Grave's disease Flashcards
Define Graves disease
Autoimmune disease associated with hyperthyroidism, eye exophthalmos and tibial myxoedema -AB agains TPO and TSH receptors
Management of Graves disease
thyroid storm-high dose carbi/polyuracil + B blockers + steroids STAT
B-blockers-symptomatic Mx-propanolol 20-40mg TDS (except in asthma)
Carbimazole 15-40mg OD
(But liver is over active due to hyperThyroid-takes a while to work and often initially destroyed fast (start with higher and go down))
or
Propylthioluracil 200-400mg OD
UK approach tends to be block and replace-kill of thyroid with prolonged use of the drugs (or radio idodine), then give levothyroxine rest of life
Aetiology and risk factors of Graves disease
Graves is autoimmune-seems to be caused by combination of genetic (80%) and environemental–but not single gene defects
Graves is an AID with AB against TSH receptors and TPO
TSHR AB activate the TSHR, causing the thyroid to overproduce massively
These AB can also latch in the eye-causing exophtalmos and soft tissue in tubia-causing non pitting oedema
Risk factors :
FHx of Thyroid AID (Hashimoto, etc)
Female
Smoke
Epidiemology of Graves disease
Graves if the most common form of hyperthyroidism in most of the world (except those with iodine deficiency)
about 2 in 1000-commonish
Signs and Sx of graves disease
can be subclinical and asymptote
Hyperthyroidism
Heat intolerance, sweating, weight loss, increased appetite, moist skin
palpitations, tachycardia, high BP, tremor
hair loss, menstrual changes
Graves specific-
25% have exopthalmos
and pretibial myxedema
Smooth, enlarged goitre
Investigations of graves disease
TSH-very low/supressed
T3/T4-high, except in subclinical then normal
Iodine uptake-faster than usual, but no hot nodules
TSHreceptor AB-positive
USS-enlarged, vascular thyroid
Complications of Graves disease
Thyroid storm-killer is heart going haywire-
Bone mineral loss
atrial fibrillation (and MI/stroke)
Congestive Heart failure
Sign threatening exophthalmos
Prognosis of Graves disease
high increase of CVD death in patient with suboptimal control
prompt treatment and good control nearly entirely removes risk
but can relapse-quite commonly,=-need monitoring