Antertior Neck Mass

Anterior Neck MassSabalvaro Dyan, Salac Carmina, Salazar Janelle , Salazar Riccel, Salcedo Von, Saldana Emmanuel, Sales Stephanie, Salonga Cryscel65 year old female with anterior neck mass

History of Present IllnessPhysical ExaminationSalient Features65 y/o Female2 X 2 cm anterior neck massProgressive increase in size lump in throatPrescribed L thyroxine 100 ug/tab 1 tab TIDtook for one month until she noted easy fatigability, palpitations, and weight lossDiscontinued medication as advised by physician

Physical ExaminationVS: BP=120/80 PR=85/min RR=28/minPink palpebral conjunctive, anicteric scleraeNeck: 8 X 6 cm firm anterior neck mass with welldefined borders and moves with deglutition; no palpable cervical adenopathiesHeart/Chest/Abdomen unremarkable1. If you were the physician who initially saw the patient one year ago, what would you have done?2. What do you think were the serum T3 ,T4, and TSH levels in the previous consult? What do you call this condition?

Low circulating levels of T4 and T3Primary Thyroid FailureRaised TSH levelsSecondary Hypothyroidism Low TSH levels that do not increase following TRH stimulation

LEVOTHYROXINE SODIUMINDICATIONHypothyroidism.Adults: Initially 50-100 mcg daily, and adjusted 4-6 week intervals by 50 mcg until attainment of clinical and biochemical euthyroidism. Normal metabolism is steadily maintained. This may require doses of 100-200 mcg daily. With patients >50 years, it is not advisable to exceed 50 mcg a day initially. Where there is cardiac disease, 50 mcg on alternate days is more suitable. In this condition, the daily dosage may be increased by 50 mcg on alternate days is more suitable. In this condition, the daily dosage may be increased by 50 mcg on alternate days, at intervals of approximately 4 weeks.OVERDOSAGE:Symptoms: In addition to exaggeration of side effects, the following symptoms may be seen: Agitation, confusion, irritability, hyperactivity, headache, sweating, mydriasis, tachycardia, arrhythmias, tachypnea, pyrexia, increased bowel movements and convulsions. The appearance of clinical hyperthyroidism may be delayed for up to 5 days. Treatment: The goal of therapy is restoration of clinical and biochemical euthyroid state by omitting or reducing the Eltroxin dosage and other measures as needed depending on clinical status.Treatment is symptomatic, and tachycardia has been controlled in adults by 40-mg doses of propranolol given every 6 hrs and other symptoms by diazepam and/or chlorpromazine as appropriate.Further management should be as clinically indicated or as recommended by the national poison centre, where available.C/I:Hypersensitivity to any component of Eltroxin. Thyrotoxicosis.SPECIAL PRECAUTIONS:Eltroxin has a narrow therapeutic index. Appropriate Eltroxin dosage is based upon clinical assessment and laboratory monitoring of thyroid function tests. During the initial titration period, careful dosage titration and monitoring is necessary to avoid consequences of under- or over-treatment. The symptoms of excessive Eltroxin dosage are the same as many features of endogenous thyrotoxicosis.Patients with panhypopituitarism or other causes predisposing to adrenal insufficiency may cause reactions including dizziness, weakness, weight loss, hypotension and adrenal crisis. It is advisable to initiate corticosteroid therapy before giving thyroxine in these cases.Special care is needed in the elderly and in patients with symptoms of myocardial insufficiency or ECG evidence of myocardial infarction or ischemia and also those with diabetes mellitus or insipidus.Eltroxin raises blood sugar levels and this may upset the stability of patients receiving antidiabetic agents.MOA:Thyroxine (T4) is a naturally occuring hormone produced by the thyroid gland and converted to the more active hormone triiodothyronine (T3) in peripheral tissues. The precise signals controlling the conversion of T4 to T3 within the cell are not known. The thyroid hormones are required for normal growth and development , particularly of the nervous system. They increase the resting or basal metabolic rate of the whole organism and have stimulatory effects on the heart, skeletal muscle, liver and kidney. Thyroid hormones enhance lipolysis and the utilization of carbohydrate.

8HYPOTHYROIDISMDeficiency in the circulating levels of thyroid hormone leads to hypothyroidism, and, in neonates, to cretinism, which is characterized by neurologic impairment and mental retardation. Hypothyroidism may also be associated with deafness (Pendred's syndrome)4 and Turner's syndrome.

