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Clinical Biochemistry > Lab Investigation of Endocrine Disorders > Flashcards

Lab Investigation of Endocrine Disorders Flashcards

1
Q

Describe the hypothalamic-pituitary-thyroid axis

A

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

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2
Q

What controls TH release?

A

Synthesis and release of TH controlled by TSH

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3
Q

Outline the HPT axis

A
  1. TRH synthesised + released from hypothalamus
  2. TRH released into pituitary portal circulation, acts on
    anterior Pituitary to release thyrotropin / TSH
  3. TSH released into general circulation, stimulates TH
    (T3/T4) production by thyroid gland
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4
Q

Describe the abundance of both T3 and T4

A

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

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5
Q

What are the actions of T3 and T4 in circulation?

A

Circulating levels of T3 & T4 act to inhibit the source of the hormones at the pituitary and hypothalamus ∴

↑T3 and T4 = ↓TRH and TSH (negative feedback)

Lack of inhibition is excitation of TSH and TRH

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6
Q

What is the significance of thyroid hormones?

A

Essential for normal growth and development

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7
Q

What is the effect of thyroid hormones on metabolism?

A

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

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8
Q

How are thyroid hormones produced?

A

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

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9
Q

How are the effects of thyroid hormone mediated?

A

Effects are mediated via activation of nuclear receptor

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10
Q

How are thyroid hormones transported in circulation?

A

Thyroid hormones in circulation are mostly bound to protein carriers (ie. thyroglobulin)

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11
Q

Describe the longevity of T3 and T4

A

T4 has 6-7 days half life

T3 has v short half life

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12
Q

Outline the terminology of thyroid function disorders

A

Euthyroid (normal range)
Hypothyroid (below)
Hyperthyroid (above)

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13
Q

What is meant by primary thyroid disorders?

A

Primary hyper/hypothyroidism: dysfunction is in thyroid gland

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14
Q

What is secondary thyroid dysfunctions?

A

Secondary: problem is with pituitary or hypothalamus (tertiary)

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15
Q

What is hyperthyroidism?

A

Excessive production of thyroid hormones (thyrotoxicosis)

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16
Q

How does hyperthyroidism effect metabolism?

A

Increased metabolic rate: Weight loss, heat intolerance, palpitations, goitre, eye changes (Graves)

In extreme: thyroid storm - treated with beta blockers and then the underlying cause

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17
Q

What is goitre?

A

Swelling in neck due to enlarged thyroid gland

many causes, excess thyroid is one

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18
Q

Outline the causes of hyperthyroidism

A
  • Graves disease (most common)
    Due to stimulatory TSH-R antibodies (act as agonist)
  • Toxic multinodular goiter
  • Toxic adenoma
  • Secondary: excess TSH production (rare)
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19
Q

What is hypothyroidism?

A

Deficient production of thyroid hormones

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20
Q

Describe the clinical features of hypothyroidism?

A

Weight gain
Cold intolerance,
Lack of energy
Goitre (due to lack of -ve feedback = inc. TSH)

Congenital - developmental abnormalities

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21
Q

Describe the investigations of hypothyroidism

A

Raised TSH, reduced fT4 = primary

Reduction in TSH and T4 suggests secondary (hypopituitarism)

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22
Q

What are the causes of hypothyroidism?

A
  • Autoimmune thyroiditis (Hashimoto’s)
    Thyroid peroxidase antibodies (anti-TPO)
    • block enzyme = no thyroid hormone synthesis
  • Iodine deficiency
  • Toxic adenoma
  • Secondary – lack of TSH
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23
Q

