Patho E4: Thyroid

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What is a goiter?

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60 Terms

1

What is a goiter?

abn enlargement of the thyroid gland; often painless

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2

What is the most common cause of goiters world-wide?

lack of iodine

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3

What is the most common cause of goiters in the US?

over/under production of thyroid hormones

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4

How does lack of iodine contribute to goiter formation?

no T3/T4 production → no inhibition of TRH/TSH → overstimulation of thyroid → enlargement

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5

What is thyrotoxicosis?

state of thyroid hormone excess, large amount in circulation

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6

What is hyperthyroidism?

thyroid hormone excess resulting form excessive thyroid gland function, large amount in circulation

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7

What are examples of Primary Hyperthyroidism?

Graves, toxic nodular goiter, toxic thyroid adenoma, functioning thyroid cancer, iodine excess

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8

What is the most common cause of hyperthyroidism?

Graves’ disease

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9

What are examples of secondary hyperthyroidism?

TSH-secreting pituitary adenoma, ovarian tumor containing ectopic thyroid tissue

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10

What are examples of Iatrogenic hyperthyroidism?

medications: interferon, amiodarone

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11

What are some examples of Thyrotoxicosis w/o hyperthyroidism?

ingestion of excess thyroid hormone, thyroid destructive processes, subacture thyroiditis (painful), silent thyroiditis, damage to thyroid causing release of T3/T4 w/o inc production

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12

Who does Graves’ disease primarily affect?

young adult women (10:1 F-M); +FHx inc risk

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13

What is the pathophysiology behind Graves’ disease?

TSH receptor auto-Ab TSH-R stimulates thyroid follicular cells to produce excessive amounts of T3/T4 → thyroid becomes hyperplastic and very vascular → inc in T3/T4 shuts down TSH, but Auto-Ab continue T3/T4 production

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14

What are the S/sx associated w/ Graves’ disease?

irritable, nervous, poor concentration, tremor, hyperreflexia, exophthalmos, ptosis, heat intolerance, wt loss, palpitations, tachycardia, diarrhea

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15

What effects can hyperthyroidism have on the cardiovascular system?

inc HR and contractility, dec PVR, inc CO, pulse pressure inc, tachycardia, CHF

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16

What metabolic effects can hyperthyroidism cause?

inc hepatic gluconeogenesis, wt loss, inc need for vitamins, inc bone fragility, inc defecation

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17

What GU/GYN effects can hyperthyroidism cause?

W: oligomenorrhea w/ dec fertility

M: dec fertility and impotence

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18

What ocular effects can hyperthyroidism cause?

proptosis, fibrotic EOMS, restricted ocular mobility, diplopia

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19

What effects can hyperthyroidism have on the skin?

warm, sweaty, velvety, non-pitting edema of LE, nodular plaques, clubbing, hyperpigmentation of LE & nail beds, pretibial myxedema or thyrotoxic dermopathy (skin thickening, orange peel texture)

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20

What is a complication of hyperthyroidism?

Thyroid storm -rare, but emergency

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21

What can cause a Thyroid Storm?

often precipitated by another illness or a surgical emergency

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22

What S/sx are associated w/ a Thyroid storm?

tachycardia, HTN, fever, agitation, N/V/D, restlessness, psychosis, CHF, hypotension, shock, can be fatal

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23

What is another term for Hypothyroidism?

Myxedema

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24

What is Hypothyroidism characterized by?

low serum T4/T3, elevated serum TSH

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25

What causes primary hypothyroidism?

damage to the thyroid gland

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26

What are some examples of primary hypothyroidism?

Cretinism, Hashimoto’s, iodine deficiency, thyroidectomy, drugs (amio)

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27

What causes secondary hypothyroidism?

deficiency of TSH secretion from the pituitary

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28

What are some examples of secondary hypothyroidism?

hypopituitarism, hypothalamic disease

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29

What is Cretinism?

congenital hypothyroidism -evident at birth or w/in a few months

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30

What are the clinical manifestation of Cretinism?

persistent jaundice, hoarse cry, delay in development, short stature, protruding tongue, broad flat nose, wide set eyes, dry skin

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31

What happens in Cretinism goes untreated?

leads to mental retardation

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32

What S/sx are associated w/ hypothyroidism?

fatigue, cold intolerance, boggy facies, puffy eyelids, edema of hands and feet (myxedema), hoarseness, trouble concentrating, slow movements, menorrhagia, wt gain, constipation

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33

What is a complication of long-standing hypothyroidism?

