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Summer Patho > Thyroid > Flashcards

Thyroid Flashcards

1
Q

name the blood supply of the thyroid

A

superior and inferior thyroid arteries

superior, middle, and inferior thyroid veins

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2
Q

name the lymph drainage from they thyroid

A

upper and lower deep cervical lymph node

pretracheal and paratracheal lymph node

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3
Q

what two nerves are in intimate proximity to the thyroid gland

A

the recurrent laryngeal nerve and the external motor superior laryngeal nerve

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4
Q

how much does the thyroid gland weigh

A

20g

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5
Q

describe the structure of the thyroid gland

A

two lobes joined by an isthmus, the upper isthmus borders the cricoid cartilage

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6
Q

THe thyroid is innervated by the

A

adrenergic and cholinergic systems

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7
Q

what does the thyroid gland do?

A

takes absorbed exogenous iodide (reduced in the gut from iodine) into itself and synthesizes T3 and T4

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8
Q

thyroid hormone production

A

depends on availability of exogenous iodine which is reduce to iodide in GI tract,
absorbed into blood
transported from plasma into thyroid follicular cells
iodide compounded with tyrosine and thyroglobulin and yields monoiodotryosine and diiodotyrosine that are then coupled to form T3 and T4
T3 and T4 are stored in the colloid until they are released

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9
Q

what are the roles of the thyroid hormone

A 
regulate metabolism
fetal development
CNS development and activity
bone and tissue growth
GI regulation
cardiac contractility myocytes
vasc smooth muscle vasodilation
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10
Q

thyroid hormone release is the interaction between

A

hypothalamic pituitary axis
thyroid gland
thyroid hormones

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11
Q

hypothalamus controls the release of what hormone

A

thyrotropin releasing hormone

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12
Q

thyrotropin releasing hormone stimulates secretion of what from where

A

thyroid stimulating hormone from anterior pituitary gland

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13
Q

what does thyroid stimulating hormone do?

A

acts on the thyroid gland to enhance synthesis and secretion of T3 and T4

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14
Q

pituitary and thyroid feedback loop

A

its CLASSIC and NEGATIVE

increased levels of thyroid hormone inhibit secretion of TSH from the pituitary

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15
Q

what is the primary determinant of TSH secretions

A

thyroid hormone levels

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16
Q

thyroid stimulating hormone structure

A

211 amino acids, 2 subunits

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17
Q

thyroid stimulating hormone function

A

controls production of T3 and T4

stimulates all aspects of thyroid hormone production (iodide uptake, incorporation, and then release of T3/T4)

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18
Q

what will happen to TSH levels in hypothyroidism

A

elevated

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19
Q

Triiodothyronine

A

t3
synthesized and released in the thyroid gland and also formed in liver and kidneys from conversion of T4 by slenodeiodinases

3-4x more active than t4

half life is 1-3 days

99.7% albumin bound

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20
Q

thryoxine

A

T4
synthesized and released by thyroid gland
serum half life of 6-7 days(1 wk)
99.9% bound to thyroid binding globulin

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21
Q

what is the percentage of T3 and T4

A

T3 - 10%

T4 - 90%

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22
Q

which thyroid hormone is more tightly bound to protein

A

T4 - that is why the longer half life

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23
Q

a larger amount of which thyroid hormone circulates in the bloodstream

A

T3

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24
Q

does the bound form of thyroid hormone matter?

A

no its the free form that drives the metabolic state

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25
Q

what are the principle thyroid function tests

A

TSH, T3, T4, radioactive iodine uptake

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26
Q

what happens to TSH with aging

A

increase in baseline

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27
Q

what is your normal TSH level

A

0.4-5.0

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28
Q

subclinical hyperthyroidism lab values

A

TSH: 0.1-0.4

normal levels of T3 and T4

29
Q

overt hyperthyroidism lab values

A

TSH: below .03

elevated T3 and T4

30
Q

subclinical hypothyroidism lab values

A

TSH: 5-10

normal T3 T4

31
Q

overt hypothyroidism lab values

A

TSH > 20

reduced T3 T4

32
Q

how do you diagnose pituitary dysfunction?

