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
Increased / decreased / unchanged in hyperthyroidism: Tubular reabsorptive maximum
Increased
26
Increased / decreased / unchanged in hyperthyroidism: Tubular secretory maximum
Increased
27
Increased / decreased / unchanged in hyperthyroidism: Total exchangeable potassium
Decreased
28
Increased / decreased / unchanged in hyperthyroidism: Potassium levels
Unchanged
29
Common / rare / very rare adverse event of antithyroid drugs: Skin rash
Common
30
Common / rare / very rare adverse event of antithyroid drugs: Urticaria
Common
31
Common / rare / very rare adverse event of antithyroid drugs: Arthralgia
Common
32
Common / rare / very rare adverse event of antithyroid drugs: Polyarthritis
Common
33
Common / rare / very rare adverse event of antithyroid drugs: Transient mild leukopenia
Common
34
Common / rare / very rare adverse event of antithyroid drugs: Gastrointestinal
Rare
35
Common / rare / very rare adverse event of antithyroid drugs: Abnormal smell and taste
Rare
36
Common / rare / very rare adverse event of antithyroid drugs: Agranulocytosis
Rare
37
Common / rare / very rare adverse event of antithyroid drugs: Aplastic anemia
Very rare
38
Common / rare / very rare adverse event of antithyroid drugs: Thrombocytopenia
Very rare
39
Common / rare / very rare adverse event of antithyroid drugs: Lupus-like, ANCA-positive vasculitis
Very rare
40
Common / rare / very rare adverse event of antithyroid drugs: Hepatitis
Very rare
41
Common / rare / very rare adverse event of antithyroid drugs: Hypoglycemia
Very rare
42
Common / rare / very rare adverse event of antithyroid drugs: Cholestatic jaundice
Very rare
43
Carbimazole / methimazole / propylthiouracil adverse event: Aplastic anemia
CBZ & PTU
44
Carbimazole / methimazole / propylthiouracil adverse event: Thrombocytopenia
CBZ & PTU
45
Carbimazole / methimazole / propylthiouracil adverse event: Lupus-like, ANCA-positive vasculitis
PTU
46
ANCA positive / negative: PTU-induced vasculitis
ANCA-positive
47
Carbimazole / methimazole / propylthiouracil adverse event: Hypoglycemia
PTU
48
Carbimazole / methimazole / propylthiouracil adverse event: Cholestatic jaundice
CBZ & MMI
49
Prevalence of adverse event of antithyroid drugs: Skin rash
1-5%
50
Prevalence of adverse event of antithyroid drugs: Urticaria
1-5%
51
Prevalence of adverse event of antithyroid drugs: Arthralgia
1-5%
52
Prevalence of adverse event of antithyroid drugs: Polyarthritis
1-5%
53
Prevalence of adverse event of antithyroid drugs: Transient mild leukopenia
1-5%
54
Characteristics (2) of leukopenia as a common adverse event of antithyroid drugs
Transient mild leukopenia
55
Prevalence of adverse event of antithyroid drugs: Gastrointestinal
0.2-1%
56
Prevalence of adverse event of antithyroid drugs: Abnormal smell and taste
0.2-1%
57
Prevalence of adverse event of antithyroid drugs: Agranulocytosis
0.2-1%
58
Prevalence of adverse event of antithyroid drugs: Aplastic anemia
<0.1%
59
Prevalence of adverse event of antithyroid drugs: Thrombocytopenia
<0.1%
60
Prevalence of adverse event of antithyroid drugs: Vasculitis
<0.1%
61
Prevalence of adverse event of antithyroid drugs: Hepatitis
<0.1%
62
Prevalence of adverse event of antithyroid drugs: Hypoglycemia
<0.1%
63
Prevalence of adverse event of antithyroid drugs: Cholestatic jaundice
<0.1%
64
Increased / decreased / unchanged: Peripheral vascular resistance in thyrotoxicosis
Decreased
65
Increased / decreased / unchanged: Cardiac output in thyrotoxicosis
Increased
66
Increased / decreased / unchanged: LV mass in thyrotoxicosis
Increased
67
Scratchy systolic sound along the left sternal border resembling a pleuropericardial effusion seen in thyrotoxicosis
Means-Lerman scratch
68
Prevalence of atrial fibrillation in patients with thyrotoxicosis
2-20%
69
Prevalence of thyrotoxicosis in patients with otherwise unexplained atrial fibrillation
~15%
70
Pathophysiology of atrial fibrillation in thyrotoxicosis (2)
Thyroid hormone excess Activating autoantibodies to beta1 adrenergic receptors
71
Individuals over the age of 60 with a suppressed TSH had a __-fold ⬆️ risk of developing atrial fibrillation
2.8-fold
72
Proportion of patients with atrial fibrillation that revert spontaneously to sinus rhythm within 4 months after treatment of thyrotoxicosis
~60%
73
60% of patients with atrial fibrillation that revert spontaneously to sinus rhythm within hoe many after treatment of thyrotoxicosis
4 months
74
In thyrotoxicosis, both synthesis and degradation rates of proteins are increased, with which of the two being increased more than the other?
