1 Thyroid Disease and the Eye: What We Must Know I The endocrine system A Goal- maintaining homeostasis 1 Organisms are exposed to constant change 2 The ability to respond to change is inherent in living things 3 Maintenance of homeostasis is vital to survival! 4 Homeostasis is the job of the of the endocrine system B Communication and homeostasis 1 Some situations require rapid, focal response (nervous system) a Speed is the critical issue b Resources used are of minimal importance 2 Some situations require slower, widespread response (endocrine system) a Speed not the critical issue b Reaching a very large number of target tissues is crucial c Resources need to be conserved 3 Selectivity-To affect a target cell receptors specific for a given hormone must be present a Cells lacking receptors to a specific hormone will not react to it, regardless of concentration b Hormonal selectivity is crucial to proper functioning of the endocrine system 4 Hormone glands and functions a Hypothalamus – region not gland I Releasing hormones II Inhibiting hormones b Pituitary gland I Hormones reach circulation & act on: II Other glands III Target organs c Adrenal glands-cortisol d Gonads- sex hormones e Thyroid I Hormones that can affect entire body II Parathyroid- parathyroid hormone f Pancreas- insulin, glucagon 5 Thyroid produces thyroxine (T4)= 90% and triiodothyronine (T3)=10% 6 Liver, kidneys convert T4 to the more powerful & rapidly acting T3 7 Thyroid hormones increase: a Heart rate b Body temperature c Mood, alertness d Protein production e Lipid metabolism f Overall metabolic rate 8 Thyroid gland anatomy, physiology a Butterfly shaped gland located on anterior larynx 2 II b Follicles- sub-units that produces thyroid hormones I Each follicle filled with colloid, site of thyroid hormone synthesis II Follicles richly supplied by fenestrated capillaries 9 Biosynthesis of thyroid hormones a TSH reaches follicle via circulation- stimulates hormone biosynthesis b Follicle epithelial cells transport iodide into colloid c Thyroglobulin binds iodide to form T3 & T4 d T3 & T4 released into circulation – act on target organs-produce desired effects 10 Functions of thyroid hormones a Increase basal metabolic rate b Stimulate fat mobilization c Increase concentrations of fatty acids in plasma d Lower cholesterol e Stimulate carbohydrate metabolism & protein synthesis f Increase heart rate, cardiac contractility and cardiac output g Increase alertness, positive mental state Thyroid diseases A Risk factors 1 Gender: women a Five to eight times more likely to suffer from a thyroid disorder b Higher risk of developing a thyroid disorder with increasing age 2 Age: a Individuals over 50 have the highest risk of thyroid disease b Male risk of developing thyroid disease increases after age 60. 3 Radiation exposure - head and neck region during childhood increases the risk of thyroid disease. B Hypothyroidism 1 Second most common endocrine disorder in the United States 2 Thyroid gland produces reduced levels of thyroid hormones 3 Body functions at a lower metabolic rate. 4 Can contribute to heart disease 5 Increased amount of LDL (bad) cholesterol 6 Hashimoto’s Disease a Autoimmune disease first described in 1912 by Dr. Hakaru Hashimoto b The immune system attacks & ultimately destroys thyroid gland c Gender: 5-10 times more common in women d Histological findings I Thyroid-specific lymphocytes attack & infiltrate the thyroid II Lymphoid cellular infiltration III Follicular epithelial cell destruction e Signs, Symptoms I Fatigue II Depression III Modest weight gain IV Cold intolerance V Excessive sleepiness 3 VI Dry, coarse hair VII Constipation C Hyperthyroidism 1 Thyroid gland produces excessive T3 & T4 2 Increases metabolic rate of the body 3 Symptoms & complications of hyperthyroidism a Nervousness b Decreased menstrual flow c Weight loss d Irregular heartbeat e Infertility and miscarriage 4 Graves’ Disease- autoimmune disease affecting thyroid gland metabolism a First described 1835-Dr. Robert Graves b Triad of: I Goiter- swelling of thyroid gland II Exophthalmos III Hyperthyroidism c Most common cause of hyperthyroid and diffuse goiter d Plasma cells make antibodies to the thyroid-stimulating hormone receptor (TSHR) e