12 Hyperthyroid Disorders Flashcards

1
Q

Mechanism of hyperthyroidism:
Graves disease

A

Excessive TSH-receptor stimulation

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2
Q

Mechanism of hyperthyroidism:
Pregnancy-associated transient hyperthyroidism

A

Excessive TSH-receptor stimulation

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3
Q

Mechanism of hyperthyroidism:
Trophoblastic disease

A

Excessive TSH-receptor stimulation

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4
Q

Mechanism of hyperthyroidism:
Familial gestational hyperthyroidism

A

Excessive TSH-receptor stimulation

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5
Q

Mechanism of hyperthyroidism:
TSH-producing pituitary adenoma

A

Excessive TSH-receptor stimulation

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6
Q

Mechanism of hyperthyroidism:
Multinodular toxic goiter

A

Autonomous thyroid hormone secretion

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7
Q

Mechanism of hyperthyroidism:
Solitary toxic thyroid adenoma

A

Autonomous thyroid hormone secretion

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8
Q

Mechanism of hyperthyroidism:
Congenital activating TSH-receptor mutation

A

Autonomous thyroid hormone secretion

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9
Q

Mechanism of hyperthyroidism:
Subacute de Quervain thyroiditis

A

Destruction of follicles with release of hormone

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10
Q

Mechanism of hyperthyroidism:
Painless thyroiditis/postpartum thyroiditis

A

Destruction of follicles with release of hormone

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11
Q

Mechanism of hyperthyroidism:
Acute thyroiditis

A

Destruction of follicles with release of hormone

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12
Q

Mechanism of hyperthyroidism:
Drug-induced thyroiditis

A

Destruction of follicles with release of hormone

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13
Q

Mechanism of hyperthyroidism:
Iatrogenic overreplacement with thyroid hormone

A

Extrathyroidal sources of thyroid hormone

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14
Q

Mechanism of hyperthyroidism:
Excessive self-administered thyroid medication

A

Extrathyroidal sources of thyroid hormone

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15
Q

Mechanism of hyperthyroidism:
Food and supplements containing excessive thyroid hormone

A

Extrathyroidal sources of thyroid hormone

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16
Q

Mechanism of hyperthyroidism:
Functional thyroid cancer metastases

A

Extrathyroidal sources of thyroid hormone

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17
Q

Mechanism of hyperthyroidism:
Struma ovarii

A

Extrathyroidal sources of thyroid hormone

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18
Q

Causes of hyperthyroidism:
Excessive TSH-receptor stimulation (5)

A

Graves disease
Pregnancy-associated transient hyperthyroidism
Trophoblastic disease
Familial gestational hyperthyroidism
TSH-producing pituitary adenoma

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19
Q

Causes of hyperthyroidism:
Autonomous thyroid hormone secretion (3)

A

Multinodular toxic goiter
Solitary toxic thyroid adenoma
Congenital activating TSH-receptor mutation

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20
Q

Causes of hyperthyroidism:
Destruction of follicles with release of hormone (4)

A

Subacute de Quervain thyroiditis
Painless thyroiditis/postpartum thyroiditis
Acute thyroiditis
Drug-induced thyroiditis

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21
Q

Causes of hyperthyroidism:
Extrathyroidal sources of thyroid hormone (5)

A

Iatrogenic overreplacement with thyroid hormone
Excessive self-administered thyroid medication
Food and supplements containing excessive thyroid hormone
Functional thyroid cancer metastases
Struma ovarii

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22
Q

Increased / decreased / unchanged in hyperthyroidism:
Renal blood flow

A

Increased

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23
Q

Hyperthyroid symptoms referable to the urinary tract (2)

A

Mild polyuria
Nocturia

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24
Q

Increased / decreased / unchanged in hyperthyroidism:
Glomerular filtration

A

Increased

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25
Q

Increased / decreased / unchanged in hyperthyroidism:
Tubular reabsorptive maximum

