Thyroid Disorders

Balkeej Kaur

M.Sc. (N)2nd year

AIMS,CON

Sri Muktsar Sahib

Thyroid Gland Second largest endocrine gland in body Small butterfly shaped gland located at

base of neck. Thyroid is controlled

by the hypothalmus

and pituitary

Functions Stimulates & maintains metabolic

processesProduces thyroid hormones T3-

triiodothyronine and T4-thyroxineThese hormones regulate metabolism & affect

the growth and function of other systems in the body

Parathyroid gland secretes PTH to raise serum calcium levels

Calcitonin Is another important hormone secreted by the thyroid gland. It is secreted in response to high plasma levels of calcium. It

reduces the plasma level of calcium by increasing its deposition in bone.

Iodine Is essential to the synthesis of the thyroid gland hormones. Is mainly used by the thyroid. Deficiency alters thyroid function. Iodide is ingested in the diet, absorbed & its ions are converted

to iodine molecules. Molecules react with tyrosine (an amino acid) to form the

thyroid hormones.

Iodine

Dietary Iodide is removed from the bloodstream by means of an active pump

The pump can concentrate iodide in the follicular sacs at 350x greater than the blood concentration

Oxidation of iodide by thyroid peroxidase converts iodide iodine

Peripheral de-iodination of T4 to T3 is regulated by many factors including health, nutritional status, and other hormones

Hormones: T3 & T4

T3 (Triiodothyronine) & T4 (TetraiodothyronineT4 is converted to T3 by peripheral organs

such as kidney, liver, and spleenT3 is 10x more active than T 4

Hormones: T4 to T3

Only 20% of total T3 is secreted by thyroid Majority is formed from catalysis of T4 by 5’-

iodthryonine deiodinase (highest activity in liver and kidney)

Hormones: T4 T4-thyroxine contains 4 iodine atoms It is a slow-acting pre-hormone T4 takes 4 days to peak in blood

Half-life 7 days Overall effects take 6 weeks T3 is the active and faster-acting hormone The immediate effects of T3 last 1-2 days

Half-life 1.5 days

Hormones- TSH TSH

TSH is a pituitary hormone Controlled by TRH-thyrotropin releasing hormone from

hypothalamusFunctions to stimulate thyroid hormone production

May enlarge thyroid (goiter) when under producing or over producing

Labs: High TSH indicates low thyroid hormone= hypo Low TSH indicates high thyroid hormone = hyper

Hormones-Calcitonin & PTH

Produced by thyroid to regulate serum calcium levels

Calcitonin stimulates movement of calcium into bone

Parathyroid hormone (PTH) opposite effect of calcitonin

Functions Metabolic stimulants of:

Neural and skeletal development Oxygen consumption at rest Stimulating bone turnover by increasing formation and

resorption Increasing number of catecholamine receptors in heart Increasing production of RBC metabolism of carbs, fats, and protein

Negative Feedback System

TRH

T3 & T4 Thyroid

TSH

The disruption of any of these mechanisms can cause abnormal levels of T3 and T4 leading to thyroid disease

Diseases Hypothyroidism-Under Activity Prevalence

Affects 5-17% of population Females> Males Higher in >60 years old

Types Hashimoto’s thyroiditis Postoperative hypothyroidism Postpartum hypothyroidism Iatrogenic hypothyroidism

Diseases Hyperthyroidism- Over activity Prevalence

Affect 5-17% of population Females> Males More common in younger persons

Types Thyroid storm Graves disease Toxic thyroid nodule Iatrogenic hyperthyroidism

Assessment and Diagnostic Findings Inspection: Identification of landmarks. Look for swelling or asymmetry. Palpation: Palpate the gland for size, shape,

consistency, symmetry, and the presence of tenderness.

Auscultate the enlarged gland to identify localized audible vibration of a bruit. This indicates increased blood flow necessitates referral to a physician.

Thyroid Function Tests Thyroid function tests, TSH and free thyroxine

(FT4), are elevated in hyperthyroidism and decreased in hypothyroidism.

Thyroid scanning. Biopsy. Ultrasonography.

