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Hyperthyroidism & Hypothyroidism. Hyperthyroidism Persistant elevation of the synthesis & release of thyroid hormones ( T3 & T4 ) leads to hyperthyroidism.

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Presentation on theme: "Hyperthyroidism & Hypothyroidism. Hyperthyroidism Persistant elevation of the synthesis & release of thyroid hormones ( T3 & T4 ) leads to hyperthyroidism."— Presentation transcript:

1 Hyperthyroidism & Hypothyroidism

2 Hyperthyroidism Persistant elevation of the synthesis & release of thyroid hormones ( T3 & T4 ) leads to hyperthyroidism.

3 Common causes: 1. Toxic Diffuse Goiter (Thyrotoxicosis, Graves Disease) 2. Toxic Multinodular Goiter ( Plummer's disease) 3. Thyroid Adenoma (Tumor--).--------- Rare Causes------

4 Graves Disease / Thyrotoxicosis Autoimmune Disorder: Immuno globulin antibodies that bind with receptors that bind TSH are found in the blood of these patients. These cause continual stimulation of cAMP system of thyroid cells leading to the development of Hyperthyroidism. These are named as Thyroid stimulating immunoglobulins ( TSI ) / LATs (long acting thyroid stimulator) having TSH like actions

5 Causes of Hyperthyroidism (Toxic Goiter, Thyrotoxicosis, Graves disease) In most cases: Thyroid gland increases in size-2-3times normal with tremendous hyperplasia, ↑ in number & size of follicles & ↑ T4, T3 secrretion TSH levels are markedly reduced

6 Hyperthyroidism / Thyrotoxicosis Symptoms-- Vary with condition, severity- Common: Due to hypermetabolic state- Loss of weight, increased heat intolerance & sweating, Excessive appetite, palpitation, tachycardia, exertional dyspnea, nervousness, tremors, diarrhea, easy fatigability, apprehension, insomnia & sometimes mental changes--

7 Examination of the neck Diffusely enlarged thyroid Feels Soft, warm, pulsatile, tender, arterial thrill & bruit- due to increased vascularity

8 Exophthalamus Most (not all) pts develop Eye disease---- ( Abnormal protusion of the eye balls)- due to swelling of the retro-orbital tissue & degenerative changes in the extraocular muscles--).

9 Symptoms 1. A high state of excitability 2. Increased BMR 3. Intolerance to heat & Increased sweating 4. Weight loss (mild to severe) 5. Diarrhoea

10 Symptoms ( Cont. ) 6. Muscle weakness 7. Extreme nervousness or other psychic disorders 8. Extreme fatigue but inability to sleep 9. Tremors of hands 10. Enhanced sensitivity to catecholamines

11 Symptoms ( Cont. ) 11. CVS Effects: Increased cardiac work load & over prolonged periods→ Heart Failure Due to direct effect on the excitability of cardiac muscle → ↑ HR, Stroke Vol., CO & indirect effects due to ↑ sensitivity to catecholamines

12 Thyroid Function Tests Isotopic Tests I 131 uptake studies, TSH stimulation & T 3 suppression tests Estimation of T3, T4 & TSH by radio immuno assay or ELISA Estimation of TSI Estimation of free T3 & T4 Thyroid scanning

13 Thyroid Function Tests (Cont.) Non Isotopic Tests: Increased BMR - (+30 to +60 ) Biopsy of thyroid gland / FNAC

14 Lab. Evaluation T4 & T3 will always be elevated in hyperthyroidism Levels of TRH & TSH will vary depending on precise cause of hyperthyroidism

15 Lab. Evaluation (Cont.) TypeExampleTRHTSHT4 PrimaryGraves ↓↓↑ Seconda ry Pituitary Adenom a. ↓↑↑ TertiaryHypoth. Tumor ↑↑↑

16 Principle underlying management Drugs (that blocks the formation of thyroid hormones) β blockers e.g. propranalol can ameliorate cvs symptoms ( tachycardia--) Surgical Treatment Radio active iodine Treatment ( can destroy secretory cells of thyroid gland )

