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Flashcards in Histopathology Endocrine Pathology Deck (94):
1

thyroid Cellular structure

Colloid – filled acini lined by follicular epithelial cells.

2

Thyroid Secretes

1. Hormone thyroxine which is secreted into the blood. The organ is highly vascular for this reason

3

Thyroid Function

2. Regulates basal metabolic rate

4

Hypothyroidism: Commonest Cause is

Hasimoto’s thyroiditis – chronic lymphocytic thyroiditis

5

Hypothyroidism: Hasimoto’s thyroiditis is

An autoimmune: anti-thryoid antibodies: lymphocytic destruction of thyroid – leads to a fibrotic scarred atrophic gland.

6

Hypothyroidism:Epi

F:M = 10:1

7

Hypothyroidism: Less often caused by

Removal of thyroid
Radioiodine treatment

8

Hypothyroidism: Symptoms

Myxoedema slowing of the mind and body
• Weight gain, constipation
• Cold intolerance
• Tiredness, depression
• Big tongue, deep voice (deposition of matrix substances in viscera and skin)
• Thin Hair
• Weak Heartbeat + low BP
• Slow reflexes

9

Hypothyroidism: Histologically

Lymphocytes destroying follicular cells
Reduced colloid in accini
Active inflammation infiltrate

10

Hyperthyroidism Common causes

85% of cases is Grave’s disease
Hyperfunctional multinodular goitre (MNG is usually euthyroid)
Hyperfunctional adenoma (benign follicular tumour) - rarely

11

Hyperthyroidism Description

Increased basal metabolic rate

12

Hyperthyroidism Symptoms

• Sweating, heat intolerance
• Weight loss despite incd appetite, diarrhoea
• Tachycardia, arrhythmias (often AF)
• Tremor, anxiety, hyperactivity, brisk reflexes
• Staring gaze, lid lag, exophthalmos

13

Graves’ disease (diffuse toxic goitre) Epi

F:M = 10:1

14

Graves’ disease (diffuse toxic goitre) Description

Autoimmune

15

Graves’ disease (diffuse toxic goitre) Caused by

Thyroid-stimulating autoantibodies (overdrive increased thyroxine production)

16

Graves’ disease (diffuse toxic goitre) Presentation

Symmetrical enlargement of thyroid – often a bruit can be heard as there is a vast increased in blood flow

17

Graves’ disease (diffuse toxic goitre) Exopthalamos due to

Deposition of connective tissue behind the eyeball = pushed forward

18

Multinodular goitre: Description

Usually euthyroid
Large goitre may cause tracheal compression or dysphagia/stridor
Cosmetic effects

19

Multinodular goitre:
Causes

Due to iodine deficiency and other reasons.
Endemic in some developing countries w/ chronic iodine deficiency.

20

Adenoma (follicular): Description

Benign tumour
Usually euthyroid (not overactive)
Rarely hyperfunctional (toxic nodule)

21

Adenoma (follicular): Treatment

Thyroid lobectomy (can survive with on elobe4)

22

Carcinoma of the thyroid: Types and incidence

• Papillary – 80%
• Follicular – 15%
• Anaplastic – 2%
• Medullary – 3%

23

Carcinoma of the thyroid: Epi

Female predominance of most types
20-30 yrs old

24

Papillary carcinoma

Spread via lympatics
Indolent, often cystic, may be multifocal.
Good prognosis

25

Papillary carcinoma description

Papillae covered by epithelial cells with pale, empty nuclei; psammona bodies
Vesicular appearance.. Cystic (fluid filled)
Well defined lesion

26

Papillary carcinoma Classical presentation

35 yr old woman presents with enlarged cervical lymph nodes: metastatic carcinoma]ultrasound showed a thyroid tumour
Resected thyroid gland: papillary carcinoma.

27

Papillary carcinoma Risk association

Radiation is associated with papillary carcinoma - chernobyl

28

Papillary carcinoma Follicular carcinoma description

Widely invasive. Spreads via bloodstream with metastases to lungs/liver/bones/brain

29

Papillary carcinoma Follicular carcinoma epi

30-50 yrs
Poorer prognosis due to spread via blood stream

30

Papillary carcinoma Clinical presentation example

45 yr old
Pathological fractures
Metastatic

31

Anaplastic carcinoma

Elderly patients
Aggressive – local invasion, metastases
No response to treatment
Fatal in a few months

32

Adenoma carcinoma histology

Spindly shaped tumour cells
Osteoclast like multinucleated → not cancer just reacting to process

