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Cardio > Histopathology Endocrine Pathology > Flashcards

Histopathology Endocrine Pathology Flashcards

1
Q

thyroid Cellular structure

A

Colloid – filled acini lined by follicular epithelial cells.

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2
Q

Thyroid Secretes

A
  1. Hormone thyroxine which is secreted into the blood. The organ is highly vascular for this reason
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3
Q

Thyroid Function

A
  1. Regulates basal metabolic rate
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4
Q

Hypothyroidism: Commonest Cause is

A

Hasimoto’s thyroiditis – chronic lymphocytic thyroiditis

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5
Q

Hypothyroidism: Hasimoto’s thyroiditis is

A

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

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6
Q

Hypothyroidism:Epi

A

F:M = 10:1

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7
Q

Hypothyroidism: Less often caused by

A

Removal of thyroid

Radioiodine treatment

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8
Q

Hypothyroidism: Symptoms

A 
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
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9
Q

Hypothyroidism: Histologically

A

Lymphocytes destroying follicular cells
Reduced colloid in accini
Active inflammation infiltrate

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10
Q

Hyperthyroidism Common causes

A 
85% of cases is Grave’s disease
Hyperfunctional multinodular goitre (MNG is usually euthyroid)
Hyperfunctional adenoma (benign follicular tumour) - rarely
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11
Q

Hyperthyroidism Description

A

Increased basal metabolic rate

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12
Q

Hyperthyroidism Symptoms

A
  • Sweating, heat intolerance
  • Weight loss despite incd appetite, diarrhoea
  • Tachycardia, arrhythmias (often AF)
  • Tremor, anxiety, hyperactivity, brisk reflexes
  • Staring gaze, lid lag, exophthalmos
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13
Q

Graves’ disease (diffuse toxic goitre) Epi

A

F:M = 10:1

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14
Q

Graves’ disease (diffuse toxic goitre) Description

A

Autoimmune

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15
Q

Graves’ disease (diffuse toxic goitre) Caused by

A

Thyroid-stimulating autoantibodies (overdrive increased thyroxine production)

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16
Q

Graves’ disease (diffuse toxic goitre) Presentation

A

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

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17
Q

Graves’ disease (diffuse toxic goitre) Exopthalamos due to

A

Deposition of connective tissue behind the eyeball = pushed forward

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18
Q

Multinodular goitre: Description

A

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

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19
Q

Multinodular goitre:

Causes

A

Due to iodine deficiency and other reasons.

Endemic in some developing countries w/ chronic iodine deficiency.

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20
Q

Adenoma (follicular): Description

A 
Benign tumour
Usually euthyroid (not overactive)
Rarely hyperfunctional (toxic nodule)
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21
Q

Adenoma (follicular): Treatment

A

Thyroid lobectomy (can survive with on elobe4)

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22
Q

Carcinoma of the thyroid: Types and incidence

A
  • Papillary – 80%
  • Follicular – 15%
  • Anaplastic – 2%
  • Medullary – 3%
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23
Q

Carcinoma of the thyroid: Epi

A

Female predominance of most types

20-30 yrs old

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24
Q

Papillary carcinoma

A

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

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25
Q

Papillary carcinoma description

A

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

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26
Q

Papillary carcinoma Classical presentation

A

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

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27
Q

Papillary carcinoma Risk association

A

Radiation is associated with papillary carcinoma - chernobyl

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28
Q

Papillary carcinoma Follicular carcinoma description

A

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

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29
Q

Papillary carcinoma Follicular carcinoma epi

A

30-50 yrs

Poorer prognosis due to spread via blood stream

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30
Q

Papillary carcinoma Clinical presentation example

A

45 yr old
Pathological fractures
Metastatic

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31
Q

Anaplastic carcinoma

A

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

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32
Q

Adenoma carcinoma histology

A

Spindly shaped tumour cells

Osteoclast like multinucleated → not cancer just reacting to process

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33
Q

Medullary Carcinoma arises from

A

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

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34
Q

Medullary Carcinoma tumour type

A

Neuroendocrine tumour

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35
Q

Medullary Carcinoma histo

A
  • Amyloid carcinoma – combination of epithelial proliferation and stromal changes in medulla.
  • Calcitonin present in tumour (brown stain = positive cells)
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36
Q

Medullary Carcinoma Epi/associated with

A

Sporadic: 70%

MEN 2A,2B or FMTC: 30%

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37
Q

Medullary Carcinoma Diagnostic test

A

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

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38
Q

Medullary Carcinoma Immuno stain

A

Confers Calcium secretion confirming medullary carcinoma

39
Q

Normal parathyroid glands

A

3-4 mm

40-60 mg

40
Q

parathyroid Secrete

A

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

41
Q

Primary hyperparathyroidism causes

A

Hyper-calcaemia

42
Q

Primary Hyperparathyroidism causes

A

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

43
Q

parathyroidism Epi

A

Most cases are sporadic

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

44
Q

Hyper Parathyroidism Symptoms are due to

A

Hypercalcaemia and increased PTH

45
Q

Hyperparathryoidism Symptoms are

A

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

46
Q

Secondary hyperparathyroidism common cause

A

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

47
Q

Less common causes of secondary hyperparathyroidism

A 
Vit D or calcium deficiency
Malabsorption
Low serum magnesium
Tissue resistance to Vit D
Pseudohypoparathyroidism (genetic resistance to PTH)
48
Q

