Anti-Diuretic Hormone PhysiologyOverviewAnti-diuretic hormone, or ADH for short, is also called "arginine vasopressin" (AVP), or, simply, vasopressin. Responsible for regulating body water and blood pressure. - Review of body water osmotic, hyperosmotic, and hypoosmotic states, and the role of blood volume in determining blood pressure.ADH assists aldosterone during hemorrhage or other hypovolemic states – it does this by raising the intravascular volume to maintain tissue perfusion. - Thus, ADH is given during hypotensive crisis. Key pathologies of ADH include: - Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH), which occurs when ADH is excessively secreted. - Diabetes insipidus, when there is too little secretion of or reaction to ADH. Anti-Diuretic Hormone PhysiologyFirst, we show the hypothalamus and pituitary and that the anterior pituitary gland comprises clusters of hormone-producing cells. The posterior pituitary comprises neural tissue.ADH pro-hormones are produced in the supraoptic and paraventricular nuclei of the hypothalamus; on their way to the posterior pituitary, these prohormones are converted to ADH. From there, ADH is secreted into the blood stream and travels to its targets.Unlike anterior pituitary hormones, the posterior pituitary hormones are not stored until needed; instead, stimulation of the hypothalamic centers triggers their production and secretion on demand.Two triggers for ADH release: - ADH is released in response to minute increases in plasma osmolality (so, above ~ 280 milliosmoles per kilogram of water), for example, in response to hypernatremia. - ADH is also released in response to decreases in intravascular pressure, such as in hypovolemia.Serum OsmolalityChanges in serum osmolality are sensed by hypothalamic osmoreceptors, which triggers the release of ADH.We show a nephron, and show that ADH binds V2-receptors in the distal nephron, causing the insertion of special water channels called aquaporins. When ADH is present, the number of aquaporins increases so that more water is reabsorbed from the distal nephron. - Because more water is resorbed, urine volume is reduced and its osmolality is increased (in other words, the small amount of urine produced contains a high concentration of solutes).When osmolality returns to baseline, ADH release stops, and urine production returns to normal. - In the absence of ADH, water reabsorption is reduced, so urine volume increases and its osmolality decreases (the larger volume of urine is more dilute). Blood PressureChanges in blood pressure are sensed by baroreceptors in the chest (review baroreceptors).In response to reduced blood pressure, ADH is released and binds to V1A-receptors in the vascular smooth muscle. ADH causes vasoconstriction, which raises the intravascular blood pressure to maintain tissue perfusion. Osmolality vs Blood Pressure - It takes a higher concentration of ADH to achieve the vascular effects than to achieve the water-balancing effects in the nephron. - In hypovolemia, ADH will be released in high quantities, regardless of the osmotic state. - In hypervolemia, ADH release will be inhibited, regardless of the osmotic state. - In other words, blood pressure homeostasis is prioritized over water balance, which underscores the importance of tissue perfusion.SIADH Diabetes insipidus

