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Endocrinology > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

Causes of thyrotoxicosis with low radio iodine uptake scan

A
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2
Q

Chronic autoimmune thyroiditis presents with

A

Hypothyroidism with elevated TSH and low T4. A small amount may have hyperthyroidism but those have suppressed TSH and elevated T4

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3
Q

Post partum painless thyroiditis happens when?

A

1-6 months after delivery

will have low radioactive iodine uptake but serum thyroglobulin is elevated.

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4
Q

factitious thyrotoxicosis will have these labs:

A

low TSH, high T3 (most supplements will have high T3) and low serum thyroglobulin. levels and suppressed TSH.

WIll not see exophthalmos (only seen in Graves dx pts) but can see lid lag.

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5
Q

Graves disease presentation

A

May not have thyromegaly or extrathyroidal manifestations. Can be ruled out based on serum thyroglobulin and radioactive iodine uptake which can be elevated in Graves dx.

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6
Q

De Quevain’s thyroiditis (subacute thyroiditis) presentation

A

moderate to severe pain and tenderness of the thyroid gland. Can by slightly hyperthyroid and this resolves over time.

TX with NSAIDs.

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7
Q

how to manage pregnant pts with hyperthyroidism

A
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8
Q

what happens to TSH in 1st trimester of pregnancy?

A

beta HcG stimulation of thyroid gland causes transient hyperthryoidism. TO mimic this physiology in pts who have grave’s dx and are on PTU, we try to avoid fetal hypothryoidism and so the goal of hyperthyroid management during prenancy is maintence of a mildly hyperthyroid state and monitor TSH every 4 weeks.

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9
Q

Management of pts who have mild or asymptomatic or subclinical Graves dx while pregnant

A

do not treatment

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10
Q

How to treat Graves dx while pregnant and with moderate to severe hyperthyroidism

A

Give thioamides (PTU or methimazole).

PTU is for 1st trimester and methimazole is associated with congenital defects (aplasia cutis, tracheoesophageal fistula and choanal atresia)

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11
Q

Why do we switch from PTU to methimazole in pregnancy?

A

1st trimester: PTU

2nd and 3rd trimester: methimazole

Switch because PTU can cause severe hepatotoxicity.

Can treat trachycardia and tremor with a short course of BB (metoprolol) and long term treatment can affect fetal growth so is avoided

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12
Q

When do we measure thyrotroponin receptor antibodies?

A

measured in Grave Dx pts who are pregnant at 18-22 wks gestation to predict risk of fetal thyrotoxicosis and determine need for U/S monitoring of fetal thyroid

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13
Q

Can we do radioactive iodine for graves dx treatment during pregnancy

A

No. actively contraindicated

Thyroidectomy is only indicated for pts who have contraindications with thioamides (allergies or agranulocytosis)

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14
Q

PTU and methimazole is associated with

A

agranulocytosis

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15
Q

presentation of hyperthyroid in geriatric pts

A

apathy rather than hyperactivity in 30% of pts

shortness of breath of unclear cause, constipation (paradoxically) and afib and weight loss or low BMI, insomnia. and can see proximal muscle weakness.

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16
Q

fever, anterior neck pain, tender thyroid gland and symptoms of thyrotoxicosis suggests

A

subacute granulomatous thyroiditis

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17
Q

what is subacute granulomatous thyroiditis

A

de quervain’s thyroiditis

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18
Q

what clinical event precedes subacute granulomatous thyroiditis?

A

generally see viral infection prior to development of de Quervain thyroiditis. and this is part of the post viral response.

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19
Q

subacute granulomatous thyroiditis clinical presentation

A

anterior neck pain that can radiate to the jaw,

tender thyroid gland and may be enlarged

may see symptoms of thyrotoxicosis

see fatigue malaise and anorexia and fever

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20
Q

predictable clinical course of subacute granulomatous thyroiditis (de Quervain’s thyroiditis)

A

see hyperthyroidism, followed by euthyroidism and hypothyroidism and thyroid functional recovery.

