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Endocrine > Pathology of Pituitary and Adrenal Glands > Flashcards

Pathology of Pituitary and Adrenal Glands Flashcards

1
Q

What are some features of the anterior pituitary?

A

Also called the adenohypophysis, derived from Rathke’s pouch, secretes trophic (TSH, ACTH, FSH, LH) and non-trophic (GH, PRL) hormones

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2
Q

What are some features of the posterior pituitary?

A

Also called the neurohypophysis, extension of neural tissue consisting of modified glial cells and axonal processes, secretes ADH and oxytocin

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3
Q

What is the appearance of the anterior pituitary histologically?

A

Islands, cords of cells
Acidophils = somatotrophs (GH, 50%), mammotrophs (PRL, 20%)
Basophils = corticotrophs (ACTH, 20%), thyrotrophs (TSH, 5%0, gonadotrophs (FSH/LH, 5%)

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4
Q

What is the histological appearance of the posterior pituitary?

A

Contains non-myelinated axons of neurosecretory neurons

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5
Q

What are some pathologies that affect the anterior pituitary?

A 
Hyperfunction = adenoma, carcinoma
Hypofunction = surgery/radiation, sudden haemorrhage into gland, ischaemic necrosis (Sheehan syndrome), tumours extending into sella, inflammatory conditions
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6
Q

What are some pathologies that can affect the posterior pituitary?

A

Diabetes insipidus = lack of ADH

Syndrome of inappropriate ADH secretion (SIADH) = ectopic ADH secretion by tumours, primary disorder of pituitary

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7
Q

What are some features of pituitary adenomas?

A

Derived from anterior pituitary cells, relatively common (10% of intra-cranial tumours), sporadic or associated with MEN1 (Wermer syndrome)

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8
Q

How are pituitary adenomas classified?

A

Cell type/hormone produced = prolatin (20-30%), ACTH (10-15%), FSH/LH (10-15%), GH (5%)

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9
Q

How many hormones can pituitary adenomas secrete?

A

Can secrete more than one = can also be hypo/non-functional (25-30%), hormone production may be at sub-clinical level

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10
Q

What are some complications of large adenomas?

A

Visual field defects, pressure atrophy of surrounding normal tissue, infarction can lead to panhypopituitarism

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11
Q

What are some examples of functional pituitary adenomas?

A

Prolactinoma, growth-hormone secreting, ACTH-secreting, carcinoma

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12
Q

What are some features of prolactinomas?

A

Most common functional tumour (30%), may cause infertility, lack of libido or amenorrhoea (25%)

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13
Q

What are some features of growth-hormone secreting adenomas?

A

Second most common functional tumour, GH causes increase in Insulin-like growth factor (IGF), stimulates growth of bone, cartilage and connective tissue (gigantism, acromegaly)

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14
Q

What are some features of ACTH-secreting adenomas?

A

Usually micro-adenomas, may cause Cushing’s disease or bilateral; adrenocortical hyperplasia

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15
Q

What are some features of pituitary carcinomas?

A

Rare (<1% of pituitary tumours), usually produce prolactin or ADH, metastasise late after multiple recurrences

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16
Q

How does pituitary hypofunction usually occur?

A

Usually panhypopituitarism = rarely affects individual hormones

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17
Q

What are the features of pituitary hypofunction?

A

Depends on the cause:
Granulomatous inflammation = sarcoidosis
Infarction = Sheehan’s syndrome
Primary or metastatic tumours

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18
Q

What are craniopharyngiomas?

A

Derived from remnants of Rathke’s pouch = 1-5% of intra-cranial tumours

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19
Q

What are some features of craniopharyngiomas?

A

Slow growing, often cystic, may calcify, some arise in sella but most are suprasellar

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20
Q

How do craniopharyngiomas present?

A

Headaches and visual disturbances, children may have growth retardation, bimodal incidence = age 5-25, 60-70s

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21
Q

What is the prognosis of craniopharyngiomas?

A

Excellent, especially if <5cm

SSC may develop after radiation (rarely)

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22
Q

What are some posterior pituitary syndromes?

A

Diabetes insipidus

SIADH secretion = ectopic production of ADH (paraneoplastic syndrome)

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23
Q

What are the types of diabetes insipidus?

A 
Central = ADH deficiency, caused by trauma (including surgery), tumours and inflammatory disorders of hypothalamus and pituitary
Nephrogenic = renal resistance to ADH effects
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24
Q

What is the anatomy of the adrenal gland?