A

TRH test - injection of exogenous TRH by rapid IV push
serum concentration of TSH is collected at 15 and 30 min intervals over 2-3 hours
normally TSH would rise in concentration

if your hypothyroidism is due to pituitary disease (secondary hypothyroidism) then the administration of TRN will NOT produce and increase in TSH

33
Q

Hyperthyroidism

A

labs: low TSH, high T4/T3

syndrome caused by an intrinsic abnormality of the thyroid

34
Q

thyrotoxicosis

A

clinical syndrome caused by increased thyroid hormone levels

35
Q

Graves Disease

A

85% of hyperthyroid cases!!!
autoimmune disease caused by thyroid-stimulating antibodies that bind to TSH receptors in the thyroid, stimulating thyroid growth, vascularity, and hyper-secretion

36
Q

what are the causes of hyperthyroidism

A 
Graves disease
toxic multinodular goiter or long standing simple goiter hyperfunctioning
autonomously functioning thyroid nodule
thyroiditis
exogenous thyroid hormone ingestion
iodine induced
37
Q

S&S of hyperthyroidism

A

hypermetabolic state - anxious, restless, tachypneic, warm skin, sweating, flushed, heat intolerance, protruding eyes, weakness, fatigue, inability to sleep, tremors, weight loss, frequent BM, increased cardiac work, tachycardia, dysrhythmias, palpitations

38
Q

morbidity and mortality of hyperthyroidism is cuased by

A

increased HR - can lead to stroke, MI, ectopy, PVC, afib
hypermetabolism - increased CO2 - increased minute vent - resp weakness
myopathies

39
Q

treatment of hyperthyroidism

A

thionamides - PTU or methimazole
radioactive iodine
thyroidectomy

40
Q

thionamides (PTU) MOA

A

interfere with synthesis (coupling) of thyroid hormones in the thyroid and prevents conversion of T4-T3 in the periphery

meds are given for weeks to months and then thyroid function tests are used to ensure euthyroid state

41
Q

when should you perform thyroidectomy

A

when the patient is in a euthyroid state

42
Q

thyroid storm

A

acute, life threatening hyperthyroid
significant mortality >20%

Temp elevation with diaphoresis
marked tachy
cerebral dysfunction
GI probs

precipitated by surgery, infection, IV dye, DKA, trauma, thyroid palpation

43
Q

when does thyroid storm most often occur

A

post op period of inadequately treated hyperthyroidism patients

44
Q

treatment of thyroid storm

A

PTU and corticosteroids (stop conversion in periphery)

supportive care - treat temp, oxygenate and ventilate, hydrate (with glucose containing fluids)

beta blockers

determine cause

avoid SNS activation (ketamine, epi, etc)

45
Q

what drugs can you use to treat thyroid storm?

A

PTU and steroids!
ALSO
- iodides - blocks release of stored thyroid hormone from thyroid gland
- beta blockers - reduces symptoms and blocks conversion of T3 to T4

46
Q

why should you avoid aspirin with hyperthyroid

A

associated with displacement of thyroid hormone binding from thyroid binding globulin = increased free thyroid hormone

47
Q

why should you avoid amiodarone with hyperthyroid

A

it contains iodine and can de-iodinate T4 to T3

48
Q

why might you use caution with beta blocker for hyperthyroid patients

A

they may need the tachycardia to maintain adequate perfusion

49
Q

what can you do preop for you emergent patient with hyperthyroid?

A

premed with benzos/narc and avoid anticholinergics which can precipitate brady

50
Q

what can you do intraop for you emergent patient with hyperthyroid?

A 
consider invasive monitoring
dif dx - MH/thyroid storm
increase depth - avoid SNS
NO to ketamine, ephedrine, epi, dopa
if hypotension - reach for fluids or direct acting pressor (neo)
succ, NDMR, N2O - OK
eye protection (exopthalmos)
51
Q

what can you do postop for you emergent patient with hyperthyroid?

