hyperthyroidism
TRANSCRIPT
HYPERTHYROIDISM
Dr.Badr Al-Sayed
Learning Objectives
To recognize the clinical features of hyperthyroidism
To enumerate a reasonable deferential diagnosis
To analyze essential laboratory finding To understand concept of treatment
Main Contents
Clinical scenario DDx Clinical approach Pathophysiology Management
Clinical Scenario
Sara is 22 year old college student presented to her family physician C/O:
Palpitation Sweating For the last one month but get worse last
week
What do you think she has more?
Associated symptoms
Heat intolerance Fever Tremor Menstrual dysfunction (oligomenorrhea,
amenorrhea) Increased appetite
Associated symptoms
Weight loss Diarrhea Anxiety Irritability Emotional liability Panic attacks
Epidemiology
Hyperthyroidism affects 2% of women and 0.2% of men in their lifetimes
Toxic multinodular goiter usually occurs in women >55 yr
Graves’ disease usually occur in women 30-50 yr
F:M is 7-10:1
P.Examination
Sinus tachycardia HR: 120/min BMI 23 Bilateral exophthalmos Moist hand Fine tremor Hyperreflexia
Thyroid Examination
Size Consistency (soft, firm or hard) Nodularity (MNG) Tenderness (subacute thyroiditis) Fixation (neoplastic) Bruit (hypervascularity) Lower border (retrosternal extension) LNE (part of neck exam.)
Definitions
Thyrotoxicosis: the state of thyroid hormone excess
Hyperthyroidism: the result of excessive thyroid function
Graves’ disease: autoimmune mediated, is caused by an activating autoantibody that targets the TSH receptor
Thyroiditis: is an inflammatory process that causes follicular disruption and release of thyroglobulin and thyroid hormone
Extrathyroidal ManifestationsGraves’ disease
Ophthalmopathy Pretibial myxedema Thyroid acropachy
Ophthalmopathy
Infiltrative orbitopathy 20% to 40% of patients who have Graves'
disease TRAb bind to TSH receptor antigen in retro-
orbital tissues Initiates subsequent T-cell inflammatory
infiltrate Cytokines stimulate Fibroblasts to produce
glycosaminoglycans (GAG) causing ophthalmopathy as a result of mass effect
Ophthalmopathy
Pretibial myxedema
Thyroid acropachy
Digital clubbing Soft tissue swelling of the hands and feet Periosteal bone formation 0.1% to 1% of patients with Graves'
disease
Thyroid acropachy
Periosteal bone formation
Clinical Approach
DDx
Anxiety disorder Pheochromocytoma Metastatic neoplasm Diabetes mellitus Atrial fibrillation due to other causes Premenopausal state High estrogen states, eg, pregnancy
(falsely increase serum thyroxine)
Etiology
Graves’ disease (diffuse toxic goiter): 80% to 90% of all cases of hyperthyroidism
Toxic multinodular goiter (Plummer’s disease)
Toxic adenoma Iatrogenic and factitious Transient hyperthyroidism (subacute
thyroiditis, Hashimoto’s thyroiditis) Rare causes
Pathophysiology
Increased thyroid hormone production Release of stored thyroid hormone
following injury to the thyroid gland (thyroiditis).
Increased RAIU
Diffuse toxic goiter (Graves' disease), Toxic multinodular goiter, Single toxic nodule (Plummer's disease) Thyroid-stimulating hormone (TSH)-
secreting tumor (rare) Hydatidiform mole (rare)
Without increased RAIU
Subacute thyroiditis Excessive ingestion of medicinal thyroid
hormone Struma ovarii Thyroid hormone-secreting metastatic
thyroid cancer
Physiology
Physiology
Physiology
Biosynthesis
Biosynthesis
LABORATORY TESTS
Low TSH (unless hyperthyroidism is a result of the rare hypersecretion of TSH from a pituitary adenoma)
Elevated free thyroxine (T4) Elevated free triiodothyronine (T3):
generally not necessary for diagnosis Thyroid autoantibodies in Graves’
disease (absent toxic MNG)
Imaging
24-hr RAIU Increased uptake: overactive thyroid Normal or decreased uptake: iatrogenic
thyroid ingestion, painless or subacute thyroiditis
The RAIU results in hyperthyroidism Graves’ disease: increased
homogeneous uptake Multinodular goiter: increased
heterogeneous uptake Hot nodule: single focus of increased
uptake
Graves’ disease
Multinodular goiter
Hot nodule
Treatment
ANTITHYROID DRUGS: Propylthiouracil (PTU) and methimazole (Tapazole)
RADIOACTIVE IODINE (RAI; 131I) SURGICAL THERAPY: (subtotal
thyroidectomy) ADJUNCTIVE THERAPY: (Propranolol)
Take Home Message
F:M is 7-10:1 If your patient is clinically thyrotoxic,
look for underlying pathology It has serous complications: AF, T.Storm Due to ignorance, some people are using
Thyroxin in addition to lasix as Wt losing medications!!
Thanks
References
Endocrine Physiology, 3e Patricia E. Molina Harrison's Online,Chapter 335. Disorders
of the Thyroid Gland J. Larry Jameson, Anthony P. Weetman
Ferri: Ferri's Clinical Advisor 2011, 1st ed RadioGraphics journal