GOITER (DISEASE OF THYRIOD GLAND)

NASIR YAHAYA JEGA (UDUS)

Thyroid gland (weighs about 30 g in adults) islocated on either side of the trachea below thelarynx. It produces two principal hormonesthyroxin (T4; 3,5,3',5'-tetraiodothyronine) and

3,5,3'-triiodothyronine (T3)-which regulate the metabolic rate of the body.

Thyroid gland also secretes calcitonin, a Hormone Concerned with calcium

homeostasis.

THYROID HORMONES REVIEW

CHEMICAL STRUCTURE OF THYROID HORMONES(T3 T4)

Influence on metabolic rate: Thyroid hormone increase the basal metabolic rate.

Effect on protein synthesis: TH activate DNA to produce RNA

Influence on CHO metabolism: TH improves glucose uptakes, gluconeogenesis, glycogenolysis

Influence on lipid metabolism: lipid turn over and utilization are stimulated by thyroid hormones.

ABNORMALITIES OF THYRIOD FUNCTION HYPOTHYROIDISM OR HYPERTHYRIODISM= ( GOITER)

METABOLIC EFFECT OF THYROID HORMONE

GOITER, disease of the thyroid gland, characterized by an enlargement of the gland, visible externally as a swelling on the front of the neck. In simple goiter the basal metabolic rate(the least amount of energy necessary to maintain the vital involuntary activities) is somewhat lowered, and in toxic goiter it is elevated.

WHAT IS GOITER?

GOITER IS CLASSIFY INTO TWO:1. Simple goiter 2. Toxic goiter SIMPLE GOITER is characterized by an enlargement

of the entire thyroid gland or one of its two lobes. It is associated with hypothyroidism, a condition caused by insufficient production of thyroid hormone. Simple goiters may be classified as either endemic or nontoxic.

TOXIC GOITER This disease, also called exophthalmic goiter, hyperthyroidism, thyrotoxicosis, or Graves' disease, for the Irish physician Robert James Graves, is caused by an excess of thyroxine secretion. The cause of the excessive secretion is obscure.

CLASSIFICATION GOITER DISEASE

Goiter is endemic in regions with low iodine level in the soil, such as countries in the mountainous areas in South-East Asia, Latin America and Central Africa.

ETIOLOGY OF THE DISEASE (CAUSES OF THE DISEASE GOITER)

Sporadic goiter can be divided in to cases with a genetic background, including individuls with congenital goiters in nonendemic areas, and other cases induced by goitrogenic drugs.

ETIOLOGY CONT’D

CAUSES OF GOITER (ENDEMIC OR SPORADIC)ETIOLOGY CONT…

ENDEMIC SPORADICIodine deficiency Genetic defects of thyroid

hormone synthesisDietary goitrogens Genetic defects of thyroid

hormone action

Environmental goitrogens Goitrogenic drugs

Thyroiditis syndromes

Acromegaly

TSH producing pituitary adenoma

DRUGS AND CHEMICALS GOITROGENIC FOODSSulfadimethoxine, propylthiouracil, potassiumperchlorate, and iopanoic acid.Some oxazolidines such as goitrin.Ions such as thiocyanate (from cigarette smoking for example) and perchlorate.Amiodarone inhibits peripheral conversion of thyroxine to triiodothyronine; also interferes with thyroid hormone action.Phenobarbitone, phenytoin, carbamazepine, rifampin induce metabolic degradation of triiodothyronine (T3) and thyroxine (T4)

CassavaSoya beansPine nutPeanutFlax seedMilletStrawberriesPearPeachesSpinachBamboo shootsSweet potatoes

GOITROGENIC DRUGS, CHEMICALS& FOOD

PHATOPHYSIOLOGY OF GOITER (CHANGES CAUSED BY DISEASE)

TEST HYPOTHYROIDISM HYPERTHYROIDISMBMR low HighSERUM CHOLESTEROL

High Low

24hr IODINE 131 UPTAKE BY THYRIOD GLAND

Low High

PLASMA THYROXINE

Low High

PROTIEN BOUND IODINE (PBI)

Low High

LAB TEST FOR THYROID ABNORMALITIES

Surgery Destruction with radioactive iondine Oral L-thyroxine Anti-thyriod drugs include; thiouracilAnd thiourea, they inhibit peroxidase activity. Others (Thryoid-Supporting Foods).

TREATMENT

SURGERY:- Removing all or part of the thyroid gland (total or partial thyroidectomy) is an option if one have a large goiter that is uncomfortable or causes difficulty breathing or swallowing, or in some cases , if you have nodular goiter causing hyperthyroidism. Surgery is also the treatment for thyroid cancer. You may need to take levothyroxine after surgery, depending on the amount of thyroid removed.

SURGERY TREATMENT

What is Radioactive Iodine?Radioactive iodine (commonly called radioiodine) is a form of iodine chemically identical to nonradioactive iodine.

How is Treatment Given?Radioactive iodine is given either in a capsule or in a tasteless solution in water.

How Does the Treatment Work?Radioactive iodine treatment makes use of the thyroid gland's natural need for iodine to make thyroid hormone.

When radioiodine is given, the thyroid gland cannot tell if the iodine is radioactive or not, and collects it in the normal way in proportion to the activity of the thyroid. Radioiodine thus accumulates in the cells that make thyroid hormone and remains there long enough to radiate the gland and to slow thyroid production.

