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PHAR255 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Describe the thyroid gland.

A

butterfly-shaped endocrine gland in front of neck
responsible for synthesis, storage, and release of T3 and T4

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2
Q

Describe thyroid gland physiology.

A

synthesis and secretion of T3 and T4 controlled by thyroid stimulating hormone (TSH), which is controlled by thyrotropin releasing hormone
creation of T3 and T4 require iodide, thyroglobulin, and tyrosine
1) iodide binds with tyrosine attached to thyroglobulin=MIT or DIT
2) MIT + DIT = T3 or DIT + DIT = T4
3) then secreted into circulation
4) some T4 converted to T3 in peripheral tissue (13:1)

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3
Q

What are the actions of T3 and T4?

A

heart: chronotropic and ionotropic
adipose tissue: catabolic
muscle: catabolic
bone: developmental
nervous system: developmental
gut: metabolic
other tissues: calorigenic

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4
Q

Describe some relevant points about circulating T3 and T4.

A

T4 in circulation is 100% from thyroid
T3 in circulation is 20% directly from thyroid
T3 is ~4x more potent than T4
45% of T4 is converted to inactive rT3
the rest of T4 and T3 circulate in active free form or protein-bound inactive form

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5
Q

Describe the thyroid hormone release process.

A

regulated by a negative feedback loop
hormone release promoted by:
-TSH (release stimulated by low T3/T4)
-low serum iodide
hormone release inhibited by:
-high circulating T3/T4
-lithium
-iodide excess

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6
Q

What is hyperthyroidism?

A

disease caused by excess synthesis and secretion of thyroid hormone
-several causes possible
-causes a constellation of symptoms

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7
Q

What are the common causes of hyperthyroidism?

A

toxic diffuse goiter (Graves)
toxic multi-nodular goiter (Plummers)
acute phase of thyroiditis
toxic adenoma

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8
Q

Describe Graves disease.

A

more common in younger, female patients (age 20-50)
most common cause of hyperthyroidism
autoimmune disorder
-immune system creates antibodies against TSH receptor
can result in hyperplasia of thyroid gland=causes goiter

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9
Q

Describe Plummers disease.

A

most common in older, female patients (>50)
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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10
Q

Describe 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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11
Q

Describe toxic adenoma.

A

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

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12
Q

What are some symptoms of hyperthyroidism?

A

all body systems overstimulated, non-specific
tremor in hands
diarrhea
heat intolerance
unintentional weight loss
weakness
tachycardia
amenorrhea

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13
Q

What are some symptoms that are specific to toxic diffuse goiter?

A

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

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14
Q

What are symptoms specific to toxic multi-nodular goiter?

A

individual thyroid nodules may be palpable
same general hyperthyroidism symptoms

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15
Q

How is hyperthyroidism diagnosed?

A

based on clinical symptoms and lab tests
-low TSH, elevated T3 and T4

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16
Q

What is an example of a drug which can influence lab tests for hyperthyroidism?

A

amiodarone
-increases synthesis and release of T3/T4

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17
Q

What are the anti-thyroid (thioamides) drugs?

A

methimazole
propythiouracil

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18
Q

What are the indications for the anti-thyroid (thioamides) drugs?

A

toxic diffuse goiter
toxic multi-nodular goiter
pre-treatment before RAI

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19
Q

What are the goals of therapy with thioamides?

A

achieve remission
-relapses are common
-about 30% remain in remission after 1-2 yrs of therapy with either drug

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20
Q

What is the MOA of the thioamides?

A

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

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21
Q

In general, how are the thioamides dosed and titrated?

A

high initial dose–>lower maintenance doses
titrating dose if TSH and T4 does not improve in 4-6wks
decrease dose gradually once euthyroid
PTU dosing is same regardless of severity, MMI doses differ based on severity

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22
Q

How should thioamides be taken?

A

take with or without food
Terrys Tips:
-if convenience a priority, give both as a single daily dose
-if lowered nausea more important, give divided doses

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23
Q

What is the onset for thioamides?

A

symptom improvement in 1-4 weeks
euthyroid in 2-3 months

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24
Q

What is the duration of therapy for thioamides?

A

12-18 months is common
may taper to d/c and see if relapse occurs

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25
Q

What are the common side effects of the thioamides?

A

dose related for MMI, but not PTU
most of these AEs will improve over 4 weeks
GI upset
rash
arthralgia
abnormal taste/smell

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26
Q

Which thioamide is more likely to produce the common adverse effects such as GI upset, arthralgia, etc?

A

PTU

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27
Q

What are the serious adverse effects of the thioamides?

