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Clinical Manifestation Of Hyperthyroidism With Details On Diffuse Goitre

Updated on February 9, 2014

Diffuse Goitre

The exact etiology is unknown. The consensus is that Grave’s disease is an autoimmune disorder. In some cases, thyroid stimulating auto-antibodies such as long acting thyroid stimulator (LATS) are demonstrable.
The exact etiology is unknown. The consensus is that Grave’s disease is an autoimmune disorder. In some cases, thyroid stimulating auto-antibodies such as long acting thyroid stimulator (LATS) are demonstrable. | Source

A General Overview

Persistent elevation of the synthesis and release of thyroid hormones (T4 and/or T3) leads to hyperthyroidism. It may be due to several causes.

Common causes: Toxic diffuse goiter (Grave’s disease) and toxic nodular goiter (plummer’s disease).

Rare causes:

  1. Neonatal hyperthyroidism due to transplacental transfer of long-acting thyroid stimulator (LATS).
  2. Thyrotoxicosis factitia caused by the self administration of thyroid hormones
  3. Iodide induced hyperthyroidism (Jod Basedow phenomenon), usually seen in regions where iodine is supplemented.
  4. Hashinomoto’s disease may be associated with thyrotoxicosis (Hashi-toxicosis).
  5. Ectopic secretion of TSH like substances by trophoblastic tumours, e.g hydatidiform mole or choriocarcinoma.

Increase Sweating In Diffuse Goiter

The symptoms may be less obvious in others. The general symptoms include loss of weight, intolerance to heat, increased sweating, excessive appetite, palpitation, tachycardia, exertional dyspnea, nervousness, tremor, diarrhea, easy fatigability, appr
The symptoms may be less obvious in others. The general symptoms include loss of weight, intolerance to heat, increased sweating, excessive appetite, palpitation, tachycardia, exertional dyspnea, nervousness, tremor, diarrhea, easy fatigability, appr | Source

Diffuse Toxic Goitre (Grave’s Disease, Parry’s Disease, Basedow’s Disease)

The disease is quite common in general practice, but the severity may vary. Females are affected more with a peak incidence between 20 and 40 years. Though neonates of thyrotoxic mothers may suffer from hyperthyroidism, usually the condition subsides within 3-6 weeks of birth.

Etiology: The exact etiology is unknown. The consensus is that Grave’s disease is an autoimmune disorder. In some cases, thyroid stimulating auto-antibodies such as long acting thyroid stimulator (LATS) are demonstrable. LATS is an auto-immunoglobulin of IgG class. It possesses TSH-like action, which is more prolonged. LATS crosses the placenta and may lead to neonatal hyperthyroidism in infants of thyrotoxic mothers. The thyroid gland shows diffuse enlargement, hyperplasia of the acinar cells and lymphocytic infiltration. The gland is highly vascular.

Clinical features: The effect of thyroid hormone is to increase metabolism and sensitise the tissues to catecholamines. The condition is florid and easily detectable in many cases. The symptoms may be less obvious in others. The general symptoms include loss of weight, intolerance to heat, increased sweating, excessive appetite, palpitation, tachycardia, exertional dyspnea, nervousness, tremor, diarrhea, easy fatigability, apprehension and insomnia. Rarely mental changes like severe agitation and frank psychosis may be the presenting features.

Examination of the neck shows the thyroid to be diffusely enlarged, but sometimes it may be asymmetrical. It is soft, warm, pulsatile and tender. Arterial thrills and bruit may be detectable. These phenomena indicate increased vascularity.

Several organs show abnormality. Though in most cases, many of them are detectable, the severity of involvement may not be uniform.

Occular Manifestations

The retro-orbital tissues and extraocular muscles are infiltrated with mucoid material, lymphocytes, and mast cells. These give rise to abnormal protrusion of the eyeball (exophthalmos) and partial or complete ophthalmoplegia.
The retro-orbital tissues and extraocular muscles are infiltrated with mucoid material, lymphocytes, and mast cells. These give rise to abnormal protrusion of the eyeball (exophthalmos) and partial or complete ophthalmoplegia. | Source

Other Clinical Manifestations

Ocular manifestations:

  1. Sympathetic overactivity leads to lid lag, stare, increased watering and infrequent blinking. These subside with correction of thyroid function.
  2. The retro-orbital tissues and extraocular muscles are infiltrated with mucoid material, lymphocytes, and mast cells. These give rise to abnormal protrusion of the eyeball (exophthalmos) and partial or complete ophthalmoplegia. Exophthalmos is generally bilateral, but can be unilateral or asymmetrical. It may precede overt hyperthyroidism, but more often it appears concurrently. In severe cases, there is chemosis of the conjunctiva, prolapsed of the eyeball, failure of closure of the eyelids, corneal ulceration and blindness. These constitute malignant exophthalmos.
  3. Papilledema may develop in advanced cases. Some cases may show optic atrophy. The exact pathogenesis of this ophthalmopathy is not clear.

Skin Changes: The skin is soft and moist. The hair is soft. Sweating is excessive. The nails show thinning (onycholysis). Sometimes localized myxedematous deposits may occur. The common site is the front of the leg (hence called pre-tibial myxedema). Over this site the skin is raised, nodular, indurated and reddish brown in colour. The lesions may be pruritic. Examination reveals “peau de Orange” (Orange Peel-like) appearance. In addition to the pretibial regions, thighs, genitalia and lower abdomen may be affected. Pretibial myxedema is attributed to local non-responsiveness of tissues to the thyroid hormones.

Some cases show clubbing of fingers and toes and hypertrophic osteoarthropathy.

Changes in Skeletal Muscles: There is excessive fatigue and weakness. The proximal muscles of pelvic and pectoral girdles show myopathy and this may incapacitate the patient. The condition recovers completely when thyrotoxicosis is controlled.

Cardiovascular system: Congestive heart failure, tachyarrhythmias like paroxysmal tachycardias, atrial fibrillation and atrial flutter are common. Severe cases develop angina pectoris.

Alimentary system: Abdominal cramps, diarrhea and vomiting are common features. The diarrhea is due to intestinal hurry. In many cases it takes the form of increased frequency of bowel movements, especially after food.

Reproductive system: In women the periods become scanty and fertility is reduced. In men libido and potency may be altered variably. Gynecomastia may develop.

Bones: Osteoporosis may develop.

The clinical picture produced by toxic diffuse goiter and toxic nodular goiter is similar in many respects. However, eye changes and pretibial myxedema are more common in toxic diffuse goiter. Other autoimmune conditions such as myasthenia gravis and chronic lymphocytic thyroiditis are associated with toxic diffuse goiter. Hypokalemic periodic paralysis is more common in thyrotoxicosis. In toxic nodular goiter, the cardiovascular manifestations may be more prominent than the other signs. In this condition, a single nodule or multiple nodules may be palpable in the thyroid.

Sometimes, the thyroid gland may produce excessive quantities of only tri-iodothyronine (T3). Such a condition is called T3-toxicosis.

© 2014 Funom Theophilus Makama

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