logging in or signing up Thyroid disease - A Medusa of sorts drmdsadiq Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 248 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: June 02, 2012 This Presentation is Public Favorites: 0 Presentation Description Management of Hyperthyroidism, Subclinical hypothyroidism, Thyroid dysfunction in pregnancy & Sick euthyroid syndrome Comments Posting comment... Premium member Presentation Transcript PowerPoint Presentation: In the Name of God, Most Gracious, Most MercifulA KALEIDOSCOPIC PRESENTATION OF THYROID DISEASE: A KALEIDOSCOPIC PRESENTATION OF THYROID DISEASE - Dr.Mohammed Sadiq Azam Postgraduate MD ( Int Med) Dept Of Internal Medicine, DCMSCase 1: Case 1PowerPoint Presentation: 35/F presented with c/o diarrhoea , palpitations and a feeling of restlessness. She has been having increased sweating since 3 months. Complaints of increased appetite and decreased weights over 6 months. On examination: Irregular pulse, 106pbm, PD 20 bpm . Thyroid Profile revealed : T3: 210 ng /dl (high) T4: 15 ug /dl (high) TSH: <0.01 (low)THE HYPERTHYROID STATE: THE HYPERTHYROID STATE - Diagnosis & TreatmentEVALUATION THYROTOXICOSIS: EVALUATION THYROTOXICOSIS Measure TSH, unbound T4 TSH ↓ unbound T4 ↑ TSH ↓ unbound T4 - N TSH - N/↑ unbound T4 ↑ TSH & unbound T4 - N No further tests Primary thryrotoxicosis F/S/O Graves? Unbound T3 High Normal T3 toxicosis Subclinical hyperthyroidism Follow up 6-12 weeks TSH secreting pituitary adenoma or thyroid hormone resistance syndrome Yes, Graves MNG or Toxic adenoma Yes, Toxic nodular hyperthyroidism No, Low RN uptake Yes, Destructive thyroiditis Iodine excess or thyroid hormone excess Rule out other causes including Stimulation by hCGPowerPoint Presentation: THYROTOXICOSIS MANAGEMENT 3 approaches Antithyroid drugs Radioactive Iodine I 131 Subtotal thyroidectomyPowerPoint Presentation: THYROTOXICOSIS MEDICAL MANAGEMENT 1. ANTITHYROID DRUGS: > Carbimazole > Propyl thiouracil Dosage of Carbimazole : 0-3 weeks 40-60 mg daily 4-8 weeks 20-40 mg daily Maintainence 5-20 mg daily for 18-24 months ADR: Rash, Agranulocytosis C/I: Lactating MothersPowerPoint Presentation: MEDICAL MANAGEMENT 2. RADIOACTIVE I 131 : MOA: > Destroys functioning thyroid cells > Inhibits their ability to replicate Dose: 180-370 MBq (5-10mCi) orally (Dep. on goitre size) 4-6 weeks to be effective (long lag period) -blockers control symptoms in lag period. Severe cases: Carbimazole within 48 hrs of I 131 THYROTOXICOSISPowerPoint Presentation: MEDICAL MANAGEMENT 3. Role of -blockers: ONLY SYMPTOMATIC RELIEF (within 12-24 h) Propronolol: 160 mg/day Nadolol: 40-80 mg/day T3 toxicosis : I 131 (555-110Mbq), Hemithyroidectomy THYROTOXICOSISPowerPoint Presentation: MANAGEMENT OF ATRIAL FIBRILLATION Ventricular Rate responds little to Digoxin. Good response to addition of - blockers. CARDIOVERSION to revert to sinus rhythm. (Only after TSH/T4 ) Anti coagulation with Warfarin / Aspirin. Generally control of serum T4 causes a return to sinus rhythm. Drugs provide symptomatic relief. THYROTOXICOSISPowerPoint Presentation: GRAVES’ OPTHALMOPATHY Gritty sensation, Discomfort, lacrymation Exopthalmous Periorbital oedema, Chemosis, Scleral injection THYROTOXICOSISPowerPoint Presentation: MANAGEMENT - GRAVES’ OPTHALMOPATHY Reassurance Methyl cellulose drops grittiness, discomfort Tinted