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PHAR 255 Exam 2 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Describe the thyroid gland structure and function

A

Butterfly-shaped endocrine gland in the front of the neck

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

Hormones produce many physiological effects (almost every system in some capacity)

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2
Q

When doing a diagnostic workup, a physician is capable of doing what to the thyroid gland?

A

A physician can palpate the thyroid gland to determine structural abnormalities

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3
Q

Describe the thyroid gland anatomy? What type of cells are present?

A

Colloid

Follicular cells

Parafollicular cells

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4
Q

What is the most important cell of the thyroid gland?

A

Colloid is the most important cell in the thyroid – stores iodine, tyrosine, and thyroglobulin

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5
Q

Function of the Colloid

A

Colloid is the most important cell in the thyroid – stores iodine, tyrosine, and thyroglobulin

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6
Q

Follicular Cell Function

A

Follicular – transport cells, pumping susbtances into colloid and secretion

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7
Q

What hormones does the thyroid gland produce? How does it produce such hormones?

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 requires iodide, thyroglobulin and tyrosine

1) Iodide binds with tyrosine attached to thyroglobulin = mono or di-iodotyrosine (MIT or DIT) (metabolically inactive)

2) MIT + DIT = T3 or DIT + DIT = T4

3) Then secreted into circulation

4) Some T4 converted to T3 in peripheral tissue (kidney/liver)
Physiologic ratio of T4:T3 is ~13:1

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8
Q

What is the physiologic ratio of T3 and T4 conversion in the periphery?

A

Enables more mechanisms for homeostatic balance – T3 is 3x the potency of T4
If body is need, can produce t3
T3 is metabolically cheaper to produce and is more potent

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9
Q

What is the best signalling hormone for T3/T4 Production?

A

TSH best signalling hormone for T3 and T4 production and secretion

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10
Q

What enzymes is required for thyroid synthesis of T3 and T4?

A

Thyroid Perioxidase

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11
Q

Chemical steps of T3 and T4 production in the thyroid

A

Thyroglobulin synthesis
Iodide trapping
Oxidation of iodide
Iodination of tyrosine
Coupling of MIT and DIT
Secretion of hormones

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12
Q

What are some actions of T3 and T4?

A

Heart – chronotropic and inotropic (Affects Hr and CO)
Adipose tissue – catabolic
Muscle – catabolic (muscle cell turnover for building muscle)
Bone – developmental
Nervous system – developmental
Gut – metabolic
Other tissues - calorigenic

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13
Q

Describe the following:
a) T4 and T3 Circulation
b) T4 and T3 Potency
c) Conversion To Inactive Forms

A

T4 in circulation is 100% from thyroid

T3 in circulation is 20% directly from thyroid (rest of peripheral conversion)

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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14
Q

T3/T4 Protein Binding

A

99.5% is in the protein bound form

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15
Q

How is the thyroid hormone process regulated?

A

Regulated by a negative feedback loop

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16
Q

Describe the regulation process of thyroid hormone (What promotes release? What inhibits release?)

A

Hormone release promoted by:
Thyroid Stimulating Hormone – TSH
Release of TSH stimulated by low circulating T3/T4 levels
Low serum iodide (initially compensatory mechanism, increases T3 and T4 production, cannot go on for ever - chronically, low serum iodine leads to hypothyroid)

Hormone release inhibited by:
High circulating T3/T4 levels
Lithium (one of the main drug induced hypothyroidism)
Iodide excess (interferes with organocation of iodide; temporary inhibition by 7 days or so)

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17
Q

Draw out the process of thyroid hormone regulation?

A
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18
Q

What are some significant epidemiology statistics of thyroid disorders?

A

~10% of Canadians have overactive or underactive thyroid glands; >50% are undiagnosed

More than 8 out of 10 patients with thyroid disease are women

1 out of 50 women are diagnosed with hypothyroidism during pregnancy

Incidence of hypothyroidism increases with age (over the age of 65, rate incraeses by 25% plus)

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19
Q

Why are thyroid disorders often undiagnosed?

A

Thyroid disorders cause non-specific sx that are hard to pinpoint on the thyroid

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20
Q

Define hyperthyroidism

A

Disease caused by excess synthesis and secretion of thyroid hormone

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21
Q

Causes of Hyperthyroidism

A

Toxic diffuse goiter (Graves disease)

Toxic multi-nodular goiter (Plummers disease)

Acute phase of thyroiditis

Toxic adenoma

  • Can be many causes
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22
Q

What is a goiter?

