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Others argue that genetic factors could be “switched on” by the hormonal changes and the particular stressors of puberty (Herpertz-Dahlman et al buy diovan 40 mg with visa 4 arteria aorta, 2011) buy diovan 40 mg free shipping blood pressure 11070. Pregnancy and perinatal complications, especially preterm birth, are risk factors. The evidence for childhood sexual abuse as an aetiological factor in AN is inconclusive (Wonderlich et al, 1997). Severe life events are found in a minority of those with onset before 25 years ant the majority of patients with onset after 25 years. Personality disorder is found in at least 70% of those with AN; obsessive- compulsive personality disorder is the most common. Personality traits are characteristic, and may represent risk factors, or an underpinning pathological process. Herpertz-Dahlmann et al (2011) describe patients as “usually good and successful”, however, often with “some peculiarities”. They describe rigidity and perfectionism, depression, anxiety. Interpersonal function may be reduced with non-assertive, submissive interpersonal style, poor theory of mind, and autistic traits, while Ahren et al (2011) found that these patients characteristically evaluate themselves by comparison with others. Patients with AN also appear to demonstrate diminished “interoceptive awareness”. Interoception includes a range of sensations beyond taste, including the perception of pain, temperature, itch, tickle, sensual touch, muscle tension, air hunger, stomach pH and intestinal tension. Integration of these provides a sense of the entire body and the self – provides a link between cognitive and affective processes and the current body state. Altered interoceptive awareness might be a precipitating and reinforcing factor in AN (Guardia et al, 2013). Alexithymia is the term applied to an impaired ability to identify and communicate emotions. A recent review indicated that when alexithymia is present in AN, the prognosis is less favourable (Pinna et al, 2015). Many such personality features improve with remission of the condition. However, tendency to negative emotional states, harm avoidance, perfectionism, desire for thinness and mild dietary preoccupation persist – suggesting these are underlying traits which contribute to the pathogenesis of AN (Kaye et al, 2009). At the same time, it must be remembered that such features are exaggerated by starvation (Keys et al, 1950). Evidence suggests that individuals with AN experience anxiety, that dietary restraint reduces this unpleasant state, and that eating stimulates dysphoric mood (Kaye et al, 2009). Others state that dieting counteracts feeling of worthlessness (Herpertz-Dahlmann et al, 2011). Socio-cultural factors have shaped “the modern cult of thinness” in Western societies. Evidence suggests a culture bound syndrome, as AN is rare in Asia and developing countries - although this pattern is probably changing (Jennings et al, 2006). Earlier reports found that the prevalence of AN was higher in higher socio-economic schools, but the evidence is now equivocal. Recent studies, however, indicate the risk for hospitalization for NA is related to mothers level of education (higher risk is associated with higher maternal education; Ahren et al, 2011). Perhaps such mothers are more demanding of their daughters. Maintaining factors Mentioned under etiology, the relief of anxiety by dieting and dysphoric mood caused by eating, may also serve as a maintaining factor. Starvation is another maintaining factor, inducing complex physiological and psychological reactions involving central and peripheral mechanisms. Such mechanism may have had evolutionary value, allowing animals to survive periods of food shortage, but in the current setting they serve only to perpetuate a vicious cycle of weight loss. Neuropsychological testing Neuropsychological testing reveals cognitive deficits (Weider et al, 2013) which are related to severity of the disorder, and may play a role in cause and outcome (Zakzanis et al, 2009). Executive control is impaired with problems in set-shifting, attention and decision-making (Treasure & Russell, 2011).

Neurons trusted 40mg diovan blood pressure medication and weight loss, of course diovan 80 mg free shipping arrhythmia newborn, FUNCTIONS must eventually reaccumulate K lost during activity using their Na pump, but only glial cells show net accumulation Ion Homeostasis of K (Fig. It is interesting to note that the neuronal One of the best-established functions of astrocytes is regula- Na pump is not sensitive to small increases in [K ] and o tion of brain [K ]. Astrocytes are also likely to participate is probably activated mainly by increases in intracellular o in the regulation of extracellular pH, but this aspect of astro- [Na ] (45). In fact, under conditions of diminished energy supply, glial cells actually contribute K to the ECS, rather than take it up (49). Transmitter Synthesis Glutamate is one of the most common amino acids in the brain, present at millimolar concentrations in brain tissue homogenate. It is also the predominant excitatory neuro- transmitter (50). Only a small fraction of total brain gluta- mate is packaged for synaptic release and astrocytes are inti- mately involved in the synthesis of this crucial vesicular pool of glutamate. Although glutamate can be derived from neuron glucose metabolism, carbon-labeling experiments reveal that astro- FIGURE 10. Schematic representation of mechanisms of K cyte-derived glutamine is the principal precursor of synapti- uptake in astrocytes. K released by firing neurons is actively cally released glutamate (51,52). The synthesis and release accumulated by astrocytes in three ways. The sodium pump and an anion transporter both take up K ; the sodium pump relies of glutamine by astrocytes is part of a biochemical shuttle directly on the availability of ATP, whereas the anion transporter mechanism called the glutamate-glutamine cycle (53) (Fig is indirectly powered by the energy stored in the transmembrane 10. After release from the presynaptic terminal, glutamate Na gradient. The presence of channels for Cl and K , allow Donnan forces to produce KCl influx. These mechanisms along is taken up primarily by astrocytes (54,55). In the glial cell, with K spatial buffering (seetext), prevent [K ] from exceeding glutamate is converted to glutamine through the ATP-de- o 12 mM. Increases in [K ] are seen during neural activity as [K ] i o pendent enzyme glutamine synthetase, located exclusively increases. In fact, glutamine synthetase is localized to astrocytic processes surrounding glutamatergic synapses The idea that focal increases in [K ] could be redistrib- o uted by glial cells was introduced by Kuffler and colleagues (46). They realized that the selective K permeability of glia coupled with their low-resistance intercellular connections (mediated by gap junctions), would permit them to trans- port K from focal areas of high [K ] , where a portion o of the glial network would be depolarized, to areas of normal [K ] , where the glial network would have a near normal o membrane potential (46). Experiments suggest that under conditions of focal increases in [K ] , five times as much o K moves by way of glial cells as through the ECS, except where only very localized K gradients are involved (25). A further specialization that contributes to spatial buffering is a nonuniform distribution of K channels on a single cell. Because the end-foot of the Muller¨ cell, which abuts the vitreous humor of the eye, has the highest density of K channels, accumulated [K ] is pref- FIGURE 10. Scheme showing how astrocytes are involved in o erentially transported to the vitreous, which acts as a dis- glutamate metabolism and uptake. Only astrocytes contain the enzyme glutamine synthetase, which converts glutamate to glu- posal site. It is not known if nonuniform K channel distri- tamine in an ATP-requiring reaction. Glutamine is transported to bution is a general feature of astrocytes. Finally, the released glutamate is recaptured o by astrocytes via a high affinity glutamate uptake system. Al- gray matter (to 60 to 80 mM) and white matter (to 12 though glutamate transporters are present in neurons, astrocytes to 15 mM in vitro) of the brain (27,47). The increases in are the most active in removing glutamate (see text). In the ab- sence of the normal transmembrane Na gradient, maintained [K ]o result because energy-dependent ion gradients can by the ATP-dependent Na pump, the glutamate transporter no longer be maintained and K entering the ECS can no ceases to remove glutamate and can run in reverse so that it longer be taken up by glial cells, which also depend on ATP pumps glutamate into the extracellular space (ECS). Glutamine is released by the glial cells and taken up sulfoximine produces a significant decrease in GABA pro- by the neurons through specific uptake carriers.