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Clinical Pathology > CP9-2 investigations of endocrine disease > Flashcards

CP9-2 investigations of endocrine disease Flashcards

1
Q

What are hormones?

A

Messenger molecules produced by endocrine glands which circulate around the body to elicit a response - short or long term - from a compatible target cell.

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2
Q

What are the three main type of hormones? Where are they produced?

A

Peptide - produced in pituitary or parathyroid hormone
Steroid - produced in adrenal glands
Tyrosine-based - produced by thyroid gland

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3
Q

What are all steroid hormones made from?

A

Cholesterol

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4
Q

What are examples of peptide hormones?

A

PTH
ACTH
TSH

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5
Q

What are the three ways that steroid hormones illicit a respons at the target cells?

A

Classical model
Receptor-mediated endocytosis
Signalling through cell-surface receptors

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6
Q

What are examples of steroid hormones?

A

Testosterone
Oestradiol
Cortisol

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7
Q

What are examples of tyrosine-based hormones?

A

Thyroxine (T4)
Triiodothyronine (T3)

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8
Q

How is the endocrine system regulated?

A

By negative feedback

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9
Q

What does thyroxine (T4) inhibit production of?

A

TRH and TSH

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10
Q

What is the TSH pathway?

A

TRH produced by hypothalamus
Stimulates production of TSH at pituitary gland.
TSH stimulates the thyroid to produce

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11
Q

What is the free hormone hypothesis?

A

Only unbound thyroxine is physiologically active and detected in a test, so if levels of thyroxine-binding globulin changes, the level of free hormone is affected. This then changes the measurement of hormone levels.

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12
Q

When is cortisol level testing inacurrate?

A

Oestrogen contains contraceptive pill

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13
Q

Where and what is the pathology if TSH is normal/low and thyroxine is low?

A

In the pituitary gland leading to secondary hypothyroidism

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14
Q

Where and what is the pathology when TSH is high but the thyroxine levels are low?

A

in the thyroid gland leading to primary hypothyroidism usually due to Hashimoto’s

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15
Q

Where and what is the pathology if TSH levels are low and thyroxine is high?

A

In the thyroid gland leading to primary hyperthyroidism usually due to Grave’s disease

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16
Q

Where and what is the pathology if TSH is high and thyroxine is also high?

A

On the pituitary gland due to a TSH producing tumour

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17
Q

What diagnosis can be missed if a normal TSH level is seen upon testing but no thyroxine testing is done?

A

Secondary hypothyroidism as around 84% of patients with this have normal TSH

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18
Q

Why is thyroxine not measured for if TSH is normal but secondary hypothyroidism is suspected?

A

As very rare and often picked up on other tests

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19
Q

Why should thyroid hormones not be tested for in acutely ill patients?

A

As TSH and thyroxine often drops and T3 increases but this is most likely to be due to their acute illness not a thyroid problem

20
Q

How often should TFTs be done?

A

Every 3 years in a healthy person
In hyperthyroidism when treating Graves’ disease, 1-2 months after radioactive iodine or 6-8 weeks post op after thyroidectomy
In hypothyroidism when minitoring treatment annually in long term thyroxine treatment or 2 months after change of dose

21
Q

How are hormones tested for in blood testes?

A

Immunoassays or mass spectrometry

22
Q

Why are immunoassays used to test for hormone levels more than mass spectrometry?

A

as its amenable to automation

23
Q

What are the two types of immunoassays?

A

Non-competitive
Competitive

24
Q

What can compromise immunoassays?

A

Interference

25
Q

What are phaeochromocytomas?

A

An adrenal medullary tumour of neuroendocrine chromaffin cells seen in adults

26
Q

What percentage of phaeochromocytomas are bilateral?

A

5%

27
Q

What percentage of phaeochromocytomas are malignant?

A

10%

28
Q

What percentage of phaeochromocytomas are in extra-adrenal neuroendocrine cells?

A

10%

29
Q

What are the clinical features of phaeochromocytoma?

A
30
Q

How is a phaeochromocytoma diagnoses?

A

Using plasmametanephrine levels
24 hour urine fractionates metanephrines
Clonidine suppression test
Plasma chromogranin A

31
Q

Why is it hard to diagnose phaeochromocytomas?

A

As it is not uncommon for false negative and false positive results of biochemical tests

32
Q

How is hypoglycaemia diagnosed?

A

Based on Whipple’s triad
- low plasma glucose
- signs and symptoms of hypoglycaemia
- resolution of symptoms once glucose levels rise

33
Q

What are autonomic signs and symptoms of hypoglycaemia?

A

Hunger
Sweating
Anxiety
Paresthesis
Palpitations
Tremulousness
Pallor
Tachycardia
Widened pulse pressure

34
Q

What are neuroglycopenic signs and symptoms of hypoglycaemia?

A

weakness + fatigue
dizziness
headache
confusion
behavioural changes
cognitive dysfunction
blurred vision and diplopia –> cortical blindness
hypothermia
seizures
coma

35
Q

What are endogenous causes of hypoglycaemia?

A

Insulin-mediated e.g. insulinoma
Insulin-independent e.g. critical organ failure, sepsis, hormone deficiency, non-islet cell tumours

36
Q

What are exogenous causes of hypoglycaemia?

A

Alcohol
Facetious
Therapeutic drugs e.g. insulin

37
Q

What is an insulinoma?

A

Most common tumours arising from islets of langerhans?

38
Q

When should blood be taken for insulin and blood glucose tests?

A

when patient is hypoglycaemic

39
Q

What type of blood test is used in diagnosing insulinomas?

A

Fasting

40
Q

What results in blood tests are seen in patients with insulinomas?

A

Low blood sugar - less than 2.2 mmol/L
High insulin - 6 micro units/ml or more
High levels of C peptide - >0.2nmol/L

41
Q

What are features of Cushing’s?

A

Obesity - centrally and on shoulders and causes moon face
Think skin with bruising and purple striate
Hypertension
Glucose intolerance
Menstrual disturbances
Thin limbs and muscle weakness
Depression

42
Q

How is cortisol produced?

A

ACTH produced by pituitary gland causes adrenal glands to produce cortisol. Negative feedback of cortisol to the pituitary gland then inhibits ACTH production.

43
Q

What causes Cushing’s syndrome?

A

Excess cortisol production due to:
- Cushing’s disease Pituitary gland tumour
- adrenal gland tumours
- exogenous gluticocorticoid therapy
- Ectopic ACTH secreting tumours e.g. small cell carcinomas, islet cell tumours of the pancreas, medullary carcinoma of the thyroid, thymus gland tumours

44
Q

What causes the contralateral adrenal gland to shrink when there is a unilateral adrenal gland tumour?

A

excess cortisol production from affected adrenal gland inhibits ACTH production of the pituitary gland so the contralateral gland is not stimulated

45
Q

If adrenal insufficiency is suspected, what test is done?

A

Synactin test

46
Q

How do you test for Cushing’s syndrome?

A

Overnight dexamethasone supression test

Clinical Pathology (65 decks)

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