A

enlargement of the thyroid

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23
Q

Hyperthyroidism Sx

A

Causes a constellation of symptoms

Sx can change over time for the same individual

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24
Q

What type of disease is toxic diffuse goiter?

A

Autoimmune disorder

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25
Q

What is the most common cause of hyperthyroidism?

A

Toxic diffuse goiter (AKA Graves disease)

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26
Q

Who is toxic diffuse goiter more common in? Explain the pathology of the condition?

A

More common in younger, female patients (ages 20-50)

Most common cause of hyperthyroidism
Autoimmune disorder

Immune system creates antibodies against the TSH receptor

Can result in hyperplasia of thyroid gland, leading to a goiter
–> Antibodies bind to receptor and cause secretion of T3 and T4
–> Negative feedback does not work – TSH levels will be low; but does not cause anything as it is the antibodies doing the elevation

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27
Q

Is toxic multi-nodular goiter an autoimmune disease?

A

NO - NOT AN AUTOIMMUNE DX

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28
Q

Describe the epidemiology of toxic-multi nodular goiter?

A

Most common in older, female patients (>50)

Second most common cause of hyperthyroidism

Temprrary iodine deficiency (not chronic) most common trigger for nodules to grow, but can be many others

Develops slowly over several years

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29
Q

Describe the pathology of toxic multi-nodular goiter?

A

Iodine deficiency –> less T4 production –> thyroid cells grow larger (multi-nodular goiter) –> TSH receptors mutate –> continually active

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30
Q

Describe acute phase of thyroiditis

A

Causes inflammation and damage to the thyroid gland

Damage causes excess hormone to be released (passive diffusion type mechanism)

Eventually leads to hypothyroidism once T3/T4 stores exhausted

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31
Q

What is 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 (no TSH receptors)

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32
Q

What are some causes of acute phase of thyroiditis?

A

Infection

Physical Trauma

Pregnancy During the Delivery Phase

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33
Q

What are some common non-specific symptoms of hyperthyroidism?

A
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34
Q

What are some less common non-specific symptoms of hyperthyroidism?

A
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35
Q

When analyzing a patients symptoms (non-specifc sx), how many can a patient have?

A

Can vary from person to person

A person may only have one of the symptoms listed

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36
Q

What are some specifc symptoms of toxic diffuse goiter?

A

Exophthalmos (or proptosis) (slow processes to reverse)

Peri-orbital edema

Diplopia

Diffuse Goiter

Pre-tibial myxedema (rash on the shins, not severe consequences but uncomfortable)

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37
Q

In toxic diffuse goiter, are the ocular symptoms permenant?

A

Ocular sx are often reversible

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38
Q

What are some specific symptoms of toxic multi-nodular goiter?

A

Same general hyperthyroidism symptoms

Individual thyroid nodules may be palpable (only difference)

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39
Q

What is unique to toxic multi-nodular goiter hyperthyroidism?

A

Individual thyroid nodules may be palpable (only difference)

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40
Q

How is hyperthyroidism diagnosed?

a) Subclinical Hyperthroidism

b) Toxic Diffuse

c) Toxic Multi-nodular

A

Diagnosis based on clinical symptoms and lab tests

T3 and T4 are inverse to TSH in toxic diffuse and toxic multi-nodular - Differentiate the two on an imaging exam

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41
Q

When diagnosing hyperthyroidism, an important consideration is to….

A

Treat the patient (sx) and not the number

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42
Q

Can drugs influence lab tests of hyperthyroidism? If so, how? Which ones?

Are these significant? If so, in who?

A

Some drugs can influence lab tests

If someone has healthy thyroid, these should not matter

Only really effects people if they have hyperthyroid or undiagnosed hyperthyroid issues

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43
Q

What are the treatment options for hyperthyroidism?

A

I. Drugs
Thioamides
Beta-blockers

II. Radioactive iodine (RAI)

III. Surgery (thyroidectomy)

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44
Q

Thioamide Examples

A

Anti-thyroid drugs:

Methimazole (MMI)

Propylthiouracil (PTU)

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45
Q

What are the clinical indications for thioamides?