glasses / Side shields excess lacrymation Complications: Corneal Ulcer: Lid lengthening Sx Papilloedema/Loss of acuity/Field defects: URGENT trt. with PREDNISOLONE 60mg/d THYROTOXICOSISPowerPoint Presentation: GRAVES’ OPTHALMOPATHY EFFECT OF THERAPY BEFORE AFTERCase 2: Case 2PowerPoint Presentation: 32/F come to hospital for routine physical examination and master heath checkup. Healthy. No specific complaints. Thyroid profile: T3: 124 ng /dl (normal) T4: 9.1ug/dl (normal) TSH: 7.5 uIU /ml (high)SUBCLINICAL THYROID DYSFUNCTION: SUBCLINICAL THYROID DYSFUNCTION - A Tricky situationINCLUDES:: INCLUDES: Subclinical hypothyroidism Commonly encountered Subclinical hyperthyroidism Rare entitySUBCLINICAL HYPOTHYROIDISM: SUBCLINICAL HYPOTHYROIDISM Defined as: “Biochemical evidence of thyroid hormone deficiency in patients who have few or no apparent clinical features of hypothyroidism.” Previously called: Mild hypothyroidism Early thyroid failure Preclinical hypothyroidism Decreased thyroid reserveSUBCLINICAL HYPOTHYROIDISM: SUBCLINICAL HYPOTHYROIDISM Associated with risk of cardiac, neuropsychiatric and dyslipidemic abnormalities. Risk of neonatal hypothyroidism if encountered in pregnancy. Risk of progression to overt hypothyroidism is high when TSH is elevated and Anti TPO Ab +SUBCLINICAL HYPOTHYROIDISM: SUBCLINICAL HYPOTHYROIDISM Recent guidelines do not recommend routine treatment when TSH levels are < 10 mU /L. ( Har 18 th ed , Pg 2922) Confirm sustained elevation of TSH over a 3 month period prior to initiating therapy. Start with low dose of 25-50ug/day with the goal of normalising TSH.Case 3: Case 3PowerPoint Presentation: 23/F, Primi Gravida , no past history of thyroid disease. TFT during ANC (12 weeks GA) revealed a normal T3, T4 but raised TSH 6.4uIU/ml. No treatment done, at term (36 weeks) her TSH increased to 8.2 uIU /ml (T3, T4 Normal). 8 months postpartum: T3: <10ng/dl T4: <0.30 ug /dl TSH: >150.00 uIU /mlTHYROID FUNCTION IN PREGNANCY: THYROID FUNCTION IN PREGNANCY - An Enigma in its own right!FACTORS ALTERING THYROID FUNCTION: FACTORS ALTERING THYROID FUNCTION Transient increase in hCG during first trimester stimulates TSH-R Estrogen induced rise in TBG during Trimester I sustained throughout pregnancy Alterations in immune system expression of an underlying thyroid disease Increased thyroid hormone metabolism by placenta Increased urinary excretion of iodide high risk of deficiency in women taking <50ug of iodide/dayThe hCG phenomenon: The hCG phenomenon Rise in hCG in first trimester is accompanied by a reciprocal fall in TSH that persists upto the middle of pregnancy. Weak binding of hCG , which is present at very high levels to the TSH-R hCG induced changes in thyroid function can result in: Transient gestational hyperthyroidism Hyperemesis gravidarum Rarely warrants use of antithyroid drugsHYPOTHYROIDISM - PREGNANCY: HYPOTHYROIDISM - PREGNANCY Maternal hypothyroidism occurs in 2-3% of women of child-bearing age. All pregnant women & those planning pregnancy ( esp with family history) must be screened for hypothyroisism in first & third trimester. Most pregnant women with primary hypothyroidism require an additional 25-50ug increase to their dose. Subclinical hypothyroidism must be treated TSH Target to treat in pregnacy : 2.5-3.0uIU/mlHYPERTHYROIDISM - PREGNANCY: HYPERTHYROIDISM - PREGNANCY Rare