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Y2 LCRS1 Endocrinology > Neurohypophysial Disorders > Flashcards

Neurohypophysial Disorders Flashcards

1
Q

Name the two main nuclei within which neurones of the neurohypophysis have their cell bodies.

A

Paraventricular Nucleus

Supraoptic Nucleus

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2
Q

What two hormones are produced by the neurohypophysis?

A

Vasopressin

Oxytocin

NB: neurohypophysis = posterior pituitary

adenohypophysis = anterior pituitary

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3
Q

What is the principal action of vasopressin and how does it carry out this action?

A

ANTI-DIURETIC (ADH)

Vasopressin’s main action is on the V2 receptors (it binds to them) in the renal cortical and medullary collecting ducts

It stimulates the synthesis and assembly of aquaporin 2 into the membrane of teh lumen, which then increases water reabsorption from the nephron and has an antidiuretic effect

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4
Q

What are the main actions of oxytocin?

A

It is a contractile molecule that binds to oxytocin receptors It causes contraction of the myometrium during parturition and is involved in milk ejection It also has central effects

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5
Q

What part of the brain is responsible for regulating vasopressin release? What enables it to have this function?

A

Organum vasculosum - has osmoreceptors (=neurones) which project to the hypothalamic PVN and SON

Organum vasculosum is devoid of a BBB so it can communicate with systemic ciruclation

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6
Q

Describe how osmoreceptors regulate vasopressin release.

A
  • Osmoreceptors ae very sensitive to changes in EC OSMOLALITY
  • An increase in EC sodium causes plasma osmolality to increase and the osmoreceptor to shrink
  • This leads to more osmoreceptor firing
  • Causing VP release from hypothalamic PVN and SON neurones
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7
Q

Describe the normal response to thirst.

A

Results –> reuced urine volume, increase in urine osmolality, reduction in serum osmolality.

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8
Q

What are the consequences of a lack of the neurohypophysial hormones?

A

(Lack of Oxytocin – not clinically significant )

Lack of Vasopressin – Diabetes Insipidus

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9
Q

What are the two forms of diabetes insipidus?

A

Central (cranial) and Nephrogenic Diabetes Insipidus

(Either th body not making enough from the poosterior pituitary or kidneys not responding to vasopressin - nephrogenic is uncommon)

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10
Q

What can cause central diabetes insipidus?

A

Acquired (more common):

  • Damage to neurohypophysial system (injury, surgery, pituitary tumours, metastasis to pituitary gland, granulomatous infiltration of median eminence e.g. sarcoidosis)

Congenital (rare)

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11
Q

What can cause nephrogenic diabetes insipidus?

A

Congenital (rare) - e.g. mutation in gene encoding V2 receptor, aquaporin 2 type water channel

Acquired - Drugs e.g. lithium

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12
Q

State some signs and symptoms of diabetes insipidus. (Recall the process that causes these).

A
  • Polyuria
  • Polydipsia
  • Hypo-osmolar urine
  • Dehydration (and its consequences)
  • Possible disruption of sleep
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13
Q

Can patients die from diabetes insipidus?

A

Yes - e.g. if they do not have access to water in a hospital and their sodium levels rise to ver high concentrations in the blood they can die.

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14
Q

State another cause of polydipsia that isn’t diabetes.

A

Psychogenic polydipsia - “dry mouth”

This is a central disturbance that increases the drive to drink

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15
Q

Describe the symptoms associated with psychogenic polydipsia. How is it different from diabetes insipidus?

A

Excess fluid intake (polydipsia) and excess urine output (polyuria) -

BUT unline DI, ability to secrete vasopressin in response to osmotic stimuli is maintained.

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16
Q

What test can be used to distinguish between normal, psychogenic polydipsia, central DI and nephrogenic DI? Describe the results you would expect.

A

Fluid deprivation test

  • Normals and psychogenic polydipsia will show a rise in urine osmolality
  • Central and nephrogenic diabetes insipidus will show little or no change in urine osmolality

Fluid deprivation with administration of DDAVP (Desmopressin)

  • Central diabetes insipidus will show a rise in urine osmolality
  • Nephrogenic DI will still have a low urine osmolality (because of end-organ resistance)
  • NB: This is bascially an injection of vasopressin
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17
Q

Why is the urine osmolality of someone with psychogenic polydipsia lower (in the fluid deprivation test) than a normal subject?

A

Over time, the constant passage of large volumes of water through the kidneys will wash out the osmotic gradient that is necessary for AVP to exert its diuretic effect

18
Q

Describe the normal change in urine osmolality as plasma osmolality increases.

A

Normally, urine osmolality will increase as plasma osmolality increases (in a graph of urine osmolality against plasma osmolality it will show a sigmoid shape)

In DI, there is little change in urine osmolality as plasma osmolality increases

19
Q

Describe changes in plasma vasopressin following administration of hypertonic saline in a normal subject, psychogenic polydipsia, central DI and nephrogenic DI.

A

Hypertonic saline will increase the plasma osmolality and hence

will increase the vasopressin secretion in patients that have the capacity to produce vasopressin (normal, psychogenic polydipsia and nephrogenic DI)

Patients with central DI can’t produce vasopressin at all so the hypertonic saline will show no change in plasma vasopressin

20
Q

List the biochemical features of diabetes insipidus.