Describe the blood flow in the adrenal cortex

A

Blood flows from outer cortex to inner medulla

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24
Q

Describe how the structure of adrenal glands effects its products

A

Outer cortex produces adrenal steroids

Inner medulla produces adrenaline

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25
What hormones
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
26
Outline the different hormones produced in each layer
Zona glomerulosa - mineralocorticosteroids (aldosterone) Zona fasciculata - glucocorticoids (cortisol) Zona reticularis - adrenal androgens
27
What is the precursor of steroids?
All adrenal steroids share a similar biochemical synthesis pathway starting with cholesterol
28
How does steroid synthesis occur
Various enzymatic modifications of cholesterol result in production of adrenal androgens, mineralocorticoid production of aldosterone or glucocorticoid production of cortisol
29
What is a significant steroidogenesis pathology associated with congenital adrenal hyperplasia
CYP21A is the gene for 21-hydroxylase. It’s deficiency is the major cause of congenital adrenal hyperplasia
30
What is the major role of aldosterone?
Mineralocorticoids (aldosterone) Salt and water balance in order to maintain plasma volume by balancing ECFV via Na+ retention - maintenance of BP long term
31
How does aldosterone maintain BP?
Increased Na+ reabsorption from distal tubule Starling's forces then distribute inc. ECFV to Plasma and ICF
32
How does salt effect water balance?
Net loss of salt ⇒ equivalent amount of water lost with it = net loss in volume, ∴ plasma volume
33
What are the functions of cortisol?
Glucocorticoids (cortisol): metabolism and immune function
34
What induces glucocorticoid cortisol release?
Stress increases release, but minimal levels essential for normal function
35
Describe the effects of cortisol on the cardiovascular system
(low cortisol = low BP) Normal regulation of BP via counterbalancing NO in endothelial cells of blood vessels to prevent vasodilation in order to lower BP
36
How does cortisol effect glucose metabolism?
Cortisol known as glucose sparing Promotes insulin resistance in skeletal muscles (blocks GLUT4) allowing more glucose in circulation Muscles use oxidative factors instead
37
Which metabolic processes are promoted by cortisol?
Cortisol promotes glucose production in liver via gluconeogenesis (from a.a.) (in)directly promotes lipolysis of stored fats into free fatty acids - muscles use FFA instead
38
Why is the glucose sparing effect of cortisol not needed as often in modern day diet?
Increased [glucose] in circulation = hyperglycemia which stimulates insulin production which in turn promotes lipogenesis
39
What are the effects of excess cortisol glucose sparing?
Excess cortisol indirectly leads to wasting appearance of arms and legs but thicker in trunk and face
40
How is cortisol production regulated?
Synthesis and release regulated by hypothalamic-pituitary-adrenal axis (CRH, ACTH)
41
What controls aldosterone release?
Controlled by RAAS
42
What mediates adrenal androgen release?
ACTH (not gonadotropins)
43
Why is measuring glucocorticoids difficult?
Measuring glucocorticoid isn’t straightforward as levels fluctuate due to circadian rhythms
44
Which hormones are involved in the cortisol HPA axis?
Corticotropin-releasing hormone (CRH) Adrenocorticotropic hormone (ACTH)
45
Describe the role of the ACTH receptor
ACTH receptor: G-protein coupled, via cAMP stimulates cholesterol uptake and steroid synthesis
46
Why is a cortisol reading not a reliable source of diagnosis?
Cortisol secretion fluctuates in a circadian rhythm, which means a random plasma cortisol reading cannot exclude abnormality, unless way outside of normal range
47
Outline the syndromes of a hyperfunctioning adrenal cortex
Aldosterone excess - Conn’s syndrome Cortisol excess - Cushing’s syndrome
48
What causes Cushings syndrome?
The feedback loop is disturbed | collective term for a number of disorders with reason of excess varying
49
What is a common cause of excess cortisol in Cushings?
Rule out glucocorticoid therapy (medication / analogs) as this may be causing excess levels
50
How does glucocorticoid medication lead to excess cortisol?
Will lead to reduced ACTH and CRH due to -ve feedback Cortisol from adrenal gland will also be reduced - feedback system is intact but exogenous glucocorticoids cause excess
51
What is a less common reason for cushings?
Excess cortisol may also be due to a tumour elsewhere in the body secreting ACTH Other possibilities for Cushing’s ie. primary adrenal hyperplasia etc.
52
What is Cushings disease?
Adenoma anterior pituitary tumour may cause increased ACTH secretion causing excess cortisol Secondary as adrenal gland not cause of problem
53
What are the effects of a pituitary adenoma in cushings?
High cortisol leads to strong -ve feedback of both hypothalamus and ant. Pituitary However no. of ACTH secreting cells increases so -ve feedback now acting at a higher set point in adenoma tumour
54
What is the purpose of a dexamethasone suppression test?
Allows us to distinguish between Cushing’s possibilities
55
What is dexamethasone?
Dexamethasone: synthetic exogenous steroid that binds to glucocorticoid receptors like cortisol
56
What is the effect of low dose dexamethasone?
Low doses will normally suppress ACTH secretion via negative feedback
57
What are the results of a dexamethasone suppression test in a Cushings patient?
Low dose fails to suppress ACTH secretion with pituitary disease (Cushing's) Higher dose will suppress ACTH secretion in Cushing's
58
What does no suppression in a dexamethasone test suggest?
No suppression with low or high dose: suggests ectopic source of ACTH e.g., tumour elsewhere
59
What is primary adrenocortical insufficiency?
Primary adrenocortical failure – Addison’s disease typically autoimmune; adrenal cortex stops functioning Addison’s - progressive disease, leads to hypotension eventually
60
What is secondary adrenaocortical failure?
Secondary – impaired ACTH release
61
What causes secondary adrenocortical failure?
Head trauma, tumour, surgery | Abrupt steroid withdrawal
62
Why can adrenocortical failure lead to adrenal failure?
Adrenal failure, in extreme due to cortisol and aldosterone lack in Addison’s as its an attack on the adrenal cortex If primary, signs are also due to ACTH excess.
63
What deficiencies cause Addisons disease?
Loss of: - Cortisol - Androgens - Aldosterone (primary adrenal failure)
64
What are the causes of primary adrenal failure?
usually autoimmune
65
What is the role of a dynamic test of adrenal function?
Assess ability of adrenal to produce cortisol in response to ACTH
66
Outline a short synacthen test
Short synacthen test (synthetic ACTH) Measure baseline cortisol (9am) and 30 min after 250 µg synacthen (synthetic ACTH) i.m.
67
Describe results of a short synacthen test
Adrenal insufficiency excluded by increased cortisol of >200 nmol/L and/or a 30 min value >550 Cortisol levels don’t increase as expected
68
Outline a long synacthen test
3-day stimulation with i.m. synacthen Adrenal cortex ‘shuts down’ in absence of stimulation by ACTH – time needed to regain responsiveness Long test not often necessary since ACTH assay can distinguish
69
Describe results of a long synacthen test
In secondary (but not primary) adrenal insufficiency cortisol increases by >200 nmol/L over baseline

Clinical Biochemistry (7 decks)

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