A

Increased

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26
Q

Increased / decreased / unchanged in hyperthyroidism:
Tubular secretory maximum

A

Increased

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27
Q

Increased / decreased / unchanged in hyperthyroidism:
Total exchangeable potassium

A

Decreased

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28
Q

Increased / decreased / unchanged in hyperthyroidism:
Potassium levels

A

Unchanged

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29
Q

Common / rare / very rare adverse event of antithyroid drugs:
Skin rash

A

Common

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30
Q

Common / rare / very rare adverse event of antithyroid drugs:
Urticaria

A

Common

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31
Q

Common / rare / very rare adverse event of antithyroid drugs:
Arthralgia

A

Common

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32
Q

Common / rare / very rare adverse event of antithyroid drugs:
Polyarthritis

A

Common

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33
Q

Common / rare / very rare adverse event of antithyroid drugs:
Transient mild leukopenia

A

Common

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34
Q

Common / rare / very rare adverse event of antithyroid drugs:
Gastrointestinal

A

Rare

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35
Q

Common / rare / very rare adverse event of antithyroid drugs:
Abnormal smell and taste

A

Rare

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36
Q

Common / rare / very rare adverse event of antithyroid drugs:
Agranulocytosis

A

Rare

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37
Q

Common / rare / very rare adverse event of antithyroid drugs:
Aplastic anemia

A

Very rare

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38
Q

Common / rare / very rare adverse event of antithyroid drugs:
Thrombocytopenia

A

Very rare

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39
Q

Common / rare / very rare adverse event of antithyroid drugs:
Lupus-like, ANCA-positive vasculitis

A

Very rare

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40
Q

Common / rare / very rare adverse event of antithyroid drugs:
Hepatitis

A

Very rare

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41
Q

Common / rare / very rare adverse event of antithyroid drugs:
Hypoglycemia

A

Very rare

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42
Q

Common / rare / very rare adverse event of antithyroid drugs:
Cholestatic jaundice

A

Very rare

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43
Q

Carbimazole / methimazole / propylthiouracil adverse event:
Aplastic anemia

A

CBZ & PTU

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44
Q

Carbimazole / methimazole / propylthiouracil adverse event:
Thrombocytopenia

A

CBZ & PTU

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45
Q

Carbimazole / methimazole / propylthiouracil adverse event:
Lupus-like, ANCA-positive vasculitis

A

PTU

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46
Q

ANCA positive / negative:
PTU-induced vasculitis

A

ANCA-positive

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47
Q

Carbimazole / methimazole / propylthiouracil adverse event:
Hypoglycemia

A

PTU

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48
Q

Carbimazole / methimazole / propylthiouracil adverse event:
Cholestatic jaundice

A

CBZ & MMI

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49
Q

Prevalence of adverse event of antithyroid drugs:
Skin rash

A

1-5%

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50
Q

Prevalence of adverse event of antithyroid drugs:
Urticaria

A

1-5%

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51
Q

Prevalence of adverse event of antithyroid drugs:
Arthralgia

A

1-5%

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52
Q

Prevalence of adverse event of antithyroid drugs:
Polyarthritis

A

1-5%

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53
Q

Prevalence of adverse event of antithyroid drugs:
Transient mild leukopenia

A

1-5%

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54
Q

Characteristics (2) of leukopenia as a common adverse event of antithyroid drugs

A

Transient mild leukopenia

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55
Q

Prevalence of adverse event of antithyroid drugs:
Gastrointestinal

A

0.2-1%

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56
Q

Prevalence of adverse event of antithyroid drugs:
Abnormal smell and taste

A

0.2-1%

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57
Q

Prevalence of adverse event of antithyroid drugs:
Agranulocytosis

A

0.2-1%

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58
Q

Prevalence of adverse event of antithyroid drugs:
Aplastic anemia

A

<0.1%

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59
Q

Prevalence of adverse event of antithyroid drugs:
Thrombocytopenia

A

<0.1%

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60
Q

Prevalence of adverse event of antithyroid drugs:
Vasculitis

A

<0.1%

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61
Q

Prevalence of adverse event of antithyroid drugs:
Hepatitis

A

<0.1%

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62
Q

Prevalence of adverse event of antithyroid drugs:
Hypoglycemia

A

<0.1%

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63
Q

Prevalence of adverse event of antithyroid drugs:
Cholestatic jaundice

A

<0.1%

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64
Q

Increased / decreased / unchanged:
Peripheral vascular resistance in thyrotoxicosis