Degradation rates
75
Both lipogenesis and lipolysis are increased in thyrotoxicosis, but the net effect is:
Lipolysis
76
Increased / decreased / unchanged in thyrotoxicosis: Plasma free fatty acids
Increased
77
Increased / decreased / unchanged in thyrotoxicosis: Plasma glycerol
Increased
78
Increased / decreased / unchanged in thyrotoxicosis: Serum cholesterol
Decreased
79
Increased / decreased / unchanged in thyrotoxicosis: Serum triglycerides
Slightly decreased
80
Increased / decreased / unchanged in thyrotoxicosis: Plasma concentrations of epinephrine and norepinephrine
Unchanged
81
Increased / decreased / unchanged in thyrotoxicosis: Urinary excretion of catecholamine metabolites
Unchanged
82
Increased / decreased / unchanged in thyrotoxicosis: Frequency of seizures in those with convulsive disorders
Increased
83
EEG finding in thyrotoxicosis
Increase in fast wave activity
84
Proximal muscle wasting out of proportion to overall loss of weight
Thyrotoxic myopathy
85
Increased / decreased / unchanged in thyrotoxicosis: Vital capacity
Decreased: Vital capacity is commonly reduced, mainly from weakness if respiratory muscles
86
Increased / decreased / unchanged in thyrotoxicosis: Ventilation during exercise
Increased
87
Increased / decreased / unchanged in thyrotoxicosis: Diffusing capacity of the lung during exercise
Unchanged: Diffusing capacity of the lung is normal
88
Increased / decreased / unchanged in thyrotoxicosis: Serum calcium
Increased Total serum calcium is increased in as many as 27% of patients, and iCa in 47%
89
Increased / decreased / unchanged in thyrotoxicosis: Parathyroid hormone
Unchanged: low-normal in most
90
Increased / decreased / unchanged in thyrotoxicosis: Plasma 25-OH vitamin D
Decreased
91
Increased / decreased / unchanged in thyrotoxicosis: Plasma volume
Increased
92
Increased / decreased / unchanged in thyrotoxicosis: Hematocrit
Unchanged
93
Major production site of thyroid autoantibodies in Graves disease
Thyroidal lymphocyte infiltrate
94
Gene that is most tightly associated with Graves disease
TSHR gene
95
Median onset of Graves hyperthyroidism in individuals treated with alemtuzumab
17 months (2-107 months)
96
Preferred imaging procedure for the diagnosis of Graves hyperthyroidism
Ultrasound with Doppler
97
Ultrasound findings in Graves disease (3)
Diffuse thyroid enlargement Hypoechogenicity Increased vascularity
98
Indications for scintigraphy in Graves hyperthyroidism (2)
Nodularity Prior to 131I therapy
99
Plasma half life of MMI
6 hours
100
Plasma half life of PTU
1.5 hours
101
Remission rate after ATD therapy in Graves disease
40-60%
102
GREAT score: Age 40 and above
0
103
GREAT score: Age <40
+1
104
GREAT score: FT4 <40 pmol/L
0
105
GREAT score: FT4 >/= 40 pmol/L
+1
106
GREAT score: TBII <6 U/L
0
107
GREAT score: TBII 6-19.9 U/L
+1
108
GREAT score: TBII >/= 20 U/L
+2
109
GREAT score: Goiter size grade 0-1
0
110
GREAT score: Goiter size grade II-III
+2
111
Class I GREAT score
0-1
112
Class II GREAT score
2-3
113
Class III GREAT score
4-6
114
Risk of Graves hyperthyroidism recurrence: Class I GREAT score
16%
115
Risk of Graves hyperthyroidism recurrence: Class II GREAT score
44%
116
Risk of Graves hyperthyroidism recurrence: Class III GREAT score
68%
117
Persistence or recurrence rate of Graves hyperthyroidism at 5 years following subtotal thyroidectomy
8%
118
Dose of lithium carbonate in the treatment of Graves hyperthyroidism
300-450 mg every 8 hours
119
High volume thyroid surgeon is define as a surgeon who does how many thyroidectomies in a year?
>25
120
Lifetime risk attributable to a 15-mCi 131I dose at the age of 20 years
0.8%
121
Fetuses exposed to I-131 after how many weeks of gestation may be born athyreotic
10 weeks
122
I-131 should not be administered for at least how many weeks after cessation of lactation?
