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PHAR 255 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

The thyroid gland synthesizes, stores, and releases what 2 thyroid hormones?

A
  1. T3
  2. T4
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2
Q

What are the 3 cell types that make up the thyroid gland? Which is the most important of the bunch?

A
  1. Colloid - most important
  2. Follicular cells
  3. Parafollicular cells - no thyroid effect, just happens to be here
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3
Q

Synthesis and secretion of T3 and T4 is controlled by _______ ___________ _______ (___), which is controlled by ___________-_________ _______

A

thyroid stimulating hormone (TSH); thyrotropin-releasing hormone

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4
Q

What are the 3 things that make up T3 and T4?

A
  1. Iodide
  2. Thyroglobulin
  3. Tyrosine
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5
Q

What are the 4 steps of T3/T4 synthesis?

A
  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 tissue (kidney/liver)
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6
Q

The physiologic ratio of T4:T3 is?

A

~13:1

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7
Q

The mechanism of T3/T4 synthesis is most mediated by what enzyme?

A

Thyroid peroxidase

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8
Q

What are the actions of T3 and T4 in the following body systems?
1. Heart
2. Adipose tissue
3. Muscle
4. Bone
5. Nervous system
6. Gut
7. Other tissue

A
  1. Heart = Chronotropic and inotropic
  2. Adipose tissue = catabolic
  3. Muscle = catabolic
  4. Bone = developmental
  5. Nervous system = developmental
  6. Gut = metabolic
  7. Other tissues = calorigenic
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9
Q

Between T3 and T4, which is more potent?

A

T3 is ~4x more potent

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10
Q

The thyroid hormone release process is regulated by a ________ _________ ____

A

negative feedback loop

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11
Q

Thyroid hormone release is promoted by: (2)

A
  1. Thyroid Stimulating Hormone - TSH
    - Release of TSH stimulated by low circulating T3/T4 levels
  2. Low serum iodide (not a huge concern in Canada)
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12
Q

Thyroid hormone release is inhibited by: (3)

A
  1. High circulating T3/T4 levels
  2. Lithium
  3. Iodide excess
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13
Q

What are 4 common disease causes of hyperthyroidism?

A
  1. Toxic diffuse goiter (Graves disease)
  2. Toxic multi-nodular goiter (Plummers disease)
  3. Acute phase of thyroiditis
  4. Toxic adenoma
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14
Q

What is THE most common cause of hyperthyroidism?
What is the 2nd most common cause?

A
  1. Graves disease (toxic diffuse goiter)
  2. Plummers disease (toxic multi-nodular goiter)
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15
Q

Graves disease (toxic diffuse goiter) is more common in which demographic?

A

Younger, female patients (ages 20-50)

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16
Q

What is the mechanism by which Graves disease (toxic diffuse goiter) works? (3)

A
  1. Autoimmune disorder
  2. Immune system creates antibodies against the TSH receptor
  3. Can result in hyperplasia of thyroid gland, leading to a goiter
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17
Q

Plummers disease (toxic multi-nodular goiter) is most common in which demographic?

A

Older, female patients (>50)

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18
Q

What is the most common trigger for Plummers disease (toxic mutli-nodular goiter)?
How long does this typically devlop?

A
  1. Iodine deficiency most common trigger for nodules to grow, but can be many others
  2. Develops slowly over several years
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19
Q

What is the mechanism by which Plummers disease (toxic multi-nodular goiter) works? (4 steps)

A

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

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20
Q

What is the mechanism by which acute phase of thyroiditis occurs? (2)

A
  1. Causes inflammation and damage to the thyroid gland
  2. Damage causes excess hormone to be released
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21
Q

What is the ironic endpoint of acute phase of thyroiditis?

