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N O — nitric oxide; PGI2 ↓ Systemic PDGF— platelet-derived growth factor; PGI2— prostacyclin 2 telmisartan 40 mg without prescription fetal arrhythmia 32 weeks. NO ↓ vasoplasm Thrombin ↑ Endothelin ↑ M itogenic factors↑ (eg discount telmisartan 20mg with mastercard arrhythmia treatment algorithm, PDGF) ↓ Organ flow Intravascular coagulation Kidney Disease and Hypertension in Pregnancy 10 generic telmisartan 20mg otc pulse pressure meaning. Preeclam psia is a m ultisystem maternal disorder order telmisartan with american express heart attack or gas, with dramatic alterations in heart, kidney, circulation, liver, and brain. Interestingly, all of these abnorm alities resolve within a few weeks of delivery. A ↓ Plasma renin Finally, sodium retention NO/PGl S1 ↓ Aldosterone 2 Endothelin owing to renal vasocon- Relaxation Contraction striction m ay further Antiproliferation Proliferation ↑ Sympathetic nervous system S2 increase blood pressure. TX ET cAM P— cyclic adenosine Vascular smooth cGM P/cAM P muscle cells monophosphate; cGM P— cyclic guanosine monophosphate; 5-HT— serotonin; PThr— parathyroid hormone; FIGURE 10-32 S2— serotonergic receptors; H ypertension in preeclam psia. Although the m echanism of the increased blood pressure in preeclampsia is Thr— thombin TX— not established, evidence suggests it may involve multiple processes. A possible scenario involves the following: thromboxane; TXA — 2 decreased placental production of estrogen and progesterone, both of which have hem odynam ic effects; thromboxane A2. These processes m ay then result in alterations in platelet– vascular and Dubey; endothelial cell function, with decrease in vasodilators such as nitric oxide and prostacyclin and increased production with permission. O n light m icroscopy, the glom eruli from preeclam p- quences of glom erular endotheliosis and of the horm onal alter- tic wom en are characterized by swelling of the endothelial and ations in preeclam psia are sum m arized in this schem atic diagram m esangial cells. This swelling results in obliteration of the capillary of the nephron in preeclam psia. Suppression of the renin- lum ina, giving the appearance of a bloodless glom erulus. O n occa- angiotensin system occurs, probably in response to vasoconstric- sion, the m esangium , severely affected, m ay expand. The glom erular lesion leads to and fibrinlike m aterial and foam cells m ay be present, and epithe- proteinuria, which m ay be heavy. Renal hem odynam ic changes lial crescents have been described in rare instances. Decreased sodium and uric acid excre- tion m ay be caused by increased proxim al tubular reabsorption. The m echanism for the m arked hypocalciuria is not known. Investigators have sought m ethods to prevent preeclam psia (eg, salt restriction, prophylactic diuretics, and high-protein Smaller studies 11 10/319 50/284 (<200 women) (3. O ne approach that has been exten- sively investigated in the last 10 years is Larger studies: therapy with low-dose aspirin. It was EPHREDA (1990) 5/156 8/74 hypothesized that such therapy reversed the Hauth (1993) 5/303 17/303 im balance between prostacyclin and throm - Italian (1993) 12/565 9/477 Sibai (1993) 69/1570 94/1565 boxane that m ay be responsible for som e of Viinikka (1993) 9/103) 11/105) the m anifestations of the disease. Several CLASP (1994) 313/4659 352/4650 large trials now have been com pleted, and Odds ratio m ost have had negative results. Shown here All larger trials 6 413/7356 491/7174 Overall results is an overview of the effects of aspirin on 25% SD 6 proteinuric preeclam psia reported from all All trials 17 423/7675 541/7458 odds reduction (5. O dds ratios (area proportional therapy therapy to am ount of inform ation contributed) and better worse 99% confidence interval (CI) are plotted for various trials. A black square to the left of the solid vertical line suggests a benefit (how- ever, this indication is significant at 2p >0. Another preventive strategy Study that has been extensively investigated, with M arya et al. The rationale for this approach is Lopez-Jaramillo et al. A recent meta-analysis of 14 trials of calcium supple- 0. In contrast, a large randomized trial of calcium supple- mentation in 4589 low-risk women failed to demonstrate a benefit of calcium