Armando Hasudungan
Biology and Medicine videos

Hyperthyroidism (Thyrotoxicosis)

Summary

Summary

Overview

Overview The most common cause of hyperthyroidism are Graves disease, multinodular goitre, an autonomously functioning thyroid nodule  (adenoma) and subacute thyroiditis. Graves Disease is more common in women. Multinodular goitre is more common in the elderly. Graves disease typically manifests in middle aged women. Thyroid diseases are more common in women.

Definition
Hyperthyroidism: denote conditions in which hyperfunction of the thyroid leads to thyrotoxicosis.
Hypothyroidism: variety of abnormalities that cause insufficient secretion of thyroid hormones. The most common cause is autoimmune thyroid disease
Thyrotoxicosis: denotes the clinical, physiological, and biochemical findings that result when the tissues are exposed to excess thyroid hormone. It can arise in a variety of ways (drugs, thyroiditis)

Anatomy and Physiology

The thyroid gland is butterfly shaped endocrine organ that sits and wraps around the trachea. Anteriorly the thyroid glands are joined by the Isthmus. Developmentally, the thyroid isthmus can give rise to a structure contiguous called the pyramidal lobe, which extends upward.

Posteriorly the thyroid gland does not connect, however 4 parathyroid glands are attached onto the thyroid gland posteriorly.

The gland is in visceral compartment of the neck, along with the trachea, oesophagus and pharynx. The compartment is enclosed in the pre- tracheal fascia, which anchors the thyroid gland to the trachea, so that the thyroid moves up on swallowing.. The thyroid gland stands at the vertebral level C5-T1.


Embryologically
, the thyroid gland begins its development at the base of the tongue before descending down to the trachea. This is the reason why thyroid ductal cysts can occur higher up on the neck, anywhere along the path of descent.

Arterial blood supply:

  • Superior thyroid artery ← External Carotid
  • Inferior thyroid artery ← Thyrocervical trunk
  • Ima Artery (~3% of people) ← Brachiocephalic artery

Venous drainage:

  • Superior thyroid vein → Internal Jugular
  • Middle thyroid vein → Internal Jugular
  • Inferior thyroid vein → Brachiocephalic Vein

Physiology The thyroid gland produces 3 hormones:

  • Tridothyronine
  • Thyroxine
  • Calcitonin

Signs and Symptoms

sands

Clinical Presentation

  • Hyperactivity, irritability, altered mood, insomnia
  • Heat intolerance, sweating
  • Palpitations
  • Fatigue, weakness
  • Dyspnea
  • Weight loss with increased appetite (weight gain in 10% of patients)
  • Pruritus
  • Increased stool frequency
  • Thirst and polyuria
  • Oligomenorrhea or amenorrhea; loss of libido

Clinical Examination

  • General: irritability, axious, weight loss, warm, moist skin, chorea, periodic paralysis (primarily in Asian males), psychosis (rare)
  • Hands: onycholysis, fine tremor
  • Face: Hair loss, Graves opthalmology
  • Cardiovascular: Sinus tachycardia, atrial fibrillation, palmar erythema, congestive (high-output) heart failure,
  • Neurological: hyperkinesia, hyperreflexia, muscle weakness and wasting
  • Legs: pretibial myxoedema

examination

Features of Severe Hyperthyroidism
Atrial fibrillation
Heart Failure
Significant weight loss
Proximal myopathy

Graves Disease Additional Manifestation

  • Diffuse goiter
  • Ophthalmopathy
  • Localised dermopathy
  • lymphoid hyperplasia
  • Thyroid acropachy

Proptosis and lid retraction from Graves’ Disease – Courtesy of Jonathan Trobe, M.D. – University of Michigan Kellogg Eye Center

Conditions associated with Graves Disease
Type 1 Diabetes
Addison’s Disease
Pernicious anaemia
Myasthenia Gravis
Celiac Disease
Vitiligo

Differential Diagnosis

  • Toxic Multinodular Goitre
  • Toxic Adenoma
  • Thyroiditis (can be painful or painless)
    • De Quervain thyroiditis (painful)
  • Graves Disease (most common cause of hyperthyroidism)
  • Myasthenia Graves – causes opthalmopathy
De Quervain’s thyroiditis is acute inflammation of the thyroid gland causing spillage of thyroid hormones into blood stream. Presents with ↑T4,T3, ↑ESR and decreased radioactive iodine uptake.

