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Peritonitis Pancreatitis Small bowel obstruction Rhabdomyolysis discount 200mg prometrium with visa, crush injury Bleeding into tissues Venous occlusion FIGURE 2-20 In volum e expansion discount prometrium 200 mg, total body sodium (N a) content is increased generic prometrium 100mg free shipping. In prim ary renal N a retention, volum e expansion is m odest and edem a does not develop because blood pressure increases until N a excretion m atches intake. In secondary N a retention, blood pres- sure m ay not increase sufficiently to increase urinary N a excretion until edem a develops. FIGURE 2-23 FIGURE 2-24 Clinical signs of volum e depletion. N ote that laboratory test results for volum e expansion and contraction are sim ilar. Serum sodium (N a) concentration m ay be increased or decreased in either volum e expansion or contraction, depending on the cause and intake of free water (see Chapter 1). Acid-base disturbances, such as m etabol- ic alkalosis, and hypokalem ia are com m on in both conditions. The sim ilarity of the lab- oratory test results of volum e depletion and expansion results from the fact that the “effective” arterial volum e is depleted in both states despite dram atic expansion of the extracellular fluid volum e in one. Unifying Hypothesis of Renal Sodium Excretion from a reduction in m ean arterial pressure M yocardial ↓ Extracellular (M AP). Som e disorders decrease cardiac dysfunction fluid volume output, such as congestive heart failure owing to m yocardial dysfunction; others – – High output decrease system ic vascular resistance, such AV fistula Cirrhosis Pregnancy failure as high-output cardiac failure, atriovenous – – fistulas, and cirrhosis. Because M AP is the – – product of system ic vascular resistance and cardiac output, all causes lead to the sam e Cardiac output × Systemic vascular resistance = M ean arterial pressure result. As shown in Figures 2-3 and 2-4, sm all changes in M AP lead to large changes + in urinary N a excretion. Although edem a- tous disorders usually are characterized as Sodium excretion resulting from contraction of the effective (pressure natriuresis) arterial volum e, the M AP, as a determ inant of renal perfusion pressure, m ay be the cru- cial variable (Figs. The m echanism s of edem a Sum m ary of m echanism s of sodium (N a) retention in volum e contraction and in depletion in nephrotic syndrom e are m ore com plex of the “effective” arterial volum e. In secondary N a retention, N a retention results prim arily and are discussed in Figures 2-36 to 2-39. Ascites A AVF B Cirrhosis FIGURE 2-26 Role of renal perfusion pressure in sodium (Na) retention. A, Results which experimental cirrhosis was induced in dogs by sporadic feeding from studies in rats that had undergone myocardial infarction (M I) or with dimethylnitrosamine. Three cirrhotic stages were identified based placement of an arteriovenous fistula (AVF). In the first, dietary Na intake was bal- large M Is were identified. Both small and large M Is induced signifi- anced by Na excretion. In the second, renal Na retention began, but cant Na retention when challenged with Na loads. Renal Na retention still without evidence of ascites or edema. In the last, ascites were occurred in the setting of mild hypotension. Because Na was retained before the appearance of ascites, cant Na retention, which was associated with a decrease in mean arte- “primary” renal Na retention was inferred. An alternative interpreta- rial pressure (M AP) [55,56]. Figure 2-3 has shown that Na excretion tion of these data suggests that the modest decrease in M AP is respon- decreases greatly for each mm Hg decrease in M AP. B, Results of two sible for Na retention in this model.

