Hyperthyroidism and thyrotoxicosis - AMBOSS.pdf

Thyrotoxicosis
refers to the symptoms caused by the excessive circulation of thyroid hormones. It is typically
caused by thyroid gland hyperactivity (i.e., hyperthyroidism
), the most common causes of which are Graves
disease (most common), toxic multinodular goiter (MNG), and toxic adenoma. It may also be caused by the
inappropriate release of thyroid hormone from a damaged or inflamed thyroid gland (e.g., thyroiditis). In rare
cases, thyrotoxicosis is caused by TSH-producing pituitary tumors (central hyperthyroidism
), excessive
production of hCG (e.g., in gestational trophoblastic disease), or oral intake of thyroid hormones (
exogenous
hyperthyroidism symptoms of thyrotoxicosis
). The most common include fatigue, anxiety, heat intolerance,
increased perspiration, palpitations, and significant weight loss despite increased appetite.
Thyroid function tests
( ) confirm , while TSH receptor TFTs thyrotoxicosis antibodies, , and
thyroid ultrasonography radioactive iodine
uptake tests are used to identify the etiology. Management of any form of thyrotoxicosis
involves the initial
control of symptoms with beta blockers and antithyroid drugs, oMen followed by definitive therapy with either
radioactive iodine ablation RAIA
( ) of the thyroid gland or thyroid surgery. An acute exacerbation of
can lead to a life-threatening hypermetabolic state known as thyroid storm
, which is diagnosed
clinically along with thyroid function tests . Patients with thyroid storm
require urgent stabilization in critical care
seRings with fluids, beta blockers, antithyroid medications (propylthiouracil, potassium iodide, and parenteral
glucocorticoids), active cooling, and management of tachyarrhythmias. Definitive therapy with RAIA
or surgery is
considered once they are stable.

1. Hyperthyroidism and thyrotoxicosis Last edited: Sep 20, 2024
Content policy
Learned
Summary
refers to the symptoms caused by the excessive circulation of thyroid hormones. It is typically
caused by thyroid gland hyperactivity (i.e., ), the most common causes of which are Graves
disease (most common), toxic multinodular goiter (MNG), and toxic adenoma. It may also be caused by the
inappropriate release of thyroid hormone from a damaged or inflamed thyroid gland (e.g., thyroiditis). In rare
cases, is caused by TSH-producing pituitary tumors (central ), excessive
production of hCG (e.g., in gestational trophoblastic disease), or oral intake of thyroid hormones (
). The most common include fatigue, anxiety, heat intolerance,
increased perspiration, palpitations, and significant weight loss despite increased appetite.
() confirm , while TSH receptor antibodies, , and
are used to identify the etiology. Management of any form of involves the initial
control of symptoms with beta blockers and antithyroid drugs, oMen followed by definitive therapy with either
() of the thyroid gland or thyroid surgery. An acute exacerbation of
can lead to a life-threatening hypermetabolic state known as , which is diagnosed
clinically along with . Patients with require urgent stabilization in critical care
seRings with fluids, beta blockers, antithyroid medications (propylthiouracil, potassium iodide, and parenteral
glucocorticoids), active cooling, and management of tachyarrhythmias. Definitive therapy with or surgery is
considered once they are stable.
COLLAPSE NOTES FEEDBACK
Definitions
QBANK SESSION
Thyrotoxicosis
hyperthyroidism
thyrotoxicosis hyperthyroidism
exogenous
hyperthyroidism symptoms of thyrotoxicosis
Thyroid function tests
TFTs thyrotoxicosis thyroid ultrasonographyradioactive iodine
uptake tests thyrotoxicosis
radioactive iodine ablationRAIA
thyrotoxicosis thyroid storm
thyroid function tests thyroid storm
RAIA
Hyperthyroidism
fact sheet
OPTIONS High-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism

2. COLLAPSE NOTES FEEDBACK
Definitions
While and are o,en used interchangeably, the two terms are not synonymous.
Thyrotoxicosis: a hypermetabolic condition caused by an inappropriately high level of circulating thyroid
hormones irrespective of the source.
Hyperthyroidism: a condition characterized by the overproduction of thyroid hormones by the thyroid
gland; can cause
Overt hyperthyroidism
↓ Serum TSH levels with ↑ serum free T and/or T levels
Patients typically experience .
Subclinical hyperthyroidism
↓ Serum TSH levels with normal serum free T and T levels
Patients are normally asymptomatic or mildly symptomatic.
May progress to
COLLAPSE NOTES FEEDBACK
Overview
fact sheet
thyrotoxicosishyperthyroidism
[1]
thyrotoxicosis
4 3
symptoms of thyrotoxicosis
4 3
overt hyperthyroidism
MAXIMIZE TABLE TABLE QUIZ
Overview of common etiologies in hyperthyroidism and thyrotoxicosis
Graves disease Toxic MNG
Subacute
granulomatous
thyroiditis (de
Quervain
thyroiditis)
Subacute
lymphocytic
thyroiditis (silent
thyroiditis)
Iodine-induced
hyperthyroidism
Thyroid status
Acute to chronic Chronic Transient followed by
features of hypothyroidism
in
patients with a
preexisting
iodine-deficiency
thyroid disorder
Epidemiology
Most common
cause of
in the US
Peak incidence:
> 50 years of age
Peak incidence: 30–50 years of age
More common in
iodine-deficient
[2][3][4][5][6][7][8]
hyperthyroidism hyperthyroidism
thyrotoxicosis
Thyrotoxicosis
hyperthyroidism
Hyperthyroidism and thyrotoxicosisDefinitions
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
Can be due to overproduction by either the thyroid gland (i.e., hyperthyroidism) or an ectopicsource, inappropriate release of
thyroid hormone (e.g., in thyroiditis), or ingestion of exogenous thyroid hormone (accidental or intentional)
I.e. synthesis and secretion

