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HYPERTHYROIDISM

mrs. magsaysay

Endocrine Gland - consist of ductless glands that secrete hormones directly into the circulatory system. Hypersecretion disorders
are those in which the bloodstreams have oversecretion of hormones.

Hyposecretion disorders
are those in which the bloodstreams have undersecretion of hormones.

TSH) Thyroid-Stimulating Hormone binds to the membrane-bound receptors on cells of the thyroid gland and cause the cell to secrete thyroid hormone.

Thyroid Gland
butterfly-shaped gland located just below the larynx (Adam's apple). small, soft gland that wraps around the trachea (windpipe). made up of two lobes connected by a narrow band called the isthmus.

Thyroid Gland
uses iodine to produce thyroid hormone, which has regulatory functions on :

1. 2. 3. 4. 5. 6.

rate of metabolism body temperature heart rate menstrual periods mental alertness growth in children

THYROID GLAND: HORMONES AND FUNCTIONS


HORMONES PRODUCED FUNCTION
acts as a catalyst; influences metabolic rate, growth and development. Controls rate of body metabolism, growth and nutrition. Controls calcium and phosphate metabolism

Thyroxine (T4) Triiodothyronine (T3) Parathyroid hormone (PTH ) Thyrocalcitonin

Assists in control of calcium levels, decreases reabsorption in bone

Thyroid hormone secretion is regulated by TSH from the anterior pituitary.


Thyroxine or Tetraiodothyronine
1 thyroid hormone contains 4 iodine atoms abbreviated as T4.

Triiodothyronine other thyroid hormone contains 3 iodine atoms - abbreviated as T3.

Thyroid Hormones are stored in combination with a special protein called thyroglobulin.

Main Function of the Thyroid Gland secretes thyroid hormones bind to intracellular receptors in cells regulate the rate of metabolism

Hypothyroidism lack of thyroid hormones

o Cretinism hypothyroidism in infants o Myxedema hypothyroidism in adults

Hyperthyroidism elevated rate of thyroid


hormone secretion o Graves' disease hyperthyroidism result of production of abnormal proteins by immune system that are similar in structure and function to TSH. - Exophthalmia bulging of the eyes

PATHOPHYSIOLOGY
normal regulatory controls of thyroid hormone secretion lost state of hypermetabolism w/sympathetic activity exists. elevated thyroid hormone levels stimulate heart HR and stroke volume CO and peripheral blood flow. adrenergic responsive at beta adreneceptor sites in heart HR or arrhythmias. thyroid hormone levels increase: Protein, carbohydrate, and lipid metabolism Vitamin metabolism tissue stores of the vitamins Peristaltic activity, leading to diarrhea Appetite (as metabolism increases)

Increased metabolism

weight loss.

Excessive sweating, flushing, heat intolerance occur.

Hair may become fine and soft; alopecia may occur. - metabolism of vit.
Nails may grow away from nail beds growth hormone CNS may react with agitation, nervousness and anxiety insomia. Eyelids elevated - exopthalmos and edema of the orbital structure= Itching pain, lacrimation, photophobia, and eventually corneal ulceration (eyelids may not close)

Menstrual irregularities - may occur in women In Graves diseased, thyroid- stimulating immunoglobulin (TSI) overrides normal regulatory mechanisms. Thyroid hypersecretion leads to pituitary suppression of TSH and hypothalamic suppression of Thyrotropin - Releasing Hormone (TRH). Iodine uptake = gland has an increased metabolic rate. When Graves disease is the caused, there are subcutaneous swelling on anterior part of the leg (pretibia myxedema) and erythematous skin , Palmar erythema .

Gland increases in size - response to thyroid hormone demand resulting from other condition (eg, pregnancy or iodine deficiency). Hypertrophy resolves when condition abates. Thyroid may return to normal / some of the thyroid cells may continue to secrete independently thyroid hormone oversecretion(toxic nodular goiter)
Thyroid storm (thyrotoxicosis) occurs when hyperthyroidism worsen to an extent in tachycardia, hypertension, heat tolerance become life threatening may happen spontaneously or result from insufficient treatment /may be induced by stress due to illness/ surgery/emotions.

