thyroid Flashcards

(45 cards)

1
Q

how are the thyroid hormones made? brief summary

A
  • dietary iodine pumped into thyroid cell via Na-I symporter, then colloid
  • thyroid peroxidase uses I + thyroglobulin > MIT and DIT&raquo_space; combos T4 and T3
  • TSH > endocytosis of thyroglobulin into follicle cell > release T4 and T3
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2
Q

T4 vs T3

A

T4:
more - 4:1 T4:T3
- 7 day half life
- more protein bound, 0.02% free

T3
- 20% from thyroid, 80% converted
- short half life, 1 day
- less protein bound - 0.5% free
- x10 more metabolically active

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3
Q

what proteins does T4/T3 bind to?

A
  1. TBG 95%
  2. TTR
  3. albumin last
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4
Q

HPA axis for thyroid hormone

A

Hypothal TRH > ant pit for TSH > thyroid for T3/T4 > neg FB to hypothal/pit

TSH also neg FB to hypothal

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5
Q

factors affecting TRH vs TSH secretion

A

TRH: inc with cold, decr with stress
TSH: inhib by - somatostatin, DA, glucocorticoids

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6
Q

what happens to thyroid hormone in fetal life vs birth

A
  • <20/40 its maternal
  • > 20/40 inc foetal production
  • at birth: serum TSH surges at 30 MINS from cold/cord clamping
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7
Q

pitfalls of the NST for thyroid dysfunction

A
  • only detects high TSH i.e. 1’ hypothyroidism
  • TSH surges in first 24-36h, so testing before 48h high false positive
  • 33% neonatal T4 from mum, so hypothyroidism may be missed
  • false neg in premmie/VLBW, bc they cant increase levels as much, and excess iodine
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8
Q

thyroid ab most likely positive in:
- graves
- AI thyroiditis
- T1DM

A
  • graves: TSHR > Tg/TPO
  • AI thyroiditis: TPO > Tg > TSHR
  • T1DM: Tg and TPO only
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9
Q

defects of TBG: when to treat

A

Abnormalities of TBG are not associated with clinical disease and do NOT require treatment (T4 will be low/high, but free T4 will be normal)

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10
Q

most congenital hypothyroidism - sporadic or hereditary?

A

sporadic 85% - most by thyroid dysgenesis

hereditary only 15% - most by inborn errors of thyroid hormone synthesis

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11
Q

levothyroxine - what can’t you mix it with?

A

soy formulas and iron - they’ll bind the T4

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12
Q

goal T4 for thyroxine treatment?

A

T4 in upper half of reference range

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13
Q

thyroid dysgenesis - key features

A
  • most common cause of permanent congenital hypothyroidism worldwide
  • 2/3 have ectopic remnants
  • most unknown cause, some monogenic causes (**congenital heart defects)
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14
Q

dyshormogenesis of thyroid hormone- key features

A
  • AR mutations
  • 15% of congenital hypothyroidism
  • always have GOITRE

causes inc:
1) defect of iodine transport
2) TPO defect **most common
3) TBG defect
4) deoidination defect

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15
Q

important example of a TPO defect

A

Pendred syndrome:
AR mutation in Cl-I transporter
triad of:
1) hypothyroid
2) SNHL
3) goitre

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16
Q

types of TSH hormone resistance

A
  1. fully compensated: via hypersecretion of TSH
  2. partially compensated: high TSH can’t fully compensate > mild hypoT: initial euthyroid, hypoT over time
  3. uncompensated: severe hypoT

WON’T have goitre

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17
Q

sick euthyroid =

A

normal TSH, low T3/T4
not from a thyroid problem e.g. prem, stress, sepsis

NO treatment required

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18
Q

Resistance to Thyroid Hormone (RTH) - key features

A
  • AD mutations, HIGHLY heterogenous
  • all: thyroid dysfunction despite high T4/T3
  • not suppressed HIGH TSH
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19
Q

Thyrotropin Receptor (= TSH Receptor) Blocking Antibody - key points

A
  • b/g maternal AI thyroid disease > placental t/f of Abs > TSH does not bind to receptor in neonates
  • half life of Ab 21 days, remission of disease in 6 months, so don’t need tx for so long!
20
Q

most common cause of acquired hypothyroidism

A

Hashimoto’s

21
Q

examples of aetiologies for accquired hypothyroidism

A
  1. AI
  2. hypothal/pituitary disease
  3. drugs e.g. amiodarone
  4. haemangiomas
  5. infiltrative e.g. LCH
  6. syndromes e.g. DiGeorge
22
Q

how often to monitor thyroxine treatment in hypothyroidism?

