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Endocrine > hyperthyroidism, hypothyroidism and thyroxitis > Flashcards

hyperthyroidism, hypothyroidism and thyroxitis Flashcards

1
Q

what cells produce TSH and where?

A

Thyrotroph cells in the anterior pituitary

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2
Q

What does TSH reflect?

A

tissue thyroid hormone action

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3
Q

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

A

80:20

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4
Q

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

A

TRUE

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5
Q

Thyroid hormones are primarily metabolised by?

A

liver

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6
Q

Free T3/4 LOW. TSH HIGH ?

A

PRIMARY HYPOTHYRODISM (opposite = primary hyper)

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7
Q

Free T3/4 HIGH and TSH HIGH/NORMAL ?

A

SECONDARY HYPERthyroidism (opposite = secondary hypo)

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8
Q

Most common cause of goitrous PRIMARY HYPOthyroidism?

A

Chronic thyroiditis (Hashimoto’s)

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9
Q

Cause of non-goitrous primary HYPOthyroidism?

A

Atrophic thyroiditis

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10
Q

Diseases of what endocrine organs cause secondary hypothyroidism?

A

Hypothalamus and pituitary

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11
Q

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

A

TPOAb

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12
Q

Diagnostic abnormalities for primary HYPOthyroidism?

A

Increased TSH and decreased fT4/3

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13
Q

Treatment of hypothyroidism?

A

Levothyroxine

-replacement therapy

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14
Q

Treatment of primary hypothyroidism?

A

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

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15
Q

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

A

T

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16
Q

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

A

T

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17
Q

How is levothyroxine treatment assesed for A) Primary

B) secondary hypothyroidism

A

A) according (dose titrated) to TSH levels

B) dose titrated to fT4 level

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18
Q

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

A

TSH is unreliable as its supply is low in secondary.

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19
Q

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

A

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

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20
Q

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

A

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

21
Q

What is a myxoedema coma a result of?

A

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

22
Q

Features of this?

A

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

23
Q

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

A

Graves

24
Q

Smoking doesnt affect graves? T/F

A

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

25
Q

3 Clinical signs specific to graves?

A
  • dysthyroid eye disease
    Pretibial myxoedema
    thyroid acropachy
    Thyroid bruit
26
Q

Diagnostic abnormalities for Graves?

A

Low TSH, HIGH fT4/3

27
Q

Graves is associated with osteoperosis? T/F

A

T , esp when poorly controlled

28
Q

What clinical signs is specific to Graves?

A

Thyroid bruit.

29
Q

Difference between nodular thyroid disease and graves?

A

Goitre is SMOOTH in graves, asymmetrical in NTD

30
Q

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

A

Multinodular thyroid goitre

31
Q

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

A

Hyperthyroidism

32
Q

Why does hyperthyroidism cause heat intolerance?

A

Basal metabolic rate is increased.

33
Q

High fT4, low fT3, normal TSH?

A

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

34
Q

If TSH is increased and fT4/3 normal ?

A

Subclinical hypothyoidism

35
Q

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

A

YES

36
Q

Subclincical hyperthyroidism TSH and fT levels?

A

LOW TSH and normal fT3/4

37
Q

SUbclincial hyperthyroidism is commonly seen in what goitre?

A

Multinodular

38
Q

Secondary conditions assoc. with subclinical hyperthyroidism?

A

Osteoporosis and AF

39
Q

How is hyperthyroidism produced in Graves?

A

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

40
Q

TSH levels are high in Graves? T/F

A

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

41
Q

1st line medication to treat hyperthyroidism ?

A

Carbimazole

42
Q

When does PTU become 1st line for hyperthyroidism?

A

In 1st trimester

43
Q

Mechanism of carbimazole?

A

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

44
Q

Mechanism of PTU?

A

Inhibits hormone synthesis and inhibits peripheral conversionof T4

45
Q

Why are BB used in hyperthyroidism treatment?

A

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

46
Q

Treatment of thyroid storm?

A

Propanalol, hydrocortisone, iodine, carbimazole.

47
Q

MEchanism of radioiodine?

A

Destroys thyroid => halts excess hormone production

48
Q

Causes of a diffuse goitre?

A

Physiological, Graves, Hashimoyos thyroiditis, subacute thyroiditis

49
Q

Causes of nodular goitre?

A

Multinodular goitre, adenoma, carcinoma

Endocrine (9 decks)

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