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PEDS ENDO RC TD 2022 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

what is required for thyroid hormone synthesis?

A

NIS, TG, and thyroid peroxidase

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2
Q

what are the steps for thyroid hormone synthesis?

A

TSH binds to TSH-R (cAMP activation)

1) TRAPPING: active transport of iodide across the basement membrane into the thyroid cell (NIS - Na I symporter)

Iodide diffuses to apex and enters colloid via PENDRID (Chloride Iodide transporter)

2) ORGANIFICATION: oxidation of iodide to iodine (by H2O2) and iodination of tyrosyl residues in TG
this forms iodothyronines (MIT and DIT)

3) COUPLING: linking pairs of iodotyrosine molecules within TG to form the iodothyronines T3 and T4
MIT + DIT = T3
DIT + DIT = T4

4) ENDOCYTOSIS: pinocytosis and then proteolysis of TG with release of free iodothyronines and iodotyrosines into the circulation

5) deiodination of iodotyrosines (MIT AND DIT) within the thyroid cell, with conservation and reuse of the liberated iodide

6) intrathyroidal 5’-deiodination of T4 to T3.

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3
Q

what are the transporters in the thyroid follicular cell?

A

NIS - Na I symporter

PENDRID (Chloride Iodide transporter)

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4
Q

what is catalyzed by TPO?

A

oxidation: iodide to iodine by H2O2

organification: iodine is bound to tyrosine residues in TG to form MIT and DIT

coupling: MIT+DIT or DIT+DIT to make T3 and T4

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5
Q

Factors that increase TBG

A

Pregnancy
Estrogen-secreting tumors
Drugs: estrogen, 5-fluourouracil
*estrogen decreases metabolic clearance and elevate TBG

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6
Q

Factors that decrease TBG

A

Nephrotic syndrome and protein-losing enteropathy -> increase clearance
Major illness (due to cleavage by leukocyte proteases and reduction in TBG’s binding affinity for thyroid hormones)
Chronic thyrotoxicosis
Hypercortisolism
Acromegaly
Drugs - androgenic steroids, glucocorticoids, danazol, L-asparaginase

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7
Q

what is the most common cause of transient CH worldwide

A

iodine deficiency

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8
Q

effect of Iodine excess on thyroid

A

Can also cause hypothyroidism caused by the Wolff-Chaikoff effect

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9
Q

how long do Drugs and Antibodies From Mother to Fetus last

A

Drugs – 2-5 days
Ab – 3-6 months

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10
Q

how do hemangioma affect thyroid function?

A

produce type 3 deiodinase
(can cause severe hypothyroidism)

in severe early-onset hypothyroidism requiring high doses of thyroxine, an abdominal ultrasound is indicated

normal T4, low T4, and high reverse T3 in serum

high output cardiac failure

need high dose thyroxine

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11
Q

congenital hypothyroidism DDX

A

1) Iodine deficiency
2) Iodine excess:
3) Transfer of Drugs or Antibodies Form Mother to Fetus
4) Transient Hypothyroxinemia of Prematurity
5) Hemangiomas
6) Defects in Thyroid Hormone Signaling Pathways
- Defects in Thyroid Hormone Metabolism
- Defects in Thyroid Hormone Transport Into Cells
- Defects in Thyroid Hormone Receptors

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12
Q

MCT8 deficiency

A

SLC16A2 gene mutation
X-linked

Impaired T4, T3 transport into cells

severe mental retardation, developmental delay, hypotonia

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13
Q

is breast feeding safe when on a antithyroid med?
how much is passed through?

A

Yes safe at low-mod doses
0.1% - very small amount

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14
Q

what are signs of neonatal hypothyroidism?

A

Portmaturity
Macrosomia
Large anterior fontanelle
Macroglossia
Hypotonia, umbilical hernia, and prolonged jaundice
Obvious symptoms are not present until 3mo

Delays osseous maturation of bones

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15
Q

most common place for ectopic thyroid

A

sublingual

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16
Q

what is the most common cause of dyshormonogenesis in CH

A

organification defect

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17
Q

Pendred syndrome

A

SLC26A4 or PDS gene mutation
encodes pendrid
pendrid transports iodine from follicular cell to the colloid

often presents with goiter
often euthyroid
sensorineural deafness

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18
Q

I-123
I-131

A

I-123 has shorter half-life

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19
Q

radionuclide scans for thyroid

A

I-123
Tc99m

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20
Q

what is the goal of treatment in congenital hypothyroidism

A

The goal of treatment is to restore normal thyroid function as quickly as possible and maintain it thereafter

goal is to maintain TSH within the age-appropriate reference range and fT4 within the upper half of the normal range.