In adults, symptoms in general are nonspecific: Tiredness, weight gain, cold intolerance, constipation, and menorrhagiaPatients with severe hypothyroidism or myxedema Facial and periorbital puffinessCharacteristic facial features as a consequence of the deposition of glycosaminoglycans in the subcutaneous tissuesThe skin becomes rough and dry and often develops a yellowish hue from reduced conversion of carotene to vitamin A. Hair becomes dry and brittle, and severe hair loss may occurLoss of the outer two-thirds of the eyebrows.

An enlarged tongue may impair speech, which is already slowed, in keeping with the impairment of mental processes. Myxedema madnessUntreated dementiaNonspecific abdominal pain accompanied by distention and constipation. Libido and fertility are impaired in both sexes. Cardiovascular changes in hypothyroidism include:Bradycardia, cardiomegaly, pericardial effusion, reduced cardiac output, and pulmonary effusionsCardiac failure is uncommon When hypothyroidism occurs as a result of pituitary failure, features of hypopituitarism such as pale, waxy skin, loss of body hair, and atrophic genitalia may be presentLABORATORY FINDINGSHypothyroidism is characterized by low circulating levels of T4 and T3. Raised TSH levels are found in primary thyroid failure, whereas secondary hypothyroidism is characterized by low TSH levels that do not increase following TRH stimulation. Thyroid autoantibodies are present and are highest in patients with autoimmune disease (Hashimoto's thyroiditis, Graves' disease), although they are also elevated in patients with nodular goiter and thyroid neoplasms. Other findings include anemia, hypercholesterolemia, and decreased voltage with flattening or inversion of T waves on electrocardiogram. Comatose patients with myxedema also have hyponatremia and CO2 retention.TREATMENTTHYROXINETreatment of choice50 to 200 mcg per day, depending upon patient's size and condition. Starting doses of 100 mcg of thyroxine daily are well toleratedElderly patients and those with coexisting heart disease and profound hypothyroidism should be started on a considerably lower dose such as 25 to 50 mcg daily because of associated hypercholesterolemia and atherosclerosis. The dose can be slowly increased over weeks to months to attain a euthyroid state.EUTHYROID - The state of having normal thyroid gland function.14

A baseline ECG should always be obtained in patients with severe hypothyroidism prior to treatment. Patients are instructed to take tablets in the morning, usually without other medications, or at mealtime to assure good absorption. Thyroxine dosage is titrated against clinical response and TSH levels, which should return to normal. Patients who present with myxedema coma, in contrast to the patients with mild to moderate hypothyroidism, require an initial emergency treatment with large doses of intravenous thyroxine (300 to 400 g), and careful monitoring in an ICU setting.3. What is your diagnosis? Other considerations? Explain.DiagnosisHyperthyroidism secondary to over dosage to L thyroxine

Other Considerations18Differential DiagnosesNodular Non-toxic GoiterGraves DiseaseToxic Multinodular GoiterToxic AdenomaSolitary Thyroid Nodule19Nodular Non-toxic GoiterFAMILIAL GOITERENDEMIC GOITERSPORADIC GOITERInherited enzyme defectImpaired iodine metabolismUsually associated with hypothyroidismDue to iodine-deficient dietMountainous regionsintake of substances (goitrogens) that inhibit production of thyroid hormonecommon goitrogens include foods such as cabbage, turnips, brussel sprouts, seaweed, and milletTx: iodized saltNo definite cause can be established20Enlargement of the thyroid glandNo toxicity; no cancerThe following factors increase your chance of developing nontoxic goiter: Sex: female (nontoxic goiter is more common in women than men)Age: over 40 years

Reference: http://www.mbmc.org/healthgate/GetHGContent.aspx21SYMPTOMSNontoxic goiters usually do not have noticeable symptoms. Swelling on the neckBreathing difficulties, coughing, or wheezing with large goiterDifficulty swallowing with large goiterFeeling of pressure on the neckHoarseness

22MANAGEMENTA goiter only needs to be treated if it is causing symptoms.Treatments for an enlarged thyroid include:Radioactive iodine to shrink the gland, particularly if the thyroid is producing too much thyroid hormoneSurgery (thyroidectomy) to remove all or part of the glandSmall doses of Lugol's iodine or potassium iodine solution if the goiter is due to iodine deficiencyTreatment with thyroid hormone supplements if the goiter is due to underactive thyroid

