Cause Amp; Effect Diagram Water Treatment |BEST|
In states of hypovolemia or hypernatremia, ADH is released from the posterior pituitary gland and binds to the type-2 receptor in principal cells of the collecting duct. Binding to the receptor triggers an intracellular cyclic adenosine monophosphate (cAMP) pathway, which causes phosphorylation of the aquaporin-2 (AQP2). After achieving water homeostasis, the ADH levels decrease, and AQP2 is internalized from the plasma membrane, leaving the plasma membrane watertight again.
cause amp; effect diagram water treatment
ADH secretion also occurs during states of hypovolemia or volume depletion. In these states, decreased baroreceptors sense arterial blood volume in the left atrium, carotid artery, and aortic arch. Information about low blood pressure sensed by these receptors is transmitted to the vagus nerve, which directly stimulates the release of ADH. ADH then promotes water reabsorption in the kidneys and, at high concentrations, will also cause vasoconstriction. These two mechanisms together serve to increase effective arterial blood volume and increase blood pressure to maintain tissue perfusion. It is also important to note that in states of hypovolemia, ADH will be secreted even in hypoosmotic states. Conversely, hypervolemia inhibits ADH secretion; therefore, in hyperosmotic hypervolemic states, ADH secretion will be reduced.
ADH principally exerts its effects by binding to the kidneys principal cells within the late distal tubule and collecting ducts. ADH binds to the V receptor on these cells and leads to the activation of adenylate cyclase, which causes a subsequent increase in the second messenger cyclic AMP (cAMP). cAMP activates protein kinase A (PKA), a phosphorylating enzyme that initiates an intracellular phosphorylation cascade. Ultimately, intracellular aquaporin-2 (AQP2) storage vesicles are phosphorylated, which promotes their movement and insertion into the apical membrane. AQP2 is a water channel that allows water to move passively into the cell guided by the osmotic gradient established by NaCl and urea, and thus promotes reabsorption of water in the kidney. This activity creates concentrated, or hyperosmotic, urine, and allows our body to conserve water in times of dehydration or loss of sufficient blood volume, as seen in hemorrhagic or edematous states.
ADH also has a second action on vascular smooth muscle. ADH binds to V receptors on vascular smooth muscle and activates G protein. G activates phospholipase C (PLC), which results in the production of inositol triphosphate (IP-3) as well as diacylglycerol (DAG) from the cell membrane. IP-3 causes a release of intracellular calcium from the endoplasmic reticulum. DAG and calcium activate protein kinase C (PKC), which, like PKA, results in a signaling phosphorylation cascade. The net effect of this signaling cascade is a contraction of vascular smooth muscle leading to increases in total peripheral resistance and thus increases in blood pressure. This mechanism is synergistic with water reabsorption in that both mechanisms elevate blood pressure. This mechanism is crucial in periods where sufficient arterial blood volume is low to maintain tissue perfusion.
There are three pathologic states related to ADH. The first is the syndrome of inappropriate ADH (SIADH) and occurs when ADH is released in excessive unregulated quantities. SIADH results in excess water reabsorption and thus creates dilutional hyponatremia. Although water is retained in quantities greater than the body's needs, these patients typically remain euvolemic and do not exhibit features of the third spacing of fluid such as edema. The mechanism behind this is that, regardless of the excess ADH present, the kidneys maintain their ability to excrete salt. As ADH signals for increased water reabsorption, the body senses the increase in extracellular volume, and natriuretic mechanisms come into play that cause increased salt excretion via the kidneys. The increased salt in the urine will osmotically attract water to be excreted as well, thus keeping the body in a euvolemic state. This increase in salt excretion also contributes to the hyponatremia seen in SIADH. Settings in which SIADH arises include malignancies (most often by autonomous production of ADH by small cell lung cancer), central nervous system (CNS) disturbances (e.g., stroke, hemorrhage, infection, trauma, etc.), drugs (e.g., selective serotonin reuptake inhibitors, carbamazepine, and others), surgery (most likely secondary to pain), and more. Patients with SIADH may be asymptomatic or present with a spectrum of severity of complaints based on their level of hyponatremia. Nausea and malaise are typically the earliest presenting symptoms and present when the sodium acutely falls below 125 to 130 mEq/L. Lower levels of sodium are associated with headache, obtundation, seizure, and even coma and respiratory arrest. These symptoms arise due to the increased movement of water into neurons as the extracellular osmolarity falls. The intracellular swelling causes neuronal dysfunction.
Unlike the excess ADH seen in SIADH, the remaining two pathologic states related to ADH result from either decreased ADH or resistance to its effects. A failure of ADH secretion causes central diabetes insipidus. In this scenario, ADH levels are low; thus, the collecting tubules are impermeable to water, resulting in excess water excretion. In nephrogenic diabetes insipidus, ADH secretion is normal, but there is a defect in the V receptor or other signaling mediators that makes the kidneys unresponsive to ADH. In either disease, the net effect is increased excretion of water. The depletion of water causes the production of large volumes of dilute water and the concentration of body fluids leading to hypernatremia and hyperosmolarity. This status results in polyuria, polydipsia, and the effects of electrolyte imbalances that ensue.
ADH is an important hormone that is responsible for water, osmolar, and blood pressure homeostasis. Its function is vital in times of thirst, hemorrhage, the third spacing of fluid, and other scenarios where there is the diminution of effective arterial blood flow. Its efforts serve to maintain volume status as well as blood pressure to continue adequate tissue perfusion. Additionally, the pathologic states discussed above are important considerations when working up patients with electrolyte imbalances. SIADH is a common cause of hyponatremia and may be a sign of an underlying occult malignancy when no other risk factor is present. Clinically, SIADH is the diagnosis in a hyponatremic patient who has evidence of decreased plasma osmolarity (less than 275 mOsm/kg), inappropriately concentrated urine (urine osmolarity greater than 100 mOsm/kg), elevated urine sodium (greater than 20 mEq/L), and euvolemia.
Diabetes insipidus is an important cause of hypernatremia. They are distinguished from each other and primary polydipsia, a disease of dysregulated thirst mechanism resulting in excess fluid intake and, therefore, polydipsia and polyuria, by a water deprivation challenge. In this test, a patient's urine and plasma osmolarity are measured at baseline and then repeatedly measured over a few hours while they are not allowed to drink water. If during this period of water deprivation, their urine osmolarity increases to above 750 mOsm/kg, then primary polydipsia is the diagnosis as this signals the body is adequately releasing ADH in response to a lack of fluid intake. If the urine osmolarity remains low, then this implies an issue with ADH is present, and diabetes insipidus is likely the culprit. To differentiate between nephrogenic and central forms of the disease, during the water deprivation challenge, one may administer desmopressin, an ADH analog. If after desmopressin administration urine osmolarity increases, then central diabetes insipidus is present as this scenario describes a working response ADH. If, however, desmopressin does not increase urine osmolarity, then we know the response to ADH is inappropriate, and it must be nephrogenic diabetes insipidus. This distinction is important to make as the treatment differs between nephrogenic and central diabetes insipidus. The treatment for the central form is to replace the inadequate ADH with desmopressin. In the nephrogenic form, the treatment of choice is thiazide diuretics. Thiazide diuretics act at the distal convoluted tubule to block sodium and chloride cotransport. The increased excretion of sodium chloride induces mild hypovolemia, which triggers increased sodium reabsorption in the proximal convoluted tubule. This increase in sodium reabsorption will promote the increase in passive water reabsorption in the same segment, resulting in a net decrease in water excretion, thus mitigating the polyuria seen in these patients.
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