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Flashcards by Hannah Tribe, updated more than 1 year ago
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Created by Hannah Tribe
almost 10 years ago
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| Question | Answer |
| Give 2 functions of the thyroid gland. | 1. Development, especially of the CNS and bone. 2. Metabolism. |
| What is the arterial supply to the thyroid gland? | Superior thyroid artery - branch of the external carotid artery. Inferior thyroid artery - branch of the thyrocervical trunk of the subclavian artery. |
| Describe the histology of the thyroid gland. | Large follicles filled with colloid, surrounded by follicular cells. Parafollicular cells exist in the interstitial spaces between follicles. |
| What is the function of the parafollicular cells? | Secrete calcitonin |
| What stimulates the synthesis of thyroid hormones? | TSH (thyroid stimulating hormone) released from the anterior pituitary gland upon stimulation from TRH (thyrotropin releasing hormone) released from the hypothalamus. |
| What is the first stage of synthesis of thyroid hormone? | 'Trapping' of iodine in the follicular cell - it enters by active transport by Na+/I- symporter (NIS) - Na+ concentrations maintained by Na+/K+ ATPase pumps at basolateral membrane. |
| How does iodide leave the cell at the apical surface? | Pendrin transporter |
| What is the first reaction that iodine undergoes? | Reacts with hydrogen peroxide (H2O2) under the action of thyroid peroxidase enzyme, to form an intermediate compound. |
| What happens to the intermediate compound? | The intermediate gets incorporated into tyrosine residues on thyroglobulin molecules within the colloid. |
| What is this process called? | Organification |
| What can inhibit this process? | Thionamides |
| What is the last stage in the synthesis of TH? | The molecules couple and form the thyroid hormone that has either 3 or 4 iodide groups, and are stored in the colloid. |
| How does TH become secreted? | Upon stimulation by TSH, droplets of colloid containing the thyroid hormone-thyroglobulin complex enter the follicular cells by pinocytosis, where they fuse with a lysosome. The lysosome hydrolyses the thyroglobulin protein and releases T3 and T4 into the circulation. |
| How does TH travel in circulation? | Mostly bound to plasma proteins |
| Which is the active form of TH? | T3 |
| So what happens to the other form? | T4 can be converted to T3 by deiodination by D2 enzyme |
| What controls the secretion of TH? | Negative feedback loop. When levels of T3 and T4 are high, TSH release from the anterior pituitary is inhibited, as is release of TRH from the hypothalamus. |
| How does TSH stimulate production of TH? | Binds to GPCRs that activate the Gs and Gq pathways. The Gs effects cause increased iodide uptake due to increased transcription of NIS. The Gq effects cause increased iodide efflux, increased H2O2 production and increased iodination. |
| How can TSH produce a diffuse goitre? | If there is iodide deficiency, less TH can be synthesised. The negative feedback loop detect low TH so tries to stimulate it by secreting more TSH. This causes all the effects of TSH to occur more, yet no increase in TH as there is still not enough iodide. Thyroid gland grows as it is trying to produce hormone. |
| Where are TH receptors found, and which form of TH do they have higher affinity for? | In the nucleus, with higher affinity for T3 |
| How does binding of TH to the receptor cause any effect? | Receptors dimerize and combine with other transcription factors to induce gene transcription. |
| What are the effects of TH binding to the THR? (2) | 1. Metabolic Rate increases (increased no. and size of mitochondria, increased enzymes and increased activity of Na+/K+ ATPase pumps) 2. Positive inotropic and chronotropic effects on the heart. |
| What is the most common cause of primary hyperthyroidism? | Grave's disease |
| What is the cause of this disease? | The body produces autoantibodies to the TSH receptor, which cause the TSH receptors in the thyroid gland to be activated even when TSH is not present, resulting in uncontrolled release of TH. |
| What would be the measured levels of TH and TSH in a person with Grave's disease? | High circulating TH levels, low levels of TSH |
| What are the pathophysiological symptoms of Grave's disease? (5) | 1. Increased heart rate (Tachycardia) 2. Weight loss (but increased appetite) 3. Feeling tired and restless 4. Diffuse goitre 5. Ophthalmopathy |
| What are the physical signs of Grave's disease? (9) | 1. Onycholysis (detaching nails) 2. Vitiligo (loss of pigment in areas of skin) 3. Acropachy (finger clubbing) 4. Dermopathy 5. Periorbital oedema 6. Lid lag 7. Chemosis (eye inflammation) 8. Proptosis (abnormal protrusion of the eye) 9. Ophthalmoplegia (paralysis of eye muscles) |
| How does Grave's cause ophthalmopathy? | The autoantibodies produced to the TSH receptor also bind to proteins in the fatty tissue behind the eye and cause inflammation. |
| What is secondary hyperthyroidism and how is it different to primary? | In secondary hyperthyroidism, there is a problem in the pituitary gland causing uncontrolled high release of TSH, which stimulates a high level of secretion of TH. This causes TH levels to be high, but not due to a problem with the thyroid gland, unlike in primary hyperthyroidism. |
