Polyuria and Polydipsia Case Study 1 (Clinical Pathology)

In this blog post, we are going to discuss Polyuria and Polydipsia Case studies in clinical pathology. Students can check their clinical pathology abilities by studying these cases.

History Polyuria and Polydipsia

A 45-year-old woman with a history of hypothyroidism A 45-year-old woman with a history of hypothyroidism visits her GP with a three-month history of urinating more frequently, even up to three times a night. She finds her constant desire for fluids, particularly cold water, and her frequent need to go to the bathroom bother him since she works as a teacher. Apart from hypothyroidism, she has no other health problems and does not take medication regularly. She presents to her GP with a three-month history of urinating more frequently, including three times a night. She finds her constant desire for fluids, particularly cold water, and her frequent need to go to the bathroom bother him since she works as a teacher. Apart from hypothyroidism, she has no other health problems and does not take medication regularly.

Examination Polyuria and Polydipsia

Peripherally, the patient is warm and well perfused, with no evidence of dehydration. Examination of her heart, lungs, and abdomen is unremarkable. Neurologic examination is normal. Urine dipstick is negative.

A water deprivation test

 

Requirements:

  1. What is the differential diagnosis for this presentation, and what further tests are required?
  2. What are the principles of a water deprivation test, and how should the results are shown in Figure 1.1 be interpreted?
  3. Discuss the pathophysiology of the likely diagnosis, and suggest how the patient may be treated.

 

ANSWER

This woman has polyuria, nocturia, and polydipsia. These symptoms have four important differential diagnoses:

(1) diabetes mellitus,

(2) diabetes insipidus, which can be of central or nephrogenic origin,

(3) hypercalcemia, which can present as the above in an acute setting, and

(4) polydipsia primary (PP).

Therefore, investigations should be aimed at elucidating one of the above diagnoses. For diabetes mellitus, a finger glucose prick may be performed, but a formal fast or random serum glucose is needed to make a diagnosis. Simple urinalysis can show the presence of glucose, which would point toward this diagnosis. Corrected serum calcium needs to be measured to look for hypercalcemia.

Diabetes insipidus is a relatively rare disease characterized by the excretion of large volumes of dilute urine as a result of a deficiency or resistance to the actions of antidiuretic hormone (ADH) of the posterior pituitary, also known as arginine vasopressin (AVP). ADH is released into the circulation from the posterior pituitary gland in response to increased serum osmolality and acts to increase water reabsorption by causing the insertion of aquaporin-2 (AQP2) channels in the apical membrane of the distal parts. of the nephron. . ADH deficiency leads to central diabetes insipidus (CDI), while kidney failure to respond to its actions causes nephrogenic diabetes insipidus (NDI).

When the diagnosis is equivocal, a fluid deprivation test may be performed. Patients are withheld from fluid intake under close supervision for a period of 8 hours, with hourly measurement of body weight, urine volume and urine osmolality. After allowing sufficient time for dehydration, desmopressin (synthetic ADH) is administered subcutaneously, and a final urine sample is taken one hour afterward to measure urine osmolality. The table below shows how the results may be interpreted:

 

Urine osmolality case study

The essence of the test is that with CDI, urine will become more concentrated once the deficient ADH is replaced, whereas, with NDI, the inability of the kidney to respond to ADH means that any further replacement by ADH has no effect. CDI is commonly idiopathic though autoantibodies against ADH-secreting cells of the hypothalamus are found in several cases. Moreover, these patients tend to exhibit other autoimmune conditions, so the patient in our case is most likely to fall into this category since she has a background of hypothyroidism. Other causes of CDI include benign or malignant tumors of the brain (such as germinomas and craniopharyngiomas), neurosurgery, head injury, and infiltrative conditions (such as Langerhans cell histiocytosis). There are also genetic forms of the disease, with the majority being inherited in an autosomal dominant fashion with mutations in the ADH gene.

Treatment of diabetes insipidus depends on whether it is cranial or nephrogenic in origin. CDI responds well to ADH replacement, usually via the synthetic analog, desmopressin (DDAVP). High-dose DDAVP may be used for mild cases of NDI, but the treatment of NDI requires management of the underlying cause (e.g. correcting metabolic abnormalities, discontinuing any offending drugs). In any case, treatment is required only if the patient is suffering from severe dehydration, with urine volumes >4 L per day.

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