Pathophysiology
Hypoosmolar plasma: The pathologies decrease the osmolality of plasma
Psychogenic polydipsia: This is a psychiatric condition characterized by self-induced water intoxication. There are 3 phases to the disease process. First, there is a polyuria and polydipsia phase in which the patient is thirsty and has excessive urine output. The second phase appears hyponatremia in the blood as the kidney cannot excrete all the water, resulting in hypo-osmolar plasma. The final phase consists of the sequelae from water intoxication and hyponatremia, including delirium, ataxia, seizures, nausea, and vomiting. Death may result if the electrolyte abnormalities are not corrected promptly. One must be aware that central pontine myelinolysis is a deadly sequelae of quick sodium correction.[9]
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Syndrome of inappropriate ADH (SIADH): This condition occurs when the human body produces and secretes an excessive amount of ADH via CNS tumors, lung cancers, and medications, resulting in the kidneys reabsorbing too much water and manifests as a dilutional hypoosmolar plasma and hypertension. Treatment can involve vasopressin receptor blockers such as tolvaptan, removing cancer, creating the ADH, removing the medications inducing SIADH, and therapy with hypertonic saline.[10]
Nephrotic syndrome: This general term describes disease processes that result in proteinuria (over 3 g/d), accompanied by hypoalbuminemia, hypertriglyceridemia, and a hypercoagulable state. The characteristic proteinuria occurs when there is damage to the glomerular basement membrane or podocyte foot processes, which results in decreased plasma osmolality and oncotic pressure. Edema is frequently a presenting sign because there is insufficient oncotic pressure to draw water into the vasculature from the extracellular matrix.[11]
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Liver cirrhosis: Albumin production occurs in the liver and is then secreted out of the hepatocytes and into the extravascular space and then returned to the blood via lymphatic drainage and directly released into a blood vessel, the space of Disse. When the liver incurs damage, it cannot produce albumin, resulting in a hypoosmolar plasma.[12]
Diabetes Insipidous (DI): This disease demonstrates excretion of a large volume of urine, which results in concentrated, hyperosmolar plasma (greater than 300 mOsm/liter) and dilute, hypoosmolar urine (less than 300mOsm/liter). It can result from central damage to the neurons, which are responsible for the creation of ADH. Examples of sources of damage include infarcts, germinomas, Langerhans histiocytosis, and sarcoidosis. Another cause for DI is end-organ resistance. Although ADH is present, the patient has a genetic mutation in the vasopressin receptors, which renders the hormone ineffective.[13]
Dehydration: see above.
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