A

Toxic diffuse goiter
Toxic multi-nodular goiter
Pre-treatment before Radioactive Iodine

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46
Q

In regards to hyperthyroidism, remission refers to?

A

Bring thyroid levels into normal range and are sx free

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47
Q

What is the goal of therapy for thioamides?

A

Goal of therapy is to achieve remission

Relapses are common

About 30% remain in remission after 1-2 years of therapy with either drug (some people can see long term success; may not be necessary to pursue curative options)

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48
Q

Describe the mechanism of action of thioamides?

A

Interferes with thyroid peroxidase-mediated processes in T3/T4 production

PTU also inhibits peripheral conversion T4 to T3

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49
Q

Of the thioamides, which drug is considered the most potent?

A

PTU

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50
Q

What is an issue with the mechanism of action of the thioamides?

A

Not targeting the route cause – likely to not be effective lifelong – temporary relief until permanent treatment

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51
Q

Draw out the mechanism of action of drugs used to treat hyperthyroidism

A

Methimazole – Not clinically significant effect on peripheralnversion to T3

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52
Q

Describe the dosing/administration of the thioamides

A

High initial dose –> lower maintenance doses

Titrate dose if TSH and T4 does not improve in 4-6w

Decrease dose gradually once euthyroid

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53
Q

Why does the MD of the thioamides decrease with continual usage?

A

Goiter should shrink so lower MD as we continue

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54
Q

When can thioamide doses be adjusted? Why?

A

Do not alter doses no more than every 4-6 weks

When a new homeostatic set point is established

55
Q

What is the dosing of the thioamides?

A
56
Q

Explain the dose to s/e relationship of the thioamides

A

Meth – Dose related s/e

PTU – same rates of s/e no matter the dose

57
Q

Can the thioamides be taken with food?

A

Take with or without food

58
Q

Onset of effect of the thioamides

A

Symptom improvement within 1-4 weeks

Euthyroid in 2-3 months

59
Q

Duration of therapy with the thioamides

A

12-18 months common

May taper to d/c and see if relapse occurs

60
Q

How can dosing of the thioamides be altered for:

a) Convenience

b) S/e Management

A

If convenience is a priority, may give both as a single daily dose

If lowered naseau more important, divide the doses

61
Q

Which thioamide has higher rates of s/e? Are they dose related?

A

Higher rates with PTU

Dose related for MMI, but not PTU

62
Q

How common are side-effects with the thioamides?

A

Occur in 5-10% of patients

Most of these side-effects improve over 4 weeks

63
Q

What are some common side effects of thioamides?

A

GI upset
Rash
Arthralgia
Abnormal taste/smell

64
Q

A patient is on a thioamide and the dose was just increased. Would you expect this individual to have s/e with the dose increase?

A

Dose escalations may cause s/e to reappear for a few weeks before disappearing

65
Q

An individual is complaining of s/e from thioamide therapy. As a pharamacist, should you encourage the patient to continue the thioamide or stop the thioamide?

A

No other options for drugs that work on the thyroid, so really want people to push through these s/e

66
Q

What are some serious side effects of thioamides?

A

Neutropenia

Agranulocytosis

Hepatotoxicity

Vasculitis

67
Q

Describe thioamide neutropenia and agranulocytosis. When does it occur? Symptoms? Is frequent monitoring required?

A

Small decline in neutrophils common (transient decrease is common)

Agranulocytosis in 0.3 – 0.4% of patients
higher with PTU

Usually occurs within the first 90 days

Fever, malaise, sore throat most common symptoms

Abrupt onset

Regular monitoring of WBC not cost-effective

68
Q

Lab value definition of neutropenia and agranulocytosis?

A
69
Q

How much a decline is required to lead to agranulocytosis?

A

Sig decline over 30-40% of baseline may lead to agranulocytosis

70
Q

Monitoring of thioamides frequenyc?

A

Only monitoring suggested – baseline and week later but no more often

71
Q

Important counselling tip for thioamides

A

Feel any illness lasting beyond a few days, go see physician

72
Q

Hepatoxocity and thioamides. Frequency? Type of injury? Does it resolve? Lab Findings?

