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212- S + OM > Graves opthamology > Flashcards

Graves opthamology Flashcards

1
Q

where is the thyroid gland located

A

highly vascular endocrine gland

lower neck anterior to trachea between the sternocleidomastoid muscles

consists of densely packed follicles

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2
Q

what is the function of the thyroid gland

A

concentrates iodide to form thyroid hormones

thyroid hormones synthesised and stored in the follicles

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3
Q

what are hormones does the thyroid secreate

A

trh stimulates the release of tsh
tsh is secreted by the anterior pituitary and stimulates the secretion of t3 - try-idothyroine
tetra idothyroonine t4 (thyroxine)

t3 and t4 recreated into bloodstream
bound to plasma proteins
free from intracellular

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4
Q

what are the roles of thyroid hormones

A

growth and development

rate of growth and many tissues
maturation of cns and bones
regulation of synthesis and some respiratory enzymes

metabolic effects
regulation of basal metabolic rate
regulation of water and ion transport
regulation of calcium and phsophorus metabolism
regulation of nitrogen metabolism

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5
Q

what is hyperthyroidism

A

enlarged thyroid gland - goitre
abnormal heart rhythms- tachycardia
increased appetite but may have weight loss
hand tremors
fine brittle hair
hyperactivity
heat intolerance and increased perspiration - warm , moist skin
lighter or less frequent periods
irratability
anxiety
muscle weakness - upper arms and thighs

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6
Q

what are symptoms of hypothyroidism ( underachieve)

A

fatigue , exhaustion
feeling run down and sluggish
unexplained / excessive weight gain
dry coarse , itchy skin and hair
slow heart rate
feeling cold , especially in extremities
goitre
more frequent periods
difficulty concentrating - brain fog
hoarse voice
muscle cramps

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7
Q

how are thyroid abnormalities diagnosed

A

tsh (considered outside normal if lower than 0.3 or higher than 3.0

calculate free t4 index (10-20)

thyroid stimulating immonoglobin (tsi)

anti thyroid antibodies

serum t3 - 2.5- 5.3 pmd

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8
Q

hyperthyroidism management

A

drug therapy

radioactive iodine treatment

thyroidectomy

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9
Q

hyperthyroidism treatment

A

thinomines - interfere with thyroid hormone synthesis by blocking the build of iodine

most effective if the onset of disease within 1 year

steroids- oral prednisone - decreases secretion of thyroid hormones and peripheral conversion of t4 and t3 - used in severe cases

immunosuppresants ( azathioprine or rituximab)

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10
Q

how is radioactive iodine used in the treatment of ted

A

radioactive iodine - taken up by thyroid gland - normal cell division = disturbed

used in patients over 45 yrs of age or in Younger patients if other treatments are contraindicated

ocular symptoms have been found to worsen following this treatement

20% of patients become hypothyroid within 1 year of the treatment

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11
Q

what effect does radioactive iodine and prohlaytic corticosteroids have on GO wheen treating hyperthyroidism

A

prevents progression of go in patients with pre- existing eye disease
eye signs worsened 6 months in

15% after ri

2.7% after antithyroid drugs

none who had ri and prednisone

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12
Q

how is a thyroidectomy used to treat hyperthyroidism

A

removal of the thyroid gland
reduces hormone production
post op recurrence in 10-15% patients
post op hypothyroidism in 40% of patients
usually performed in younger patients

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13
Q

what is used in patients with hypothyroidism

A

oral thyroxine

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14
Q

what is graves disease

A

autoimmune disorder that causes hyperthyroidism - the immune system attacks the thyroid and causes it to make more thyroid hormone the body needs
3 patients

all with enlargement of the thyroid gland
all with palpations
1 with protusion of the eyes

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15
Q

what is graves orbitoptahy

A

auto immune disease
disease of the orbit affecting the orbital soft tissues
closely correlated to auto immune systemic thyroid disease
presence of circulating antibodies that bind and stimulate the thyroid hormone receptor (tsh) leading to hyperthyroidism and goitre

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16
Q

what are risk factors of graves orbitopathy

A

genetic

environmental- smoking , stress

immune factors

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17
Q

what are risk factors of graves orbitopathy

A

female - 86%
16/10 000 women
3/ 10 000 men

Age- women - 40- 50 years

men 50- 55 years

greater severity with age

smoking- may known risk factor

severity of eye signs and symptoms with increased tobacco consumption

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18
Q

what thyroid abnormalities are associated with graves orbitopathy

A

hyperthyroidism - 90%

hypothyroid - 3-5%

euthyroid- 5% - sensitivity of detection]

patients hyperthyroid without eye signs - 50- 60 % - 80- 90% have eom changes on ct imaging