Reference: http://www.nlm.nih.gov/medlineplus/ency/article/001178.htm23INDICATIONS FOR SURGERYHuge goiter which is cosmetically unacceptableCompression symptomsSuspicion of malignancy24GRAVES DISEASEA type of hyperthyroidism, is caused by a generalized overactivity of the entire thyroid gland. An autoimmune disease; thyroid-stimulating antibodies directed at TSH receptors on follicular cells.It is named for Robert Graves, an Irish physician, who was the first to describe this form of hyperthyroidism about 150 years ago.

25ETIOLOGYThe trigger for auto-antibody production is not known. Genetic predisposition HLA DR3Since Graves' disease is an autoimmune disease which appears suddenly, often quite late in life, it is thought that a viral or infection may trigger antibodies which cross-react with the human TSH receptor (a phenomenon known as antigenic mimicry, also seen in some cases of Type I diabetes).Yersinia enterocolitica

Reference: http://en.wikipedia.org/wiki/Graves%27_disease26CLINICAL FEATURESTriad:Goiter including the pyramidal lobeThyrotoxicosisExophthalmos

Symptoms:Heat intoleranceThirstSweatingWeight loss despite adequate caloric intakeAmenorrheaTachycardia or atrial fibrillationCongestive heart failure27PE:Weight lossFlushingWarm and moist skinInappropriate sweatingTachycardiaWidening of pulse pressureFine tremorMuscle wastingHyperactive tendon reflexesPretibial myexedemaGynecomastiaAudible bruit over the gland

Laboratory Findings:Decreased TSHIncreased circulating T3/T4 levelsIncreased circulating thyroid autoantibodiesThyroid stimulating immunoglobulins (TSI)Tyhroid stimulating antibodies (TSAb)Radioactive iodine scan shows diffuse uptake through the gland of 45-90 percent.

28GRAVES OPHTHALMOPATHYThyroid-associated ophthalmopathy is one of the most typical symptoms of Graves' disease. Thyroid eye disease is an inflammatory condition, which affects the orbital contents including the extraocular muscles and orbital fat. It is almost always associated with Graves' disease but may rarely be seen in Hashimoto's thyroiditis, primary hypothyroidism, or thyroid cancer.The ocular manifestations that are relatively specific to Grave's disease include soft tissue inflammation, proptosis (protrusion of one or both globes of the eyes), corneal exposure, and optic nerve compression. There are more general symptoms include lid retraction, lid lag, and a delay in the downward excursion of the upper eyelid, during downward gaze.It is believed that fibroblasts in the orbital tissues may express the Thyroid Stimulating Hormone receptor (TSHr). This may explain why one autoantibody to the TSHr can cause disease in both the thyroid and the eyes.Reference: http://en.wikipedia.org/wiki/Graves%27_disease29Classification of Graves Eye DiseaseMnemonic: "NO SPECSClass 0: No signs or symptomsClass 1: Only signs (limited to upper lid retraction and stare, with or without lid lag)Class 2: Soft tissue involvement (oedema of conjunctivae and lids, conjunctival injection, etc)Class 3: ProptosisClass 4: Extraocular muscle involvement (usually with diplopia)Class 5: Corneal involvement (primarily due to lagophthalmos)Class 6: Sight loss (due to optic nerve involvement)

Reference: http://en.wikipedia.org/wiki/Graves%27_disease30MANAGEMENTMedical:Propylthiouracil (PTU)Methimazole (Tapazole)CarbimazoleBeta-blockers (Propanolol)