A

0.1-0.2% incidence (higher with PTU)

MMI – reversible cholestatic jaundice

PTU – allergic type hepatocellular damage

Resolves once drug d/c, but can result in death

Both can increase AST/ALT, concern if >3x upper limit normal, or alcoholic

73
Q

When monitoring for hepatoxicity in the thioamides? Watch for? Which drug primarily?

A

Watch for fatigue, darker urine, yellowing of skin/eyes, ruq pain – Definetely for PTU would warn someone about these s/e

Abrupt onset, so regular testing unlikely to catch it happening

74
Q

Testing of hepatoxcity thiamoides?

A

Baseline and a week later

75
Q

Thioamides vasculitis? More common with….. What type of condition is it? What does it lead to?

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

76
Q

OVERALL COUNSELLING TIPS OF 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

77
Q

Drug Interactions of Thioamides

A

Warfarin: Decrease in INR
Digoxin: Increase in digoxin levels

Methimazole weakly inhibits 2D6, 2C9, 2E1 – Clinically insignificant

78
Q

How should the effectiveness of thioamides be monitored? What if discontinuing a thioamide?

A

1-4 weeks for symptom improvement
Assess TSH, T3 and T4 at 4-6 week intervals until stable; then q2-3 months for 6-12m, then q4-6 months

If discontinuing, must watch for relapse:
TSH at 3 months –> 6 months –>12 months –> anually
Relapse most likely within first 3 months
If suppressed TSH and normal T4/T3 seen, relapse likely

79
Q

How can thioamides safety be monitored?

A

CBCs: baseline and 1 week later

LFTs: baseline and 1 week later
watch for AST/ALT >3x ULN and symptoms of hepatotoxicity

80
Q

Compare methimazole and PTU

a) Onset of euthyroid
b) Clinical Response
c) S/e and toxicity
d) Compliance
e) C.I.
f) Pregnancy

A
81
Q

In hyperthyroidism, beta-blockers are used for….

A

Reduces symptoms of hyperthyroidism:

Palpitations
Tachycardia
Tremors
Anxiety
Heat intolerance

Just related to cardiovascular symptom improvement

82
Q

What beta-blocker should be used in hyperthyroidism?

A

Choose propranolol if no other compelling indication for a beta-blocker – short acting and easy to titrate and withdraw – can use on PRN basis if not constant cardiovascular indication

Most beta-blockers effective

83
Q

When can a beta-blo0cker be started for hyperthyroidism?

A

Can be started as soon as hyperthyroidism suspected and added to other treatment

  • If other beta-blocker on board, just continue to use it
84
Q

What conditions should be watched for in hyperthyroidism and beta-blocker usage? Which beta-blocker should be used?

A

COPD or Asthma – propranolol not recommended as a short acting beta-blocker, use atenolon OD beta-blocker that is cardioselective

85
Q

Radioactive Iodine Usage in Hyperthyroidism

A

Radioactive Iodine 131 (I131)
Used commonly
I131 is taken up by the thyroid in its normal process, but the I131 causes tissue damage and ablation of gland
Is a definitive treatment compared to thioamides

86
Q

When is radioactive iodine given in hypethyroidism?

A

Only give when:

Mild hyperthyroidism (tx with thioamides prior to radioactive iodine)
Normal or only slightly enlarged gland
No exopthalmous

87
Q

What are some downsides/complications of radioactive iodine?

A

Permanent hypothyroidism (Treating hypo is easier and safer lifelong than hyper)
Can trigger thyroid storm / thyrotoxicosis
Worsen exopthalmous

88
Q

Radioactive Iodine C.I.

A

In pregnancy / lactation
Severe hyperthyroidism / exopthalmous

89
Q

What are some adverese effects of hypothyroidism

A

Initial hyperthyroidism exacerbation likely
Followed by hypothyroidism symptoms

90
Q

What is the most common usage of radioactive iodine?

A

Pre-treatment with thioamides

Given to achieve euthyroid status and avoid thyroiditis

Recommended for all, but must pretreat: Elderly patients, cardiac disease or severe hyperthyroidism

91
Q

A permenant solution of hyperthyroidism is….

A

Surgery (thyroidectomy)

91
Q

How should radioactive idoine be given to patients persuing pre-tx in hyperthyroidism?

A

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

92
Q

A thyroidectomy should be pursued be used as an option in individuals when….