Myxedema coma -high mortality rate

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34

What causes a Myxedema coma?

often precipitated by infection (sepsis), stroke, sedative-hypnotic meds

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35

What are S/sx of a Myxedema coma?

sx of hypothyroidism + dec level of consciousness, possibly seizures

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36

What is the most common form of hypothyroidism?

Hashimoto’s thyroiditis

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37

Who is more likely to be effected by Hashimoto’s?

3x more common in women, 3rd-5th decade

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38

What helps distinguish Hashimoto’s from other forms of hypothyroidism?

presence of anti thyroidperoxidase (antiTPO) and antithyroglobulin antibodies (Tg Ab)

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39

What is one of the first sx of Hashimoto’s?

painless enlarged goiter-lymphocytic infiltrate

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40

What is the pathophysiology behind Hashimoto’s?

T cell mediated follicular cell destruction + Anti-TSH block TSH action + Anti-TPO blocks peroxidase → no synthesis of T4/T3 + Tg Ab don’t allow for storage of T3/T4

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41

What signs may be present on the PE in pts w/ Hashimoto’s?

painless, symmetric enlarged thyroid, can impair swallowing, may be only one firm palpable lobe/nodule due to atrophy

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42

What labs would be seen in pts w/ Hashimoto’s?

90% have anti-TPO, 50% have Tg Ab, cell membrane Ab, normal T4 and TSH, no T3

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43

What are the neurological signs associated w/ Hashimoto’s?

slowed mentation, forgetfulness, dec hearing, ataxia, sluggish DTRs, paresthesias

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44

What MSK sx are associated w/ Hashimoto’s?

muscle weakness, cramps, stiffness

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45

What cardiac sx are associated w/ Hashimoto’s?

dec CO, bradycardia

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46

What other sx are associated w/ Hashimoto’s?

inc incidence of sleep apnea, inc cholesterol & TGs, Normo normo anemia, constipation, brittle hair, loss of body hair

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47

What skin sx are associated w/ Hashimoto’s?

cool, dry, diffuse non-pitting edema, puffy face w/ coarse features

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48

What is Nodular Disease characterized by?

disordered growth of thyroid cells → gradual development of fibrosis

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49

Who is more likely to develop a nontoxic multinodular goiter?

females, inc incidence w/ age, develop over many yrs

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50

What S/sx are associated w/ nontoxic multinodular goiters?

Asx, often felt on PE, ± dysphagia

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51

What complications can arise from nontoxic mulinodular goiters?

sudden pain → hemorrhage or malignancy ± hoarseness if laryngeal nerve involved

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52

What is a toxic Nodular goiter?

enlarged thyroid gland w/ nodules that produce too much thyroid hormone

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53

What is more likely to develop a toxic Nodular goiter?

elderly, develop from a simple goiter over yrs

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54

How might a pt w/ a toxic Nodular goiter present?

A fib, palpitations, tachycardia, nervousness, tremor, wt loss

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55

What can cause a toxic Nodular goiter?

receiving IV or oral iodine, medicines that contain iodine (amio)

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56

What is a toxic Adenoma?

single solitary nodule that autonomously produces thyrotoxicosis

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57

What would be seen on the PE of a pt w/ a toxic Adenoma?

large enough to palpate nodule, No S/sx of Grave’s dz

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58

What would a thyroid scan show in pts w/ a toxic Adenoma?

focal uptake in the hyper-functioning nodule and diminished uptake in the remainder of the gland; “HOT nodule“

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59

What are the tumor characteristics of a toxic Adenoma?

rapidly enlarging nodule, vocal cord involvement, fixed hard nodule, cervical LAD, dysphagia, stridor

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60

What risk factors increase the likelihood of someone developing a toxic Adenoma?

radiation exposure (head/neck radiation, nuclear disaster/test sites), FMHx of papillary or medullary thyroid cancer, male

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