Reply to classmates post. At least 125 words each and 1 scholarly reference for each within last 5 years

Post 1

Diabetes insipidus (DI) is an insufficiency of anti-diuretic hormone (ADH), which leads to polyuria and polydipsia. This can be neurogenic (central) or nephrogenic. Neurogenic, or central DI is caused by insufficient secretion of ADH, caused by any organic lesion of the hypothalamus, pituitary stalk, or posterior pituitary, which interferes with ADH synthesis, transport, or release. Lesions include primary or metastatic brain tumors, hypophysectomy, aneurysms, thrombosis, infections and immunologic disorders. This is a recognized complication of traumatic brain injury or pituitary surgery. In the case of surgery, DI may be permanent or transient. In addition, this can also be a complication of pregnancy, and in rare cases, be caused by hereditary disorders (McCance & Huether, 2018). Neurogenic DI can be inherited as an autosomal dominant trait, in which about 10% of cases are familial (Schub & Parks-Chapman, 2018).
Nephrogenic DI is a result of an inadequate response of the renal tubules to ADH and is typically acquired or may be genetic. Acquired is related to disorders and drugs that damage the renal tubules or inhibit the generation of cAMP in the tubules. Examples of disorders that would cause this include pyelonephritis, amyloidosis, destructive uropathies, polycystic disease, and intrinsic renal disease, all of which lead to irreversible DI. Drugs that may cause a reversible form of nephrogenic DI include lithium, colchicine, amphotericin B, loop diuretics, general anesthesia and demeclocycline (McCance & Huether, 2018).
Individuals with DI have a partial or complete inability to concentrate urine. Large excretion of dilute urines leads to increased plasma osmolality. The thirst mechanism is stimulated, and patients typically have a craving for cold drinks. Dehydration can develop rapidly without ongoing fluid replacement. If the individual is unable to conserve enough water as is lost in the urine, serum hypernatremia and hyperosmolality can occur (McCance & Huether, 2018).
Patients with DI may require pharmacologic treatment, while others may be treated with fluid replacement (McCance & Huether, 2018). Proper hydration and nutrition should be encouraged. Healthcare professionals should promote decreased sodium and protein, and increased potassium. For those individuals that require pharmacologic treatment, proper use of the medication and potential side effects/management of these effects should be discussed. Also, intake and output may need to be recorded, as well as monitoring of urine specific gravity, dehydration and electrolyte imbalances. Furthermore, patients anxiety level should be assessed and emotional support and education about DI and its management should be discussed, setting realistic long-term goals to promote adjustment to chronic endocrine dysfunction (Schub & Parks-Chapman, 2018).

Post 2

Desmopressin (DDVAP) is a synthetic analog of vasopressin used to treat diabetes insipidus. DDVAP is a selective vasopressin V2 receptor agonist present throughout the collecting ducts and distal convoluted tubules of the kidneys. When the V2 receptor is activated, a cascade occurs that prompts an increase in cyclic adenosine monophosphate (cAMP) it the renal tubules, resulting in increased water permeability. This leads to a decrease in urine volume and increase in urine osmolality (McCarthy & Shah, 2020). DDVAP is available as an intranasal spray, oral tablet, oral disintegrating tablet and can also be administered intravenous. The oral tablets have advantages over the intranasal formulation as they can be easily used in infants, elderly patients, patients with visual disturbances and chronic rhinitis. The tablet is absorbed unaltered from the GI tract after oral administration, reaching peak plasma concentration in 90 minutes. Urine volumes decrease about 1 hour after administration, with diuretic activity remaining low 3-6 hours after administration. Although the nasal spray has a more rapid onset and longer duration of action, according to a study, the oral route was more available and more easily consumed according to patients. Also, intranasal absorption is erratic due to changes of the nasal mucosa, such as atrophy, scarring, congestion or discharge. Furthermore, disintegrating oral tablets have 60% greater bioavailability than tablets (Klara et al., 2016).
Desmopressin use requires weekly outpatient dose adjustments during the first month due to individual variations in pharmacokinetics (Klara et al., 2016). The major adverse effect from this drug is hyponatremia. In certain situations, hyponatremia can precipitate seizures. Signs and symptoms like nausea, confusion, or altered mental status should be reported. Routine monitoring of sodium levels should be performed, as well periodic renal function, as the therapeutic index and clearance of the drug can change according to renal function. Furthermore, water intoxication can occur due to overdose of desmopressin. This can result in a delayed loss of consciousness and seizures. This requires immediate hospital admission and electrolyte correction (McCarthy & Shah, 2020). Use of this medication and reinforcement of routine follow up should be encouraged.