hyperthyroidism

Question 1

2 causes of hyperthyroidism

Answer 1

graves disease nodular goitre/plummers disease

Question 2

features of graves (types of antibodies)

Answer 2

autoimmune as well- antibodies bind to TSH receptor in thyroid antibody 1 causes thyroid gland to grow and make thyroxine (goitre)= hyperthyroidism antibody 2 causes eyes to swell- binds to muscles behind eye= exopthalmos 3 causes swollen shins (pretibial myxoedema)- non-pitting when you press on it

Question 3

features of graves eye disease

Answer 3

pushes eyes forward, keeping eyes open eyelids also kept open by adrenaline

Question 4

feature of goitre and uptake test

Answer 4

smooth as whole gland enlarges- thats why in thyroid uptake test, radioactive iodine taken up by whole gland

Question 5

features of plummers disease

Answer 5

not autoimmune, caused by benign tumour which is overactive, producing excessive T4 therefore no pretibial myxoedema or exophthalmos

Question 6

neck in plummers disease and thyroid uptake test DIAGRAM

Answer 6

not smooth, a bulge forms on one side- the rest of the thyroid is fine and TSH is low, so it becomes smaller (although overall due to tumour patient still has hyperthyroidism) in radioactive uptake test, only the HOT TOXIC NODULE takes iodine, rest of gland doesn’t

Question 7

effect of T4 on SNS

Answer 7

beta adrenoreceptors sensitised to normal levels of adrenaline/NA= tachycardia, tremor in hands, palpitations and lid lag (eye lid doesn’t come down with eyeball as adrenaline holds it back)

Question 8

features of hyperthyroidism

Answer 8

weight loss with increased appetite SNS symtpoms sweating heat intolerance diarrhoea breathlessness

Question 9

thyroid storm: danger and symptoms

Answer 9

excessive levels T4, with half of mortality untreated, so aggressive treatment needs hyperpyrexia (above 41 degrees), excessive tachycardia/arrhythmia, cardiac failure, confusion and jaundice- any 2 of these+ hyperthyroidism= admission into hospital

Question 10

treatment of hyperthyroidism and their effect

Answer 10

thioamides (antithyroid drugs) potassium iodide radioiodine beta blockers first 3 reduce T4, last reduces symptoms

Question 11

use of thioamines

Answer 11

daily treatment of hyperthyroidism (graves/toxic nodule) treatment before thyroidectomy (keeps thyroid function normal- also better to cause anaesthesia and patient less anxious) reduces symptoms whilst waiting for radioiodine to work

Question 12

thyroid hormone synthesis DIAGRAM

Answer 12

uptake of iodide by active transport, then iodination of thyroglobulin using thyroperoxidase and H2O2 coupling reaction occurs then storage in colloid iodinated thyroglobulin then endocytosed using same enzyme and secreted as T4/3

Question 13

mechanism of thionamides and problem, and solving problem

Answer 13

inhibits thyroid peroxidase= T3/4 synthesis and secretion store of thyroid hormone in colloid can still be used, thionamides simply stop production of new T3/4, hence clinical effect (reduction in symptoms) takes weeks thus, treatment involves beta blocker called propranolol to rapidly reduce tremor and tachycardia

Question 14

other mechanisms of thioamides

Answer 14

reduces antibody production reduces conversion of T4 to T3 in peripheral tissues (PTU)

Question 15

unwanted effects of thionamides

Answer 15

agranulocytosis- rare but can cause lower neutrophils (although reversible) rashes- common

Question 16

pharmacokinetics of thionamides

Answer 16

orally active ie tablet carbimazole is prodrug which is converted to methimaole can cross placenta and is passed in breastmilk- so PTU preferred to carbimazole for pregnant women and breastfeeds its broken down in liver and excreted in urine

Question 17

follow up from thionamides

Answer 17

after 18months, it is stopped, and patient reviewed periodically with thyroid function tests for relapse

Question 18

role of beta blockers in thyrotoxicosis and when not given

Answer 18

it is non-selective which is good, stops many symptoms like tremors, heart rate etc not used for those with asthma, as blocks beta receptors in bronchial tree

Question 19

potassium iodide- when is it used

Answer 19

only given when rapid reduction in symptoms is required for either preparing patients for surgery, or if they have a thyroid storm

Question 20

mechanism of KI

Answer 20

dosage 30 times greater than daily requirement- causes autoregulatory effect called WOLFF-CHAIKOFF effect- prevents H202 and peroxidase, and inhibits iodination

Question 21

effect of KI

Answer 21

symptoms reduced in a day, and size of glad/vascularity reduced after 10 days- better for surgery as smaller, and fact that symptoms are lower, so anaesthesia easier prior to surgery

Question 22

unwanted action of KI

Answer 22

allergic reaction like rash, but rare

Question 23

pharmacokinetics of KI

Answer 23

given orally (liquid/tablet)

Question 24

radioiodine in high doses- mechanism and usefulness

Answer 24

emits beta particles in colloid to destroy follicular cells- thyroid gland permanently destoryed, so daily lifetime thyroxine needed

Question 25

pharmacokinetics of radioiodine and differences in dosage

Answer 25

anti-thyroid drugs discontinued 10 days before treatment, and single tablet given half life 8 days, with little radioactivity after 2 months higher dosage for thyroid cancer compared to graves

Question 26

cautions of radioiodine

Answer 26

avoid contact with small children (as neck emits radiation) not good for pregnancy/breastfeeding (emits radiation)