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21
Q

Starting dose of synthroid in congenital hypothyroidism

A

15 mcg/kg/d

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22
Q

neonatal graves - Fetal Signs

A

Tachycardia
IUGR
Fetal goiter with tracheal compression
Thrombocytopenia
Cholestasis
Hypertension
Tachyarrhythmia

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23
Q

neonatal graves - Neonatal signs

A

irritability,
tachycardia,
hypertension,
heart failure/heart block,
poor weight gain,
thyroid enlargement/compression, and
exophthalmos

low birth weight
periorbital edema
lid retraction
hyperthermia
diarrhea
craniosynostosis

Thrombocytopenia,
hepatosplenomegaly,
jaundice,
hypoprothrombinemia, &
cardiac failure

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24
Q

what is the usual course of Neonatal graves

A

The usual clinical course of neonatal Graves disease extends from 3 to 12 weeks

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25
Q

when and how to treat neonatal graves

A

if symptomatic hyperthyroidism
admit for monitoring
propranolol (1–2 mg per kilogram per day, divided in 4 doses) and methimazole in a dose of 0.5 to 1 mg/kg daily in divided doses at 8-hour intervals.

Iodine is also often used, because it rapidly inhibits hormone release: Lugol’s solution (5% iodine and 10% potassium iodide; 126 mg of iodine per milliliter) is given orally in a dose of one drop (about 8 mg) 3 times daily

A therapeutic response should be observed within 24 to 36 hours.
If no response, can increase antithyroid drug and iodine by 50%
Glucocorticoids in high doses diminish T4 to T3 conversion and may therefore be helpful.
In severe cases, sedatives and digitalization may be necessary.

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26
Q

Diffuse thyroid enlargement DDX

A
  • chronic lymphocytic thyroiditis (Hashimoto)
  • colloid goiter
  • thyroid hormone resistance
  • subacute or acute thyroiditis
  • Graves disease
  • congenital hypothyroidism. (dyshormonogenesis)
  • iodine deficiency (endemic goitre)
  • excessive iodine ingestion (Wolfe-Chaikoff effect)
  • infiltrative dysorders
    — histiocytosis
    —cystinosis
    —neoplasms (lymphoma, teratoma)
    —adults: sarcoidosis, amyloidosis
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27
Q

etiologies of 1ary hypothyroidism

A
  • Hashimoto (autoimmine)
  • iodine deficiency/excess
  • neck irradiation
  • drugs
  • syndromes
  • infiltrative process
  • cystinosis
  • congenital
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28
Q

etiologies of 2ary hypothyroidism

A
  • hypopit
  • cranial radiation
  • CNS process (tumour, infection, injury)
  • isolated TSH B gene mutation
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29
Q

drugs that increased clearance of thyroid hormone

A

phenobarbitol
phenytoin
carbamazines
oxcarbemazipine
rifampin

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30
Q

what decreases and increases TSH in hypothal-pit-thyr axis

A

decreases TSH:
- dopamine
- dopamine agonist (bromocriptine, carbegoline)
- glucocoirticoids
- opiates
- octreotide

increases TSH:
- hypocortisolism
- dopamine receptor blockers (meoclopramide)

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31
Q

what are the Thyroid hormone-binding proteins

A

thyroxine-binding globulin (TBG),
prealbumin or transthyretin,
and albumin

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32
Q

what percent of T3 is derived from thyroid and from conversion from T4

A

70% to 90% of circulating T3 is derived from peripheral conversion of T4

10% to 30% of circulating T3 is from the thyroid gland

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33
Q

what happens to the thyroid gland in Hashimoto thyroiditis

A

lymphocytic infiltration

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34
Q

if severe hypothyroidism, what is the concern w treating

A

psuedotumour cerebri
often start at lower dose of synthroid

treatment is often initiated with one-third to one-half of the usual dose of levothyroxine.

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35
Q

what is the Wolff-chaikoff effect?