Imaging for diagnosis of hyperparathyroidism

A 
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
Q

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

A

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
Q

Parathyroid Carcinoma: Incidence

51
Q

Parathyroid Carcinoma: Features

A 
Very high Calcium >3.5 mmol/l
Bone disease
Renal Stones
Metastasis (via bloodstream)
Adherent at surgery - fibrosis difficult to dissect off
52
Q

Cortex

A

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

53
Q

Medulla

A

Produces catecholamines, mainly adrenaline

54
Q

Primary Adrenocortical insufficiency (Addison’s disease):

Causes

A 
Autoimmune destruction
Tuberculosis
Removal
Metastatic Cancer – need both glands involved to have any underactivity
AIDS (CMV, Mycobacterium, Kaposi’s)
Congenital hypoplasia
55
Q

Secondary Adrenocortical insufficiency causes

A

Disorders of hypothalamus or pituitary – reduced output of ACTH

56
Q

Treatment of secondary adrenocortical insufficiency

A

Steroids, long term

57
Q

Addison’s disease symptoms

A

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
Q

Hyperpigmentation of the skin due to

A

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

59
Q

Acute renal crisis with addison’s disease

A

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

60
Q

Cushing’s Syndrome – Definition

A

Most commonly iatrogenic due to glucocorticoid administration

61
Q

Cushing’s Syndrome – overactive adrenal cortex Causes

A

Iatrogenic –due to glucocorticoid administration.

Endogenous

62
Q

Cushing’s Syndrome – overactive adrenal cortex Endogenous

A

ACTH dependent

ACTH independent

63
Q

Cushing’s Syndrome – overactive adrenal cortex ACTH dependent

A 
Pituitary adenoma (Cushing’s disease) (70%)
Ectopic ACTH production e.g. small cell Carcinoma (10%)
64
Q

Cushing’s Syndrome – overactive adrenal cortex ACTH independent

A 
Adrenal adenoma (10%)
Adrenal carcinoma (5%)
Nodular hyperplasia (<3%)
65
Q

Cushings Syndrome

A

Excessive cortisol

Adrenal cortical hyperplasia, nodular (involves both glands)

66
Q

Hyperaldosteronism

A

Excessive aldosterone

67
Q

Adrenogenital or virilising synromes

A

Excess androgens

68
Q

Conn’s syndrome

A

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

69
Q

Adrenal Cortical Carcinoma –

A
  • Most are functional and usually cause virilism.
  • Often large and invasive.
  • Venous and lymphatic spread.
70
Q

Pheochromocytoma

A

Tumour arising in adrenal medullar

71
Q

medullar Produces

A

Catecholamines, mainly adrenaline

72
Q

Pheochromocytoma Treatment

A

Surgically correctable hypertension

73
Q

Pheochromocytoma Main feature

A

Hypertension is often paroxysmal (not continuous therefor in spurts)

74
Q

Pheochromocytoma Diagnosis

A

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

75
Q

Pheochromocytoma Macroscopic changes

A

Haemorrhagic and necrotic areas

76
Q

Pheochromocytoma Rule of 10’s

A
  • 10% Extra-adrenal (paragangliomas)
  • 10% Bilateral
  • 10% Malignant (no histological features predict behaviour)
  • 10% NOT associated with hypertension
77
Q

Multiple Endocrine Neoplasia (MEN) Syndrome → Inheritance

A

Genetically inherited diseases

78
Q

Multiple Endocrine Neoplasia (MEN) Syndrome → Features

A

Proliferative lesions (hyperplasia, adenoma or carcinoma)

79
Q

Multiple Endocrine Neoplasia (MEN) Syndrome → Involves

A

Multiple endocrine organs

80
Q

Multiple Endocrine Neoplasia (MEN) Syndrome → Types

A

1, 2A, 2B, FMTC

81
Q

Multiple Endocrine Neoplasia (MEN) Syndrome

A

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

82
Q

MEN 1 (Wermer)

features
Genetic Abnormality

A

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

Chromosome 11q, tumour suppressor gene

83
Q

MEN 2 A (Sipple)
Features
Genetic abnormality

A

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

84
Q

MEN 2B
Features
Genetic Abnormality

A

Medullary carcinoma of the thyroid/phaeochronocytoma

Chromosome 10q, ret oncogene

85
Q

Hypothyroidism: causes

A

Hasimoto’s thyroiditis
Thyroidectomy
Radioiodine treatment

86
Q

Hypothyroidism Symptoms

A 
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
Q

Hyperthyroidism: causes

A

Graves
Nodular goitre
Follicular Adenoma

88
Q

Hyperthyroidism: Symptoms

A 
‘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
Q

Hyperplastic epithelium causes

A

Graves
Iodine deficiency
Goitrogen/ PUT effect

90
Q

Colloid-filled follicles

A

Idiopathic nodular goitre

91
Q

Anaplastic cells

92
Q

Lymphocytes

A

Hashimoto’s

93
Q

Foreign-body granulomas

A

DeQuervain’s

94
Q

Fibrous tissue

A

Riedel’s

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