacrolimus-based immunosuppression may be one way to reduce the severity of hypertension in transplant recipients. Conversion to a tor inhibitor or belatacept, which are not associated with hypertension, may also be an alternative to the cnis in patients with difficult-to-treat hypertension.

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Continue to be used to treat tremors in pd. T ey are not e ective against other motor symptoms and have an un avorable side e ect pro le, particularly in the elderly (con usion, hallucinations). T is class o medications have limited utility in the management o pd but can be considered or younger patients with medication-resistant tremor-predominant pd. Dyskinesia,23 although it may not be sustained. Amantadine is usually given at a starting dose o 100 mg twice daily, which can be titrated up to 400 mg total per day. Side e ects include livedo reticularis, leg swelling, con usion, and visual hallucinations. There ore, it has to be used with caution in elderly patients and those with pre-existing dementia. It should also be used with caution among patients with renal insuf ciency. Monoamine oxidase b inhibitors dopamine agonists anticholinergics medications such as trihexiphenydyl and benztropine t ese include selegiline, zydis selegiline and rasagiline. T ese are selective, irreversible monoamine oxidase (mao) type 2 inhibitors. T ey can be used or mild symptomatic monotherapy in early pd, and also used as an adjunct to levodopa in patients with motor uctuations. T ey were evaluated as possible neuroprotective agents, but studies have remained inconclusive or both selegiline and rasagiline.21,22 t e usual dose or selegiline is 5 mg in the morning and noon.

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35 (acidemia) ph > 7. 45 (alkalemia) paco2 > 45 mm hg hco−3 < 22 mmol/l paco2 < 35 mm hg hco−3 > 26 mmol/l respiratory acidosis metabolic acidosis respiratory alkalosis metabolic alkalosis figure 28–1. An algorithmic approach to acid–base disorders. Normal values. Ph 7. 35 to 7. 45, paco2 35 to 45 mm hg (4. 7–6. 0 kpa), hco3 – 22 to 26 meq/l (26 mmol/l), anion gap less than 12 meq/l (12 mmol/l). Note that paco2 should be in millimeters of mercury to use the equations in the figure. (cl–, chloride ion. Hco3 –, bicarbonate. Na+, sodium ion. Paco2, partial pressure of arterial carbon dioxide. ) step 2. Assess adequacy of compensation respiratory acidosis metabolic acidosis respiratory alkalosis expected paco2 = (1. 5 × hco−3 ) + 8 metabolic alkalosis expected paco2 = (0. 9 × hco−3 ) + 15 acute chronic acute chronic expected ∆hco−3 = (0. 1 × ∆paco2 ) expected ∆hco−3 = (0. 35 × ∆paco2 ) expected ∆hco−3 = (0. 2 × ∆paco2 ) expected ∆hco−3 = (0. 4 × ∆paco2 ) step 3. Calculate the anion gap anion gap = na+ − (cl− + hco−3) anion gap < 12. No anion gap metabolic acidosis anion gap 12 or more. Anion gap metabolic acidosis step 4.

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−2 parasomnias can, at times, be dif cult to di erentiate rom nocturnal seizures. Sleep walking and night terrors are typically noted among children during the rst hal o the night, but may persist into adulthood when they become dif cult to distinguish rom ictus. Rapid eye movement (rem) behavior disorder is associated with parkinson disease (pd). T e absence o paralysis during rem sleep allows the patient to “act out” patients were diagnosed as having seizures if the point score was ≥ 1, and diagnosed with syncope if the point score was < 1. Adapted with permission from sheldon r, rose s, ritchie d, et al. Historical criteria that distinguish syncope from seizures, j am coll cardiol 2002 jul 3;40(1):142-148. Epileps y his/her dreams with o en a violent and rightening tone. Epileptic seizures may have similar symptomatology, and video-eeg monitoring with emg may be necessary to rule out seizures. Variations in the level o vigilance during the day associated with a sleep disorder, such as sleep apnea or periodic limb movements, may have an abrupt onset. Patients typically have their eyes closed, and are easily arousable. In younger patients, the association with cataplexy and sleep paralysis may indicate narcolepsy. Partial seizures case 31-1 the patient is a 24-year-old woman ollowed up or 4 years by a psychiatrist or bipolar disorder and anxiety. She has been treated with lamotrigine or mood stabilization, and is taking alprazolam or anxiety attacks. A ter discussing her symptoms with a riend who was a physician, she decided to consult a neurologist. What elements in the history and the examination may point to seizures being the cause of these spells?.