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Endocrine > Pathology of Endocrine Diseases > Flashcards

Pathology of Endocrine Diseases Flashcards

1
Q

what is the endocrine system?

A

Integrated network of GLANDS - secrete chemical messengers – hormones - directly into bloodstream

HORMONES act on target cells distant from site of synthesis - bind to receptors – change cell activity

REGULATION of metabolism, growth and development, tissue function

maintain functional balance

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2
Q

where are hormones synthesised and stored?

A

glands

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3
Q

how are endocrine glands described?

A

packets of cells with secretory granules
vascular
ductless

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4
Q

how is balance of the endocrine system maintained?

A

negative feedback

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5
Q

what makes up the classical endocrine system?

A

Pineal gland
Hypothalamus
Pituitary gland

Thyroid gland
Parathyroid gland
Adrenal glands
Pancreas

but several organs eg ovary, testes, kidneys, produce hormones also endocrine type cells scattered throughout body lung, GI tract, paraganglia (under neuropeptide control)

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6
Q

what can dysregulated hormone release lead to?

A

HYPERFUNCTION
HYPOFUNCTION

effect of a mass lesion

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7
Q

what disease processes affects endocrine organs?

A

HYPERPLASIA
increased number and secretory activity of cells
ATROPHY
diminution of cells due to lack of stimulation
TISSUE DAMAGE
inflammation, autoimmune disease, compression, trauma, infarction
NEOPLASIA
Adenoma – functioning or non functioning
Carcinoma – 1ry or metastatic
CONGENITAL ABNORMALITY

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8
Q

what is a benign neoplasm?

A

Often circumscribed, localised, cannot invade, don’t usually transform

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9
Q

what is malignant neoplasm?

A

Synonymous with cancer, invades, metastasises, if untreated, will often prove fatal

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10
Q

what does the thyroid gland synthesise store and release?

A

thyroxine (T4), triiodothyronine (T3)
Regulates basal metabolic rate

calcitonin
Regulates calcium homeostasis

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11
Q

what is the role of thyroxine (T4), triiodothyronine (T3)?

A

Regulates basal metabolic rate

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12
Q

what is the role of calcitonin?

A

Regulates calcium homeostasis

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13
Q

what physiological effects do thyroxine (T4), triiodothyronine (T3) have?

A

Increases BMR; Accelerates protein synthesis in children; Enhances sympathetic tone (sympathomimetic effect on heart, brown fat) carbohydrate and lipid metabolism

stimulates protein synthesis

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14
Q

what are manifestations of thyroid diseases?

A

Hyperthyroidism
Thyrotoxicosis*

Hypothyroidism
Myxoedema, Cretinism
Subclinical

Thyroid enlargement
Goitre
Isolated nodule/mass

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15
Q

what are primary and secondary causes of thyroid diseases?

A

Thyroiditis
Autoimmune
Others

Gland destruction

Multinodular goitre
Tumours
Benign
Malignant

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16
Q

what are causes of hyperthyroidism?

A

Diffuse toxic hyperplasia (Graves disease) – 70%

Toxic multinodular goitre – 20%

Toxic adenoma

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17
Q

what is graves disease?

A

F>M, peak 20-40 yrs, genetic predisposition

Autoimmune production of anti- TSH receptor antibodies
stimulate activity, growth, inhibit TSH binding
ophthalmopathy immune mediated – ocular fibroblasts have TSH receptor

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18
Q

what affect does graves disease have on the thyroid?

A

diffuse hyperplasia and hyperfunction

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19
Q

how does graves disease affect the thyroid gland?

A

enlarged gland (meaty)

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20
Q

what are causes of hypothyroidism?

A

Hashimoto’s thyroiditis
(auto-immune destruction)

Iatrogenic – surgery, drugs

Iodine deficiency

Congenital hypothyroidism

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21
Q

what is hashimotos thyroiditis?

A

F>M , 45-65yrs

Autoimune destruction of thyroid epithelial cells
Cytotoxic T cells, cytokine and antibody mediated destruction
Circulating autoantibodies to
thyroglobulin ,
thyroid peroxidase

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22
Q

what effect does hashimotos thyroiditis have on the thyroid?

A

Diffuse enlargement gradual failure

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23
Q

describe the manifestation of a multinodular goitre?

A

Iodine deficiency, goitrogens
↓
Impaired synthesis of T3,T4
↓
↑TSH
↓
Hypertrophy and hyperplasia of thyroid epithelium

Simple → → multinodular

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24
Q

what are causes of multinodular goitre?

