sprint123
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SIADH--->Increased ECF--->Sensed by atrium-->Secretes ANF-->Natriuretic effect--->Normovolemic--->No edema
I am not sure about the lymphedema..?
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| Medusin
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Thats right sprint123...
We must remember that the diagnosis of SIADH must only be considered if the five cardinal features are met:
1. hypotonic hyponatremia
2. Natriuresis
3. Urine osmolality in excess of plasma osmolality
4. Absence of edema and volume depletion
5. Normal renal and adrenal function
We must remember that edema does not become clinically evident untils the interstistitial volume has been increased by 2.5 to 3 L. In SIADH there is a moderate increase in the extracelular volume due to water retention but sodium excretion is normal. The mechanism of natriuresis is complex and involves increased glomerular filtration; pressure natriuresis, and natriuretic factors, especially atrial natriuretic peptide (as you pointed out) and brain natriuretic peptide.
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| Medusin
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Therefore the ECF might be normal or a litle expanded but not enough to become clinically evident edema.
Agree?
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| Medusin
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Anyone want to try the pathophyis for the absence of pitting edema in Lymphedema?
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| Medusin
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In lymphedema, the lymphatic transport capacity is reduced. This causes the normal volume of interstitial fluid formation to exceed the rate of lymphatic return, resulting in the stagnation of high molecular weight proteins in the interstitium. It usually occurs after flow has been reduced by 80% or more. The result, as compared to other forms of edema that have much lower concentrations of protein, is high-protein edema, or lymphedema, with protein concentrations of 1.0-5.5 g/mL. This high oncotic pressure in the interstitium favors the accumulation of additional water.
Accumulation of interstitial fluid leads to massive dilatation of the remaining outflow tracts and valvular incompetence that causes reversal of flow from subcutaneous tissues into the dermal plexus. The lymphatic walls undergo fibrosis, and fibrinoid thrombi accumulate within the lumen, obliterating much of the remaining lymph channels. Spontaneous lymphovenous shunts may form. Lymph nodes harden and shrink, losing their normal architecture.
In the interstitium, protein and fluid accumulation initiates a marked inflammatory reaction. Macrophage activity is increased, resulting in destruction of elastic fibers and production of fibrosclerotic tissue. Fibroblasts migrate into the interstitium and deposit collagen. The result of this inflammatory reaction is a change from the initial pitting edema to the brawny nonpitting edema characteristic of lymphedema. Consequently, local immunologic surveillance is suppressed, and chronic infections, as well as malignant degeneration to lymphangiosarcoma, may occur.
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| rock
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hmm...good discussion.
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