A

when excess iodine
inhibits organification of iodine which decreases T4 and T3 synthesis

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36
Q

how do hemangioma affect thyroid?

A

endothelium of these vascular structures produces type 3 iodothyronine deiodinase, which degrades circulating T4

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37
Q

Thyroid hormone resistance
- mutation in which gene

A

thyroid hormone receptor Beta gene

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38
Q

lab findings in hypothyroidism

A
  • hypercholesterolemia (incr LDL)
  • hyponatremia (increased TBW)
  • anemia (decr erythropoietin, decr O2 req)
  • elevated CK and LDH (from skeletal muscle)
  • reduced GFR
  • elevated liver transaminases
  • elevated PRL (TRH stim from the hypothalamus)
  • decreased/impaired GH secretion
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39
Q

Hyperthyroidism DDx

A
  • Grave Disease
  • Autonomously functioning thyroid nodules
  • Hashitoxicosis
  • neonatal thyrotoxicosis
  • infections of the thyroid - acute thyroiditis and subacute thyroiditis
  • thyroid hormone ingestion
  • McCune–Albright syndrome
  • struma ovarii
  • TSH-producing pituitary adenomas
  • activating mutation of the TSH receptor
  • amiodarone
  • excess iodine intake

Mimicers: thyroid hormone resistance and thyroid hormone- binding protein disorders

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40
Q

How do antithyroid drugs work
which is more potent

A

inhibiting oxidation and organic binding of thyroid iodide to impair thyroid hormone production

methimazole (MMI) and propylthiouracil (PTU)
MMI is 10- to 20-fold more potent than PTU and has a longer half-life

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41
Q

do antithyroid drugs cure hyperthyroidism

A

no just palliate

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42
Q

Betablocker in hyperthyroidism
- which is preferred
- what if they have asthma

A

atenolol - does not cross the blood barrier as much as propranolol, patients will not feel as tired on this medication

metaprolol (cardiac selective)

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43
Q

MMI doses

A

MMI is available in 5, 10, and 20 mg tablets
infants, 1.25 mg/day;
1 to 5 years, 2.5 to 5.0 mg/day;
5 to 10 years, 5 to10 mg/day;
10 to 18 years, 10 to 20 mg/day.

once T4 normal, can cut in half to maintain euthyroidism

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44
Q

MMI side effects

A

Low neutrophil count

Most common minor adverse side effects related to MMI:
hives/skin reaction
arthralgia
gastric distress, nausea
abnormal sense of taste/smell
sialadenitis

Major side effects:
agranulocytosis
Stevens-Johnson syndrome
vasculitis
cholestatic jaundice
acute arthritis
pancreatitis
immunoallergic hepatitis

MMI adverse events most commonly occur within 6 months of therapy onset

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45
Q

factors that make remission of graves disease less likely

A

thyroid gland is large (>2 times normal size for age),
the child is young (<12 years),
not Caucasian,
serum TRAb/TSI levels are elevated, or
the patient presents with profound hyperthyroidism at presentation

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46
Q

what are remission rates for graves disease

A

15% to 30% in 1-2 years

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47
Q

at what point if there is no remission from graves should you move on from ATD

A

2 years

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48
Q

what is the goal for 131I therapy for GD

A

to induce hypothyroidism (not euthyroidism because increased risk of neoplasm)

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49
Q

how long after 131I treatment for the patient to become biochemically euthyroid or hypothyroid

A

It usually takes 6 to 12 weeks

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50
Q

how to treat after 131-I for graves disease

A

beta blocker

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51
Q

what is the risk of recurrence after subtotal thyroidectomy in graves

A

hyperthyroidism recurs in 10% to 15% of patients

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52
Q

familial non-autoimmune hyperthroidism

A

activating mutation of the TSH receptor

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53
Q

Sick euthyroid syndrome

A

signficant decrease in TBG
decrease in type 1 deiodinase (T4->T3)
increase in type 3 deiodinase (T4->rT3)

as gets more sick:
TSH normal to low
T4 normal to low
T3 low to very low
rT3 high to very high

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54
Q

thyroid nodule - what % benign

A

75%

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55
Q

benign thyroid nodule ddx

A

Colloid nodule (aka adenodmatoid nodule)
Follicular or Hurthle Cell adenoma
Simple cyst