A

Iodine deficiency commonest cause – also goitrogens like cabbage brussels sprouts and cassava which contains thiocyanate
Endemic/Sporadic Endemic >10% population

Physiological
Puberty
Pregnancy
Autoimmune
Graves’ disease
Hashimoto’s disease
Thyroiditis
Acute (de Quervain’s )
Chronic fibrotic (Reidel’s)
Iodine deficiency (endemic goitre)
Dyshormogenesis
Goitrogens

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25
Q

what can a thyroid nodule be?

A

Dominant nodule in multinodular goitre
Cyst

Follicular adenoma

Carcinoma (5% of nodules)
Differentiated thyroid carcinoma
Papillary carcinoma 75-85%
Follicular carcinoma 10-20%
Anaplastic carcinoma <5%
Medullary carcinoma 5%
(lymphoma)

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26
Q

how should a thyroid nodule be investigated?

A

TFTs

Ultrasound

FNA - cytology

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27
Q

how are thyroid carcinomas often found?

A

inicdentally

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28
Q

what are risk factores for thyroid carcinoma?

A

Family Hx
Chronic inflammatory conditions
Radiation exposure
Obesity

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29
Q

what is follicular adenoma?

A

Most non-functioning
Circumscribed, encapsulated tumour
Histology often small microfollicles

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30
Q

how would you describe follicular carcinoma?

A

Rare, usually solitary
Malignant cells breach capsule
Metastases – blood, bones

invasion through thyroid capsule

31
Q

how would you describe a papillary carcinoma?

A

Usually <50yrs
BRAF mutation or RET/PTC gene rearrangement
Associated with exposure to ionizing radiation
Spreads via lymphatics… but
Excellent prognosis - 85% survival 10 yrs (esp <55yrs)

32
Q

how would you describe a thyroid medullary carcinoma?

A

Malignant tumour of C – cells

produces calcitonin (+/- other polypeptides)

70% sporadic

30% MEN 2A, 2B, familial FMTC – mutations in RET proto-oncogene – prophylactic thyroidectomy

33
Q

how are thyroid carcinomas treated?

A

Surgery

Radioactive iodine

External radiotherapy

Chemotherapy

34
Q

what are parathyroid glands?

A

4 small glands – 120mg
Produce PTH – regulates plasma Ca2+

35
Q

what is Primary hyperparathyroidism?

A

often asymptomatic hypercalcaemia
Sporadic or familial (MEN-1)
Adenoma (85-95%)
Hyperplasia (5-10%)
Carcinoma (rare)

36
Q

what is Secondary hyperparathyroidism?

A

Physiological response to ↓ Ca2+ renal failure

37
Q

describe the pitiutary gland?

A

Small gland, located in sella turcica

Connected to hypothalamus by pituitary stalk

Critical role in regulating other endocrine glands

38
Q

what are the two distinct components of the pituiatary gland?

A

anterior pituitary
posterior pituitary

39
Q

describe the function of anterior pituitary?

A

adenohypophysis 80%

secretes ACTH, TSH, GH, PROLACTIN, FSH/LH

blood supply from hypothalamus

controlled by release factors from hypothalamus

40
Q

describe the function of the posterior pituitary?

A

neurohypophysis

downgrowth of hypothalamus
Secretes ADH, OXYTOCIN

41
Q

what is the most common cause of pituitary hyperfunction?

A

pituitary adenoma

(pituitary carcinomas v rare and some hypothalamic disorders)

42
Q

what is the aetiology of pituitary adenoma?

A

usually adults, 35 to 60 yrs

most sporadic; 5% inherited eg MEN1

43
Q

how does a pituitary adenoma appear macroscopically?

A

soft, well-circumscribed lesion

small microadenomas may be incidental

eg at post mortem

44
Q

what are the effects of pituitary adenoma?

A

If functioning - hormone excess

Prolactinoma - 20-30%
galactorrhoea, menstrual disorders

GH secreting
acromegaly, gigantism

ACTH secreting
Cushing’s disease

Non-functioning - 25-30% of detected tumours
immunohistochemical demonstration (mostly prolactin)

45
Q

describe clinically some effects of a pituitary adenoma?

A
46
Q

if the pituitary tumour is large what affect might this have?

A

Local mass effects: may be confined to the sella turcica but as adenoma expands, may lead to
radiographic abnormalities of the sella turcica, including sellar expansion, bony erosion of sella turcica and anterior clinoid processes, and disruption of the diaphragma sella

visual field abnormalities, classically in the form of defects in the lateral (temporal) visual fields, so-called bitemporal hemianopsia. – as tumour extend superiorly through the diaphragm sella into the suprasellar region, where they often compress the optic chiasm
elevated intracranial pressure, including headache, nausea, and vomiting
compression damage – hypopituitarism esp non functioning which present later

47
Q

describe pituitary hypofunction?

A

75% needs to be lost

Compression by tumours – craniopharyngioma. metastatic

48
Q

what can be caused by pituitary hypofunction?

