RED Endocrine 7 Learning objectives PDF

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Summary

1. Describe the regulation of thyroid hormone secretion (endocrine axis).The hypothalamus secretes thyrotropin releasing hormone TRH and this positively impacts the anterior pituitary to secrete TSH thyroid stimulating hormone. TSH has a positive effect on the thyroid gland and stimulates the synthe...

Description

1. Describe the regulation of thyroid hormone secretion (endocrine axis). The hypothalamus secretes thyrotropin releasing hormone TRH and this positively impacts the anterior pituitary to secrete TSH thyroid stimulating hormone. TSH has a positive effect on the thyroid gland and stimulates the synthesis and release of the thyroid hormones T3 and T4. There is a short feedback loop where high levels of TSH have a negative effect on the hypothalamus so there is less secretion of TRH. There is a long feedback loop and this negative feedback occurs if there are high levels of T3 and T4, inhibiting 1 and 2 levels above the thyroid gland to reduce the stimulation on the thyroid gland to produce more thyroid hormone.

2. State how the thyroid hormones are transported in the plasma and briefly describe the peripheral conversion of T4 to T3 or reverse T3. Thyroid hormones are lipophilic and therefore insoluble in blood plasma and must be protein bound to travel around the body. T3 and T4 are highly protein bound with less than 1 % in the free unbound form which is the only active form, the protein bound form is biologically inert. T4 functions as a prohormone and in target cells and tissues T4 is converted into T3 by deiodinase enzymes which convert T4 into mostly T3 and rT3 ( inactive)

3. Describe briefly the effects of thyroid hormone and the consequences of excessive or deficient hormone action. Actions of thyroid hormones   

Increase metabolism in the body - Generalized increase in functional activity of almost all tissues Stimulate growth and development (particularly important for normal development and maturation of CNS) Thyroid hormones upregulate Beta-adrenoceptors, synergistic with actions of SNS / catecholamines

Excessive action: High metabolic activity, increased maturation of CNS, increased growth and development and more Beta- adrenoceptors Deficient action: low metabolic activity, decreased maturation of CNS, decreased growth and development and less Beta- adrenoceptors

4. State the main causes, signs and symptoms of hyperthyroidism and hypothyroidism, and how these thyroid disease conditions can be treated. Hyperthyroidism- high thyroid hormone levels= more metabolic activity 

Graves Disease- Abnormal levels of thyroid-stimulating immunoglobulins ( TSI) Get HIGH levels of T3 and T4 and LOW TSH ( TSI activates the TSH receptors therefore you still get a diffuse goitre) Get build up of lymphocytes in the soft tissues of the eye causing exophthalmos

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Secondary to excess hypothalamic or ant. pituitary secretion. Get LOW T3 and T4 and HIGH TSH, get a diffuse goitre

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Hyper-secreting thyroid tumour- (Toxic multinodular goitre, toxic adenoma) HIGH T3 and T4, LOW TSH ( due to negative feedback on the hypothalamus and ant pit) but get goitre because the tumour as a mass is causing an enlarged thyroid gland get nodular goitre

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Iatrogenic causes (e.g. amiodarone, lithium)

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Excessive action: Nervousness, palpitations, tremor, sweating, goitre, anxiety , Heat intolerance, diarrhoea, increased HR and Arterial blood pressure, weight loss due to high metabolic rate (BMR)

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Treatment : -

Radioactive iodine- First line for older patients with nodular goitres

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Single drink or capsule, max effect 2-4 months after

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Surgery- Thyroidectomy, for severe thyrotoxicosis ( severely high levels of T3 and T4) with a large goitre or concern about tumour development

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Anti-thyroid drugs o Decrease the production of thyroid hormones by inhibiting the iondination and coupling process via TPO. Used for 1218 months o Carbimazole and propylthiouracil ( thionamides)

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Non selective Beta Blockers- propranolol and nadolol o Reduce the actions of the catecholamines and get rapid sympathetic relief of tremours, palpitations and anxiety

Hypothyriodism – low thyroid hormone levels= less metabolic activity 

Hashimoto’s thyroiditis - Primary failure of thyroid gland LOW T3 and T4, HIGH TSH get a goitre. Chronic autoimmune disease against substances like thyroglobulin and thyroid peroxidase (TPO)

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Secondary to hypothalamic or ant. pituitary failure- LOW T3 and T4, LOW TSH due to ant pit and hypth failure

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Lack of dietary iodine (simple non-toxic goitre)- LOW T3 and T4, HIGH TSH Drug-induced (e.g. anti-thyroid drugs, lithium, amiodarone) Radioactive iodine therapy Thyroid hormone resistance Deficient action: confusion, depressed, cold intolerance, constipation, decreased HR and arterial blood pressure, dry skin, hoarse voice and menstrual problems, weight gain due to low BMR Management – synthetic thyroid hormones o With T4- levothyroxine- treatment of choice

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o With T3- liothyronine- can induce heart failure due to rapid onset and potency. Used in severe hypothyroid states when rapid response is neededgiven by IV

5. State where parathyroid hormone (PTH) and calcitonin are produced, and their roles on calcium homeostasis (PTH also in Lecture K6). The parathyroid hormone is produced by the 4 small parathyroid glands located on the posterior surface of the thyroid gland. Parathyriod hormone acts to increase Ca2+ plasma levels and therefore opposes the actions of calcitonin Calcitonin is produced by the parafollicuar C cells and acts to reduce plasma Ca2+ levels. Cali- calcium, tonin- to bring down. Not a thyroid hormone as it isn’t based on tyrosine....