Labs

Thyroid Function Test

Measurement Normal Range

Total T4 (TT4) Bound & Free T4 4.5-12.5mg/dL

Free T4 (FT4) Free T4 0.8-1.5 ng/dL

Total T3 (TT3) Bound & Free T3 80-220ng/dL

T3 Resin Uptake Binding capacity of TBG

22-34%

TSH Thyroid stimulating hormone

0.25-6.7U/mL

Total(T3) Bound & Free T3 80-220ng/dL

Labs

HyperthyroidismFT4 TSH

HypothyroidismFT4 TSH

Hyperthyroidism-Types Graves disease

Most common form (70-80%)-autoimmune disorder. Autoimmune disorder in which thyroid-stimulating antibodies are

circulating in blood. These bind to thyroid cells and activate cells in the same manner as TSH. E.g TSH does decrease slightly in the first trimester. This corresponds with increased beta HCG levels. The changes in TSH levels may be explained by the fact that beta HCG is not only structurally quite similar to TSH, but it also has thyrotropic activity. It should also be noted that the thyroid gland itself may increase slightly in size during pregnancy. 7 times greater in women Peak onset is 20-30’s(in younger)

Hyperthyroidism-Types

Can be caused by:Toxic multinodular goiterSolitary toxic noduleThyroiditisDrug-induced thryotoxicosisPituitary or trophoblastic tumors

Hyperthyroidism-Symptoms

Weight loss Tachycardia Bulging eyes Nervous/Anxious Insomnia Intolerant of heat Goiter

Patients exhibit a characteristic group of signs and symptoms (thyrotoxicosis). The presenting symptom is often nervousness.

Emotionally hyperexcitable, irritable, and apprehensive; cannot sit quietly; palpitations; tachycardia at rest and on exertion.

Poor heat tolerance and unusual perspiration. The skin is flushed continuously. Skin is dry and diffuse pruritus. Exophthalmos

Increased appetite and dietary intake, weight loss, abnormal muscular fatigability and weakness, amenorrhea, and changes in bowel function.

Elevation of systolic blood pressure Atrial fibrillation. Osteoporosis and fracture.

Assessment and Diagnostic Findings Enlarged thyroid. It is soft and may pulsate; with a bruit. Diagnosis is made on the basis of the

symptoms and ↑ in serum T4 and an increased 123I or 125I uptake by the thyroid in excess of 50%.

Nursing InterventionsImproving Nutritional Status

Up to six well-balanced meals of small size are offered daily.

Foods and fluids are selected to replace fluid lost through diarrhea and diaphoresis.

To reduce diarrhea, highly seasoned foods and stimulants such as coffee, tea, cola, and alcohol are discouraged.

High-calorie, high-protein foods are encouraged.

Monitor weight, dietary intake, and nutritional status.

Enhancing Coping Measures Reassure the patient that the emotional reactions will

be controlled with effective treatment. Similar reassurance needs to be made to family and

friends. Minimise stressful experiences for the patient. Keep the patient’s environment quiet and noiseless. The nurse encourages relaxing activities if they do

not overstimulate the patient. Educate patient about medications to be taken in

anticipation for surgical intervention.

Improving Self-esteem The patient with hyperthyroidism may lose self-

esteem due to changes in appearance, appetite, and weight, and due to his inability to cope well with family and the illness.

Cover or remove mirrors. Remind family members and personnel to avoid

bringing these changes to the patient’s attention. Explain the temporary nature of these changes. Provide eye care as appropriate. Instruct the patient

on how to use eye preparations.

Maintaining Normal Body Temperature The patient with hyperthyroidism frequently

finds a normal room temperature too warm because of an exaggerated metabolic rate and increased heat production.

The nurse maintains the environment at a cool, comfortable temperature and changes bedding and clothing as needed. Cool baths and cool or cold fluids may provide relief.

Teaching Patients Self-Care Provide instruction and written plan about the

medications. Provide verbal and written instruction about the

actions and possible side effects of the medications.

Identify adverse effects that should be reported. Provide information to the patient about what to

expect if total or subtotal thyroidectomy is anticipated.

Goiter A diet deficient in

iodine Increase in thyroid

stimulating hormone (TSH) in response to a defect in normal hormone synthesis within the thyroid gland.