A

neutropenia/agranulocytosis
hepatotoxicity
vasculitis

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28
Q

Describe neutropenia/agranulocytosis as serious adverse effects of the thioamides.

A

small decline is neutrophils is common
agranulocytosis is rare (more common with PTU)
usually occurs within the first 90 days
WBC falls to < 0.5 x 10 to the 9
fever, malaise, sore throat most common symptoms
abrupt onset
regular monitoring is not cost effective

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29
Q

Describe hepatotoxicity as a serious adverse effect of thioamides.

A

rare (more common with PTU)
MMI can cause reversible cholestatic jaundice
PTU can cause allergic hepatocellular damage
resolves once drug d/c but can result in death
both can increase AST/ALT, concern if > 3x ULN or alcoholic

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30
Q

Describe vasculitis as a serious adverse effect of thioamides.

A

more common with PTU
auto-immune process
damages vascular tissue causing inflammation and destruction of blood vessels
leads to:
-acute renal dysfunction
-arthritis
-skin ulcers/rashes
-respiratory problems

31
Q

What are the drug interactions of the thioamides?

A

warfarin: decrease in INR
digoxin: increase in levels
methimazole weakly inhibits 2D6, 2C9, and 2E1

32
Q

How can we monitor the thioamides for effectiveness?

A

1-4 weeks for symptom improvement
assess TSH, T3 and T4 at 4-6 wk intervals until stable; then q2-3 months for 6-12 months, then q4-6 months
if d/c, watch for relapse:
-TSH at 3 mo –> 6 mo –> 12 mo –> annually
-relapse most likely within first 3 months

33
Q

How can we monitor the thioamides for safety?

A

CBCs: baseline and 1 week later
LFTs: baseline and 1 week later
-watch for AST/ALT > 3x ULN, and signs of hepatotoxicity

34
Q

What is the use of beta-blockers in hyperthyroidism?

A

reduces symptoms of hyperthyroidism (mainly CV)
-palpitations, tachycardia, tremor, anxiety, heat intolerance

35
Q

Which beta-blockers are used in hyperthyroidism?

A

most are effective
Terrys Tips:
-choose propranolol if no compelling indication for a BB
-short acting and easy to titrate/withdraw

36
Q

What is the use of radioactive iodine for hyperthyroidism?

A

definitive treatment compared to thioamides
-causes tissue damage and ablation of gland
-used commonly

37
Q

When is radioactive iodine given for hyperthyroidism?

A

mild hyperthyroidism
normal or only slightly enlarged gland
no exophthalmos

38
Q

What are the downsides/complications of radioactive iodine?

A

permanent hypothyroidism
can trigger thyroid storm/thyrotoxicosis
worsen exophthalmos

39
Q

What are the contraindications to radioactive iodine?

A

pregnancy/lactation
severe hyperthyroidism/exophthalmos

40
Q

What are the adverse effects of radioactive iodine?

A

initial hyperthyroidism exacerbation likely
followed by hypothyroidism symptoms

41
Q

Why do we pre-treat with thioamides prior to radioactive iodine?

A

to achieve euthyroid status and avoid thyroiditis
recommended for all, but must pre-treat:
-elderly patients, cardiac disease or severe hyperthyroidism

42
Q

How do we initiate and stop treatment with thioamides prior to radioactive iodine?

A

initiate 4-6 weeks before RAI
stop three days prior to RAI
restart three days after RAI
taper and d/c once thyroid hormone levels decline

43
Q

When do we use thyroidectomy for hyperthyroidism?

A

pregnant pts who cant tolerate medication
patients who want “curative” therapy but not RAI
patients with large goiters

44
Q

What are the complications of thyroidectomy?

A

hypoparathyroidism
vocal cord paralysis
thyrotoxicosis

45
Q

What is subclinical hyperthyroidism?

A

TSH of 0.1-0.3, normal FT3/FT4, asymptomatic

46
Q

Why is subclinical hyperthyroidism important?

A

osteoporosis risk increases
cardiac abnormalities
increase in mortality

47
Q

What is the treatment for subclinical hyperthyroidism?

A

if at risk for complications:
-strongly consider treatment or check levels again in 3 mo
if at low risk for complications:
-recheck levels in 4-6 mo unless TSH < 0.1

48
Q

What is the management of thyroiditis?

A

self-limiting
beta-blockers for symptom control
NSAIDs for pain
course of steroids for severe cases

49
Q

What are the causes of hypothyroidism?

A

results from a defect anywhere on the HPT axis
-chronic autoimmune thyroiditis (Hashimotos)
-drug induced
-iatrogenic disease
-post-partum thyroiditis
-chronic iodine deficiency
-central hypothyroidism
-hypopituitarism

50
Q

Describe Hashimotos.

