Thyroid Flashcards
1
Q
what is required for thyroid hormone synthesis?
A
NIS, TG, and thyroid peroxidase
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.
3
Q
what are the transporters in the thyroid follicular cell?
A
NIS - Na I symporter
PENDRID (Chloride Iodide transporter)
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
5
Q
Factors that increase TBG
A
Pregnancy
Estrogen-secreting tumors
Drugs: estrogen, 5-fluourouracil
*estrogen decreases metabolic clearance and elevate TBG
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
7
Q
what is the most common cause of transient CH worldwide
A
iodine deficiency
8
Q
effect of Iodine excess on thyroid
A
Can also cause hypothyroidism caused by the Wolff-Chaikoff effect
9
Q
how long do Drugs and Antibodies From Mother to Fetus last
A
Drugs – 2-5 days
Ab – 3-6 months
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
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
12
Q
MCT8 deficiency
A
SLC16A2 gene mutation
X-linked
Impaired T4, T3 transport into cells
severe mental retardation, developmental delay, hypotonia
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
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
15
Q
most common place for ectopic thyroid
A
sublingual
16
Q
what is the most common cause of dyshormonogenesis in CH
A
organification defect
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
18
Q
I-123
I-131
A
I-123 has shorter half-life
19
Q
radionuclide scans for thyroid
A
I-123
Tc99m
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.
21
Q
Starting dose of synthroid in congenital hypothyroidism
A
15 mcg/kg/d
22
Q
neonatal graves - Fetal Signs
A
Tachycardia
IUGR
Fetal goiter with tracheal compression
Thrombocytopenia
Cholestasis
Hypertension
Tachyarrhythmia
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
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
25
when and how to treat neonatal graves
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.
26
Diffuse thyroid enlargement DDX
- 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
27
etiologies of 1ary hypothyroidism
- Hashimoto (autoimmine)
- iodine deficiency/excess
- neck irradiation
- drugs
- syndromes
- infiltrative process
- cystinosis
- congenital
28
etiologies of 2ary hypothyroidism
- hypopit
- cranial radiation
- CNS process (tumour, infection, injury)
- isolated TSH B gene mutation
29
drugs that increased clearance of thyroid hormone
phenobarbitol
phenytoin
carbamazines
oxcarbemazipine
rifampin
30
what decreases and increases TSH in hypothal-pit-thyr axis
decreases TSH:
- dopamine
- dopamine agonist (bromocriptine, carbegoline)
- glucocoirticoids
- opiates
- octreotide
increases TSH:
- hypocortisolism
- dopamine receptor blockers (meoclopramide)
31
what are the Thyroid hormone-binding proteins
thyroxine-binding globulin (TBG),
prealbumin or transthyretin,
and albumin
32
what percent of T3 is derived from thyroid and from conversion from T4
70% to 90% of circulating T3 is derived from peripheral conversion of T4
10% to 30% of circulating T3 is from the thyroid gland
33
what happens to the thyroid gland in Hashimoto thyroiditis
lymphocytic infiltration
34
if severe hypothyroidism, what is the concern w treating
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.
35
what is the Wolff-chaikoff effect?
when excess iodine
inhibits organification of iodine which decreases T4 and T3 synthesis
36
how do hemangioma affect thyroid?