Thyroid Storm Life threatening syndrome Decompensated hyperthyroidism Symptoms

Hyperthyroid symptoms with agitation, confusion, delirium, psychosis

Gastrointestinal: Nausea/Vomiting, Abdominal pain

Tachycardia associated with CHF

Thyroid Storm Treatment Antithyroids

PTU 200-400mg po/NG q4-8h Methimazole 60-120mg/d PO/NG divided q6-8h

Potassium Iodide 2-5 drops PO/NG q6h Lugol Solution-Strong Iodine10 drops po TID Glucorticoids: block conversion of T4 to T3

Hydrocortisone succinate 100-200mg IV q6-8 Dexamethasone 2mg Po/IV q6-8h

BB Esmolol: 500mcg/kg/min Propranolol 20-80mg/dose PO/NG q4-6h

Hyperthyroidism-Treatment

Drug TherapyBeta blocker

Atenolol 50mg-100mg po daily Propranolol 20-40mg po TID

Antithyroids Methimazole 15-30mg po daily Propylthiouracil (PTU) 300mg TID

Hyperthyroid-Treatment

Procedural TherapyRadionuclide albation of thyroid glandTotal thyroidectomy

Methimazole

Reduces T3 & T4 production. Dosage

15-30mg PO daily

Methimazole Adverse Effects

Skin rashLoss of tasteGI upsetDrowsinessDecreased Platelets

Propylthiouracil -PTU Thio-urea derivative Preferred agent in pregnant women severe thyrotoxicosis Dosage

Adults: 300-450mg/day divided q8h Severe cases: 600-1200mg/day Maintenance dose 100-150mg/day divided q 8-12

hours

PTU

Adverse reactionsRash Itchinghives(urticaria-redness,swelling,itching)Agranulocytosis (when bone marrow is unable to

produce mature white cells that neutrophills)vasculitis(inflammation pf blood vessels)

Carbimazole Dosage

15-40mg PO daily until normal function Reduce to 5-15mg po daily maintenance dose

Adverse EffectsBone marrow suppressionNeutropeniaAgranulocytosis

Sodium Iodide I-131 (Iodotope) Quickly absorbed and taken up by thyroid No other tissue capable of retaining radioactive

iodine therefore low adverse effects Dose

Adult 75-150mCi/g of thyroid x estimated thyroid gland size

24hour radioiodine uptakeDiscontinue antithyroid therapy 3-4days before

Hypothyroidism Types:

Primary hypothyroidism Most common cause Failure of thyroid gland Occurs primarily in women aged 30-50 years old

Chronic autoimmune thyroiditis or Hashimotos disease is the most common primary hypothyroidism AND hypothyroidism overall

Secondary HypothyroidismTertiary HypothyroidismOther causes

Hypothyroidism-Symptoms

Early symptoms are nonspecific. Extreme fatigue. Hair loss, brittle nails, dry skin, and numbness and tingling of

the fingers may occur. Voice may become husky [hoarse and dry]. Menstrual disturbances & loss of libido. In severe hypothyroidism:

Hypothermia & bradycardia. Weight gain even without ↑ in food intake. Thick skin, thin hair that falls out. Expressionless and masklike face.

Hypothyroidism-Symptoms

Fatigue Depression Bradycardia Constipation Intolerant to cold

Subdued emotional responses, and dull mental processes. Slow speech and enlarged tongue, hands, and feet. Constipation. Sleep apnea, pleural effusion, and pericardial effusion. ↑cholesterol level, atherosclerosis, coronary artery disease,

and poor left ventricular function. Intraoperative hypotension and postoperative heart failure may

occur to undiagnosed patients. Myxedema coma describes the most extreme, severe stage of

hypothyroidism, in which the patient is hypothermic and unconscious.

The patient would develop respiratory complications culminating in coma.

Cardiovascular collapse and shock. Mortality rate is high.

