Thyroid Flashcards

(78 cards)

1
Q

Treatment Options of Hypothyroidism

A

desiccated thyroid
liothyronine
levothyroxine
combined T3/T4

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2
Q

Treatment options of hyperthyroidism

A

Drugs - thioamides & beta blockers
radioactive iodine (RAI)
surgery (thyroidectomy)

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3
Q

How to optimally initiate and titrate levothyroxine doses

A

start with 12.5 mcg and increase by 12.5-25 mcg q4-6w

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4
Q

What is the anatomy of thyroid gland?

A

butterfly shaped endocrine gland in the front of the neck

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5
Q

What is the responsibility of the thyroid?

A

responsible for synthesis, storage and release of the two thyroid hormones, T3 and T4

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6
Q

What are the three types of cells in the thyroid?

A

colloid, follicular cells, parafollicular cells

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7
Q

Why would the thyroid produce two different thyroid hormones?

A

T3 is 4x more potent, can address shortages quickly with smaller amount of molecules produced. Plus T4 can be converted into T3 with a loss of an iodine

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8
Q

Steps of Creation of T3 and T4

A

Requires iodide, thyroglobulin and tyrosine
1. iodide binds with tyrosine attached to thyroglobulin = mono or di iodotyrosine (MIT or DIT)
2. MIT + DIT = T3 or DIT + DIT = T4
3. then secreted into circulation
4. some T4 converted to T3 in peripheral tissues

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9
Q

What is the physiologic ratio of T4:T3

A

is ~13:1

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10
Q

What are some things that promote hormone release

A

TSH
Low serum iodide

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11
Q

What are some things that inhibited hormone release

A

high circulating T3/T4 levels
lithium
iodide excess

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12
Q

List some common causes of Hyperthyroidism

A

Toxic diffuse goiter (Graves disease)

Toxic multi-nodular goiter (Plummers disease)

Acute phase of thyroiditis

Toxic adenoma

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13
Q

What is toxic diffuse goiter

A

autoimmune disorder
immune system creates antibodies against the TSH receptor
can result in hyperplasia of thyroid gland leading to a goiter
most common cause of hyperthyroidism

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14
Q

Toxic multi-nodular goiter

A

second most common cause of hyperthyroidism
iodine deficiency most common trigger for nodules to grow, but can be many others
develops slowly over several years

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15
Q

Acute phase of thyroiditis

A

causes inflammation and damage to the thyroid gland
damage causes excess hormone to be released
eventually leads to hypothyroidism once T3/T4 stores exhausted

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16
Q

Toxic Adenoma

A

benign tumors growing on thyroid glands
become active and act just like thyroid cells, secreting T3/T4 but not responding to negative feedback

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17
Q

List some common non-specific hyperthyroidism symptoms

A

tremor in hands
diarrhea
heat intolerance
unintentional weight loss
weakness
tachycardia
amenorrhea

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18
Q

Symptoms of toxic diffuse goiter specific

A

exophthalmos
peri-orbital edema
diplopia
diffuse goiter
pre-tibial myxedema

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19
Q

For Serum TSH, Free T3, Free T4 which are high, normal, or low for subclinical hyperthyroidism

A

low
normal
normal

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20
Q

For Serum TSH, Free T3, Free T4 which are high, normal, or low for toxic diffuse

A

very low
high
normal to very high

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21
Q

For Serum TSH, Free T3, Free T4 which are high, normal, or low for toxic multinodular

A

very low
high
high

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22
Q

List some drugs that can influence lab tests by increases TSH secretion

A

1st gen antipsychotics

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23
Q

List some drugs that can influence lab tests by increases synthesis and release of T3/T4

A

amiodarone, iodine (chronic use)

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24
Q

List some drugs that can influence lab tests by decrease thyroxin binding globulin (TBG)

A

androgens (likely clinically insignificant)
glucocorticoids - supraphysiologic doses