A

This eventually leads to hypothyroidism once T3/T4 levels are exhausted (spike in release, stores run out, go hypo)

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22
Q

What is the mechanism by which toxic adenoma occurs? (2)

A
  1. Benign tumors growing on thyroid gland
  2. Become active and act just like thyroid cells, secreting T3/T4 but not responding to negative feedback (leading to hyperthyroidism)
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23
Q

What are 7 non-specific symptoms of hyperthyroidism? (Remember to think of how thyroid affects each body system and what excess might result in)

A
  1. Tremor in hands
  2. Diarrhea
  3. Heat intolerance
  4. Unintentional weight loss
  5. Weakness
  6. Tachycardia
  7. Amenorrhea
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24
Q

Graves disease (toxic diffuse goiter) has some specific symptoms that you should be aware of. What are they? (5)

A
  1. Exophthalmos (or proptosis) = eyes bulging
  2. Peri-orbital edema = swelling around the eyes
  3. Diplopia = seeing double
  4. Diffuse goiter = big, wide goiter
  5. Pre-tibial myxedema = swelling around tibia bone in leg
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25
Q

Diagnosing a hyperthyroid disease cannot be done strictly from lab results alone, but what is one important thing to keep in mind about the relationship between TSH and T3/T4 which appears in these results?

A

Since there is a negative feedback loop, TSH and T3/4 will have an inverse relationship with one another.

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26
Q

In terms of lab values, what TSH and T3/4 levels do we expect to see in:
1. Toxic diffuse (Graves)
2. Toxic multi-nodular (Plummers)

A
  1. Decreased TSH, increased free T3, normal or increased free T4
  2. Decreased TSH, increased free T3 and T4
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27
Q

There are a few drug which can induce hyperthyroidism. What is the important one to remember for our purposes?

A

Amiodarone (can actually cause hyper or hypo depending)

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28
Q

What are the 3 treatment options for hyperthyroidism?

A
  1. Drugs
    - Thioamides
    - Beta-blockers
  2. Radioactive iodine (RAI)
  3. Surgery (thyroidectomy)
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29
Q

The 2 thioamide anti-thyroid drugs for HT treatment are?

A
  1. Methimazole (MMI)
  2. Propylthiouracil (PTU)
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30
Q

What are the 3 indications for MMI and PTU?

A
  1. Toxic diffuse goiter (Graves)
  2. Toxic multi-nodular goiter (Plummers)
  3. Pre-treatment before RAI
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31
Q

The goal of therapy for thioamide use is?

A

To achieve remission from HT

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32
Q

Why is only remission the goal of using thioamides?
What is the caveat?

A
  • The drugs are not targeting the root cause of the HT, they only give temporary symptomatic relief. So, over time the underlying cause will still be causing issues, and the drugs will stop working eventually.
  • The caveat being that some people respond very well to these medications and can actually use them long-term, just make sure to monitor them
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33
Q

What is the MOA of thioamides?
What is the additional PTU-specific action?

A
  • Interferes with thyroid peroxidase-mediated processes
  • PTU also inhibits peripheral conversion of T4-T3 (more potent of the two meds)
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34
Q

What is the unique dosing property of thioamides? Why is it like this?

A
  • Start with high initial dosing then end up with lower maintenance doses
  • Most medications we start low go high, but here, as the goiter shrinks, the dose necessary to maintain HT control decreases
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35
Q

Methimazole (MMI) is dosed how often?

A

Once daily

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36
Q

Propylthiouracil (PTU) is dosed how often?

A

BID - TID

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37
Q

Thioamides - take with or without food?

A

Either is fine

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38
Q

How long is onset of effect of thioamides?
- Symptom improvement
- Euthyorid

A
  1. Symptom improvement within 1-4 weeks (days in some people)
  2. Euthyroid in 2-3 months
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39
Q

What is the typical duration of therapy of thioamides?

A

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

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40
Q

What is Terry’s Tip on dosing based on convenience or nausea prevention?

A
  • If convenience is a priority, may give both doses as a single daily dose
  • If nausea more important divide the doses
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41
Q

What are the common side-effects for thioamides? (4)

A
  1. GI upset
  2. Rash
  3. Arthralgia
  4. Abnormal taste/smell
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42
Q

True or False? Common thioamide side-effects do not resolve on their own?

A

False - most improve over 4 weeks

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43
Q

True or False? Common side-effects of thioamides are dose related for PTU, but not for MMI?

A

False - dose related for MMI, not PTU

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44
Q

True or False? PTU has higher rates of common side-effects than MMI

A

True

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45
Q

What are the 3 serious side-effects of thioamides?

