pathophysiology of thyroid disorders.pptx

MYXOEDEMA
Adult onset severe hypothyroidism
Non pitting edema due to accumulation of hydrophilic mucopolysaccharides

Decreased serum levels of T3 & T4, increased serum levels of TSH (thyroid stimulating hormone)

Etiopathogenesis:
Ablation (decreasing the function) of the thyroid gland by surgery or radiation
Autoimmune (lymphocytic) thyroiditis
Endemic or sporadic goitre
endemic goitre= occurs when thyroid enlargement (iodine deficiency) is seen in more than 10% population in an area.
sporadic goitre= enlargement of thyroid gland in iodine sufficient area due to genetic or environment factors.
Hypothalamic pituitary lesions
Prolonged administration of anti thyroid drugs
Dyshormonogenesis (abnormal hormone synthesis due to genetic defects)

Clinical features:
Having cold intolerance
Mental and physical lethargy
Constipation
Slowing of speech and intellectual fuction
Puffiness of face
Loss of hair
altered texture of skin

Treatment:
substitution of thyroid hormones by taking thyroxine (T4) tablets usully in the form of levothyroxine.
HYPERTHYROIDISM:
Characterised by excess production of thyroid hormones
More frequent in females
Increased serum levels of T3 & T4.
T3 levels increase more than T4
when hyperthyroidism results in toxic clinical features , it is called as thyrotoxicosis

Etiopathogenesis:
Caused by many diseases
1. Primary cause= graves disease, toxic adenoma (overproduction of thyroid hormones from one or more nodules in thyroid gland)
2. secondary causes= thyroiditis, tumours of thyroid gland
Congenital hyperthyroidism in the newborn of mother with graves disease
Clinical features:
Emotional instability
Nervousness
Palpitations
Fatigue
Weight loss inspite of good appetite
Heat intolerance
Perspiration (loss of fluid through skin pores / sweating)
Menstrual disturbances
Tremors of hands
Tachycardia and cardiomegaly
Skeletal muscle weakness and osteoporosis (decrease in bone mass, bones become weak and brittle)
Exophthalmos (bulging eyes)

Treatment:
anti thyroid drugs (carbimazole, methimazole)
Partial or total removal of thyroid gland
Radioactive iodine therapy (radioactive iodine kill any remaining thyroid cancer cells that remain after surgery)
THYROIDITIS
Inflammation of thyroid gland

Types:
Acute thyroiditis:
Bacterial infection= staphylococcus, streptococcus
Fungal infection= aspergillus
Radiation injury

Chronic thyroiditis:
Autoimmune thyroiditis (Hashimoto thyroiditis)
Invasive fibrous thyroiditis

Hashimoto thyroiditis
Characterised by 3 features
Goitrous enlargement of the thyroid gland
Lymphocytes infiltration in thyroid gland
Presence of thyroid autoantibodies

Etiopathogenesis:
it occurs in association with graves disease, pernicious anaemia, diabetes mellitus type 1
Immune destruction of thyroid cells.
Presence of genes associated with this disease
Ex: DR3,DR4,DR5 genes
Activation of CD4 T cells, which induces CD8 T cell infiltration that destroys thyroid cells producing hormones.
Production of autoantibodies

1. PATHOPHYSIOLOGY OF THYROID DISEASES HYPOTHYROIDISM HYPERTHYROIDISM GRAVES DISEASE THYROIDITIS GOITRE

2. HYPOTHYROIDISM a) cretinism b) myxoedema MYXOEDEMA Adult onset severe hypothyroidism Non pitting edema due to accumulation of hydrophilic mucopolysaccharides Decreased serum levels of T3 & T4, increased serum levels of TSH (thyroid stimulating hormone) Etiopathogenesis: Ablation (decreasing the function) of the thyroid gland by surgery or radiation Autoimmune (lymphocytic) thyroiditis Endemic or sporadic goitre endemic goitre= occurs when thyroid enlargement (iodine deficiency) is seen in more than 10% population in an area. sporadic goitre= enlargement of thyroid gland in iodine sufficient area due to genetic or environment factors.

3. Hypothalamic pituitary lesions Prolonged administration of anti thyroid drugs Dyshormonogenesis (abnormal hormone synthesis due to genetic defects) Clinical features: Having cold intolerance Mental and physical lethargy Constipation Slowing of speech and intellectual fuction Puffiness of face Loss of hair altered texture of skin Treatment: substitution of thyroid hormones by taking thyroxine (T4) tablets usully in the form of levothyroxine.