A

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

93
Q

Complications of thyroidectomy

A

Hypoparathyroidism (parathyroid located on back side of thyroid) – rates are low

Vocal cord paralysis

Thyrotoxicosis

94
Q

What is subclinical hyperthyroidism?

A

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

95
Q

Subclinical hypothyrodism is ________. Tx shoudl occur in those who…

A

Clinically important! Tx those such as:
Osteoporosis risk increase
Cardiac abnormalities
Increase in mortality

96
Q

Treatment and monitoring of subclinical hyperthyroidism?

A

If at risk for complications: strongly consider treatment, or check levels again in 3 months (then treat if confirmed result)

If at low risk for complications: recheck levels in 3-6 months unless TSH <0.1 (then consider treating)

97
Q

Thyroiditis Management?

A

Self-limiting
B-blocker for Symptom control
NSAIDs for pain
Course of steroids for severe cases

DO NOT USE THIOAMIDES

98
Q

What are some causes of hypothyroidism?

A

Results from a defect anywhere on the HPT axis

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

99
Q

What is the most common cause of hypothyrpoidism?

A

Chronic autoimmune thyroiditis (Hashimoto’s)

100
Q

Whis is chronic autoimmune thyroiditis?

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

101
Q

What are some drug-induced causes of hypothyroidism?

A

Lithium
Blocks iodine transport into the thyroid & prevents hormone release
May cause subclinical or overt hypothyroidism (~20%)
Patients with history of thyroid dysfunction at risk, elderly
Monitor at 3m, then q6-12m

Amiodarone
Can cause hyper (<5%) or hypothyroidism (5-25%)
Increased risk if history of thyroid dysfunction
Monitor q1m x 3 m, then q3m x 6 m, then q6-12m

102
Q

What is the most common presentation of hypothyroidism?

A

Weight gain and fatigue

103
Q

What are some signs of early hypothyroidism and advanced hypothyroidism?

A
104
Q

Hypothyroidism presentation in the elderly?

A

Elderly patients – atypical presentation – cognitive related signs and symptoms

105
Q

What are some lab tests for sub-clinical hypothyroidism and hashimoto’s?

A
106
Q

What are some drugs that can influence the lab results in hypothyroidism? Management?

A

Don’t panic if you see someone on one of these and is being treated for hypothyroidism. It can be managed.

Not a contraindication if start one of these meds if someone has hypo.

107
Q

What is the treatment of hypothyroidism? What are the treatment options?

A

Treatment
Replacement of thyroid hormone necessary

Options:
Desiccated thyroid
Liothyronine
Levothyroxine
Combined T3/T4

108
Q

What was the first agent available for hypothyroidism?

A

Desiccated thyroid
First agent available

109
Q

What is dessicated thyroid?

A

Prepared from thyroid glands of animals
Contains T3 and T4
Causes high peak T3
Not well standardized batch to batch
Short t1/2

110
Q

What is the ratio of dessicated thyroid concerning T3 and T4?

A

Dessicated has a ration of 4 T4 : 1 T3 – more potent than body would prefer

111
Q

What is a PK parameter of dessicated thyroid? Implication?

A

Short t1/2 – tends to cause rollercoaster effect – high than low, repeat – prefer more stable levels of thyroid hormones – increase risk of CV effect; however, no long term studies

112
Q

Effectivenesss of dessicated thyroid

A

People do have positive effects quickly – questions about long term

113
Q

What is liothyronine?

A

Contains T3, no effect on T4

Short half-life - causes wide fluctuations in serum levels

Costly

Higher incidence of cardiac adverse effects

Try to dose close to physiologic ratio of T4:T3

114
Q

When should liothyronine be considered?

A

Some people who take levothyroxine, some people will not get control of hypo.

In rare cases, adding it here it may be added – May not convert in person, add on to levothyroxine

  • Only comes in 5 mcg increments
  • 100 mg of levothyroxine, add on 10 mcg of liothyronine
115
Q

What are some issues with liothyronine?

A

Wherever possible prefer body handles conversion of T4 to T3 to ensure homeostatic setpoint

Not family physician territory

116
Q

What is levothyroxine?

A

Analogue of T4
Standard 1st therapy
Half life of 7 days
Conversion to T3 regulated by body

117
Q

What PK parameter is important for levothyropxine? Whast does it allow us to do?

