Thyroid Flashcards

1
Q

which type of hypothyroidism is most common?

A

primary

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2
Q

why is TSH normal-range w/ secondary hypothyroidism?

A
  1. inappropriately low TSH given low T4
  2. glycosylation machinery is dependent on TRH
    w/out TRH –> make TSH still, but it is inactive –> low T4
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3
Q

causes of primary hypothyroidism

A

iodine deficiency
hashimoto’s
resistance to thyroid hormone - uncommon

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4
Q

cretinism

A

thyroid hormone is needed for CNS development of infant. dx w/in 4-6 wks –> catch up with normal development

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5
Q

target genes for thyroid hormone

A

developmental: CNS, long bone growth
metabolism: mito # and function, metabolic clearance of endogenous (LDL, CPK, cortisol, hyaluronic acid) and exogenous molecules (digoxin, anesthetics)
expression of beta-adrenergic receptors: skeletal and cardiac striated muscle

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6
Q

galactorrhea may occur in primary hypothyroidism. why?

A

high TRH –> causes production of prolactin

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7
Q

ddx primary hypothyroidism

A
iodine deficiency
hashimoto's
congenital 
subacute thyroiditis
surgical or radioiodine ablation
drugs - amiodarone, PTU, methimazole, lithium
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8
Q

ddx secondary hypothyroidism

A

hypothalamic disease
pituitary disease
genetic (TSH deficiency, pit-1/prop-1 mutations)

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9
Q

draw pit-1, prop-1 lineage diagram

A

see notes

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10
Q

resistance to thyroid hormone

A

rare
dominant negative mutation
high T4 and TSH, but hypothyroid appearing organs

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11
Q

how to tx hypothyroidism w/ coexisting hypoadrenalism

A

DON’T prescribe thyroid hormone. may precipitate adrenal crisis from increased turnover of cortisol.

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12
Q

treating hypothyroidism in pregnancy

A

increase dosage b/c increased T4 degradation by the placenta

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13
Q

how might initiation of thyroxine worsen underlying myocardial ischemia?

A

increases HR –> increase oxygen demand

- replace gradually

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14
Q

effect of thyroid hormone on heart

A
  1. increase HR
  2. decrease BP and peripheral resistance
  3. increase myocardial efficiency
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15
Q

causes of thyrotoxicosis in order of prevalence

A

Graves
TMG
toxic adenoma
thyroiditis

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16
Q

how does thyrotoxicosis cause sympathetic sx?

A

increases beta adrenergic receptors –> enhanced cAMP response

17
Q

graves sx

A
enlarged gland
goiter, sometimes w/ hums/bruits
graves triad:
1. diffuse thyroid hyperplasia
2. infiltrative opthalmopathy
3. infiltrative dermopathy = pretibial myxedema
18
Q

thyrotoxicosis factitia - labs

A

high thyroid hormone, low TSH
low thyroglobulin
0% iodine uptake nuclear scan due to suppression

19
Q

how much of thyroid hormone is bound to binding protein

A

> 99% = bound and inactive

20
Q

conditions that increase thyroid hormone binding to TBG

A
  • -> HIGH total T4/T3
  • pregnancy
  • estrogen
  • acute hepatitis
  • congenital > TBG
  • mutant albumin molecule
21
Q

conditions that reduce thyroid binding to TBG

A
--> LOW total T4/T3
androgens
corticosteroids 
salicylates
barbituates
major illness/trauma
nephrotic syndrome
congenital low TBG
22
Q

euthyroid sick syndrome

A

low free T3 and T4 w/ low or normal TSH in severe illness

23
Q

diagnostic features of papillary carcinoma

A
  1. papillary architecture
  2. psamomma bodies
  3. unique nuclear features: nuclear pseudo inclusions, nuclear grooves
24
Q

diagnostic features of follicular adenoma

A
  1. capsule surrounding a solitary nodule
  2. no evidence of invasion
  3. commonly micro follicular pattern
25
Q

diagnostic features of follicular carcinoma

A
  1. INVASION - vascular and transcapsular

often has a micro follicular pattern

26
Q

most common thyroid malignancy

A
  1. papillary (85%-90%)

2. follicular (10-15%)ll

27
Q

thyroid malignancy - fastest progression and worst prognosis

A

anaplastic

28
Q

thyroid malignancy - medullary

A

intermediate growth, mets can happen, prognosis good to poor

rare

29
Q

met patterns in thyroid malignancies

A

papillary = local common, distant rare
follicular = local rare, distant common
anaplastic and medullary = common everywhere