8 weeks
123
Prevention of worsening GO after 131I therapy of high risk patients
Prednisone 0.3-0.5 mg/kg daily for 3 months
124
Prevention of worsening GO after 131I therapy of low risk patients
Prednisone 0.2 mg/kg daily for 6 weeks
125
Treatment of very severe GO or dysthyroid optic neuropathy
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
Most orbital surgeons require stable thyroid eye disease for how long prior to surgery
6 months
127
Target of the autoimmune attack in Graves orbitopathy
Dermal fibroblasts
128
In vitro potency of hCG in terms of stimulating TSHR
1 U hCG = 0.7 uU TSH
129
Hallmark of the immune effects initiated by the placenta in pregnant patients with Graves disease
Fall in thyroid autoantibody secretion
130
Values of TRAb associated with neonatal thyrotoxicosis
>3.7x ULN
131
ATA guidelines recommend fetal monitoring of thyroid function in mothers who have this level of TRAb
>3x ULN
132
Iodide, when used in treating pregnant women, should not exceed this duration
2-3 weeks
133
Large amounts of iodide are containdicated during this period of pregnancy
Last month
134
ULN of total serum FT3 and FT4 are usually how many times that of nonpregnant levels
1.5x
135
Maternal T4 is the major source of fetal thyroid hormone prior to:
20 weeks of gestation
136
Prevalence of congenital defects in children of women treated with MMI
~1 in 30
137
Prevalence of congenital defects in children of women treated with PTU
~1 in 40
138
Period of risk when antithyroid drugs may be teratogenic
Weeks 6-10 of pregnancy
139
Target during antithyroid drug therapy in pregnant patient with Graves disease
At or above upper normal nonpregnant range
140
Possible adverse effects to the fetus of beta blocker therapy in the treatment of Graves hyperthyroidism in the mother (3)
Intrauterine growth restriction Delayed lung development Neonatal hypoglycemia or depression
141
Postpartum period when transient postpartum thyroiditis occurs
4-12 months postpartum
142
Most common genetic cause of toxic multinodular goiter
Somatic mutations in TSHR gene
143
Somatic mutations in TSHR gene occur in __% of toxic nodules in TMNGA
60%
144
TMNG usually occurs after the age of:
50 years
145
Treatment of choice for TMNG
Radioiodine
146
It is unusual for adenomas to produce thyrotoxicosis until they achieved a diameter of:
>3 cm
147
Usual RAI dose in the treatment of toxic adenoma
300-370 MBq or 8-10 mCi
148
Preferred treatment modality for toxic adenomas in those younger than 18
Hemithyroidectomy
149
Leading cause of increased cardiovascular mortality in both overt and subclinical hyperthyroidism
Heart failure
150
Consider treatment of subclinical hypothyroidism with TSH >0.1 mU/L in:
Over age 65 with cardiac disease or osteoporosis
151
Consider treatment of subclinical hypothyroidism with TSH <0.1 mU/L in: (2)
Over age 65 Younger than age 65 with cardiac disease or risk factors for cardiac disease or significant risk for osteoporosis
152
More prevalent amiodarone induced thyroid dysfunction in iodine sufficient regions
Amiodarone induced hypothyroidism
153
More prevalent amiodarone induced thyroid dysfunction in iodine deficient regions
Amiodarone induced thyrotoxicosis
154
Most useful diagnostic test in differentiating type 1 and type 2 AIT
Color flow Doppler sonography
155
Preferred treatment for AIT type 2
Prednisone 30 mg daily
156
Sodium perchlorate should not be used longer than
4-6 weeks
157
Median onset of AIT type 1
3.5 months
158
Median onset of AIT type 2
30 months
159
Preferred treatment for patients with RTH beta
Beta blockers
160
In women found to be TPOAb positive prenatally, postpartum assessment of thyroid function si recommended to be done at: (3)
3, 6, and 12 months
161
A hypothyroid phase following transient autoimmune thyrotoxicosis usually lasts:
2-9 months
162
Primary events in the pathophysiology of subacute thyroiditis (2)
Apoptosis of follicular epithelium Loss of follicular integrity
163
ESR in subacute thyroiditis
>100 mm/hr
164
Increased / decreased / unchanged: RAIU in acute pyogenic thyroiditis
Unchanged “RAIU and thyroid function are usually preserved in acute pyogenic thyroiditis”
165
This laboratory finding is a clear indication that thyrotoxicosis results from exogenous hormone
Low Tg
166
Thyrotoxicosis may result from metastasis of this type of thyroid cancer
Follicular thyroid carcinoma