endothelium of these vascular structures produces type 3 iodothyronine deiodinase, which degrades circulating T4
37
Thyroid hormone resistance
- mutation in which gene
thyroid hormone receptor Beta gene
38
lab findings in hypothyroidism
- 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
39
Hyperthyroidism DDx
- 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
40
How do antithyroid drugs work
which is more potent
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
41
do antithyroid drugs cure hyperthyroidism
no just palliate
42
Betablocker in hyperthyroidism
- which is preferred
- what if they have asthma
atenolol - does not cross the blood barrier as much as propranolol, patients will not feel as tired on this medication
metaprolol (cardiac selective)
43
MMI doses
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
44
MMI side effects
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
45
factors that make remission of graves disease less likely
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
46
what are remission rates for graves disease
15% to 30% in 1-2 years
47
at what point if there is no remission from graves should you move on from ATD
2 years
48
what is the goal for 131I therapy for GD
to induce hypothyroidism (not euthyroidism because increased risk of neoplasm)
49
how long after 131I treatment for the patient to become biochemically euthyroid or hypothyroid
It usually takes 6 to 12 weeks
50
how to treat after 131-I for graves disease
beta blocker
51
what is the risk of recurrence after subtotal thyroidectomy in graves
hyperthyroidism recurs in 10% to 15% of patients
52
familial non-autoimmune hyperthroidism
activating mutation of the TSH receptor
53
Sick euthyroid syndrome
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
54
thyroid nodule - what % benign
75%
55
benign thyroid nodule ddx
Colloid nodule (aka adenodmatoid nodule)
Follicular or Hurthle Cell adenoma
Simple cyst
56
RF for thyroid cancer
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
gold standard for dx thyroid Ca
FNA
58
when to do I123 thyroid scan and uptake for a thyroid nodule
if TSH suppressed or low normal
59
are most thyroid Ca hot or cold nodules
cold
60
Bethesda scoring
1. unsatisfactory - repeat FNA
2. benign
3. atypia/follicular lesion of undetermined significance
4. follicular neoplasm
5. suspicious for malignancy
6. malignant
61
what to do with each Bethesda scoring
1. repeat FNA
2. clinical follow up
3. lobectomy
4. lobectomy
5. thyroidectomy
6. thyroidectomy
62
TIRADS
- what does it stand for
- what does it include
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
what is the single, most reliable feature associated with a lower risk of thyroid malignancy
Cystic or mixed composition, with a greater than 75% cystic component
64
what are features associated with a higher risk of malignancy on thyroid ultrasound
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
what are features associated with a higher likelihood of being benign on thyroid ultrasound
egg shell calcifications
iso- to hyper echoic
translucent halo
smoother border
peripheral vascular flow
66
what are the % of thyroid ca
papillary 90+%
Follicular 5-10%
medullary <5%
67
what can be dx on thyroid nodule fna
Papillary can be dx on FNA
Follicular cannot be dx on FNA, will be indeterminate
68
Thyroid Ca prognostic factors
male sex
non papillary histology (MTC)
distant disease
no surgery
69
does papillary thyroid cancer get mets?
high rate of LN mets
lungs too
70
preop stagings for PTC?
Neck US w FNA
CXR (ID microscopic mets)
Thyroglobulin and Tg Ab
CT neck (+/- chest) w contrast for bulky or fixed neck dz
71
I 131 for DTC
RAI to treat persistent disease
not for remnant ablation
ie not for everyone, just give if needed for residual disease
72
post op staging for PTC?
1) diagnostic whole body scan
2) stimulated Tg and Tg Ab
73
ATA pediatric risk level: Low
- what does it mean
- initial post op staging
- TSH goal
- surveillance
- 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
ATA pediatric risk level: Intermediate
- what does it mean
- initial post op staging
- TSH goal
- surveillance
- 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
ATA pediatric risk level: High
- what does it mean
- initial post op staging
- TSH goal
- surveillance
- 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
Follicular Cell Thyroid Ca - assoc w?
iodine deficiency
77
Histopathology of Follicular Cell Thyroid Ca
Hurthle Cell, clear cell
78
what is Medullary Thyroid Cancer
neuroendocrine cancer that derives from the neural crest and originated parafollicular C-cells of the thyroid gland
79
tumour markers for MTC?
calcitonin and carcinoembryonic antigen (CEA)
do not express the sodium-iodine symporter, and do not produce TG.
80
are MTC responsive to TSH?
no
81
Hematogenous spread of MTC
Lungs, bone liver
82
gene assoc w MTC?
RET protooncogene
83
syndrome assoc w MTC?
MEN2
84
symptoms of MTC?