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56
Q

RF for thyroid cancer

A

Radiation exposure - <30 Gy (lower dose worse)
- Increasing years since rad’n
- Younger age at ca dx
- Female
Autoimmune thyroid dz
Iodine insufficiency
FHx
Genetic d/o (MEN2, PTEN mut’n, DICER, FAP)

57
Q

gold standard for dx thyroid Ca

A

FNA

58
Q

when to do I123 thyroid scan and uptake for a thyroid nodule

A

if TSH suppressed or low normal

59
Q

are most thyroid Ca hot or cold nodules

A

cold

60
Q

Bethesda scoring

A
  1. unsatisfactory - repeat FNA
  2. benign
  3. atypia/follicular lesion of undetermined significance
  4. follicular neoplasm
  5. suspicious for malignancy
  6. malignant
61
Q

what to do with each Bethesda scoring

A
  1. repeat FNA
  2. clinical follow up
  3. lobectomy
  4. lobectomy
  5. thyroidectomy
  6. thyroidectomy
62
Q

TIRADS
- what does it stand for
- what does it include

A

Thyroid Imaging and Reporting Data System

  • composition (cystic, spongiform, mixed or solid)
  • echogenicity, (anechoic, hyperechoic, isoechoic, or hypoechoic),
  • shape on transverse imaging (taller than wide or wider than tall),
  • margin (smooth, ill-defined, lobulated, or with extrathyroidal extension)
  • echogenic foci (none, comet-tail, macrocalcifications, rim calcifications, or punctate calcifications)
63
Q

what is the single, most reliable feature associated with a lower risk of thyroid malignancy

A

Cystic or mixed composition, with a greater than 75% cystic component

64
Q

what are features associated with a higher risk of malignancy on thyroid ultrasound

A

solid composition,
hypoechogenicity (darker)
micro calcifications
taller than wide shape on transverse imaging
lobulated or irregular margin (jagged)
punctate echogenic foci
intranodular vascular flow

65
Q

what are features associated with a higher likelihood of being benign on thyroid ultrasound

A

egg shell calcifications
iso- to hyper echoic
translucent halo
smoother border
peripheral vascular flow

66
Q

what are the % of thyroid ca

A

papillary 90+%
Follicular 5-10%
medullary <5%

67
Q

what can be dx on thyroid nodule fna

A

Papillary can be dx on FNA
Follicular cannot be dx on FNA, will be indeterminate

68
Q

Thyroid Ca prognostic factors

A

male sex
non papillary histology (MTC)
distant disease
no surgery

69
Q

does papillary thyroid cancer get mets?

A

high rate of LN mets

lungs too

70
Q

preop stagings for PTC?

A

Neck US w FNA
CXR (ID microscopic mets)
Thyroglobulin and Tg Ab
CT neck (+/- chest) w contrast for bulky or fixed neck dz

71
Q

I 131 for DTC

A

RAI to treat persistent disease
not for remnant ablation
ie not for everyone, just give if needed for residual disease

72
Q

post op staging for PTC?

A

1) diagnostic whole body scan
2) stimulated Tg and Tg Ab

73
Q

ATA pediatric risk level: Low
- what does it mean
- initial post op staging
- TSH goal
- surveillance

A
  • Disease grossly confined to the thyroid with N0 (no lymph node metastasis) or NX (no lymph nodes assessed) disease or patients with incidental metastatic lymph nodes in the central neck (N1a)
  • Tg
  • 0.5-1.0

-US at 6months then annually x5 years
- Tg on T4 q3-6 months for 2 years then annually

74
Q

ATA pediatric risk level: Intermediate
- what does it mean
- initial post op staging
- TSH goal
- surveillance

A
  • Extensive N1a or minimal N1b disease
  • Presence of extrathyroidal extension or >6 metastatic lymph nodes (N1a) or lateral neck lymph node metastasis (N1b).
  • TSH- stimulated Tg and diagnostic I123 scan
  • 0.1-0.5
  • US at 6 months, every 6-12 months for 5 years and then less frequently
  • Tg on LT4 q3-6 months for 3 years and then annually
  • consider TSH stimulated Tg +/- diagnostic I123 scan in 1-2 years in patients tx w I131
75
Q

ATA pediatric risk level: High
- what does it mean
- initial post op staging
- TSH goal
- surveillance

A
  • regionally extensive disease or locally invasive disease, with or without distant metastasis
  • Presence of more than 10 metastatic lymph nodes or distant metastasis.
  • TSH stimulated Tg and diagnostic I123 scan in all patients
  • <0.1
  • US at 6 months, every 6-12 months for 5 years and then less frequently
  • Tg on LT4 every 3-6 months for 3 years and then annually
  • TSH stimulated Tg +/- diagnostic I123 scan in 1-2 years in patients tx w I131
76
Q

Follicular Cell Thyroid Ca - assoc w?

