hope olson. the incidence of thyroid disease is increasing, predominately among women. up to 5% of...

THYROID DISORDERS: A CLOSER LOOK AT HYPER- & HYPOTHYROIDISM

Hope Olson

FAST FACTS

The incidence of thyroid disease is increasing, predominately among women.

Up to 5% of the U.S. female population has altered thyroid function.

An estimated 15% of the general population have physical thyroid abnormalities, and 30% of undetected cases are affected by the disease daily.

Pinto, Andres. Glick, Michael. (2002). Management of patients with thyroid disease. Journal of American Dental Association. 133(7), 849-858.

OBJECTIVES

Describe the thyroid gland and its functions

Cover two types of thyroid disorders: hyperthyroidism and hypothyroidism

Become familiar with common medications and their resulting nutritional implications

Effectively use the NCP to treat thyroid disorders

Examine ethical issues and standards of practice

Summary/Questions

THE THYROID

Q: What is it? A: A butterfly-shaped, bilobular gland that lies

over the top of the trachea. The lobes are connected by a 2-cm wide isthmus (Pinto, 2002).

Functions of Thyroid and its hormones: Controlling metabolic rate (Nelms, 2007).

Influences growth and maturation of tissue, as well as the turnover of cells and nutrients (Pinto, 2002).

Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole.Pinto, Andres. Glick, Michael. (2002). Management of patients with thyroid disease. Journal of American Dental Association.

133(7), 849-858.

HORMONES ASSOCIATED WITH THE THYROID

Thyroglobulin: building block for thyroid hormones Triiodothyronine (T3) and Thyroxine (T4)(Pinto, 2002).

In addition to thyroglobulin, Iodine is needed for T3 and T4 synthesis (Pinto,

2002).

T3 is the main metabolic effector T3 found more prominently in the body than T4 (Pinto, 2002)

T3 at the molecular level: activates genetic material for gene expression assists in translation of proteins coding for multiple hormonal and

constituent tissues such as growth hormone activates myosin, and the calcium pump complex of the sarcoplasmic

reticulum (Pinto, 2002).

Thyroid stimulating hormone (TSH): produced by pituitary gland, stimulates hormone production by the thyroid. (Nelms, 2007).

Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole.Pinto, Andres. Glick, Michael. (2002). Management of patients with thyroid disease. Journal of American Dental Association. 133(7),

849-858.

HYPERTHYROIDISM: AN OVERVIEW

The clinical state resulting from excessive secretion of thyroid hormones. The most common cause of hyperthyroidism is Grave’s disease.

There is an abnormal presence of thyroid-stimulating immunoglobulin (an antibody that mistakenly targets TSH receptors on thyroid cells).

TSI stimulates secretion and growth of thyroid similar to TSH, but it isn’t subject to the negative-feedback inhibition by the thyroid like TSH would be. This results in excess T4 production, and higher plasma T3 concentrations than normal.

Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole.

RISK FACTORS FOR HYPERTHYROIDISM

Grave’s Disease – overproduction of thyroid hormone by the entire thyroid gland due to antibodies in the blood causing growth and stimulation of the thyroid (Nelms, 2007)

Grave’s is hereditary, and it occurs more often in young women It’s unknown why specific individuals contract Grave’s Grave’s is the most common cause of Hyperthyroidism (Hyperthyroidism, 2005)

Be aware that other risks exist! multinodular goiter, thyroiditis, surgical removal of

part or all of the thyroid gland, radiation treatment (Hyperthyroidism, 2005).

Hyperthyroidism: What is hyperthyroidism? 2005. Retrieved September 20, 2008, from American Thyroid Association Web Site: http://www.thyroid.org

Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole

http://www.thyroid.org/

SYMPTOMS AND SIGNS

The hypermetabolic effects of hyperthyroidism affect every organ in the body.

Key symptoms include: Heart palpitation, nervousness, sweating,

hyperdefication, heat intolerance, oligomenorrhea General signs include:

Weight loss despite increased appetite, drooping eyelids and stare, atrial fibrillation, tremor, and muscle weakness(Nelms, 2007).

Increased cardiac output, hypertension, & emotional instability are additional signs (Pinto, 2002).

Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole.Pinto, Andres. Glick, Michael. (2002). Management of patients with thyroid disease. Journal of American Dental Association. 133(7), 849-858.