3. Thyroid status
Acute to chronic Chronic Transient followed by
features of hypothyroidism
in
patients with a
preexisting
iodine-deficiency
thyroid disorder
Epidemiology
Most common
cause of
in the US
Peak incidence:
20–30 years of
age
♀
>
♂
(8:1)
Peak incidence:
> 50 years of age
♀
>
♂
Peak incidence: 30–50 years of age
♀
>
♂
(3:1)
More common in
iodine-deficient
regions
Causes
Autoimmune
due to TSH
receptor
autoantibodies
Chronic iodine
deficiency
Viral infections
causing damage
to follicular
cells
Postpartum
thyroiditis
Autoimmune
diseases
Drugs:
α–interferon,
lithium,
amiodarone,
interleukin–2,
tyrosine kinase
inhibitors
Iodine excess from
diet, contrast, or
amiodarone
Goiter
Consistency
Diffuse and
smooth
Multinodular Diffuse and firm
Depends on
underlying thyroid
disorder
Pain Painless Painless Painful Painless Painless
Other findings
Graves
ophthalmopathy
Pretibial
myxedema
Nonspecific
↑ ESR
Fever, malaise
Possible history of upper respiratory tract
infections a few weeks prior to the onset of
subacute thyroiditis
Nonspecific
↓/Undetectable
TSH
↑ T3/T4
↓ TSH
↑ T3/T4
Thyrotoxic phase: ↓ TSH, ↑ T3/T4, and
↑ thyroglobulin
Hypothyroid phase: ↑ TSH and ↓ T3/T4
↓ TSH
↑ T3/T4
Antibodies
↑ TRAbs,
anti-TPO
antibody, and
anti-Tg
Absent Anti-TPO antibody
Possible ↑ TRAb
in patients with
Graves disease
Iodine uptake on
scintigraphy
Diffuse
Multiple focal areas
of increased uptake
Reduced Reduced
Histopathological
findings
Diffuse
hyperplasia and
hypertrophy of
follicular cells
Patches of enlarged
follicular cells
distended with
colloid and
fla\ened
epithelium
Granulomatous
inflammation,
multinucleated
giant cells on
histology
Absence of
germinal follicles,
lymphocytic
infiltration on
histology
Depends on
underlying thyroid
disorder
hyperthyroidism hyperthyroidism
thyrotoxicosis
Thyrotoxicosis
hyperthyroidism
Thyroid function tests
Hyperthyroidism and thyrotoxicosisOverview
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
ESR is normal among patients with
postpartum thyroiditis.

4. COLLAPSE NOTES FEEDBACK
Epidemiology
Prevalence
: ∼ 1%
: 2–3%
Sex:
♀
>
♂
(5:1)
Age range at presentation
Graves disease: 20–30 years of age
Toxic adenoma: 30–50 years of age
Toxic MNG: peak incidence > 50 years of age
References:
Epidemiological data refers to the US, unless otherwise specified.
COLLAPSE NOTES FEEDBACK
Etiology
Hyperfunctioning thyroid gland
Graves disease (∼ 60–80% of cases)
Toxic MNG (∼ 15–20% of cases)
Toxic adenoma (3–5% of cases)
TSH-producing pituitary adenoma (thyrotropic adenoma)
hCG-mediated : e.g., gestational transient thyrotoxicosis (GTT), gestational trophoblastic disease (GTD)
Destruction of the thyroid gland (destructive thyroiditis)
Thyroiditis (see “Subacute thyroiditis”)
Subacute granulomatous thyroiditis (de Quervain thyroiditis)
Subacute lymphocytic thyroiditis (e.g., postpartum thyroiditis)
Drug-induced thyroiditis (e.g., amiodarone, lithium)
Contrast-induced thyroiditis (Jod-Basedow phenomenon)
Hashitoxicosis (see “Hashimoto thyroiditis”)
Palpation thyroiditis: due to thyroid gland manipulation during parathyroid surgery.
Riedel thyroiditis
Ectopic (extrathyroidal) hormone production
epithelium histology
[9]
Overt hyperthyroidism
Subclinical hyperthyroidism
[10]
[11][12]
hyperthyroidism
Radiation thyroiditis
Exogenous thyrotoxicosis
Hyperthyroidism and thyrotoxicosisEpidemiology
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
Overproduction, i.e., synthesis and secretion, of thyroid hormones by the thyroid gland
Very high amounts of hCG may lead to
hyperthyroidism because hCGstructurally
resembles TSH.
Inflammation/destruction of the thyroid cells results in inappropriate release of thyroid hormone.
I
2
3
4 ↑
TSH
-
*Ts
,
T4
H
.
Mole
B
I
2
3
4
-

5. Hashitoxicosis (see “Hashimoto thyroiditis”)
Palpation thyroiditis: due to thyroid gland manipulation during parathyroid surgery.
Riedel thyroiditis
Ectopic (extrathyroidal) hormone production
Struma ovarii
Metastatic follicular thyroid carcinoma
References:
COLLAPSE NOTES FEEDBACK
Pathophysiology
Hypothalamic-pituitary-thyroid axis
The hypothalamus, anterior pituitary gland, and thyroid gland, together with their respective hormones, make up a
self-regulating circuit known as the hypothalamic-pituitary-thyroid axis.
Physiological regulation: See “Thyroid gland” in “General endocrinology.”
Disorders of the thyroid gland → excess production of T/T → compensatory decrease of TSH
Thyrotropic adenoma → ↑ TSH levels → ↑ T/T levels
Other causes of
Excess intake/ectopic production of thyroid hormone → ↑ levels of circulating T/T → compensatory decrease of TSH
Trigger → inflammation of the thyroid gland → cellular damage and destruction → inappropriate release of T/T
Effects of
Generalized hypermetabolism (increased substrate consumption)
↑ Number of Na/K-ATPase → elevation of basal metabolism → promoted thermogenesis
Upregulation of β-adrenergic receptors → hyperstimulation of the sympathetic nervous system
Cardiac effects (increased cardiac output)
↑ Numbers of ATPase on cardiac myocytes; ↓ amount of phospholamban (PLB) → ↑ transsarcolemmal Ca movement →
enhanced myocardial contractility
↓ Peripheral vascular resistance
COLLAPSE NOTES FEEDBACK
Clinical features
Radiation thyroiditis
Exogenous thyrotoxicosis
[2][13][14]
Hyperthyroidism
34
34
thyrotoxicosis
34
34
thyrotoxicosis
++
[15]
2+
Hyperthyroidism and thyrotoxicosisPathophysiology
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
This state of hyperthyroidism is called central hyperthyroidism.
E.g., infection, radiation, autoimmune disease, trauma, surgery, medication
No evidence suggests that catecholaminesecretion is elevated in hyperthyroidism.

6. ↓ Peripheral vascular resistance
COLLAPSE NOTES FEEDBACK
Clinical features
General
Heat intolerance
Excessive sweating because of increased cutaneous blood flow
Weight loss despite increased appetite
Frequent bowel movements (because of intestinal hypermotility)
Weakness, fatigue
Skin
Infiltrative dermopathy, especially in the pretibial area (pretibial myxedema)
Onycholysis
An early cutaneous manifestation of
Thickened nails with distal white discoloration and separation of the nail plate
Initially develops in the fourth fingers, but can involve all nails, including the toenails
Thyroid acropachy: nail clubbing seen in late stages of Graves disease
Eyes
Lid lag: caused by adrenergic overactivity, which results in spasming of the smooth muscle of the levator palpebrae
superioris
Lid retraction: “staring look”
Graves ophthalmopathy (exophthalmos, edema of the periorbital tissue)
Goiter
Diffuse, smooth, nontender goiter
ONen with an audible bruit at the superior poles
Also seen in subacute thyroiditis, toxic adenoma, and toxic MNG
Cardiovascular
Tachycardia
Palpitations, irregular pulse (due to atrial fibrillation/ectopic beats)
Hypertension with widened pulse pressure
Systolic pressure is increased due to increased heart rate and cardiac output.
Diastolic pressure is decreased due to decreased peripheral vascular resistance.
Thyrotoxicosis-induced cardiac failure: elderly patients oNen present with features of cardiac failure (e.g., pedal edema,
exertional dyspnea).
Abnormal heart rhythms, including atrial fibrillation
Chest pain
Musculoskeletal
Fine tremor of the outstretched fingers
hyperthyroidism
Hyperthyroidism and thyrotoxicosisClinical features
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
Results from glycosaminoglycans deposition
Sclera visible above the cornea when looking down.
Sclera visible above the cornea when looking straight ahead.
Mainly seen in Graves disease, the most common cause of hyperthyroidism
System most affected in the elderly
Tachycardia may be masked in the elderly by beta-blockers since these are often taken for hypertension/angina
LL/LR
"Atherosc"160/70
=
PP
+
90↑Go
PUR

7. Thyrotoxicosis-induced cardiac failure: elderly patients o6en present with features of cardiac failure (e.g., pedal edema,
exertional dyspnea).
Abnormal heart rhythms, including atrial fibrillation
Chest pain
Musculoskeletal
Fine tremor of the outstretched fingers
Hyperthyroid myopathy: a condition of muscle weakness, pain, and atrophy associated with (e.g., from
Graves disease, thyroiditis)
Predominantly affects individuals > 40 years of age
Can develop acutely or several weeks to months a6er the onset of .
Typically affects proximal muscles (e.g., hip flexors, quadriceps) more than distal muscles
Serum creatine kinase levels are most o6en normal
o6en reverses myopathy
Osteopathy: osteoporosis due to the direct effect of T on osteoclastic bone resorption , fractures (in the elderly)
Endocrinological
Female: oligomenorrhea, amenorrhea, anovulatory infertility, dysfunctional uterine bleeding
Male: gynecomastia, decreased libido, infertility, erectile dysfunction
Glucose intolerance
↓ Insulin sensitivity of peripheral tissue
Impaired insulin secretion
Neuropsychiatric system
Anxiety
Emotional instability
Depression
Restlessness
Insomnia
Tremoulousness (results from the hyperadrenergic state)
Hyperreflexia
COLLAPSE NOTES FEEDBACK
Subtypes and variants
hyperthyroidism
hyperthyroidism
Treatment of hyperthyroidism
3
[16]
Graves ophthal-
mopathy
Patient with goiterSurface anatomy of
the thyroid gland
Examination of the
Thyroid - Clinical
Examination
Hyperthyroidism and thyrotoxicosisClinical features
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
The tremor can also involve the face, tongue, and head, and responds well to treatment with beta blockers.
In long-standing hyperthyroidism
Serum sex hormone-binding globulin (SHBG)
levels are high in hyperthyroidism ? low
serum free (unbound) estradiol concentrations
High serum SHBG levels ? low serum free (unbound) testosterone
concentrations and increased extragonadal conversion of testosterone to
estradiol

8. COLLAPSE NOTES FEEDBACK
Subtypes and variants
Exogenous thyrotoxicosis
Etiology
is caused by excessive intake of thyroid hormone.
Intentional
Therapeutic: suppressive doses of thyroid hormones for thyroid cancer treatment
Related to psychiatric illness (e.g., eating disorders, body dysmorphia, or factitious disorders)
AAempting weight loss
Unintentional
Iatrogenic
Accidental ingestion (primarily in children)
Dietary supplements
Clinical features
Goiter is absent.
Diagnostics
Low/undetectable TSH
High levels of T and/or T
Low Tg levels
Low RAI uptake on scintigraphy
Treatment
Taper and stop the exogenous thyroid hormone.
Consider with beta blockers if symptoms are severe.
For severe , consider:
Cholestyramine (which binds to T and T in the intestine and interrupts the enterohepatic circulation)
COLLAPSE NOTES FEEDBACK
Diagnosis
mopathy the thyroid glandThyroid - Clinical
Examination
[17][18]
Exogenous thyrotoxicosis
[19]
[17]
[17][20]
Symptoms of thyrotoxicosis
[21]
[17][20]
4 3
[17]
[22]
[17]
[19]
symptomatic therapy for thyrotoxicosis
thyrotoxicosis
[17]
3 4
[17]
Hyperthyroidism and thyrotoxicosisSubtypes and variants
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
This condition is sometimes referred to as exogenous or factitious
hyperthyroidism. These are misnomers, as hyperthyroidisminvolves an
overproduction of thyroid hormones, not excess intake.
A prescribed or dispensed dose is too high.
Supplements may contain thyroid hormones.
Suppression of TSH causes thyroid glandatrophy rather than growth.
An imaging procedure in which low doses of radioactive
substances are injected into the bloodstream and then detected by
a device (gamma camera), providing information about the
metabolic activity of body structures. The selection of the
radioactive agent depends on the structure to be scanned (e.g.,
thyroid gland, bowel, bones, heart, lungs).
Bound T3 and T4 are excreted
with feces
08
00
If
of

9. Cholestyramine (which binds to T and T in the intestine and interrupts the enterohepatic circulation)
COLLAPSE NOTES FEEDBACK
Diagnosis
For neonates or pregnant individuals, see “Special patient groups” for additional information.
Approach
Initial evaluation: perform clinical assessment and screen () alongside routine laboratory studies.
Consider alternate diagnoses if are normal.
If characteristic features of Graves disease are present: can stop investigations and begin management of Graves disease.
Identify any tachyarrhythmia requiring treatment (see also “Atrial fibrillation” and “Acute management of tachycardia”).
Subsequent evaluation depends on the clinical picture . Options include:
: first-line for most patients with uncertain diagnoses, e.g., suspected thyroid adenoma or toxic MNG
TSH receptor antibody (TRAb): for suspected Graves disease without characteristic features
: first-line for pregnant/lactating patients, palpable nodules or suspected thyroiditis
Further evaluation: based on initial results
Normal imaging and negative TRAb: consider serum thyroglobulin to identify
Inconclusive imaging and negative TRAb: consider thyroid peroxidase antibodies to identify thyroiditis
Suspicious nodules visible on imaging: refer for FNAC (see also “Thyroid nodules”)
Initial evaluation
Thyroid-stimulating hormone (TSH) level (initial screening test): Typically low/undetectable; a normal TSH level usually rules
out .
Free T (FT) and total T levels: Typically both elevated; indicated when is strongly suspected or TSH is
abnormal
3 4
[17]
thyroid function testsTFTs
TFTs
Thyroid scintigraphy
Thyroid ultrasound
exogenous thyrotoxicosis
Diagnosis of hyper-
thyroidism
[17][23]
Thyroid function tests
hyperthyroidism
4 4 3 thyrotoxicosis
MAXIMIZE TABLE TABLE QUIZ
Interpretation of elevated thyroid hormones
Condition TSH level Free T Total T
[17][23]
Hyperthyroidism and thyrotoxicosisDiagnosis
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
+ve TRAb may obviate the need for imaging
Exceptions include a thyrotropic adenoma or thyroid hormone resistance.
Levels of total T3 and T4 are both affected by levels of thyroid-binding globulin. To improve diagnostic accuracy, measuring free T4 is preferred. Assays to measure free T3 are
less reliable; in clinical practice, measurement of total T3 is recommended.
H
9
4
TG
TPGAB
*
32 I Normal
-
Grav
.
Grav
TRAb
Hash
TPoAb
&
TG
Exo
.
Thyrox
.-Low
TG
De
Q
After
Viral
Inf
MESR
I
-
I