A
  1. Neutropenia/agranulocytosis
  2. Hepatotoxicity
  3. Vasculitis
46
Q

If you were counseling a patient on thioamides, what general things would you mention first?

A

Discuss common side-effects, management strats, and reassurance they usually improve after 1 month

47
Q

If you were counseling a patient on thioamides, what would you talk about when discussing the serious side-effecs?

A

Low risk, but watch for:
- Signs of infection i.e., fever, headache, malaise, sore throat
– May need to see doc immediately depending on severity
- PTU specifically: Liver related issues (fatigue, weakness, RUQ pain, jaundice)
– See doc immediately

48
Q

What are the most common symptoms of neutropenia/agranulocytosis? (3)

A
  1. Fever
  2. Malaise
  3. Sore throat
49
Q

Neutropenia is defined as <____ neutrophils per microliter
Agranulocytosis is defined as <___ neutrophils per microliter

A

<1500;
<100

50
Q

What sort of hepatoxicities might be seen with MMI and PTU?

A

MMI - reversible cholestatic jaundice
PTU - allergic type hepatocellular damage

51
Q

Vasculitis is more common with PTU use. What is it? (2)

A
  1. Auto-immune process
  2. Damages vascular tissue causing inflammation and destruction of blood vessels
52
Q

What are the 2 DIs seen with thioamides?

A
  1. Warfarin: Decrease in INR
  2. Digoxin: Increase in digoxin levels
53
Q

What is the approach to monitoring for effectiveness in thioamides? (2)

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
54
Q

If discontinuing a thioamide, how would we monitor for relapse? (2)

A
  1. TSH at 3 months –> 6 months –> 12 months –> annually
  2. Relapse most likely within first 3 months
    - If suppressed TSH and normal T4/T3 seen, relapse likely
55
Q

What 2 things should be monitored safety-wise for patients on thioamides?

A
  1. CBCs: baseline and 1 week later
  2. LFTs: baseline and 1 week later
    - Watch for AST/ALT >3x upper limit of normal and symptoms of hepatotoxicity
56
Q

Comparing MMI to PTU:
Onset of euthyroid

A
  • MMI faster (~8 weeks)
  • PTU slower (~12 weeks)
57
Q

Comparing MMI to PTU:
Clinical response time

A

Same at 1-4 weeks

58
Q

Comparing MMI to PTU:
Side effects/toxicity commonality

A
  • MMI less common
  • PTU more common
59
Q

Comparing MMI to PTU:
Compliance

A
  • MMI - better (OD dosing likely)
  • PTU worse (usually BID-TID)
60
Q

Comparing MMI to PTU:
Cost

A
  • MMI - $25/month
  • PTU - $50/month
61
Q

Comparing MMI to PTU:
Contraindications

A
  • MMI - thioamide allergy
  • PTU - thioamide allergy and liver disease
62
Q

Comparing MMI to PTU:
Pregnancy

A

MMI
- 1st trimester: less safe
- 2nd and 3rd trimester: more safe
PTU
- 1st trimester: more safe
- 2nd and 3rd trimester: less safe

63
Q

Beta-blockers are used to treat symptoms of hyperthyroidism, such as? (5)

A
  1. Palpitations
  2. Tachycardia
  3. Tremors
  4. Anxiety
  5. Heat intolerance
64
Q

When can beta-blockers be initiated for hyperthyroid treatment?

A

As soon as it’s suspected and it can be added to other treatment

65
Q

Thyroidectomy (hyperthyroidism) surgery is an option if: (3)

A
  1. Pregnant patients who cannot tolerate medication
  2. Patients who want “curative” therapy, but not RAI
  3. Patients with large goiters (resistant to RAI)
66
Q

What are 3 complications associated with thyroidectomy?

A
  1. Hypoparathyroidism
  2. Vocal cord paralysis
  3. Thyrotoxicosis
67
Q

What are the 3 factors of subclinical hyperthyroidism?

A
  1. TSH of 0.1-0.3
  2. Normal FT3/FT4
  3. Asymptomatic
68
Q

Why is subclinical hyperthyroidism clinically important? (3)

A
  1. Osteoporosis risk increase
  2. Cardiac abnormalities
  3. Increase in mortality
69
Q

What is the treatment/monitoring of subclinical hyperthyroidism if at risk for complications?

