hyperthyroidism

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