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Endocrine MBCHB > Pituitary Disorders > Flashcards

Pituitary Disorders Flashcards

1
Q

What is a pituitary adenoma?

A

Benign tumour derived from cells of anterior pituitary

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2
Q

What is the aetiology of pituitary adenoma?

A

sporadic or associated with MEN1

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3
Q

What are micro-adenomas?

A
  • adenomas<1cm
  • much less aggressive than macroadenomas
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4
Q

What are macroadenomas?

A
  • adenomas >1cm
  • can present with visual field defects due to compression of the optic chiasma
  • can cause pressure atrophy of normal surrounding cell tissue
  • infarction can lead to panhypopituitarism
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5
Q

What are aggressive pituitary adenomas?

A
  • a subset of adenomas behave aggressively and enlarge more rapidly (but don’t metastasise as still benign)
  • features which indicate an aggressive lesion include lots of mitotic figures and p53 mutations
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6
Q

What are pituitary carcinomas?

A
  • rare, account for <1% of pituitary tumours
  • often functional (prolactin or ACTH usually)
  • metastasise late after multiple recurrences
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7
Q

What is the presentation of a pituitary adenoma?

A

Non-functioning adenomas

  • present due to mass effects

Functioning adenomas

Functioning pituitary adenomas are classified by cell type/hormone produced:

  • prolactin (20-30%) - most common
  • FSH/LH (10-15%)
  • GH (5%) → GIGANTISM (Children) or acromegaly (adults)
  • ACTH - usually a microadenoma → Cushing’s, bilateral adrenocortical hyperplasia
  • can produce more than one hormone
  • hormone production may be at subclinical levels
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8
Q

What is the investigation for a pituitary adenoma?

A

Prolactinoma

  • serum prolactin raised
  • MRI pituitary - micro vs macro, involvement of pituitary stalk/optic chiasm
  • visual fields - bitemporal hemianopia
  • other pituitary hormone tests to assess whether other hormones are being affected
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9
Q

What is the management of a prolactinoma?

A
  • Bromocriptine - three times a day oral
  • Quinagolide - once a day oral
  • Cabergoline - once to twice per week oral - least side effects
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10
Q

What is acromegaly?

A

Growth hormone (GH) stimulates skeletal and soft tissue growth - GH excess therefore produces gigantism in children (if acquired before epiphyseal fusion) and acromegaly in adults

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11
Q

What is the aetiology of acromegaly?

A

nearly always due to a GH-secreting pituitary adenoma

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12
Q

What is the presentation of acromegaly?

A
  • giant (before epiphyseal fusion)
  • thickened soft tissues - skin, large jaw, sweaty, large hands
  • snoring/sleep apnoea
  • hypertension, cardiac failure → early CV death
  • headaches (vascular)
  • diabetes mellitus
  • local pituitary effects - visual fields, hypopituitarism
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13
Q

What are the investigations for acromegaly?

A
  • IGF1 - age and sex matched, nearly always raised
  • Gold standard - GTT suppression test
    • 75g oral glucose - check GH at 0, 30, 60, 90, 120 min
    • Normally GH suppresses to <0.4 yg/l after glucose
    • acromegaly indicated if GH unchanged/no suppression or paradoxical rise
  • Visual fields
  • CT/MRI Pituitary scan to check size of adenoma
  • Pituitary function tests for other hormones
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14
Q

What is the management of acromegaly?

A

1st line - pituitary surgery
2nd line - Somatostatin analogues
3rd line - dopamine agonists
4th line - GH Antagonists

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15
Q

Describe pituitary surgery for acromegaly?

A
  • transsphenoidal approach first line
  • 90% cure if microadenoma
  • 50% cure if macroadenoma
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16
Q

Describe the management of acromegaly using pharmacological management.

A
  • Somatostatin analogues e.g., sandostatin LAR reduce GH in most patients, can be used before surgery to relieve symptoms and marginally improve outcomes
    • given by subcutaneous injection
    • side effects → diarrhoea, abdominal pains, gallstones and risk of biliary colic

Dopamine Agonists:
- Cabergoline up to 3g weekly
- works in around 10-15% of patients
- better if co-secreting prolactin

GH Antagonists:
- Pegvisomant
- SC injection - 10-30mg
- binds to GH receptor - blocks GH activity
- Tumour size does not decrease - occasional small increase in tumour size
- IGF-1 decreases but serum GH concentrations may increase

17
Q

What are the complications of acromegaly?

A
  • GH excess can result in the formation of colon polyps and colon cancer - may be presenting feature
  • Increased risk of hypertension and cardiac failure can lead to early CV death
18
Q

What is hypopituitarism?

A

Inadequate production of one or more pituitary hormone as a result of damage to the pituitary gland and/or hypothalamus

19
Q

What is the aetiology of hypopituitarism?

