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diseases of the endocrine system Flashcards

1
Q

what do endocrine glands do?

A

they secrete hormones directly into the blood and act systemically

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2
Q

what do autocrine glands gRathke’s pouch through adenohypophosis o?

A

they affect the cell that is secreting the protein

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3
Q

what do paracrine glands do?

A

they act locally

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4
Q

where is the pituitary gland located?

A

in the stella turcica beneath the hypothalamus

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5
Q

what does the pituitary gland incoroporate?

A

it has an anterior and posterior lobe and weighs 500-1000mg. 75% of it is the anterior lobe that is formed by an outpouching of the oral cavity - adenohypophysis and 25% is posterior gland by the downgrowth of the hypothalamus through neurohypophysis

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6
Q

what are the main causes of anterior pituitary hypofunction?

A

trauma, tumour, inflammation, infarction and iatrogenic

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7
Q

what tumours can cause anterior hypofunction in the pituitary?

A

metastatic carcinoma, non secretory adenoma

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8
Q

what inflammation can cause anterior hypofunction in the pituitary?

A

granulomatous, autoimmune and other infections

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9
Q

what are the vast majority of primary pituitary tumours due to?

A

benign and adenoma - derived from any hormones producing cells

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10
Q

what are the functional clinical and local effects due to?

A

functional clinical are secondary to the human being produced
local are due to pressure on the optic chiasma or adjacent pituitary

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11
Q

what are ACH, GH secreting and prolactinoma examples of?

A

they are types of anterior pituitary adenomas

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12
Q

in prolactinomas what are the effects?

A

they are the commonest types and they result in galactorrhoea and menstrual disturbance

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13
Q

what does GH secreting lead to?

A

gigantism in children and acromegaly in adults

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14
Q

what does ACTH secreting lead to?

A

cushings syndrome

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15
Q

what is the thyroid gland?

A

it is a bilobed organ that is joined by an isthmus that is encapsulated in a thin fibrous capsule located at the level of the 5, 6 and 7th verterbae in the anterior neck and is in close proximity to the trachea. The average weight is 18g for males and 15 for females and it abuts the thyroid cartilage of the largnyx and the recurrent laryngeal nerve is located in the tracheo-oesophageal groove close to the posterior lateral lobes of the thyroid

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16
Q

how is the thyroid formed?

A

it is formed from two parts - the main part migrates from the foregut to the anterior neck and it’s remnant is the foramen caecum at the junction between the anterior 2/3 and posterior 1/3 of the tongue. The utimobranchial part forms branchial arches and fuses with the main bit laterally

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17
Q

what are the muscles anterior to the thyroid?

A

there is first the thyrohyoid, then the sternohyoid and lateral to this is the omohydoid. These are all paired muscles

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18
Q

what muscles are arond the vertebral body?

A

there is the longus colli, anterior and lateral and the scalenus anterior lateral to this. They are both paired.

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19
Q

what is chronic lymphocytic thyroiditis?

A

it is hashimotos. It is an autoimmune chronic inflammatory disorder that is associated with diffuse enlargement and thyroid autoantibodies. It is more common in females and has a peak age of 59 years old.

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20
Q

what are the signs of hashimotos?

A

there is a diffusely enlarged non tender gland with serum thyroid autoantibodies elevated. There is lymphocytic infiltration of thyroid parenchyma often with germinal centre formation and most will have hypothyroidism.

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21
Q

what are the risks of hashimotos?

A

there is an 80 fold increased risk of thyroid lymphoma and increased risk of papillary carcinoma of the thyroid

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22
Q

what is diffuse hyperplasia of the thyroid?

A

graves - an autoimmune process that results in clinical hyperthyroidism and diffuse hyperplasia of the follicular epithelium - it affects more woman and peak incidence is 30-50ys with an incidence of 1% worldwide

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23
Q

what are the complications of graves?

A

it is responsible for 80% of hyperthyroidism and can be permanent.

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24
Q

what are the findings with graves?

A

symptoms of hyperthyroidism - T3 and T4 are elevated and TSH is suppressed. There will be the presence of thyroid autoantibodies especially thyroid stimulating immunoglobulin. The physical findings with be tibial myxoedema, proptosis or wide eyes stare, tachycardia and hyperactive reflexes

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25
Q

what is a multinodular goitre?

A

it is enlargement of the thyroid with varying degrees of nodularity and there is 1 or more nodules that are discovered by the person or health care professional

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26
Q

what is meant by euthyroid?