A

continue beta blocker\

T1/2 of T4 = 7 dys

52
Q

primary hypothyroid

A

90-95% of all hypo cases
decreased production of thyroid hormones despite normal TSH
most common causes are ablation of gland by radioactive iodine therapy or surgery

53
Q

autoimmune hypothyroidism

A

autoantibodies block TSH receptors in the thyroid and destroys receptors

54
Q

secondary hypothyroidism

A

secondary to hypothalamic or pituitary disease

55
Q

Hashimoto’s

A

autoimmune disorder, goiter, hypothyroidism

common in middle aged women

56
Q

S&S hypothyroidism

A

slow, progressive, tires easily, weight gain, fatigue, apathy, listlessness, slow speech, cond intolerance, decreased sweating, constipation, menorrhagia, slow motor function, slowed GI function, dry hair, skin, large tongue, periorbital edema
cardiomyopathy, impaired baroreceptor function, brady, hyponatremia, impaired ventilatory response to hypoxia and hypercarbia

57
Q

diagnosis of hypthyroid

A

primary - reduced T4, T3 and elevated TSH

secondary (pituitary) - reduced T4, T3, and TSH

58
Q

TRH stimulation test to determine primary or secondary hypothyroidism

A

can confirm pituitary pathology as a cause

in primary hypothyroidism: basal levels of TSH are elevated and elevation is exaggerated after TRH administration
pituitary dysfunction: blunted or absent response to TRH

59
Q

L-thyroxine/synthroid

A

levothyroxine is synthetic T4 which can be converted to T3
OA: 3-5d
peak: 4-6wk
IV: 6-8h

60
Q

anesthetic consideration hypothyroid

A

airway issue - goiter, edematous cord, swollen oral cavity
decreased gastric emptying increases risk of aspiration
hypodynamic CV system
decreased vent responsiveness to hypoxia and hypercarbia
risk for hypothermia
heme abnorms
increasee narc/sedation sensitivity

61
Q

that are the hematologic abnormals with hypothyroid

A

anemia, platelet dysfunction, lyte imbalance, hypoglycemia

62
Q

what can you do for your emergent patient with hypothyroid?

A

IV thyroid replacement, steroid coverage

phosphodiesterase inhibitors for decreased myocardial contracility

63
Q

why are phosphodiesterase inhibitors better for hypothyroid patients with reduced cardiac contractility than beta blockers?

A

patients may have reduced sensitivity at beta receptors

64
Q

myxedema coma

A

rare hypothyroid crisis
delirium, unconsciousness, hypovent, hypotherm, brady, hypotension, dilutional hyponatremia

most common in elderly women with history of hypothyroid

50% mortality

65
Q

what do you do for myxedema coma

A

IV thyroxine or triiodothyronine and IV steroids for possible adrenal insufficiency

66
Q

Goiter

A

swelling of thyroid gland
can be with hypo or hyper
causes: deficient intake of iodine, ingestion of a dietary (cassava), pharm, defect in hormonal biosynthetic pathway

compensatory hypertrophy and hyperplasia of follicular epithelium secondary to a reduction in thyroid hormone output

67
Q

thyroid surgery anesthetic consideration

A

patient needs to be euthyroid (1-2 months med treatment followed by recent TSH T3/T4)
airway compromise with large goiters may be present with nerve compression, tracheal deviation, and erosion
use RLN monitor

68
Q

complications of thyroid surgery

A

RLN injury
- unilateral: hoarse
- bilateral: obstruction
SLN injury
- weakness of voice and inability to create high tones
Hypoparathyroidism
- d/t damage to blood supply of parathyroid gland
- hypocalcemia 24-48h
- stridor/laryngospasm - treatment is IV calcium
Tracheal compression
- from expanding hematoma (hematoma evacuation is first line treatment)

Summer Patho (10 decks)

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