Pathology of The Endocrine System Flashcards

1
Q

How is balance in the endocrine system maintained?

A

Feedback inhibition

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2
Q

What is included in the endocrine system?

A

Pineal gland, hypothalamus, hypothalamus, pituitary gland, thyroid gland, parathyroid gland, adrenal glands, pancreas
Also ovary, testes and kidneys

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3
Q

What are some disease processes in endocrine organs?

A

Hyperplasia
Atrophy
Tissue damage
Neoplasia
Congenital abnormality

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4
Q

What is the differences between benign and malignant neoplasia?

A

Benign - often circumscribed, localised, cant invade and don’t usually transform
Malignant - cancer, invades, metastasises, and can be fatal

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5
Q

What are some important aspects of endocrine diseases?

A

Endocrine organs have high reserve capacity
Feedback effects may cause endocrine changes
Can have multiorgan effects

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6
Q

Describe the anterior pituitary

A

Adenohypophysis
Secretes ACTH, TSH, GH, prolactin, FSH/LH
Blood supply from hypothalamus
Controlled by release factors from hypothalamus

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7
Q

Describe the posterior pituitary

A

Neurohypophysis
Downgrowth of hypothalamus
Secretes ADH and Oxytocin

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8
Q

What is the most common cause for pituitary hyperfunction?

A

Pituitary adenoma

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9
Q

Describe a pituitary adenoma

A

Usually adults - 35-60years
Most sporadic - 5% inherited
Macroscopic - soft, well circumscribed and mainly an incidental finding

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10
Q

What are the effects pituitary adenoma?

A

If functioning then hormone excess
Prolactinoma, GH secreting and ACTH secreting (Cushing’s)
Non functioning

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11
Q

What large pressure effects can an pituitary adenoma give?

A

Radiograhic abnormalities
Visual field abnormalities
Elevated intracranial pressure
Compression damage - hypopituitarism

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12
Q

What is pituitary hypofunction?

A

75% needs to be lost
Can be compression by tumours
Trauma, infection, TB or sarcoidosis
Sheehan’s syndrome - post partum ischaemic necrosis

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13
Q

Describe the histology of thyroid gland

A

Follicles
Colloids containing thyroglobulin
Epithelial cells - TG synthesis, iodination resorption and release of T3/4
C cells - secrete calcitonin

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14
Q

What are manifestation of thyroid disease?

A

Hyperthyroidism - thyrotoxicosis
Hypothyroidism - myxoedema, cretinism, subclinical
Enlargement - goitre and isolated mass/ nodule

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15
Q

What are the causes of hyperthyroidism?

A

Graves disease - diffuse toxic hyperplasia
Toxic multinodular goitre
Toxic adenoma

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16
Q

Describe Graves disease

A

Autoimmune production of anti-TSH receptor antibodies
Stimulate growth, activity and inhibit TSH binding
More females - peak 20-40yrs
Genetic predisposition
Hyperplasia and hyperfunction

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17
Q

What is the histology for Graves disease?

A

Increased cell activity and cell numbers
Scalloping of colloids

18
Q

What are some causes of hypothyroidism?

A

Hashimoto’s thyroiditis
Iatrogenic - surgery and drugs
Iodine deficiency
Congenital hypothyroidism

19
Q

Describe Hashimoto’s thyroiditis

A

Autoimmune destruction of thyroid epithelial cells
More females - 45-65 yrs
Cytotoxic T cells, cytokine and antibody mediated destruction
Circulating autoantibodies to thyroglobulin and thyroid peroxidase

20
Q

What happens to the thyroid gland in Hashimoto’s thyroiditis?

A

Diffuse enlargement gradual failure

21
Q

Describe the histology of Hashimoto’s thyroiditis

A

Hurthle cell change - ore pink and rounded (more cytoplasm)
Intense infiltration of lymphocytes and plasma cells

22
Q

Describe the process of formation of multinodular goitre

A

Iodine deficiency and goitrogens - impaired synthesis of T3 and T4 - increased TSH - hypertrophy and hyperplasia of epithelium
Then simple to multinodular

23
Q

Describe the histology of multinodular goitre

A

Crowded follicles
Distended colloid filled follicles
Haemorrhage, fibrosis and cystic change
Nodular appearance

24
Q

What can a thyroid nodule be?

A

Dominant nodule in multinodular goitre
Cyst
Follicular adenoma
Carcinoma - differentiated - papillary, medullary, follicular and anaplastic

25
Q

What are the investigations for thyroid nodules?

A

TFTs
US
FNA - cytology

26
Q

What are the risk factors for thyroid carcinoma?

A

FH, chronic inflammatory disease, radiation exposure and obesity

27
Q

Describe follicular adenoma

A

Mostly non-functioning
Circumscribes and encapsulated
Histology - small micro-follicles

28
Q

Describe follicular carcinoma

A

Rare and usually solitary
Malignant cells breach capsule
Metastases - blood and bones
RAS mutation or PAX8/PPARG translocation

29
Q

Describe papillary carcinoma

A

Usually over 50 yrs
BRAF mutation or RET/PTC gene rearrangement
Spreads via lymphatics but good prognosis
Associated with ionising radiation

30
Q

What is the histology of papillary carcinoma?

A

Papillary projections, empty nuclei, psammoma bodies and may be cystic

31
Q

Describe medullary carcinoma

A

Malignant tumour of c cells
Produces calcitonin
70% sporadic
Some MEN2a, b and familial FMTC - mutations in RET proto-oncogene

32
Q

What is the histology of medullary carcinoma?

A

Tumour cells
Amyloids

33
Q

What is the treatment for thyroid carcinoma?

A

Surgery, radio-active iodine, external radiotherapy and chemo

34
Q

What is primary hyperparathyroidism?

A

Often asymptomatic hypercalcaemia
Sporadic or familial (MEN1)
Adenoma mainly, hyperplasia or carcinoma (rare)

35
Q

What is secondary hyperparathyroidism?

A

Physiological response to decreased Ca renal failure
As feedback loop so increases PTH

36
Q

What are multiple endocrine neoplasia (MEN)?

A

Inherited disorders with underlying genetic mutation
Hyperplasia/ neoplasms of endocrine organs - younger age and multifocal
Autosomal dominant

37
Q

Describe MEN1

A

MEN1 tumour suppressor gene mutation - defect in menin protein involved in regulating cell growth

38
Q

What is affected in MEN1?

A

Parathyroid hyperplasia and adenomas
Pancreatic (hypoglycaemia) and duodenal (ulcers) endocrine tumours
Pituitary adenoma

39
Q

Describe MEN2

A

RET proto-oncogene mutation
Medullary carcinoma of thyroid
Pheochromocytoma

40
Q

What is involved in MEN2A?

A

Sipple syndrome
Parathyroid hyperplasia
Extracellular domain auto-dimerization of RET receptor

41
Q

What is involved in MEN2B?

A

Neuromas of skin and mucous membrane
Skeletal abnormalities
Younger patients and aggressive
Autoactivation of tyrosine kinase pathway