A

iodine deficiency

77
Q

Histopathology of Follicular Cell Thyroid Ca

A

Hurthle Cell, clear cell

78
Q

what is Medullary Thyroid Cancer

A

neuroendocrine cancer that derives from the neural crest and originated parafollicular C-cells of the thyroid gland

79
Q

tumour markers for MTC?

A

calcitonin and carcinoembryonic antigen (CEA)

do not express the sodium-iodine symporter, and do not produce TG.

80
Q

are MTC responsive to TSH?

A

no

81
Q

Hematogenous spread of MTC

A

Lungs, bone liver

82
Q

gene assoc w MTC?

A

RET protooncogene

83
Q

syndrome assoc w MTC?

A

MEN2

84
Q

symptoms of MTC?

A

diarrhea
flushing
Cushing syndrome

85
Q

mgmt of MTC

A

Surgical (TT + LN dissection)
No RAI
Normal TSH
Long term monitoring with blood tests and imaging
- Calcitonin,CEA
- US, CT
Genetic testing
- MEN2 screening

86
Q

thyroid storm - criteria

A
  • temperature elevated
  • tachycardia
  • atrial fibrillation
  • congestive heart failure
  • GI-hepatic dysfunction (diarrhea, abdo pain, N/V, jaundice)
  • CNS disturbance (agitation, delirium, psychosis, extreme lethargy, seizure, coma)
  • precipitant history
87
Q

how to treat thyroid storm

A

MMI
PTU
B-blocker
corticosteroids
potassium iodide
cholestyramine

88
Q

NBS TSH False positive

A

Presence of macro TSH (from mum to baby)
Intercurrent illness/stress
Sample drawn early (<24h of life)

89
Q

NBS TSH False negative

A

Low BW infants
Very low BW infants
Central hypothyroidism
Monozygotic twins

90
Q

what enzyme converts T4 into T3

A

type 1 and 2 monodeiodinase

91
Q

what enzyme converts T4 into rT3

A

type 3 monodeiodinase

92
Q

what does Deiodinase type 1 do

A

Creates T3 in liver, kidney, and thyroid from rT3 and T4

92
Q

what does Deiodinase type 2 do

A

Creates T3 from T4 and rT3

93
Q

what does Deiodinase type 3 do

A

: Causes break own of T3 and T4 (into r,r’T2 and rT3 respectively

94
Q

myxoedema coma from hypothyroidism

A

-Altered LOC (semi/comatose)
-Dry, coarse skin
-hoarse voice
-thin scalp and eyebrow hair
-Hyperreflexic (hung reflexes)
-Pericardial, pleural, peritoneal effusions
-Marked hypothermia
-QT prolongation and Torsades
-Disorientation
-Depression
-Psychosis

95
Q

what are Thionamides

A

MMI, PTU

96
Q

what does illness do to thyroid hormones

A

decrease T3, increase rT3

as it gets more severe, decrease T4

97
Q

what affects absorption of thyroxine

A

i) Iron
ii) Fibre
iii) Coffee
iv) Calcium
v) PPI
vi) Bile acid binding resins
vii) Soy
viii) Sucralfate
ix) Aluminum (in antacids)
x) Phosphate binders

98
Q

what drugs increase clearance of synthroid

A

i) Carbamazepine
ii) Phenobarbitol
iii) Rifampin
iv) Hydantoins
v) Phenytoin
vi) Sertraline

99
Q

medical conditions were thyroxine needs are increased

A

i) Nephrotic syndrome - due to increased urinary losses (mentioned in ATA guidelines)
ii) Celiac disease (mentioned in ATA guidelines)
iii) Vascular tumors (198), fibroblastic tumors (199), and gastrointestinal stromal tumors
iv) Consumptive hemangioma
v) Pregnancy
vi) Pseudohypoparathyroidism type 1