DIAGNOSIS OF HYPERTHYROIDISM

The physician examining the thyroid patient will notice an enlarged thyroid gland and a rapid pulse.

If the patient has Grave’s disease, they will have eye abnormalities.

Lab tests: T3/T4 & TSH tests High levels of the thyroid hormones, and low levels of TSH is

typical of this thyroid disorder

Digital scan of thyroid to find out if the entire gland is overactive



HYPERTHYROIDISM

•Testing for elevated T3 levels is essential to determining the patient’s thyroid dysfunction

•In some individuals with a low TSH, only the T3 is elevated, and T4 is normal.

•TSH is in low concentrations

•T4 (in the form of T3) is in high concentrations

Thyroid Function Tests. 2005. Retrieved September 20, 2008 from American Thyroid Association Website http://www.thyroid.org.


LAB TESTS

Background: because >90% of T4 & T3 in the blood are bound to serum proteins, it makes sense to test only the active, free thyroid hormones (FT4, and FT3).

When hyperthyroidism is suspected, the combination of a FT4 estimate and a total- or free- T3 estimate provides the most complete assessment of severity. The goal is to identify “T3 toxicosis” or a selective increase of the

serum T3 concentration. Too much T3 leads to the signs and symptoms of the disease.

Kaplan, M. (1999). Clinical Perspectives in the Diagnosis of Thyroid Disease. Clinical Chemistry, 45, 1377-1383.

TREATMENT AND NUTRITIONAL IMPLICATIONS

Thyroidectomy: possible hypothyroidism without synthetic T4. Hypothyroidism would lead to slower metabolism of nutrients.

Antithyroid drugs: May be taken with or without food; yet consistency is key Methimazole (Tapazole,MMI) & Propylthiouracil (PTU) (Nelms,2007)

These drugs can cause loss of taste (ageusia) Aplastic Anemia (AA) can be induced by antithyroid drugs, with

concomitant agranulocytosis. To date, there are 34 reported cases of AA, and 2 deaths due to this

reaction to antithyroid drugs. However, this is not the norm. Cease exposure to antithyroid drugs, and supplement with

Cobalamin(B-12) and Folic Acid (B-9)

Thomas, D., Moisidis, A. et al. 2008. Antithyroid Drug-Induced Aplastic Anemia. Journal of the American Thyroid Association, 15, 317-320.Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole.

TREATMENT AND NUTRITIONAL IMPLICATIONS CONTINUED… Importance of B-12 & B-5 after adverse reaction to antithyroid

drug: B-12: Helps in the formation & regeneration of red blood cells, thus helping

prevent anemia B-9: essential to the formation of red blood cells by its action on the bone

marrow (Moisidis, et al., 2008)

Radioactive Iodine Treatment Because thyroid cells need iodine to make hormones, they

will uptake any form of iodine, radioactive or not. Administered by mouth, radioiodine quickly absorbed by thyroid cells,

and the cells are killed slowly over several weeks or months. Remaining radioiodine is excreted, or decayed to nonradioactive

form. No complications apparent from this treatment means, although

patient may become Hypothyroid.

Thomas, D., Moisidis, A. et al. 2008. Antithyroid Drug-Induced Aplastic Anemia. Journal of the American Thyroid Association, 15, 317-320.



NUTRITION CARE PROCESS FOR HYPERTHYROIDISM

Assessment: gather anthropometrics, but also ask your patient if they are experiencing any of the following: Nervousness, irritability, increased perspiration,

racing heart, hand tremors, thin skin, fine brittle hair, and muscular weakness in upper arms and thighs.

Unwarranted weight loss, and increased appetite will be key side effects to note, so you can help the patient maintain/improve their nutritional status.

NCP CONTINUED…

Diagnosis: Lab tests will include assessment of FT4 and FT3, as well as monitoring TSH levels.

Since the metabolism will be higher than usual, adequate Kcal will need to be assessed to avoid malnourishment.

NCP CONTINUED…

Implementation: To treat Hyperthyroidism, antithyroid drugs can be prescribed, the patient can have Radioactive Iodine treatment, surgery, and/or beta-blockers to slow heart rate. A patient is at risk of developing Hypothyroidism if

over-treated for Hyperthryoidism by any of the means listed above. Then the nutritional risks for Hypothyroidism would cause concern.