31Relapse rate in 12-18 monthsRisk for fetal goiter, hypothyroidismNo morbidity related after surgeryTreatment of choice for small goiters and pregnant patients (PTU)Euthyroid state is achieved in 4-6 weeks32Radioactive IodineEase of treatmentHighly effective especially in diffuse goitersNo morbidity related to surgeryTreatment of choice for failed surgical managementThe effect is seen in 1.5-4 monthsStandard dose = 10 mCl = 8500 cGy33SurgeryComplete and permanent control of toxicityRapid control of symptomsRemoval of massTreatment of choice for huge goitersNeeds pre-operative preparationOverall morbidity of 1-2%34Toxic Multinodular GoiterUsually occur in individuals older than 50 years of age who often have a prior history of a nontoxic multinodular goiterOver several years, enough thyroid nodules become autonomous to cause hyperthyroidism.Similar to Graves disease, but symptoms and signs of hyperthyroidism are less severe and extrathyroidal manifestations are absent.May present with atrial fibrillation or palpitations, tachycardia, nervousness, tremor or weight loss.Low TSH, normal or minimally increased T4, elevated T3, T3>T4.35Toxic Multinodular GoiterThyroid scan heterogenous uptake with multiple regions of increased and decreased uptake.24hr uptake of radioiodine may not be increased. ManagementAntithyroid drugs + beta blockers normalize thyroid function and address the clinical features of thyrotoxicosis, but often stimulates the growth of the goiter; spontaneous remission does not occur.Radioiodine treat areas of autonomy, decrease the mass of the goiterA trial of radioiodine should be considered before subjecting patients to surgery.36Toxic Multinodular GoiterSurgeryDefinitive treatment of underlying thyrotoxicosis and goiter.Subtotal thyroidectomy is the standard procedure.Patients should be rendered euthyroid using antithyroid drugs before operation.

37Toxic AdenomaA solitary, autonomously functioning thyroid noduleTypically occurs in younger patients(+) thyroid nodule with symptoms of hyperthyroidismSize is at least 3cm before hyperthyroidism occurs.Absent clinical features suggestive of Graves disease or other causes of thyrotoxicosis

38Toxic AdenomaThyroid scan definitive diagnostic testFocal uptake in the hyperfunctioning nodulesDiminished uptake in the remained of the glandSuppression of the activity of the normal thyroid

39Toxic AdenomaRadioiodine ablation treatment of choice131I is concentrated in the hyperfunctioning nodule with minimal uptake and damage to normal thyroid tissue.Relatively large doses correct thyrotoxicosis in about 75% of patients within 3 months.Hypothyroidism occurs in 5 sessionsReduce nodule size42Solitary Thyroid NodulePresent in approximately 4 percent of the populationPain is unusual. When present, it should raise suspicion for intrathyroidal hemorrhage in a benign nodule, thyroiditis, or malignancy.History of hoarseness - may be secondary to malignant involvement of the recurrent laryngeal nervesRisk factors for malignancy exposure to ionizing radiation and family history of thyroid and other malignancies associated with thyroid cancer.

43Solitary Thyroid NoduleMass moves with swallowing.Hard, gritty of fixed nodules are more likely to be malignant. Most are euthyroid.If a patient with a nodule is found to be hyperthyroid, the risk of malignancy is approximately 1 percent.FNAB most important diagnostic testBenign 65% (includes cysts and colloid nodules)Suspicious 20%Malignant 5%Nondiagnostic 10%

44Solitary Thyroid NoduleUltrasoundFor detecting nonpalpable thyroid nodulesFor differentiating solid from cystic nodulesFor diagnosing suspicious nodules with microcalcificationsFor identifying adjacent lymphadenopathyCT and MRI unnecessary in except for large, fixed, or substernal lesions. 123I or 99mTc rarely necessary, unless evaluating patients for hot or autonomous thyroid nodules

45Solitary Thyroid NoduleMalignant tumors generally treated by total or near-total thyroidectomySimple thyroid cysts - resolve with aspiration in approximately 75 percent of casesUnilateral thyroid lobectomy - if the cyst persists after three attempts at aspirationLobectomy For cysts >4 cm in diameterFor complex cysts with solid and cystic components46Solitary Thyroid NoduleColloid nodule should be observed with serial ultrasound and Tg measurementsRepeat FNAB if nodule enlargesL-thyroxine in doses sufficient to maintain a serum TSH level between 0.1 and 1.0 U/mL.50% decrease in sizeThyroidectomy if a nodule enlarges on TSH suppression, causes compressive symptoms, or for cosmetic reasonsExceptions: Patient who has had previous irradiation of the thyroid gland or who has a family history of thyroid cancer.In these patients total or near-total thyroidectomy is recommended. High incidence of thyroid cancer ( 40%) Decreased reliability of FNA biopsy