A

Monitor 4-6 monthly as well as 6 weeks after dose change

23
Q

sick euthyroid neonate - what to do?

A

if T21, treat
if no T21:
- TSH > 10: treat if persists

24
Q

compare:
Transient hypothyroxinaemia
Transient primary hypothyroidism
Transient hyperthyrotropinaemia

A

Transient hypothyroxinaemia:
- low T4, =/low TSH
- from prems, immature HPA axis, will self-correct over 1-2mo

Transient primary hypothyroidism:
- low T4, high TSH
- idiopathic/prems, self-corrects over 2-3 mo

Transient hyperthyrotropinaemia:
- high TSH, self-correct after 9mo, but must follow up to exclude dyshormonogenesis / ectopia

25
Hashimoto's - 4 genetic syndromes to think of
i. APS-1 (10%) and APS-2 (70%) ii. IPEX syndrome iii. Turner syndrome and T21 iv. Klinefelter syndrome
26
hashimoto's - key features
= chronic lymphocytic thyroiditis - **goitre + growth retardation** most common, with mental dullness - most children clinically asymptomatic - NO ophathalmopathy!! - TPO and Tg-Abs in 95% - heterogenous echogenicity on USS
27
prominent nodules in Hashimoto's - what to do?
should have FNA as thyroid carcinoma or lymphoma can occur
28
Subacute granulomatous thyroiditis (= Dequervain disease) - key features
- rare in kids - acute: URTI + *thyroid pain* - weeks-months: hypothyroid - then normalisation in most
29
acute suppurative thyroiditis: most common cause?
alpha-haemolytic strep
30
acute suppurative thyroiditis: recurrent episodes suggest?
infection from piriform sinus fistula / thyroglossal duct remnant
31
congenital goitre =
Pendred syndrome (unless mum was on thyroxine/iodides)
32
most common cause of acquired goitre
Hashimotos (i.e. lymphocytic thyroiditis)
33
what is cretinism?
= severely stunted physical and mental growth due hypothyroidism
34
types of cretinism
1. neurologic: ID, pyramidal signs. Euthyroid, normal growth. GOITRE 2. myxedematous: ID, AND delayed growth with NO GOITRE, and low T4/high TSH
35
common causes of primary hypethyroidism
AI: Grave's Initial Hashimoto's (hashitoxicosis) sub-acute thyroiditis (after virus) Autonomous: McCune-Albright adenoma (Plummer) / MNG carcinoma Exogenous: iodine/thyroxine
36
grave's disease - key features
- HLA-B8 and DR3 - Th cells produce TRSAb > bind to TSH receptor > hyperthyroid - also anti-TPO
37
hyperthyroid + ophthalmopathy = what?
grave's = due to antigens to eye muscle too, and may NOT resolve when euthyroid!
38
which anti-thyroid med to give in grave's? key points.
carbimazole > PTU - block TPO to reduce stores in 2-6 weeks - trial cessation after 1-2y
39
important AE of anti-thyroid medications
carbimazole: 1. agranulocytosis 2. pancreatitis 3. reversible cholestatic jaundice - teratogen! 4. GN 5. lupus like polyarthritis PTU: 1. ANCA vasculitis 2. **fulimnant hepatic necrosis **
40
complications of thyroidectomy
1. Hypothyroidism (50%) 2. Recurrent thyrotoxicosis (10-20%) 3. Hypoparathyroidism (1-2%) 4. RLN palsy (1%), ELN palsy – husky voice (30%) 5. BLEEDING 6. Thyroid storm – if not prepared for surgery adequately
41
thyroid storm
increased TH from stress, infection surgery or radio-iodine therapy >> inc SNS drive EMERGENCY - IV PTU/carbimazole beta-blocker, steroids and rehydrate.
42
most common cause of neonatal hyperthyroidism?
neonatal grave's
43
key features of neonatal grave's
- from maternal graves: transplacental TSHR-IgG - hyperthyroid at birth unless mum taking Rx (~D7-10) - test TSHR-Ab in 3rd trim, and TFTs D1, D7-10 - give carbimazole if needed, or iodide
44
key features of thyroid carcinoma in childhood
- F>M, adolescents - high rate of mets, but usually indolent - highest risk 15y post radiation - papillary differentiated most common > follicular > medullary
45
medullary thyroid carcinoma = ??
MEN2! RET mutation, high calcitonin in serum/FNA