Radioiodine Side EffectsThere are no immediate side effects from radioiodine treatment. Do not expect nausea, vomiting, hair loss, and allergic reactions to iodine; they do not occur. Rarely, the thyroid gland may develop a slight tenderness which may last for a day or two.

RADIOACTIVE IODINE TREATMENT

Levothyroxine (L-thyroxine) is typically used to treat goiter via its ability to lower thyroid-stimulating hormone (TSH), a hormone that is considered goiter-inducing.

IUPAC name: (S)-2-Amino-3-[4-(4-hydroxy-3,5-diiodophenoxy)-3,5-diiodophenyl]propanoic acid

Other names: 3,5,3',5'-Tetraiodo-L-thyronine

LEVOTHYROXINE TREATMENT

L-THYROIXINE MECHANISM OF ACTIONLevothyroxine is a synthetic form of thyroxine (T4), an

endogenous hormone secreted by the thyroid gland, which is converted to its active metabolite, L-triiodothyronine (T3). T4 and T3 bind to thyroid receptor proteins in the cell nucleus and cause metabolic effects through the control of DNA transcription and protein synthesis.

Absorption:Levothyroxine absorption is increased by fasting and decreased in certain malabsorption syndromes, by certain foods, and with age. The bioavailability of the drug is decreased by dietary fiber.

DISTRIBUTION: Greater than 99% of circulating thyroid hormones are bound to plasma proteins including thyroxine-binding globulin, thyroxine-binding prealbumin, and albumin.

Only free hormone is metabolically active. METABOLISM: The primary pathway of thyroid hormone

metabolism is through sequential deiodination. The liver is the main site of T4 deiodination, and along with the kidneys are responsible for about 80% of circulating T3. In addition to deiodination, thyroid hormones are also excreted through the kidneys and metabolized through conjugation and glucuronidation and excreted directly into the bile and the gut where they undergo enterohepatic recirculation.

ELIMINATION: Half-life elimination is 9–10 days for hypothyroid patients; 3–4 days for hyperthyroid patients. Thyroid hormones are primarily eliminated by the kidneys (approximately 80%), with urinary excretion decreasing with age. The remaining 20% of T4 eliminated in the stool

PHARMACOKINETICS OF L-T4

LEVOTHYROIXINE DOSAGE

Generic levothyroxine, 25 µg oral tablet

Dosages vary according to the age groups and the individual condition of the patient, body weight and compliance to the medication and diet. Monitoring of the patient's condition and adjustment of the dosage is periodical and necessary. Levothyroxine is taken on an empty stomach approximately half an hour to an hour before meals. As such, thyroid replacement therapy is usually taken 30 minutes prior to eating in the morning. For patients with trouble taking levothyroxine in the morning, bedtime dosing is effective as well.

Dosing, which is generally straightforward, must be controlled to achieve free T4 and free T3 levels within the normal reference range and elimination of hypothyroid and hyperthyroid symptoms.

Long-term suppression of TSH values below normal values will frequently cause cardiac side-effects and contribute to decreases in bone mineral density (low TSH levels are also well known to contribute to osteoporosis)

Overdose can result in heart palpitations, abdominal pain, nausea, anxiousness, confusion, agitation, insomnia, weight loss, and increased appetite.

Allergic reactions to the drug are characterized by symptoms such as difficulty breathing, shortness of breath, or swelling of the face and tongue.

Acute overdose may cause fever, hypoglycemia, heart failure, coma, and unrecognized adrenal insufficiency.

The effects of overdosing appear 6 hours to 11 days after ingestion.

ADVERSE EFFECTS

There are several foods that will support thyroid health. Among them are those high in iodine and tyrosine.

Foods Rich In IodineFoods that are high in iodine include kelp and other sea vegetables,

fennel, Jerusalem artichokes, cow’s milk, eggs, iodized salt.Foods Rich in TyrosineTyrosine is an amino acid that is found in a lot of goitrogenic foods

like wheat, peanuts, and soybeans. It’s important to get tyrosine without those goitrogenic properties tagging along. Some good sources include pumpkin seeds, beef, fish, dairy products, eggs, bananas, avocados, poultry, and almonds.

Non-Cruciferous Veggies and FruitIf you’ve got thyroid issues, some of the best foods you can eat

(aside from those already mentioned) include non-cruciferous vegetables and fruit. Vegetables and fruit, in general, tend to contain high amounts of antioxidants, especially when eaten fresh.

Antioxidants help protect your body against damage from free radicals. Most also have high amounts of electrolytes like potassium and sodium, which contribute to the movement of fluid in body tissues.

THYROID-SUPPORTING FOODS TREATMENT

In view of all (hypothyriodism and hyperthyriodism) iodine supplementation shows great significance in disputing the adverse effect of iodine deficiency, iodine supplementation can be recommended to manage the adverse effect.

yahaya_nasir@yahoo.com

CONCLUSION

Harington (1926). "Chemistry of Thyroxine: Constitution and Synthesis of Desiodo-Thyroxine". Biochem J 20 (2): 300–313.

Verhoeven DT, Verhagen H, Goldbohm RA, van den Brandt PA, van Poppel G (February 1997). "A review of mechanisms underlying anticarcinogenicity by brassica vegetables". Chem. Biol. Interact. 103 (2): 79–129

U.Satyanarayana, U.Chakrapani “ Biochemistry textbook” third edition page 425-442

EXTERNAL LINK Microsoft encarta premium 2009

REFERENCES