474. How would you manage this patient now?Goal: restoration of clinical and biochemical euthyroid state by omitting or reducing the dosage of medications and other measures as needed depending on clinical status.ECGBlood test: TSH, T3, T4 levels, monitored regularlySYMPTOMATIC TREATMENT: To control tachycardia, hypertension and atrial fibrillation: 20 - 40 mg doses of propranolo Q 6hours; dIf beta blockers are contraindicated: Diazepam and/or chlorpromazine RADIOACTIVE IODINEingestion of a radioactive iodine tablet (6-12 wks) which is then taken up by thyroid cells. These overactive cells are destroyed so that the thyroid can shrink in size and produce hormone at normal levels.In patients with underlying heart disease and in elderly patients, it is desirable to treat with antithyroid drugs (methimazole) until the patient is euthyroid. The medication is then stopped for 5-7days before the appropriate dosage of 131I. Although it is a safe treatment, most people become hypothyroid after radioactive iodine therapy and therefore require lifelong thyroid hormone replacement therapy.

THYROIDECTOMYNow uncommonly performed; the surgeon removes most or all of the glandCandidates for surgery: include pregnant hyperthyroid patients intolerant of anti-thyroid drugs, patients desiring definitive therapy without the use of radioactive iodine, children, and patients with very large or multinodular goiters.Patients are treated with antithyroid drugs until euthyroid (about 6wks). In addition, 10-14 days prior to surgery, they receive saturated solution of potassium iodide 5 drops BID, to diminish vascularity of the gland and simplify surgeryHowever, in cases of total removal of the thyroid gland, patient must take thyroid replacement pills for the rest of his or her life

NON-PHARMACOLOGICALHigh calorie diet in order to replace all the energy burned by the body in hyperthyroid stateDrink plenty of water and juices to replace all the fluid losses. Avoid or limit caffeinated drinks for such could produce anxiety.Journals on Diagnosis and Treatment of Drug Induced HyperthyroidismDiagnosisNewly diagnosed thyrotoxicosis in hospitalized patients: clinical characteristics

Rotman-Pikielny P et. Al

Background:Thyrotoxicosis is often diagnosed in an outpatient setting. Most common symptoms include irritablility, heat intolerance ,palpitations and weaknessThe prevalent symptoms in hospitalized patients with newly diagnosed thyrotoxicosis have not been fully characterizedObjectiveTo determine the clinical characteristics of patients with thyrotoxicosis newly diagnosed during hospitalization. DesignRetrospective computer-based search was undertaken to detect patients that were hospitalized in our medical centre during 1999-2006, and discharged with thyrotoxicosis or thyroiditis primary diagnosis.

ResultsFifty-eight patients (36F/22M; mean age 52.1 +/- 17.5 years) were identified. Weakness, weight loss and palpitations were the most common manifestations (50, 40 and 35%, respectively) and were predominantly present in patients with hyperthyroidism. Sore throat was present in 41% of patients with thyroiditis. Sinus tachycardia and atrial fibrillation occurred in 65.5 and 15.5% of the patients, more common in those with hyperthyroidism. The diagnoses on discharge were Graves' disease, subacute thyroiditis and multinodular goiter in 39.7, 34.5 and 8.9%, respectively.ConclusionWeakness, weight loss and palpitations were the main symptoms in patients diagnosed with thyrotoxicosis during hospitalization. Thyrotoxicosis should be included in the differential diagnosis when patients are admitted to the hospital with those symptoms.

TreatmentDrug induced thyrotoxicosis: the surgical optionLorberboym M., Schacter P. Background:Drug induced thyrotoxicosis is not uncommon, It may worsen life threatening arrythmias and become refractory to medical treatment

SummaryThe Article talks about a near total thyroidectomy as valid alternative to medical therapyThe article pursues to promote near total thyroidectomy as an early management of the diseaseMethodsThe study included 12 patients 7 men and 5 women aged 63-82 years of age with drug induced fulminant thyrotoxicosisDrugs such as Iodine containing Amiodarone or IFN a treatmentPatients has adjunct medical therapy of an anti thyroid Propylthiouracil 1200 mg and a Beta receptor antagonist

Thyroid scan was performed in all patients using Tc-99m pertechnate

Results4 patients did not respond to 3 months of medical therapy required surgical thyroidectomy due to unremitting thyrotoxicosis.Near total thyroidectomy resulted into rapid correction of thyrotoxicosis enabling continuation of anti-arrythmic drugsAll patients recovered rapidly and remained well and euthyroid on thyroxine replacement therapy