100
Q

what is the most common cause of congenital hypothyroidism

A

Maternal iodine deficiency (worldwide most common)

ii) Ectopic or absent thyroid (in iodine sufficient regions)

101
Q

if you have graves ophthalmopathy, what’s the preferred tx

A

ATD or surgery

not RAI

102
Q

what nerve do you worry about with thyroid sx

A

Recurrent laryngeal nerve damage

103
Q

what is Struma ovarii

A

a variant of dermoid tumors of the ovary in which thyroid tissue components is the major constituent

can secrete thyroid hormone

104
Q

High uptake on thyroid scan with high TH

A
  • Graves
  • Trophoblastic disease (molar pregnancy, etc.)
  • TSH producing adenoma
  • Thyroid hormone resistance (beta mutation)
  • Thyroid adenoma or toxic multinodular goiter
105
Q

Low uptake on thyroid scan with high TH

A

painless (silent) thyroiditis
amiodarone-induced thyroiditis
subacute (granulomatous) thyroiditis
palpation thyroiditis
iatrogenic thyrotoxicosis
factitious ingestion of TH
struma ovaria
acute thyroiditis
extensive metastases from follicular thyroid ca

106
Q

a) Type 1 Amiodarone-induced
b) Type 2 Amiodarone-induced

A

a) Type 1 Amiodarone-induced
i) iodine-induced hyperthyroidism – due to the high iodine content of amiodarone (tends to occur in patients with underlying thyroid autonomy in a nodular goiter, or GD)

b) Type 2 Amiodarone-induced
i) destructive thyroiditis – due to direct toxicity of amiodarone on follicular cells. (occurs as a result of direct damage or induction of apoptosis in thyrocytes by amiodarone)
decrease in iodine transportation into a cell

107
Q

what is subacute thyroiditis

A

viral URI and small painful goitre

thyrotoxic to hypothyroid to recovery

decreased RAI uptake

108
Q

what is silent thyroiditis

A

small painless goiter

thyrotoxic to hypothyroid to recovery

probably autoimmune

decrease RAI

109
Q

Treatment for Graves ophthalmopathy

A

i) Smoking cessation
ii) Refer to ophthalmology
iii) Symptom relief (topical lubrication, etc)
iv) Ensure rapid treatment of hyperthyroidism (since the sooner a patient is euthyroid the better the ophthalmopathy will be)
v) Avoid RAI (worsens outcomes)
vi) If RAI is done consider course of corticosteroids
vii) If thyroidectomy or RAI done, ensure rapid initiation of Synthroid (more time euthyroid improves outcomes)
viii) Consider elevating head of the bed and diuretics for periorbital edema
ix) Consider eye radiation therapy

110
Q

what happens with thyroid function during pregnancy

A

rise in TGB and total T4 due to increase in HCG (acts as TSH)

111
Q

how does PTU work?

A

inhibits PTU:
Peroxidase/peripheral deiodination
Tyrosine iodination
Union (ie coupling)

112
Q

how is T4 measured in a lab

what is the gold standard

A

immunometric assay

Equilibrium dialysis

113
Q

what is TRH stimulation

A

you give IV TRH to a patient and measure TSH, FT4

primary hypothyroid: stimulates TSH but fT4 is low

pituitary: no rise in TSH

hypothalamic: TRH produces delayed (60-120min vs 15-30min) increase in TSH
(because TRH was deficient before, so TSH was not being made, so now it takes longer
b/c needs to be made from the start, rather than some present and released right away)

thyroid hormone resistance: both TSH and free thyroid hormones are high (b/c body
is not responding to free thyroid hormones so TSH ramping up)

114
Q

remnant from thyroid budding

A

Foramen cecum

115
Q

remnant from thyroid migration

A

Thyroglossal duct

116
Q

risk of a thyroid nodule being malignant?

A

22-26% vs. 5-10% in adult

117
Q

Follicular thyroid Ca - what syndromes are assoc

A

Carney complex
DICER1
PTEN hamartoma syndrome
Werner syndrome

118
Q

Cowden syndrome

A

Autosomal dominant
-PTEN gene → LOF contributes to oncogenesis

Breast Ca
Follicular Thyroid Ca
Mucocutaneous symptoms

other malignancies like GU (endometrial cancer, RCC), testicular lipomatosis in men, esophageal glycogen acanthosis, polyps (gastric and duodenal), colorectal CA, colonic polyps, tumours and neurovascular malformations (dysplastic gangliocytoma of cerebellum), venous and cavernous angiomas, macrocephaly, ID, immune dysregulation

119
Q

How do you differentiate between follicular adenoma and carcinoma?

