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255B > Thyroid > Flashcards

Thyroid Flashcards

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
Q

List examples of thioamides

A

Anti-thyroid drugs
- methimazole (MMI)
- propylthiouracil (PTU)

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26
Q

Indications for Thioamides

A

Toxic diffuse goiter
Toxic multi-nodular goiter
Pre-treatment before RAI

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27
Q

What is the GoT for thioamides

A

to achieve remission
relapses are common
about 30% remain in remission after 1-2 years of therapy with either drugs

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28
Q

MOA of Thioamides

A

interferes with thyroid perozidase-mediated processes in T3/T4 production
PTU also inhibits peripheral conversion T4-T3

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29
Q

Explain basic theory of dosing for Thioamides

A

Methimazole - has higher dose the more severe
PTU - the same dose as all severities
Starts high initial dose then lower maintenance dose for both

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30
Q

Administration, Onset of effect and duration of therapy for thioamides

A

take with or without food
sx improvement within 1-4 weeks
euthyroid in 2-3 months
duration of therapy - 12-18 months

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31
Q

Common S/E of Thioamides

A

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)

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32
Q

Serious S/E with Thioamides

A

Neutropenia / Agranulocytosis
hepatotoxicity
vasculitis

33
Q

What to tell patients for S/E for thioamides

A

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
Q

DDI for Thioamides

A

Warfarin - decrease INR
Digoxin - increase in digoxin levels

35
Q

Monitoring for Thioamides

A

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
Q

What trimesters are PTU and MMT safe in?

A

MMT - 1 less safe, 2/3 more safe
PTU - 1 more safe, 2/3 less safe

37
Q

What is the best beta blocker for hyperthyroidism and why?

A

choose propranolol if no other comorbidities
it is short acting & easy to titrate/withdrawal so it can be taken PRN

38
Q

What is the effective of beta blockers for hyperthyroidism?

A

reduce sxm of hyper in cardio
palpitations, tachycardia, tremors, anxiety, heat intolerance

39
Q

Radioactive Iodine (131)

A

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
Q

When should Radioactive iodine be used?

A

mild hyperthyroidism
normal or only slightly enlarged glad
no exophthalmos

41
Q

List some downsides and complication for radioactive iodine

A

permanent hypothyroidism
can trigger thyroid storm/ thyrotoxicosis
worsen exopthalmous

42
Q

CI for Radioactive Iodine

A

in pregnancy / lactation
severe hyperthyroidism / exopthalmous

43
Q

A/E for Radioactive iodine

A

initial hyperthyroidism exacerbation likely
followed by hypothyroidism symptoms

44
Q

Describe pre tx with thioamides

A

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
Q

Patient instructions for RAI

A
  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
Q

When is surgery an option

A

Pregnant patients who cannot tolerate medication
Patients who want “curative” therapy, but not RAI
Patients with large goiters (resistant to RAI)

47
Q

List the management strategies for thyroiditis

A

self limiting
b-blocker for symptom control
NSAIDs for pain
course of steroids for severe cases

48
Q

What is the thyroid storm?

A

also known as thyrotoxicosis
Rare, life-threatening condition
Characterized by severe manifestations of hyperthyroidism
Can occur in patients with untreated hyperthyroidism

49
Q

List some triggers of thyroid storm

A

Often triggered by an acute event, like:
Thyroid surgery or RAI
Trauma
Infection
Giving birth

50
Q

List some causes of hypothyroidism

A

Chronic autoimmune thyroiditis (Hashimoto’s)
Drug induced
Iatrogenic disease (e.g. thyroidectomy/RAI)
Post-partum thyroiditis
Chronic iodine deficiency
Central hypothyroidism
Hypopituitarism

51
Q

Describe chronic autoimmune thyroiditis (hashimoto’s)

A

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
Q

What drugs can induced hypothyroidism?

A

lithium
amiodarone

53
Q

Sx of hypothyroidism

A

weight gain
fatigue
sluggishness
cold intolerance
bradycardia
constipation
heavy menses

54
Q

In terms of serum TSH, free T3, free T4 as high, low, and normal for sub-clinical hypothyroidism

A

high
normal
normal

55
Q

In terms of serum TSH, free T3, free T4 as high, low, and normal for hashimotos

A

very high
low
very low

56
Q

What drug may cause a decrease in TSH

A

amiodarone
glucocorticoids
metformin

57
Q

What drugs can cause decreases T4-T3 conversion

A

amiodarone
beta blockers
glucocorticoids

58
Q

what drugs can cause decreases synthesis and release of T3 and T4

A

amiodarone
lithium
iodine (acute use)

59
Q

What drug can increase T4/T3 metabolism

A

carbamazepine
phenobarbital
phenytoin
rifampin

60
Q

What are some limitations to desiccated thyroid?

A

High levels of subjective benefit, but lab values do not show same level of benefits

61
Q

What should you know about desiccated thyroid?

A

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
Q

What should you know about liothyronine

A

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
Q

When can liothyronine be considered?

A

Perhaps they are unable to achieve their optimal range
Endocrinologist management

64
Q

What should you know about levothyroxine

A

analogue of T4
standard 1st therapy
half life of 7 days
conversion to T3 regulated by body

65
Q

What is the average replacement dose per weight?

A

1.6 mcg/kg/d

66
Q

What is the starting dose ranges

A

12.5 mcg/day to max wt. based

67
Q

what is often the starting dose for a young, healthy patients

A

100 mcg

68
Q

why are some reasons to starting low and titrating up

A

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
Q

Administration instructions for levothyroxine

A

on empty stomach,
30 min before meals or 1 hour after, QAm best

70
Q

S/E for levothyroxine

A

Hyperthyroidism symptoms
Cardiac risk increase
Aggravate existing CVD
BMD reduction

71
Q

list some categories of DDI for Levothyroxine

A

Absorption reduction
Potent CYP inducers increases thyroid hormone metabolism
TCAs

72
Q

What does DDI for TCAs happen with levo?

A

increased risk of arrhythmias

73
Q

Monitoring Plan for Levothyroxine

A

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
Q

What if tx with levothyroxine fails? Consider

A

decreased bioavailability
increased need
other conditions

75
Q

What to consider for decreased bioavailability with levo?

A

poor adherence
malabsorption
improper administration

76
Q

What to consider for increased need for levo?

A

recent weight gain
pregnancy
new medications that increase metabolism of T3/T4

77
Q

What to consider for other conditions for levo dosing?

A

addison’s disease
altered hypothalamic-pituitary-thyroid axis
insufficient peripheral conversion of T4 to T3

78
Q
A

255B (5 decks)

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