NCP CONTINUED…

Monitor: Make sure the patient has no adverse medication reactions, and that their taste has not been impaired by the medication. Supplement with B-12 & B-5 while the patient

recovers from rare adverse reaction so bone marrow, RBC and WBC can be restored quickly.

Monitor Kcal, so when medicine takes effect, weight can stabilize.

Check appetite (lack of possibly due to aguesia) Monitor for continuing weight loss, or weight gain

HYPOTHYROIDISM: AN OVERVIEW

The clinical state resulting from decreased production and secretion of thyroid hormones (Nelms, 2007).

An underactive thyroid inhibits normal function of the body (Hypothyroidism, 2005).

Hypothyroidism is the most common pathologic hormone deficiency (Hypothyroidism, 2005).

Hypothyroidism: What is hypothyroidism? 2005. Retrieved September 20, 2008, from American Thyroid Association Web Site: http://www.thyroid.org

Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole.


RISK FACTORS FOR HYPOTHYROIDISM In the U.S & other areas where iodine is sufficient in

the foods we eat, autoimmune thyroid disease and previous treatment for hyperthyroidism are the most common causes (Nelms, 2007).

Autoimmune disease of the thyroid is referred to as Hashimoto’s Thyroiditis.

The immune system can mistake thyroid gland cells and their enzymes as threatening foreign material.

Once the thyroid gland cells are attacked, stores of the cells and their enzymes are depleted, rendering the body in a state of inadequate thyroid hormone production. (Hypothyroidism, 2005).

A severe iron deficiency will also induce hypothyroidism (Pinto, 2002).


Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/ColePinto, Andres. Glick, Michael. (2002). Management of patients with thyroid disease. Journal of American Dental Association. 133(7), 849-858.


SYMPTOMS SIGNS

Abdominal distension

Easily fatigued Intolerance of cold Reduced basal

metabolic rate (BMR) Slow mental

responsiveness Loss of hairNelms, M., & Sucher, K. (2007). Diseases of the Endocrine

System. Belmont: Thomson Brooks/Cole

Myxedema Overweight Depression Bradycardia Slow reflexes &

movement Periorbital puffiness Goiter

DIAGNOSIS OF HYPOTHYROIDISM

There are no characteristic symptoms that all patients have, and a lot of the signs and symptoms associated with the disease are common in other diseases.

Medical/Family History, and a physical exam will help determine diagnosis

Blood Tests: TSH & FT4 tests are necessary to determine just how high TSH levels are, and how few T4 is left to enter cells to become T3.



HYPOTHYROIDISM

A high TSH level indicates that the thyroid gland is failing because of a problem directly affecting the thyroid.

With this disease, most T4 is attached to thyroxine-binding globulin, making T4unable to get into cells to make the much needed T3.

This is why so much TSH is secreted by the pituitary.

Thyroid Function Tests. 2005. Retrieved September 20, 2008, from American Thyroid Association Web Site: http://www.thyroid.org


LAB TESTS

Besides elevated TSH and decreased FT4, other abnormal lab values are associated with Hypothyroidism

Increased LDL, serum cholesterol, creatine, aspartate aminotransferase, serum lactate dehydrogenase, and increased risk for pernicious anemia.

Gastric antiparietal antibodies have been found in some people, which explains achlorhydria in various hypothyroid patients.


LAB TESTS CONTINUED…

Serum lactate dehydrogenase (LDH) is a blood test used to check for tissue damage. The enzyme LDH is in many body tissues, especially the heart, liver, kidney, skeletal muscle, brain, blood cells, and lungs.

LDH is used by the body to convert lactate to glucose in the liver.

Avg is 105-333 IU/L; higher than normal levels code for potential heart attack, low blood pressure, hemolytic anemia, and muscular dystrophy/weakness.

In hypothyroidism, high levels signify the body is working too hard (lactate is a product of this) so there is high amounts of LDH to convert lactate back to energy the cells can use. Often a patient experiences fatigue and slow reflexes. (Nelms, 2007).

Levin, M. (2007). LDH. Retrieved September 16, 2008, from MedlinePlus Medical Encyclopedia Website: www.medlineplus.gov. Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole

http://www.medlineplus.gov/

LAB TESTS CONTINUED…

Gastric antiparietal antibodies: Parietal cells secrete HCl which is needed for the stomach to properly break down food. If antiparietal anitbodies are present, the formation of parietal cells will be inhibited.