33

Medullary Carcinoma arises from

C cells of thyroid,, which secrete calcitonin (calcium metabolism)

34

Medullary Carcinoma tumour type

Neuroendocrine tumour

35

Medullary Carcinoma histo

• Amyloid carcinoma – combination of epithelial proliferation and stromal changes in medulla.
• Calcitonin present in tumour (brown stain = positive cells)

36

Medullary Carcinoma Epi/associated with

Sporadic: 70%
MEN 2A,2B or FMTC: 30%

37

Medullary Carcinoma Diagnostic test

Ret oncogene = overativity of the MEN 2A, 2B

38

Medullary Carcinoma Immuno stain

Confers Calcium secretion confirming medullary carcinoma

39

Normal parathyroid glands

3-4 mm
40-60 mg

40

parathyroid Secrete

Parathyroidhormone (PTH) is secreted in response to low serum calcium levels = increased calcium release from resorption

41

Primary hyperparathyroidism causes

Hyper-calcaemia

42

Primary Hyperparathyroidism causes

Adenoma (85-95%) – benign
Hyperplasia (5-25%)
Carcinoma (<1%) 0 rare

43

parathyroidism Epi

Most cases are sporadic
Hyperplasia or adenoma seen in MEN 1 and 2A (part of these syndromes)

44

Hyper Parathyroidism Symptoms are due to

Hypercalcaemia and increased PTH

45

Hyperparathryoidism Symptoms are

Painful bones – osteoporosis, osteitis, fibrosa cystic
Renal stones – increased calcium
Abdominal groans – various
Pyschic moans – depression, lethargy, seizures

46

Secondary hyperparathyroidism common cause

Chronic renal failure. Hypocalcaemia causes comoensatory overactivity (hyperplasia of all 4 glands)

47

Less common causes of secondary hyperparathyroidism

Vit D or calcium deficiency
Malabsorption
Low serum magnesium
Tissue resistance to Vit D
Pseudohypoparathyroidism (genetic resistance to PTH)

48

Imaging for diagnosis of hyperparathyroidism

Localisation:
1. Sestambi scan: uses radioactive technetium – 99 to look at parathyroids
⇒ Highlightd hyperadctive P/T glands
⇒ 1 = tumour (adenoma more likely)
⇒ 4 or more = hyperplasia
2. Ultrasound

49

Hyperplasia, Primary and secondary – four big ones (usually variably sized):

Enlargement to different degrees
• Primary: Take all four as stimulus to hyperplasia still there.
• Secondary: Unsure of cause therefore take 3 ½ to aim to leave some behind – maintains calcium

50

Parathyroid Carcinoma: Incidence

Rare

51

Parathyroid Carcinoma: Features

Very high Calcium >3.5 mmol/l
Bone disease
Renal Stones
Metastasis (via bloodstream)
Adherent at surgery - fibrosis difficult to dissect off

52

Cortex

Produces 3 types of steroids
• Glucocorticoids, mainly cortisol
• Mineralocorticoids, mainly cortisol
• Sex steroids: oestrogens and androgens

53

Medulla

Produces catecholamines, mainly adrenaline

54

Primary Adrenocortical insufficiency (Addison’s disease):
Causes

Autoimmune destruction
Tuberculosis
Removal
Metastatic Cancer – need both glands involved to have any underactivity
AIDS (CMV, Mycobacterium, Kaposi’s)
Congenital hypoplasia

55

Secondary Adrenocortical insufficiency causes

Disorders of hypothalamus or pituitary – reduced output of ACTH

56

Treatment of secondary adrenocortical insufficiency

Steroids, long term

57

Addison’s disease symptoms

Symptoms due to low levels of glucocorticoids and mineralocorticoids:
• Weakness, tiredness
• GI disturbance: nausea, vomiting, wt loss, diarrhoea
• Hyperpigmentation of skin
• Potassium retention and sodium loss; hypotension
• Adrenal cortex atrophy

58

Hyperpigmentation of the skin due to

Pro-opiomelanocortin from pituitary – a precursor of ACTH and melanocyte stimulating hormone – hyperactivity.

