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Phase 2 3. Endocrinology > Pituitary gland and regulation of the endocrine system > Flashcards

Pituitary gland and regulation of the endocrine system Flashcards

1
Q

Describe the pituitary gland

A

2 lobes:

  • anterior
  • posterior
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2
Q

Describe the anterior lobe of the pituitary gland

A

linked to the hypothalamus by a portal circulation system

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3
Q

Describe the posterior lobe of the pituitary gland

A

Direct extension of the cns

- axons extend down directly from the hypothalamus

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4
Q

What hormones are stored in the posterior pituitary gland?

A
  • ADH

- Oxytocin

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5
Q

What stimulates many of the pituitary gland actions?

A

in response to actions in the hypothalamus

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6
Q

What connects the hypothalamus and the pituitary gland?

A

hypophyseal portal

system

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7
Q

What hormone released from the hypothalamus stimulates growth hormone production in the pituitary gland?

A

Growth hormone releasing hormone (GHRH)

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8
Q

What hormone released from the hypothalamus stimulates FSH/LH production in the pituitary gland?

A

Gonadotrophin releasing hormone (GnRH)

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9
Q

What hormone released from the hypothalamus stimulates ACTH production in the pituitary gland?

A

corticotrophic releasing hormone

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10
Q

What hormone released from the hypothalamus stimulates TSH production in the pituitary gland?

A

Thyroid releasing hormone

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11
Q

What hormone released from the hypothalamus inhibits prolactin hormone production in the pituitary gland?

A

Dopamine

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12
Q

How is GH secretion described?

A
  • pulsatile

- mainly overnight

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13
Q

How can GH be measured in the blood?

A

By IGF-1, as it is longer acting

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14
Q

What stimulates the hypothalamus to alter its activity in relation to GH?

A

external/environmental factors

NOT PITUITARY

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15
Q

How is GH and IGF-1 regulated?

A

Through a negative feedback loop

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16
Q

What is the effect of GH?

A

Multiple physiological effects, mostly in childhood
- Either direct effects or via production of insulin-like
growth factor-1 (IGF-1) from liver

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17
Q

What is the effect of somatostatin production on GH?

A
  • inhibits GH production by the anterior pituitary
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18
Q

What cells of the anterior pituitary produce growth hormone?

A

somatotrophs

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19
Q

What is the result of excess GH?

A

Gigantism = growth hormone excess in childhood/puberty

Growth hormone excess after puberty will not cause
people to grow taller, grow wider instead

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20
Q

What is the result of GH deficiency?

A

Dwarfism in childhood

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21
Q

Describe the normal lactotroph axis state

A

under negative hypothalamic control as dopamine inhibitsd prolactin release

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22
Q

How is the normal lactotroph axis state altered in pregnancy?

A

high oestrogenic states overcome inhibition by dopamine

=> enhances lactation

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23
Q

What is ADH?

A

vasopressin

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24
Q

What is oxytocin?

A

stimulates cervical dilatation and uterine contractions

25
Q

Name disorders of the posterior pituitary

A
  • diabetes insipidus

- syndrome of inappropriate anti-diuretic hormone (SIADH)

26
Q

Name disorders that can result from pituitary tumours

A

overproduction/under function

  • anterior pituitary excess hormones
  • hypopituitarism
27
Q

What is diabetes insipidus?

A
  • lack of ADH and inability to reabsorb water

- passage of large volumes of dilute urine

28
Q

What are the clinical features of diabetes insipidus?

A
  • polyuria
  • polydipsia
  • nocturia
  • low urine osmolality
  • high plasma osmolality

(must exclude hyperglycaemia and hypercalcaemia)

29
Q

What symptoms are common between diabetes insipidus and diabetes mellitus?

A
  • polyuria

- polydipsia

30
Q

Describe the action of ADH

A
  • acts on ADH receptor (AVPR2)
  • stimulates GPCR and PKA activation

= insertion of aquaporin channels
inhibition of endocytosis of channel

31
Q

Where are ADH receptors found?

A

basolateral membrane of kidney collecting ducts

32
Q

What are the two causes of diabetes insipidis?

A
  • cranial (deficiency)

- nephrogenic (resistance)

33
Q

Describe cranial diabetes insipidis

A

Deficiency of ADH:

  • Can be idiopathic or genetic (mutation in ADH gene)
  • Trauma, tumours, infections, inflammatory conditions of the posterior pituitary
  • Usually patients who have had pituitary surgery
34
Q

Describe nephrogenic diabetes insipidis

A

Resistance to ADH

  • Genetic (usually AVPR2 mutation)
  • secondary to drugs (e.g. lithium used to treat various forms of mental instability), metabolic upset (profound hypokalaemia or hypercalcaemia), renal disease
35
Q

How is diabetes insipidus diagnosed?

A

water deprivation test

36
Q

What is the water deprivation test?