A

Decreased

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65
Q

Increased / decreased / unchanged:
Cardiac output in thyrotoxicosis

A

Increased

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66
Q

Increased / decreased / unchanged:
LV mass in thyrotoxicosis

A

Increased

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67
Q

Scratchy systolic sound along the left sternal border resembling a pleuropericardial effusion seen in thyrotoxicosis

A

Means-Lerman scratch

68
Q

Prevalence of atrial fibrillation in patients with thyrotoxicosis

A

2-20%

69
Q

Prevalence of thyrotoxicosis in patients with otherwise unexplained atrial fibrillation

A

~15%

70
Q

Pathophysiology of atrial fibrillation in thyrotoxicosis (2)

A

Thyroid hormone excess
Activating autoantibodies to beta1 adrenergic receptors

71
Q

Individuals over the age of 60 with a suppressed TSH had a __-fold ⬆️ risk of developing atrial fibrillation

A

2.8-fold

72
Q

Proportion of patients with atrial fibrillation that revert spontaneously to sinus rhythm within 4 months after treatment of thyrotoxicosis

A

~60%

73
Q

60% of patients with atrial fibrillation that revert spontaneously to sinus rhythm within hoe many after treatment of thyrotoxicosis

A

4 months

74
Q

In thyrotoxicosis, both synthesis and degradation rates of proteins are increased, with which of the two being increased more than the other?

A

Degradation rates

75
Q

Both lipogenesis and lipolysis are increased in thyrotoxicosis, but the net effect is:

A

Lipolysis

76
Q

Increased / decreased / unchanged in thyrotoxicosis:
Plasma free fatty acids

A

Increased

77
Q

Increased / decreased / unchanged in thyrotoxicosis:
Plasma glycerol

A

Increased

78
Q

Increased / decreased / unchanged in thyrotoxicosis:
Serum cholesterol

A

Decreased

79
Q

Increased / decreased / unchanged in thyrotoxicosis:
Serum triglycerides

A

Slightly decreased

80
Q

Increased / decreased / unchanged in thyrotoxicosis:
Plasma concentrations of epinephrine and norepinephrine

A

Unchanged

81
Q

Increased / decreased / unchanged in thyrotoxicosis:
Urinary excretion of catecholamine metabolites

A

Unchanged

82
Q

Increased / decreased / unchanged in thyrotoxicosis:
Frequency of seizures in those with convulsive disorders

A

Increased

83
Q

EEG finding in thyrotoxicosis

A

Increase in fast wave activity

84
Q

Proximal muscle wasting out of proportion to overall loss of weight

A

Thyrotoxic myopathy

85
Q

Increased / decreased / unchanged in thyrotoxicosis:
Vital capacity

A

Decreased: Vital capacity is commonly reduced, mainly from weakness if respiratory muscles

86
Q

Increased / decreased / unchanged in thyrotoxicosis:
Ventilation during exercise

A

Increased

87
Q

Increased / decreased / unchanged in thyrotoxicosis:
Diffusing capacity of the lung during exercise

A

Unchanged: Diffusing capacity of the lung is normal

88
Q

Increased / decreased / unchanged in thyrotoxicosis:
Serum calcium

A

Increased
Total serum calcium is increased in as many as 27% of patients, and iCa in 47%