Each phase can last up to 8 weeks

Some pts may only have hyper or hypothyroid start before thyroid recovery and only 5% have permanent hypothyroidism

will see elevated ESR and CRP, follow TSH and T4 2-8 weeks

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21
Q

subacute granulomatous thyroiditis lab findings

A

will have ESR and CRP elevated

radioactive iodide uptake scan during hyperthyroid phase will have low uptake (<1%)

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22
Q

Treatment of subacute thyroiditis and subacute granulomatous thyroiditis

A

high dose NSAIDS (1200-3200 mg/day) are usually helpful but if pain is not relieved in 2-3 days with NSAIDS they should be discontinued and tx of prednisone 40 mg/day should be started

Don’t need to thionamides as these symptoms are a result of release of preformed thyroid hormones. Also people don’t need tx for hypothyroid state.

measure TSH every 2-8 weeks in all pts. Only 5% of pts develop permanent hypothyroidism.

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23
Q

subacute granulomatous thyroiditis and mild thyroxoticosis management

A

present in early stages of disease with subacute thyroiditis (seen 50%)

treat symptoms with beta blockers. Don’t need to thionamides (PTU or methimazole) as these symptoms are a result of release of preformed thyroid hormones. Also people don’t need tx for hypothyroid state.

measure TSH and T4 every 2-8 weeks in all pts. Only 5% of pts develop permanent hypothyroidism.

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24
Q

acute infectious thyroiditis management

A

thyroid u/S and fine needle aspiration biopsy in pts presenting with fever leukocytosis, thyroid pain and tenderness.

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25
Q

algorithm for hyperthyroidism evaluation

A
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26
Q

in pts who do not have obvious features of graves dx, but have symptoms and signs of hyperthyroidism (low TSH and high T4) need to order

A

a Radioactive iodine uptake (RAIU) scan as initial evaluation as this will explain etiology.

Normal or elevated RAIU indicates de novo thyroid hormone synthesis

decreased or absent uptake indicates thyroid destruction (thyroiditis leading to preformed hormone.

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27
Q

hyperthyroid on labs but negative RAIU uptake scan means

A

Normal or elevated RAIU indicates de novo thyroid hormone synthesis

decreased or absent uptake indicates thyroid destruction (thyroiditis) leading to preformed hormone.

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28
Q

if patient has a palpable nodule and hyperthyroid, what should be done?

A

RAIU to clarify if there’s only localized uptake at nodule, patchy nodular uptake or diffuse uptake (grave’s dx)

also need a thyroid scan to help clarify where the iodine is being uptook.

29
Q

why do we check serum thyroglobulin in hyperthyroid cases?

A

serum thyroglobulin is checked when suspected surreptitious ingestion of thyroid hormone is suspected. This will be low in pts who take exogenous thyroid hormone.

30
Q

when do we check thyrotropin receptor antibodies

A

check if graves dx is strongly suspected but extrathyroidal manifestations are not present.

antibody tests with recombinant thyrotroponin receptor have high sensitivity for grave’s dx.

31
Q

If suspecting amiodarone induced thyroid dx need to check TSH and follow algorithm

A
32
Q

when do Graves dx pts who get radioactive iodine therapy starto improve

A

4-8 weeks and up to 80% of pts develop hypothyroidism betwen 2-6 months following tx.

Post treatment hypothyroidism can sometimes be transient and self limited

33
Q

what happens to TSH after radioactive iodine therapy in Graves pts?

A

it can remain suppressed for months after resolution of hyperthyroidism and may not indicate ongoing hyperthyroidism .

IF concerned about ongoing hypothyroid in post radioactive iodine therapy, follow the T3 and T4 levels. monitor pt symptoms and clinical exam.

If T3 and T4 levels are low and pt has symptoms needs levothyroxine.

34
Q

when can someone get pregnant after they get radioactive iodine ablative treatment

A

avoid pregnancy for at least 6 months after radioactive iodine therapy / ablation

35
Q

if pt has graves dx s/p radioactive iodine therapy and has symptoms of hypothyroid best lab to check

A

T3 and T4 and not TSH as this can be low for several months (2-6 months). If T3 and T4 are normal repeat T3 and T4 in four weeks if symptoms of hypothyroid continue. If low can start levothyroxine.

36
Q

thyrotropin receptor antibody (TRab) levels will do what after a radioactive ablative treatment

A

they will remain high even if pt develops hypothyroidism.

37
Q

What do we check in third trimester of pregnancy when someone has Grave’s dx

A

Thyrotropin receptor antibody to predict fetal hyperthyroidism.

38
Q

what does positive thyroid stimulating hormone antibody (TRab)?

A

indicates you may have auotimmune disorder like Graves or Hashimoto’s

39
Q

can hyperthyroidism cause hypercalcemia?