Anti-Diuretic Hormone PhysiologyOverviewAnti-diuretic hormone, or ADH for short, is also called "arginine vasopressin" (AVP), or, simply, vasopressin. Responsible for regulating body water and blood pressure. - Review of body water osmotic, hyperosmotic, and hypoosmotic states, and the role of blood volume in determining blood pressure.ADH assists aldosterone during hemorrhage or other hypovolemic states – it does this by raising the intravascular volume to maintain tissue perfusion. - Thus, ADH is given during hypotensive crisis. Key pathologies of ADH include: - Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH), which occurs when ADH is excessively secreted. - Diabetes insipidus, when there is too little secretion of or reaction to ADH. Anti-Diuretic Hormone PhysiologyFirst, we show the hypothalamus and pituitary and that the anterior pituitary gland comprises clusters of hormone-producing cells. The posterior pituitary comprises neural tissue.ADH pro-hormones are produced in the supraoptic and paraventricular nuclei of the hypothalamus; on their way to the posterior pituitary, these prohormones are converted to ADH. From there, ADH is secreted into the blood stream and travels to its targets.Unlike anterior pituitary hormones, the posterior pituitary hormones are not stored until needed; instead, stimulation of the hypothalamic centers triggers their production and secretion on demand.Two triggers for ADH release: - ADH is released in response to minute increases in plasma osmolality (so, above ~ 280 milliosmoles per kilogram of water), for example, in response to hypernatremia. - ADH is also released in response to decreases in intravascular pressure, such as in hypovolemia.Serum OsmolalityChanges in serum osmolality are sensed by hypothalamic osmoreceptors, which triggers the release of ADH.We show a nephron, and show that ADH binds V2-receptors in the distal nephron, causing the insertion of special water channels called aquaporins. When ADH is present, the number of aquaporins increases so that more water is reabsorbed from the distal nephron. - Because more water is resorbed, urine volume is reduced and its osmolality is increased (in other words, the small amount of urine produced contains a high concentration of solutes).When osmolality returns to baseline, ADH release stops, and urine production returns to normal. - In the absence of ADH, water reabsorption is reduced, so urine volume increases and its osmolality decreases (the larger volume of urine is more dilute). Blood PressureChanges in blood pressure are sensed by baroreceptors in the chest (review baroreceptors).In response to reduced blood pressure, ADH is released and binds to V1A-receptors in the vascular smooth muscle. ADH causes vasoconstriction, which raises the intravascular blood pressure to maintain tissue perfusion. Osmolality vs Blood Pressure - It takes a higher concentration of ADH to achieve the vascular effects than to achieve the water-balancing effects in the nephron. - In hypovolemia, ADH will be released in high quantities, regardless of the osmotic state. - In hypervolemia, ADH release will be inhibited, regardless of the osmotic state. - In other words, blood pressure homeostasis is prioritized over water balance, which underscores the importance of tissue perfusion.SIADH Diabetes insipidus

Reference sheet for the nursing care of patients with ARDS (Acute Respiratory Distress Syndrome). ARDS is a serious disease with high mortality.

SIADH- syndrome of inappropriate anti-diuretic hormoneOccurs when ADH is secreted in excess.In the distal nephron, we show that excessive ADH secretion results in unregulated aquaporin creation and insertion in the nephron, which leads to increased water reabsorption. - Thus, the urine produced is highly concentrated (low volume, high osmolality). Signs and Symptoms: Patients present with hyponatremia and low serum osmolality.We might expect that the patients would be hypervolemic, but this is often only a transient state due to natriuretic mechanisms that respond to expanded body water volume. Some patients are asymptomatic, but if serum sodium levels fall too low and/or too rapidly, patients can experience nausea/vomiting, obtundation (a state of reduced alertness due to diminished consciousness), headaches, seizures, respiratory arrest, even coma and death.Neurologic symptoms occur when excessive water reabsorption causes brain swelling and neuron dysfunction; this typically occurs at serum sodium levels below 120 mEq/L. Causes: SIADH can be caused by CNS disorders (including stroke, infection, hemorrhage), tumors that secrete ectopic ADH (particularly in Small Cell Lung Cancer), drugs (including some analgesics, antiseizures meds, SSRIs, and antipsychotics), surgery, infections (particularly lung infections like TB and pneumonia, or HIV), and, that there are some inherited disorders that cause SIADH. For more details, please see the links in our notes. Treatment for SIADH includes ADH antagonists, treatment of underlying causes, and fluid restriction.More complete list of causes: - Ectopic tumor secretion Carcinoma of bronchi, duodenum, pancreas, ureters, bladder, uterus. Thymoma Mesothelioma Lymphoma/leukemia - Drugs Tricyclic and SSRI antidepressants MOAIs Chlorpropamide Carbamazepine Clofibrate Ecstasy Vinca alkaloids Cisplatin Cyclophosphamide Desmopressin Oxytocin - Neural pathway disruption CNS disorders (infection, trauma/surgery, hemorrhage, inflammatory and degenerative diseases) Pulmonary disorders (TB, pneumonia, fungal infections, empyema, and positive pressure ventilation) - Nephrogenic SIADH: mutation that causes chronic activation of V2 receptor - Other (AIDS, strenuous physical activity, such as marathon running, psychosis)

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