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Endocrinology > Disorders of vasopressin > Flashcards

Disorders of vasopressin Flashcards

1
Q

Where is vasopressin released from?

A
  • Arginine vasopressin (AVP) is produced in the hypothalamus, as well as Oxytocin and both are stored in the posterior pituitary
  • The posterior pituitary is anatomically continuous with the hypothalamus
  • Connected via hypothalamic magnocellular neurons
  • AVP is located in the supraoptic hypothalamic nuclei of the hypothalamus, go down the neurons, then to the P.P
  • Oxytocin is located in the paraventricular hypothalamic nuclei of the hypothalamus, go down the neurons, then to the P.P
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2
Q

What is the main physiological action of vasopressin?

A

Stimulation of water reabsorption in the renal collecting duct
- Concentrates urine (reduces urine volume)
- Acts through the V2 receptor in the kidney
- Also acts as a vasoconstrictor (via V1 receptor) to increase b.p
- Also stimulates ACTH release from the anterior pituitary

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3
Q

Describe the mechanism by which vasopressin stimulates water reabsorption

A
  1. AVP in the blood travels to the renal collecting duct and binds to V2 receptors on the basolateral membrane of the duct
  2. Binding stimulates cascade
  3. Cascade stimulates the formation of aquaporin-2 channels on the apical membrane
  4. More H2O molecules taken into the lumen and out of the basolateral membrane into the blood
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4
Q

How does the posterior pituitary appear on an MRI?

A
  • “bright spot”
  • Not visulaised in all healthy individuals, so absence may be normal variant
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5
Q

What 2 factors stimulate vasopressin release?

A
  1. OSMOTIC:
    Rise in plasma osmolality sensed by osmoreceptors
  2. NON-OSMOTIC: (stretch)
    Decrease in atrial pressure sensed by atrial stretch receptors
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6
Q

Where are the osmoreceptors located?

A

Situated in 2 nuclei:
1. Organum vasculosum (of the lamina terminalis)
2. Subfornical organ
- both nuclei sit around the 3rd ventricle (circumventricular)
- No blood brain barrier (so neurons can respond to changes/ v. good at sensing conc of blood)
- Highly vascularised
- Neurons project to the supraoptic nucleus- site of vasopressinergic neurons

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7
Q

How do osmoreceptors regulate vasopressin?

A
  1. There is an increase in extracellular Na+
  2. Water flows out of the osmoreceptors
  3. Osmoreceptors change in shape (shrink)
  4. Leads to osmoreceptor firing
  5. Stimulates vasopressin release from hypothalamic neurons (AVP will increase the water to decrease the Na+ conc)
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8
Q

Describe the mechanism by which Non- osmotic stimulation of vasopressin release?

A
  1. Atrial stretch receptors detect pressure in the right atrium
  2. Inhibit vasopressin release via vagal afferents to hypothalamus
  3. Reduction in circulating volume (e.g. haemorrhage) means less stretch of these atrial receptors, so less inhibition of vasopressin (vasopressin can increase Na+ conc/ b.p)
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9
Q

Why is vasopressin released following a haemorrhage (ie reduction in circulating volume)

A
  • Vasopressin release results in increased water reabsorption in the kidney (some restoration of circulating volume) V2 receptors (INCREASES BLOOD VOL)
  • Vasoconstriction via V1 receptors (INCREASES BP)
  • Renin-aldo system also activated
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10
Q

Describe the physiological response to water deprivation

A
  1. Increased plasma osmolality (conc of plasma)
  2. Simulates osmoreceptors
  3. Can lead to thirst OR increased AVP release
  4. Increased AVP= increased water rebasoption from renal collecting ducts
  5. Leads to reduced urine volume, increase in urine osmolality (conc)
  6. Leads to reduction in plasma osmolaltiy (more water reabsorbed from the blood)
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11
Q

What is diabetes insipidus?

A

When an individual expereinces symptoms of poyluria, extreme thirst, nocturia and polydipsia due to a problem with arginine vasopressin (NOTHING TO DO WITH INSULIN/ TYPE 1 OR 2 DIABETES MELLITUS)

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12
Q

What are the symptoms of Diabetes Insipidus?

A
  1. Polyuria
  2. Nocturia
  3. Polydipsia (extreme thirst)
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13
Q

What are the different types of diabetes insipidus a person can have?

A
  1. Cranial (central) diabetes insipidus
  2. Nephrogenic diabetes insipidus
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14
Q

What is the difference between cranial and nephrogenic diabetes insipidus?

A
  1. CRANIAL:
    - Problem with hypothalamus &/ or posterior pituitary
    - Unable to MAKE arginine vasopressin
    “vasopressin insufficiency”
    - More common
  2. NEPHROGENIC:
    - Can make arginine vasopressin (normal hypothalamus & posterior pituitary)
    - Kidney (collecting duct) unable to RESPOND to it
    “ vasopressin resistance”
    - Less common
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15
Q

What are some causes of cranial diabetes insipidus?

A

ACQUIRED:
- Traumatic brain injury
- Pituitary surgery
- Pituitary tumours
- Metastasis to the pituitary gland (e.g breats)
- Granulomatous infiltration of pituitary stalk (e.g. TB, sarcoidosis) [vasopressin cannot travel via stalk from the hypothalamus to the posterior pituitary]
- Autoimmune
CONGENITAL: rare

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16
Q

What are some causes of nephrogenic diabetes insipidus?