A

Bilateral glands of 4-5g each, sit superior and medial to upper pole of kidneys, composed of outer cortex and inner medulla

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25
Q

What pathology can affect the adrenal gland?

A

Hypo/hyperfunction = both cortex and medulla

ACTH secretion from functional adenoma, shock/DIC, any condition that damages adrenal tissue

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26
Q

How is the adrenal cortex organised?

A

Into three zones = zona glomerulosa (mineralocorticoids, aldosterone), zona fasciculata (glucocorticoids, cortisol), zone reticularis (sex steroids, glucocorticoids)

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27
Q

What pathologies can affect the adrenal cortex?

A 
Hyperfunction = hyperplasia, adenoma, carcinoma
Hypofunction = acute (Waterhouse-Friderichsen), chronic (Addison's)
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28
Q

What causes congenital adrenocortical hyperplasia?

A

Group of autosomal recessive disorders = deficiency of enzyme required for steroid biosynthesis

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29
Q

What does congenital adrenocortical hyperplasia cause?

A

Altered biosynthesis leads to increased androgen = masculination, precocious puberty

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30
Q

What does the reduced cortisol caused by congenital adrenocortical hyperplasia cause?

A

Stimulate ACTH and causes cortical hyperplasia (10-15 times normal weight)

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31
Q

What are causes of acquired adrenocortical hyperplasia?

A

Endogenous ACTH production = pituitary adenoma (Cushing’s disease), ectopic ACTH (paraneoplastic)
Bilateral adrenal enlargement (up to 30g)
Diffuse (ACTH driven) or nodular (non-ACTH dependent)

32
Q

What are some features of adrenocortical tumours?

A

Mainly adults (Li-Fraumeni syndrome in young), more common in men, present with incidental finding, hormonal effects or mass lesion

33
Q

What can carcinomas with necrosis cause?

A

A fever

34
Q

How do adrenocortical adenomas appear?

A

Well circumscribed, encapsulated lesions, usually small (2-3cm), yellow/yellow-brown cut surface (lipid), small nuclei

35
Q

What are some features of adrenocortical adenomas?

A

Composed of cells resembling adrenocortical cells, usually non-functional, mitoses are rare

36
Q

What are some features of adrenocortical carcinomas?

A

Rare, more likely to be functional, virilising tumours usually malignant, can closely resemble adenoma

37
Q

How can adrenocortical carcinomas spread?

A

Local invasion to retroperitoneum or kidney, metastases usually vascular to liver, lung and bone, may spread to peritoneum, plura or regional lymph nodes

38
Q

What is the prognosis of adrenocortical carcinomas?

A

% years survival = 20-35%

50% dead in two years

39
Q

What features of a tumour are suggestive of an adrenocortical carcinoma?

A

Large size (>50g, >20cm), haemorrhage and necrosis, frequent and atypical mitoses, lack of clear cells, capsular or vascular invasion

40
Q

What are the causes of primary hyperaldosteronism?

A

Conn’s syndrome, 60% associated with diffuse/nodular hyperplasia of both adrenal glands, 35% adenomas, rarely carcinoma

41
Q

What are some features of adenomas associated with primary hyperaldosteronism?

A

Solitary, small, bright yellow and buried within the gland, don’t suppress ACTH so adjacent and contralateral tissue is not atrophic

42
Q

What are some features of causes of primary aldosteronism that are glucocorticoid remediable?

A

Uncommon genetic disorder with production of hybrid steroids, cortisol and aldosterone, under influence of ACTH

43
Q

What are some examples of adrenocortical hyperfunction?

A

Primary hyperaldosteronism ad hypercortisolism

44
Q

What are some causes of hypercortisolism?

A

Cushing’s syndrome or disease, exogenous (iatrogenic i.e steroids), endogenous

45
Q

What are some endogenous causes of hypercortisolism?

A

ACTH dependent = ACTH secreting pituitary adenoma (70%), ectopic ACTH (10%)
ACTH independent = adrenal adenoma (10%) or carcinoma (5%), non-lesional adrenal gland atrophies

46
Q

What does ACTH-dependent endogenous hypercortisolism cause?

A

Gives rise to adrenal hyperplasia

47
Q

What are secondary causes of adrenocortical hypofunction?

A

Failure to stimulate adrenal cortex (hypopituitarism), suppression of adrenal cortex (steroids)

48
Q

What are some acute causes of primary adrenocortical hypofunction?

A

Rapid withdrawl of steroids, crisis in patient’s with chronic adrenocortical insufficiency, massive adrenal haemorrhage

49
Q

In what cases would massive adrenal haemorrhage cause acute primary adrenocortical hypofunction?