A

Strongly consider treatment, or check levels again in 3 months (then treat if confirmed result)

70
Q

What is the treatment/monitoring of subclinical hyperthyroidism if at low risk for complications?

A

Recheck levels in 3-6 months unless TSH <0.1 (then consider treating)

71
Q

What are the management options for thyroiditis? (4)

A
  1. Self-limiting
  2. Beta-blocker for symptom control
  3. NSAIDs for pain
  4. Course of steroids for severe cases
72
Q

Thyroid Storm/Thyrotoxicosis is a rare, life-threatening condition. What is it characterized by? Can occur in which patients?

A
  1. Characterized by severe manifestations of hyperthyroidism
  2. Can occur in pts with untreated hyperthyroidism
73
Q

Thyroid Storm/Thyrotoxicosis is often triggered by an acute event, like: (4)

A
  1. Thyroid surgery or RAI
  2. Trauma
  3. Infection
  4. Giving birth
74
Q

Why exactly is Thyroid Storm/Thyrotoxicosis life-threatening?

A

Due to liver damage, cardiovascular collapse and shock

75
Q

What is the treatment for thyroid storm/thyrotoxicosis? (4)

A
  1. Supportive care (oxygen, ventilator, IV fluids)
  2. Treat underlying condition
  3. Treat cardiac arrhythmias
  4. Administer beta-blockers to reduce symptoms
    More, but not listed
76
Q

Hypothyroidism results from a defect anywhere on the HPT axis. What are 7 examples? (Will go through each)

A
  1. Chronic autoimmune thyroiditis (Hashimoto’s)
  2. Drug induced
  3. Iatrogenic disease (e.g., thyroidectomy/RAI)
  4. Post-partum thyroiditis
  5. Chronic iodine deficiency
  6. Central hypothyroidism
  7. Hypopituitarism
77
Q

The most common cause of hypothyroidism is?

A

Hashimoto’s disease (Chronic autoimmune thyroiditis)

78
Q

What is chronic autoimmune thyroiditis (Hashimoto’s)? (3)

A
  1. Autoimmune disorder where antibodies form
  2. Antibodies bind to TSH receptors which directly destroy thyroid cells
  3. Other antibodies may form that interfere with production of T3 and T4
79
Q

What are the 2 big drugs that cause drug-induced hypothyroidism?

A
  1. Lithium
  2. Amiodarone
80
Q

Explain how lithium can cause drug-induced hypothyroidism (2)

A
  1. Blocks iodine transport into the thyroid and prevents hormone release
  2. May cause subclinical or overt hypothyroidism (~20%)
81
Q

What patients are more prone to drug-induced hypothyroidism when taking lithium? (2)
How often should they be monitored?

A
  1. Patients with history of thyroid dysfunction at risk
  2. Elderly
  3. Monitor at 3m, then q6-12m
82
Q

What are 5 clinical presentations of early hypothyroidism?

A
  1. Weight gain
  2. Fatigue
  3. Sluggishness
  4. Cold intolerance
  5. Bradycardia
83
Q

What are 5 clinical presentations of advanced hypothyroidism?

A
  1. Myxedema
  2. Hypothermia
  3. Confusion
  4. Stupor, coma
  5. CO2 retention
84
Q

With sub-clinical hypothyroidism, what is the serum TSH level?
What is the serum TSH level of Hashimoto’s?
Reference range is 0.45-4.5 mlU/L

A

Sub-clinical hypothyroidism: slight increase (4.5-10)
Hashimoto’s: significant increase (>10)

85
Q

With sub-clinical hypothyroidism, what is the free T3 level?
What is the free T3 level of Hashimoto’s?
Reference range is 2.6-5.7 pmol/L

A

Sub-clinical hypo: Normal
Hashimoto’s: slightly decreased

86
Q

With sub-clinical hypothyroidism, what is the free T4 level?
What is the free T4 level of Hashimoto’s?
Reference range is 9-19 pmol/L

A

Sub-clinical hypo: Normal
Hashimoto’s: moderately decreased

87
Q

Amiodarone and lithium can influence lab results (hypothyroidism) by what 3 mechanisms?