89
Q

Increased / decreased / unchanged in thyrotoxicosis:
Parathyroid hormone

A

Unchanged: low-normal in most

90
Q

Increased / decreased / unchanged in thyrotoxicosis:
Plasma 25-OH vitamin D

A

Decreased

91
Q

Increased / decreased / unchanged in thyrotoxicosis:
Plasma volume

A

Increased

92
Q

Increased / decreased / unchanged in thyrotoxicosis:
Hematocrit

A

Unchanged

93
Q

Major production site of thyroid autoantibodies in Graves disease

A

Thyroidal lymphocyte infiltrate

94
Q

Gene that is most tightly associated with Graves disease

A

TSHR gene

95
Q

Median onset of Graves hyperthyroidism in individuals treated with alemtuzumab

A

17 months (2-107 months)

96
Q

Preferred imaging procedure for the diagnosis of Graves hyperthyroidism

A

Ultrasound with Doppler

97
Q

Ultrasound findings in Graves disease (3)

A

Diffuse thyroid enlargement
Hypoechogenicity
Increased vascularity

98
Q

Indications for scintigraphy in Graves hyperthyroidism (2)

A

Nodularity
Prior to 131I therapy

99
Q

Plasma half life of MMI

A

6 hours

100
Q

Plasma half life of PTU

A

1.5 hours

101
Q

Remission rate after ATD therapy in Graves disease

A

40-60%

102
Q

GREAT score: Age 40 and above

A

0

103
Q

GREAT score: Age <40

A

+1

104
Q

GREAT score: FT4 <40 pmol/L

A

0

105
Q

GREAT score: FT4 >/= 40 pmol/L

A

+1

106
Q

GREAT score: TBII <6 U/L

A

0

107
Q

GREAT score: TBII 6-19.9 U/L

A

+1

108
Q

GREAT score: TBII >/= 20 U/L

A

+2

109
Q

GREAT score: Goiter size grade 0-1

A

0

110
Q

GREAT score: Goiter size grade II-III

A

+2

111
Q

Class I GREAT score

A

0-1

112
Q

Class II GREAT score

A

2-3

113
Q

Class III GREAT score

A

4-6

114
Q

Risk of Graves hyperthyroidism recurrence: Class I GREAT score

A

16%

115
Q

Risk of Graves hyperthyroidism recurrence: Class II GREAT score

A

44%

116
Q

Risk of Graves hyperthyroidism recurrence: Class III GREAT score

A

68%

117
Q

Persistence or recurrence rate of Graves hyperthyroidism at 5 years following subtotal thyroidectomy

A

8%

118
Q

Dose of lithium carbonate in the treatment of Graves hyperthyroidism

A

300-450 mg every 8 hours

119
Q

High volume thyroid surgeon is define as a surgeon who does how many thyroidectomies in a year?

A

> 25

120
Q

Lifetime risk attributable to a 15-mCi 131I dose at the age of 20 years

A

0.8%

121
Q

Fetuses exposed to I-131 after how many weeks of gestation may be born athyreotic

A

10 weeks

122
Q

I-131 should not be administered for at least how many weeks after cessation of lactation?

A

8 weeks

123
Q

Prevention of worsening GO after 131I therapy of high risk patients

A

Prednisone 0.3-0.5 mg/kg daily for 3 months

124
Q

Prevention of worsening GO after 131I therapy of low risk patients

A

Prednisone 0.2 mg/kg daily for 6 weeks

125
Q

Treatment of very severe GO or dysthyroid optic neuropathy

A

IV methylprednisolone 1 g IV on 3 consecutive days in the first week followed by 1 g IV on 3 consecutive days in the second week

126
Q

Most orbital surgeons require stable thyroid eye disease for how long prior to surgery

A

6 months

127
Q

Target of the autoimmune attack in Graves orbitopathy

A

Dermal fibroblasts

128
Q

In vitro potency of hCG in terms of stimulating TSHR

A

1 U hCG = 0.7 uU TSH

129
Q

Hallmark of the immune effects initiated by the placenta in pregnant patients with Graves disease

A

Fall in thyroid autoantibody secretion

130
Q

Values of TRAb associated with neonatal thyrotoxicosis

A

> 3.7x ULN

131
Q

ATA guidelines recommend fetal monitoring of thyroid function in mothers who have this level of TRAb

