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incom > Thyroid eye disease (TED) > Flashcards

Thyroid eye disease (TED) Flashcards

1
Q

what is graves

A
  • Systemic autoimmune disorder
  • Hyperthyroid - px starts with having this - over acting thyroid
  • Orbitopathy - eye movement disorders, swelling due to graves disease - blood tests don’t always prove
  • Myxoedema (lumpy red skin) - extreme situation
  • Acropachy (finger clubbing) - extreme situation
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2
Q

epidemiology of graves

A
  • Prevalence of hyperthyroidism in the general population is 1.2%
    • 0.7% subclinical hyperthyroidism
    • 0.4% Graves’ Disease – most common etiology; note there is overlap with the subclinical group
  • Graves’ Disease is more common in females (7:1 ratio)
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3
Q

what is normal thyroid hormone control

A

2 hormones produced by the Thyroid Gland
* T4 Thyroxine
* T3 Triiodothyronine

They are responsible for the metabolic regulation in all cells

Normal control

  • Thyrotropin releasing hormone (TRH)is produced by the hypothalamus - sends message of how much hormone is to be produced
  • Acts on the anterior pituitary gland
  • Releasing thyroid stimulating hormones (TSH) - if too much produced, increases T3 AND T4 production resulting in a goitre (swelling of gland)
  • TSH binds to the TSH receptors in the thyroid gland releasing Thyroid hormone
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4
Q

Abnormal Control

A
  • Hyperthyroidism in Graves disease is a direct result of an Abnormal Circulating Antibody (Ab) (TSH receptor AB)
  • This targets the TSH receptor and mimics the effect of normal TSH resulting in overstimulation of the Thyroid gland
  • Goitre – swelling of the gland may occur
  • Over production of T4 and T3
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5
Q

causes

A

→ Graves Disease
→ Thyroiditis
→ Toxic Multinodular goitre - cancerous tumor in gland
→ Toxic Thyroid nodule
→ Self administered thyroid hormones - overdose on thyroid meds

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6
Q

Systemic symptoms Hyperthyroid

A
  • Weight loss
  • Increased appetite
  • Intolerance of heat
  • Anxiety
  • Tremor - never had this before/ sudden onset
  • Sweating
  • Increased heart rate
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7
Q

Systemic Symptoms Hypothyroidism

A

Not producing enough T3 and T4

  • Weight gain
  • Decreased appetite
  • Intolerance of cold
  • Lethargy - tired/ fatigue - can also have MG
  • Hair loss
  • Reduced heart rate
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8
Q

what is Graves Orbitopathy

A

enetics play a large role in the development of GO
* High levels of TSH Ab linked to severe GO
* Smoking increases the severity of GO in hyperthyroidism

→ Not all patients with hyperthyroidism develop GO
→ Approx 20% of patients develop GO prior to the diagnosis of thyroid disorder
→ 20% are diagnosed with GO at the same time as their Thyroid disorder
→ 20% develop GO 6 months after the thyrioid is diagnosed
→ 40% can develop GO more than 6 months after their hyperthyroidism
A very small percentage of patients can be Hypothyroid or Euthyroid

Anybody attending endocrinology or presenting signs/ symptoms think TED

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9
Q

Pathophysiology - NEED TO KNOW!!

A
  • Acute/Active - Inflammatory Phase - used to be called wet phase
  • Late/Inactive Phase - 18 months after disease has started - can be known as dry phase
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10
Q

active phase of ted

A
  • Connective Tissue Inflammation
  • Activation of Extraocular Muscle Fibroblasts - EOM
    start to swell up can be 8-10x bigger than normal size leading to PROPTOSIS, EXOPTHALMUS
  • Increasing Orbital volume by differentiating into orbital fat and secreting glycosaminoglycans
  • These then attract water
  • Inflammatory Myopathy resulting from the Autoimmune process
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11
Q

Connective Tissue Inflammation symptoms

A
  • Redness
  • Mild Ocular discomfort
  • Periorbital swelling
  • Pain on motility - usually on elevation as pain is on opposite direction of area affected
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12
Q

