BALANCE HIDROELECTROLITICO PDF
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It is, therefore, appropriate that thirst tends to be satisfied quickly by consumption of water but recurs in bursts. Thirst is also stimulated. Other natriuretic peptides Hiddroelectrolitico Osmoreceptors and the hypothalamo-pituitary tract, which regulates secretion of anti-diuretic hormone Paraventricular neurones Third ventricle Supraoptic neurone Optic chiasm Anterior hypophyseal artery Portal venous system Hidroelectroljtico pituitary Posterior pituitary Systemic venous drainage Anti-diuretic hormone, synthesized in the supraoptic osmoregulatory and paraventricular volume-sensitive nuclei adjacent to the third ventricle, is transported along axons and secreted in the posterior pituitary, the portal venous system and into the cerebrospinal fluid Figure 2 Changes in plasma anti-diuretic hormone Changes in plasma anti-diuretic hormone ADH with increasing plasma osmolality a and volume depletion b.
Actions of aldosterone Aldosterone acts on the principal cells of the cortical collecting tubule in the distal nephron. See more popular or the latest prezis.
A randomized clinical trial. Water is able to pass freely between these compartments and the distribution of water is therefore determined by osmotic pressure. Present to your audience.
Calculated and measured osmolality In normal circumstances, plasma osmolality can be derived from the concentrations of the three principal solutes as follows: Regulation of salt balance and effective circulating volume Sodium is the principal solute acting to preserve water within the extracellular compartment.
The response to ADH can take several hours to restore normality.
ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus, and then migrates along the axons of these neurones into the posterior pituitary Figure 2. In the absence of ADH, these channels are cleared by endocytosis. Neither balanve, nor the coeditors you shared it with will be able to recover it again.
It might be responsible for the cerebral salt wasting sometimes seen after severe neurological damage. After reading this article, you should be able to: Conversely, rapid development of severe hypernatraemia causes cells balancee shrink with potential for permanent neurological damage. However, sodium is able to move freely across the capillary walls.
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Actions of atrial natriuretic peptide The physiological role of ANP is not well understood. ADH also stimulates distal tubular potassium excretion. Clinical physiology of acid-base and electrolyte disorders, 5th edn. This parameter effectively represents the volume which is perfusing the tissues. Total body water and extracellular volume are dependent on total body sodium. If this were not the case, the thirst stimulus would persist for some hours, resulting in excess water consumption.
Activation of V2 receptors on the basolateral membrane of principal cells triggers cyclic adenosine monophosphate, causing activation of a protein kinase and insertion of water channels aquaporin-CD into the luminal membrane, which is otherwise impermeable to water.
Balacne documents to beautiful publications and share them worldwide. The RAS plays a central role in regulation of salt excretion and thus in maintenance of extracellular fluid volume. It bwlance the permeability of the luminal membrane to sodium, thereby increasing passive diffusion of sodium into the cells. Baroreceptors do not sense volume directly; rather, they sense pressure, through stretch.
Renin secretion is also stimulated whenever effective circulating volume falls, and is suppressed when it is restored.
It is not surprising that the osmoreceptors controlling ADH release are highly sensitive; this is because maintenance of plasma osmolality within a small range is essential to preserve cell volume and thus normal function. RAS activation and ADH release result in salt and water retention with the objective of restoring a perceived volume deficit, although the result is salt and water overload and sometimes hyponatraemia dilutional effect.
REGULACION DE FLUIDOS Y BALANCE HIDROELECTROLITICO
A discrepancy between the calculated and measured osmolalities indicates the presence of a solute that is not routinely measured e. Increased water intake driven by thirst, together with water preservation driven by ADH release, returns elevated osmolality to normal or, if bslance is volume driven, helps to correct volume depletion. Electroneutrality is preserved either by passive reabsorption of chloride or by secretion of potassium into the tubular lumen.
Experimental evidence indicates that ANP effects an increase in sodium and water excretion by increasing GFR and decreasing sodium absorption in both balancee proximal and distal nephron segments.
Conversely, volume depletion stimulates RAS activity and aldosterone in order to increase sodium and water retention, but aldosterone-driven potassium secretion might be expected to cause potassium depletion. Thirst Like ADH release, thirst can be stimulated independently by either hyperosmolality or hypovolaemia. The requirement for potassium secretion in order to reabsorb the greater part of the filtered load of magnesium might explain hidroelsctrolitico severe potassium wasting that can occur in states of magnesium depletion.
The responses to the perceived reduction in effective circulating volume tend to increase the already expanded extracellular volume, exacerbating ascites and generating hyponatraemia through ADH Table 2. Present to your audience Start hidroelectrklitico presentation. Although plasma osmolality is determined principally by plasma sodium concentration, osmolality is regulated by changes in water balance that bring about dilution or concentration of solute.