Thyroid Gland Physiology And Disorders.pptx

yohannesfetene2 49 views 31 slides Jun 29, 2024
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About This Presentation

This slides describes on thyroid gland phsiology and disorders including manifestations and clinical presentations


Slide Content

Thyroid Gland Physiology And Disorders Gizeshwork (MD)

Thyroid Development and Physiology Fetal bilobed thyroid shape is recognized by 7 wk of gestation Colloid formation is seen by 10 wk Iodine trapping occurs by 8-10 wk, T 4 and to a lesser extentT 3 synthesis and secretion occur from 12 wk of gestation Maturation of the HP-thyroid axis occurs over the 2nd half of gestation Normal feedback r/ships are not mature until approximately 3 mo of postnatal life

Follicles: the Functional Units of the Thyroid Gland Follicles Are the Sites Where Key Thyroid Elements Function: Thyroglobulin ( Tg ) Tyrosine Iodine Thyroxine (T 4 ) Triiodotyrosine (T 3 )

The Thyroid Hormones Two principal hormones Thyroxine (T 4 ) and triiodothyronine (T 3 ) Required for homeostasis of all cells Influence cell differentiation, growth, and metabolism Considered the major metabolic hormones because they target virtually every tissue

Hormone secretion TRH Produced by Hypothalamus Release is pulsatile , circadian Down regulated by T 3 Travels through portal venous system to adenohypophysis Stimulates TSH formation

TSH Produced by Adenohypophysis Thyrotrophs Up regulated by TRH Down regulated by T 4 , T 3 Travels through portal venous system to cavernous sinus& to thyroid gland Stimulates several processes Iodine uptake Colloid endocytosis Growth of thyroid gland

PHYSIOLOGY THYROID GLAND REGULATION “negative Feed-back” axis Hypothalamus (TRH positive effect) Pituitary gland ( TSH, positive effect ) Thyroid gland T3 & T4 ( negative effect )

Hypothalamic-Pituitary-Thyroid Axis Negative Feedback Mechanism

Thyroid Hormone Majority of circulating hormone is T 4 98.5% T 4 1.5% T 3 Total Hormone load is influenced by serum binding proteins Albumin 15% Thyroid Binding Globulin 70% Transthyretin 10% Regulation is based on the free component of thyroid hormone

T 4 is the primary secretory product of the thyroid gland, which is the only source of T 4 The thyroid secretes approximately 70-90 g of T 4 per day T 3 is derived from 2 processes The total daily production rate of T 3 is about 15-30 g About 80% of circulating T 3 comes from deiodination of T 4 in peripheral tissues About 20% comes from direct thyroid secretion

T 4 is biologically inactive in target tissues until converted to T 3 T 3 then becomes the biologically active hormone responsible for the majority of thyroid hormone effects The liver is the major extra thyroidal T 4 conversion site for production of T 3 Some T 4 to T 3 conversion also occurs in the kidney and other tissues

T 4 Disposition Normal disposition of T 4 About 41% is converted to T 3 38% is converted to reverse T 3 (rT 3 ), which is metabolically inactive 21% is metabolized via other pathways, such as conjugation in the liver and excretion in the bile Normal circulating concentrations T 4 4.5 -11 g/ dL T 3 60-180 ng / dL (~100-fold less than T 4 )

Free Hormone Concept Only unbound (free) hormone has metabolic activity and physiologic effects Free hormone is a tiny percentage of total hormone in plasma (about 0.03% T 4 ; 0.3% T 3 ) Total hormone concentration Normally is kept proportional to the concentration of carrier proteins Is kept appropriate to maintain a constant free hormone level

Effect of the Hormone Calorigenesis Affects growth and development CNS development and function Affects CH2O,fat and protein metabolism Muscle metabolism Electrolyte balance Affects every organ function

Thyroid Evaluation TRH TSH Total T 3 , T 4 Free T 3 , T 4 RAIU Thyroglobulin Antibodies: Anti-TPO, Anti- TSHr

THYROID GLAND DISORDERS HYPOTHYROIDISM Primary Iodine defficiency Congenital (1 in 3000 to 4000 ) Infiltrative disorders Autoinmune (Hashimoto´s) Iatrogenic Surgery or 131 I Drugs: amiodarone, lithium

