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Week-7 Discussion Response

Week-7 Discussion Response


I like your post on Diabetes Insipidus (DI). As you have stated, the level of serum sodium increases due to excessive loss of water in the form of urine. Urine levels vary based on the type of condition. Polyuria involves excessive urine production. Polydipsia refers to excess thirst, which results from excessive consumption of water. Nocturia affects the sleeping patterns due to frequent visits to the toilet at night. Dehydration is common if a patient fails to consume water to meet the body’s demands. The osmolality increases due to the inappropriate dilution of urine.

Central DI results from diminished or non-existent vasopressin (The Royal Children’s Hospital Melbourne, n.d). This occurrence is often a result of brain damage, making it difficult to produce or regulate vasopressin. It is inborn or acquired later in life. Therefore, fluid is lost at a higher-than-normal rate and could lead to dehydration. Nephrogenic DI occurs when kidneys cannot concentrate urine appropriately. This anomaly is present because the kidney does not respond to vasopressin leading to the production of more fluid as urine. As you have explained, desmopressin is ideal for the treatment of Diabetes Insipidus. It acts as a controlling agent, which reduces the amount of water lost through urine. The anti-diuretic hormone can be in tablet or spray forms. The dose depends on the condition’s severity. However, it is not recommended for nephrogenic DI (Gubbi & Hannah-schmouni, 2019).


Gubbi, S., & Hannah-schmouni, F. (2019). Diagnostic Testing for Diabetes Insipidus. Retrieved from

The Royal Children’s Hospital Melbourne. (n.d). Diabetes insipidus. Retrieved from


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Week-7 Discussion Response


Week-7 Discussion Response

Week-7 Discussion Response

  • -Length: A minimum of 200 words per post, not including references
  • Citations: At least one high-level scholarly reference in APA per post from within the last 5 years

A 23-year-old female presents with frequency absent of infection. The final diagnosis is Diabetes
Insipidus. She is treated with dDAVP.

Diabetes insipidus (DI) is a result of low-level ADH due to posterior pituitary disorder. This
disease leads to excess fluid output and excessive thirst.
1. What would you expect her sodium level would be, high or low? Defend your answer.
Her sodium level will be high, >145mEq/L. the sodium level will be high due to excessive loss
of water up to 2 L/day in adults. As the body system is trying to compensate for excessive loss of
water, the brain is stimulated to produce excessive thirst as well. Hypernatremia can worsen if a
patient with DI has impaired thirst or inability to drink water or if fluids are not replaced
(Dlugasch & Story, 2020).
2. Her osmolarity is elevated. Why?
Osmolality is a term used when referring to fluids inside the body, and the normal serum level is
282-295 mosm/kg. Her osmolarity will be elevated because Diabetes Insipidus causes
dehydration dies to excessive volume loss leading to hypertonic dehydration and increases
3. Compare and contrast central vs/ neurogenic Diabetes Insipidus.
Central diabetes insipidus (CDI) results from causes that impair the synthesis, transport, or
release of ADH dues to hypothalamus or pituitary disorder. It can be Idiopathic, Autoimmune,
Tumours Hypoxic brain injury, damage to the pituitary gland or hypothalamus can be caused by
surgery, head injury, inflammation, infection, or in rare cases genetic disorders. Nephrogenic
Diabetes Insipidus is mostly due to a genetic or inherited disorder. Kidneys do not respond to
ADH and there is Impairment of urine concentrating ability and free water conservation. It May
also be due to disorders such as bilateral urinary tract obstruction and polycystic kidney disease
4. Explain the mechanism of dDAVP.
Desmopressin acetate is a synthetic analog of antidiuretic hormone (ADH). It works as an
antidiuretic by limiting the amount of water that is eliminated in the urine; that is, it is an
antidiuretic. It works at the level of the renal collecting duct by binding to V2 receptors, which
signal for the translocation of aquaporin channels via cytosolic vesicles to the apical membrane
of the collecting duct (Fralick, et al. 2019). The presence of these aquaporin channels in the
distal nephron causes increasing water reabsorption from the urine, which becomes passively re-
distributed from the nephron to systemic circulation by way of basolateral membrane channels.

Dlugasch, L., & Story, L. (2019). Applied pathophysiology for the advanced practice nurse (1st
ed.). Jones & Bartlett Learning.

Fralick, M., Schneeweiss, S., Wallis, C.D., Jung, E. H., & Kesselheim, A. S (2019)
Desmopressin and the risk of hyponatremia: A population-based cohort study. PLOS Medicine

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