A

(Much less common than cranial diabetes insipidus)
ACQUIRED:
- Drugs (e.g. lithium- reason not known, but lithium is often used as treatment for manic depression)
CONGENITAL:
-rare (e.g. mutation in gene encoding V2 receptor, aquaporin 2 type water channel)

17
Q

What are the presentations of diabetes insipidus?

A
  1. Polyuria, nocturia, polydipsia (extreme thirst)

URINE:
- Very dilute (hypo-osmolar- less vasopressin so less reabsorption of H20)
- Large volumes

PLASMA:
- Increased concentratiom (hyper-osmolar) as patient becomes dehydrated
- Increased sodium (hypernatraemia)
- Glucose normal (make sure you ALWAYS check this in a patient with these symptoms to rule out diabetes mellitus)

18
Q

Why do the symptoms of diabetes insipidus occur?

A
  1. Arginine vasopressin problem (either not enough AVP or not responding to AVP)
  2. Leads to impaired (reduced) concentration of urine renal collecting duct
  3. So large volumes of dilute (hypotonic) urine
  4. Leads to an increase in plasma osmolality (and sodium)
  5. Stimulates osmoreceptors
    (In this case vasopressin release cannot be stimulated/ has no effect)
  6. Leads to polydipsia (thirst)
  7. Maintains circulating volume as long as patient has access to water
    (if no access to water, can lead to dehydration and death)
19
Q

Diabetes insipidus is a cause of death, true or false?

A

TRUE, if patient has no access to water in extreme thirst

20
Q

What is Psychogenic polydipsia?

A

Problem= the patient drinks all the time, so passes large volume of dilute urine
- Experiences similar presentations to diabetes insipidus (polydipsia, polyuria, nocturia)
- Unlike DI- no problem with arginine vasopressin
- No problem with insulin

21
Q

Why does drinking too much water cause the symptoms of psychogenic polydipsia?

A
  1. Increased drinking
  2. Leads to plasma osmolality falls (reduced conc)
  3. Less AVP secreted by posterior pituitary (we have too much H20, don’t want to reabsorb anymore)
  4. Large volumes of dilute (hypotonic) urine
  5. Plasma osmolality returns to normal
22
Q

How do we distinguish between diabetes insipidus & psychogenic polydipsia?

A

WATER DEPRIVATION TEST
- No access to anything to drink
- Over time, measure
* Urine volumes
* Urine concentration (osmolality)
* Plasma concentration (osmolality)

  • In NORMAL response: urine conc will start low from the water deprivation but increases via vasopressin release (rebsorbing more water) there is sigmoidal increase in urine osmolality
  • In psychogenic polydipsia the urine conc will increase but not as much as normal
  • In Diabetes Insipidus the urine conc DOES NOT INCREASE AT ALL (no AVP)
23
Q

How do we distinguish between cranial & nephrogenic diabetes insipidus?

A

(conduct the water deprivation test)
- This time, give the patient ddAVP (Desmopressin is a man-made form of vasopressin)
- Cranial DI will respond to the ddAVP (urine conc will increase)
- With Nephrogenic DI (no urine conc change)

24
Q

What plasma osmolality is seen in diabetes insipidus?

A

NORMAL (HYDRATED) RANGE= 280 mOsm/kg H20
DI= 290 mOsm/kg H20

25
Q

What plasma osmolality is seen in psychogenic polydipsia?

A

NORMAL (HYDRATED) RANGE= 280 mOsm/kg H20
Psychogenic polydipsia= 270 mOsm/kg H20

26
Q

What is the treatment of Cranial diabetes insipidus?

A

AIM= want to replace vasopressin
- ddAVP (Desmopressin- man made vasopressin)
- Selective for V2 receptor (V1 receptor activation would be unhelpful)
- Different preparations
*Tablets
*Intranasal (nasal spray)

27
Q

What is the treatment of Nephrogenic diabetes insipidus?

A

(VERY RARE- difficult to treat successfully)
- Thiazide diuretics (e.g. bendofluazide) used but mechanism is unclear

28
Q

What is “Syndrome of Inappropriate Anti- Diuretic Hormone” (SIADH)

A

“Too much arginine vasopressin”
- Reduced urine output
- Water retention
- High urine osmolality (conc)
- Low plasma osmolality
- Dilutional hypoatraemia

29
Q

What are the causes of SIADH?

A

“Syndrome of Inappropriate Anti- Diuretic Hormone”
CNS:
- Head injury, stroke, tumour
Pulmonary disease:
- Pneumonia, bronchiectasis
Malignancy:
- Lung cancer (can make vasopressin)
Drug related:
- Carbamazepine, Serotonin Reuptake Inhibitors (SSSRIs)
Idiopathic (arises spontaneously- cause unknown)

30
Q

How is SIADH managed?

A

“Syndrome of Inappropriate Anti- Diuretic Hormone”
- Common cause of prolonged hospital stay
- Fluid restrict (difficult to adhere to)
- Can use a vasopressin antagonist (vaptan)- binds to the V2 receptors in the kidney (v. expensive)

Endocrinology (14 decks)

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