 

Investigations

 

ix

The clinical presentation of hyperthyroidism is diverse. Neither nuclear thyroid scanning not thyroid ultrasound is a mandatory investigation in hyperthyroidism. If hyperthyroidism has been confirmed by biochemical test (TFT), nuclear thyroid scanning should be considered if the thyroid is no palpable, a single thyroid nodule is detected or thyroiditis is suspected. A normal concentration of TSH rules out a diagnosis of hyperthyroidism.

 

Grave’s Disease De Quervain’s thyroiditis (↑ESR)
TFT’s Increased Increased
Scintiscanning Increased Decreased
Management Antithyroid, B-blocker, radioactive iodine, thyroidectomy Symptomatic treatment because self resolving – b-blocker, steroids.

Aetiology

  • Graves Disease (most common cause of hyperthyroidism)
  • Multinodular goitre (toxic)
  • Thyroid adenoma (toxic)
  • Thyroiditis (postpartum, bacterial, postviral, subacute, chronic)
  • Exogenous (Amiodarone, Iodine excess, thyroid hormone medication)
  • Pituitary adenoma → TSH → Thyroid gland → ↑Thyroid Hormone

Aetiology

Side note 1/3 of Amiodarone is Iodine and so can cause hyperthyroidism because iodine is an ingredient for thyroid hormone production

Pathology

pathology

microscopic changes seen in graves disease

Pathophysiology

pathophysiology

The main cause of hyperthyroidism is graves disease, an autoimmune disease. In Graves disease, autoantibodies are produced that mimic thyroid stimulating hormone resulting in increase thyroid hormone production leading to hyperthyroidism

Management

mgx

Treatment of hyperthyroidism is medical (pharmacological), radioiodine therapy or surgery

Medical Treatment aim is to induce remission in Graves’ disease, monitor for relapse of treatment and for patients who relapse to consider other treatment options such as radioiodine or surgery.

  • Antithyroid drugs (treat for 18 months and review)
    • Thionamides – inhibits thyroid hormone production
    • B-blockers – to decrease the sympathetic activity
Pharmacology Thionamides actively accumulates in thyrotoxic tissue and inhibits the action of thyroid peroxidase. Thyroid peroxidase is an enzyme that helps in thyroid hormone synthesis. Agranulocytosis is a life threatening side-effect. Itch and urticarial rash are common side-effects.
Remember Treat patient with antithyroid drug for 18months the aim is remission and prevent relapse. If relapse consider radioiodone or surgery
  • Radioiodine therapy
Side note Contraindications of radioiodine therapy:

  • Young children, because of the potential risk of thyroid carcinogenesis
  • Pregnant and lactating women
  • Situations where it is clear that the safety of other people cannot be guaranteed

Surgical treatment Thyroidectomy is rarely recommended for patients with Graves’ disease

Indications for thyroidectomy
Suspicious or malignant thyroid nodule by FNAC
Pregnant mothers who are not adequately controlled by ATD
Patient reject or fear exposure to radiation
Poor compliance to medical treatment
Patients who wants rapid control of symptoms

Complications

Complications of thyroidectomy

  • Recurrent laryngeal nerve damage
  • Hypoparathyroidism
  • Thyroid crisis
  • Local hemorrhage, causing laryngeal edema
  • Wound infection
  • Hypothyroidism
  • Keloid formation

Thyroid Crisis (Storm)

Thyroid crisis represents a rare but life-threatening exacerbation of the manifestations of thyrotoxicosis.

Clinical signs suggestive of a thyroid storm

  • Alteration in mental status
  • High fever
  • Tachycardia or tachyarrhythmias
  • Severe clinical signs of hyperthyroidism
  • Vomiting, jaundice, and diarrhea
  • Multisystem decompensation: cardiac failure, respiratory distress, congestive hepatomegaly, dehydration, and renal failure

Management

  • General supportive therapy
  • Antiarrhythmic drugs may need to be used – digoxin (watch for Hypokalemia)
  • Broad-spectrum antibiotics should be given if infection is suspected.
  • Antithyroid drugs in large doses- to inhibit thyroid hormone synthesis completely.
  • Potassium iodide 10 drops, twice daily, after starting antithyroid drugs, will inhibit thyroid hormone release.
  • B-Adrenergic blocking agents are essential in management to control tachycardia, tremor, and other adrenergic manifestations.
  • High doses of glucocorticoids are capable of blocking T4-to-T3conversion

References

Therapeutic Guidelines Version 4 2009
Best Practice
UpToDate
Oxford Handbook of Endocrinology and Diabetes