Physiologic Responses to Endocrine System Dysfunction

A. Fatigue: tired, exhausted feeling resulting in


decreased physical and mental functioning.

B. Anorexia in hypo
C. Change in libido: increase or decrease in the instinctual energy or drive related to the desired for sexual D. Myxedema: condition resulting from advanced hypothyroidism or thyroxin deficiency

E. Exopthalmos

F. Chvosteks sign: facial muscle spasm

resulting from tapping the muscles or the branches of the facial nerve; seen in hypocalcemia. G. Integumentary changes
In hyposecretion

skin - cool, pale, yellowish, dry, coarse, scaly nails - brittle, thick hair - dry, coarse.
In hypersecretion disorders,

skin - warm, moist ,and smooth nails and hair - fine and soft

H. Cardiovacular Changes
hyposecretion- decreased activity or exercise tolerance with hypotension and an enlarged heart, bradycardia

In hypersecretion- changes may include chest pain, with tachycardia arryhymias.

I. Gastrointestinal Changes
Anorexia with weight loss or increased appetite, weight gain may present, depending on the disease.

Constipation and abdominal distention or diarrhea may also occur, depending on the disease.

Hyperthyroidism
gland enlargement (goiter)
- oversecretion of thyroid hormone ; thyroid

Causes - result from a number of diseases


1. Graves disease (toxic diffuse goiter): familial case that affects the thyroid:abnormal proteins by immune system that are similar in structure and function to TSH. 2. Thyroiditis- inflammation of thyroid affects the T4 and T3 secretion.

3. Toxic multinodular goiter: multiple thyroid results in thyroid hyperfunctioning.


4. Thyroid cancer: uncommon, can occur with large carcinomas

Clinical Manifestation of Hyperthyroidism Increased body metabolism Nervousness/ restlessness personality changes Short attention span : insomnia Tachycardia (> 100 bpm; bounding heart sounds) cardiac dysrhythmia, HPN Increased blood pressure Enlargement of the thyroid gland Skin warm, moist ,and smooth Hair fine, nails soft Weakness and fatigue Demineralization of bones Hypercalcemia Brisk reflexes Increased stools, diarrhea
Increased libido Decreased fertility Higher body temperature heat intolerance

Clinical Manifestation of Hypothyroidism Decreased body metabolism Lethargy and headaches Memory deficit Bradycardia (>60 bpm; weak heart sounds) Decreased blood pressure Lowered respiratory rate Skin, cool, dry and rough Hair coarse, nails brittle Weakness and fatigue Stiff joints Decreased appetite/weight gain Muscular stiffness Diabetics need (less insulin) Constipation

Decreased libido Decreased fertility Lower body temperature cold intolerance

DIAGNOSTIC EXAM
measurement of thyroid function T3 and T4 levels sensitive assay for TSH - an excellent screening test for thyrotoxicosis. physical examination fine-needle thyroid aspiration may be used (if there was a dominant nodule suspicious for malignancy). Radioiodine uptake (RAIU) is indicated in order to estimate the therapeutic dose in the treatment . Imaging modalities - nuclear scans - CT or MRI, are more expensive but ultrasound, provide no indication of function so offer no advantage.

Laboratory Value - Normal Adult Range


Increased Serum T3 =70 205 ng/dL Increased Serum T4 = 4-12 mcg/dL Increased Free T4 index = 0.8-2.4 ng/dL Increased resin uptake =24%-34% Increased Calcium = 4.5-5.5 mEq /dl Decreased Magnesium = 1.5-2.6mEq/L Decreased Potassium = 3.5-5.0mEq/L Decreased Bicarbonate = 22-30mEq/L

B. Treatment 1. Drug therapy- inhibit hormone synthesis / release, reduce the amount of thyroid hormone. a. Methimazole(Tapazole): started at 5 mg -15 mg bid up to 30 mg bid in pts who are very toxic, w/ maintenance doses 5 mg -10 mg. b. Propylthiouracil (Propyl-Thyracil):inhibit hormone synthesis;causes cytotoxic -hepatitis (unknown reason) SE: abnormal taste, pruritus, urticaria, fever, arthralgia; hepatotoxicity c. Propranolol (Inderal) Beta- adrenergic Blocker counteracts symptoms of inc. met. rate. tachycardia, tremors