A

Half-life – Miss a dose (not a big deal), can take totally week dose as one dose – not as effective but can be done to improve adherence

118
Q

How is the dosage and administration of levothyroxine determined?

A

Depends on age, weight, cardiac status, severity and duration of hypothyroidism

Higher baseline TSH usually predicts higher T4 dose

119
Q

AVERAGE DOSE OF LEVOTHYROXINE

A

Average replacement (target) dose is 1.6mcg/kg/d

Starting dose ranges from 12.5mcg/day to max wt. based

Often give 100mcg empirically to young, healthy patients (not CV)

If subclinical, 25-50mcg empirically

120
Q

Why is a high empirical dos eof 100 mg of levothyroxine given to young healthy patients and not elderly patients?

A

Hypothyroidism for long time – CV system not use to higher amounts of stimulation – theoretical risk of causing too much stress on CV system

121
Q

Levothyroxine should be started slow and titrated up if: Recommended Dose?

A

Any CVD (eg. ischemic heart disease)
Rhythm disorders (e.g a-fib)
>50 years old
Severe, long-standing hypothyroidism

Start low (12.5-25mcg) and titrate up by 12.5 – 25mcg q4-6 weeks

122
Q

How should levothyroxine be administered?

A

Administer on empty stomach, 30 min before meals or 1 hour after, QAM best (small bioavailability) – spaced away from other meds

123
Q

If someone does meet the criteria for starting slow, what dose should be started of levothyroxine?

A

Not this criteria – anyone else, higher empiric of max weight based – achieve control faster

Consistency is best here

-Unsure of what dose to start someone one
- If non-urgent, start slow and go slow
- Often not life threatning condition

124
Q

What are some side effects of levothyroxine? Are these common?

A

Hyperthyroidism symptoms
Cardiac risk increase
Aggravate existing CVD
BMD reduction

If initiate appropriately, should not notice anything – NO s/e with medications unless dosed too high

125
Q

What are some drug interactions with levothyroxine absorption? How are these drug interactions managed?

A

Antacids / H2 blockers / PPIs
Iron
Calcium / mineral supplements
Cholestyramine / colestipol

Manage by spacing levothyroxine 2-4 hours away from these meds
Raloxifene –> space by 12h

126
Q

A patient just started a PPI and is on levotyhyroxine, what is the cocnern? What6 should be monitored?

A

PPI’s – mechanism of impairment changes pH of levothyroxine – PPI is okay on with levothyroxine (small effect), newly initiated be aware and dose change may be necessary for levothyroxine

127
Q

Drug interactions of levothyroxine clerance?

A

Drug Interactions
Potent CYP inducers increases thyroid hormone metabolism

Ciprofloxacin (short term, so clinically significance is low)
Phenytoin
Carbamazepine
Rifampin
Pregnancy

TCAs: increased risk of arrhythmias

128
Q

Monintroing of levothyroxine TFT’s

A

TSH –> aim for low normal value (~<2.5mIU/L)
Lower values can increase risk of cardiac toxicity (younger patient, may be better for more aggressive)
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

129
Q

Subclinical Hyothyroidism Test Diagnosis and TX

A

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

Treatment is controversial (often do not treat)

130
Q

Subclinical hypothyroidism can be potentially clinically relevant when….

A

Potentially clinically relevant. Increased risk of:
Atherosclerosis
Heart failure
MI
Depression
Low BMD
Metabolic syndrome

131
Q

When is subclinical hypothyroidism often treated?

A

Treat if patient develops symptoms, planning pregnancy, heart failure, very young patient

132
Q

When treatment with levothyroxine fails, one should consider?

A

Decreased bioavailability
Poor adherence
Malabsorption (PPI therapy, gastritis, H.pylori, Celiac)
Improper administration (taking with food, milk, other meds)

Increased need
Recent weight gain
Pregnancy
New medications that increase metabolism of T3/T4

Other conditions:
Addison’s disease
Altered hypothalamic-pituitary-thyroid axis
Insufficient peripheral conversion of T4 to T3

133
Q

Comapre leveothyroxine and thioamides?

a) Expect/Sx Improvement
b) Monitoring
c) S/e
d) When to see MD
e) Meds to Watch For

A

PHAR 255 Exam 2 (5 decks)

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