Hypothyroidism ………….. Secondary Pituitary gland destruction Isolated TSH deficiency Hypothalamic disorders

Hypothyroidism Cause Hormone concentrations Goitre Primary failure of thyroid gland T 3 and T 4 ,  TSH Yes Secondary to hypothalamic or pituitary failure T 3 and T 4,  TSH and/or  TRH No Dietary iodine deficiency T 3 and T 4 ,  TSH Yes

HYPOTHYROIDISM Symptoms: Tiredness Weakness Dry skin Sexual dysfunction Hair loss Difficulty concentrating Signs: Bradycardia Dry coarse skin Puffy face, hands and feet Diffuse alopecia Peripheral edema Delayed tendon reflex & relaxation Carpal tunel syndrome Serous cavity effusions .

HYPOTHYROIDISM CONGENITAL HYPOTHYROIDISM Prevalence: 1 in 3000 to 4000 newborns Cause - Dysgenesis 85% - Inborn error of thyrosine synthesis-10% Dx: Blood screning (TSH &/or T4) Treatment: Supplemental Rx. With Levothyroxine is “essential” for a normal C.N.S. Development and prevention of mental retardation

Goiter Chronic enlargement of the thyroid gland not due to neoplasm Euthyroidism , Hypothyroidism or Hyperthyroidism Goiter may be congenital or acquired, endemic, or sporadic Endemic goiter Areas where > 5% of children 6-12 years of age have goiter Common in China and central Africa Sporadic goiter Areas where < 5% of children 6-12 years of age have goiter Familial

Iodine deficiency Iodide uptake is a critical first step in thyroid hormone Synthesis. Iodine deficiency , there is an increased prevalence of Goiter. When deficiency is severe, hypothyroidism and cretinism develops. Iodine deficiency remains the most common cause of preventable mental deficiency

IDD Problem Pyramid It's worldwide major public health problem. Globally 1.5 billion- risk of Iodine deficiency disorders. The pyramid shows the visible effects of Iodine Deficiency Disorders (IDD) Goitre and Cretinism account only for 1--10% of these, Whereas 90% of the effects remain hidden . 1%-10% 5% -30% 30% - 70% Goitre & Cretinism Some brain damage Less active population due to decreased thyroid function (hypothyroidism )

Effect of Iodine Deficiency World’s single most significant cause of preventable brain damage and M.R. is Deficiency of Iodine.

Current Research indicates that iodine deficiency result in lowering the average intelligence of the entire school age population by as much as 10 to 15 points so 400 millions IQ points are missed by 40 million children. So preventing deficiency raises the learning capacity of school children and improves school performance.

Iodine Deficiency Iodine deficiency in pregnant woman may cause miscarriages, stillbirths, and birth defects. Iodine deficiency impairs growth and development of children .

Iodine Deficiency Decreased IQ, mild neurological deficits, cretinism, goitre stillbirths & neonatal deaths

Cretinism It results in MR and stunted growth. Shows up in young child or infants Can be caused by lack of iodine in the patients diet, medicines such as Nitroprusside, lithium, or iodides Endemic cretinism includes 2 different but overlapping syndromes — a neurologic type and a myxedematous type Symptoms: Constipation, thickening skin Signs: trouble feeding the patient, choking on their food, thick tongue, dry brittle hair, short thick neck, hoarse voice, Cure/Treatment: Treatable if it is caught in the early stages of childbirth. Replacement therapy with thyroxin is a common treatment

Before after treatment in myxedematous cretinism

Iodine requirement To meet iodine requirements, the current recommended daily iodine intakes are: 50mg for infants (first 12 months of age) 90mg for children (2-6 years of age) 120mg for school children (7-12 years of age) 150mg for adults (beyond 12 years of age) 200mg for pregnant and lactating women

  Prevention of Iodine Deficiency Salt iodization is mandatory at the level of 20-60 ppm . The estimated percent of households consuming salt with some iodine is 91%.  The estimate of households consuming adequately iodized salt (15ppm or above) is 63%.