therapy. Close surveillance is best accom plished in the hospital in all but the m ildest cases. Close monitoring of maternal and fetal conditions M aternal hypertension should be treated to avoid cerebrovascular and cardiovascular Hospitalization in most cases com plications. M agnesium sulfate is the treatm ent of choice for seizure prophylaxis and usually is instituted im m ediately after delivery. W hen the fetus is m ature, delivery is indi- Lower blood pressure for maternal safety cated in all cases. W hen the fetus is im m ature, the decision to deliver is m ade after careful- Seizure prophylaxis with magnesium sulfate ly assessing both the m aternal and fetal condition. W hen m aternal health is in jeopardy, Timely delivery delivery is necessary, even with a prem ature fetus. FIGURE 10-38 ANTIHYPERTENSIVE THERAPY Som e controversy exists regarding when to institute antihypertensive therapy in wom en IN PREECLAM PSIA with preeclam psia. The basis for this controversy is that decreased uteroplacental perfusion is believed to be im portant in the pathophysiology of this disorder, and concern exists that lowering m aternal blood pressure m ay com prom ise uteroplacental blood flow and lead to Decreased uteroplacental blood flow and placental fetal distress. Furtherm ore, lowering m aternal blood pressure does not cure preeclam psia. Lowering blood pressure does not prevent or cure For m ost physicians, this treatm ent threshold is at approxim ately 150/100 m m H g. Lowering blood pressure is appropriate for maternal safety: maintain blood pressure at 130–150/85–100 mm Hg. FIGURE 10-39 ANTIHYPERTENSIVE THERAPY IN PREECLAM PSIA W hen blood pressure increases acutely and delivery is likely within the next 24 hours, use of a parenteral antihypertensive agent is preferable. Intravenous hydralazine or labetalol are acceptable Imminent delivery Delivery postponed agents for pregnant wom en, and both have been used successfully in preeclam psia. Calcium channel blockers should be used with Hydralazine (intravenous, intramuscular) Methyldopa caution because they m ay act synergistically with m agnesium sul- Labetalol (intravenous) Labetalol, other blockers fate, resulting in precipitous decreases in blood pressure. Rarely, Calcium channel blockers Calcium channel blockers agents such as diazoxide m ay be needed; however, when hyperten- Diazoxide (intravenous) Hydralazine sion is severe, m aternal safety takes priority over pregnancy status. M ethyldopa is one of the safest drugs in preg- nancy and has been used extensively with excellent m aternal and fetal outcom e. Labetalol and other blockers have been used suc- cessfully in preeclam psia. Calcium channel blockers also m ay be used as either second- or third-line agents. Lim ited experience exists with blockers or cloni- dine, although anecdotal reports suggest these agents are safe. W om en with preexisting or chronic hypertension Diastolic BP, mm Hg during pregnancy have a favorable prognosis, unless preeclam psia <90 90–100 ≥ 100 develops.

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Long term follow-up of therapy in the short-term treatment of anorexia nervosa order telmisartan overnight delivery heart attack ekg. Neuroleptics in the short-term treatment of vosa in women with obsessive compulsive disorder 80 mg telmisartan mastercard prehypertension at 20. Int J Eating anorexia nervosa: a double-blind purchase cheapest telmisartan and telmisartan blood pressure medication cialis, placebo controlled study with Dis 1986;5:1069–1075 order telmisartan without a prescription blood pressure medication used for opiate withdrawal. J Clin Psy- activity in anorexia nervosa after long-term weight restoration. Obsessive-compulsive disorder: psychobiologi- treatment of anorexia nervosa. Int J Eating Dis 2000;27(3): cal approaches to diagnosis, treatment, and pathophysiology. Antiserotonin-antihista- 9-tetrahydrocannabinol in primary anorexia nervosa. J Pharmacol Exp Ther 1961; chopharmacol 1983;3:165–171. Cyproheptatadine in an- crossover study of oral clonidine in acute anorexia nervosa. Biol Psychiatry 2001;49(7): cisapride accelerates delayed gastric emptying and increases antral 644–652. Does fluoxetine augment the Garner DM, Garfinkel PE, eds. Diagnostic issues in anorexia ner- inpatient treatment of anorexia nervosa? Effects