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

51
Q

What are some drug-induced causes of hypothyroidism?

A

lithium
amiodarone

52
Q

Describe lithium as a drug-induced cause of hypothyroidism.

A

blocks iodine transport into the thyroid & prevents hormone release
may cause subclinical or over hypothyroidism
patients with a history of thyroid dysfunction at risk, elderly
monitor at 3mo, then q6-12mo

53
Q

Describe amiodarone as a drug-induced cause of hypothyroidism.

A

can cause hyper or hypothyroidism
increased risk if history of thyroid dysfunction
monitor q1mo x 3mo, then q3mo x 6mo, then q6-12mo

54
Q

What are some symptoms of hypothyroidism?

A

weight gain
fatigue
cold intolerance
bradycardia
constipation

55
Q

What are the expected labs for Hashimotos?

A

elevated TSH
low T3 and T4

56
Q

Which drugs can influence lab results for hypothyroidism?

A

amiodarone
-decreases TSH
-decreases synthesis/release of T3/T4
lithium
-decreases synthesis/release of T3/T4

57
Q

What are the options for therapy of hypothyroidism?

A

desiccated thyroid
liothyronine
levothyroxine

58
Q

Describe desiccated thyroid.

A

first agent available
prepared from thyroid glands of animals
contains T3 and T4
causes high peak T3
not well standardized batch to batch

59
Q

What are the limitations of desiccated thyroid?

A

4:1 ratio (much more potent)
short t1/2

60
Q

Describe liothyronine.

A

contains T3, no effect on T4
short t1/2 (causes wide fluctuations in serum levels)
costly
higher incidence of cardiac adverse effects
try to dose close to physiologic ratio of T4:T3

61
Q

When can liothyronine be considered?

A

people uncontrolled on levothyroxine

62
Q

Describe levothyroxine.

A

analogue of T4
standard 1st therapy
t1/2 of 7 days
conversion to T3 regulated by body

63
Q

What should be considered when determining an initial dose of levothyroxine?

A

age
weight
cardiac status
severity and duration of hypothyroidism
higher baseline TSH usually predicts higher T4 dose

64
Q

What is the average dose of levothyroxine?

A

1.6mcg/kg/d

65
Q

What is the starting dose range for levothyroxine?

A

12.5mcg/day to max wt. based
if subclinical, 25-50mcg empirically
often give 100mcg empirically to young, healthy patients

66
Q

When do we recommend starting low and titrating up for levothyroxine?

A

any CVD
rhythm disorders
> 50 years old
severe, long-standing hypothyroidism
start low (12.5-25mcg) and titrate up by 12.5-25mcg q4-6 weeks

67
Q

How should levothyroxine be administered?

A

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

68
Q

What are the side effects of levothyroxine?

A

hyperthyroidism symptoms
cardiac risk increase
aggravate existing CVD
BMD reduction

69
Q

What are drug interactions of levothyroxine?

A

absorption reduction
-antacids/H2 blockers/PPIs
-iron
-calcium/mineral supplements
-cholestyramine/colestipol
space levothyroxine 2-4 hours away from these meds (raloxifene space by 12h)
potent CYP inducers increases thyroid hormone metabolism
-ciprofloxacin
-phenytoin
-carbamezepine
-rifampin
-pregnancy
TCAs: increased risk of arrhythmia

70
Q

How should levothyroxine be monitored?

A

TSH–>aim for low normal value (~2.5mlU/L)
-lower values can increase risk of cardiac toxicity
-may take 4-6 wks to stabilize with each dose change
free T4–>normal to slightly elevated
free T3–>normal
symptoms–>improvement in 2-3 wks, maximum effect in 4-6 wks
once stable and symptom free, monitor TSH q6-12-24mo

71
Q

What is subclinical hypothyroidism?

A

TSH of 4.5-10mlU/L, normal T3/T4, “asymptomatic”

72
Q

What does subclinical hypothyroidism increase the risk for?

A

atherosclerosis
heart failure
MI
depression
low BMD
metabolic syndrome

73
Q

When do we treat subclinical hypothyroidism?

A

if patients develop symptoms, planning pregnancy, HF, very young

74
Q

What should we do if levothyroxine treatment fails?

A

consider:
decreased F:
-poor adherence
-malabsorption
-improper administration
increased need:
-recent weight gain
-pregnancy
-new meds that increase metabolism of T3/T4
other conditions:
-Addisons
-altered HPT axis
-insufficient conversion of T4 to T3

PHAR255 (24 decks)

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