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25
List examples of thioamides
Anti-thyroid drugs - methimazole (MMI) - propylthiouracil (PTU)
26
Indications for Thioamides
Toxic diffuse goiter Toxic multi-nodular goiter Pre-treatment before RAI
27
What is the GoT for thioamides
to achieve remission relapses are common about 30% remain in remission after 1-2 years of therapy with either drugs
28
MOA of Thioamides
interferes with thyroid perozidase-mediated processes in T3/T4 production PTU also inhibits peripheral conversion T4-T3
29
Explain basic theory of dosing for Thioamides
Methimazole - has higher dose the more severe PTU - the same dose as all severities Starts high initial dose then lower maintenance dose for both
30
Administration, Onset of effect and duration of therapy for thioamides
take with or without food sx improvement within 1-4 weeks euthyroid in 2-3 months duration of therapy - 12-18 months
31
Common S/E of Thioamides
occur in 5-10% most of these s/e improve over 4 weeks - GI upset - rash - arthralgia - abnormal taste and smell (higher rates with PTU)
32
Serious S/E with Thioamides
Neutropenia / Agranulocytosis hepatotoxicity vasculitis
33
What to tell patients for S/E for thioamides
Discuss common side-effects, management strategies, and reassurance they usually improve after 1 month Discuss risk of severe side-effects are low, but watch for: - Signs of infection: fever, headache, malaise, sore throat - Depending on severity of symptoms, may need to see doctor immediately PTU: Liver related issues (fatigue, weakness, RUQ pain, yellowing of eyes/skin, dark urine) Should be seen by doctor immediately for evaluation
34
DDI for Thioamides
Warfarin - decrease INR Digoxin - increase in digoxin levels
35
Monitoring for Thioamides
1-4 weeks for Sxm improvement assess TSH, T3 and T4 at 4-6 weeks until stable then q2-3m for 6-12m, then q4-6m CBCs - baseline and 1 week later LFTs - baseline and 1 week later
36
What trimesters are PTU and MMT safe in?
MMT - 1 less safe, 2/3 more safe PTU - 1 more safe, 2/3 less safe
37
What is the best beta blocker for hyperthyroidism and why?
choose propranolol if no other comorbidities it is short acting & easy to titrate/withdrawal so it can be taken PRN
38
What is the effective of beta blockers for hyperthyroidism?
reduce sxm of hyper in cardio palpitations, tachycardia, tremors, anxiety, heat intolerance
39
Radioactive Iodine (131)
used commonly taken up by the thyroid in its normal process, but the I131 causes tissue damage and ablation of gland is a definitive tx compared to thioamides
40
When should Radioactive iodine be used?
mild hyperthyroidism normal or only slightly enlarged glad no exophthalmos
41
List some downsides and complication for radioactive iodine
permanent hypothyroidism can trigger thyroid storm/ thyrotoxicosis worsen exopthalmous
42
CI for Radioactive Iodine
in pregnancy / lactation severe hyperthyroidism / exopthalmous
43
A/E for Radioactive iodine
initial hyperthyroidism exacerbation likely followed by hypothyroidism symptoms
44
Describe pre tx with thioamides
Given to achieve euthyroid status and avoid thyroiditis Recommended for all, but must pretreat: Elderly patients, cardiac disease or severe hyperthyroidism Initiate 4-6 weeks before RAI Stop three days prior to RAI Restart three days after RAI Taper and discontinue once thyroid hormone levels decline
45
Patient instructions for RAI
1. Do not kiss, exchange saliva, or share food or eating utensils for 5 days. Your dishes should be washed in a dishwasher, if one is available. 2. Avoid close contact with infants, young children (under 8 years), and pregnant women for 5 days. (You can be in the same room with them.) 3. If you have an infant, no breast-feeding is allowed. 4. Flush the toilet twice after urinating, and wash your hands thoroughly. 5. If a sore throat or neck pain develops, take acetaminophen or aspirin. 6. If you note increased nervousness, tremors, or palpitations, call a physician
46
When is surgery an option
Pregnant patients who cannot tolerate medication Patients who want “curative” therapy, but not RAI Patients with large goiters (resistant to RAI)
47
List the management strategies for thyroiditis