Achlorhydria: absence of gastric acid secretion

Nutritional Implication: If food is not broken down, it may sit in the stomach and cause discomfort. Lack of stomach acid to hydrolyze nutrients will lead to malabsorption and nutrient deficiencies.

TREATMENT AND NUTRITIONAL IMPLICATIONS

In general, levothyroxine sodium, or L-thyroxine is the first drug of choice: (Lovothroid, Levoxyl, Synthroid are brands) Implemented at .25mg/day, and is adjusted according to patient’s

response at monthly intervals. The appropriate initiating dose should be 1.6ug/kg

Synthetic T3 hormone replacement can be used, and a combination of synthetic T3 & T4 is used if severe deficiency of both hormones is present. T3 is not preferred, especially with the elderly population, simply

because it’s not as safe if the patient has cardiac complications. Common for patients to have high LDL/ total cholesterol, and

overweight due to slowed metabolic processes.Pinto, Andres. Glick, Michael. (2002). Management of patients with thyroid disease. Journal of American Dental Association. 133(7), 849-858.

TREATMENT AND NUTRITIONAL IMPLICATIONS CONTINUED…

USDA Human Nutrition Research Center on Aging at Tufts University compared the rate of bone mineral loss in thyroxine-treated women with low TSH levels to women without known thyroid disease.

Conclusion over the 2-yr trial illustrated thyroxine-treated women with low TSH lose bone mineral from the spine more rapidly than do women without known thyroid disease.

These patients therefore, are at increased risk for osteoporosis, and it is the dietitian’s role to make sure they are getting adequate calcium, as well as a calcium supplement.

Stall, G.M., Harris,S. Sokoll, L.J., Dawson-Hughes, B. (1990). Accelerated bone loss in hypothyroid patients overtreated with L-thyroxine. Ann Intern Med., 113(4), 265-269.


Healthy weight maintenance is an important goal for hypothyroid patients as evidenced by a meta-analysis of 6 previously published works, one of which works is shown below: Astrup A et al (1996): 56 females (28 wt stable/post-obese,

and 28 never obese) with similar average %body fat, %FFM, and age range 35-41 were examined for FT3 (our main metabolic effector).

There was a statistically significant (P<0.01) lower concentration of FT3 in the post-obese compared to the control individuals

T3 is a thermogenic hormone that contributes to the lower RMR of the post-obese subjects.

RMR was 8% lower in post-obese than in control subjects (p<0.02)

Astrup A., Buemann B., et al. (1996). Low resting metabolic rate in subjects predisposed to obesity. Retrieved September 14, 2008, from ADA evidence library Website: http://www.adaevidencelibrary.com/evidence.cfm?evidence_summary_id=88.

http://www.adaevidencelibrary.com/evidence.cfm?evidence_summary_id=88


Although a fiber-rich diet may aid in management of body weight, be sure to note the adverse effects on levothyroxine bioavailability.

In this study, dietary fiber supplements were withheld from patients requiring disproportionately high doses of T4, in whom diet history revealed ingestion of fiber supplements.

Liel, Y., Harman-Boehm, I., Shany, S. (1996). Evidence for a clinically important adverse effect on fiber-enriched diet on the bioavailability of levothyroxine in adult hypothyroid patients. Journal of Clinical Endocrinology & Metabolism, 81, 857-859.


The dose of T4 was maintained, and serum TSH was assessed before and after supplement removal. Decreased serum TSH was noted, or the increased dose

of T4 was reduced because of dietary fiber reduction. There is absorption of T4 by wheat bran. Results show a decrease in T4 bioavailability by dietary

fiber . Increased intake of dietary fiber may account for larger

than expected doses of T4 in some hypothyroid patients.Liel, Y., Harman-Boehm, I., Shany, S. (1996). Evidence for a clinically important adverse effect on fiber-enriched diet on the

bioavailability of levothyroxine in adult hypothyroid patients. Journal of Clinical Endocrinology & Metabolism, 81, 857-859.

NUTRITION CARE PROCESS FOR HYPOTHYROIDISM

ASSESSMENT DIAGNOSIS

Gather anthropometrics, but also ask your patient about being intolerant to cold, if they have gained more weight than usual, if they notice they are easily fatigued in their ADL’s, if their memory is poor, or if they are experiencing hair loss, or any edema (myxedema).