4. HYPERTHYROIDISM: Characterised by excess production of thyroid hormones More frequent in females Increased serum levels of T3 & T4. T3 levels increase more than T4 when hyperthyroidism results in toxic clinical features , it is called as thyrotoxicosis Etiopathogenesis: Caused by many diseases Primary cause= graves disease, toxic adenoma (overproduction of thyroid hormones from one or more nodules in thyroid gland) 2. secondary causes= thyroiditis, tumours of thyroid gland Congenital hyperthyroidism in the newborn of mother with graves disease

5. Clinical features: Emotional instability Nervousness Palpitations Fatigue Weight loss inspite of good appetite Heat intolerance Perspiration (loss of fluid through skin pores / sweating) Menstrual disturbances Tremors of hands Tachycardia and cardiomegaly Skeletal muscle weakness and osteoporosis (decrease in bone mass, bones become weak and brittle) Exophthalmos (bulging eyes) Treatment: anti thyroid drugs (carbimazole, methimazole) Partial or total removal of thyroid gland Radioactive iodine therapy (radioactive iodine kill any remaining thyroid cancer cells that remain after surgery)

6. GRAVES DISEASE Diffuse toxic goitre (consists of diffusely enlarged thyroid gland with rubber like consistency) Also known as Basedow disease/ exophthalmic goitre Characterised by triad of features: hyperthyroidism, thyroid enlargement, ophthalmopathy (eye diseases including exophthalmos) Usually occurs in people of 30- 40yrs age more prevalent in women

7. Etiopathogenesis It is an autoimmune disease having similarities with Hashimoto thyroiditis and these two diseases may coexist in the same patient. Development of the disease is associated with presence of genes DR3 & CTLA-4 (cytotoxic lymphocyte associated antigen gene) Production of autoantibodies ex: thyroid stimulating immunoglobin (antibody) = stimulates TSH receptor on the thyroid gland and stimulates the release of thyroid hormones. Clinical features: Enlarged thyroid gland Exophthalmic eyes Lid retractions, weakness of eye muscles, stare, and in extreme cases the lids can no longer close and may produce corneal injuries and ulcerations. Palpitations Irregular heart rate Fatigue Menstrual irregularities Hand tremors Treatment: Antithyroid drugs Surgery Radioactive iodine therapy

8. THYROIDITIS Inflammation of thyroid gland Types: Acute thyroiditis: Bacterial infection= staphylococcus, streptococcus Fungal infection= aspergillus Radiation injury Chronic thyroiditis: Autoimmune thyroiditis (Hashimoto thyroiditis) Invasive fibrous thyroiditis

9. Hashimoto thyroiditis Characterised by 3 features Goitrous enlargement of the thyroid gland Lymphocytes infiltration in thyroid gland Presence of thyroid autoantibodies Etiopathogenesis: it occurs in association with graves disease, pernicious anaemia, diabetes mellitus type 1 Immune destruction of thyroid cells. Presence of genes associated with this disease Ex: DR3,DR4,DR5 genes Activation of CD4 T cells, which induces CD8 T cell infiltration that destroys thyroid cells producing hormones. Production of autoantibodies which form a coat over thyroid cells leading to their destruction, decreasing hormone production

10. Clinical features: Enlarged thyroid gland, usually associated with hypothyroidism low serum levels of T3, T4 Only a few cases develop hyperthyroidism, called as Hashitoxicosis Increased risk of thyroid carcinoma Weight gain or weight loss Excess sweating Cold intolerance Menstrual irregularities Treatment: Levothyroxine Radioactive iodine therapy

11. GOITRE Refers to thyroid enlargement caused by compensatory hyperplasia and hypertrophy of the follicular epithelium in response to thyroid hormone deficiency. There are 2 forms of goitre: simple goitre nodular or multinodular goitre (end stage goitre) Simple goitre This type of goitre occurs when the entire thyroid gland swells and feels smooth to touch. defects in hormone synthesis and production due to lack of iodine Increase in TSH levels Often appears at puberty or in adolescence In some patients it may progress to nodular goitre Etiopathogenesis: occurs in 2 forms Endemic goitre: Defined as prevalence of goitre in an area in more than 10% of the Population. Ex: in mountain region where there is iodine deficiency in food and water. Caused by goitrogens which interfere with synthesis of thyroid hormones.

12. b) Sporadic (non-endemic) goitre Occurs due to: Hereditary defect in thyroid hormone synthesis and transport Dietary goitrogens Low intake of iodine or sufficient Errors in iodine metabolism Nodular goitre Characterised by most extreme degree of tumour-like enlargement of the thyroid gland and presence of nodules Causes cosmetic disfigurement, dysphagia and choking due to compression of the oesophagus and trachea Etiopathogenesis: Follicular epithelial cell hyperplasia (generation of new follicles) Irregular accumulation of colloid in follicles leading to increased tension and stress in thyroid gland causing rupture of follicles. > leading to haemorrhage scarring and sometimes calcification resulting in development of nodular pattern.

13. We can also classify goitre into: Hyperthyroid goitre: increased TSH causes enlargement of thyroid and also secretes more T4, resulting in hyperthyroidism with goitre ex: graves disease b) Euthyroid goitre: inadequate iodine in food decreases the secretion of T4 which causes the pituitary to secrete more TSH. Now TSH causes the thyroid gland to enlarge enough to make sufficient T4 c) Hypothyroid goitre: if dietary iodine is severely reduced , even an enlarged gland will not be able to make enough T4. The gland will keep on growing under the influence of TSH but may never be able to make enough T4 Clinical features: Difficulty in breathing and swallowing Heat intolerance Weight gain Palpitations Mental retardation Treatment : goitre with hypothyroidism treated with levothyroxine and goitre with hyperthyroidism is treated with antithyroid drugs. If goitre is due to lack of iodine then iodine intake should increase