17 Hypothyroidism Insufficient synthesis & release of thyroid hormones-- Congenital hypothyroidism → Cretinism In adults → Myxedema

18 Causes Non Goitrous Spontaneous atrophy (autoimmune) Congenital Surgical or I 131 Treatment Goitrous Dietary I deficiency - Endemic Antithyroid drugs given during pregnancy, goiterogenic subst. Hashimoto's disease (Autoimmune destruction of thyroid gland)

19 Cretinism Hypothyroidism from fetal life, infancy, childhood --detected after several months Infant remains dull, lethargic, Retarded growth, Some features include: Large protruding tongue, broad flat nose, widely set eyes, sparse hair, dry skin, protuberant abdomen, physiological jaundice, croaky voice, problems in feeding→ suspicion of cretinism

20 Cretinism ( Cont. ) As the baby becomes older- - Retardation of growth & Milestones Mental development severely retarded Other neurological abnormalities-may be present- deafness, spastic limbs--- ( If not treated within a few wks after birth the new born will lose 3-5 IQ points every month)

21 Primary hypothyroidism in adults: Myxedema Manifestations: Slowing of activities, Lethargy, somnolence, constipation, general disinterestedness, weight gain, Increased sensitivity to cold, Hair- Coarse, dry & scanty Skin- Lusterless, thick & dry & scanty hair Non pitting edema / edematous appearance throughout the body called myxedema in severe cases, Macroglossia, Husky voice---

22 Myxedema In pts with almost total lack of thyroid hormones: Swelling all over, bagginess under the eyes, ↑ hyaluronic acid,chondroitin sulphate bound with proteins form excessive tissue gel in the interstitial spaces→↑ fluid, gel→non pitting edema

23 Myxedema: Manifestations ( Cont. ) Neurological Features: (Prominent in some): Slowness of mental & physical activities Slowed speech, Muscle cramps, Muscle hypertrophy, Paresthesias & entrapment neuropathies, Carpel tunnel syndrome, Altered tendon reflexes, Slowed Nerve conduction, Psychic disturbances (Myxedema madness)------

24 Myxedema: Manifestations ( Cont. ) Cardiovascular disturbances Cardiomegaly, Pericardial effusion, Mild to moderate hypertension, predisposition to ischemic heart disease. ↑ in blood cholestrol due to altered fat & cholesterol metabolism & ↓ cholestrol excretion by Liver predisposes pts to atherosclerosis→peripheral vascular disease--

25 Hypothyroidism: Laboratory Investigations ↓ BMR ↑ Serum Cholesterol ↑ Creatine phosphokinase ↓ 131 I uptake by thyroid gland ↑ TSH levels ECG- Slow rate, low voltage, T wave changes. Immunological Markers---

26 Lab. Evaluation (Cont.) TypeExampleTRHTSHT4 PrimaryHashim- oto ↑ ↑↓ Seconda ry Pituitary↑↓↓ TertiaryHypoth.↓↓↓

27 Treatment- Principle of therapy Replacement of thyroid hormone to achieve full clinical remission & normal biochemical parameters Replacement therapy is started with synthetic levothyroxine sodium ( T4 ) & T 3 ----proper treatment → normality Monitoring the treatment- By clinical assessment & TSH levels (kept at lower levels of normal)

28 Treatment- Principle of therapy Patients with long h/o untreated hypothyroidism → Severe Manifestations → Myxedema Coma Patient presenting with profound lethargy, weakness, hypothermia, hypoglycemia would require immediate / emergency treatment to prevent myxedema coma

29 Learning Outcomes Review the functions of the Thyroid gland Describe the clinical features & investigations of Thyrotoxicosis Describe the principles of management of Thyrotoxicosis Describe the clinical features & investigations of Myxedema Describe the principles of management of Myxedema

30 Thank You


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