of carbohydrate depressive illness: a review of 11 studies. Comp Psychiatry 1988; and protein meals on plasma large neutral amino acids, glucose 29:427–432. Am J Psychol weight subjects normalize after weight gain. Amitriptyline in the increases serotonin transporter (SERT) binding sites and SERT treatment of anorexia nervosa: a double-blind placebo-controlled mRNA expression in discrete regions of female rat brain. In: Schatz- trial of lithium carbonate in primary anorexia nervosa. Washington, monoamine metabolism in anorexia nervosa. Arch Gen Psychiatry DC: American Psychiatric Press, 1993:49–70. Personality and symptomatological features in young, 68. Relationship of depres- nonchronic anorexia nervosa patients. J Psychosom Res 1980;24: sion, anxiety, and obsessionality to state of illness in anorexia 353–359. Practice guideline for the treat- ship of eating disorders to major affective disorder. Psychiatry Res ment of patients with eating disorders (revision). Chapter 116: Psychopharmacology of Eating Disorders 1683 70. Intensive nutritional bulimia nervosa, and binge eating. In: Bloom FE, Kupfer DJ, counseling in bulimia nervosa: a role for supplementation with eds. Psychopharmacology: the fourth generation of progress. Flouxetine Bulimia Nervosa Collaborative Study Group. Fluoxe- pharmacological treatments of bulimia nervosa: predictors and tine in the treatment of bulimia nervosa: a multicenter, placebo- processes of change. A double-blind, placebo- treatment of bulimia nervosa. Pharmacologic and treatment of obese binge eaters and non-binge eaters. Am J Psy- cognitive-behavioral treatment for bulimia nervosa: a controlled chiatry 1990;147:876–881. Comparison of cognitive- tricyclic antidepressant and opiate antagonist on binge-eating in behavior therapy and desipramine in the treatment of bulimia normoweight bulimic and obese, binge-eating subjects. Fluvoxamine in controlled trial of fluoxetine and cognitive behavioral therapy for the treatment of binge-eating disorder: a multicenter placebo- bulimia nervosa: short-term outcome. Behav Res Ther 1997;9: controlled, double-blind trial. LECKMAN to conceptualize tics in TS as 'movement-equivalents' of Each movement is preceded by certain preliminary sensory obsessions and compulsions, and the apparent connections signals and is in turn followed by sensory impressions at the with OCD and attention-deficit/hyperactivity disorder end of the action. Each movement is the result of a voluntary capitulation to a demanding and relentless urge accompanied (ADHD) raise hope that by solving the TS 'model,' we by an extraordinarily subtle sensation that provokes and fuels will understand a family of disorders that collectively affects the urge. Successively sharper movements build up to a cli- close to 10% of the population. By all accounts, the TS max—a climax that never comes (1). Al- though we still lack clear answers for many of the complex questions raised by this syndrome, this chapter reviews the A MODEL NEUROPSYCHIATRIC DISORDER current state of progress in understanding the clinical fea- tures and neurobiology of TS and related tic disorders. Biological models allow investigators to extrapolate from simple to complex systems, to generate and test hypotheses, and to grasp schema that are within range of our intellect, TICS: MOTOR, PHONIC, AND BEYOND as we reach to conceptualize things beyond this range. Tourette syndrome (TS) is a 'model neuropsychiatric disor- The DSM-IV describes tics as 'sudden, rapid, recurrent, der' (2,3) that seems tantalizing in its simplicity. The ge- nonrhythmic, stereotyped movements or vocalizations,' but netic basis is stronger than any common neuropsychiatric the self-assessments by Dr. Joseph Bliss (quoted earlier) and disorder other than Huntington disease. The age of onset others (4) make it clear that tics in TS have a depth and and the sex distribution of TS are strong clues that neurode- dimension far beyond their motor or vocal components. Tics can be characterized by their anatomic location, fre- Emerging evidence suggests a role of epigenetic (e. The clinical sounds by the expulsion of air through the upper airways. These may include blinking, facial grimacing, studied and best understood in the neuropsychiatric litera- mouth movements, head jerks, shoulder shrugs, and arm ture.

