Neurohypophysial (Posterior Pituitary) Disorders Flashcards
What is the term for a group of neuronal cell bodies?
Nucleus
What are the names of the two hypothalamic nuclei that supply the neurohypophysis?
Supraoptic
Paraventricular
What are the two main hormones produced by the neurohypophysis?
Vasopressin (ADH)
Oxytocin
What is the principal effect of vasopressin/ADH and how does it do this?
Anti-diuretic
- Increases water reabsorption from renal cortical and medullary collecting ducts via V2 receptors
- Decreases urine production
What is the name of the small region of the brain which regulates vasopressin release?
Organum Vasculosum
What is located in the Organum Vasculosum which allows regulation of vasopressin release and what do they project to/communicate with?
Osmoreceptors (neurones)
- Project to hypothalamic paraventricular and supraoptic nuclei which then control posterior pituitary action and thus vasopressin release
Osmoreceptors are very sensitive to extracellular osmolality. What sequence of events takes place when there is an increase in extracellular sodium?
Osmoreceptor shrinks as water flows out of them
- Increased osmoreceptor firing
- Stimulates vasopressin release from hypothalamic paraventricular and supraoptic neurones
What is the normal response to water deprivation?
- No water is drank
- Serum osmolality is increased
- Osmoreceptors are stimulated
- Thirst is stimulated as well as increased vasopressin release
- More water is reabsorbed from renal collecting ducts
- Reduced urine volume, increased urine osmolality, reduced serum osmolality
What is the name of the disorder where you have insufficient vasopressin or vasopressin unable to work?
Diabetes Insipidus
What are the two types of diabetes insipidus?
Cranial (or central)
Nephrogenic (much less common)
Where does the problem lie in cranial and nephrogenic diabetes insipidus?
Cranial - absence of lack of circulating vasopressin
Nephrogenic - end-organ (kidneys) resistant to vasopressin, vasopressin unable to work
What are the acquired (more common than congenital) causes of cranial diabetes insipidus?
Damage to neurohypophysial system
- Traumatic brain injury
- Pituitary surgery
- Pituitary tumours, craniopharyngioma
- Metastasis to the pituitary gland e.g. breast
- Granulomatous infiltration of median eminence e.g. TB, sarcoidosis
What are the congenital and acquired causes of nephrogenic diabetes insipidus?
Congenital - rare, e.g. mutation in gene encoding V2 receptor, aquaporin 2 type water channel
Acquired - drugs, e.g. lithium
What are the signs and symptoms of diabetes insipidus?
- Large volumes of urine (polyuria)
- Urine very dilute (hypo-osmolar0
- Urinating in the night (nocturia) (disrupted sleep as presenting complaint)
- Thirst and increased drinking (polydipsia)
- Dehydration (and its consequences) if fluid intake not maintained - can lead to DEATH
What is the physiological sequence of events in diabetes insipidus starting with inadequate production of/response to vasopressin leading to symptoms when the patient has access to water?
- Inadequate response to/production of vasopressin
- Large volumes of dilute (hypotonic) urine
- Increase in plasma osmolality (and sodium)
- Reduction in extracellular fluid volume
- Thirst and then polydipsia (drinking a lot)
- Extracellular fluid volume expands, sort of keeping up with the diabetes insipidus when access to water is provided
What is the difference in physiological events when the patient does NOT have access to water?
All the steps up to reduction in extracellular fluid volume occur the same way.
- Thirst is stimulated but patient has no access to water.
- Sodium goes up and up and patient becomes dehydrated and possibly dies
What is the other cause of polydipsia in patients with healthy vasopressin release and kidneys?
Psychogenic polydipsia
Who is psychogenic polydipsia most frequently seen in, what is the cause, how do health professionals end up making it worse, and what are the two main symptoms despite what?
- Most frequently seen in psychiatric patients
- Causes are unclear, may be due to anti-cholinergic drug side effects e.g. dry mouth
- Healthcare professionals tell patients to drink plenty
- Excess fluid intake (polydipsia) and excess urine output (polyuria)
- DESPITE ability to secrete vasopressin in response to osmotic stimuli is normal
What is the physiological sequence of events in psychogenic polydipsia?
Normal response to drinking, no thirst stimulus except mental stimulus to drink
- Increased drinking (polydipsia)
- Expansion of extracellular fluid, reduction in plasma osmolality
- Less vasopressin secreted by neurohypophysis
- Large volumes of dilute (hypotonic) urine
- Extracellular fluid volume returns to normal, starts again with excessive drinking
How tightly is plasma osmolality controlled, what are the boundaries of the normal range and what conditions cause movement outside these boundaries?
- Very tightly controlled
- 270-290 mOsm/kg H2O
- Diabetes insipidus >290
- Psychogenic polydipsia <270
How is diabetes insipidus diagnosed and differentiated from psychogenic polydipsia? (since signs/symptoms are the same)
Water deprivation test
- Patient is asked to not drink water at all and take samples of urine throughout the day when they go to the toilet
- Results are plotted on a graph of urine osmolality when normally hydrated, fluid deprived, and after DDAVP (vasopressin drug) administration)
How does the osmolality and volume of urine change in a normal person after fluid deprivation?
- Osmolality increases
- Volume decreases
How does the osmolality of urine change in a psychogenic polydipsia patient after fluid deprivation?
- Osmolality increases but not as concentrated as normal person (due to polydipsia reducing the gradient in the kidney thus less water moves out)
- Volume decreases
How does the concentration and volume of urine change in a diabetes insipidus patient after fluid deprivation?
- Osmolality doesn’t increase as unable to (no VP/VP response)
- Central and nephrogenic DI around the same osmolality after deprivation as they were hydrated
