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Endocriknowlogy > Thyroid: Hyperthyroidism > Flashcards

Thyroid: Hyperthyroidism Flashcards

1
Q

Most common cause of thyrotoxicosis

A

Graves’ disease (60-80%)

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2
Q

Concordance for Graves’ disease in twins

A

20-30% in monozygotic twins

<5% in dizygotic twins

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3
Q

Is smoking a risk factor for Graves’ disease?

A

Smoking is a minor risk factor for Graves’ disease and a major risk factor for the development of ophthalmopathy.

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4
Q

What is the pathogenesis of Graves’ disease?

A

The hyperthyroidism of Graves’ disease is caused by thyroid-stimulating immunoglobulin (TSI) that are synthesized in the thyroid gland, as well as in bone marrow and lymph nodes.

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5
Q

What is the term that refers to thyrotoxicosis which occurs primarily in the elderly and which presents mainly as fatigue and weight loss.

A

Apathetic thyrotoxicosis

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6
Q

What are the most frequent symptoms of thyrotoxicosis?

A

Hyperactivity, irritability, dysphoria

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7
Q

What are the most frequent signs of thyrotoxicosis?

A

Tachycardia; atrial fibrillation in the elderly

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8
Q

Characteristic muscle weakness in thyrotoxicosis

A

Proximal myopathy

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9
Q

Most common cardiovascular manifestation of thyrotoxicosis

A

Sinus tachycardia

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10
Q

In thyrotoxicosis, where is the thrill or bruit best detected?

A

Inferolateral margins of the thyroid lobes

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11
Q

How is proptosis best detected?

A

By visualization of the sclera between the lower border of the iris and the lower eyelid, with the eyes in the primary position

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12
Q

Most serious manifestation of Graves’ ophthalmopathy

A

Compression of the optic nerve at the apex of the orbit, leading to papilledema; peripheral field defects; and if left untreated, permanent loss of vision

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13
Q

“NO SPECS” scoring system for ophthalmopathy

A 
0 = No signs or symptoms
1 = Only signs (lid retraction or lag), no symptoms
2 = Soft tissue involvement (periorbital edema)
3 = Proptosis (>22 mm)
4 = Extraocular muscle involvement (diplopia)
5 = Corneal involvement
6 = Sight loss
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14
Q

Scoring system more preferable than NO SPECS for monitoring and treating Graves’ orbitopathy

A

European Group On Graves’ Orbitopathy (EUGOGO)

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15
Q

Most frequent site of thyroid dermopathy

A

Anterior and lateral aspects of the lower leg (“pretibial myxedema”)

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16
Q

Typical lesion of thyroid dermopathy

A

Noninflamed, indurated plaque with a deep pink or purple color and an “orange skin” appearance

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17
Q

Term used to denote a form of clubbing found in <1% of patients with Graves’ disease

A

Thyroid acropachy

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18
Q

TRUE OR FALSE: Thyroid acropachy is strongly associated with thyroid dermopathy, which is almost always develops with moderate or severe ophthalmopathy.

A

TRUE. An alternative cause of clubbing should be sought in a Graves’ patient without coincident skin and orbital involvement.

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19
Q

TRUE OR FALSE: A normal TSH doesn’t exclude Graves’ disease as a cause of diffuse goiter.

A

FALSE. A normal TSH excludes Graves’ disease as a cause of diffuse goiter.

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20
Q

What is the typical clinical course of Graves’ ophthalmopathy?

A

Ophthalmopathy typically worsens over the initial 3-6 months, followed by a plateau phase over the next 12-18 months, and then some spontaneous improvement, particularly in the soft tissue changes.

