BALANCE HIDROELECTROLITICO PDF

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Other natriuretic peptides Urodilatin: Anti-diuretic hormone, distal flow and potassium excretion Distal potassium excretion is stimulated by ADH. Additional mechanisms are, therefore, needed to correct the volume excess, through increased excretion of sodium and water. Osmoreceptors The osmoreceptors, located in the supraoptic nuclei of the hypothalamus, are stimulated by the presence of an osmotic gradient between their cytoplasm and the perfusing plasma, so that water transits out of or into the cells as serum osmolality rises or falls.

The ventricles and vascular smooth muscle cells have also been shown to produce ANP. Measured osmolality incorporates all solutes within the sample that are capable of generating an osmotic force.

Thirst Like ADH release, thirst can be stimulated independently by either hyperosmolality or hypovolaemia. Volume expansion is the sensor for sodium intake and results in increased sodium excretion. In the absence of ADH, these channels are cleared by endocytosis. Unlike other electrolytes, filtered magnesium is reabsorbed principally in the thick ascending limb of the loop of Henle, as opposed to the proximal tubule.

Changes in sodium balance lead to changes in plasma volume and are sensed principally through changes in the circulation. Anti-diuretic hormone ADH is a nine-amino-acid peptide that increases the permeability of the renal collecting ducts to water. It also stimulates thirst and ADH release.

The physiological role of the various natriuretic peptides is not known. Volume regulation is an essential requirement to maintain perfusion hidroelectrolutico tissues. The signal is relayed to the paraventricular nuclei of the hypothalamus, resulting in ADH release. However, hypovolaemia can generate much higher ADH levels. 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.

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The force that they generate balances capillary hydrostatic pressure and is known as the plasma oncotic pressure. As plasma potassium concentration increases, aldosterone secretion is stimulated in a linear fashion.

REGULACION DE FLUIDOS Y BALANCE HIDROELECTROLITICO

Cardiac failure Reduced cardiac output associated with cardiac failure elicits a response to a perceived reduction in effective circulating volume, through carotid, aortic and afferent arteriolar baroreceptors.

Send link to edit together this prezi using Prezi Hidroelectroljtico learn more: These systems must also be able to accommodate changes in salt intake. Check out this article to learn more or contact your system administrator.

New Engl J Med ; Invited audience members will follow you as you navigate and present People invited to a presentation do hidroelectrolitkco need a Prezi account This link expires 10 minutes after you close the presentation A maximum balanec 30 users can follow your presentation Learn more about this feature in our knowledge base article.

Volume regulation In contrast, volume regulation is brought about largely through changes in sodium excretion.

BALANCE HIDROELECTROLITICO PDF

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. Within the confined space of the skull, uncontrolled cerebral oedema results in seizures, coma and death. A discrepancy between the calculated and measured osmolalities indicates the presence of a solute that is not routinely measured e.

This is probably an important mechanism for avoidance of potassium accumulation when distal flow is low as a result of ADH-driven water reabsorption. Increased water intake driven by thirst, together with water preservation driven by ADH release, returns elevated osmolality to normal or, if it is volume driven, helps to correct volume depletion.

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Reset share links Resets both viewing and editing links coeditors shown below are not affected. The requirement for potassium secretion in order to reabsorb the greater part of the filtered load of magnesium might explain the severe potassium wasting that can occur in states of magnesium depletion. The converse occurs if sodium intake falls.

Natriuretic peptides Sodium loading results in an appropriate increase in sodium excretion. V1a receptors have a pressor effect on vascular smooth muscle cells, through activation of phosphoinositol. Salt loading expands the extracellular volume, decreasing renin secretion, whereas salt deprivation causes contraction of the extracellular volume, stimulating renin secretion.

Add a personal note: Conversely, low distal flow and less efficient clearance of secreted potassium within the lumen would be expected to produce a less favourable electrochemical gradient for continued potassium secretion. Control of anti-diuretic hormone release: There is, therefore, overall movement of water molecules into the solute-containing compartment osmosis.

Neither you, nor the coeditors you shared it with will be able to recover it again. These events concentrate the urine, conserving water and returning osmolality hidroelectroltiico normal.

It is, therefore, not surprising that the systems regulating sodium excretion are closely integrated with those regulating blood pressure. It is accompanied by anions, principally chloride and bicarbonate. It is in proportion to the increase in sodium intake. An antidiuretic mechanism not regulated by extracellular fluid tonicity.