A

Newborn, anticoagulation therapy, DIC, septicaemic infection

50
Q

What are some causes of chronic primary adrenocortical hypofunction?

A

Addison’s, autoimmune adrenalitis, infection (TB, histoplasma, HIV), metastatic malignancy (lung, breast)
Unusual causes = amyloid, sarcoidosis, haemochromatosis

51
Q

When do signs and symptoms of chronic primary adrenocortical hypofunction present?

A

Once >90% of the gland has been destroyed

52
Q

How does Addison’s disease present?

A

Insidious onset = manifests once significant decrease in glucocorticoid and mineralocorticoid levels

53
Q

What are the symptoms of Addison’s disease?

A

Weakness, fatigue, anorexia, nausea, vomiting, weight loss, diarrhoea, pigmentation (raised POMC)

54
Q

What do the decreased mineralocorticoid levels in Addison’s disease cause?

A

K+ retention, Na+ loss, hyperkalaemia, hyponatraemia, volume depletion, hypotension

55
Q

What does the decreased glucocorticoids in Addison’s disease cause?

A

Hypoglycaemia

56
Q

What occurs in Addison’s disease crisis?

A

Triggered by stress (infection, surgery, trauma) = vomiting, abdominal pain, hypotension, shock, death

57
Q

What is the anatomy of the adrenal medulla?

A

Central core of adrenal, innervated by pre-synaptic fibres from sympathetic nervous system, contains neuroendocrine (chromaffin) cells (secrete catecholamines)

58
Q

What are some tumours of the adrenal medulla?

A

Phaeochromocytoma, neuroblastoma

59
Q

What are some features of neurofibromas of the adrenal medulla?

A

Usually diagnosed at 18 months, 40% diagnosed in infancy, 40% arise in adrenal medulla, remainder mostly along sympathetic chain

60
Q

What is the histological appearance of neurofibromas?

A

Composed of primitive appearing cells but can show maturation and differentiation towards the ganglion cells

61
Q

What is associated with a poorer prognosis in neurofibromas?

A

Amplification of N-myc and expression of telomerase

62
Q

What are phaeochromocytomas?

A

Neoplasm derived from chromaffin cells of adrenal medulla = secret catecholamines, rare cause of secondary hypertension

63
Q

What are features of the hypertension associated with phaeochromocytomas?

A

Occur in 90%, paroxysmal episodes common, episodes triggered by stress, exercise, posture or palpation of tumour, associated with micturition when in bladder

64
Q

What are complications of phaeochromocytomas?

A

Cardiac failure, infarction and arrhythmias

65
Q

How are phaeochromocytomas diagnosed?

A

Detection of urinary excretion of catecholamines and metabolites

66
Q

What is the “rule of 10” of phaeochromocytomas?

A

10% extra-adrenal (paragangliomas), 10% bilateral (up to 50% in familial), 10% malignant (more common in extra-adrenal), 10% not associated with hypertension

67
Q

What are some features of familial phaeochromocytomas?

A

25% of cases, germline mutations, often bilateral, malignant if associated with germline mutations of B subunit of succinate dehydrogenase

68
Q

What is the appearance of phaeochromocytomas?

A

Range from small to large (average 100g), may see adrenal remnants on surface, yellow, red/brown to haemorrhagic and necrotic

69
Q

What effect does K2Cr2O7 have on phaeochromocytomas?

A

Turns the tumour dark brown

70
Q

What do cells characteristically form in phaeochromocytomas?

A

Tumour cells form nests (zellballen)

71
Q

How do phaeochromocytomas spread?

A

Propensity for skeletal metastasis = also regional lymph nodes, liver and lung

72
Q

What does MEN2a (Sipple syndrome) cause?

A

Phaeochromocytomas (40-50%), medullary thyroid carcinoma (100%), parathyroid hyperplasia (10-20%)

73
Q

What are the phaeochromocytomas that occur dues to Sipple syndrome like?

A

May be bilateral and extra-adrenal

74
Q

What is the mutation that causes MEN2a?

A

Linked to germline gain of function mutation in RET oncogene on chromosome 10q11.2

75
Q

What occurs in MEN2b?

A

Phaeochromocytoma, meduallry thyroid cancer, neuromas and gangliomas, marfanoid habitus

76
Q

What mutation causes MEN2b?

A

Germline mutation in RET oncogene = almost always activating point mutation in the catalytic domain of the encoded enzyme

Endocrine (42 decks)

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