| From investigations, how would you distinguish between primary and secondary hyperthyroidism? | In primary hyperthyroidism, levels of TH would be high but TSH low, whereas in secondary hyperthyroidism, both levels would be high, as the problem is with the pituitary gland secreting high levels of TSH. |
| What are 3 drug options for patients with hyperthyroidism? | 1. Thiocarbamides such as Carbimazole, which prevent iodination of tyrosine residues by TPO 2. Beta blockers to reduce cardiovascular effects 3. Glucocorticoids to reduce eye inflammation. |
| What are the other 2 options for more severe cases? | 1. Thyroidectomy 2. Radioactive iodine, which destroys thyroid cells. |
| What is Hashimoto's? | An autoimmune disease causing primary hypothyroidism. |
| What causes it? | Autoantibodies are produced which attack the thyroid gland itself, causing it to be unable to produce TH. |
| What are the characteristic levels of TH and TSH in a person with Hashimoto's? | Low levels of TH, but high levels of TSH, as the negative feedback loop detects low TH so tries to stimulate more to be secreted. |
| What are the symptoms of Hashimoto's? | 1. Lethargy (due to low energy and slow metabolism) 2. Intolerance to the cold 3. Lack of growth and development (hair loss, late puberty) 4. Diffuse goitre (due to effects of high TSH and infiltration of lymphocytes due to damage done by autoantibodies) |
| What is euthyroidism? | Normal thyroid function |
| What is the difference between primary and secondary hypothyroidism, and how can they be distinguished on investigation? | Primary hypothyroidism is a result of defective thyroid gland, so TH levels would be low, yet high levels of TSH due to negative feedback loop. On the other had, levels of both TH and TSH would be low in secondary hypothyroidism, as there is also a problem in the pituitary gland causing decreased production of TSH. |
| What is the main treatment for hypothyroidism? | Thyroxine (T4) |
| What are 3 types of thyroiditis? | 1. Hashimoto's thyroiditis 2. Post-partum thyroiditis (resolves after a year or so) 3. Acute thyroiditis (due to infection) |
| Depending on the size of the goitre, what could 3 possible effects be? | 1. Dysphagia 2. Dysphonia (trouble speaking) 3. Dyspnoea |
| If tumours or nodules are suspected in the thyroid, what can be done to test this? | Fine Needle Aspiration (FNA) to take a small sample from the nodule and examine it under the microscope. If tumours are found, surgery is usually performed to remove them. |
| What is thyroid storm? | An extreme case of hyperthyroidism in which levels of TH reach dangerously high levels. |
| What causes thyroid storm? (3) | 1. Severely undertreated hyperthyroidism 2. Untreated hyperthyroidism 3. Infection associated with hyperthyroidism |
| What are the symptoms? (5) | 1. Very high HR, BP 2. Fever 3. Confusion 4. Diarrhoea/Vomiting 5. Unconsciousness |
| What can stimulate a thyroid storm in patients with hyperthyroidism? (3) | 1. Trauma 2. Emotional distress 3. Surgery |
| How is thyroid storm diagnosed? | High TH levels with very low TSH levels |
| What is the treatment for thyroid storm? | Admit to hospital, and give beta blockers to reduce cardiovascular effects, give carbimazole to lower TH levels. Also give supportive care such as hydration, cooling blankets and antipyretics (not aspirin) to make patient more comfortable. |
| What is myxoedema coma? | A state of severe hypothyroidism, associated with high mortality. |
| What are the symptoms of this? (8) | 1. Dry skin 2. Thin hair 3. Hoarse voice 4. Myxoedema 5. Fatigue, apathy or unconsciousness 6. Usual symptoms of hypothyroidism 7. Extreme low HR and BP 8. Low core temperature |
| What can bring on myxoedema coma? (3) | 1. Hypothermia 2. Infections 3. Drugs |
| What are the 3 main causes of myxoedema coma? | 1. Undiagnosed hypothyroidism 2. Discontinuation of therapy or running out of medication for hypothyroidism 3. Iatrogenic causes |
| What will the levels of TH and TSH be? | Low TH and very very high TSH |
| What is the treatment for myxoedema coma? | 1. Supportive care to bring up their vitals 2. Thyroxine based drugs to raise TH levels |
| What hormone helps to regulate calcium levels in the body? | Parathyroid hormone (PTH) |
| Where is this secreted from? | Parathyroid glands, on posterior surface of thyroid (4 in total) |
| When they detect low levels of Ca++, what is the response? | Low levels of Ca++ cause release of PTH, to stimulate bone resorption (allowing release of Ca++ and phosphate), increased reabsorption of Ca++ from the kidneys and increased absorption of Ca++ from the gut. |
| If parathyroid function is impaired, what can this lead to? | Hypercalcaemia |
| What are possible clinical features of this? (4) | 1. Kidney stones 2. Weak bones 3. Abdominal pain 4. Impaired cognition |
| What are possible drug treatments for hypercalcaemia? | 1. Saline (enhances kidney filtration and thus excretion of Ca++) 2. Furosemide (inhibits Ca++ reabsorption in the DCT of kidney) 3. Bisphosphonate (inhibit activity of osteoclasts) 4. Glucocorticoids (inhibit conversion of vit D to calcitriol) |
| When might you consider surgery for patients with hyperparathyroidism? (3) | 1. If they are younger than 50 2. If they have severe symptoms of hypercalcaemia 3. If they have significantly decreased bone mass |
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