Auto-antibodies not subject to negative feedback f Unlimited thyroid hormones are produced, released into circulation III Thyroid associated eye disease (TAED) A 20% of patients state ocular morbidity troublesome than thyroid disease B Dry eye (with hyperthyroid and hypothyroid) 1 Gilbard JP, Farris RL. Ocular surface drying & tear film osmolarity in thyroid eye disease. Acta Ophth 1983 a Evaluated 17 patients w/ Graves’ DZ b 94% had dry eye symptoms c 42% had increased tear film osmolarity d Increased palpebral fissure width e Rose bengal staining proportional to PFW f Increased blink rate associated w/ Rose bengal staining 2 Management a Well designed artificial tears I Goebels & Spitzmas- NO BAK II Blink Tears- CMC based, comfort excellent, duration issues? III Soothe- lipid component for reduction of evaporative dry eye IV Systane Balance- lipid component present up to 90 minutes b Punctal occlusion I Positive prognostic indicators II Moderate to adequate aqueous layer III Minimal inflammatory indicators IV Anterior blepharitis and or posterior blepharitis V Meibomian gland & lid margin scarring c Negative prognostic indicators I Minimal to no aqueous layer 4 II Significant inflammatory indicators III Anterior blepharitis and or posterior blepharitis IV Meibomian gland & lid margin scarring V Lid configuration issues VI Punctal ectropion d Restasis- Excellent therapy for thyroid-associated dry eye A Expect a three month lag between TX & improvement B Prescribe for optimal financial benefit C Ophthalmopathy 1 Upper lid retraction (Dalrymple sign) #1 sign 2 Proptosis- sympathetic drive of Müller muscleCompressive neuropathy a Increased surface area > drying 3 Visual field loss 4 Diplopia a Upgaze restriction- fibrosis of the levator b Estropia- fibrosis of medial rectus c Contralateral ptosis (myasthenia) D Management/Triage 1 Lid evaluation at office visits 2 EOM evaluation, history of diplopia 3 Proptosis, EOM changes a May change significantly over time b Obtain (and bill for) baseline photos for future reference c Work with a competent and conservative lid specialist d Protect the anterior surface from dryness secondary to exposure 4 Surgical options a Botulinum toxin injections I Duration @ 3 months-40 months II Complications- ptosis, diplopia b Surgery I May use weights or relaxing procedure to reduce lid lag II Delay consultation until stable IV Thyroid-associated ophthalmopathy A Definition B Pathogenesis 1 Lymphocytic infiltration of orbital tissue release of cytokines i.e. IL-1 2 Cytokines activate quiescent fibroblasts, secrete hyaluronic acid 3 Doubling hyaluronic acid content 5-fold increase in osmotic load 4 Osmotic damage results in muscle edema 5 May occur despite well controlled hyperthyroidism 6 Usually a self-limited course over one or more years. 7 Strongly associated with smoking C Treatment options D Goals of therapy 1 Cosmetic (disfiguring proptosis, exophthalmos, strabismus) 2 Functional (reduce dryness, diplopia) 3 Sight preservation (compressive optic neuropathy) 4 Approx 5% of TAO patients require surgery 5 5 Orbital decompression a Surgery generally delayed until after the inflammatory phase b May be forced to operate sooner if vision loss is present c Two orbital walls decompressed I Traditional: the medial wall and floor of the orbit II Decompression of the medial & lateral orbital walls is gaining popularity d Three walls orbital decompression increasingly common a Delay until patient is stabilize V The optometrist’s role in thyroid associated ocular conditions A Detection 1 High index of suspicion especially in females 2 Recent onset severe dry eye no other 3 Weight gain, loss, pretibial edema 4 Changes in mentation, personality 5 Obvious changes in lids, adnexae B Consultation when indicated 1 Internist or endocrinologist 2 Send reports after your visits: (Forms in MS Word) C Long-term care, reassurance, remediation VI Conclusion A OD’s may be the first health care providers with the opportunity to detect thyroid disease B ODs may be the first health care providers to diagnose TAED C Management of most patients with these conditions within our scope and expertise D Have an index of suspicion for any patient who presents with the diverse signs & symptoms of TAED