A
  • Hypernatraemia
  • Raised urea
  • Increased plasma osmolality
  • Dilute (hypo-osmolar) urine - ie low urine osmolality
21
Q

What are the biochemical features of psychogenic polydipsia?

A
  • Mild hyponatraemia – excess water intake
  • Low plasma osmolality
  • Dilute (hypo-osmolar) urine - ie low urine osmolality
22
Q

Where are V1 and V2 receptors found?

A

V1

  •  Vascular smooth muscle
  •  Non-vascular smooth muscle
  •  Anterior pituitary
  •  Liver
  •  Platelets
  • CNS

V2

  •  Kidney
  •  Endothelial cells
23
Q

State two selective peptidergic vasopressin selective agonists.

A

V1 – Terlipressin

V2 - Desmopressin (DDAVP)

24
Q

How is desmopressin administered?

A
  • Nasally
  • Orally
  • SC
25
Q

What are the effects of desmopressin? What must you tell a patient who is taking desmopressin?

A
  • Effects: Reduction in urine volume and concentration in cranial DI
  • CARE – to tell patient starting this NOT to continue drinking large amounts of fluid – risk of hyponatraemia
26
Q

State one treatment used for nephrogenic diabetes insipidus and its possible mechanism of action.

A

Thiazide Diuretics (e.g. bendroflumethiazide)

  • This inhibits the Na+/Cl- pump in the DCT leading to a diuretic effect
  • This leads to volume depletion resulting in a compensatory increase in Na+ reabsorption from the PCT (plus small decrease in GFR etc)
  • This increases proximal water reabsorption so less water reaches the collecting duct
  • This ultimately leads to reduced urine volume
27
Q

What is SIADH?

A

Syndrome of Inappropriate ADH = when the plasma vasopressin concentration is inappropriately HIGH for the existing plasma osmolality

28
Q

State some signs of SIADH.

A
  • Decreased urine volume (initially)
  • Increased urine osmolality
  • Decreased p[NA+] (hyponatraemia) mainly due to increased water reabsorption
29
Q

State some symptoms of SIADH that are caused by the hyponatraemia.

A

Can be symptomless

At relatively mild hyponatraemia (p[Na+]<120mM) = generalized weakness, poor mental function, nausea

Severe hyponatraemia (p[Na+]<110mM) = confusion, coma, death

30
Q

What is the main consequence of SIADH?

A

HYPONATRAEMIA

31
Q

State some causes of SIADH.

A
  • CNS - SAH, stroke, tumour, TBI
  • Pulmonary disease - Pneumonia, bronchiectasis
  • Malignancy –Lung (small cell)
  • Drug-related –Carbamazepine, SSRI
  • Idiopathic
32
Q

How is SIADH treated?

A

Provide appropriate treatment when the cause is identified (e.g. surgery for a tumour)

To reduce immediate concern i.e. hyponatraemia:

  1. Immediate: Fluid Restriction
  2. Long term: use drugs wihich prevent vasopressin action in kidneys
    • e.g. induce nephrogenic DI - DEMECLOCYLINE (reduces renal water reabsorption)
    • inhibit action of ADH - V2 RECEPTOR ANTAGONIST
33
Q

What are vaptans?

A

Non-competitive V2 receptor antagonists

Inhibit AQP2 synthedid and transport to collectig duct apical membrane, preventing renal water reabsorption

34
Q

How are vaptans better than diuretics?

A

They cause aquaresis = solute sparing renal excretion of water.

Diuretics produce electrolyte loss

35
Q

What stops the use of vaptans more?

A

although they are licensed for use of hyponatraemia with SIADH in the UK they are VERY EXPENSIVE - limits their use.

36
Q

State some drugs that increase or decrease vasopressin secretion.

A

Increase vasopressin secretion = nicotine

Decrease vasopressin secretion = alcohol + glucocorticoids

37
Q

State some other actions of vasopressin.

A
  • Vasoconstriction
  • Corticotrophin release
  • Factor VIII and von Willebrand factor
  • Central effects
38
Q

Diabetes insipidus:

    • may be due to a deficiency of circulating vasopressin
    • can be a consequence of lithium treatment
    • is characterised by the excretion of large volumes of dilute urine
    • can usually be diagnosed on the basis of the response - to a water deprivation test
    • is treated with a V1 receptor agonist
A
  • True
  • True
  • True
  • True
  • False
39
Q

Desmopressin:

    • is an analogue of aldosterone
    • promotes water reabsorption in the collecting ducts
    • is a treatment for diabetes mellitus
    • is used in the treatment of cranial diabetes insipidus
    • is normally administered by subcutaneous injection
A
    • False
  • -True
  • -False
  • -True
  • -False
40
Q

The Syndrome of Inappropriate ADH (SIADH):

    • is associated with a low urine osmolality
    • is associated with a hyponatraemia
    • is associated with fluid overload
    • causes polyuria
    • is usually treated by surgical removal of the posterior pituitary
A
    • False
    • True
    • False
    • False
    • False

Y2 LCRS1 Endocrinology (18 decks)

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