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Although usually short-lived discount 200 mg prometrium with amex, this phenom- Various metabolic and hormonal conditions can be responsi- enon is reported by patients to be a very frightening experi- ble for psychotic symptoms in children buy 100mg prometrium amex. Support purchase prometrium 100 mg without a prescription, reassurance, and ensuring safety at the time may include disorders of the adrenal, thyroid, or parathyroid are usually sufficient in the management of patients after glands. Exogenous metabolic disturbances leading to psy- anesthesia. MANAGEMENT AND TREATMENT Toxic Psychoses Assessment Toxic psychosis or delirium usually occurs secondary to bacte- rial or viral infections, high fevers, and exogenous toxins Effective treatment requires knowledge of the psychotic dis- including medications, illicit drugs, alcohol, and poison- orders, diagnostic criteria, symptoms, and longitudinal ings. Auditory hallucinations can also also addressing any comorbid disorders or biopsychosocial occur, but their content is qualitatively different from those stressors. The physician must prioritize symptoms and diag- experienced in childhood schizophrenia or mood disorders. Children and adolescents often question about delusions and hallucinations and whether describe the experience as 'losing their mind'—a frighten- the child endorses the psychotic symptoms only to please the ing concept, and they can become disoriented, unable to interviewer or to get attention. In addition, it is important to orient to person or place, or comprehend why they are be- determine whether the child acts on the basis of the delu- having in an unusual manner. They may also experience sional or hallucinatory perceptions—associated with an af- fluctuating levels of alertness. In children, infections (bacterial or viral) can cause en- The assessment of the child with psychotic symptoms cephalitis, meningitis, and human immunodeficiency vi- should include a careful, comprehensive, and thoughtful 620 Neuropsychopharmacology: The Fifth Generation of Progress evaluation. The assessment when the clinical picture is dominated by frank delusions should include a detailed evaluation of the symptom presen- and hallucinations and other positive symptoms such as a tation, course of illness, and phenomenology. A develop- formal thought disorder or strange and idiosyncratic behav- mental history of the child and a detailed family psychiatric iors. A positive family history, especially for an affec- to remit and dissipate. However, often there may still be tive disorder or schizophrenia because these disorders tend the presence of some psychotic symptoms, although they to run in families, often helps the clinician with the differen- are less disturbing to the child. In this phase, the child may tial diagnosis in the child. This will, in large part, determine tinue to subside, but the child continues to experience apa- the management and treatment of the child presenting with thy, lack of motivation, withdrawal, and restricted or flat psychosis. A thorough physical examination is essential, and affect. These may include imaging studies, an electroen- chronically impaired, despite what would be considered ad- cephalogram, toxicology screens, and renal and liver func- equate treatment. Usually, such impairment is characterized tion tests. Some children may require consultation with by persistent symptoms, which occur especially if the psy- other pediatric specialists. However, they can be helpful for intellectual assess- both the parents and the child. Interventions targeted at ment and to determine developmental delays, because these improving family functioning, problem solving, communi- deficits may influence the presentation or interpretation of cation skills, and relapse prevention have been shown to symptoms. Routine use of adaptive function measures is decrease relapse rates in adults (82). Children may benefit important for understanding actual function in social, daily from social skills training and may require specialized educa- living, and communication domains. These can be quite tional programs, academic adjustments, and support at helpful in planning and maintaining developmentally rele- school. Ongoing illness teaching and medication education, vant treatment goals. Similarly, speech and language evalua- are important to promote compliance with treatment and tions are often helpful, especially with a child who appears to help in coping with the daily and sometimes long-term to have linguistic impairments on examination. Every effort should be made for the child to be maintained in the least restrictive setting, such as home.

