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Endocrinology > Pathology of Pituitary and Adrenal Glands > Flashcards

Pathology of Pituitary and Adrenal Glands Flashcards

1
Q

what is the anterior pituitary derived from

A

Rathkes pouch

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2
Q

what trophic hormones does the anterior pituitary produce

A

TSH, ACTH, FSH, LH

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3
Q

what non trophic hormones are produced by the anterior pituitary

A

GH and prolactin

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4
Q

what is a trophic hormone

A

one that has a growth affect on endocrine glands and stimulates them to produce their hormones

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5
Q

what is the andenohypophysis

A

anterior pituitary gland

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6
Q

what is the neurohypophysis

A

posterior pituitary gland

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7
Q

what does posterior pituitary tissue consist of

A

is an extension of neural- consists of modified glial cells and axonal processes

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8
Q

what does the posterior pituitary secrete

A

vasopressin and oxytocin

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9
Q

describe the histology of the posterior pituitary gland

A

non- myelinated axons of neurosecretory neurones

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10
Q

describe the histology of the anterior pituitary gland

A

islands, cords of cells,
acidophils,
basophils,
chromophobes

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11
Q

what cells produce GH

A

type of acidophil called somatotrophs

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12
Q

what type of cell produces PRL

A

type of acidophil called mammotrophs

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13
Q

what type of cell produces ACTH

A

type of basophil called corticotrophs

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14
Q

what type of cell produces TSH

A

type of basophil called thyrotrophs

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15
Q

what type of cell produces FSH, LH

A

type of basophil called gonadotrophs

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16
Q

what can cause hyperfunction of the anterior pituitary

A

adenoma, carcinoma

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17
Q

what can cause hypofunction of the anterior pituitary

A 
surgery/ radiation,
sudden haemorrhage into gland,
ischaemic necrosis (sheehan syndrome in pregnancy),
tumours extending into sella,
inflammatory conditions (sarcoidosis)
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18
Q

what causes SIADH

A

ectopic secretion of ADH by tumours

primary disorder int the pituitary

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19
Q

what condition can

pituitary adenomas be associated with

A

MEN1- werner syndrome

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20
Q

what are pituitary adenomas classified by

A

cell type/ hormone produced

can be hypo/non functional (mass lesion which compresses surrounding normal pituitary tissues which will atrophy)
can produce more than 1 hormone

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21
Q

what are features of large pituitary adenomas

A

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

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22
Q

what are the functional pituitary adenomas

A

prolactinoma (most common), GH secreting, ACTH secreting

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23
Q

what are the symptoms of a prolactinoma

A

infertility, lack of libido, amenorrhea

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24
Q

what are the features of a growth secreting hormone

A

GH causes increase in insulin like growth factors (IGF)
stimulates growth of bone, cartilage and connective tissue
gigantism or acromegaly

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25
Q

what are the symptoms of an ACTH tumour

A

cushings disease

bilateral adrenocortical hyperplasia

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26
Q

what do functional pituitary carcinomas usually secrete

A

prolactin or ACTH

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27
Q

what can cause panhypopituitarism

A

granulomatous inflammation- sarcoidosis
infarction- sheehans syndrome
primary or metastatic tumours

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28
Q

what is a craniopharyngioma

A

intracranial tumour derived from remnants of rathke’s pouch, often suprasellar

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29
Q

who gets craniopharynogioma

A

5-15 years

eldery- 6th to 7th decades

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30
Q

what are the symptoms of craniopharyngioma

A

visual disturbances, children may have growth retardation

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31
Q

what is the prognosis like for craniopharyngioma

A

very good (especially if under 5cm)

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32
Q

what are the central causes of diabetes insipidus

A

ADH deficiency

trauma (including surgery), tumours, inflammatory disorders of the hypothalamus an pituitary

33
Q

what are the nephrogenic causes of diabetes insipidus

A

renal resistance to ADH effects

34
Q

what causes SIADH

A

ectopic production of ADH- paraneoplastic syndrome

35
Q

how much does an adrenal gland weigh

A

4-5 grams each

36
Q

where are the adrenal glands

A

sit superior and medial to the upper pole of the kidneys

37
Q

what are the components of the adrenal glands

A

outer cortex enclosing a central medulla

38
Q

what diseases can manifest as adrenal pathologies

A

pituitary disease (ACTH secretion from function adenoma)
Shock, DIC
conditions that damage/ destroy adrenal tissue

39
Q

is it the cortex or medulla of the adrenal glands that can be affected by hypo/hyper function

A

both

40
Q

what can cause hyperfunction of the adrenal cortex

A

hyperplasia, adenoma, carcinoma

41
Q

what can cause hypofunction of the adrenal cortex

A

acute: waterhouse-friderichsen
chronic: addisons disease

42
Q

what are the congenital causes of adrenocortical hyperplasia - how does it cause it

A

group of autosomal recessive disorders

where there is a deficiency or lack of enzyme required for steroid biosynthesis which leads to increased androgen production (masculinisation and precocious puberty)

stimulates ACTH release and cortisol hyperplasia

43
Q

what are the causes of acquired adrenocortical hyperplasia

A

endogenous ACTH production: cushings disease (pituitary adenoma), ectopic ACTH (paraneoplastic syndrome)