A
  • Pituitary tumours - non-functioning pituitary macroadenomas are the most common cause of hypopituitarism among adults
  • Other local brain tumours - astrocytomas, meningiomas, gliomas, clival chordoma
  • Iatrogenic - surgery or radiation
  • Secondary metastatic lesions - lung, breast
  • Traumatic brain injury
  • Vascular diseases - polyarteritis
  • Subarachnoid haemorrhage
  • Hypothalamic diseases - syphilis, meningitis
  • Autoimmune - Sheenan (post pregnancy)
  • Granulomatous inflammation - sarcoidosis, histiocytosis X tuberculosis, meningitis
  • Infarction/haemorrhage
20
Q

What are the consequences of hypopituitarism?

A
  • ↓ GH → growth failure
  • ↓ TSH → secondary hypothyroidism
  • ↓ LH/FSH → hypogonadism
  • ↓ ACTH → hypoadrenal
  • ↓ prolactin → unknown
  • ↓ ADH → diabetes insipidus
21
Q

What is panhypopituitarism?

A
  • Refers to deficiency of all anterior pituitary hormones
  • It is most commonly caused by pituitary tumours, surgery or radiotherapy
22
Q

What is the presentation of hypopituitarism?

A
  • Variable - depend on the specific hormone deficiency, age of onset, the rate at which hypopituitarism develops, and the underlying cause of hypopituitarism
  • As well as hormonal effects, intra/parasellar masses (e.g. pituitary macroadenomas, craniopharyngiomas) can present with headaches and visual field defects (bitemporal hemianopia)
  • Secondary hypothyroidism, hypoadrenalism, hypogonadism and GH deficiency lead to tiredness and general malaise, and reduced quality of life
23
Q

What is the presentation of hypothyroidism?

A

Hypothyroidism causes weight gain, slowness of thought and action, dry skin, cold intolerance, constipation and potentially bradycardia and hyperthermia

24
Q

What is the presentation of hypoadrenalism?

A

Hypoadrenalism causes mild hypotension, hyponatraemia and CV collapse (during severe intercurrent stressful illness)

25
Q

What is the presentation of hypogonadism?

A

Hypogonadism leads to loss of libido, loss of secondary sexual hair, amenorrhoea and erectile disfunction, and eventually osteoporosis

26
Q

What are the investigations for hypopituitarism?

A

Basal Tests

  • LH, FSH, oestradiol/testosterone
  • IGF-1
  • Prolactin
  • TSH, free T4, T3
  • ACTH, cortisol
  • Plasma/urine osmolality

Dynamic Tests

  • Growth - insulin tolerance test, glucagon test
  • HP-adrenal - insulin tolerance test, short ACTH stimulation test
  • Water deprivation test

Imaging

  • If a pituitary hormone deficiency is identified, perform cranial imaging (preferably MRI) to identify pituitary adenomas
27
Q

What is the management of TSH deficiency?

A

levothyroxine

28
Q

What is the management of ACTH deficiency?

A
  • Hydrocortisone
  • Cortisol is the most important hormone to replace because its deficiency can make patients the most unwell and often presents with an ‘Addisonian’ type clinical picture
29
Q

What is the management of growth hormone deficiency?

A
  • Needs to be given in children for growth
  • May be considered in adults to improve work capacity and psychological well-being
    • Decreases abdominal fat, increases muscle mass, strength, exercise, capacity and stamina, improves cardiac function, decreases cholesterol, increases LDL, increases bone density
  • Daily SC injection
30
Q

What is the management for hypogonadism?

A
  • HRT/oest/prog pill for female
  • Testosterone for males - sustanon (IM every 3-4 weeks) or skin gel (testogel, tostral) or nebido (prolonged IM injection 10-14 weeks)
31
Q

What happens in diabetes insipidus?

A

Kidneys are unable to concentrate urine

32
Q

What is the aetiology of diabetes insipidus?

A

Cranial DI

  • Occurs when there is insufficient levels of circulating ADHFamilial - very rare
  • Isolated in most causes
  • DIDMOADAcquired
  • Idiopathic in 50% - often autoimmune
  • Tumours - craniopharyngioma, hypothalamic tumour, metastases, pituitary (very rare)
  • Trauma - road accidents, skull fracture, external irradiation
  • Infiltrations - sarcoidosis
  • Infections - tuberculosis, meningitis, inflammatory disorders of hypothalamus and pituitary
33
Q

What is the presentation of diabetes insipidus?

A
  • Polydipsia
  • Polyuria with dilute urine
34
Q

What are the investigations of diabetes insipidus?

A

Water deprivation test

  • After obtaining baseline lab values, patients stop drinking water for 2–3 hours before the first measurement
  • Check serum and urine osmolarities hourly for 8hr, then 4hr after giving DDAVP
  • If Ur/serum osmol ratio >2 it is normal, otherwise DI
  • If Ur/serum osmol ratio is low and improves after DDAVP then it is due to cranial DI (not nephrogenic)

Imaging

  • If CDI is diagnosed, a CT scan or MRI of the head should be conducted to rule out brain tumours (especially craniopharyngioma)
35
Q

What is the management of diabetes insipidus?

A
  • Desmospray (nasally) or desmopressin oral tablets
  • Desmopressin IM injection - generally reserved for emergency or post pituitary surgery

Endocrine MBCHB (13 decks)

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