59

Acute renal crisis with addison’s disease

• Precipitated by infection, trauma, and surgical procedures.
• Causes vomiting, abdo pain, hypotension, coma
Rapidly fatal unless treated promptly with corticosteroids

60

Cushing’s Syndrome – Definition

Most commonly iatrogenic due to glucocorticoid administration

61

Cushing’s Syndrome – overactive adrenal cortex Causes

Iatrogenic –due to glucocorticoid administration.
Endogenous

62

Cushing’s Syndrome – overactive adrenal cortex Endogenous

ACTH dependent
ACTH independent

63

Cushing’s Syndrome – overactive adrenal cortex ACTH dependent

Pituitary adenoma (Cushing’s disease) (70%)
Ectopic ACTH production e.g. small cell Carcinoma (10%)

64

Cushing’s Syndrome – overactive adrenal cortex ACTH independent

Adrenal adenoma (10%)
Adrenal carcinoma (5%)
Nodular hyperplasia (<3%)

65

Cushings Syndrome

Excessive cortisol
Adrenal cortical hyperplasia, nodular (involves both glands)

66

Hyperaldosteronism

Excessive aldosterone

67

Adrenogenital or virilising synromes

Excess androgens

68

Conn’s syndrome

Adrenal cortical adenoma: often non-functional or function = Cushing’s Syndrome or hyperaldosteronism

69

Adrenal Cortical Carcinoma –

• Most are functional and usually cause virilism.
• Often large and invasive.
• Venous and lymphatic spread.

70

Pheochromocytoma

Tumour arising in adrenal medullar

71

medullar Produces

Catecholamines, mainly adrenaline

72

Pheochromocytoma Treatment

Surgically correctable hypertension

73

Pheochromocytoma Main feature

Hypertension is often paroxysmal (not continuous therefor in spurts)

74

Pheochromocytoma Diagnosis

Raised level of catecholamines excreted in urine (24 hr screen)

75

Pheochromocytoma Macroscopic changes

Haemorrhagic and necrotic areas

76

Pheochromocytoma Rule of 10’s

• 10% Extra-adrenal (paragangliomas)
• 10% Bilateral
• 10% Malignant (no histological features predict behaviour)
• 10% NOT associated with hypertension

77

Multiple Endocrine Neoplasia (MEN) Syndrome → Inheritance

Genetically inherited diseases

78

Multiple Endocrine Neoplasia (MEN) Syndrome → Features

Proliferative lesions (hyperplasia, adenoma or carcinoma)

79

Multiple Endocrine Neoplasia (MEN) Syndrome → Involves

Multiple endocrine organs

80

Multiple Endocrine Neoplasia (MEN) Syndrome → Types

1, 2A, 2B, FMTC

81

Multiple Endocrine Neoplasia (MEN) Syndrome

MEN 1 (Wermer)
MEN 2 A (Sipple)
MEN 2B

82

MEN 1 (Wermer)


features
Genetic Abnormality

Parathyroid adenoma or hyperplasia/adenoma or hyperplasia o other endocrine glands/carcinoid tumours.

Chromosome 11q, tumour suppressor gene

83

MEN 2 A (Sipple)
Features
Genetic abnormality

Medullary Carcinoma of the thyroid// phaeochromocytoma/parathyroid adenoma or hyperplasia
Chromosome 10q, ret oncogene

84

MEN 2B
Features
Genetic Abnormality

Medullary carcinoma of the thyroid/phaeochronocytoma
Chromosome 10q, ret oncogene

85

Hypothyroidism: causes

Hasimoto’s thyroiditis
Thyroidectomy
Radioiodine treatment

86

Hypothyroidism Symptoms

Slowing of the mind and body
Weak Heartbeat
Constipation
Myxoedema
High LDL
Slow reflexes
Hair thinning
Depression “schizophrenia” irritability
Big Tongue
Croaky voice
Dry Skin
Cold Skin
Cold intolerance

87

Hyperthyroidism: causes

Graves
Nodular goitre
Follicular Adenoma

88

Hyperthyroidism: Symptoms

‘Lid Lag”
Hot Adenoma
Graves
Factitous
Rapid “I” replacement
Ectopic tSH
Sweating “Neurotic anxiety”
Fine Tremor (Paper test)
Brisk Reflexes
Low LDL
Diarrhoea
Wt loss despite increased appetite
Osteoporosis
Atrial fibrillation

89

Hyperplastic epithelium causes

Graves
Iodine deficiency
Goitrogen/ PUT effect

90

Colloid-filled follicles

Idiopathic nodular goitre

91

Anaplastic cells

Cancer

92

Lymphocytes

Hashimoto’s

93

Foreign-body granulomas

DeQuervain’s

94

Fibrous tissue

Riedel’s

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