Look at medical and family history (genetic): see if the patient has had radiation to the neck for cancer treatment, if they were previously hyperthyroid, or if family members have had it.

Blood tests will show high TSH and low amounts of FT4

Blood tests may also show high levels of total cholesterol, LDL, LDH, etc.

NCP CONTINUED…

IMPLEMENTATION MONITOR

To prevent obesity secondary to hypothyroidism, monitor nutritional status and correct over-nutrition. Give the patient education about maintaining a healthy weight.

To prevent osteoporosis, recommend calcium supplementation, and adequate dairy intake. Calcium can also control hypertension and weight.

Check consistently to see how the patient is doing, since medication will be adjusted monthly until a balance is reached.

Be sure to continue education about the latest information for the hypothyroid drugs and their nutrient interactions

Monitor weight and lipid profile to asses risks of cardiovascular disease

ETHICS / STANDARDS OF PRACTICE

The Research Unit of the Royal College of Physicians in London, the Endocrinology and Diabetes Committee of the college, and the Society of Endocrinology set up a working group to produce a consensus statement for good practice with associated adult audit measures which could be used to ensure purchasers of health care are obtaining an acceptable standard of care for thyroid patients.

This statement about the development of ethical standards can be found at http://bmj.com/cgi/content/full/313/7056/539 or at www.bmj.com under “Consensus statement for good practice and audit measures in the management of hypothyroidism and hyperthyroidism.”

http://bmj.com/cgi/content/full/313/7056/539

http://www.bmj.com/

SUMMARY / QUESTIONS Thyroid hormones T4 and T3 play a critical role in

metabolism of nutrients THS is responsible for signaling the release of thyroid

hormones from the thyroid Hyperthyroidism results from low levels of TSH and high

levels of FT4, most common cause is Grave’s disease Key signs include palpitations, unwanted weight loss, increased

appetite, nervousness, mood alterations, rapid pulse. Hypothyroidism results from high levels of TSH and low

levels of FT4, most common cause is autoimmune disease referred to as Hashimoto’s Thyroiditis. Key signs include fatigue, myxedema, weight gain, abdominal

distension, depression.

QUESTIONS?

BIBLIOGRAPHY Astrup A., Buemann B., et al. (1996). Low resting metabolic rate in subjects predisposed to obesity. Retrieved

September 14, 2008, from ADA evidence library Website: http://www.adaevidencelibrary.com/evidence.cfm?evidence_summary_id=88.



Kaplan, M. (1999). Clinical Perspectives in the Diagnosis of Thyroid Disease. Clinical Chemistry, 45, 1377-1383.

Levin, M. (2007). LDH. Retrieved September 16, 2008, from MedlinePlus Medical Encyclopedia Website: www.medlineplus.gov.

Liel, Y., Harman-Boehm, I., Shany, S. (1996). Evidence for a clinically important adverse effect on fiber-enriched diet on the bioavailability of levothyroxine in adult hypothyroid patients. Journal of Clinical Endocrinology &

Metabolism, 81, 857-859.

Nelms, M., & Sucher, K. (2007). Diseases of the Endocrine System. Belmont: Thomson Brooks/Cole


http://www.adaevidencelibrary.com/evidence.cfm?evidence_summary_id=88



http://www.medlineplus.gov/

BIBLIOGRAPHY CONTINUED…

Stall, G.M., Harris,S. Sokoll, L.J., Dawson-Hughes, B. (1990). Accelerated bone loss in hypothyroid patients overtreated with L-thyroxine. Ann Intern Med., 113(4), 265-269.

Thyroid Function Tests. 2005. Retrieved September 20, 2008, from American Thyroid Association Web Site: http://www.thyroid.org

Thomas, D., Moisidis, A. et al. 2008. Antithyroid Drug-Induced Aplastic Anemia. Journal of the American Thyroid Association, 15, 317-320.

http://bmj.com/cgi/content/full/313/7056/539 “Consensus statement for good practice and audit measures in the management of hypothyroidism and hyperthyroidism.” BMJ 1996, 313: 539-544


http://bmj.com/cgi/content/full/313/7056/539

hope olson. the incidence of thyroid disease is increasing, predominately among women. up to 5% of...

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