A
  1. Decreases TSH
  2. Decreases T4 –> T3 conversion
  3. Decreases synthesis/release of T3/T4
88
Q

The treatment of hypothyroidism is replacement of thyroid hormone. What are the 4 options?

A
  1. Dessicated thyroid
  2. Liothyronine
  3. Levothyroxine
  4. Combined T3/T4
89
Q

The first thyroid replacement medication was dessicated thyroid. What is it made from?
What does it contain?
What are the problems? (2)

A
  1. Prepared from thyroid glands of animals
  2. Contains T3 and T4
    Problems:
  3. Causes high peak T3
  4. Not well standardized batch to batch
90
Q

What are the characteristics of liothyronine?
How much T3/T4?
Half-life
Cost
Problem

A
  1. Contains T3, no effect on T4
  2. Short half-life - causes wide fluctuations in serum levels
  3. Costly
  4. Higher incidence of cardiac adverse effects
91
Q

The standard 1st line therapy thyroid replacement medication is?

A

Levothyroxine

92
Q

What is levothyroxine?
Half-life?

A
  1. Analogue of T4 - conversion to T3 regulated by body
  2. Half-life of 7 days
93
Q

What does dosage/administration of levothyroxine depend on? (4)

A
  1. Age
  2. Weight
  3. Cardiac status
  4. Severity and duration of hypothyroidism
94
Q

When giving levothyroxine, higher baseline TSH usually predicts ______ __ ____

A

higher T4 dose

95
Q

The average replacement dose for levothyroxine is _._mcg/kg/d

A

1.6

96
Q

The starting dose of levothyroxine ranges from __._mcg/d to ___ ______ based

A

12.5; max weight

97
Q

Often, ___mcg levothyroxine is given empirically to young, healthy patients.
If subclinical, __-__mcg empirically

A

100;
25-50

98
Q

When giving levothyroxine, we recommend starting low and titrating up if: (4)

A
  1. Any CVD (e.g., ischemic heart disease)
  2. Rhythm disorders
  3. > 50 years old
  4. Severe, long-standing hypothyroidism
99
Q

What is the guideline for levothyroxine dosing titration? I.e., what are we starting at, and how much do we increase and how often?

A

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

100
Q

How should levothyroxine be administered?

A

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

101
Q

What are 4 potential side effects of levothyroxine?

A
  1. Hyperthyroidism symptoms
  2. Cardiac risk increase
  3. Aggravate existing CVD
  4. BMD reduction
102
Q

Levothyroxine drug interactions: What medications cause absorption reduction? (4)

A
  1. Antacids/H2 blockers/PPIs
  2. Iron
  3. Ca/mineral supplements
  4. Cholestyramine/colestipol
103
Q

How are levothyroxine absorption reduction drug interactions managed?

A

Managed by spacing levothyroxine 2-4 hours away from these meds

104
Q

Levothyroxine and TCAs what is the risk here?

A

Increased risk of arrhythmias

105
Q

Potent CYP inducers _________ thyroid hormone metabolism (levothyroxine)

A

increases

106
Q

When on levothyroxine what are we monitoring in terms of TSH?

A

Aim for low normal value (~<2.5mlU/L)
- Lower values can increase risk of cardiac toxicity
- May take 4-6 weeks to stabilize with each dose

107
Q

When on levothyroxine what are we monitoring in terms of Free T4/T3 levels? (i.e., what should the levels be?)

A

Free T4 –> normal to slightly elevated
Free T3 –> normal

108
Q

When on levothyroxine how long until patients should start seeing symptom improvement?
How long until maximum effect takes place?

A
  1. Improvement in 2-3 weeks
  2. Maximum effect in 4-6 weeks
109
Q

Subclinical hypothyroidism treatment is more controversial than subclinical hyperthyroidism. When are the only times we should really consider treatment? (4)

A
  1. Pt develops symptoms
  2. Planning pregnancy
  3. Heart failure
  4. Very young patient
110
Q

What if levothyroxine fails? What are some things to consider first? (3)

A
  1. Decreased bioavailability
  2. Increased need
  3. Other conditions:
    - Addison’s disease
    - Altered hypothalamic-pituitary-thyroid axis
    - Insufficient peripheral conversion of T4 to T3

PHAR 255 (14 decks)

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