10. Free T (FT) and total T levels: Typically both elevated; indicated when is strongly suspected or TSH is
abnormal
Routine laboratory studies
CBC: leukocytosis and/or mild anemia
BMP
Hyperglycemia
Mild hypercalcemia
Liver chemistries: mildly elevated AST, ALT, ALP, and bilirubin
Serum cholesterol: decreased total cholesterol, LDL, and HDL
ESR: typically elevated (> 100 mm/hour) in subacute thyroiditis
ECG findings
Tachycardia
Atrial fibrillation
LBBB and ECG signs of LVH in patients with dilated cardiomyopathy
Subsequent evaluation
Indicated if the diagnosis remains uncertain aQer clinical assessment and initial evaluation. The choice and priority of studies
depends on the clinical picture, patient characteristics and test availability.
TSH receptor antibody (TRAb)
Indication: if Graves disease is suspected but classic clinical features are absent
Interpretation
Positive: Diagnosis of Graves disease is established.
Negative: Further investigation is necessary.
Nuclear medicine thyroid scan and radioactive iodine uptake measurement
Definitions
: a nuclear medicine imaging technique that visualizes the distribution of thyroid function
using an oral or IV radiotracer (most commonly Tc-99m pertechnetate or iodine-123)
( ): a test that quantifies the percentage of the administered amount of
4 4 3 thyrotoxicosis
MAXIMIZE TABLE TABLE QUIZ
Interpretation of elevated thyroid hormones
Condition TSH level Free T Total T
and thyrotoxic-phase thyroiditis ↓ ↑ In 90% of cases ↑
↓ Normal Normal
Exogenous thyrotoxicosis ↓ ↑ Normal or ↑
Thyrotropic adenoma Normal or ↑ ↑ ↑
[17][23]
4 3
Overt hyperthyroidism
Subclinical hyperthyroidism
[17]
[17]
[24]
Nuclear medicine thyroid scan
Radioactive iodine uptake measurementRAIU test
Hyperthyroidism and thyrotoxicosisDiagnosis
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
E.g., Graves disease, toxic MNG, and toxic adenoma
If the negative feedback regulation mechanism is intact,
increased T3 and T4 lead to TSH suppression, which in turn
leads to reduced stimulation of thyroid follicular cells. Thyroid
hormone levels may then be normal.
Levels of β-hCG (similar molecular structure to TSH) peak at the end
of the first trimester, leading to a decrease in serum TSH levels.
Secondary to increased glyconeogenesis and inhibition of insulin by catecholamines
Bone resorption in hyperthyroidism is increased; therefore, even subclinical hyperthyroidism should be treated to reduce the risk of osteoporosis.
Most common cardiac finding
In 13% of patients with hyperthyroidism> 65 years of age
Dilated cardiomyopathy is a complication that can
occur as a result of a high cardiac output state.
In patients with characteristic features of Graves disease
(hyperthyroidism with new orbitopathy and a symmetrically
enlarged thyroid), further testing is not required. If the patient
does not have these features but Graves disease is still
suspected, TRAb levels can be measured to confirm the
diagnosis.
TRAbs can be negative in very mild Graves disease.
I.e., even distribution of
function, hyperfunctioning
areas, or suppressed areas
2
3
Y
&
=> -

11. Nuclear medicine thyroid scan and radioactive iodine uptake measurement
Definitions
: a nuclear medicine imaging technique that visualizes the distribution of thyroid function
using an oral or IV radiotracer (most commonly Tc-99m pertechnetate or iodine-123)
( ): a test that quantifies the percentage of the administered amount of
radioactive iodine taken up by the thyroid gland
Indications
First-line test for most patients with uncertain etiology of aGer initial evaluation
Assessment of functional status of thyroid nodules
Thyroid malignancy
Identification of ectopic thyroid tissue (e.g., lingual thyroid, struma ovarii)
Evaluation of retrosternal goiters
Evaluation of thyroglossal cysts
Contraindications: pregnant or breasLeeding women
Findings
Hot nodule: Hyperfunctioning tissue takes up large amounts of radioactive iodine
Cold nodule: Non-functioning nodules do not take up any radioactive iodine and appear "cold”, but the surrounding normal
thyroid tissue takes up radioactive iodine and appears "warm"
See also “Diagnostics” in “Thyroid cancer” and “Diagnostic steps for thyroid nodules”
[24]
Nuclear medicine thyroid scan
Radioactive iodine uptake measurementRAIU test
[25]
[17]
thyrotoxicosis
[25]
[17]
MAXIMIZE TABLE TABLE QUIZ
Characteristic findings of nuclear medicine thyroid scan and RAIU measurement
Appearance of thyroid
Normal thyroid tissue Normal-sized gland with evenly distributed activity Normal
Graves disease Diffusely enlarged gland with increased activity ↑
Toxic MNG
Heterogeneous appearance
Several hyperfunctioning (hot) nodules
Suppression of the rest of the gland
Normal or ↑ (mild)
Toxic adenoma
One or two hot nodules
Suppression of the rest of the gland
↑ (Mild to moderate)
No or minimal activity throughout the gland ↓
Overall decreased activity ↓
Thyrotropic adenoma Enlarged gland with increased activity ↑
[24]
RAIU measurement
Destructive thyroiditis
Exogenous thyrotoxicosis
Hyperthyroidism and thyrotoxicosisDiagnosis
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
Reference ranges vary because the average iodine intake differs according to geographical location.
Should be performed before thyroglossal cystexcision as in some cases,
thyroglossal cystsmay contain the only functioning thyroid tissue within the body.
The rest of the glandular tissue is
suppressed and does not take up the RAI
Solid, hypoechoic nodules with irregular margins,
microcalcifications, taller-than-wide shape,
extrathyroidal growth, and/or cervical
lymphadenopathy should raise suspicion for
malignancy and require further evaluation with
FNAC.
Evaluate for indications for FNAC
Only the functional
parts of the gland take
up radioactive iodine
A cold nodule in a toxic MNG
must be further investigated with
fine needle aspiration cytology.
The inflammatory disruption of the
follicle membranes inhibits the
transport of iodine across the thyroid
cells.
Excess intake of thyroid hormones
causes TSH suppression and therefore
prevents radioactive iodine uptake.
Excess TSH production from the
pituitary tumor stimulates the entire
gland. Unlike in Graves disease,
however, TRAbs will be negative in
these patients.
I
2
3
Y
S
ca