Corneal Exposure symptoms

A
  • Grittiness
  • Photophobia
  • Epiphora - over production of tears to counteract gritiness
  • Reduction in vision
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13
Q

enlarged EOM symptoms

A

→ Diplopia
→ Reduced field of BSV
→ Reduced uniocular field of fixation

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14
Q

Typical order of limitations - MEMORISE

A

Will usually follow this pattern
OBLIQUES ARE NOT INVOLVED

  • Inferior Rectus - unable to elevate/ pain
  • Medial Rectus - unable to pull eye out to side - may have hypo and eso deviation/ pain
  • Superior Rectus
  • Lateral Rectus

Diplopia in opposite direction

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15
Q

Clinical Features

A
  • AHP of chin elevation
  • Hypophoria/tropia usually first deviation
  • With/Without Head Turn - when MR affected will have head turn to move eye away from problem as cant abduct
  • Enlarged Vertical fusion range - anything above 5^ - longstanding 4th or TED, if normal vertical fusion range (2-3^) then recently acquired
  • Raised IOP on elevation/attempted elevation - px may have spike in IOP on direct elevation (USUALLY EXTREME CASES)
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16
Q

Increased Orbital Volume

A
  • PROPTOSIS - key sign - usually one eye
  • COMPRESSION ON OPTIC NERVE
  • Reduced Colour Vision - colour or contrast sensitivity may be reduced before reduced VA
  • Loss of vision
17
Q

Muller’s muscle hyperactivity

A
  • Upper eyelid retraction
  • Lower eyelid lag

→ Upper eyelid retraction - check palpebral aperture
→ Caused by overactivity of Muller’s muscle and finally by fibrosis of the levator muscle
Upper lid lag on downgaze - not depressing at same rate as eye

18
Q

Soft Tissue Inflammation types

A
  • Periorbital swelling
  • Conjunctival swelling
  • Conjunctival injection
19
Q

Increased Orbital Volume

A
  • Proptosis
  • Lower eyelid retraction
  • Corneal exposure
  • Diplopia
  • Compressive Optic Neuropathy
20
Q

PROPTOSIS

A
  • Proptosis
  • Exophthalmos - both eyes protruding - using ex-ophthalmometer
  • Unilateral/Bilateral
  • Symmetrical/Asymmetrical
21
Q

Signs of Optic Nerve Compression

A
  • Loss of VA - can be loss of color sensitivity first
  • This may be due to Corneal exposure and Punctate Keratitis
  • Pinhole to ensure not refractive
  • Reduction in color Vision - big sign of compression on optic nerve
  • Visual Field defects – paracentral/arcuate/any - can be due to rise in IOP
  • RAPD – unilateral/asymmetrical - compression of ON
  • Mild or no disc swelling
  • Extreme cases Optic atrophy develops
  • VEP – showing reduced amplitude
  • CT scan- crowding of orbital apex with enlarged muscles

Active phase can last 18 months - 2 years
Need to know day of initial symptoms

22
Q

Inactive Phase

A

Cant manage with steroids in inactive stage - can only use in active and inflammatory phase
* Cicatrical phase - can also be known as this or inactive phase
* Fibrosis and muscle contraction - become tight and fibrotic, contract, muscle cant move UP or DOWN
* Reduction in proptosis/swelling
* Corneal exposure persists due to retraction of lids - due to insufficient lid closure

23
Q

CAS SCORE

A
24
Q

EUGOGO SCORE

A

For initial CAS, only score items 1-7

  1. Spontaneous orbital pain.
  2. Gaze evoked orbital pain.
  3. Eyelid swelling that is considered to be due to active (inflammatory phase)
  4. Eyelid erythema
  5. Conjunctival redness that is considered to be due to active (inflammatory phase
  6. Chemosis.
  7. Inflammation of caruncle OR plica. Patients assessed after follow-up can be scored out of 10 by including items 8-10.
  8. Increase of > 2mm in proptosis.
  9. Decrease in uniocularocular excursion in any one direction of > 8
  10. Decrease of acuity equivalent to 1 Snellen line
25
Q

Score of severity

A
  • RAPD - may have optic atrophy
  • Eyelid measurements
  • Proptosis
  • Risk of Corneal Ulceration

incom (14 decks)

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