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19
Q

what are symptoms of thyroid eye disease

A

most common is change in appearance and/or ocular irritation

dry eyes

epiphora

grittiness

diplopia

photophobia/ flashing lights

reduced vision/ colour vision

pain/ ache on extreme gaze

distress at changing apperance

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20
Q

what lid abnormalities are seen in thyroid eye disease

A

upper or lower lid retraction

palpebral appeture - measurement can be taken

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21
Q

how to measure lid retraction

A

position patients head
ask patient to fixate on target positioned at their eye level and in the distance

ask patient to relax as much as possible to record the minimum amount of retraction for that patient (I.e Mullers muscle as relaxed as possible)

observer holds vertical clear plastic ruler near to visual axis without touching patients eyelashes

observer should consistently use only one of their eyes near to visual axis without touching eyelashes

observer should consistently use only one of their eyes and on the same horizontal level as the patients eye

for patients with manifest strabismus the contralateral visual axis is occluded prior to measurement

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22
Q

what instrument is used to measure exophthalmos/ proptosis

A

hertel mirror exopthalmometer

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23
Q

what should be noted about exopthalmos

A

if its bilateral
asymmetric
unilateral
normal

amount depends on severity of disease and inflammation and the structure of anterior orbital septum

axial/ non axial

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24
Q

what relating to oedema is caused by ted

A

lid oedema / periorbital odema

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25
Q

what relating to the conjuctiva can be caused by ted

A

inflamamation of caruncle
chemises, conjuctiva redness and swelling

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26
Q

what is affected in the eyes by graves orbitopathy

A

extra ocular muscles

orbit

lids

sight

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27
Q

what happens during the wet phase (active phase) to extraocular muscles

A

wet phase- active phase

cellular infiltration with gags (glycosminoaglycans( and osmotic inhibition of water

this leads to eom becoming up to 8- 10x enlarged

may compress optic nerve leading to visual loss

subsequent degeneration of muscle fibres leads to fibrosis resulting in restricted motility and diplopia

this phase tends to settle within 3 years

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28
Q

what is the fibrotic phase

A

muscle fibres become distorted , contracted and damaged due to fibrosis

eyes are white and quiet

painless restrictive myopathy may be present

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29
Q

what details need to be noted/ assessed regarding eom

A

limitation

reversal

saccades

cog wheel pursuit

fatigue

pain

retraction

bilateral involvment

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30
Q

what is the order of eoms involved in ted

A

inferior rectus

medial rectus

superior rectus, lateral rectus

superior oblique and inferior oblique

vertical , horizontal and torsional diplopia

swelling of eom results in restriction : if ir affected then patient unable to elevate as eye becomes tethered down

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31
Q

what is graves orbitpoathy and how is diagnosed

A

go is an autoimmune condition diagnosed by blood tests along with clinical history and assesment

MRI scans can aid diagnosis

patients are usually hyperthyroid but can be hypothyroid or euthyroid

management of thyroid levels is an important first step in treatmenr 3 phases

multiple distinctive eye signs

can result in painful eye movements diplopia or visual loss

upgaze typically affected first

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32
Q

what signs need to be present for a patient to be diagnosed with ted

A

clinical orbital signs `(lid retraction/ proptosis/ optic neuropathy)

laboratory tests (positive bloods for autoantibodies)

typical orbital imaging finding = swollen eoms

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33
Q

what are the signs and symptoms seen in the mild and early stages of ted

A

symptoms include—–
foreign body sensation

dry ete - excessive tearing , conjunctival or eyelid redness and swelling

blurred vision

retro - orbital pain
clinical signs include ——-

mild soft tissue inflammation

dilated conjunctival vasculature

keratoconjuctivitis

corneal staining

34
Q

what signs and symptoms seen in the moderate stage

A

pulling sensation around the eye

eyelid redness and swelling

34
Q

what signs and symptoms seen in the moderate stage

A

pulling sensation around the eye

eyelid redness and swelling

eyelid retraction and bulging eyes

swelling of eom s

cheomosis

eyelid oedema

proptosis

35
Q

what symptoms would you see in advanced ted

A

horizontal, vertical and torsional strabismus with double vision

deteriorating blurred vision

fading colour vision in one or both eyes

decrease in va , visual field and colour vision

signs of optic neuropathy

progressive proptosis with eyelid retraction

corneal ulceration

inflammation og eom and scarring leading to strabismus and opthalmolplegia

increased top

36
Q

describe the summary of the orthoptic role

A

diagnosis

assessment of visual function

document effects of ocular muscles

record disease progress

establish when ocular signs stabilise

explaining and information signposting

eliminate symptoms / diplopia

plan long term management

37
Q

outline the orthoptic investigation

A

ct , visual function , note any app - most common , head elevation

om and measure pa

bsv tests (inc vpfr)

pct + torsion

(synoptophore or torsionometer)

funicular field of fixation

field of bsv

lees screen / hess (not useful in bilateral cases)

measure 9 position of gaze due to them having an incomitiant deviation

38
Q

what parts of visual function would be assessed

A

visual acuity
colour vision - 100 hue , d15
Ishihara is used for congenital conditions
visual fields
contrast sensitivity
pupils - checks for optic nerve , damage which may occur if on compression

