Thyroid Eye Disease/Graves Disease Flashcards
Describe Graves’ Disease?
- Systemic autoimmune disorder
- Hyperthyroid – overactive thyroid
- Orbitopathy – all eye signs/features of proptosis, upper lid retraction, chemosis, periorbital oedema
- Myxoedema (lumpy red skin)
- Acropachy (finger clubbing)
What is the epidemiology of Graves’ Disease?
- Prevalence of hyperthyroidism in general pop. is 1.2%
Have clinical features & +ve thyroid test that would say that they were hyperthyroid
o 0.7% subclinical hyperthyroidism
Cannot prove on blood test that px has overactive thyroid with too much stimulating hormone but they have all the signs & symptoms
o 0.4% Graves’ Disease – most common aetiology – note there is overlap w/ subclinical group - Graves’ Disease is more common in females (7:1 ratio)
Describe normal thyroid hormone control and normal control?
- 2 hormones produced by Thyroid Gland
o T4 – Thyroxine
o T3 – Triiodothyronine - They are responsible for metabolic regulation in all cells
- When everything is working normally, should not be any thyroid disfunction
- Hypothalamus is where everything is starting – pituitary gland sits under it
- Thyrotropin releasing hormone (TRH) is produced by hypothalamus – need normal production of this
o This acts on anterior pituitary gland
o This results in releasing thyroid stimulating hormones (TSH) - TSH binds to TSH receptors in thyroid gland releasing Thyroid hormone (T3 & T4)
o Gives increased metabolism, growth in development – gives you an overstimulation of metabolic cells in body
o Note: there is a negative feedback loop involving T4 and T3 & the pituitary regulates the circulating hormone levels
Negative feedback where its going back to pituitary gland – upsetting normal function if there is a thyroid problem
Describe abnormal control?
- Hyperthyroidism (overactive thyroid) in Graves disease is a direct result of an Abnormal Circulating Antibody (Ab) (TSH receptor AB are producing far too much circulating antibody)
o This targets the TSH receptor & mimics the effect of normal TSH resulting in overstimulation of Thyroid gland
This is when px is producing too much thyroid hormone - Goitre – swelling of gland may occur – swelling around neck
- Over production of T4 and T3 & gland itself is swollen & enlarged
What are the causes of overstimulation of thyroid gland?
- Graves’ Disease – autoimmune disfunction of normal hormone control
- Thyroiditis – inflammation of thyroid gland producing more thyroid hormone
- Toxic Multinodular goitre – something has attacked/poisoned thyroid gland
- Toxic Thyroid nodule
- Self-administered thyroid hormones – to give increased metabolic result
Describe Graves’ Orbitopathy (GO)?
- Genetics play a large role in development of GO – ask in hx
o Typical px is lady in her 40s, she will have other female family members that have GO - High levels of TSH Ab linked to severe GO
- Varying levels of severity of the condition
- Smoking increases the severity of GO in hyperthyroidism – ask in hx
o Smoking known to affect immune system – either by altering function of T cell, changing immune chain or products of cigarette having a direct immunological effect - Not all pxs with hyperthyroidism develop GO
o ~20% of pxs develop GO prior to diagnosis of thyroid disorder
Px presents with proptosis, lid oedema, conjunctival oedema but GP reports blood tests are normal
o 20% are diagnosed with GO at same time as their Thyroid Disorder
Px goes to GP & GP notices eye signs – blood result comes back +ve
o 20% develop GO 6 months after thyroid is diagnosed
See endocrinologist before seeing is
o 40% can develop GO more than 6 months after their hyperthyroidism - A v small percentage of pxs can be Hypothyroid (underactive thyroid gland) or Euthyroid (normal thyroid function – neither elevated or depressed in the thyroid function test)
Describe the acute/active inflammatory phase/ wet phase of Graves’ Disease?
Process is developing
* Usually 1st 18 months of px suffering from thyroid condition
* Connective tissue inflammation:
o Inflamed conj, inflamed caruncle
Redness
Mild ocular discomfort – don’t tend to come with severe pain (pain thresholds vary from px to px though)
Periorobital swelling
Pain on motility
* Activation of EOM fibroblasts causing swelling within muscle itseld
o Increasing orbital volume (due to muscle swelling) by differentiating into orbital fat & secreting glycosaminoglycans
These secreting glands then attract water
o Inflammatory myopathy resulting from autoimmune process that px is going through
Describe corneal exposure in the acute phase of Graves’ Disease?
