Thyroid gland
Bilobed gland in the neck Largest of all endocrine glands : Produces hormones Thyroxine (T4) and tri-iodothyronine (T3)When the Thyroid Doesn’t Work Hyperthyroidism Too Much Thyroid Hormone Metabolism Speeds Up
Hypothyroidism Too Little Thyroid Hormone Metabolism Slows Down
G O I T E R
The functions of thyroid hormone are1- Facilitated growth and development. 2- Interfere with carbohydrate protein and fat metabolism. 3- Increase oxygen consumption by the tissue, basal metabolic rate, and heat production. 4- Increase oxygen release from HB. 5- Augmentation of adrenalin and noradrenalin function.
Thyrotoxicosis))Hyperthyroidism
“Hyperthyroidism” refers to overactivity of the thyroid gland leading to excessive synthesis of thyroid hormones and accelerated metabolism in the peripheral tissues. The secretion of thyroid hormone is no longer under the regulatory control of the hypothalamic-pituitary center.1- Graves' disease 2- Multinodular goitre 3- Toxic adenoma
1- Graves' disease
2- Multinodular goitre
3- Toxic adenoma
Pathogenesis
An autoimmune phenomenon – presentation determined by ratio of antibodies TSH ReceptorThyroid Stimulating Ab (TSAb)
Thyroid Stimulation Blocking Ab (TSBAb)
Thyroid
+
-
Graves’ Disease AutoimmuneHypothyroidism(Hashimoto’s) Thyroglobulin Ab
Thyroid peroxidase Ab (anti TPO)
GRAVES' DISEASE
The most common manifestation is thyrotoxicosis with or without a diffuse goitre. Graves' disease also causes ophthalmopathy and rarely pretibial myxoedema These features usually occur in thyrotoxic patients,. Graves' disease can occur at any age but is unusual before puberty and most commonly affects women aged 30-50 yearsThe Classic Triad of Graves’ Disease 1-Hyperthyroidism (90%) 2-Ophthalmopathy (20-40%) 3-Dermopathy (0.5-4.3%)
Graves’ Ophthalmopathy Antibodies to the TSH receptor also target retroorbital tissues T-cell inflammatory infiltrate -> fibroblast growth(exophthalmus) Severe: exposure keratopathy, diplopia, ,com-pressive optic neuropathy
Pretibial myxedema
Asymmetric, raised, firm, pink-to-purple, brown plaques of nonpitting edema on the anterior surface of the legFeatures of Hyperthyroidism
General : Weight loss, heat intolerance Thinning of hair, softening of nails Cardiac Atrial fibrillation Sinus tachycardia Dyspnoea on exertion Angina Ankle swellingSystolic hypertension/ increased pulse pressure Cardiac failure Gastroenterology Diarrhoea, steatorrhoea, hyperdefecation Dermatological Sweating Pruritis
Neuromuscular Anxiety, irritability, emotional lability, psyachosis Tremor Muscle weakness Hyper-reflexia sustained clonus Proximal myopathy Bulbar myopathy
Eyes 1) Lid lag slowly moving point from above eye level to below and see if eyelid smoothly follows movement of eye - 2) Lid retraction Lid retraction due to exophalmos (protrusion)Alopecia
Reproductive Amenorrhoea/oligomenorrhoe Infertility, spontaneous abortion Loss of libido, impotence
Signs and Symptoms of Hyperthyroidism
Bulging Eyes/Unblinking StareMenstrual Irregularities or Light Period
Excessive Vomiting in Pregnancy
First-Trimester Miscarriage
Family History of Thyroid Disease or Diabetes
Nervousness
Irritability
Difficulty Sleeping
Swelling (Goiter)
Frequent Bowel Movements
Warm, Moist Palms
Hoarseness or Deepening of Voice
Difficulty Swallowing
Rapid or Irregular Heartbeat
Infertility
Weight Loss
Heat Intolerance
Increased Sweating
Persistent Sore or Dry Throat
Thyroid function tests Total T3 = 1.2 to 2.8 nmol\L Total T4 = 150 nmol\L TSH 0.5 to 5 mU\L.
recently 1-free T4=10-30nmol\L 2-free T3=0.3-3.3nmol\L which is the most sensitive and specific test Autoantibody assessment: include TPH (thyroid peroxidase) normally less than 25nmol\l, and anti thyroglobulin anti body.
Diagnostic Imaging
Radioactive Iodine Uptake Shows distribution of uptake Technetium-99 Distinguishes high-uptake from low-uptake Thyroid ultrasonography Identifies nodulesThyroid scanning: iodine 123 (123I) and iodine 131 (131I) Technetium Tc 99m The imagesobtained by these studies provide the size and shape of the gland and the distribution of functional activity.
Thyrotoxicosis treatment
The choice of therapy depends on: 1-Age of the patient 2-Size of the thyroid 3-Type of thyroxicosis1- Age less than 45
Antithyroid drugs carbimazole 40-60 mg daily or prophylthiouracil 400-600 mg daily. There is subjective improvement within 10-14 days and the patient is usually clinically and biochemically euthyroid at 3-4 weeks, when the dose can be reduced. The maintenance dose is determined by measurement of T4 and TSH, Unfortunately, thyrotoxicosis recurs in at least 50%, usually within 2 years of stopping treatment.In all patients with thyrotoxicosis a non-selective β-adrenoceptor antagonist (β-blocker), such as propranolol (160 mg daily) or nadolol (40-80 mg daily), will alleviate but not abolish symptoms within 24-48 hours. Beta-blockers cannot be recommended for long-term treatment, but they are extremely useful in the short term, e.g. for patients awaiting hospital consultation or following 131I therapy.