2. Radioactive iodine Therapy radioactive isotopes given p.o to destroy thyroid gland and reduce thyroid activity. - use of RAI is limited to patients aged above 50 yrs because of the risk of atrial fibrillation.
3. Thyroidectomy -performed after thyroid function has returned to normal ( 4 6 wks); preferable to prepare the patient with antithyroid drugs preoperatively so that they are euthyroid, Excellent results have been obtained by using propranolol alone or in combination with potassium iodide to prepare patients for operation.

C. NURSING INTERVENTIONS
1 . Provide adequate rest 2 . Provide cool, quiet environment 3 . Provide high-calorie diet. evaluate nutritional status 4 . Weight client daily 5 . Provide emotional support 6 . Provide eye protection; monitor vision changes of eye. 7 . Elevate head of bed 8 . Administer antithyroid medications 9 . Administer nonsalicylate antipyretics, as prescribed, for fever. 10. Administer medications, as ordered, for cardiac dysrhythmias. 11. Be alert for complications.

D. NURSING INTERVENTIONS post Thyroidectomy


a. Semi-Fowlers position. b. Check dressing. c. Observe for respiratory distress. d. Be alert for signs of hemorrhage. e. Talking limited, note any hoarseness f. Observe for signs of tetany caused by reduction in the blood Ca. g. Calcium gluconate IV at bedside-needs Ca. h. Observe for thyroid storm. i. Gradually increase range of motion to neck

Thyrotoxicosis - clinical and biochemical manifestations of exposure to excessive quantities of thyroid hormones. Usually caused by Graves Disease. In 1956, Adams and Purves, using a bioassay for thyroid-stimulating hormone (TSH), reported finding a substance in the serum of patients with Graves' disease that behaved differently from TSH, which they named the long-acting thyroid stimulator, or LATS. In due time, this was identified as a gamma globulin or antibody, which attaches to the thyrotropin receptor on thyroid follicular cells. These thyroid-stimulating immunoglobulins TSIs - mimic the action of TSH, binding to and activating the thyrotropin receptor, producing not only excess secretion of thyroid hormones, but hypertrophy and hyperplasia of the thyroid follicle

Thyroid storm is precipitated by the following factors in individuals with thyrotoxicosis: Sepsis Surgery Anesthesia induction4 Radioactive iodine (RAI) therapy5 Drugs (anticholinergic and adrenergic drugs such as pseudoephedrine; salicylates; nonsteroidal anti-inflammatory drugs [NSAIDs]; chemotherapy6 ) Excessive thyroid hormone (TH) ingestion Withdrawal of or noncompliance with antithyroid medications Direct trauma to the thyroid gland Vigorous palpation of an enlarged thyroid

Distinctive signs and symptoms in acute situations of thyroid crisis 1. heart failure 2. hypothermia 3. cardiogenic shock 4. restlessness & agitation 5. delirium and coma

SIGNS
Fever Temperature consistently exceeds 38.5C. Patients may progress to hyperpyrexia. Temperature frequently exceeds 41C. Excessive sweating Cardiovascular signs Hypertension with wide pulse pressure, with shock Tachycardia disproportionate to fever Signs of high-output heart failure Cardiac arrhythmia (Supraventricular arrhythmias are more common, [eg, atrial flutter and fibrillation], but ventricular tachycardia may also occur.) Neurologic signs Agitation and confusion Hyperreflexia and transient pyramidal signs Tremors, seizures, Coma

Nursing Management a. Monitor diagnostic studies of serum levels of


T4, T3, TSH, TRH b. Pharmacotherapy Anti-thyroid drugs is adrenergic blockers radioactive iodine c.cardiogenic drugs d. Surgery once stabilized e. Monitoring Measures f. Spiritual Care

Complications Opthalmic pathology


due to edema and inflammation involving the extraocular muscles, as well as increased orbital fat and connective tissue. skin lesion or dermopathy. patches of thickened skin, most

commonly in the pretibial area, to an elephantiasic involvement of the entire lower leg and foot