12. Thyroid ultrasound with Doppler
Indications
Palpable abnormality, e.g., goiter or nodules
Additional study following or second-line initial imaging study
Preferred imaging technique in pregnant or breas<eeding women
Typical findings
Changes to morphology: diffuse enlargement or nodules
Increased perfusion: either diffuse (Graves disease, toxic adenoma) or nodular (toxic MNG)
Decreased perfusion:
Hypoechoic areas in acute thyroiditis and malignancy
Further evaluation
These additional tests are not routinely required but may be performed depending on the suspected underlying etiology.
Ultrasound-guided FNAC
Consider for suspicious nodules (see “Diagnostic steps for thyroid nodules” and “Indications for FNAC in thyroid nodules”).
Can help confirm etiology if diagnosis remains uncertain (see “Pathological findings” in “ ”)
Other thyroid antibodies
Thyroid peroxidase antibodies (TPOAb)
Indication: suspected subacute lymphocytic thyroiditis, including postpartum thyroiditis
Elevated levels may also be seen in Graves disease.
Thyroglobulin antibodies (TgAb): not routinely indicated but can be elevated in Graves disease, autoimmune conditions, and
Overall decreased activity ↓
Thyrotropic adenoma Enlarged gland with increased activity ↑
Exogenous thyrotoxicosis
Thyroid scintigraphyHyperthyroidism Hyperthyroidism in
Graves disease
[22]
nuclear medicine thyroid scan
[22]
destructive thyroiditis
Autonomous thy-
roid adenoma
Thyroid nodule with
peripheral calcifica-
tion
Graves disease Hypervascularity in
Graves disease
Thyroid gland in
Graves disease
Common causes of thyrotoxicosis
[17]
Hyperthyroidism and thyrotoxicosisDiagnosis
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
manum
"

13. Other thyroid antibodies
Thyroid peroxidase antibodies (TPOAb)
Indication: suspected subacute lymphocytic thyroiditis, including postpartum thyroiditis
Elevated levels may also be seen in Graves disease.
Thyroglobulin antibodies (TgAb): not routinely indicated but can be elevated in Graves disease, autoimmune conditions, and
thyroid cancer
See also “Thyroid antibodies.”
Serum thyroglobulin (Tg): indicated for suspected with unclear history
Serum Tg should be assessed alongside TgAb because a TgAb-positive result indicates an unreliable serum Tg finding.
Findings
: ↓ Tg due to production that is suppressed by the administered thyroid hormones
Endogenous : normal or ↑ Tg
COLLAPSE NOTES FEEDBACK
Differential diagnoses
The are nonspecific and overlap significantly with other common conditions. If there is any clinical
uncertainty, TSH should be assessed.
Neuropsychiatric symptoms: anxiety/panic disorders
Hyperadrenergic symptoms: intoxication with anticholinergics; cocaine/amphetamine misuse; withdrawal syndromes
Weight loss: diabetes mellitus, malignancy
Cardiac symptoms: congestive cardiac failure
References:
The differential diagnoses listed here are not exhaustive.
COLLAPSE NOTES FEEDBACK
Treatment
Symptomatic therapy for thyrotoxicosis
The treatment of hyperadrenergic symptoms is important for decreasing the risk of cardiac complications in , such
as atrial fibrillation and heart failure.
Indication: all symptomatic patients
Treatment of hyperadrenergic symptoms: beta blockers (first line)
Provide immediate control of symptoms, e.g., neuropsychiatric and/or hyperadrenergic symptoms
Treatment options
First line: propranolol
[17]
exogenous hyperthyroidism
[17]
Exogenous hyperthyroidism
hyperthyroidism
symptoms of thyrotoxicosis
[2][4][5][6][7][8][14]
[17]
thyrotoxicosis
Hyperthyroidism and thyrotoxicosisDifferential diagnoses
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
If the patient can confirm accidental or
intentional overdose of thyroid hormones,
further testing is unnecessary. However, in
patients who are unable or unwilling to
provide a history, serum Tg may help to
confirm the diagnosis
In such cases,
fecal T4 levels can
be recorded, with
elevated levels
suggesting
exogenous
hyperthyroidism.
Especially important in elderly patients or patients with resting heart rates > 90/minuteor concomitant cardiovascular disease
#
propanolol
-
BB-
metoP
,
At t
[CBi
.

14. Indication: all symptomatic patients
Treatment of hyperadrenergic symptoms: beta blockers (first line)
Provide immediate control of symptoms, e.g., neuropsychiatric and/or hyperadrenergic symptoms
Treatment options
First line: propranolol
Alternatives: atenolol OR metoprolol
Severe or treated in ICU: esmolol
If there are contraindications to beta blockers, e.g., severe asthma, Raynaud phenomenon , consider CCBs: verapamil OR
diltiazem.
Antithyroid drugs
Antithyroid drugs can effectively render a patient euthyroid. 20–75% of patients with Graves disease achieve permanent
remission aRer 1–2 years of treatment; however, some patient groups have a higher likelihood of remission than others.
Indications
: initial management as well as prevention in at-risk patients prior to surgery or
Graves disease: Patients with high remission likelihood , and/or moderate to severe active Graves ophthalmopathy
Contraindications to both and surgery
Other: hyperthyroidism in pregnancy, limited life expectancy, patient preference
Contraindication:
Medication for hyperthyroidism
The choice of medication depends on the severity of symptoms and patient factors.
Most patients: methimazole
or first trimester of pregnancy: propylthiouracil
Monitoring
CBC, liver chemistries, and bilirubin
Obtain baseline prior to therapy.
Repeat if febrile illness or symptoms of liver injury, e.g., jaundice.
See also “Adverse effects” in “Antithyroid drugs”.
thyrotoxicosisthyroid storm
[26]
Thyroid storm RAIA
RAIA
destructive thyroiditis
[17]
Thyroid storm
[17]
Obtain a CBC and liver chemistries immediately if patients develop fever or signs of hepatotoxicity while taking
ATD.
[17]
ATDs are ineffective in the management of -induced , which is caused by a
release of preformed thyroid hormones by the damaged follicles
destructive thyroiditis thyrotoxicosis
[17]
Hyperthyroidism and thyrotoxicosisTreatment
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
Nonselective beta blocker. In high doses, propranolol also decreases the peripheral conversion of T4 to T3 by inhibiting the 5'-monodeiodinase enzyme.
When heart rate control is essential, these beta-1 selective beta blockers are preferred for
patients with stable asthma, mild obstructive airway disease, or Raynaud phenomenon.
A cardioselective beta blocker (ß1 selective) without intrinsic sympathomimetic activity commonly used in
surgery to treat tachycardia and in the acute treatment of supraventricular tachycardia.
For rapid disease control before evaluating further treatment options
E.g., those with female sex, mild disease, small goiter, negative or low TRAb titer
E.g., high surgical risk due to age and comorbidities, or inability to adhere to radiation safety regulations
It is recommended to achieve a
euthyroidstate prior to these
interventions as they can
transiently worsen symptoms and
trigger thyroid storm.
Agranulocytosis and
hepatotoxicity are potential
adverse effects of
antithyroid drugs.
I
2
3
4 5
"¥
TRAb