A

> 3x ULN

132
Q

Iodide, when used in treating pregnant women, should not exceed this duration

A

2-3 weeks

133
Q

Large amounts of iodide are containdicated during this period of pregnancy

A

Last month

134
Q

ULN of total serum FT3 and FT4 are usually how many times that of nonpregnant levels

A

1.5x

135
Q

Maternal T4 is the major source of fetal thyroid hormone prior to:

A

20 weeks of gestation

136
Q

Prevalence of congenital defects in children of women treated with MMI

A

~1 in 30

137
Q

Prevalence of congenital defects in children of women treated with PTU

A

~1 in 40

138
Q

Period of risk when antithyroid drugs may be teratogenic

A

Weeks 6-10 of pregnancy

139
Q

Target during antithyroid drug therapy in pregnant patient with Graves disease

A

At or above upper normal nonpregnant range

140
Q

Possible adverse effects to the fetus of beta blocker therapy in the treatment of Graves hyperthyroidism in the mother (3)

A

Intrauterine growth restriction
Delayed lung development
Neonatal hypoglycemia or depression

141
Q

Postpartum period when transient postpartum thyroiditis occurs

A

4-12 months postpartum

142
Q

Most common genetic cause of toxic multinodular goiter

A

Somatic mutations in TSHR gene

143
Q

Somatic mutations in TSHR gene occur in __% of toxic nodules in TMNGA

A

60%

144
Q

TMNG usually occurs after the age of:

A

50 years

145
Q

Treatment of choice for TMNG

A

Radioiodine

146
Q

It is unusual for adenomas to produce thyrotoxicosis until they achieved a diameter of:

A

> 3 cm

147
Q

Usual RAI dose in the treatment of toxic adenoma

A

300-370 MBq or 8-10 mCi

148
Q

Preferred treatment modality for toxic adenomas in those younger than 18

A

Hemithyroidectomy

149
Q

Leading cause of increased cardiovascular mortality in both overt and subclinical hyperthyroidism

A

Heart failure

150
Q

Consider treatment of subclinical hypothyroidism with TSH >0.1 mU/L in:

A

Over age 65 with cardiac disease or osteoporosis

151
Q

Consider treatment of subclinical hypothyroidism with TSH <0.1 mU/L in: (2)

A

Over age 65
Younger than age 65 with cardiac disease or risk factors for cardiac disease or significant risk for osteoporosis

152
Q

More prevalent amiodarone induced thyroid dysfunction in iodine sufficient regions

A

Amiodarone induced hypothyroidism

153
Q

More prevalent amiodarone induced thyroid dysfunction in iodine deficient regions

A

Amiodarone induced thyrotoxicosis

154
Q

Most useful diagnostic test in differentiating type 1 and type 2 AIT

A

Color flow Doppler sonography

155
Q

Preferred treatment for AIT type 2

A

Prednisone 30 mg daily

156
Q

Sodium perchlorate should not be used longer than

A

4-6 weeks

157
Q

Median onset of AIT type 1

A

3.5 months

158
Q

Median onset of AIT type 2

A

30 months

159
Q

Preferred treatment for patients with RTH beta

A

Beta blockers

160
Q

In women found to be TPOAb positive prenatally, postpartum assessment of thyroid function si recommended to be done at: (3)

A

3, 6, and 12 months

161
Q

A hypothyroid phase following transient autoimmune thyrotoxicosis usually lasts:

A

2-9 months

162
Q

Primary events in the pathophysiology of subacute thyroiditis (2)

A

Apoptosis of follicular epithelium
Loss of follicular integrity

163
Q

ESR in subacute thyroiditis

A

> 100 mm/hr

164
Q

Increased / decreased / unchanged:
RAIU in acute pyogenic thyroiditis

A

Unchanged
“RAIU and thyroid function are usually preserved in acute pyogenic thyroiditis”

165
Q

This laboratory finding is a clear indication that thyrotoxicosis results from exogenous hormone

A

Low Tg

166
Q

Thyrotoxicosis may result from metastasis of this type of thyroid cancer

A

Follicular thyroid carcinoma