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Patients dem on- strating m ore than 75% stenosis of a renal artery are at highest risk for progression to com plete occlusion buy telmisartan 20mg free shipping arteria auricular posterior. RENOVASCULAR DISEASE Clinical clues to the high-risk patient are sim ilar to the clinical presentations of ischemic renal disease shown in Figure 3-25 80mg telmisartan visa prehypertension 38 weeks. Nearly 75% of adults with a unilateral sm all kidney have sustained this renal atrophy due to large vessel occlusive disease from atherosclerosis telmisartan 20 mg with mastercard hypertension and exercise. Generalized atherosclerosis obliterans O ne third of these patients with a unilateral sm all kidney have Presumed renovascular hypertension high-grade stenosis of the artery involving the contralateral normal- Unilateral small kidney sized kidney buy 20mg telmisartan with mastercard hypertension 38 weeks pregnant. Flash pulm onary edem a is another clue to bilateral Unexplained azotemia renovascular disease or high-grade stenosis involving a solitary Deterioration in renal function with BP reduction and/or ACE inhibitor therapy functioning kidney. These patients, usually hypertensive and with Flash pulmonary edema docum ented coronary artery disease and underlying hypertensive heart disease, present with the abrupt onset of pulm onary edem a. Left ventricular ejection fractions in these patients are not seriously im paired. Flash pulm onary edem a is associated with atherosclerotic FIGURE 3-28 renal artery disease and may occur with or without severe hypertension. Clinical clues to bilateral atherosclerotic renovascular disease. Renal revascularization to preserve kidney function or to prevent The patient at highest risk for developing renal insufficiency from life-threatening flash pulmonary edema may be considered in patients renal artery stenosis (ischem ic nephropathy) has sufficient arterial with high-grade arterial stenosis to a solitary kidney or high-grade stenosis to threaten the entire renal functioning m ass. Pecutaneous translum inal renal risk patients have high-grade (m ore than 75% ) arterial stenosis angioplasty (PTRA), renal artery stenting, or surgical renal revascu- to a solitary functioning kidney or high-grade (m ore than 75% ) larization m ay be em ployed. Patients with chronic total renal artery bilateral renal artery stenosis. Patients with two functioning occlusion bilaterally or in a solitary functioning kidney are candidates kidneys with only unilateral renal artery stenosis are not at for surgical renal revascularization, but are not candidates (from a significant risk for developing renal insufficiency because the technical standpoint) for PTRA or renal artery stents. Clinical clues suggesting PREDICTORS OF KIDNEY SALVAGEABILITY renal viability include 1) kidney size greater than 9 cm (pole-to- pole length) by lam inography (tom ography); 2) som e function of the kidney on either urogram or renal flow scan; 3) filling of distal renal arteries (by collaterals) angiographically, when the Kidney size >9 cm (laminography) m ain renal artery is totally occluded proxim ally (see Fig. Patients with m oderately severe Glomerular histology on renal biopsy azotem ia, eg, serum creatinine m ore than 3-4 m g/dL, are likely to have severe renal parenchym al scarring (see Fig. Exceptions to this observation are cases of FIGURE 3-29 total m ain renal artery occlusion wherein kidney viability is Predictors of kidney salvageability. In evaluating patients as m aintained via collateral circulation (see Figure 3-30). A kidney candidates for renal revascularization to preserve or im prove biopsy m ay guide subsequent decision m aking regarding renal renal function, som e determ ination should be m ade of the revascularization for the goal of im proving kidney function. FIGURE 3-30 This abdom inal aortogram reveals com - plete occlusion of the left m ain renal artery (panel A) with filling of the distal renal artery branches from collateral supply on delayed film s (panel B). The observation of collateral circulation when the m ain renal artery is totally occluded proxim ally suggests viable renal parenchym a. The biopsy in a patient with severe bilateral renal artery stenosis and a serum shows hypoperfused retracted glomeruli consistent with ischemia. The biopsy dem onstrates glom erular scle- There is no evidence of active glomerular proliferation or glomerular rosis, tubular atrophy, and interstitial fibrosis. Note intact tubular basement membranes and negligible glom erular and interstitial scarring predict irreversible loss of kidney interstitial