A

Trauma
Infection (rare)
TB
Sarcoidosis

49
Q

what syndrome is characterised by post partum ischaemic necrosis?

A

Sheehan’s syndrome

50
Q

what is produced by the adrenal cortex?

A

Steroid hormones

51
Q

what is produced by the adrenal medulla?

A

Neuroendocrine (chromaffin) cells

Adrenaline/ noradrenaline

response to stress maintain BP

Extra adrenal paraganglia similar

52
Q

what is the adrenal cortex made up of?

A
53
Q

what are different adrenal pathologies?

A

Hyperfunction
clinical syndromes depend on which adrenal hormones stimulated

Hypofunction

Mass lesion - effect late

Effect on adrenal gland –hyperplasia (diffuse or nodular), atrophy, mass lesion

54
Q

what three syndromes are characterised by adrenal cortical hyperfunction?

A

Hypercortisolism– CUSHING’S SYNDROME

Hyperaldosteronism (Conn’s syndrome)

Adrenogenital syndormes

55
Q

what are different causes of cushings syndrome (hypercortisolism)

A

Exogenous -Iatrogenic steroids

Endogenous
ACTH dependent
pituitary adenoma Cushings disease – 70%
ectopic ACTH

ACTH independent
functioning adrenal adenoma 10%

56
Q

what is ACTH independent hypercortisolism?

A
57
Q

what is ACTH dependent hypercortisolism?

A
58
Q

what is hyperaldosteronism (conns syndrome)?

A

Bilateral idiopathic hyperplasia
Functioning adrenal adenoma
(2ry hyperaldosteronism – physiological due to ↓renal perfusion ↑renin-angiotensin)

Increases sodium retention in the nephron

59
Q

what is adrenogenital syndrome?

A

Functioning adrenal tumour
Pituitary tumour Cushings disease
Congenital adrenal hyperplasia – steroid enzyme deficiency

60
Q

what is acute adrenal insufficiency caused by?

A

destruction of the glands through:

meningococcal septicaemia
Waterhouse Friderichsen

61
Q

what is chronic adrenal insufficiency caused by?

A

1ry - Addison’s disease
Autoimmune : autoimmune polyendocrine syndromes – spare medulla
Infections: TB, fungus HIV-related infections
Replacement: metastatic carcinoma amyloidosis,
Atrophy: prolonged steroid therapy
Congenital hypoplasia

2ry - Pituitary failure

[causing destruction of the glands]

62
Q

what affect do functioning adrenocortical tumours have?

A

hyperadrenal syndromes, atrophy of adjacent cortex

63
Q

how are non functioning adrenocortical tumours found?

A

often incidental – imaging/autopsy

64
Q

what are the appearance of adrenocortical tumours?

A

Yellow-brown circumscribed
Most 2-3cm <30g

65
Q

what are primary adrenocortical carcinomas?

A

rare, any age
More likely functional – virilising
Most large >20cm , haemorrhage and necrosis, cystic
Metastasises by lymphatics and blood – invades adrenal vein

66
Q

what are metastatic carcinomas?

A

More common
lung, breast

67
Q

what is a type of adrenal medullary tumour?

A

PHAEOCHROMOCYTOMA

68
Q

describe PHAEOCHROMOCYTOMA?

A

Adrenal medulla neuroendocrine cells
secrete catecholamines → hypertension
Usually benign behaviour, can be bilateral
Up to 30% inherited – eg MEN 2, SDH
10% extra adrenal (paraganglioma)

69
Q

what is multiple endocrine neoplasia?

A

Inherited disorders with underlying genetic mutation

Hyperplasia/ neoplasms of endocrine organs –
younger age, multifocal

Several distinct syndromes

70
Q

what distinct syndromes does multiple endocrine neoplasia have?

A

MEN 1 (Wermer syndrome)
MEN 2

71
Q

describe MEN 1 (wermers syndrome)

A

MEN 1 tumour suppressor gene mutation -defect in menin protein involved in regulating cell growth

Parathyroid hyperplasia and adenomas

Pancreatic and duodenal endocrine tumours (hypoglycaemia and ulcers)

Pituitary adenoma (prolactinoma)

72
Q

what is MEN 2?

A

RET proto-ongogene mutations

Medullary carcinoma of thyroid
Phaeochromocytoma

73
Q

what is MEN 2A?

A

MEN 2A (Sipple syndrome)
+ Parathyroid hyperplasia

Extracellular domain auto dimerisation of RET receptor

74
Q

what is MEN 2B?

A

+ Neuromas of skin &mucous membrane, skeletal abnormalities

+ Younger patients, aggressive
Autoactivation of tyrosine kinase pathway

Endocrine (35 decks)

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