self limiting b-blocker for symptom control NSAIDs for pain course of steroids for severe cases
48
What is the thyroid storm?
also known as thyrotoxicosis Rare, life-threatening condition Characterized by severe manifestations of hyperthyroidism Can occur in patients with untreated hyperthyroidism
49
List some triggers of thyroid storm
Often triggered by an acute event, like: Thyroid surgery or RAI Trauma Infection Giving birth
50
List some causes of hypothyroidism
Chronic autoimmune thyroiditis (Hashimoto’s) Drug induced Iatrogenic disease (e.g. thyroidectomy/RAI) Post-partum thyroiditis Chronic iodine deficiency Central hypothyroidism Hypopituitarism
51
Describe chronic autoimmune thyroiditis (hashimoto's)
Most common cause of hypothyroidism Autoimmune disorder where antibodies form Antibodies bind to TSH receptors which directly destroy thyroid cells Other antibodies may form that interfere with production of T3 and T4
52
What drugs can induced hypothyroidism?
lithium amiodarone
53
Sx of hypothyroidism
weight gain fatigue sluggishness cold intolerance bradycardia constipation heavy menses
54
In terms of serum TSH, free T3, free T4 as high, low, and normal for sub-clinical hypothyroidism
high normal normal
55
In terms of serum TSH, free T3, free T4 as high, low, and normal for hashimotos
very high low very low
56
What drug may cause a decrease in TSH
amiodarone glucocorticoids metformin
57
What drugs can cause decreases T4-T3 conversion
amiodarone beta blockers glucocorticoids
58
what drugs can cause decreases synthesis and release of T3 and T4
amiodarone lithium iodine (acute use)
59
What drug can increase T4/T3 metabolism
carbamazepine phenobarbital phenytoin rifampin
60
What are some limitations to desiccated thyroid?
High levels of subjective benefit, but lab values do not show same level of benefits
61
What should you know about desiccated thyroid?
first agent available short half life prepared from thyroid glands of animals contains T3 and T4 causes high peak T3 not well standardized batch to batch
62
What should you know about liothyronine
contains T3 no effect on T4 short half life - causes wide fluctuations costly higher incidence of cardiac a/e try to dose close to physiologic ratio of T4:T3
63
When can liothyronine be considered?
Perhaps they are unable to achieve their optimal range Endocrinologist management
64
What should you know about levothyroxine
analogue of T4 standard 1st therapy half life of 7 days conversion to T3 regulated by body
65
What is the average replacement dose per weight?
1.6 mcg/kg/d
66
What is the starting dose ranges
12.5 mcg/day to max wt. based
67
what is often the starting dose for a young, healthy patients
100 mcg
68
why are some reasons to starting low and titrating up
any CVD rhythm disorders >50 years old severe, long standing hypothyroidism start low (12.5-25 mcg) and titrate up by 12.5-25 mcg q4-6w
69
Administration instructions for levothyroxine
on empty stomach, 30 min before meals or 1 hour after, QAm best
70
S/E for levothyroxine
Hyperthyroidism symptoms Cardiac risk increase Aggravate existing CVD BMD reduction
71
list some categories of DDI for Levothyroxine
Absorption reduction Potent CYP inducers increases thyroid hormone metabolism TCAs
72
What does DDI for TCAs happen with levo?
increased risk of arrhythmias
73
Monitoring Plan for Levothyroxine
TSH  aim for low normal value (~<2.5mIU/L) Lower values can increase risk of cardiac toxicity May take 4-6 weeks to stabilize with each dose change Free T4  normal to slightly elevated Free T3  normal Symptoms  improvement in 2-3 weeks, maximum effect in 4-6 weeks Once stable and symptom free, monitor TSH q6-12-24m
74
What if tx with levothyroxine fails? Consider
decreased bioavailability increased need other conditions
75
What to consider for decreased bioavailability with levo?
poor adherence malabsorption improper administration
76
What to consider for increased need for levo?
recent weight gain pregnancy new medications that increase metabolism of T3/T4
77
What to consider for other conditions for levo dosing?
addison's disease altered hypothalamic-pituitary-thyroid axis insufficient peripheral conversion of T4 to T3
78