- Due to upper lid retraction – may have inadequate lid closure – leaving cornea exposed
o Grittiness feeling
o Photophobia
o Epiphora – watering eyes onto cheek
o Reduction in vision (in end stages – due to corneal epithelium drying out & creating a cloud cornea) - Ocular discomfort can be due to inflammatory agents in the tears & drying of conreal epithelium from proptosis, eyelid retraction, poor blink pattern or reduced Bell’s due to contracture of inferior rectus
- Look for corneal staining especially lower third with fluorescein
- Swollen & hyperaemic conjunctiva over horizontal rectus insertion sites & caruncle
- Superior limbal keratoconjunctivitis often seen
Describe the inactive phase/later phase/ dry phase of Graves’ Disease?
- Need to know hx – when did they start to experience these problems? Helps differentiate between active & inactive phase
- Cicatricial phase
- Subsequent fibrosis & muscle contraction
- In direct reaction to swelling & inflammatory process that had in v active phase
- Reduction in proptosis/swelling when have fibrosis & muscle contraction
- Corneal exposure persists due to retraction of lids
o When levator fibroses – lid retraction can be worse – causes more problems with diplopia as eye will not move now
What happens in the vision due to enlarged EOM’s in Graves’ Disease?
- Diplopia – could be horizontal/vertical/torsional
- Reduced field of BSV – px will be able to maybe maintain BSV in depression but not in elevation
o V important that is continued to be monitored - Reduced uniocular field of fixation
o Mechanical restrictive orbitopathy
o Monitor each eye independently to see exactly the range of movement that each eye has
Describe uniocular field of fixation (UFOF) for Graves’ Disease?
Can be carried out on Goldmann Perimenter
When looking at this, consider where each muscle should b e working at its maximum
LR & MR are working on horizontal meridian
Ask px to follow light target on machine, at each distance of degrees, testing how far the eye is allowed to complete the certain action
Want to know when px is able to maintain central fixation from their fovea
When central fixation fails then that is the mark made where the extent of the movement ends – repeated for all EOMs
What is the typical order of limitations of EOMs in Graves’ Disease?
- Inferior rectus – pxs initial complaint is looking up
- Medial rectus – pxs initial complaint is abducting
- Superior rectus – px will have problem looking down
- Lateral rectus – lastly px will have problem adducting
Limitation will always be in the opposite direction to 1st muscle affected
Describe symptoms and signs of a px with Graves’ Disease? What is clinically significant for these pxs?
- AHP of chin elevation (usually) – e.g. if struggling to elevate eyes, tilt head up then eyes looking down
- Hypophoria/tropia usually 1st deviation – one eye slightly lower than the other – if tropia and become manifest then will have vertical diplopia
- With/without head turn – depends if MR is affected (will turns head accordingly to take eyes away from adducting position)
- Enlarged vertical fusion range – CLINICALLY SIGNIFICANT – normal vertical fusion range is between 3 & 4D of elevation & depression – in many thyroid pxs, vertical fusion range could be range of 20-30D – v slow progressing disorder, allows brain to connect to fact that eyes are moving out of alignment, brain is fighting with all the fusion it can muster to keep the eyes together
- Raised IOP an elevation/attempted elevation – px may be unable to elevate the eye – sheer force of attempting to elevate the eye will show a peak in IOP when tested
What can result due to increased orbital volume from swollen fat & muscles?
- Proptosis (aka exophthalmos) – in a bony orbit there is nowhere to go but out
o Can be unilateral
o Can be bilateral (but asymmetric – one eye protrudes more than other) - Compression on optic nerve – Compressive Optic Neuropathy – ALWAYS look out for this - if px does not get proptosis then due to the increased orbital volume in the bony space – if eyes don’t come forward & relieve some pressure then optic nerve is in danger of being compressed which will result in:
o Initially a reduction in colour vision
o Loss of vision (ultimately if left untreated) - Upper & Lower eyelid retraction
- Corneal exposure – eyelids are unable to close adequately
- Diplopia – asymmetrical swelling of EOMs – one eye may be higher or lower than other & may have ESO/EXO deviation
- These pxs need monitored v closely to ensure that they do not have permanent visual loss while in process of having Graves Disease
Describe Muller’s Muscle Hyperactivity in Graves’ Disease?
- Upper eyelid retraction – slightly staring look
o Retracted up over globe & due to proptosis this can be very exaggerated
Pxs can appear as though they have proptosis when their eyelids are retracted
o Caused by overactivity of Muller’s muscle & finally by fibrosis of levator muscle
Results in Upper lid lag on downgaze - Eye moves down slowly & lid follows very very slowly behind
- Lower eyelid lag
