Thyroid-Hyperthyroid Flashcards

1
Q

Thyroid

A

Hormone secretion T3, T4

has to uptake iodine, produce thyroglobulin

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2
Q

Thyroid Hormone Function

A
growth & development
maintenance 
metabolism
temp homeostasis
heart rate
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3
Q

Normal levels Free T4

A

.8-2.7 ng/dL

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4
Q

Normal Free T3

A

230-420 pg/dL

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5
Q

Normal TSH

A

.404 mIU/L

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6
Q

Drugs that increase TGB, therefore decreasing free thyroid hormone levels

A
Estrogen
tamoxifen
heroin
methadone
mitotane
fluorouracil
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7
Q

Drugs that decrease TGB therefore increasing free thyroid hormone levels

A

Androgens
anabolic steroids
slow release nicotinic acid
glucocorticoids

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8
Q

Drugs decreasing secretion of TSH

A

dopamine
glucocorticoids
octreotide

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9
Q

Drugs that decrease thyroid hormone secretion

A

lithium
iodide & iodine preparations
radiocontrast dyes
amiodarone (can increase or decrease because its 37% iodine and it stays in your system for a year)

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10
Q

Dx criteria for Hyperthyroidism

A

lows TSH
elevated free T3/T4
Increased radioactive iodine uptake

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11
Q

Treatments for Hyperthyroidism

A

anti-thyroid meds
radioactive iodine
thyroidectomy
symptomatic tx (B-blockers)

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12
Q

Anti-thyroid drugs

A

possible remission
low cure rate (40-50%)
can have ADR’s
1st line in children and pregnant

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13
Q

Radioactive Iodine

A

curative
will prob become HYPOthyroid and need meds for life (l-thyroxine)
best for people with goiter

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14
Q

Surgery

A

rapid effect, useful if you have to Bx anyway

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15
Q

First Line Anti-thyroid (Thioamides)

A

Methimazole

PTU if someone is in thyroid storm or 1st trimester

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16
Q

Predictors of remission on Thioamides

A

small goiter
mild dz
low or negative thyroreceptor antibody titer

17
Q

Thioamide MOA

A

inhibits thyroid hormone synthesis (blocks incorporation of iodine into hormone)

PTU–>also inhibits peripheral T4–>T3 conversion within hours

depletion of stored hormone & prevention of new hormone synthesis

18
Q

Absorption of Thioamides

A

in Gi tract

reach peak level in 1 hour

19
Q

Distribution of Thioamide

A

concentrated in the thyroid
PTU–> 80% protein binding
half life is 2-3 houra

20
Q

Metabolism of Thioamide

A

Liver

21
Q

Elimination of Thioamide

A

renal (eliminated as metabolites)
Methimazole 1/2 life= 5-13 hrs
PTU 1/2 life= 1-2 hrs

22
Q

Common Adverse Effects of Thioamides

A

GI upset
arthralgia
rash, urticaria, pruritis

23
Q

Agranulocytosis

A

serious adverse effect of Thioamide
more likely to occure in higher doese, and with older paptients

0.2-.05%

S&S= fever, sore throat, bleeding, brusing, malaise, stomatitis

24
Q

Hepatotoxicity

A

Serious adverse affect of thioamide
higher risk in PTU
should do LFT’s, if high d/c

S&S–> ligth colored stool, dark urine, yellowing of the skin and eyes

25
Q

Monitoring Free T4 Levels

A

4 mo after initiation of therapy

every 4-8 wks until normal–> then every 2-3 months

26
Q

LFT’s

A

when pt is having symptoms (jaundice, joint pain, abd pain, light stoll, dark urine, GI upset, fatigue

27
Q

MOA of Iodides

A

Inhibits thyroid hormone release
decrease thyroid release
decrease vascularity of thyroid gland –> for pre-op

symptoms improve within a week

28
Q

Uses of Iodides w/Thyroid dz

A

pre-op (reduce vasculatiry)
Thyrotoxic crisis–>decrease iodine accumulation
prevents thyroid uptake of radioactive iodine

29
Q

Adverse affects of Iodide

A
rash
gi upset
paresthesia
immune hypersensitivity rxns
salivary gland swelling

Overdose–>burning in mouth, metallic taste, sore teeth, cold sx

30
Q

Beta Blocker use in Hyperthyroidism

A

Tx’s Symptoms (palps, tachy, tremor, heat intolerance)
used esp if pt;s resting HR is over 90 and thy are elderlu, postpartum, or child

can also be used in thyroidstorm (to decrease their HR)

31
Q

Beta Blockers MOA

A

block B adrenergic receptors–>mitigates symptoms of thyrotoxicosis

Propranolol and nadolol can decrease conversion of T4 to T3

32
Q

Radioactive Iodine (RAI) MOA

A

disrupts hormone synthesis, incorporites itself into the thyroid hormone, and thyroglobulin

Works in a couple weeks–>follicles begin to necrose

can be in a person’s system for up to a month (because its half life is 5 days

contraindicated in pregnany, breast feeding, thyroid CA

33
Q

Indications of RAI

A

ablation for graves

pt’s with surgical risk

34
Q

Benefits of RAI

A

well tolerated, low risk thyroid storm

35
Q

What to monitor with RAI

A

T3/T4: 1-2 mo’s after treatment (hypothyroidism usually occurs 4 weeks after tx)

36
Q

Adverse Effects in RAI

A

dysphagia, thyroid tenderness

37
Q

Tx of Thyroid storm

A

PTU–> med of choice (prevents T4–>T3 conversion)

SSKI–> blocks new hormone

Hydocortisone–> blocks T4 conversion

Beta Blocker–> propranolol (blocks T4 conversion)
Esmolol infusion when po isnt possible

Corticosteroid (dexamethasone) to stabilize BP

38
Q

Subclinical Hyperthyroidism

A

low TSH but normal levels of thyroid hormone (T3/T4)

can cause A-Fib (and increasing risk for strokes)

39
Q

Tx of Subclinical Hyperthyroidism

A

If its caused by amiodarone tx with methimazole (type 1) or glucocorticoids (type 2) or both.

if not from amiodarone–. usually dont tx, monitor hr and TSH