Figure 113

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Natural Hypothyroidism Cure and Treatment

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Pathogenesis of dysnatremias. The countercurrent mechanism of the kidneys in concert with the hypothalamic osmoreceptors via antidiuretic hormone (ADH) secretion maintain a very finely tuned balance of water (H2O). A defect in the urine-diluting capacity with continued H2O intake results in hyponatremia. Conversely, a defect in urine concentration with inadequate H2O intake culminates in hypernatremia. Hyponatremia reflects a disturbance in homeostatic mechanisms characterized by excess total body H2O relative to total body sodium, and hypernatremia reflects a deficiency of total body H2O relative to total body sodium [11]. (From Halterman and Berl [12]; with permission.)

pseudohyponatremia, since, in most but not all situations, hypona-tremia reflects hypo-osmolality.

The nature of the solute plays an important role in determining whether or not there is an increase in measured osmolality or an actual increase in effective osmolality. Solutes that are permeable across cell membranes (eg, urea, methanol, ethanol, and ethylene glycol) do not cause water movement and cause hypertonicity without causing cell dehydration. Typical examples are an uremic patient with a high blood urea nitrogen value and an ethanol-intoxicated person. On the other hand, in a patient with diabetic ketoacidosis who is insulinopenic the glucose is not permeant across cell membranes and, by its presence in the extracellular fluid, causes water to move from the cells to extracellular space, thus leading to cell dehydration and lowering serum sodium. This can be viewed as translocational at the cellular level, as the serum sodium level does not reflect changes in total body water but rather movement of water from intracellular to extracellular space Glycine is used as an irrigant solution during transurethral resection of the prostate and in endometrial surgery. Pseudohypo-natremia occurs when the solid phase of plasma (usually 6% to 8%) is much increased by large increments of either lipids or proteins (eg, in hypertriglyceridemia or paraproteinemias).

X Reabsorption of sodium chloride in distal convoluted tubule Thiazide diuretics

HQO)

GFR diminished

Renal disease Congestive heart failure Cirrhosis

Nephrotic syndrome Volume depletion

X Reabsorption of sodium chloride in thick ascending limb of loop of Henle Loop diuretics Osmotic diuretics Interstitial disease

X Reabsorption of sodium chloride in thick ascending limb of loop of Henle Loop diuretics Osmotic diuretics Interstitial disease

-NaCl

T ADH release or action Drugs

Syndrome of inappropriate antidiuretic hormone secretion, etc.

Pathogenesis of hyponatremia. The normal components of the renal diluting mechanism are depicted in Figure 1-3. Hyponatremia results from disorders of this diluting capacity of the kidney in the following situations:

1. Intrarenal factors such as a diminished glomerular filtration rate (GFR), or an increase in proximal tubule fluid and sodium reabsorption, or both, which decrease distal delivery to the diluting segments of the nephron, as in volume depletion, congestive heart failure, cirrhosis, or nephrotic syndrome.

2. A defect in sodium chloride transport out of the water-impermeable segments of the nephrons (ie, in the thick ascending limb of the loop of Henle). This may occur in patients with interstitial renal disease and administration of thiazide or loop diuretics.

3. Continued secretion of antidiuretic hormone (ADH) despite the presence of serum hypo-osmolality mostly stimulated by nonosmotic mechanisms [12].

NaCl—sodium chloride.

Renal losses

Diuretic excess Mineralcorticoid deficiency Salt-losing deficiency Bicarbonaturia with renal tubal acidosis and metabolic alkalosis Ketonuria Osmotic diuresis

Assessment of volume status

Renal losses

Diuretic excess Mineralcorticoid deficiency Salt-losing deficiency Bicarbonaturia with renal tubal acidosis and metabolic alkalosis Ketonuria Osmotic diuresis

Assessment of volume status

Glucocorticoid deficiency

Hypothyroidism

Stress

Drugs

Syndrome of inappropriate antidiuretic hormone secretion

Glucocorticoid deficiency

Hypothyroidism

Stress

Drugs

Syndrome of inappropriate antidiuretic hormone secretion

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