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32 Cards in this Set
- Front
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What are the main cells which make up the thyroid gland? Describe how they change in shape unde the infuence of TSH |
- thyroid follicles -when follicular cells are inactive, their shape is low cuboidal tosqaumous; when influenced by TSH, their shape is low columnar tocuboidal |
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What hormones are produced in the thyroid and from what cells types? |
- tetraiodothyronine (T4) and triiodothyronine (T3) (follicular cells) - calcitonin (parafollicular cells) |
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Describe the formation, and release of thyroid hormone (essay answer) |
(1) iodide taken up from blood into follicular cells by Na/I symporter (2xNa/1xI) (2) Iodide is secreted from follicular cells into the colloid via pendrin channels (Cl/I- symporters), and thyroglobulin is secreted by exocytosis. (3) iodide is conveted iodine (I2) by thyroid perxidase in the thyroglobulin (4) in the presence of thyroid oxidase, iodine and thyroglobulin combine via a iodination reaction on tyrosines, producing monoiodotyrosine (T1) and diiodotyrosine (T2) (5) thyroid peroxidase catalyses the conjugation of monoiodityrosine and diiodotyrosine, forming tetraiodothyronine (T4) and triiodotyrosine (T3). T4 can also be broken down to Reverse T3 (RT3) (6) megalin receptors enable the endocytosis of colloid back into the follcular cells (7) vesicles fuse with lysosymes and and proteolytic enzymes cleave bonds holding T3 and T4 to the thyroglobulin (8) T3 and T4 are both lipid-soluble so are able to diffuse directly from the follicular cells into the blood vessels |
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Describe how the production of thyroid hormones is stimulated and regulated (essay answer) |
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Describe how thyroid hormones interact with target cells and exert their effect (4) |
- T3 and T4 diffuseacross target cell membranes - T4 converted to T3 by5-deiodinase - T3 binds to a nucelarthyroid receptor that complexes with a retinoid X receptor (RXR) -the receptor complex binds to thyroid-response elements on DNA,inducing transcription |
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Give 8 functions of thyroid hormones |
-increase basal metabolic rate -increase synthesis of Na-K ATPases -increase body temperature (calorigenic effect) -stimulate protein synthesis -increase consumption of glucose and fatty acids for ATP synthesis -stimulate lipolysis -enhance some actions of catecholamines -regulate growth and development of nervous tissue and bones |
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Describe how thyroid hormones increase metabolic rate (4) |
-increased consumption of O2 at rest -produces heat -increased consumption of carbohydrate, lipids and proteins -increased expression of “always on” Na K ATPase |
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Describe how thyroid hormones are involved in growth and development |
-thyroid hormones stimulate the growth of nervous tissue and bone -influences timing and rate of development of nerves -influences bone growth in children (ossification and linear growth) |
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Describe how thyroid hormones are involved in macronutrient metabolism |
-T3 and T4 increase the rate of glucogenolysis and gluconeogenesis -increases lipogenesis by promoting production of lipolytic enzymes |
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List 10 presentations of hyper/hypo thyroidism and they are affected in the 2 states |
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List >10 symptoms of hypothyroidism List >10 symptoms of hyperthyroidism |
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What is the difference between primary and secondary hypothyroidism |
- primary is due to a problem with the thyroid - second\ry is due to a problem with the hypothalamic-pituitary axis |
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Other than Hashimoto's thyroiditis, list and briefly describe 7 causes of hypothyroidism. |
- congenital hypothyroidism: deficiency in thyroid hormones from birth - iatrogenic hypothyroidism: whenpeople have been treated for hyperthyroidism, causing hypothyroidism - De Quervain's thyroiditis: inflammation of the thyroid due to viral infection e.g. mumps, adenovirus - atrophic (autoimmune): anti-thyroidautoantibodies resulting in lymphoid infiltration of the thyroidgland. Causes atrophy and fibrosis of the gland - post partum thyroiditis: cancause hypo or hyper thyroidism – or both (one followed by theother)-thought to be due to necessary modifications to the immune systemwhich occur during pregnancy - iodine deficiency: lackof dietary iodine means there is an increase in TSH to try andstimulate production of more T3 and T4. Overstimulation of thethyroid is what causes goitre |
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What gender is most likely to have atrophic (autoimmune) hypothyroiditis, and by how much? |
- 6times more common in woman than men and increases with age |
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Other than Graves disease, list and briefly describe 5 causes of hyperthyroidism |
- De Quervain's thyroiditis: inflammation of the thyroid due to viral infection e.g. mumps, adenovirus - Toxicmultinodular goitre: benign tumour of the thyroid-hormone that arises from follicular cells causing excessive thyroid hormone production - Thyroiditis: typically due to infection of lymphocytic infiltration. Inflammation causes leakage of stored steroid hormone – causingthyrotoxicosis. Inflammation can also hinder hormone production and damage caneventually result in hypothyroidism. Hashimoto's thyroiditis is anexample of this - Drug-induced: thyroxine overdose is the most common. Amiodarone (anti-arrhythmic) can cause both - Hamburgerhyperthyroidism: causedby eating beef contaminated with thyroid gland |
