Endocrine OSCEs Flashcards
Role of cortisol
Glucocorticoid from the adrenal gland
Increase blood sugar via gluconeogenesis
Fat, protein, and carb metabolism
Anti-inflammatory action
Maintain vascular tone and catecholamine responsiveness
Na retention
Where does cortisol come from
Adrenal Cortex - zona fasiculata
CRH - hypothalamus
ACTH - ant pituitary
ACTH to cortex - glucocorticoid secretion - negative feedback
Cortisol regulation through the day
Peak in the morning, fall throughout the day, diurnal variation
Levels increased by activity/stress
Pattern reversed in night workers
What patterns do you expect in a synacthen test
Pituitary failure -
No ACTH, little cortisol. Low baseline with exaggerated response
Addisons - gland is failing, high ACTH, low cortisol, no response
Commonest cause of primary adrenal failure
Auto immune - Addisons
Tumour - myeloid,
TB
Meningococcal sepsis causing Waterhouse Friedrichsen syndrome
Ischaemia
What else could you do to establish why a low cortisol
Serum hormones - ACTH, aldosterone, renin
Electrolytes - potassium, sodium
CT adrenals
21-hydroxylase antibody for autoimmune
Secondary and tertiary failures
Secondary - no ACTH from pituitary issues -
Tumour, surgery, ischaemia, infarct, Sheehans
Suppression of exogenous glucocorticoid
Tertiary failure of CRH
When might we replace cortisol in ITU
Vasopressor refractory shock
Geniuine pit/adrenal failure
When they need long term steroids
BSD
When steroids would be used in medical purposes - anaphylaxis, asthma, COPD, meningococcal disease,
Why don’t we do synacthen tests routinely in Itu
Adrenal axis malfunctions therefore cortisol levels vary widely
Cannot identify who really has insufficiency
What do you make of normal TSH and T4 with low T3
No raised TSH, so not primary hypothyroid
Sick euthyroid, seen in starvation and critical illness
What is sick euthyroid
Abnormal thyroid function tests in the setting of a non-thyroid illness
Without pre-exiting HP axis dysfunction
After recovery, TFTs should reverse (trickier in pre-existing disease)
Most T3 is made outside the thyroid by peripheral conversion from T4. Mechanism fails, so low T3 with normal/high T4. Sometimes T4 low due to low transport protein levels
Which hormones are secreted from the pituitary gland?
- Anterior lobe - TSH, ACTH, GH, FSH, LH, prolactin, gamma-melanocyte
stimulating hormone, β lipotropin - Posterior lobe - vasopressin, oxytocin
- Intermediate lobe – α and βMSH, γ-lipotropin
What happens to thyroid function in critical illness?
- Acute illness - rapid decline in T3 and rise in (inactive) reverse T3 (rT3).
Brief rise in TSH/T4, but nocturnal rise in TSH absent. - Chronic illness - decreased T4 and T3 diminished pulsatile TSH, reduced TRH. T4 is converted peripherally to rT3 (inactive) rather than T3 because of altered enzyme action.
- This low T3 syndrome is also called sick euthyroid syndrome.
- Thyroid function tests are therefore unreliable in the critically ill.
What hormones are secreted from the adrenal gland?
- Catecholamines - adrenaline, noradrenaline, dopamine - controlled by
sympathetic discharge as part of stress response - Glucocorticoids - cortisol, corticosterone
- Androgens - dehydroepiandrosterone, androstenedione
- Mineralocorticoids – aldosterone
How is the hypothalamic-pituitary-adrenal-axis affected by critical illness?
- Early stages - CRH and ACTH are increased, leading to a rise in cortisol, diurnal release is lost.
- Chronic stages - Cortisol levels remain high, but ACTH decreases. Cortisol levels only return to normal in recovery phase.
- Cortisol binding globulin levels decrease so the proportion of free cortisol is much higher
