Lab Investigation of Endocrine Disorders Flashcards

1
Q

Describe the hypothalamic-pituitary-thyroid axis.

A
  • Circulating TH levels are under negative feedback control at hypothalamic and pituitary levels
  • Synthesis and release of TH is controlled by TSH
  • T4 is the main hormone secreted by thyroid, T3 is more biologically active – mostly formed by peripheral conversion from T4
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2
Q

Describe thyroid hormones.

A
  • essential for normal growth and development
  • increase basal metabolic rate (BMR) and affect many metabolic processes
  • synthesized in thyroid via series of enzyme catalysed reactions, beginning with uptake of iodine into gland
  • synthesis and release controlled by TSH
  • T4 is main hormone secreted by thyroid, T3 is more biologically active – mostly formed by peripheral conversion from T4
  • effects are mediated via activation of nuclear receptor
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3
Q

What are the two types of disorders of thyroid function?

A

PRIMARY HYPER/HYPOTHYROIDISM:
dysfunction is in the thyroid gland

SECONDARY HYPER/HYPOTHYROIDISM:
problem is with pituitary or hypothalamus (tertiary)

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4
Q

What is hyperthyroidism?

A

It is the excessive production of thyroid hormones (thyrotoxicosis).

Clinical features:

  • weight loss
  • heat intolerance
  • palpitations
  • goitre
  • eye changes (Graves)
  • extreme: thyroid storm
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5
Q

List some causes of hyperthyroidism.

A
  • Graves disease (most common; due to stimulatory TSH-R antibodies)
  • Toxic multinodular goiter
  • Toxic adenoma
  • Secondary: excess TSH production (rare)
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6
Q

What is hypothyroidism, and how would you investigate it?

A

it is the deficient production of thyroid hormones.

Clinical features:

  • weight gain
  • cold intolerance
  • lack of energy
  • goitre
  • congenital - developmental abnormalities

Investigations:

  • Raised TSH, reduced fT4
  • Reduction in TSH and T4 suggests secondary (hypopituitarism)
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7
Q

List some causes of hypothyroidism.

A
  • Autoimmune thyroiditis (Hashimoto’s)
  • Thyroid peroxidase antibodies (anti-TPO)
  • Iodine deficiency
  • Toxic adenoma
  • Secondary – lack of TSH
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8
Q

What are the steroids of the adrenal cortex?

A

Zona Glomerulosa: ALDOSTERONE

Zona Fasiculata: CORTISOL

Zona Reticularis: ANDROSTENEDIONE/DHEA

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9
Q

What are the actions of adrenal steroids?

A

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

Glucocorticoids: metabolism and immune function
- Stress increases release, but minimal levels essential for normal function

Androgens: so called ‘weak androgens’

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10
Q

What are organs on which cortisol acts?

A
  • brain
  • bone
  • CVS
  • immune system
  • kidney
  • skin/connective tissue
  • foetus
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11
Q

How is the secretion of the hormones of the adrenal cortex controlled?

A

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

Aldosterone: controlled by RAAS

Adrenal androgens: ACTH (not gonadotropins)

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12
Q

What is the disease called with excess aldosterone?

A

Conn’s syndrome

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13
Q

What is the disease called with excess cortisol?

A

Cushing’s syndrome

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14
Q

Describe the dexamethasone suppression test.

A

Dexamethasone is an exogenous steroid.

Low doses will normally suppress ACTH secretion via negative feedback.
Low doses will fail to suppress ACTH secretion with pituitary disease (Cushing’s).

Higher dose will suppress ACTH secretion in Cushing’s.

If there is no suppression with low or high dose: suggests ectopic source of ACTH (e.g., tumour elsewhere

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15
Q

What are two ways in which you can get adrenocortical insufficiency?

A

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

Secondary – impaired ACTH release

  • head trauma, tumour, surgery
  • abrupt steroid withdrawal
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16
Q

Describe the 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.
17
Q

Describe the long synacthen 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