15. Definitive therapy for hyperthyroidism and thyrotoxicosis
Radioactive iodine ablation ()
Definition: destruction of thyroid tissue via radioactive iodine (iodine-131) through a sodium/iodine symporter
Technical background: Radioactive iodine-131 emits both gamma and beta rays.
Gamma rays: diagnostic effect
Beta rays: therapeutic effect
Indications
Toxic MNG and toxic adenoma with high nodular radioactive iodine uptake
Failure to achieve euthyroidism with antithyroid drugs (ATDs) in Graves disease, due to:
Refractory disease
Contraindications to ATDs, e.g., liver disease
Major adverse reactions to ATDs
High surgical risk due to comorbidities or previous surgery or radiation of the neck
Limited life-expectancy
Other: thyrotoxic periodic paralysis
Contraindications
Pregnant/breasHeeding women
Children < 5 years of age
Initial treatment for confirmed or suspected thyroid malignancy
Moderate to severe Graves ophthalmopathy
Preparation for
can cause a transient worsening of .
Prophylactic treatment can reduce the risk of complications in high-risk patient groups, e.g., severe , older
patients, and those with comorbid conditions.
Consider beta blockers even in asymptomatic patients (see “ ” for dosages).
Administer methimazole to rapidly achieve a euthyroid state; must be discontinued 2–3 days before is started.
Avoid excess iodine for 7 days prior to .
In women of childbearing potential, a negative pregnancy test must be confirmed within 48 hours before .
ATDs are ineffective in the management of -induced , which is caused by a
release of preformed thyroid hormones by the damaged follicles
destructive thyroiditis thyrotoxicosis
[17]
Mechanisms of ac-
tion: antithyroid
drugs
[17][29]
RAIA
[30]
RAIA
RAIA hyperthyroidism
hyperthyroidism
Symptomatic therapy for thyrotoxicosis
RAIA
RAIA
RAIA
Hyperthyroidism and thyrotoxicosisTreatment
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
E.g., congestive heart failure, pulmonary hypertension
And women planning a pregnancy within the next 4–6 months
RAIA can worsen Graves ophthalmopathy.
23
In
d

16. patients, and those with comorbid conditions.
Consider beta blockers even in asymptomatic patients (see “ ” for dosages).
Administer methimazole to rapidly achieve a euthyroid state; must be discontinued 2–3 days before is started.
Avoid excess iodine for 7 days prior to .
In women of childbearing potential, a negative pregnancy test must be confirmed within 48 hours before .
Procedure: Single oral dose of iodine-131 → isotope uptake by thyroid gland → emission of beta radiation that slowly destroys
the thyroid tissue
Complications
Early
Most patients with Graves disease become hypothyroid aRer and require life-long thyroid hormone replacement
Gastritis: nausea and vomiting
Sialadenitis
Other: transient loss of taste or smell, stomatitis, transient bone marrow suppression
Late
Radiation-induced thyroiditis: a form of acute thyroiditis that occurs a few days aRer the thyroid gland is exposed to
radiation
It is most commonly seen following in patients with Graves disease, or following external beam
radiotherapy for head and neck cancers.
Patients present with pain in the thyroid region and (due to the release of T and T following rapid
destruction of thyroid tissue).
Secondary malignancy or leukemia
Dry mouth (xerostomia)
Thyroid surgery for hyperthyroidism
The efficacy of antithyroid drugs and has reduced the need for thyroid surgery.
Indications
Large goiters (≥ 8 g) or obstructive symptoms
Confirmed or suspected thyroid malignancy
Graves disease with:
Concomitant primary hyperparathyroidism or periodic paralysis
Moderate to severe active Graves ophthalmopathy
Toxic MNG or toxic adenoma with: concomitant primary hyperparathyroidism, insufficient , or retrosternal extension
Other: large thyroid nodules , refractory amiodarone-induced , planned pregnancy within next 6 months
, or patient preference
Symptomatic therapy for thyrotoxicosis
RAIA
RAIA
RAIA
[32][33]
RAIA
radioiodine therapy
thyrotoxicosis
3 4
Thyroid scan before
and aRer radioio-
dine therapy in
…
Graves disease
[34]
RAIA
[35]
[27]
RAIA
thyrotoxicosis
Hyperthyroidism and thyrotoxicosisTreatment
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
Patients with hyperthyroidism due
to other conditions typically do
not become hypothyroid, since
only the hyperfunctioning tissue
takes up RAI and is destroyed by
RAIA.
Iodine-131 is usually administered orally.
In addition to the thyroid gland, the salivary glands also absorb low amounts of
radioactive iodine. The decreased production of saliva leads to inflammation
Especially after high-dose radioiodine therapy
Due to salivary gland destruction
Thyroid scan before and after radioiodine therapy in Graves disease
Nuclear medicine thyroid scan (99mTc pertechnetate; left: before
radioiodine therapy; middle: three months after therapy; right: 10 months
after therapy) of a patient with Graves disease
A decline in thyroid gland size and radioactivity over time is seen after
radiotherapy.
Iodine uptake is represented by a color scale (blue > green > yellow > red)
When surgery is indicated, it should be
performed by a high-volume thyroid surgeon,
which significantly improves patient
outcomes (i.e., lower complication rates and
shorter hospital stay).
Obstructive symptoms include dyspnea, stridor (tracheal compression), hoarseness(recurrent laryngeal nerve
compression), and/or dysphagia (esophageal compression).
In addition to receiving thyreostatic treatment or undergoing surgery, patients with moderate or severe Graves
ophthalmopathyare treated with glucocorticoids or teprotumumab (FDA-approved for Graves ophthalmopathy in 2020).
-
-
=>
&
4
-

