Laboratory Investigation of Endocrine Disorders Flashcards Preview

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Flashcards in Laboratory Investigation of Endocrine Disorders Deck (32)
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1
Q

Briefly describe hypothalamic-pituitary-thyroid axis

A

Circulating TH levels under negative feedback control at hypothalamic and pituitary levels

Synthesis and release of TH controlled by TSH

T4 main hormone secreted by thyroid, T3 is more biologically active – mostly formed by peripheral conversion from T4

2
Q

Thyroid hormones - use

A

Essential for normal growth and development

3
Q

Thyroid hormones - effect

A

Increase basal metabolic rate (BMR) and affect many metabolic processes

Effects are mediated via activation of nuclear receptor

4
Q

Thyroid hormones - synthesis

A

Synthesized in thyroid via series of enzyme catalysed reactions, beginning with uptake of iodine into gland

Synthesis and release controlled by TSH

5
Q

Thyroid hormones - T3 vs T4

A

T4 main hormone secreted by thyroid, T3 is more biologically active – mostly formed by peripheral conversion from T4

6
Q

Disorders of thyroid function - describe the names

A

Terminology: euthyroid (normal range), hypothyroid (below), hyperthyroid (above)

Primary hyper/hypothyroidism: dysfunction is in thyroid gland

Secondary: problem is with pituitary or hypothalamus (tertiary)

7
Q

Hyperthyroidism - define

A

Excessive production of thyroid hormones (thyrotoxicosis)

8
Q

Hyperthyroidism - clinical features

A

Weight loss, heat intolerance, palpitations, goitre, eye changes (Graves)
In extreme: thyroid storm

9
Q

Causes of hyperthyroidism

A
Graves disease (most common)
  - due to stimulatory TSH-R antibodies
Toxic multinodular goiter
Toxic adenoma
Secondary: excess TSH production (rare)
10
Q

Hypothyroidism - define

A

Deficient production of thyroid hormones

11
Q

Hypothyroidism - clinical features

A

Clinical features

weight gain, cold intolerance, lack of energy, goitre

congenital - developmental abnormalities

12
Q

Hypothyroidism - investigations

A

Raised TSH, reduced fT4

Reduction in TSH and T4 suggests secondary (hypopituitarism)

13
Q

Causes of hypothyroidism

A
Autoimmune thyroiditis (Hashimoto’s)
- thyroid peroxidase antibodies (anti-TPO)
Iodine defficiency
Toxic adenoma
Secondary – lack of TSH
14
Q

Describe functional zonation of cortex

A

Blood flows from outer cortex to inner medulla

Layer-specific enzymes; steroid synthesis in one layer can inhibit different enzymes in subsequent layers

Results in functional zonation of cortex with different hormones made in each layer

15
Q

CYP21A - function and deficiency

A

CYP21A is the gene for 21-hydroxylase. It’s deficiency is the major cause of congenital adrenal hyperplasia.

16
Q

Mineralocorticoids: action

A

Mineralocorticoids: salt and water balance in order to maintain plasma volume: maintenance of blood pressure over the long term

17
Q

Glucocorticoids: action

A

Glucocorticoids: metabolism and immune function

Stress increases release, but minimal levels essential for normal function

18
Q

Control of adrenal steroid secretion - list

A

Cortisol: synthesis and release regulated by hypothalamic-pituitary-adrenal axis (CRH, ACTH)

Aldosterone: controlled by RAAS

Adrenal androgens: ACTH (not gonadotropins)

19
Q

Explain effect on cortisol reading due to its rhythm

A

Cortisol secretion fluctuates in a circadian rhythm, which means a random plasma cortisol reading cannot exclude abnormality, unless way outside of normal range.

20
Q

Hyper-function of the adrenal cortex

A

Aldosterone excess:
Conn’s syndrome

Cortisol excess:
Cushing’s syndrome

21
Q

What could cause hyperaldosteronism

A

Possibilities: renal artery stenosis, renin-producing tumour (reninoma – rare, but well-described), anything that stimulates RAAS.

22
Q

Dexamethasone suppresion test - high vs low dose comparison

A

Dexamethasone: exogenous steroid

Low doses will normally supress ACTH secretion via negative feedback

Low dose fails to supress ACTH secretion with pituitary disease (Cushing’s)

Higher dose will supress ACTH secretion in Cushing’s

No supresssion with low or high dose: suggests ectopic source of ACTH (e.g., tumour elsewhere

23
Q

Cushing’s disease - dexamethasone suppression test + plasma ACTH result

A

DST:
Low dose = no suppression
High dose = suppression

Plasma ACTH = high

24
Q

Adrenal tumour disease - dexamethasone suppression test + plasma ACTH result

A

DST:
Low dose = no suppression
High dose = no suppression

Plasma ACTH = low

25
Q

Ectopic ACTH - dexamethasone suppression test + plasma ACTH result

A

DST:
Low dose = no suppression
High dose = no suppression

Plasma ACTH = very high

26
Q

Adrenocortical insufficiency - primary vs secondary

A

Primary adrenocortical failure – Addison’s disease (typically autoimmune)

Secondary – impaired ACTH release
Head trauma, tumour, surgery
Abrupt steroid withdrawal

27
Q

Addison’s disease effects

A

Loss of:
Cortisol
Androgens
Aldosterone

High ACTH

28
Q

Addison’s disease - action

A

Loss of –ve fb from cortisol will compromise the VP system

29
Q

Addison’s disease - cause

A

Usually autoimmune

30
Q

Dynamic tests of adrenal function - purpose

A

Assess ability of adrenal to produce cortisol in response to ACTH

31
Q

Describe short synacthen test

A

Measure baseline cortisol (9am) and 30 min after 250 µg synacthen (synthetic ACTH) i.m.

Adrenal insufficiency is excluded by an increase in cortisol of >200 nmol/L and/or a 30 min value >550

32
Q

Describe longs ynacthen test

A

Adrenal cortex ‘shuts down’ in absence of stimulation by ACTH – time needed to regain responsiveness

3-day stimulation with i.m. synacthen

In secondary (but not primary) adrenal insufficiency cortisol increases by >200 nmol/L over baseline

Long test not often necessary since ACTH assay can distinguish

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