Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endo > thyroid > Flashcards

thyroid Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what proteins does T4/T3 bind to?

A
  1. TBG 95%
  2. TTR
  3. albumin last
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

factors affecting TRH vs TSH secretion

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

levothyroxine - what can’t you mix it with?

A

soy formulas and iron - they’ll bind the T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

goal T4 for thyroxine treatment?

A

T4 in upper half of reference range

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

sick euthyroid =

A

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

NO treatment required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Hashimoto’s - 4 genetic syndromes to think of

A

i. APS-1 (10%) and APS-2 (70%)
ii. IPEX syndrome
iii. Turner syndrome and T21
iv. Klinefelter syndrome

26
Q

hashimoto’s - key features

A

= 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
Q

prominent nodules in Hashimoto’s - what to do?

A

should have FNA as thyroid carcinoma or lymphoma can occur

28
Q

Subacute granulomatous thyroiditis (= Dequervain disease) - key features

A
  • rare in kids
  • acute: URTI + thyroid pain
  • weeks-months: hypothyroid
  • then normalisation in most
29
Q

acute suppurative thyroiditis: most common cause?

A

alpha-haemolytic strep

30
Q

acute suppurative thyroiditis: recurrent episodes suggest?

A

infection from piriform sinus fistula / thyroglossal duct remnant

31
Q

congenital goitre =

A

Pendred syndrome (unless mum was on thyroxine/iodides)

32
Q

most common cause of acquired goitre

A

Hashimotos (i.e. lymphocytic thyroiditis)

33
Q

what is cretinism?

A

= severely stunted physical and mental growth due hypothyroidism

34
Q

types of cretinism

A
  1. neurologic: ID, pyramidal signs. Euthyroid, normal growth. GOITRE
  2. myxedematous: ID, AND delayed growth with NO GOITRE, and low T4/high TSH
35
Q

common causes of primary hypethyroidism

A

AI:
Grave’s
Initial Hashimoto’s (hashitoxicosis)
sub-acute thyroiditis (after virus)

Autonomous:
McCune-Albright
adenoma (Plummer) / MNG
carcinoma

Exogenous: iodine/thyroxine

36
Q

grave’s disease - key features

A
  • HLA-B8 and DR3
  • Th cells produce TRSAb > bind to TSH receptor > hyperthyroid
  • also anti-TPO
37
Q

hyperthyroid + ophthalmopathy = what?

A

grave’s = due to antigens to eye muscle too, and may NOT resolve when euthyroid!

38
Q

which anti-thyroid med to give in grave’s? key points.

A

carbimazole > PTU
- block TPO to reduce stores in 2-6 weeks
- trial cessation after 1-2y

39
Q

important AE of anti-thyroid medications

A

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
Q

complications of thyroidectomy

A
  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
Q

thyroid storm

A

increased TH from stress, infection surgery or radio-iodine therapy&raquo_space; inc SNS drive

EMERGENCY - IV PTU/carbimazole beta-blocker, steroids and rehydrate.

42
Q

most common cause of neonatal hyperthyroidism?

A

neonatal grave’s

43
Q

key features of neonatal grave’s

A
  • 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
Q

key features of thyroid carcinoma in childhood

A
  • F>M, adolescents
  • high rate of mets, but usually indolent
  • highest risk 15y post radiation
  • papillary differentiated most common > follicular > medullary
45
Q

medullary thyroid carcinoma = ??

A

MEN2! RET mutation, high calcitonin in serum/FNA

Endo (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions