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Endocrine > Disorders of Thyroid Gland > Flashcards

Disorders of Thyroid Gland Flashcards

1
Q

When does the fetal thyroid develop and begin to form?

A

development finishes around week 11; HPT axis begins to work by week 18 and peak levels of hormone production are not seen until late in gestation

developing fetus is dependent up

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2
Q

Where is the anatomical location of the thyroid?

A

anterior to the trachea, below the cricoid cartilage; composed of left and right lobes connected by an isthmus, and pyramidal lobe as the thyroglossal remnants

located with much vascular tissue, left laryngeal nerve and parathyroid glands

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3
Q

Describe the histology of thyroid follicles.

A

thyroid is composed of multiple follicles composed of colloid (thyroglobulin) used in hormonogenesis

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4
Q

Describe the structure and homology of TRH and TSH.

A

TRH is a hypothalamic tri-peptide

TSH contains alpha and beta sub-units, alpha subunit is common to TSH, LH, FSH and hCG

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5
Q

TRH stimulation of TSH is inhibited by what molecules/hormones?

A

glucocorticoids (high levels)
dopamine (in excess)
somatostatin
negative feedback from T4 and T3

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6
Q

Describe the mechanism and specificity of TSH receptor.

A

G protein linked receptor with binding sites for TSH, TSI, hCG and blocking antibodies

once stimulated it increases follicle growth and vascularity of the thyroid gland as well as stimulating all stages of thyroid hormone production, release and increases TG

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7
Q

Describe the basic steps of thyroid hormone synthesis.

A

iodine is trapped via import through sodium/iodide symporter (requires energy)
iodine is trapped by oxidation and incorporation into thyroglobulin (organification) by TPO
coupling of MIT and DIT occurs to form T3 and T4

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8
Q

What regulates thyroid hormone release from the colloid.

A

T3 and T4 are released through hydrolyzation by proteolytic enzymes and released under stimulation of TSH

*excessive iodine inhibits proteolysis and thyroid hormone release

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9
Q

Starting with T4, what will you get with deiodinization of 5’ or 5 iodine?

A

take off 5’ I –> T3 (considered up regulation due to increased potency)
take off 5 I –> reverse T3 (considered down regulation because it is not biologically active

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10
Q

What enzyme is primarily responsible for the metabolism of thyroid hormone?

A

monodeiodinases (MDIs)

converts T4 to T3 and reverse T3; half life of T4 is 7-8d, T3 is 24h

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11
Q

T4 to T3 conversion is inhibited in which situations?

A 
PTU
beta-blockers (propranolol)
starvation
illness
glucocorticoids
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12
Q

Contrast the Wollf-Chaikoff effect and the Jod-Basedow Phenomenon

A

Wolff Chaikoff Effect: mechanism by which excess iodine induced hypothyroidism which is protective against iodine excess

Jod- Basedow Phenomenon: iodine induced hyperthyroidism which is protective against iodine deficiency

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13
Q

Point mutations in the ligand binding domain of TR _____ result in ______ ______ _______ ______.

A

point mutations in binding domain of (nuclear hormone receptor) TR-b result in thyroid hormone resistance syndromes (3 domains: ligand independent, DNA binding and ligand binding domain)

(TR alpha 2 does not bind T3, receptors include a1,2, B1,2 )

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14
Q

What role does TH play in regulating fetal neural development?

A

absence of TH during active neurogenesis (put to 6mo postpartum) leads to irreversible mental retardation (cretinism) and multiple morphological changes in the brain, reduced levels lead to defective myelinization

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15
Q

How does TH regulate basic metabolism (glucose, lipids etc)?

A

stimulates metabolism, heat production and O2 consumption

stimulates catabolism but also increases appetite

stimulates glucose absorption, increased gluconeogenesis and glycogenolysis

increases lipolysis (hypercholeterolemia in hypothryoid states

increases drug metabolism

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16
Q

How does TH effect bone formation?

A

TH stimulates bone formation and bone resorption, over time resorption tends to prevail and chronic hyperthyroidism can lead to osteoporosis

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17
Q

What is the effect of TH on GI and GU symptoms?

A

stimulate gut motility (hyperdefecation in hyperthyroidism and constipation in hypothyroidism)

thyroid hormone also affects ovulation and both excess and deficiency can result in menstrual irregularities and infertility

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18
Q

When would you order the following tests:

TSH, free T4 and T3, reverse T3, TPO antibodies, TSI, TG and calcitonin?

A

TSH: initial screening tests
free T4 and T3 if TSH is abnormal
reverse T3 in lines
TPO or TSI with suspected autoimmune disease
TG used to follow thyroid cancer- follicular cell origin
calcitonin used to follow medullary CA

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19
Q

Distinguish primary from central hyperthyroidism using TSH and T4 levels.

A

primary hypothyroidism: TSH is hight, free T4 is normal/low (T3 often remains normal)
central hypothyroidism: hypothalamic pituitary failure- TSH is low/normal, and free T4 is low

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20
Q

Distinguish thyrotoxicosis and TSH secreting tumor using TSH and T4 levels.

A

thyrotoxicosis/hyperthyroid: TSH is low, free T4 is high (can be normal or low in T3 thyrotoxicosis)

TSH secreting tumor (and central thyroid hormone resistance syndrome: TSH is normal or high (autonomous), T4 and T3 are high

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21
Q

Describe the TSH and T4/T3 in patients with subclinical thyroid failure v. subclinical hyperthryoid.

A

(note subclinical does not imply asymptomatic)

mild thyroid failure: TSH is high, free T4 and T3 normal (compensation)
subclinical thyrotoxicosis: TSH low and free T4/T3 is normal (compensation)

22
Q

Who should be considered for TSH screening (higher risk)?

A 
women > 60y
\+ FH of thyroid disease
those with hyperprolactinemia (issue of hypothyroididsm)
hypercholesterolemia
infertility or menstrual irregularity
cardiomyopathy/ cardiac arrhythmia
osteoporosis

dx:
anyone with hyper/hypthryodism
presence of goiter

23
Q

What does the presence of a goiter tell you about the thyroid?

A

thyroid enlargement implies nothing about the function of the gland

condition may be seen in thyrotoxicosis, hypothyroidism, euthyroid state (most benign)

24
Q

What are the clinical signs of hyperthryodism?

A 
nervousness, agitation, irritability 
palpations, tachycardia, arrhythmia
exertion dyspnea
heat intolerance, increased perspiration, dehydration
tremor, muscle weakness
**fatigue
weight loss, increased appetite
hyperdefecation
decreased menstrual flow, infertility, increased spon. abortion
insomnia
lid lag, stare
orbitopathy, dermopathy and bruit (Graves' disease)
25
Q

Describe the presentation of apathetic thyrotoxicosis.

A

more common in older individuals, symptoms are not classic, usually cardiac manifestations (atrial fib. and CHF)

26
Q

What is thyroid storm?

A

life threatening medical emergency which includes severe thyrotoxicosis with mental status changes and fever

can occur with trigger (omission of anit-thyroid drug therapy, drug therapy, surgery, MI, CVA) on top of underlying thyrotoxicosis

27
Q

How is I-131 used in differentiation of causes of thyrotoxicosis?

A

I-131 is used to differentiate causes of thyrotoxicosis, but by itself it says nothing about thyroid function

28
Q

List etiologies of etiologies of thyrotoxicosis: high iodine v. low iodine uptake causes.

A

high uptake: Grave’s disease, autoimmune polyglandular syndrome 1 and 2, toxic multi nodular goiter, solitary hyperfucitoning nodule, TSH secreting tumors, thyroid hormone resistance syndromes

Low uptake: thyroiditis (subacute and silent), post part thyroiditis, drug induced

29
Q

What is the pathogenesis and unique symptoms of Grave’s disease?

A

auto-immune disorder resulting from production of a circulating TSI, resulting in excess thyroid hormone production

Orbitopathy (50%), smoking and I-131 worsen orbitopathy— exposure karatopathy, diplopia/gaze paralysis, loss of color vision, dryness, photosensisitvity, periorbial edema

dermopathy (1%) peau’d orange

spongy texture, often associated with other autoimmune endocrine disorders

30
Q

Describe possible cause and appearance on nuclear imaging studies or toxic multi nodular goiter.

A

may be due to activating mutations of the TSH receptor

appears as hot and cold areas of the thyroid on nuclear imaging

31
Q

What is the inheritiance pattern of TH resistance syndromes?

A

AD (patients are clinically thyrotoxic, normal/high TSH, elevated T4, MRI reveals no evidence of tumor)

32
Q

What is the classic presentation of sub acute thyroiditis?

A

often presents after URI with thyrotoxic symptoms
patient’s neck will be exquisitely tender due to inflammation
is usually self-limiting and can be treated with NSAIDs, prednisone and beta blockers

(silent thyroid’s occurs without pain)

33
Q

When does postpartum thyroiditis occur?

A

in 5-8% of post-partum women usually w/in 6mo after delivery and is self-limited but tends to recur with subsequent pregnancies; resolution may be preceded by hypothyroid phase

can be misdiagnosed as post part anxiety and depression

34
Q

What drugs are known to precipitate thyrotoxicosis?

A

iodine
amiodarone
thyroid hormone

35
Q

What medical treatments are available for thyrotoxicosis?

A

propylthiouracil (PTU): faster, 1st trimester use, liver damage
methimazole: can cause aplasia cutis, use in 2nd and 3rd trimester

both interfere directly with hormone synthesis (iodination and coupling and only work in high uptake states (PTU also blocks T4 -> T3 conversion), both risk of agranulocytosis, urticaria, rash and arthralgias

36
Q

What medical treatment is indicated in thyroid storm treatment?

A

PTU, propanol (B-blocker), potassium iodine (after PTU), glucocorticoids (block T4/T3 conversion)

37
Q

When is radioactive iodine I-131 indicated?

A 
Grave's disease
toxic multi nodular goiter
toxic adenoma
thyroid cancer
dx thyroid uptake (I-123- no B-emission and short half life)
38
Q

How does I-131 act as treatment?

A

cytotoxic effects of B-rays of radio active iodine are delayed 1-2mo, treatment results in hypothyroidism (must be managed by replacement therapy with levothryroxine)

single dose PO, can cause dry mouth and eyes; contraindicated in pregnancy (consider thyroidectomy)
antithyroid drugs have to be discontinued for 3d prior and iodine diet is recommended for 1-2 weeks prior to treatment

39
Q

What are the signs and symptoms of hypothyroidism?

A

fatigue, depression, cognitive impairment
cold intolerance, weight gain
dry skin, coarse hair, dry brittle nails, lateral eyebrow thinning
constipation
menorrhagia, infertility, galactorrrhea
dyslipidemia- high cholesterol
bradycardia, pericardial effusion
exertion dyspnea
delated relaxation of deep tendon reflexes
hypothermia
high cholesterol, high CK, hyponatremia

40
Q

What are the symptoms of myxedema coma ?

A

serve hypthyroidism with mental status changes, hypothermia, respiratory failure, common in older women

can be triggered by omission of T4 replacement therapy, MI, CVA, sepsis etc

41
Q

Name different causes of hypothyroidism.

A 
surgical 
ablative therapies: I-131 or XRT
infiltrative disease (amyloid)
autoimmune destruction
congenital, hereditary malformations
inflammatory- thyroiditis
iodine deficiency 
neoplasm
42
Q

Describe the pathogenesis of Hashimoto’s thyroiditis?

A

chronic lymphocytic thyroiditis with antibodies directed at TPO
PE: thyroid may be atrophic or enlarged, thyroid texture is irregular and firm

43
Q

What drugs are known to cause hypothyroidism?

A

lithium- impairs release of T4 and T3
amiodarone- excess iodine
PTU, MMI
interferon: causes reversible presentation similar to Hashimoto’s thyroiditis

44
Q

What complications can hypothyroidism during pregnancy cause?

A

higher rates of: spontaneous abortion, pre-eclampia, placental abruption, LBW, prematurity, still birth, fetal cognitive delay/impairment

**check a TSI in pregnant women previously treated for Graves’ disease with I-131

45
Q

What treatments are available for hypothyoridism?

A

levothyroxine T4: synthetic and identical to endogenous; DOC due to consistent potency and long duration

liothryonin: T3: not routinely used, has a faster onset of action and in rare cases of impaiared T4-T3 conversion

desiccated thyroid: derived from crude bovine thyroid glands (content of T4 and T3 varies)

46
Q

What are causes of suboptimal T4 treatment?

A 
inadequate dose
poor compliance
increased metabolism (rifampin, phenytoin, carbamazepine)
poor absorption (Fe, calcium, soy, sucralfate, chromium, espresso
increased requirement (estrogen states, pregnancy)
capecitabine, thalidomide, TKIs
formulation change
47
Q

What medications are indicated in myxedema coma?

A

levothryoxine
liothyronine (not in cardiac patients)
glucocoritocoids IV
supportive care (i.e. ventilation)

48
Q

How should physicians approach treating thyroidal changes due to non-thyroidal illnesses?

A

they do not represent abnormal thyroid function and do not require specific therapy other then addressing underlying disease states

examples: endogenous or exogenous glucocorticoids, dopamine (pressor) or catecholamines

patients will show an increased TSH in recovery phase of illness

49
Q

During unrelated illness, why are T4 possibly low?

A

decreased binding protein levels, increased clearance
(low T4 in illness is indicative of a poor prognosis

can run high due to decreased T4 to T3 conversion, decreased tissue uptake

50
Q

What are the common causes of low T3 in non thyroidal illness?

A

poor nutrition, increased circulating glucocoriticoids
drugs: amiodarone, steroids
cytokine, circulating inhibitors of 5’MDI

low T3 levels are almost universal with NTI

reverse T3 levels will be increased due to decreased clearance (major) and increased production (minor)- except in HIV (have high total T4 due to and increase in TBG)

Endocrine (28 decks)

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