44
Q

what happens to the adrenal gland in acquired adrenocortical hyperplasia

A

bilateral adrenal enlargement

diffuse (ACTH driven) or nodular (ACTH independent)

45
Q

what is produced by the adrenal cortex

A

aldosterone, cortisol and testosterone

46
Q

who gets adrenocortical tumours

A

usually adults, males more than females

47
Q

what is the usual presentation of an adrenocortical tumour

A

incidental finding
hormonal effects
mass lesion (almost always carcinomas)
carcinomas with necrosis can cause fever

48
Q

describe what adenocortical adenomas are like

A

well circumscribed, encapsulated lesions
usually small
yellow/ brownish surface (lipids)
cells resemble adrenocortical cells
are well differentiates, small nuclei, rare mitoses
can be function, usually not

49
Q

what are virulising adrenocortical carcinomas usually

A

malignant

50
Q

describe the spread of an adrenocortical carcinoma

A

local invasion (retroperitoneum, kidney)
metastasis (vascular- to liver, lung and bone)
peritoneum and pleura
regional lymph nodes

51
Q

what is the survival for adrenocortical carcinomas

A

5 year 20-35%

52
Q

what is the only definite discriminating factor between adrenocortical tumours

A

whether or not they metastasis

53
Q

what features suggest a adrenocortical tumour

A 
large 
haemorrhage and necrosis 
frequent mitosis 
atypical mitosis 
lack of clear cells 
capsular or vascular invasion
54
Q

what is primary hyperaldosteronism

A

conns- hypersecretion of aldosterone

55
Q

is conns under the influence of ACTH

A

yes

56
Q

what changes to the adrenal gland is conns associated with

A

diffuse or nodular hyperplasia of both adrenal glands

57
Q

what can cause hypercortisolism

A

cushings syndrome

exogenous (iatrogenic) or endogenous (ACTH dependent and independent)

58
Q

what are the ACTH dependent causes of hypercortisolism

A 
ACTH secreting pituitary adenoma (cushings) 
ectopic ACTH (small cell lung cancer)
59
Q

what are the ACTH independent cause of hypercortisolism

A

adrenal adenoma or carcinoma

non lesional adrenal gland atrophies

60
Q

what can cause secondary adrenocortical hypofunction

A

failure to stimulate adrenal cortex (hypothalamic-pituitary disorder)

suppression of adrenal cortex (treatment with steroids)

61
Q

what can cause acute primary adrenocortical insufficiency

A

rapid withdrawal of steroid treatment
addisons crisis
adrenal haemorrhage (newborn, antocoagulatant treatment, DIC, septicaemic infection, waterhouse friderichsen)

62
Q

what can cause chronic primary adrenocortical insifficiency

A

addisons disease: autoimmune adrenalitis, infections (TB, fungal, HIV), metastases

rare: amyloid, sarcoidosis, haemochromatosis

63
Q

describe the onset of addisons disease

A

insidious - manifests once there is a significant decrease in glucocorticoid and mineralocorticoid levels

64
Q

what are the symptoms of addisons disease

A

weakness, fatigue, anorexia, nausea, vomiting, weight loss, diarrhoea

pigmentation

65
Q

what is decreased in addisons

A

mineralocorticoids (K+ retention, Na+ loss, hyperkalaemia, hyponatraemia, volume depletion and hypotension)

decreased glucocorticoids (hypoglycaemia)

66
Q

what are the symptoms of addisons crisis

A

vomiting, abdo pain, hypotension, shock and death

67
Q

what is the precipitating factor in addisons crisis

A

stress- infection, trauma, surgery

68
Q

what is the adrenal medulla innervated by

A

pre-synaptic fibres from sympathetic nervous system

69
Q

what cells in the adrenal medulla secrete catecholamines

A

neuroendocrine (chromaffin) cells

70
Q

what are the two tumours seen in the adrenal medulla

A

phaochromocytoma and neuroblastoma

71
Q

where can neuroblastomas arise

A

40% in adrenal medulla

remainder along sympathetic chain

72
Q

what cells make up neuroblastomas

A

primitive appearing cells, can show maturation and differentiation towards ganglion cells

73
Q

what cells are pheochromocytomas derived from

A

chromaffin cells of the adrenal medulla

74
Q

explain the triad of symptoms of a phaeochromocytoma

A

headache, hypertension (paroxysmal episodes) and sweating

as secretes catcholamines

75
Q

what are the complications of phaeochromocytomas

A

cardiac failure, infarction, arrhythmias, cerebrovascular accident

76
Q

how do you lab diagnose a phaeochromocytoma

A

urinary excretion of catecholamines and metabolites

77
Q

what are the 10%s in phaeochromocytoma

A 
10% are extra-adrenal
10% are bilateral 
10% are biologically malignant
10% are NOT associated with hypertension
25% are familial
78
Q

where do phaeochromocytoma spread to

A

skeletal metastasis, regional lymph nodes, liver and lung

79
Q

what genetic condition is phaeochromoytoma a feature of

A

MEN2

Endocrinology (46 decks)

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