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21
Q

Mechanism of action of antithyroid drugs

A

1) Inhibit the function of TPO, reducing oxidation and organification of iodide
2) Also reduce thyroid antibody levels by mechanisms that remain unclear

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22
Q

Additional mechanism of action of propylthiouracil aside from TPO inhibition

A

Inhibits deiodination of T4 to T3

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23
Q

Half-life of antithyroid drugs

A

Propylthiouracil - 90 mins

Methimazole - 6 hours

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24
Q

3 indications for use of propylthiouracil (limited due to hepatotoxicity)

A

1) first trimester of pregnancy
2) thyroid storm
3) minor adverse reactions to methimazole

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25
Q

When to check TFTs after starting treatment for hyperthyroidism

A

4-6 weeks after starting treatment (most do not achieve euthyroidism until 6-8 weeks after treatment is initiated)

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26
Q

Dose titration of antithyroid drugs is based on ________ levels

A

Unbound T4 levels (TSH levels often remain suppressed for several months)

27
Q

Duration until maximum remission rates are achieved in hyperthyroidism

A

12-18 months

28
Q

Risk factors for relapse after treatment for hyperthyroidism is stopped

A

Younger patients
Males
Smokers
Patients with a history of allergy, severe hyperthyroidism, or large goiters

29
Q

Major side effects of antithyroid drugs

A

Hepatitis (especially with propylthiouracil)
Cholestasis (especially with methimazole and carbimazole)
Vasculitis
Agranulocytosis (<1%)

30
Q

Symptoms of possible agranulocytosis

A

Sore throat, fever, mouth ulcers (stop treatment pending an urgent CBC)

31
Q

Dose requirement for 1) warfarin and 2) digoxin is ______ (increased/decreased) in the thyrotoxic state.

A

Warfarin - decreased doses are required

Digoxin - increased doses are required

32
Q

How many days before RAI must carbimazole or methimazole be stopped, and when can they be restarted?

A

Carbimazole or methimazole must be stopped 2-3 days before radioiodine administration to achieve optimum iodine uptake, and can be restarted 3-7 days after radioiodine in those at risk of complications from worsening thyrotoxicosis.

33
Q

After RAI, the patient must avoid close, prolonged contact with children and pregnant women for ___ days.

A

5-7 days

34
Q

Hyperthyroidism can persistent for ___ months before radioiodine takes full effect.

A

2-3 months

35
Q

Pregnancy and breastfeeding are absolute contraindications to radioiodine treatment, but patients can conceive safely ___ months after treatment.

A

6 months

36
Q

TRUE OR FALSE: Radioiodine should generally be avoided in those with active moderate to severe eye disease.

A

TRUE

37
Q

Target T4 levels in pregnant patients with Graves’ disease

A

Just above the pregnancy reference range

38
Q

Congenital defects caused by methimazole/carbimazole

A

Aplasia cutis, choanal atresia, tracheoesophageal fistulae

39
Q

Conversion of PTU to methimazole

A

Ratio of 15-20mg PTU to 1mg methimazole

40
Q

What is the Wolff-Chaikoff effect

A

It is an autoregulatory phenomenon that occurs upon initial exposure to iodine, which inhibits iodine organification and release of thyroid hormones into the bloodstream

SSKI is given 1 hour after PTU because the delay allows the antithyroid drug to prevent the excess iodine from being incorporated into the new hormone

41
Q

Initial treatment for severe ophthalmopathy, with optic nerve involvement or chemosis resulting in corneal damage

A

Pulse therapy with IV methylprednisolone

42
Q

Most common cause of suppurative infection of the thyroid that leads to acute thyroiditis in children and young adults

A

Presence of a piriform sinus, a remnant of the 4th branchial pouch that connects the oropharynx with the thyroid

43
Q

3 distinct phase of subacute thyroiditis

A

1) thyrotoxic phase
2) hypothyroid phase
3) recovery phase
Over about 6 months

44
Q

TRUE OR FALSE: In subacute thyroiditis, there is a high uptake of radioactive iodine.

A

FALSE

45
Q

Treatment of subacute thyroiditis

A

Large doses of aspirin and NSAIDs

If inadequate or if with marked local or systemic symptoms, glucocorticoids should be given

46
Q

Factors that differentiate silent thyroiditis from subacute thyroiditis

A

In silent thyroiditis:

1) Goiter is painless
2) ESR is normal
3) TPO antibodies are present
4) Glucocorticoid treatment is not indicated

47
Q

Characteristics of Riedel’s thyroiditis

A

Rare

Typically occurs in middle-aged women

Insidious, painless goiter with local symptoms due to compression of the esophagus, trachea, neck veins, or recurrent laryngeal nerves

Dense fibrosis disrupts normal gland architecture

Thyroid dysfunction is uncommon

Goiter is hard, non-tender, often asymmetric, and fixed, leading to suspicion of malignancy