A

thyroid normally functions such as normally in multinodular goitres

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27
Q

what are the complications of multinodular goitres?

A

dominant can be mistakened for carcinoma, or tracheal compression or dysphagia may develop with large nodules

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28
Q

what is a follicular adenoma?

A

it is a benign encapsulated tumour with evidence of follicular cell differentiation - it affects females more than males usually in the 5th and 6th decades but a wide age range

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29
Q

what are the signs of follicular adenomna?

A

painless neck mass that is often present for years, solitary nodule involving only one lobe and usually cold nodule on radioactive iodine imaging

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30
Q

what are the statistics of malignant tumours of the thyroid?

A

they are accounting for 1.1% of new tumours, 0.32% of cancer deaths, 85% are differentiated thyroid carcinomas, 5-9% medullary, 1-2% anaplastic carcinoma, 1-3% malignant lymphoma

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31
Q

what is the epidemiology of papillary carcinomas?

A

they are the commonest thyroid carcinomas of over 70% with a female predominance of 2.5:1 - wide age range but peak at 43 years.

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32
Q

what is a papillary carcinoma?

A

it is a familial AD non medullary thyroid carcinoma

33
Q

what are causes of PC?

A

FAP, cowdens syndrome, therapeutic irradiation and radiation exposure, activation of RET and MTRK1, a variety of chromosomal translocations or inversions, fusion of the RET tyrosine kinase regions with thyroid proteins
BRAF V600E mutation and RAS mutations

34
Q

what are the thyroid proteins that RET tyrosine kinases fuse with to make PC?

A

PTC1 in inversion(10)q11;q21 and PTC2 in t(10;17q11.2q21)

35
Q

what is the macroscopic appearance of PC?

A

some are cystic, some are granular, some are encapsulated and they are ill defined and infiltrative

36
Q

what are the main types of follicular neoplasms?

A

Ras mutation types, widely or minimally invasive follicular carcinomas, follicular adenomas and hurthle cell neoplasms

37
Q

what are the epidemiology and stats of follicular carcinomas?

A

they represent 10-20% of thyroid cancers and 90% present with a solitary nodule in thyroid and 10% with distant mets. Off all the mets <5% are local and >60% are widely invasive

38
Q

what is the epidemiology of hurthle cell carcinomas?

A

they represent 3% of all differentiated thyroid cancers and the median age is 53 with a range of 24-85 years. the male to female ratio is F7:M3

39
Q

what is the clinical behaviour of hurthle cell carcinoma?

A

there is a significant incidence of lymph node mets and haematogenous spread sites are bone liver and lung

40
Q

what types of hyperparathyroidism is there?

A

primary secondary and tertiary

41
Q

what is primary hyperparathyroidism?

A

it is excessive secretion of parathyroid hormones from one or more glands

42
Q

what is the difference between secondary and tertiary hyperparathyroidism?

A

secondary is in response to hypocalcaemia (renal insufficiency, malabsorption or Vit D deficiency) and is hyperplasia of the glands with elevated PTH. Tertiary is in association with long standing secondary

43
Q

what is the incidence of primary hyperparathyroidism?

A

25-28 per 100000 but in caucasian women over 60 is 190 per 100000

44
Q

what is the pathogenesis of primary hyperparathyroism?

A

aging, tumourigenesis in general, association with ionising radiation and MEN 2a syndrome

45
Q

what are the causes of primary hyperparathyroidism?

A

asymptomatic mostly, arterial hypertension, hypercalcaemia, psychiatric problems, decreased renal function, osteoporosis, hyperparathyroid bone disease, urolithiasis, hypercalcaemia symptoms
the conditions are single adenomas, diffuse chief or clear cell hyperplasia or carcinoma

46
Q

what is parathyroid adenoma?

A

it is an encapsulated benign neoplasms of parathyroid cells that occurs in 1 in 1000 people and has symptoms of hypercalcaemia - it is a single enlarged parathyroid gland and the others supressed and small

47
Q

what is parathyroid adenoma associated with?

A

MEN1 and MEN2 syndrome and hyperparathyroidism and jaw tumour syndrome

48
Q

what is secondary and tertiary hyperparathyroidism?

A

it is a non neoplastic increase in parathyroid parenchymal cell mass within all parathyroid tissue with a known stimulus

49
Q

what are the features of secondary and tertiary hyperparathyroidism?

A

they are similar pathological symptoms to primary and are sometimes associated with massive gland enlargement

50
Q

where is secondary and tertiary hyperparathyroidism found?

