Week 12 - Diabetes insipidus, hyperparathyroidism, hypoparathyroidism Flashcards
what are the two reasons as to why diabetes insipidus occurs
A lack of antidiuretic hormone (cranial diabetes insipidus)
A lack of response to antidiuretic hormone (nephrogenic diabetes insipidus)
where is antidiuretic hormone produced
in the hypothalamus and secreted by the posterior pituitary gland
it is also known as vasopressin
what does ADH do
stimulates water reabsorption from the collecting ducts in the kidneys
what happens in diabetes insipidus due to the kidneys being unable to reabsorb water and concentrate the urine
Polyuria (excessive amounts of urine)
Polydipsia (excessive thirst)
what is primary polydipsia
Primary polydipsia is when the patient has a normally functioning ADH system but drinks excessive amounts of water, leading to excessive urine production (polyuria). This is not diabetes insipidus.
what is nephrogenic diabetes
is when the collecting ducts of the kidneys do not respond to ADH. it can be idiopathic without a clear cause, or it can be caused by other things
what are the other things that can cause nephrogenic diabetes insipidus
Medications, particularly lithium (used in bipolar affective disorder)
Genetic mutations in the ADH receptor gene (X-linked recessive inheritance)
Hypercalcaemia (high calcium)
Hypokalaemia (low potassium)
Kidney diseases (e.g., polycystic kidney disease)
what is cranial diabetes insipidus
when the hypothalamus does not produce ADH for the pituitary gland to secrete. it can be idiopathic, without a clear cause or…
what else can cranial diabetes insipidus be caused by
Brain tumours
Brain injury
Brain surgery
Brain infections (e.g., meningitis or encephalitis)
Genetic mutations in the ADH gene (autosomal dominant inheritance)
Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
what are the presenting features of diabetes insipidus
Polyuria (producing more than 3 litres of urine per day)
Polydipsia (excessive thirst)
Dehydration
Postural hypotension
what do investigations into diabetes insipidus
Low urine osmolality (lots of water diluting the urine)
High/normal serum osmolality (water loss may be balanced by increased intake)
More than 3 litres on a 24-hour urine collection
what is the test of choice for diagnosing diabetes insipidus
water deprivation test
what is included in the water deprivation test
The patient avoids all fluids for up to 8 hours before the test (water deprivation). After water deprivation, urine osmolality is measured. If the urine osmolality is low, synthetic ADH (desmopressin) is given. Urine osmolality is measured over the 2-4 hours following desmopressin.
what happens to the results of the water deprivation test in patients with primary polydipsia
In primary polydipsia, water deprivation will cause urine osmolality to be high. Desmopressin does not need to be given. A high urine osmolality after water deprivation rules out diabetes insipidus.
what happens to the results of the water deprivation test in cranial diabetes insipidus
In cranial diabetes insipidus, the patient lacks ADH. The kidneys are still capable of responding to ADH. Initially, the urine osmolality remains low as it continues to be diluted by the excessive water lost in the urine. After desmopressin is given, the kidneys respond by reabsorbing water and concentrating the urine. The urine osmolality will be high
what happens to the results of the water deprivation test in nephrogenic diabetes insipidus
In nephrogenic diabetes insipidus, the patient is unable to respond to ADH. The urine osmolality will be low both before and after the desmopressin is given.
how is cranial diabetes insipidus treated
desmopressin can be used to replace the absent ADH hormone. the serum sodium needs to be monitored, as there is a risk of hyponatraemia with desmopressin
what does management of nephrogenic diabetes insipidus include
Ensuring access to plenty of water
High-dose desmopressin
Thiazide diuretics
NSAIDs
what does the parathyroid hormone act to do
raise the blood calcium level
how does the PTH raise the blood calcium level
Increasing osteoclast activity in bones (reabsorbing calcium from bones)
Increasing calcium reabsorption in the kidneys (less calcium is lost in urine)
Increasing vitamin D activity, resulting in increased calcium absorption in the intestines
what does vitamin D do to calcium absorption from the intestines
acts to increase calcium absorption
what does PTH do to vitamin D
converts it into its active form.
therefore, vitamin D and parathyroid hormone act to raise blood calcium level
what are the symptoms of hypercalaemia
Kidney stones
Painful bones
Abdominal groans (constipation, nausea and vomiting)
Psychiatric moans (fatigue, depression and psychosis)
what is primary hypoerparathyroidism caused by
uncontrolled PTH production by a tumour of the parathyroid glands.
this leads to a raised blood calcium.
what is secondary hyperparathyroidism
Secondary hyperparathyroidism is where insufficient vitamin D or chronic kidney disease reduces calcium absorption from the intestines, kidneys and bones. This result in low blood calcium (hypocalcaemia). The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone. The serum calcium level will be low or normal, but the parathyroid hormone will be high. Treatment is to correct the underlying vitamin D deficiency or chronic kidney disease (e.g., renal transplant).
what is tertiary hyperparathyroidism
Tertiary hyperparathyroidism happens when secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated. Hyperplasia (growth) of the parathyroid glands occurs as they adapt to producing a higher baseline level of parathyroid hormone. Then, when the underlying cause of the secondary hyperparathyroidism is treated, the baseline parathyroid hormone production remains inappropriately high. In the absence of the previous pathology, this high parathyroid hormone level leads to the inappropriately high absorption of calcium in the intestines, kidneys and bones, causing hypercalcaemia. Treatment is surgically removing part of the parathyroid tissue to return the parathyroid hormone to an appropriate level.
in what cases is hyperparathyroidism most clinically signifiant in
chronic kidney disease