17. Graves disease with:
Concomitant primary hyperparathyroidism or periodic paralysis
Moderate to severe active Graves ophthalmopathy
Toxic MNG or toxic adenoma with: concomitant primary hyperparathyroidism, insufficient , or retrosternal extension
Other: large thyroid nodules , refractory amiodarone-induced , planned pregnancy within next 6 months
, or patient preference
Contraindications
Severe comorbidities that influence surgical risk
Pregnancy
Preparation for thyroid surgery
Achieving euthyroidism prior to surgery: preoperative application of antithyroid drugs (and beta blockers if necessary) for at
least 4–8 weeks if possible.
Patients with Graves disease: potassium iodide solution for 10 days preoperatively (harnesses the Wolff-Chaikoff effect)
Procedure
Graves disease or toxic MNG: near-total or total thyroidectomy
Isolated toxic adenoma: lobectomy
See also “Procedure/application” in “Thyroid surgery.”
Postprocedural care for thyroid surgery
Measure serum calcium and PTH levels .
Wean beta blockers.
COLLAPSE NOTES FEEDBACK
Special patient groups
differs slightly in select patient groups (e.g., individuals who are pregnant or planning
pregnancy, newborns). For more information on management of Graves disease, the most common cause of ,
see “Special patient groups” in “Graves disease.”
COLLAPSE NOTES FEEDBACK
Thyroid storm
Definition
An acute exacerbation of that results in a life-threatening hypermetabolic state.
Also known as
Etiology
Iatrogenic
[35]
[27]
RAIA
thyrotoxicosis
[17]
Management of hyperthyroidism
hyperthyroidism
[17]
hyperthyroidism
thyrotoxic crisis
[17]
Hyperthyroidism and thyrotoxicosisTreatment
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
≥ 4 cm and nonfunctioning or hypofunctioning appearance on scintigraphyPrognosis is poor due to frequent cardiac comorbidities.
Normal thyroid hormone levels are a prerequisite for pregnancy.
Those who value fast and definitive disease control over the possibility of living without lifelong thyroid hormone replacement.
E.g., cardiopulmonary disease, end-stagecancer
Anesthetic agents are teratogenic in the first trimester and there is an increased risk of preterm labor in the third trimester. Surgery in the second
trimester, while considered to be the safest time to operate during pregnancy, still has a ∼ 5% chance of preterm labor and a higher rate of complications
(e.g., hyperparathyroidism and recurrent laryngeal nerve injury) than if performed in nonpregnant patients.
To reduce the intraoperative risk of thyroid storm
Inhibits the release of T3/T4 and decreases thyroid blood flow, which reduces
intraoperative blood loss
In young patients who prefer a rapid resolution or have a large adenomaproducing obstructive symptoms
Transient hypoparathyroidism due to injury of the parathyroid gland is a common complication.
Calcium and calcitriolsupplementation can be tailored to results or given as a prophylactic set dose.
Weaning prevents symptoms such as headache and rebound tachycardia.
5
6 7
g

18. Definition
An acute exacerbation of that results in a life-threatening hypermetabolic state.
Also known as
Etiology
Iatrogenic
Thyroid surgery
Exogenous iodine from contrast media or amiodarone
Discontinuation of antithyroid medication
Stress-related catecholamine surge
Nonthyroidal surgery
Anesthesia induction
Labor
Intercurrent illness, e.g., sepsis, myocardial infarction, diabetic ketoacidosis
Clinical features
Hyperpyrexia with profuse sweating
Tachycardia (> 140/minute) and (possibly severe) arrhythmia (e.g., atrial fibrillation), hypertension with wide pulse pressure,
congestive cardiac failure
Hypotension/shock secondary to high output heart failure or hypovolemia as a result of GI and insensible losses
Abdominal pain
Severe nausea, vomiting, diarrhea, possibly jaundice
Severe agitation and anxiety, delirium and psychoses, seizures, coma
Diagnostics
A is diagnosed on the basis of classic clinical features and supporting abnormalities, e.g., low/undetectable
TSH, elevated free T/T.
Further tests should be performed to identify any underlying precipitants and to assess for complications, e.g.:
ECG to assess for atrial fibrillation
Liver chemistries to assess for evidence of jaundice
Treatment of thyroid storm
has a high mortality rate and patients should receive aggressive treatment to manage complications and restore
normal thyroid function.
Approach
Start symptomatic treatment to manage hypotension, hyperpyrexia, and tachycardia.
Administer medication to reduce thyroid hormone synthesis and release, and inhibit their peripheral action.
hyperthyroidism
thyrotoxic crisis
[17]
RAIA
[17]
Symptoms of thyrotoxicosis
[17]
thyroid storm TFT
34
[17][37]
Thyroid storm
Hyperthyroidism and thyrotoxicosisThyroid storm
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
Manipulation of the thyroid causes the release of thyroid hormones. Pretreatment with beta blockers, antithyroid drugs,
and potassium iodide has drastically decreased the incidence of thyroid storm in patients undergoing surgery.
Most commonly discontinuation of medication in Graves disease
Worsens the preexisting hyperadrenergic state of hyperthyroidism
The cardiovascular system is often most severely affected.
Neuropsychiatric symptoms are seen in most cases of thyroid storm.
Consult critical care for ICU admission and monitoring
IV
FluidParacetamolBB*

19. thyroid function.
Approach
Start symptomatic treatment to manage hypotension, hyperpyrexia, and tachycardia.
Administer medication to reduce thyroid hormone synthesis and release, and inhibit their peripheral action.
Identify and treat any precipitating cause.
Once the patient is stable, initiate .
Consider plasmapheresis or emergency surgery as life-saving treatment for rare refractory cases
Symptomatic treatment
Hyperadrenergic symptoms: beta blockers are first-line
Preferred: Propranolol, due to combined beta-blockade and antithyroid effects
Alternatives
Preexisting heart failure: esmolol
Mild obstructive airway disease/stable asthma: atenolol or metoprolol
Beta blocker contraindications: consider CCBs, e.g., diltiazem
Hyperthermia
External cooling techniques (e.g., ice packs, cooling blankets, alcohol washes)
Antipyretics, e.g., acetaminophen
Hypotension and hypovolemia: fluid resuscitation to treat insensible and GI losses
Electrolyte disturbances: (see “Electrolyte repletion”)
Antithyroid drugs in
Inhibition of thyroid hormone synthesis
First line: propylthiouracil
Alternative: methimazole
Inhibition of thyroid hormone release (through the Wolff-Chaikoff effect)
First line: iodine solutions given at least 1 hour aTer antithyroid drugs
Potassium iodide solution
Lugol solution
In patients with iodine allergy or iodine-induced , lithium can be used.
Inhibition of peripheral conversion of T to T
Propranolol
Glucocorticoids: can also treat concurrent adrenal insufficiency
First line: hydrocortisone
Alternative: dexamethasone
definitive therapy for hyperthyroidism and thyrotoxicosis
[23][38]
[37]
If has led to congestive heart failure, esmolol is the preferred beta blocker. All patients receiving beta blockers
should be monitored carefully for signs of heart failure.
thyroid storm
thyroid storm
[17][23][26]
thyrotoxicosis
4 3
Treat with PROverbial PROficiency and POetic GLU^ony: PROpranolol, PROpylthiouracil, POtassium iodide,
and GLUcocorticoids.
thyroid storm
Hyperthyroidism and thyrotoxicosisTips and Links
OPTIONSHigh-yieldStandard Clinician Key exam info on EN
TSTUDENT Hyperthyroidism
Patients should be carefully monitored while on beta-blocker therapy because it may precipitate heart failure.
In patients with preexisting heart failure or those at high risk, esmolol may
be preferred because of its short half-life and higher beta-1 selectivity.
Propylthiouracil is generally preferred over methimazole for the initial treatment of thyroid storm
because it additionally inhibits peripheral conversion of T4 to T3.
To avoid exacerbation of thyroid storm due to increased iodine uptake.
Inhibition of peripheral T4 hormoneconversion is a secondary effect or propranolol in addition to beta blockade.
Relative adrenal insufficiency can occur during thyroid storm because of hypermetabolism and
accelerated turnover of cortisol; cortisol levels are thus inappropriately low or normal compared
to other situations with significant stress.
&
&
③
?
①
&
*
&
#
*
#

