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E24 Endocrinology
Thyroid Toronto Notes 2019
Graves’ Ophthalmopathy
NO SPECS (in order of changes usually) No signs
Only signs: lid lag, lid retraction
Soft tissue: periorbital puffiness, conjuctival injection, chemosis Proptosis/exophthalmos
Extraocular (diplopia)
Corneal abrasions (since unable to close eyes) Sight loss
Clinical Features
Table 19. Clinical Features of Thyrotoxicosis
General Fatigue, heat intolerance, irritability, fine tremor
CVS Tachycardia, atrial fibrillation, palpitations
Elderly patients may have only cardiovascular symptoms, commonly new onset atrial fibrillation
GI Weight loss with increased appetite, thirst, increased frequency of bowel movements (hyperdefecation)
Neurology Proximal muscle weakness, hypokalemic periodic paralysis (more common in Asians)
GU Oligomenorrhea, amenorrhea, decreased fertility
Dermatology Fine hair, skin moist and warm, vitiligo, soft nails with onycholysis (Plummer’s nails), palmar erythema, pruritis Graves’ disease: clubbing (acropachy), pretibial myxedema (rare)
MSK Decreased bone mass, proximal muscle weakness
Hematology Graves’ disease: leukopenia, lymphocytosis, splenomegaly, lymphadenopathy (occasionally)
Eye Graves’ disease: lid lag, retraction, proptosis, diplopia, decreased acuity, puffiness, conjuctival injection NOTE: Lid lag is a reflection of a hyperadrenergic state and can be present in any form of thyrotoxicosis
Treatment
• antithyroidals (thionamides): propylthiouracil (PTU) or methimazole (MMI); MMI recommended (except in first trimester pregnancy); block thyroid hormone production
• β-blockersforsymptomcontrol
• radioactiveiodinethyroidablationforGraves’diseaseandtoxicnodules/adenoma
• surgeryintheformofhemi,subtotal,orcompletethyroidectomy
Graves’ Disease
Definition
• anautoimmunedisordercharacterizedbyautoantibodiestotheTSHreceptorthatleadstohyperthyroidism
Epidemiology
• mostcommoncauseofthyrotoxicosis
• occursatanyagewithpeakin3rdand4thdecade
• F:M=7:1,1.5-2%ofU.S.women
• familialpredisposition:15%ofpatientshaveaclosefamilymemberwithGraves’diseaseand50%have
family members with positive circulating antibodies
• association with HLA B8 and DR3
• maybeassociatedwithotherinheritedautoimmunedisorders(e.g.perniciousanemia,Hashimoto’sdisease)
Etiology and Pathophysiology
• autoimmunedisorderduetoadefectinT-suppressorcells
• Blymphocytesproducethyroid-stimulatingimmunoglobulin(TSI)thatbindsandstimulatestheTSH
receptor and stimulates the thyroid gland
• immuneresponsecanbetriggeredbypostpartumstate,iodineexcess,lithiumtherapy,viralorbacterial
infections, glucocorticoid withdrawal
• ophthalmopathy(thyroidassociatedorbitopathy)isaresultofincreasedtissuevolumedueto
inflammation and accumulation of glycosaminoglycans, stimulated by TSI, that increase osmotic
pressure within the orbit; this leads to fluid accumulation and forward displacement of the eyeball
• dermopathy(pretibialorlocalizedmyxedema)mayberelatedtocutaneousglycosaminoglycan
deposition
Clinical Features
• signsandsymptomsofthyrotoxicosis
• diffusethyroidgoitre±thyroidbruitsecondarytoincreasedbloodflowthroughthegland
• ophthalmopathy: proptosis, diplopia, conjunctival injection, corneal abrasions, periorbital puffiness, lid
lag, decreased visual acuity (plus signs of hyperthyroidism: lid retraction, characteristic stare)
• dermopathy(rare):pretibialmyxedema:thickeningofdermisthatmanifestsasnon-pittingedema • acropachy:clubbingandthickeningofdistalphalanges
Investigations
• lowTSH
• increased free T4 (and/or increased T3)
• positiveforTSI(specificbutnotsensitiveforGraves’disease) • increasedradioactiveiodine(I-131)uptake
• homogeneousuptakeonthyroidscan
Treatment
• treatmentforGrave’sdiseaseincludesthionamides,radiodine,orsurgery.Thesetreatmentoptionsare not mutually exclusive. Patients will start with medical management, but eventually require a definitive treatment with surgery