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Who is most likely to be affected by Hashimoto's thyroiditis? List 5 environmental triggers of Hashimoto's What gene is associated with Hashimoto's? |
- morecommon in women than men and more common in late middle age - iodine,medications, infection, smoke and possibly stress - HLA-DR5 (Goitrous form) |
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What are the three mechanisms of damage in Hashimoto's |
(1)CD8+ cytotoxic T-cell mediated death: target follicular cells(thyrocytes) (2)cytokine-mediated cell death: due to a result of T-cell mediatedproduction of inflammatory Th1 cytokines. Causes recruitment ofmacrophages and subsequent damage. (3)binding of anti-thyroid antibodies followed by antibody-dependentcell-mediated cell toxicity |
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What is Grave's disease? Whatare the most common risk factors (2)? What is protective? |
- autoimmuneassociated with stimulating TSH receptor antibodies - femalegender and smoking is a risk factor - moderate alcoholconsumption is protective |
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Describe the pathophysiology of Grave's disease |
(1)Thyroid stimulating immunoglobulin: -IgG antibody which binds to TSH receptor and mimics TSH -stimulates adenyl cylcase, increasing hormone production -thyroid-stimulating antibodies are relatively specific to Grave's (2)Thyroid growth-stimulating antobodies: - also directed against TSH receptor -implicated in proliferation of the thyroid follicular epithelium (3)TSH-binding inhibitor immunoglobulins: -anti-TSH receptor antibodies prevent TSH from binding normally to theTSH receptor -this can result in abnormal activity or binding -in some cases it can inhbit thyroid cell function, which may explainwhy people with Grave's have periods of hypothyroidism |
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Describe the pathophysiology of Grave's ophthalmology |
(1)infiltration of the retro-orbital space by mononuclear cells –mainly T cells (2)inflammatory oedema and swelling of extraocular muscles (3)accumulation of extracellular matrix components e.g. hyaluronic acidand chondroitin sulphate (4)increased deposition of fatty deposits -displaces the eyeballs forward and can interfere with vision |
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List the diagnostic criteria of hypothyroidism (3) |
-high serum TSH confirms primary hypothyroidism -low free T4 confirms hypothyroid state -thyroid and organ-specific antibodies may be present |
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List the supportive clinical features of hypothyroidism (5) |
-anaemia -increased serum aspartate transferase (from muscle and/or liver) -increase serum creatine kinase levels -hypercholesterolaemia -hyponatraemia |
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What is the diagnostic criteria for hyperthyroidism (3) |
-suppressed serum TSH (<0.05 mU/L) – rarely hypersecreted -raised free T3 or T4 confirms diagnosis (T3 is more sensitive) -thyroid peroxidase and thyroglobulin antibodies (Grave's) |
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What are the 3 main types of treatment for hyperthyrodism? |
- antithyroiddrugs - radioiodine - surgery |
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Name 3 antithyroid drugs How do they work? |
-carbimazole (most common), propylthiouracil and thiamazole (methimazole) -inhibit the formation of thyroid hormones (methimazole also acts as a immunosuppressive) -thought to inhibit iodination of tyrosyl residues in thyroglobulin -competitively inhibits interaction with tyrosine -propylthiouracil has an additional effect: reduces deiodination of T4to T3 |
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What is the benefit of beta blockers in hyperthyroidism (2)? |
-reduces risk of embolli -reduces atrial fibrilation |
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Describe the use of surgery in hyperthyrodism |
-thyroidectomy -reduce levels of T3 and T4 -has associated risks:damage to the recurrent laryngeal nerve (risk ofhoarseness) and risk of hypothyroidism |
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What groups are contrindicated for treatment with radoiiodine (2) |
- those pregnant and breatfeeding |
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Describe the use of radioiodine for treatment |
-131 iodine is given in an empirical dose as it has variable uptakeand there is radiosensitivity of the gland -mechanism is to accumulate in the gland and gradually destroy it vialocalised radiation-takes several months -antithyroid drugs are contraindicated 4 days before and days after -many do not need to re-start antithyroid medication after -short term side effects; discomfort in the neck; worsening ofhyperthyroidism (can be given propranolol and carbimazole can berestarted); eye problems may get worse in people with dythyroid eye -long-term: many will have hypothyroidism; 75% are euthyroid in theshort term; some may remain hyper thyroid and require second dose;risk of carcinogenesis though no strong evidence |
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Describe the treatment of hypothyroidism |
-no drugs used to specifically augment the function of the thyroidgland -instead, thyroid hormones are administered directly as a replacement -thyroxine and triodothyronine are given orally -the latter has a faster onset though shorter duration of action. |