39
Q

what are the clinical; signs of optic nerve compression

A

on compression = a ocular emergency

reduced va
reduced contrast sensitivity
reduced colour viision
visual field defect
rapd- relative afferent pupillary defect
optic disc exam - normal/ swelling/ pallor

optic neuropathy - approx - 5 %

40
Q

with an acute presentation of ted what could you differentially diagnose it with

A

carotid - cavernous fistula

mystic pseduotumour

ocular myosotis

leukemia

orbital myositis

chronic progressive external opthalmalplegia

idiopathic orbital inflmmatory disease

lymphoprolferative disorders

carticocavernous fistula

myasthenia gravis (in elderly males with inactive disease)

41
Q

what classifications are seen for the diagnosis

A

Werners classification

mouritis cas

eugogo

42
Q

what is Werners classification of ted

A

stage 1 - no ocular signs - stage 7 - sight loss

43
Q

how does the European group on graves orbitpopathy

A

combines clinical activity score with measures of severity

1- spontaneous retrobulbar pain

7- conjunctival odema

44
Q

what are the surgical mangement options

A

surgical - sight saving , strabismus, lid

45
Q

what are the aims of orthoptic management

A

perserve visual function
keep patient comfortable and symptom free
allow comfortable bsv in primary position and reading poistion where possible

46
Q

what are the management options for ted

A

encourage use of ahp

47
Q

what are the management options for orthoptic management

A

encourage use of ahp
prisms - tempoary / incorporated

occlusion - blendaderm / patch / frosted lens

surgery

BT

48
Q

What needs input from a opthamologist- non urgent

A

non urgently - gritty sensation/ and or eyes sensitive to light progressive change in eye appearance

pain in or behind the eyes

diplopia

eyelid retraction

swelling / redness of eyelids or conductive

restriction of eye movement

tilting of head to avoid double vision

49
Q

what urgently needs input from the opthamologist

A

sudden deterioration in vision
problems with colour vision
sudden onset proptosis
failure of full eye closure
corneal opacity
abnormal disc possible described referral to eye/ casualty or optmetrist

50
Q

what surgical interventions can be suggested

A

on compression - orbital surgery

strabismuss / ocular realignment surgery

lid surgery

multidiscpilanory approach - may involve maxillary facial surgeons , strabismologist and orbital surgeons

51
Q

what orbital changes are seen in ted

A

retrobulbar adipose tissue is increased in volume and may have lymphocytic infiltrate

increased volume of orbital contents typically leads to exophthalmos

51
Q

what orbital changes are seen in ted

A

retrobulbar adipose tissue is increased in volume and may have lymphocytic infiltrate

increased volume of orbital contents typically leads to exophthalmos

may lead to on compression / neuropathy

52
Q

what are the treatment options for optic neuropathy

A

steroids
radiation
orbital decompression

53
Q

what type of steroids are given for optic neuropathy

A

mechanisms - anti-inflammatory
immune response - immunosuppressive
decrease mucopolysaccharide production by orbital fibroblasts

indications -

acute inflammatory disease
optic neuropathy - mid va loss
recent onset
following other treatments - pre/post decompression

54
Q

what are the effects of steroids + azthioprine

A

another immunosuppressants
allowing reduction of steroid if prolonged large doses - reduces side effects of steroids
effects modest

55
Q

what are the effects of radiation therapy

A

well tolerated
no short term side affects
reduces symptoms but not the course of disease

referral to oncologist
face mask to immobilise patient and allow accurate delivery of radiation
planning with ct
2 weeks of treatment delivered daily

