The number of TFTs checked in hospital has ⬆️⬆️⬆️ in recent years.
We are always looking for easily reversible thyroid problems as the cause for symptoms, but how often do we find this?
In one study, ~15% of inpatients have mildly abnormal TSH but only 1-2% a true underlying thyroid abnormality.
+ many with abnormal TFTs have no follow up of this anyway!
Acutely unwell patients often have abnormal TFTs – said to be a metabolic compensation.
We called this “sick euthyroid syndrome” or “non-thyroidal illness” (NTI).
This is seen with lots of serious illnesses e.g. sepsis, and also with starvation.
The key feature of NTI = ⬇️⬇️ in T3 (active thyroid hormone)
(this is actually metabolised to “reverse T3” -we don’t measure this)
T4 and TSH can be ➡️ or ⬇️ in NTI
A fall in T4 indicates more severe illness
See image below from Medscape:
So in severe cases with low/N TSH, low T4 and low T3 – this looks like central (secondary) hypothyroidism
As the person recovers, TSH rises to restore normality again
We don’t know if NTI should be treated or not (like a secondary hypothyroidism), so currently this is NOT routine.
It is good practice to ensure patients have their TFTs checked again when they recover (typically at 6 weeks) to ensure there is no underlying abnormality
• • •
Missing some Tweet in this thread? You can try to
force a refresh
- a control centre in 🧠 (hypothalamus & pituitary) which integrate feedback & send signals (⬇️⬆️) to the
- primary endocrine glands (e.g. thyroid) re. how much “effector hormone” to make
"Tropic" hormones (e.g. corticotropin aka ACTH) signal to another endo gland.
"Effector" hormones have widespread targets throughout the body & usually affect processes e.g. growth, metabolism 👶👧👩🦰
They also ‘feed back’ on the control centre 🔄
Tropic hormones include ACTH, TSH, FSH, LH and GH (anterior pituitary) 🧠.
Their respective effector hormones are cortisol, thyroid hormones (T3/T4), oestradiol/testosterone & IGF-1.
Diabetes insipidus (DI) is the inability to hold onto water due to lack of /resistance to ADH.
Remember ADH is released as serum osmolality ⬆️ to ⬆️ renal water reabsorption, but in patients with DI this doesn’t occur and so they pass large vol watery urine - can be >10L/day!🛁
Note diabetes insipidus has nothing to do with glucose/sugar like diabetes mellitus! ⛔️❌⛔️
Misunderstandings are so common (even with HCPs) that there is a campaign to change the name to "pituitary insipidus"