Hashimoto’s Disease

Autoimmune disorder in which antibodies are directed against a thyroid sites to : Inhibit thyroid peroxidase(T4 –T3) Inhibit effects of TSHStimulate thyroid growth

Lymphocytes are attracted to attacking thyroid gland leading to inflammation and swelling

Hypothyroidism-Primary Drug induced

PTU & methimazole Iatrogenic

Surgical removal of the thyroid gland and radiation treatment

Primary Hypothyroidism

Thyroid gland failureDecrease T3 & T4 Increase TRH inspite of negative feedback Increased TSH due to decreased TRH

Secondary Hypothyroid

Pituitary failure Insufficient TSH release as a result of:

Pituitary tumors Surgery Pituitary radiation Pituitary necrosis Autoimmune mechanisms

Tertiary Hypothyroidism

Hypothalamic Failure- very rare Insufficient TRH release as a result of:

Trauma IrradiationTumors

Hypothyroidism-Treatment Drug Therapy

Levothyroxine Sodium-DOC synthetic T4 Adults 1-1.5mcg/kg/day orally initially, adjust as

needed. Average dose 1.6-1.8mcg/kg/day Pediatrics 1-1.5mgc/kg/day. Average 4 mcg/kg/day

Hypothyroidism-Treatment

Adverse EffectsMIOsteopeniaHA

ContraindicatedAcute MITreatment of obesityUncontrolled HTN

Monitoring

Obtain baseline FT4, TSH, LFT, CBCs before initiation of therapy

Repeat FT4 and TSH after 4-6 weeks on therapy and 4-6 weeks after adjustments

Once euthyroid state obtain thyroid function test after 3-6 months

Nursing Implications for Thyroid tests Determine whether the patient has taken drugs or agents that contain

iodine. These include: Contrast agents (radiopaque, dye-like substances that may contain

iodine) and medications used to treat thyroid disorders. Topical antiseptics, multivitamin preparations, cough syrups; an

antiarrhythmic agent. Estrogens, salicylates, amphetamines (drugs that produce increased

wakefulness and focus ),chemotherapeutic agents, antibiotics, and corticosteroids.

Ask the patient about the use of these drugs and note their use on the laboratory requisition.

Nursing ManagementModifying Activity

The patient experiences decreased energy and lethargy. As a result, the risk for complications from immobility increases.

The patient has decreased ability to exercise and participate in activities due to changes in cardiovascular and pulmonary status.

The nurse’s role is to assist with care and hygiene while encouraging the patient to participate in activities as tolerated to prevent the complications of immobility.

Modifying Activity The patient experiences decreased energy and

lethargy. As a result, the risk for complications from immobility increases.

The patient has decreased ability to exercise and participate in activities due to changes in cardiovascular and pulmonary status.

The nurse’s role is to assist with care and hygiene while encouraging the patient to participate in activities as tolerated to prevent the complications of immobility.

Monitoring Physical Status Close monitoring of the vital signs and cognitive level to

detect the following: Deterioration of physical and mental status Signs and symptoms indicating that treatment has resulted

in the metabolic rate exceeding the ability of the cardiovascular and pulmonary systems to respond

Continued limitations or complications of myxedema

Promoting Physical Comfort Extra clothing and blankets are provided. Use of heating pads and electric blankets is

avoided. This is because the patient could be burned by these items without being aware of it because of delayed responses and decreased mental status.

Providing Emotional Support

The patient may experience severe emotional reactions. The nonspecific, early symptoms may produce negative reactions by family members and friends, who may have labeled the patient mentally unstable, uncooperative, or unwilling to participate in self-care activities.

The nurse informs the patient and family that the symptoms and inability to recognize them are common but treatment is successful and symptoms are reversible. The patient and family may require assistance and counseling to deal with the emotional concerns and reactions that result

Teaching Patients Self-Care The patient and family require information and

instruction that will enable them to monitor the patient’s condition and response to therapy.

The nurse instructs the patient and a family member about medications.

The nurse provides written instructions and guidelines for the patient and family.

Dietary instruction is provided to promote weight loss once medication has been initiated.

Before discharge, arrangements are made to ensure that the patient returns to an environment that will promote adherence to the prescribed treatment plan. The nurse: Assists in devising a schedule or record to ensure accurate

and complete administration of medications. Reinforces the importance of continued thyroid hormone

replacement and periodic follow-up testing and instructs the patient and family members about the signs of overmedication and undermedication.

May refer the patient for home care. Documents and reports to the patient’s primary health care

provider, subtle signs and symptoms that may indicate either inadequate or excessive thyroxine hormone.

THYROID DISORDERS IN PREGNANCY: TSH does decrease slightly in the first trimester. This

corresponds with increased beta HCG levels. The

changes in TSH levels may be explained by the fact that beta HCG is not only structurally quite

similar to TSH, but it also has thyrotropic activity. It should also be noted that the thyroid gland

itself may increase slightly in size during pregnancy.