A

You can only differentiate after surgical resection. Follicular cancer is identified when there are follicular cells in an encapsulated and/or one with vascular invasion

120
Q

after TTx for papillary thyroid Ca, who should get WBS?

A

moderate and high risk

121
Q

after TTx for papillary thyroid Ca, who should get RAI

A

high risk

122
Q

what is the delayed TSH rise in prematurity?

A

in some babies with congenital hypothyroidism, extreme prematurity, and low birth weight, the TSH rise may not be seen before the age of 30 days (delayed TSH rise)

123
Q

what age can get RAI?

A

> 5
below 5, risk of malignancy

124
Q

Thyroglobulin - what is the level in exogenous T4 and in subacute thyroiditis

A

Thyroglobulin is low in the setting of exogenous T4 and normal in subacute thyroiditis

125
Q

who should get a beta blocker in hyperthyroidism

A

everyone who is symptomatic

126
Q

contraindications to RAI?

A

pregnancy,
lactation,
coexisting thyroid cancer, or suspi- cion of thyroid cancer,
individuals unable to comply with radiation safety guidelines
used with informed caution in women planning a pregnancy within 4–6 months.

127
Q

if getting RAI for hyperthyroidism, how to prepare

A

Beta blockade even if aSx
MMI- stop 2-3 days prior to RAI

128
Q

after RAI for hyperthyroidism, what to do

A

consider resuming MMI 3-7 days after RAI if symptomatic

Follow-up within the first 1–2 months after RAI
-> do free T4, total T3, and TSH

Biochemical monitoring should be continued at 4- to 6-week intervals for 6 months
Continue until stable hypothyroidism

129
Q

after starting MMI for Graves, how to f/u

A

serum free T4 and total T3 should be obtained about 2–6 weeks after initiation of therapy, depending on the severity of the thyrotoxicosis, and the dose of medication should be adjusted accordingly

Serum T3 should be monitored because the serum free T4 levels may normalize despite persistent elevation of serum total T3

Once the patient is euthyroid, the dose of MMI can usually be decreased by 30%–50%, and biochemical testing repeated in 4–6 weeks

Once euthyroid levels are achieved with the minimal dose of medication, clinical and laboratory evalua- tion can be undertaken at intervals of 2–3 months. If a patient is receiving long-term MMI (>18 months), this interval can be increased to 6 months

130
Q

how long to continue on MMI before stopping MMI

A

should be continued for approximately 12–18 months, then discontinued if the TSH and TRAb levels are normal at that time.

If a patient with GD becomes hyperthyroid after com- pleting a course of MMI, consideration should be given to treatment with RAI or thyroidectomy.

131
Q

how to prepare for surgery to Hyperthyroidism
what to do with meds

A

Render euthyroid

KI- containing preparation should be given in the immediate preoperative period

ATD should be stopped at the time of thyroidectomy for GD

b-adrenergic blockers should be weaned follow- ing surgery

132
Q

what will TFTs look like if taking estrogen

A

Estrogen can cause an increase in TBG and total T4, but freeT4 and TSH should be normal

133
Q

how does hypothyroidism affect growth

A

longstanding severe hypothyroidism is associated with only partial catch up growth; some association with bone maturation without skeletal growth

134
Q

when to do TRAbs if maternal graves

A

day 3-5
day 10-14

135
Q

patient with congenital hypothyroidism treated with synthroid - if asymptomatic but biochemically hyperthyroid, what is biggest risk

A

advanced skeletal maturation
but should not affect final height

136
Q

sx of hypothyroidism

A

myopathy

137
Q

after Tax for MTC, when to reimage?

A

If the postoperative serum calcitonin level exceeds 150 pg/mL patients should be evaluated by imaging procedures, including neck US, chest CT, contrast-enhanced MRI or three-phase contrast-enhanced CT of the liver, and bone scintigraphy and MRI of the pelvis and axial skeleton

PEDS ENDO RC TD 2022 (14 decks)

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