A

yes. Thyroid hormone acts on osteoclasts to increase bone turnover and leads to decreased bone density and osteoporosis and increased fracture risk .

40
Q

Pathyphysiology of how hyperthyroidism can cause bone disease

A
41
Q

what is seen in labs related to hyperthyroid induced hypercalcemia and bone disease?

A

see hypercalciuria, mild hypercalcemia.

PTH levels are low (causing renal calcium wasting and negative calcium balnce)

1,25 vit D will be low due to increased catabolism and decreased PTH mediated renal conversion from 25 vit D.

42
Q

how to treat hyperthyroid induced bone disease?

A

treat hyperthyroidism. May not restore the bone density lost.,

43
Q

Amiodarone’s effects on thyroid

A
44
Q

how does amiodarone cause thyrotoxicosis?

A

it can cause problems for thyroid due to high iodine content and direct effects on thyroid follicular cells and alteration of thyroid hormone metabolism.

It can increase thyroid hormone synthesis (Amiodarone induced thyrotoxicosis type 1) or destruction of thyroid follicles with release of preformed hormone (Amiodarone induced thyrotoxicosis type 2) and pts can have both

45
Q

how to tell difference between amiodarone induced thyrotoxicosis Type 1 or Type 2?

A

AIT type 1 see - increased thyroid hormone synthesis

AIT type 2 see release of preformed thyroid hormone

Use a Radioactive iodine uptake (RAIU) scan to tell the difference between the two. If type 1, RAIU will be low but detectable. If type 2 RAIU will be <5% or none.

Doppler U/S of thyroid- show hypervascularitiy with type 1 and decreased vascularity in type2

46
Q

How to treat amiodarone induced thyrotoxicosis type 1?

A

because result of amiodarone causing increased thyroid hormone synthesis, treat with methimazole to decrease new hormone synthesis.

47
Q

How to treat amiodarone induced thyrotoxicosis type 2?

A

Type 2 is result of amiodarone releasing more preformed thyroid hormone.

Treat with high dose glucocorticoid therapy

48
Q

what is euthyroid sick syndrome?

A

refers to altered thyroid metabolism in pts with severe acute illness. Pts will have low T3 levels (low T3 syndrome) due to decreased T4 to T3 but will have normal T4 and TSH.

49
Q

extra thyroidal symptoms of Graves’s dx?

A

see extrathyroidal disease (Exophthalmos, pretibial myxedema, acropachy)

50
Q

what does this radioactive iodine uptake scan show?

What to do next in management?

TSH is <0.3 and T3 serum 200. At 24 hrs is 30% (normal is 10-30%)

A

toxic adenoma / nodule.

It doesn’t matter that the uptake scan shows that only 30% absorbed. What’s important is the fact that there’s one area of uptake on RAIU means there’s a toxic nodule since the TSH is low tells you they’re hyperthyroid.

Graves would show diffuse uptake. Toxic nodules would show one area of uptake.

Treatment is radioactive iodine ablation low TSH and increased T4. The radioactive iodine in the nodular thyroid dx is taken up primary in the abnormal tissue and does little damage to the surrounding healthy tissue. Most pts are euthyroid after tx.

Do not use methimazole or PTU only reserved for people who can’t get surgery or decline definitive tx.

51
Q

what does prednisone do in hyperthyroid state or thyroxicosis

A

prevents conversion of T4 to active T3 and helpful in Graves dx, severe hyperthyroidism and thyroid storm.

52
Q

when do we use thionamides (methimazole and PTU) in hyperthyroidism

A

can be used to prep for radiodine ablation or surgery but also used as primary therapy for pts with Graves dx who have mild hyperthyroidism and small goiters. Don’t use it chronic use for toxic nodular dx.

53
Q

when do we consider surgery to treat toxic thyroid nodules or adenomas?

A

only if there’s a large goiter, coexisting malignancy, primary hyperparathyroidism or those who need rapid correction of hyperthyroidism.

54
Q

chart comparing painless thyroiditis and Grave’s dx

A
55
Q

what is painless thyroiditis?

A

transient hyperthyroidism followed by possible hypothyroidism adn then recovery

painless thyroiditis happens >1 year after pregnancy but can also happen in non postpartum men and women. Certain meds like lithium, interferon alpha, interleukin-2 and amiodarone can cause this.

Need to get a RAIU to distinguish between Graves dx in any pt without exophthalmos since both have similar presentations and different tx.

56
Q

What meds cause painless thyroiditis?