scarring. Left renal revascularization resulted in recovery viability. This abdominal aortogram demonstrates a ragged aorta, total occlusion of the right main renal artery, and subtotal occlusion of the proximal left main renal artery. Such patients are at high-risk for atheroembolic renal disease following aortography, selective renal arteriography, pecutaneous transluminal renal angioplasty, renal artery stenting, or surgical renal revascularization. FIGURE 3-34 (see Color Plate) “Purple toe” syndrom e reflecting peripheral atheroem bolic disease in the patient in Figure 3-33 (ragged aorta), following an abdom inal aortogram. M icroem boli of atherom atous m aterial are readily identified by the characteristic appearance of cholesterol crystal inclusions that appear in a biconvex needle-shaped form. In routine paraffin-em bedded histologic sections, the cholesterol is not seen because the m ethods used in preparing sections dissolve the crystals; the characteristic biconvex clefts in the glom eruli (or blood vessels) persist, allowing easy identification. Several patterns of renal failure in patients with AERD are recognized: 1) insult (eg, abdom inal aortogram ) leads to end-stage renal disease (ESRD) over weeks to m onths; 2) insult leads to chronic stable renal insufficiency; 3) m ultiple insults (repeated angiographic procedures) lead to a step-wise rise in serum creatinine eventuating in end-stage renal failure; and 4) insult leading to ESRD over several weeks to m onths with recovery of som e renal function allowing for discontinuance of dialysis. FIGURE 3-36 Renal biopsy dem onstrating severe arteriolar nephrosclerosis. Arteriolar nephrosclerosis is intimately associated with hypertension. The histology of the kidney in arteriolar nephrosclerosis shows considerable variation in intensity and extent of the arteriolar lesions. Thickening of the vessel wall, edem a of the sm ooth m uscle cells, hypertrophy of the sm ooth m uscle cells, and hyaline degenera- tion of the vessel wall m ay be apparent depending on the severity of the nephrosclerosis. In addition to the vascular lesions of arteriolar nephrosclerosis there are abnorm alities of glom eruli, tubules, and interstitial areas that are believed to be secondary to the ischem ia that results from arteriolar insufficiency. Arteriolar nephrosclerosis is observed in patients with longstanding hypertension; the m ore severe the hypertension, the more severe the arteriolar nephrosclerosis. Arteriolar nephrosclerosis m ay also be seen in elderly norm otensive individuals and is frequently observed in elderly patients with gener- alized atherosclerosis or essential hypertension. FIGURE 3-37 Schematic representation of ischemic nephropathy. Patients with atherosclerotic renal artery Atherosclerosis Nephrosclerosis disease (ASO-RAD) often have coexisting renal parenchymal disease with varying degrees of nephrosclerosis (small vessel disease) or atheroembolic renal disease. W hether or not the renal insufficiency is solely attributable to renal artery stenosis, nephrosclerosis, or atheroembolic renal disease is difficult to determine. The term “ischemic nephropathy” is more complex than being simply due to atherosclerotic renal artery stenosis. In addition, in the azotemic patient with ASO- Atheroembolism RAD, one should exclude other potential or contributing causes of renal insufficiency such as obstructive uropathy, primary glomerular disease (suggested by heavy proteinuria), drug-related renal insufficiency (eg, nonsteroidal anti-inflammatory drugs), and uncontrolled blood pressure. Renovascular Hypertension and Ischemic Nephropathy 3. Atherosclerotic renal artery disease (ASO- 11% Other RAD) has been claimed to contribute to the ESRD population. This diagram from the US Renal Data System Coordinating Center 1994 report indicates that 29% of calendar year 12% 1991 incident patients entered ESRD programs because of “hypertension (HBP). Crude estimates of the percentage of patients entering DM ESRD programs because of ASO-RAD range from 1. Precise bases for making 5% these estimates are both unclear and confounded by the high likelihood of coexisting arterio- Urology 29% lar nephrosclerosis, type II diabetic nephropathy, and atheroembolic renal disease. ASO-RAD High blood as a major contributor to the ESRD population is probably small on a percentage basis, occu- 3% pressure Cyst pying some portion of the ESRD diagnosis “hypertension (HBP). Treatment of Renovascular Hypertension and Ischemic Nephropathy FIGURE 3-39 TREATM ENT OPTIONS FOR RENOVASCULAR Treatment options for renovascular hypertension and ischemic HYPERTENSION AND ISCHEM IC NEPHROPATHY nephropathy.