56
Q

how does radiotherapy work

A

reduce the cells which cause inflammation so reduce swelling behind the eye

it may take up to year to notice the full effect

10 radiotherapy treatments given over two weeks

face mask to immbolise patient and allow accurate delivery of radiation

risk of cataract

risk of dry eyes

57
Q

how is radiation therapy utilised in the treatment of ted

A

daily doses od radiation beams directed at the orbital area
low dose of 26y x ten days

destroys lymphocytes and fribroblasts reducing auto immune response
first weeks often in conjunction with steroids

increased chemises in the first week of treatment

improvement after 2 weeks of treatment

if no improvement in 1 month treatment unlikely to improve

58
Q

in what type of patients is radiation therapy indicated

A

indicated in patients with

severe acute soft tissue signs ( steroids initially as radiotherapy not intermediate)

recent onset progressive proptosis

acute opthalmoplegia

acute vision loss

where steroid treatment has failed

59
Q

in what type of patients is radiation therapy contraindicated

A

contraindicated/ not effective in patients with

chronic ted
minimal or no inflammation
proptosis without inflammatory changes
longstanding restrictive myopathy or rapid progression of disease
male patients / smokers
age under 50 years

60
Q

how does radiotherapy treatment effect the clinical activity score

A

patients with a score lower than a 4 see a 80% chance of improvement

patients with a score higher than a 4 see a 36% chance of improvement

4= swelling of lid (erythema)

61
Q

what is orbital decompression

A

an operation to remove bone from the walls of the orbit- the eye socket- in order to reduce the amount of protusion in the eye

this can be done laterally

transantral

transfrontal

ethmoidal

maxillary

62
Q

what are indications for orbital decompression

A
  • sight threatening situations improve cosmesis (40%, Lyons and footman)
63
Q

what type of orbital compressions willl be perfumed

A

lateral orbital wall (single) - moderate proptosis

medial wall and medial half of the floor and lateral wall are removed (severe proptosis)

patients with sight threatening orbitopathy

orbital fat decompression alone - mild proptosis

64
Q

what are some of the complications regrading orbital decompression

A

complications include - temporary lib numbness

sinusitis

orbital cellulitis

meningitis

lower lid entropic

blindness 1/10000

asymmetric correction of proptosis

apparent upper lid retraction
epiphora

diplopia

65
Q

how is strabismus associated with ted

A

occurs in 15-51% with ted

diplopia which impacts on work/ driving ability to function independlty

vertical

66
Q

what are indications for strabismus surgery

A

medical condition stable

eye condition stable

problematic diplopia

uncomfortable head posture

centralise/ and or enlarge field of bsv

67
Q

what type of eom surgery can be performed

A

forced auction testing - pre, intra and post up

recession of muscles , avoid resections

free adhesions

undercorrection

adjustable sutures - allow fine tuning and adjustment of app

inferior rectus dissected from attachments to lower lid

inferior rectus recession

medial rectus recession -

preferably wait for 6 months of stability

68
Q

how are the lids affected in ted

A

lids retraction
(upper and lower lid)

levator palpeerde superioris muscle fibre enlargement oedema - rarely affects function

overaction of mullers muscle (sympathetic overaction)

innervation to superior rectus and levator palpable superioris

69
Q

what drugs can be given for lid retraction

A

guanethidine
topical drops -alpha adrenergic blocking agent

triamcinolone - oral

anti- inflammatory - anti fibrotic effect

70
Q

what procedures can be done for lid retraction

A

levator muscles procedures
mullers muscles procedures
combination of above
aim to leave ptotic - gradually elevates

lateral tatsoophary- not effective - not used - may prevent exopthalmos

71
Q

what levator muscle procedures can be done

A

recession

tetnotomy

72
Q

what is Hendersons operation

A

lid retraction - weakening of mullers muscles

73
Q

what can be done to help peri- orbital oedema

A

blepharoplasty- surgical correction of lid deformity

mark out excessive skin

excuse skin and obicularis

remove fat

74
Q

what are the complications of a belphorplasty

A

infection
bleeding

dry / irrated eyes

difficulty closing eyelids

75
Q

what can be done to protect the cornea

A

tape lids

glasses with Side protection

hypromellose

steroids

orbital decompression

tarsorraphy

76
Q

what is rituiximab used for

A

ritxumab is a drug which depletes B cells promoting antibody dependent cellular toxicity

sustained resolution of optic neuropathy and inflammation was found - no improvement of proptosis and strabismus

77
Q

what is tepezza used for

A

new medicine to treat go

human monoclonal antibody

approved for use in use in jan 2020

expensive -

78
Q

what does tepezza do

A

reverses proptosis by reducing inflammation and preventing tissue expansion - reduces diplopia and strabismus and orbital soft tissue volume in patients chronic ted

imaging studies show reduction in eom size

possibly Better strabismus outcomes

79
Q

what are the side effects of tepezza

A

only medication that reduces fat and muscle expansion within the orbit

only medicine to possibly reduce on compression

some patients remain non responders to treatment

possible side effects - hearing los , hypergluceima and muscle spasm

212- S + OM (10 decks)

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