Hypothyroidism

Significant hypothyroidism is unusual in pregnancy as untreated hypothyroid patients rarely conceive and carry a pregnancy. The few patients who do become pregnant and remain untreated have an increased risk for miscarriage, fetal loss, preeclampsia and low birth weight.Treated hypothyroidism generally does not confer an increased risk for pregnancy. check thyroid function tests once per trimester. If this frequency of testing shows that a patient requires an increase in thyroxine replacement, we then consider checking the patient’s thyroid function more frequently,there are individuals who will require dose increases up to as high as 200 micrograms of levothyroxine per day. Patients should also be instructed not to take their thyroid supplement at the same time as their prenatal vitamins since iron can decrease its absorption.

Hyperthyroidism

The signs and symptoms of hyperthyroidism in pregnancy are the same as they are for the nonpregnant individual but the clinical diagnosis is made more difficult by normal changes in pregnancy which mimic hyperthyroidism. These include increased heart rate, heat intolerance, warm skin, and systolic flow murmurs. Findings more suggestive of hyperthyroidism, however, are tremor, weight loss, hyper defecation, thyroid bruit, and eye findings consistent with Graves’ Disease.

Patients with good control are likely to have a good

pregnancy outcome. In contrast, patients with untreated hyperthyroidism have decreased fertility and an increased risk of miscarriage, intrauterine growth retardation (IUGR), premature labor,and perinatal mortality. Thyroid storm can also occur in patients with poorly controlled thyrotoxicosis especially at labor and delivery. Thus the appropriate treatment of hyperthyroidism in pregnancy is very important for both maternal and fetal health.

To minimize fetal exposure to PTU and it’s associated risk of fetal hypothyroidism and

fetal goiter, treatment favors use of lower doses of medication which allow the patient to be mildly hyperthyroid. Despite improvement antepartum, Graves’ Disease often relapses after delivery and, if needed, both beta blockers and PTU can be used in nursing mothers.

Postpartum Thyroiditis

It frequently begins approximately 4 months postpartum and usually starts with a period of acute inflammation that manifests itself as a non-tender goiter associated with hyperthyroidism. Over the course of time, the hyperthyroidism is often followed by many months of hypothyroidism. This hypothyroidism usually resolves within a year following delivery. Antithyroid antibodies are positive in 85% of the cases. At times it may become important to distinguish postpartum thyroiditis from a postpartum exacerbation of Graves’ disease. A radioactive iodine uptake scan can easily make the distinction as there will be little uptake in postpartum thyroiditis.

Postpartum thyroiditis may masquerade as postpartum depression so it is essential to consider it in any woman presenting with depressive symptoms in the year after delivery.

Hyperemesis Gravidarum

In the majority of cases, it is felt that the hyperthyroidism is caused by the hyperemesis itself. Beta HCG, the placental hormone which is believed to be partially responsible for the nausea and vomiting of hyperemesis, is only one amino acid different from Thyroid Stimulating Hormone (TSH). It is therefore believed that in some cases of hyperemesis, the high levels of Beta HCG may stimulate the thyroid. Hyperthyroidism associated with hyperemesis usually resolves at the end of the first trimester when the beta HCG levels start to decline and the symptoms of hyperemesis tend to resolve.

Thyroid Nodules

new thyroid nodules always need to be aggressively investigated in the gravid woman. There appears to be a very high incidence of malignancy in new thyroid nodules appearing during pregnancy. Therefore, fine needle aspirations should never be delayed because a woman is pregnant. Despite the increased incidence of malignancy in thyroid nodules identified in pregnancy, pregnancy does not have an adverse effect on the course of the disease. Likewise, women with a history of thyroid carcinoma who become pregnant do not have a worsened prognosis overall.

Thyroid Investigations

The fetal thyroid avidly binds iodine starting at 10-12 weeks gestation so that administering radioactive iodine to pregnant women results in doses to the fetus which are much greater than the exposure to the mother. It should be completely avoided in pregnancy. Nursing mothers who have radioactive iodine scans should be counseled to pump and discard their milk for 48-72 hours before resuming breastfeeding. If needed, thyroid ultrasounds and fine needle aspirations may be done safely in the pregnant woman.