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Subsequently buy prometrium 100 mg amex, other researchers lieved to involve not only dopamine uptake blockade but reported a number of observations suggesting that PCP is also actions of PCP in the frontal cortex and consequent neurotoxic buy prometrium 100 mg free shipping. In particular buy 200 mg prometrium amex, following PCP administration, neuromodulatory effects of the frontal cortex on the basal vacuolization of neurons in hippocampal fields CA1 and ganglia (45). Actions at and opiate receptors are thought CA3 and the subiculum has been demonstrated (56). PCP to underlie the anesthetic effect of PCP, whereas actions at induces a microglial response and a 70-kilodalton heat shock serotonin receptors may underlie its hallucinogenic effects protein in cerebellar Purkinje cells (57); most recently, it (40). Notably, cross-tolerance occurs between PCP and the has been found that PCP induces apoptosis in striatopallidal classic hallucinogens LSD, mescaline, and psilocybin (46), cells in rats (58). The mechanisms for the actions of PCP at and PCP substitutes for LSD or mescaline in two-level drug these various anatomic sites are likely to differ, with cortical discrimination studies in rats. PCP also binds to two specific injury involving activity of cholinergic, GABAergic, and ad- PCP sites in the brain. One PCP receptor, located within renergic neuronal systems (59) and apoptotic changes ob- the NMDA receptor-gated ion channel, is stimulated by served in striatopallidal cells involving excess corticosteroids NMDA-receptor agonists such as L-glutamate and can be (58). Research is needed to determine whether PCP-in- modulated by a variety of modulatory agents, such as gly- duced neurotoxicity underlies the memory deficits seen in cine-like amino acids and polyamines (47). SUBSTITUTED AMPHETAMINES (MDMA, Behavioral Effects in Humans 'ECSTASY') Phencyclidine produces a mixture of stimulant, depressant, Chemistry anesthetic, and hallucinogenic effects, with the particular 3,4-Methylenedioxymethamphetamine bears structural presentation dependent, in part, on dosage. In particular, similarity to both the psychomotor stimulant amphetamine low doses are associated with anticholinergic symptoms (red and the hallucinogen mescaline. Of the two optical isomers and dry skin, nystagmus, amnesia, conceptual disorganiza- of MDMA, the dextrorotatory isomer exhibits more potent tion); moderate doses are more likely to be associated with central nervous system activity (60). In contrast, most po- opiate receptor activity (anesthesia, dreamlike states); at tent hallucinogenic amphetamines are more potent in their high doses, dopaminergic symptoms predominate (halluci- levorotatory forms (61). The aromatic methylenedioxy sub- nations, paranoia). However, this rule of thumb should not stituent of MDMA is similar to the substance found in oils be considered diagnostic. The mnemonic RED DANES of the natural products safrole and myristicin, once pro- was coined by Giannini and colleagues (48,49) to character- posed to be the intoxicants of sassafras and nutmeg (62). It is important to note that the toxic effects of PCP may persist for days because the half-life of PCP after Data from the most recent Monitoring the Future Study overdose may be as long as 3 days (50). For example, annual use of MDMA among college have reported persistent cognitive deficits in long-term PCP students rose from 2. Notably, figures from 1996 to or months after PCP ingestion have been reported. Olney and colleagues (55) were the first to report that single doses of PCP and related compounds (MK-801 and keta- Patterns of Use mine) lead to neurotoxic damage of neurons in layers III and IV of the posterior cingulate and retrosplenial cortex in At present, MDMA is used primarily for recreational pur- rats. These cells display abnormal cytoplasmic vacuolization poses, although some still advocate the use of MDMA for that is directly correlated with the potency of noncompeti- psychotherapeutic purposes (63). Initially, these were believed to be the most frequently reported use of MDMA has been in short-term changes, but higher doses of MK-801 were ob- the context of large, organized social events known as served to cause necrotic changes persisting at least 48 hours 'raves,' often held in warehouses or dance clubs. Festively 1550 Neuropsychopharmacology: The Fifth Generation of Progress dressed 'ravers' use MDMA as their drug of choice and than cocaine (79). In rats, MDMA lowers the electric typically dance through the night to music accompanied threshold for self-stimulation in the medial forebrain bundle by computer-generated videos and laser light shows. Thus, in three different behavioral paradigms, amount of MDMA typically used during raves varies widely, MDMA appears to have significant potential for abuse. Human Studies with MDMA Acute Neurochemical Effects As would be predicted from studies in animals, MDMA The most pronounced acute biochemical effect of MDMA exhibits both stimulant and hallucinogen-like activity. The is increased 5-HT neurotransmission, brought about by a stimulant effects of MDMA, typically noted shortly after calcium-independent release of 5-HT from nerve endings drug ingestion, include increased heart rate, increased blood (64). MDMA-induced 5-HT release involves both vesicular pressure, decreased appetite, increased alertness, and eu- and plasma membrane monoamine transporter (65).

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