A

Certain meds like lithium, interferon alpha, interleukin-2 and amiodarone can cause this.

57
Q

what study is important to get with painless thyroiditis?

A

Need to get a RAIU to distinguish between Graves dx in any pt without exophthalmos since both have similar presentations and different tx.

Graves dx and toxic nodular goiter are due to excessive thyroid hormone production from hyperactive thyroid tissue and so see high RAIU

Painless thyroiditis is likely a varient of Hashimoto’s thyroiditis with autoimmune thyroid inflammation and likely the thyrotoxic state is from release of preformed thyroid hormone. RAIU is <1% or low uptake.

58
Q

painless thyroiditis will have these antibodies

A

elevated serum anti TPO antibodies and thyroglobulin

Painless thyroiditis is likely a varient of Hashimoto’s thyroiditis with autoimmune thyroid inflammation and likely the thyrotoxic state is from release of preformed thyroid hormone.

59
Q

Management of painless thyroiditis

what is the prognosis for painless thyroiditis?

A

pts will have mild thyrotoxic symptoms for 1-3 months (usually no exophthalmos) and followed by hypothyroid symptoms that last for 3-6 months.

Most recover but 20% will have permanent hypothyroidism (with higher antiTPO antibody titers) and 10% will have recurrent thyroiditis.

Mild symptoms - no tx, just check TSH labs 6-8 weeks

Significant symptoms like tachycardia - give beta blockers for relief

60
Q

amiodarone induced destructive thyroiditis (Type 2) tx

A

high dose steroids

61
Q

subacute (de Quervain’s thyroiditis) tx if unresponsive to NSAIDs

A

high dose steroids

62
Q

if someone on methimazole for Grave’s disease develops a fever and sore throat within 3 months of starting it what to do?

A

get CBC with diff and stop agranulocytosis

agranulocytosis from methimizole generally happens within several months of starting therapy and not seen with doses <20 mg per day

If ANC <500 need to stop methimazole and need to get hospitalized for broad spectrum antibiotics nad hematopoietic growth factor therapy.

63
Q

when starting someone on methimazole you need to :

A

counsel on potential side effect of methimazole agranulocytosis and counsel on symtpoms and need to call physician quickly

this is potentially fatal condition and needs to be checked upon.

64
Q

23 F has palpitations and increased frequency of bowel movements and weight loss. Has redness of eyes, see tearing, grittiness and photophobia and intermittent diplopia when reading. Smokes.

Has thyroid bruit and diffuse enlargement of thyroid goiter.

TSH is 0.005 and free T4.1 and thyroid scintigraphy shows 24 hr radioactive iodine uptake is 56% (normal is 10-30%) in a diffuse pattern.

What to do?

A

start beta blocker and oral prednisone

Then start methimazole. Stop smoking.

Pt has Grave’s disease due to the diffuse goiter and increased radioiodine uptake and hyperthyroidism.

Needs beta blocker (propranolol) 1st to control the adrenergic symptoms. Needs steroids for moderate (oral) or severe/progressive (IV) ophthalmopathy and to stop conversion of T4 to T3. Also smoking stops ophthalmolpathy.

Needs to start an antithyroid drug to stop synthesis of thyroid hormone (methimazole preferred due to increased risk for hepatoxicity with PTU)

Can’t treat Graves with eye issues with radioactive iodine ablation because RAI can worsen ophthalmolopathy and should be avoided in significant eye symptoms.

65
Q

how to decide to treat Graves hyperthyroidism?

A

Depends on severity of dx and if they have eye involvement.

Can either treat with anti thyroid drugs, radioactive iodine, or thyroidectomy

66
Q

is there a role in selenium supplementation with grave’s disease

A

yes. Selenium deficiency appears to increase the risk for Graves ophthalmopathy.

Thus there’s a role for supplementation of selenium as it appears to reduce the symtpoms but the benefits of this are unclear in people who don’t have this deficiency.

67
Q

When do we choose to use thyroidectomy for pts who have Graves disease?

A

when there’s large goiters,

obstructive symptoms of breathing,

suspected thyroid cancer

for people who have significant ophthalmopathy or people (pregnant) who fail methimazole

68
Q

first medication to give for thyroid storm is:

A

PTU and beta blocker

then give sterods.

69
Q

side effects of thionamides?

A

methimazole and PTU

agranulocytosis

drug induced hepatitis

nausea

rash

vasculitis

Endocrinology (26 decks)

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