A

in patients with renal failure and on dialysis

51
Q

what is parathyroid carcinoma?

A

it is a malignant tumour derived from the parathyroid parenchymal cells of which 1% are of primary hyperparathyroidism. The symptoms are from excess calcium and it is indolent with a recurrence rate of 50%

52
Q

how is parathyroid carcinoma treated?

A

with surgery - 50% TYSR

53
Q

what is cushings syndrome?

A

it is a collection of signs and symptoms that is due to prolonged exposure to cortisol

54
Q

what can cause cushings syndrome?

A

exogneous - excessive glucocorticoid medication
endogenous - adrenal cortical tumours or hyperplasia and ACTH secreting pituitary adenomas, paraneoplastic cushings from small cell lung carcinoma

55
Q

what are the signs and symptoms of cushings syndrome?

A

hypertension, sweating, central obesity, moonface, headaches, mood swings, insomnia, buffalo hump, weak muscles, osteoporosis and chronic fatigue. Women may also have excessive hair growth - hirsuitism and irregular menstruation

56
Q

what is the structure of the adrenals?

A

there is an outer cortex that is made up of the outer most layer - the glomerulosa, then the fasciculata and then the reticularis
the inner core is the medulla

57
Q

what secretes hormones in the adrenal glands?

A

the medulla secretes catecholamines, the reticularis androgens, the fasciculata cortisol and the glomerulosa aldosterone

58
Q

what is conns?

A

it is hyperaldosteronism that can be primary or secondary and is more common in women than men in 30-50years. It results in the excess production of aldosterone hormones from the adrenal cortex leading to low renin that is controlled by the RAAS.

59
Q

what are the causes of conns?

A

adrenal cortical hyperplasia, adenoma and familial hyperaldosteronism

60
Q

what are the signs and symptoms of conns?

A

high BP, headache, muscular weakness, muscle spasms, excessive urination and cardiac arrhythmias

61
Q

what is addisons disease?

A

it is primary adrenal cortical insufficiency caused by adrenal dysgenesis, destruction and autoimmune adrenalitis and TB, the secondary is due to failure of ACTH secretion

62
Q

what is the epidemiology of addisons?

A

5.3 per million with a high mortality is undiagnosed

63
Q

what is the most common form of addisons?

A

autoimmune

64
Q

what are the symptoms of addisons?

A

it is a triad of postural hypothension, hyponatraemia and hyperpigmentation

65
Q

how is addisons treated?

A

through long term steroid replacement

66
Q

what is an adrenal cortical nodule?

A

it is a benign non functional nodule of the adrenal cortex that affects between 1.5 and 3% of the population but higher in the elderly, those with hypotension and diabetics

67
Q

what are the symptoms of adrenal cortical nodules?

A

no clinical symptoms

incidental discovery on radiographic studies - no treatment required

68
Q

what are adrenal cortical adenomas?

A

the are benign neoplastic proliferations of adrenal cortical tissue with an incidence of 1-5% of the population

69
Q

what are the symptoms of adrenal cortical nodules from?

A

related to endocrine hyperfunction - hypertensions, cushings and virilisation - aldosterone producing cause Conns, cortisol producing - cushings and rare cause virilisation

70
Q

what are adrenal cortical carcinomas?

A

they are the malignant counterpart of adrenal cortical adenoma. They represent 3% of the endocrine neoplasms and have an incidence of about 1 million per population.

71
Q

what are the symptoms of adrenal cortical carcinomas?

A

they are related to hormone excess and present with abdo masses

72
Q

what does the treatment of adrenal cortical carcinoma depend on?

A

the stage, age and prognosis

73
Q

what is the 5YSR of adrenal cortical carcinoma?

A

around 70%

74
Q

what is a phaeochromocytoma?

A

it is a catecholamine secreting tumour arising from the adrenal medulla with an incidence of 8 per million in population and 10% are bilateral 10% are extraadrenal, 10% are in children, 10% are malignant and 10% are familial

75
Q

what are the causes of phaeochromocytoma?

A

most are sporadic but familial syndrome MEN2a and 2b, Von Hippel-Lindau and von Recklinghausens disease are related

76
Q

what are the symptoms of phaeochromocytoma?

A

the have symptoms of hypertension, palpitations, headaches and anxiety

77
Q

what are the signs of phaeochromocytoma?

A

elevated urine catecholamines, adrenaline, noradrenaline

78
Q

what is the prognosis of phaeochromocytoma?

A

excellent prognosis when benign and properly manages, malignant tumour pursue and aggressive course

CP (38 decks)

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