A

patient to keep diary of urine production to determine genuine polyuria before testing

(may just be urinating frequently but small
amounts = not DI)

  • Deprive fluid for 8h
  • Measure plasma and urine osmolality every 2-4h
  • Then give synthetic ADH (ddAVP) and reassess urine osmolality
  • Will correct cranial DI but not nephrogenic DI (due to resistance rather than deficiency)
37
Q

How is cranial diabetes insipidistreated?

A

Desmopressin (vasopressin/ADH analogue)

  • Can be given orally/nasal spray/injection
  • Monitor plasma sodium and osmolality
38
Q

How is nephrogenic diabetes insipidis treated?

A

Treat underlying cause

  • High doses of ddAVP
  • Very difficult to treat
39
Q

What is a non-functioning pituitary adenoma?

A

Pituitary tumour that does not secrete active hormones

‘incidentalomas’

40
Q

What further tests should be carried out on non-functioning pituitary adenoma?

A
  • exclude hormone function (excess/hypo)
  • Ensure no effect on visual fields (Pituitary located just below optic chiasm)

Tumour can expand upwards and push on chiasm causing loss of peripheral vision (‘bitemporal hemianopia’)

  • Tunnel vision
  • May require urgent surgery to decompress optic nerve
41
Q

What are secretory pituitary adenomas?

A

Pituitary tumour that secretes active hormones

42
Q

What are the different types of secondary pituitary adenomas?

A
  • prolactinomas
  • somatotrophic adenomas
  • corticotrophic adenomas
  • gonadotrophic adenomas
  • thyrotrophic adenomas
43
Q

What is a prolactinoma?

A
  • most common pituitary tumour

- secretes prolactin

44
Q

What are the clinical features of prolactinomas?

A

Clinical features result from suppression of gonadotrophic hormones => hypogonadrotrophic
hypogonadism (negative feedback on gonadotropins)
- Galactorrhoea – milky discharge from breasts
- Menstrual disturbance and subfertility in women
(present earlier in women)
- Rare in men, but presents with reduced libido/erectile dysfunction in men

45
Q

How are prolactinomas managed?

A

Dopamine agonists (cabergoline) – dopamine inhibits prolactin production

  • Virtually always pharmacologically managed
  • Surgery if large tumour with visual field effects (very unusual - normally small and
    shrink with cabergoline)
46
Q

What is a somatotrophic adenoma?

A

pituitary tumour that secretes growth hormone?

47
Q

What are the effects of a somatotrophic adenoma?

A

increased growth hormone secretion

= acromegaly

48
Q

What is acromegaly?

A

Excessive production of GH (and IGF-1) in adults (causes ‘gigantism’ in children)
o Growth plates have fused, and therefore cannot cause increase in height
o Cartilage, muscles and tendons can still grow

  • Rare, UK annual incidence is 4/million
  • Usually due to pituitary adenoma (often large - macroadenomas)
49
Q

What are the symptoms of acromegaly?

A

Sweats, headache, tiredness, increase in ring or
shoe size, joint pains
- Impaired function of the rest of the pituitary

50
Q

What are the signs of acromegaly?

A

Coarse facial appearance
o Enlarged tongue
o Enlarged hands and feet
o Visual field loss

51
Q

What are the complications of acromegaly?

A

Hypertension
o diabetes or impaired glucose tolerance
o Increased risk of bowel cancer – GH is thought to be carcinogenic
o heart failure

52
Q

How is acromegaly diagnosed?

A
  • glucose tolerance test
  • IGR-1 level
  • pituitary MRI
53
Q

How is a glucose tolerance test used to diagnose acromegaly?

A

glucose normally suppresses GH

o Glucose load fails to suppress GH
o May reveal underlying DM or IGT

54
Q

How is an IGF-1 level used to diagnose acromegaly?

A

Produced by liver in response to GH
o long half-life, protein bound
o So more useful than plasma GH
o NB: because of short half-life, GH might even be normal if measured

55
Q

How is an MRI used to diagnose acromegaly?

A

Tumour usually large (macroadenoma, > 1 cm) and often extends into surrounding structures
(cavernous sinus)

56
Q

How is acromegaly managed?

A
  • surgery (not curative but reduces tumour)
  • somatostatin analogues to inhibit GH secretion
  • radiotherapy to treat residual tumour, but increases risk of hypopituitarism
57
Q

What is hypopituitarism?

A

Failure of (usually anterior) pituitary function

 Can affect a single hormonal axis (FSH/LH most commonly) or all hormones (panhypopituitarism)
 Leads to secondary gonadal/thyroid/adrenal failure

58
Q

How is hypopituitarism treated?

A

Need multiple hormone replacement (give cortisol first if all axes affected)
o Lack of cortisol is life threatening

8

o Controversy over need for GH in adults

59
Q

What are the causes of hypopituitarism?

A
  • tumours
  • radiotherapy
  • infarction
  • infiltrations
  • trauma/surgery
  • congenital

Phase 2 3. Endocrinology (25 decks)

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