20. HINT USED
A 6-day-old male newborn is brought to the physician because he has become increasingly irritable and
restless over the past 2 days. During this period, he has had 12 bowel movements. He feeds 10 to 12 times a
day. He was born at 38 weeks' gestation and weighed 1800 g (3 lb 15 oz); he currently weighs 1700 g
(3 lb 12 oz). His mother has Graves disease and received propylthiouracil during the last trimester of
pregnancy. She has a history of intravenous heroin use. His temperature is 36.9°C (98.4°F), pulse is 180/min,
and respirations are 50/min. Examination shows mild diaphoresis and a firm 2-cm midline neck swelling. The
lungs are clear to auscultation. Which of the following is the most appropriate next step in management?
ADD NOTES MARK GET ANKI CARDS
This , born to a mother with , has features highly suggestive of
: irritability, restlessness, , , , increased bowel movement, and poor
weight gain despite an adequate appetite.
GIVE FEEDBACK
SHOW ALL EXPLANATIONS RESET QUESTION HIDE STATS
KEY INFO ATTENDING TIP LABS
neonate Graves disease neonatal
thyrotoxicosis tachycardiagoiterdiaphoresis
13%B Potassium iodide therapy
7%C Naloxone therapy
3%D Dextrose therapy
1%E Ampicillin and gentamicin therapy
2%F Calcium gluconate therapy
75%
Up to 5% of infants born to mothers with Graves disease develop thyrotoxicosis due to the
transplacental passage of maternal stimulatory TSH receptor antibodies (TRAb). Symptoms may appear
directly a^er birth or can be delayed up to 10 days as a result of transplacental maternal antithyroid
medication (e.g., propylthiouracil, carbimazole). The thyrotoxicosis is transient and usually resolves
within 12 weeks, when the maternal TRAb disappears from the infant's circulation. Before resolution,
though, neonatal thyrotoxicosis should be treated as soon as it is diagnosed to prevent complications
such as cardiac failure, intellectual disability, and craniosynostosis. Methimazole is administered to
achieve a euthyroid state, which can take up to a few weeks. During this period, a beta blocker (e.g.,
propranolol) should be coadministered to rapidly control the thyrotoxic symptoms.
Graves disease GIVE FEEDBACK
A Methimazole and propranolol therapy
EXIT SESSION NEXTPREVIOUS
TSTUDENT Ctrl+KAsk a medical question
Graves disease
milddiaphoresis midlineneckswelling

21. HINT USED
A 3-week-old male newborn is brought to the hospital because of poor weight gain since birth. He was born
at 38 weeks' gestation via normal vaginal delivery. He weighed 3005 g (6 lb, 10 oz) at birth and currently
weighs 2835 g (6 lb, 4 oz). He has been latching on and breasIeeding well since birth. His mother has a
history of Graves disease and underwent near-total thyroidectomy in the second trimester of her pregnancy
aKer her symptoms could not be controlled with antithyroid drugs. She is currently receiving L-thyroxine
therapy. The patient's temperature is 38.9°C (102°F), pulse is 176/min, and respirations are 42/min. He
appears irritable. Examination shows a diaphoretic infant with a paucity of subcutaneous fat. There is swelling
of the neck at the midline. Which of the following is the most likely cause?
ADD NOTES MARK GET ANKI CARDS
This has features highly suggestive of : irritability, , ,
, and poor weight gain since despite an adequate appetite. The mother's history of
provides a clue for the diagnosis.
GIVE FEEDBACK
SHOW ALL EXPLANATIONS RESET QUESTION HIDE STATS
KEY INFO ATTENDING TIP LABS
neonate neonatal thyrotoxicosis tachycardiagoiter
diaphoresis birth Graves
disease
6%A Transplacental passage of thyroglobulin antibodies
1%B Activating mutation of the TSH receptor gene
7%C Transplacental passage of thyroid peroxidase antibodies
13%E Transplacental passage of L-thyroxine
73%
Up to 5% of infants born to mothers with Graves disease develop thyrotoxicosis due to the
transplacental passage of maternal stimulatory TSH-receptor antibodies (TRAbs). TRAbs are present in
∼ 90% of patients with Graves disease and cause increased growth and function of the thyroid gland
and the subsequent development of hyperthyroidism and goiter. Neonatal thyrotoxicosis is transient
and usually resolves within 12 weeks, when maternal TRAbs disappear from the infant's circulation.
Although the condition is transient, symptomatic neonatal thyrotoxicosis should be treated as soon as
it is diagnosed to prevent complications such as cardiac failure, intellectual disability, and
craniosynostosis. Therapy consists of methimazole to achieve a euthyroid state and a beta blocker (e.g.,
propranolol) to rapidly control the thyrotoxic symptoms.
Graves disease GIVE FEEDBACK
D Transplacental passage of TSH receptor antibodies
EXIT SESSION PREVIOUS NEXT
TSTUDENT Ctrl+KAsk a medical question
historyofGravesdisease
swelling
of
theneckofthe
midline
TG
TRAb

22. HINT USED
A 25-year-old woman, gravida 2, para 1, at 36 weeks' gestation comes to the physician because of irritability,
palpitations, heat intolerance, and frequent bowel movements for the last 5 months. She has received no
prenatal care. Her pulse is 118/min and blood pressure is 133/80 mm Hg. She appears anxious. There is a fine
tremor in the hands and ophthalmologic examination shows bilateral exophthalmos. The skin is warm and
moist to touch. This patient’s child is most likely to have which of the following complications at birth?
ADD NOTES MARK GET ANKI CARDS
This patient's symptoms of irritability, , heat intolerance, in conjunction with
findings of , , and warm moist are highly suggestive of .
GIVE FEEDBACK
SHOW ALL EXPLANATIONS RESET QUESTION HIDE STATS
KEY INFO ATTENDING TIP LABS
palpitations physical exam
tachycardiaexophthalmos skin Graves disease
11%A Bradycardia and annular rash
14%B Umbilical hernia and erosive scalp lesion
12%C Macrosomia and shoulder dystocia
12%D Mechanical holosystolic murmur and tetany
51%
Poor weight gain and stridor are serious neonatal manifestations that may be seen in untreated
maternal Graves disease. During pregnancy, TSH receptor antibodies cross the placenta, leading to
neonatal Graves disease and thyrotoxicosis. Neonatal thyrotoxicosis is most oSen self-limiting, but
severe disease can result in tachycardia, diaphoresis, failure to thrive, hyperphagia, stridor (due to
compressive goiter), and microcephaly (aVributable to craniosynostosis).
Graves disease GIVE FEEDBACK
E Poor weight gain and stridor
EXIT SESSION PREVIOUS SEE ANALYSIS
TSTUDENT Ctrl+KAsk a medical question
irritability
,
palpitations
,
heatintolerance
fine
tremor exophthalmosskin
isworm
and
moist