diarrhea
flushing
Cushing syndrome
85
mgmt of MTC
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
thyroid storm - criteria
- 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
how to treat thyroid storm
MMI
PTU
B-blocker
corticosteroids
potassium iodide
cholestyramine
88
NBS TSH False positive
Presence of macro TSH (from mum to baby)
Intercurrent illness/stress
Sample drawn early (<24h of life)
89
NBS TSH False negative
Low BW infants
Very low BW infants
Central hypothyroidism
Monozygotic twins
90
what enzyme converts T4 into T3
type 1 and 2 monodeiodinase
91
what enzyme converts T4 into rT3
type 3 monodeiodinase
92
what does Deiodinase type 1 do
Creates T3 in liver, kidney, and thyroid from rT3 and T4
92
what does Deiodinase type 2 do
Creates T3 from T4 and rT3
93
what does Deiodinase type 3 do
: Causes break own of T3 and T4 (into r,r’T2 and rT3 respectively
94
myxoedema coma from hypothyroidism
-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
what are Thionamides
MMI, PTU
96
what does illness do to thyroid hormones
decrease T3, increase rT3
as it gets more severe, decrease T4
97
what affects absorption of thyroxine
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
what drugs increase clearance of synthroid
i) Carbamazepine
ii) Phenobarbitol
iii) Rifampin
iv) Hydantoins
v) Phenytoin
vi) Sertraline
99
medical conditions were thyroxine needs are increased
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
what is the most common cause of congenital hypothyroidism
Maternal iodine deficiency (worldwide most common)
ii) Ectopic or absent thyroid (in iodine sufficient regions)
101
if you have graves ophthalmopathy, what's the preferred tx
ATD or surgery
not RAI
102
what nerve do you worry about with thyroid sx
Recurrent laryngeal nerve damage
103
what is Struma ovarii
a variant of dermoid tumors of the ovary in which thyroid tissue components is the major constituent
can secrete thyroid hormone
104
High uptake on thyroid scan with high TH
- Graves
- Trophoblastic disease (molar pregnancy, etc.)
- TSH producing adenoma
- Thyroid hormone resistance (beta mutation)
- Thyroid adenoma or toxic multinodular goiter
105
Low uptake on thyroid scan with high TH
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
a) Type 1 Amiodarone-induced
b) Type 2 Amiodarone-induced
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
what is subacute thyroiditis
viral URI and small painful goitre
thyrotoxic to hypothyroid to recovery
decreased RAI uptake
108
what is silent thyroiditis
small painless goiter
thyrotoxic to hypothyroid to recovery
probably autoimmune
decrease RAI
109
Treatment for Graves ophthalmopathy
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
what happens with thyroid function during pregnancy
rise in TGB and total T4 due to increase in HCG (acts as TSH)
111
how does PTU work?
inhibits PTU:
Peroxidase/peripheral deiodination
Tyrosine iodination
Union (ie coupling)
112
how is T4 measured in a lab
what is the gold standard
immunometric assay
Equilibrium dialysis
113
what is TRH stimulation
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
remnant from thyroid budding
Foramen cecum
115
remnant from thyroid migration
Thyroglossal duct
116
risk of a thyroid nodule being malignant?
22-26% vs. 5-10% in adult
117
Follicular thyroid Ca - what syndromes are assoc
Carney complex
DICER1
PTEN hamartoma syndrome
Werner syndrome
118
Cowden syndrome
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
How do you differentiate between follicular adenoma and carcinoma?
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
after TTx for papillary thyroid Ca, who should get WBS?
moderate and high risk
121
after TTx for papillary thyroid Ca, who should get RAI
high risk
122
what is the delayed TSH rise in prematurity?
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
what age can get RAI?
>5
below 5, risk of malignancy
124
Thyroglobulin - what is the level in exogenous T4 and in subacute thyroiditis
Thyroglobulin is low in the setting of exogenous T4 and normal in subacute thyroiditis
125
who should get a beta blocker in hyperthyroidism
everyone who is symptomatic
126
contraindications to RAI?
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
if getting RAI for hyperthyroidism, how to prepare
Beta blockade even if aSx
MMI- stop 2-3 days prior to RAI
128
after RAI for hyperthyroidism, what to do
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
after starting MMI for Graves, how to f/u
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
how long to continue on MMI before stopping MMI
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
how to prepare for surgery to Hyperthyroidism
what to do with meds
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
what will TFTs look like if taking estrogen
Estrogen can cause an increase in TBG and total T4, but freeT4 and TSH should be normal
133
how does hypothyroidism affect growth
longstanding severe hypothyroidism is associated with only partial catch up growth; some association with bone maturation without skeletal growth
134
when to do TRAbs if maternal graves
day 3-5
day 10-14
135
patient with congenital hypothyroidism treated with synthroid - if asymptomatic but biochemically hyperthyroid, what is biggest risk
advanced skeletal maturation
but should not affect final height
136
sx of hypothyroidism
myopathy
137
after Tax for MTC, when to reimage?
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