Diagnosis requires OPEN biopsy

Treatment: Surgery

Tamoxifen may be beneficial

48
Q

Most common hormone pattern in sick euthyroid syndrome / nonthyroidal illness

A

Low T3

Normal T4 and TSH

49
Q

Pathophysiology of sick euthyroid syndrome

A

T4 conversion to T3 via peripheral 5’ (outer ring) deiodination is impaired, leading to increased reverse T3 (rT3)
- probably an adaptive response to limit catabolism in starved or ill patients

50
Q

Pattern of thyroid hormone abnormalities in acute liver disease

A

Initial rise in total (but not unbound) T3 and T4 due to TBG release –> become subnormal with progression to liver failure

51
Q

Pattern of thyroid hormone abnormalities in acutely ill psychiatric patients

A

Transient increase in total and unbound T4 levels, usually with a normal T3 level

52
Q

Pattern of thyroid hormone abnormalities in HIV infection

A

Early stage: Elevated T3 and T4

Progression to AIDS: T3 levels fall, but TSH remains normal

53
Q

Pattern of thyroid hormone abnormalities in renal disease

A 
Low T3
Normal rT3 (due to an unknown factor that increases uptake of rT3 into the liver)
54
Q

Treatment of sick euthyroid syndrome

A

Monitor TFTs without administering thyroid hormone, unless there is historic or clinical evidence suggestive of hypothyroidism

55
Q

Amiodarone is structurally related to thyroid hormone and contains __% iodine by weight.

A

39%

56
Q

Amiodarone is stored in adipose tissue, hence high iodine levels persist for >__ months after discontinuation of the drug.

A

> 6 months

57
Q

What are the 3 effects of amiodarone on thyroid function?

A

1) Acute, transient suppression of thyroid function
2) Hypothyroidism in patients susceptible to the inhibitory effects of a high iodine load
3) Thyrotoxicosis that may be caused by either a Jod-Basedow effect from the iodine load, in the setting of MNG or incipient Graves’ disease, or a thyroiditis-like condition

58
Q

Expected TFTs after initiation of amiodarone treatment

A

Transient decrease of T4 levels (reflecting the inhibitory effect of iodine on T4 release)

Increased T4, decreased T3, increased rT3, and transient TSH increase (escape from iodide-dependent suppression of the thyroid (Wolff-Chaikoff effect), and the inhibitory effects on deiodinase activity and thyroid hormone receptor action become predominant)

TSH levels normalize or are slightly suppressed within 1-3 months

59
Q

Treatment of amiodarone-induced hypothyroidism

A

Levothyroxine can be used to normalize thyroid function

TSH levels should be monitored (because T4 levels are often increased)

Usually unnecessary to discontinue amiodarone

60
Q

Types of amiodarone-induced thyrotoxicosis (AIT)

A

Type 1 AIT

  • Associated with underlying thyroid abnormality (preclinical Graves’ disease or nodular goiter)
  • Thyroid hormone synthesis becomes excessive as a result of increased iodine exposure (Jod-Basedow phenomenon)
  • Increased thyroid gland vascularity

Type 2 AIT

  • No intrinsic thyroid abnormalities
  • The result of drug-induced lysosomal activation leading to destructive thyroiditis with histiocyte accumulation in the thyroid
  • Decreased thyroid gland vascularity
61
Q

Treatment of amiodarone-induced thyrotoxicosis (AIT)

A

Amiodarone should be stopped if possible

Type 1 AIT

  • Potassium perchlorate (associated with agranulocytosis)
  • High doses of antithyroid drugs are often ineffective

Type 2 AIT

  • Glucocorticoids and lithium (block thyroid hormone release) have modest benefit
  • Near-total thyroidectomy (may be the most effect long-term solution)
62
Q

Most common clinically apparent cause of chronic thyroiditis

A

Hashimoto’s thyroiditis

63
Q

How can you distinguish silent thyroiditis from subacute thyroiditis (since they have the same clinical course)?

A

Normal ESR and the presence of TPO antibodies (silent thyroiditis usually occurs in patients with underlying autoimmune thyroid disorder)

Endocriknowlogy (9 decks)

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