hyperthyroidism, hypothyroidism and thyroxitis

Question 1

what cells produce TSH and where?

Answer 1

Thyrotroph cells in the anterior pituitary

Question 2

What does TSH reflect?

Answer 2

tissue thyroid hormone action

Question 3

Thyroid hormones are secreted in a ratio of ? (T4:T3)

Answer 3

80:20

Question 4

Most (99%) thyroid hormones are bound to plasma? TRUE or FALSE?

Answer 4

TRUE

Question 5

Thyroid hormones are primarily metabolised by?

Answer 5

liver

Question 6

Free T3/4 LOW. TSH HIGH ?

Answer 6

PRIMARY HYPOTHYRODISM (opposite = primary hyper)

Question 7

Free T3/4 HIGH and TSH HIGH/NORMAL ?

Answer 7

SECONDARY HYPERthyroidism (opposite = secondary hypo)

Question 8

Most common cause of goitrous PRIMARY HYPOthyroidism?

Answer 8

Chronic thyroiditis (Hashimoto’s)

Question 9

Cause of non-goitrous primary HYPOthyroidism?

Answer 9

Atrophic thyroiditis

Question 10

Diseases of what endocrine organs cause secondary hypothyroidism?

Answer 10

Hypothalamus and pituitary

Question 11

The presence of what antibody suggests the cause of thyroid disease is autoimmune?

Answer 11

TPOAb

Question 12

Diagnostic abnormalities for primary HYPOthyroidism?

Answer 12

Increased TSH and decreased fT4/3

Question 13

Treatment of hypothyroidism?

Answer 13

Levothyroxine

-replacement therapy

Question 14

Treatment of primary hypothyroidism?

Answer 14

Levothyroxine
Young - 50-100
Old w IHD - 25-50

Question 15

Precipitation of cardiac arrhythmias may occur if metabolic rate (TSH levels) are restored rapidly? T/F

Answer 15

T

Question 16

TSH level falls to normal when optimum dose of Levothyroxine is achieved? T/F

Answer 16

T

Question 17

How is levothyroxine treatment assesed for A) Primary

B) secondary hypothyroidism

Answer 17

A) according (dose titrated) to TSH levels

B) dose titrated to fT4 level

Question 18

Why are fT4 (instead of TSH)levels monitored to asses levothyroxine treatment , in secondary HYPOthyroidism?

Answer 18

TSH is unreliable as its supply is low in secondary.

Question 19

Why might dose of replacemt therapy have to increase in pregnancy?

Answer 19

In pregnancy the TBG levels increase => More thyroid hormone bound and less free thyroid hormone.

Question 20

How does destruction of thyroid follicular cells –> decreased thyroid hormone?

Answer 20

T3 and T4 are made from tyrosine residues on thyroglobulin. Follicular cells contain thyroglobulin => their destruction inhibits the production of T3/T4.

Question 21

What is a myxoedema coma a result of?

Answer 21

Loss of brain function as a result of longstanding severe hypothyroidism.

Question 22

Features of this?

Answer 22

Possible Hypothermia, Type 2 resp failure, severe cardiac failure/pericardial effusions, hyponatreamia, arrhythmias

Question 23

Autoimmune condition that is the most common cause of P hyperthyroidism?

Answer 23

Graves

Question 24

Smoking doesnt affect graves? T/F

Answer 24

False. It leads to a more severe graves that is harder to treat

Question 25

3 Clinical signs specific to graves?

Answer 25

- dysthyroid eye disease Pretibial myxoedema thyroid acropachy Thyroid bruit

Question 26

Diagnostic abnormalities for Graves?

Answer 26

Low TSH, HIGH fT4/3

Question 27

Graves is associated with osteoperosis? T/F

Answer 27

T , esp when poorly controlled

Question 28

What clinical signs is specific to Graves?

Answer 28

Thyroid bruit.

Question 29

Difference between nodular thyroid disease and graves?

Answer 29

Goitre is SMOOTH in graves, asymmetrical in NTD

Question 30

What thyroid pathology is the most common cause of tracheal &/or esophageal compression?

Answer 30

Multinodular thyroid goitre

Question 31

Thinning hair, sweaty palms, fine tremor, tachycardia, lid retraction (wide stare)...are all signs of what?

Answer 31

Hyperthyroidism

Question 32

Why does hyperthyroidism cause heat intolerance?

Answer 32

Basal metabolic rate is increased.

Question 33

High fT4, low fT3, normal TSH?

Answer 33

Drug induced thyroiditis. No peripheral conversion of T4 --> T3 due to inhibition of DeIodinase enzyme 1 by amiodarone.

Question 34

If TSH is increased and fT4/3 normal ?

Answer 34

Subclinical hypothyoidism

Question 35

Is the risk of progression to OVERT HYPOthyriodism greater if stongly TPO antibody positive?

Answer 35

YES

Question 36

Subclincical hyperthyroidism TSH and fT levels?

Answer 36

LOW TSH and normal fT3/4

Question 37

SUbclincial hyperthyroidism is commonly seen in what goitre?

Answer 37

Multinodular

Question 38

Secondary conditions assoc. with subclinical hyperthyroidism?

Answer 38

Osteoporosis and AF

Question 39

How is hyperthyroidism produced in Graves?

Answer 39

Graves antibodies bind to and prolong activation of TSH receptors => excessive secretion of T3 and T4

Question 40

TSH levels are high in Graves? T/F

Answer 40

F. Low because pituitary is trying to compensate for thyrotoxic state.

Question 41

1st line medication to treat hyperthyroidism ?

Answer 41

Carbimazole

Question 42

When does PTU become 1st line for hyperthyroidism?

Answer 42

In 1st trimester

Question 43

Mechanism of carbimazole?

Answer 43

Inhibitis TPO => inhibits deiodination of tyrosine residues --> T3 and T4

Question 44

Mechanism of PTU?

Answer 44

Inhibits hormone synthesis and inhibits peripheral conversionof T4

Question 45

Why are BB used in hyperthyroidism treatment?

Answer 45

Hyperthyroidism Increases S action => BB Decrases this, and have and added benefit of inhibiting DIO1 (Lowers conversion to T3)

Question 46

Treatment of thyroid storm?

Answer 46

Propanalol, hydrocortisone, iodine, carbimazole.

Question 47

MEchanism of radioiodine?

Answer 47

Destroys thyroid => halts excess hormone production

Question 48

Causes of a diffuse goitre?

Answer 48

Physiological, Graves, Hashimoyos thyroiditis, subacute thyroiditis

Question 49

Causes of nodular goitre?

Answer 49

Multinodular goitre, adenoma, carcinoma