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
what are the principle thyroid function tests
TSH, T3, T4, radioactive iodine uptake
26
what happens to TSH with aging
increase in baseline
27
what is your normal TSH level
0.4-5.0
28
subclinical hyperthyroidism lab values
TSH: 0.1-0.4 | normal levels of T3 and T4
29
overt hyperthyroidism lab values
TSH: below .03 | elevated T3 and T4
30
subclinical hypothyroidism lab values
TSH: 5-10 | normal T3 T4
31
overt hypothyroidism lab values
TSH > 20 | reduced T3 T4
32
how do you diagnose pituitary dysfunction?
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
Hyperthyroidism
labs: low TSH, high T4/T3 syndrome caused by an intrinsic abnormality of the thyroid
34
thyrotoxicosis
clinical syndrome caused by increased thyroid hormone levels
35
Graves Disease
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
what are the causes of hyperthyroidism
``` Graves disease toxic multinodular goiter or long standing simple goiter hyperfunctioning autonomously functioning thyroid nodule thyroiditis exogenous thyroid hormone ingestion iodine induced ```
37
S&S of hyperthyroidism
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
morbidity and mortality of hyperthyroidism is cuased by
increased HR - can lead to stroke, MI, ectopy, PVC, afib hypermetabolism - increased CO2 - increased minute vent - resp weakness myopathies
39
treatment of hyperthyroidism
thionamides - PTU or methimazole radioactive iodine thyroidectomy
40
thionamides (PTU) MOA
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
when should you perform thyroidectomy
when the patient is in a euthyroid state
42
thyroid storm
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
when does thyroid storm most often occur
post op period of inadequately treated hyperthyroidism patients
44
treatment of thyroid storm
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
what drugs can you use to treat thyroid storm?
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
why should you avoid aspirin with hyperthyroid
associated with displacement of thyroid hormone binding from thyroid binding globulin = increased free thyroid hormone
47
why should you avoid amiodarone with hyperthyroid
it contains iodine and can de-iodinate T4 to T3
48
why might you use caution with beta blocker for hyperthyroid patients
they may need the tachycardia to maintain adequate perfusion
49
what can you do preop for you emergent patient with hyperthyroid?
premed with benzos/narc and avoid anticholinergics which can precipitate brady
50
what can you do intraop for you emergent patient with hyperthyroid?
``` 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
what can you do postop for you emergent patient with hyperthyroid?
continue beta blocker\ | T1/2 of T4 = 7 dys
52
primary hypothyroid
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
autoimmune hypothyroidism
autoantibodies block TSH receptors in the thyroid and destroys receptors
54
secondary hypothyroidism
secondary to hypothalamic or pituitary disease
55
Hashimoto's
autoimmune disorder, goiter, hypothyroidism common in middle aged women
56
S&S hypothyroidism
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
diagnosis of hypthyroid
primary - reduced T4, T3 and elevated TSH | secondary (pituitary) - reduced T4, T3, and TSH
58
TRH stimulation test to determine primary or secondary hypothyroidism
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
L-thyroxine/synthroid
levothyroxine is synthetic T4 which can be converted to T3 OA: 3-5d peak: 4-6wk IV: 6-8h
60
anesthetic consideration hypothyroid
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
that are the hematologic abnormals with hypothyroid
anemia, platelet dysfunction, lyte imbalance, hypoglycemia
62
what can you do for your emergent patient with hypothyroid?
IV thyroid replacement, steroid coverage | phosphodiesterase inhibitors for decreased myocardial contracility
63
why are phosphodiesterase inhibitors better for hypothyroid patients with reduced cardiac contractility than beta blockers?
patients may have reduced sensitivity at beta receptors
64
myxedema coma
rare hypothyroid crisis delirium, unconsciousness, hypovent, hypotherm, brady, hypotension, dilutional hyponatremia most common in elderly women with history of hypothyroid 50% mortality
65
what do you do for myxedema coma
IV thyroxine or triiodothyronine and IV steroids for possible adrenal insufficiency
66
Goiter
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
thyroid surgery anesthetic consideration
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
complications of thyroid surgery
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)