Pregnancy has an attenuating influence on hyperthyroidism due to associated immunosuppression Medical therapy is the trt of choiceHYPERTHYROIDISM - PREGNANCY: HYPERTHYROIDISM - PREGNANCY PTU or Carbimazole ? Both cross placenta, can cause low T4 and high TSH in fetus Maternal T4 flux across placenta is highly variable PTU > 200mg / Carbimazole >15mg is undesirable ( esp in III trim) Serum free T4 should be maintained in upper limit of normal and no attempt at normalisation must be made.HYPERTHYROIDISM - PREGNANCY: HYPERTHYROIDISM - PREGNANCY In most cases maintainence dose must be 200mg PTU or less in early pregnancy. PTU preferred to methimazole due to risk of fetal aplasia cutis with the latter. Emerging reports of a “ carbimazole embryopathy ” have made PTU the drug of choice. ( LeBeau et al. Thy dis dur preg . Endo Clin North Am 2006;35:117-136, vii)Case 4: Case 4PowerPoint Presentation: 65/M, admitted with c/o severe abdominal pain and vomintings . High grade fever+. On examination, RIF tenderness + with Guarding and rigidiity +. Patient was taken up or emergency laparotomy for perforated appendix. Post op case kept in SICU, Thyroid profile revealed: T3: 43 ng /dl (low) T4: 8.7 ug /dl (normal) TSH: 3.8 uIU /ml (normal)SICK EUTHYROID SYNDROME: SICK EUTHYROID SYNDROME - To treat or not to treat?SICK EUTHYROID SYNDROME: SICK EUTHYROID SYNDROME Abnormalities of circulating TSH or thyroid hormone levels as a consequence of any acute, severe illness. Major cause of these hormonal changes is the release of cytokines such as IL-6. Unless a thyroid disorder is strongly suspected, the routine testing of thyroid function should be avoided in acutely ill patients.SICK EUTHYROID SYNDROME (SES): SICK EUTHYROID SYNDROME (SES) Most common hormone pattern in SES: Low T3 (total & free) Normal T4 Normal TSH Magnitude of fall in T3 correlates with the severity of the illness. Decreased peripheral conversion of T4 T3. leading to increased rT3 (more due to decreased clearance rather than increased production). Low T3 also seen in fasting. (Decreased catabolism)SICK EUTHYROID SYNDROME (SES): SICK EUTHYROID SYNDROME (SES) Very sick patients exhibit a fall in total T4 as well (low T4 syndrome). Poor prognosis Fall in T4 is due to altered binding to TBG. (Normal unbound fraction) TSH may range from <0.1 to >20 mIU /L. These alterations maybe due to IL-12 and IL-18.SICK EUTHYROID SYNDROME (SES): SICK EUTHYROID SYNDROME (SES) Acute liver failure: Initial rise in total T3 and T4 (but not unbound hormone), due to TBG release. Levels become subnormal with progression to liver failure. Acute psychiatric states (5-30%): Transient increase in total & unbound T4 Normal T3, Low, normal or high TSH HIV: Early disease T3, T4 rise, TSH normal. T3 falls with progression to AIDS. Renal disease: Low T3, normal rT3 (NOT increased rT3) due to increased rT3 uptake by liver.SICK EUTHYROID SYNDROME (SES): SICK EUTHYROID SYNDROME (SES) Based on history, severity of patient state, thyroid hormone assays (including rT3) Diagnosis is frequently presumptive Treatment is controversial. Most of the abnormalities recover with recovery from the acute crisis. Monitor TFT during recovery. No need of hormonal replacement unless clinical evidence of hypothyroidism + or low T4 levels.THANK YOU: THANK YOU You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.