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PHARM 220 > Thyroid Disorders: Pharmacology + Therapeutics > Flashcards

Thyroid Disorders: Pharmacology + Therapeutics Flashcards

1
Q

What are the goals of therapy when treating hypothyroidism?

A

1) Normalize TSH levels/ euthyroid state
- normally high in hypothyroidism patients but we want to normalize it

2) Manage symptoms

3) If pregnant, achieve optimal TSH levels

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2
Q

What are the 3 treatment options used to treat hypothyroidism

A

1) Levothyroxine/Synthetic T4
- Synthyroid: brand name; Eltroxin - generic

2) Triodothyronine or liothyronine/ Synthetic T3
- Brand name: Cytomel

3) Desiccated thyroid: animal based product with mix of T3 + T4

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3
Q

T or F: A combo of Levothyroxine and liothyronine have been used to treat patients with hypothyroidism

A

T - can use combo of the 2 but really no studies showing the benefit

  • some people just feel better when have combo of T3 and T4
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4
Q

T or F: Levothyroxine has a shorter half life than liothyronine and therefore requires multiple daily doses

A

False
Levothyroxine: 7 day half life === able to maintain stable + predictable levels of T4 in the blood

Liothyronine: 1.5 day half life; requires multiple daily dosing == more fluctuation in T3 levels (can cause too high of levels = toxic in some cases)

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5
Q

What impacts/decreases the absorption of levothyroxine?

A

Iron + aluminum containing products
Calcium
PPIs
Cholesterol resin
Phosphate binders
Coffee
Soy + bran

Solution to this interaction: try to take on empty stomach in morning (30-60 mins before you eat) or take at night 3-4 hrs after last meal

— need to try and be consistent with timing

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6
Q

T or F: Desiccated thyroid has unpredictable levels of T3 + T4

A

true

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7
Q

What is the main risk of over-treatment of hypothyroidism

A

symptoms of hyperthyroidism

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8
Q

Starting dose of levothyroxine: healthy adult

A

1.6-1.7 mcg/kg/day

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9
Q

Starting dose of levothyroxine: adult >50 years

A

12.5 -25 mcg/day OR 1 mcg/kg/day
—- decrease in dosing compared to healthy adult

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10
Q

Starting dose of levothyroxine: Adult with cardiac disease or > 60 yrs

A

12.5-25 mcg/day

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11
Q

T or F: Levothyroxine dosing should be adjusted for renal and liver dysfunction

A

F- don’t need to change

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12
Q

T or F: IV dosing of levothyroxine is the same as oral dosing

A

F - should be 75- 80% of oral dose

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13
Q

For obese patients, how should levothyroxine dose be determined

A

using IBW

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14
Q

How is levothyroxine dosing changed over time

A

Normally start low + slow
- adjust dose by 12.5-25mcg per day every 4- 8 wks (for people with cardiac disease or elderly == change every 6-8wks)

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15
Q

Typically trend seen with dosing of levothyroxine with age

A

Infants - need a higher mcg/kg dose
- range from 8-15 mcg/kg/day

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16
Q

How soon after starting levothyroxine should patients experience symptom relief?

A

Some improvement: 2-3 wks

Max effect: 4-5 weeks

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17
Q

T or F: Levothyroxine can cause a transient increase in FT4

A

Yes - due to how it is a synthetic form of T4; blood work can show an increase in FT4 or TT4
- can be nothing to worry about especially if TSH is normal (euthyroid)

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18
Q

Lab test monitoring for hypothyroidism patients once start therapy

A

Check TSH + FT4 every 6-8 weeks to ensure we get to steady state

  • TSH: most reliable measure to ensure doses of meds are good

FT4: less important, more of a diagnostic tool

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19
Q

What are some important clinical points about desiccated thyroid when it comes to being a treatment option for hypothyroidism?

A
  • derived from animal thyroid glands
  • unknown ratio of T4 + T3 in it that can vary based on batch
  • increase allergic reaction risk to animal protein
  • tabs may lose potency over time
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20
Q

What is the rough equivalent to use when switching a patient from desiccated thyroid to Levothyroxine?

A

75-100mcg of T4 per 60mg of desiccated thyroid

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21
Q

T or F: A patient with hypothyroidism that is pregnant with normally need an increase in their levothyroxine dose

A

T: normally need an increase in dose in first trimester due to how there is an increase in thyroid binding protein, volume of distribution, + T4 movement to fetus in pregnant women (need to increase dose)

  • Often 30-50% dose increase —- equivalent to taking 2 extra tabs of levothyroxine spread out through the week
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22
Q

What is the general treatment plan for hypothyroidism in pregnancy?

A

1) Generally increase Levothyroxine dose by 30-50% (2 extra tabs/week)

2) Reassess TSH q4wks during first half of pregnancy

3) Assess TSH at least once in 2nd half of pregnancy

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23
Q

T or F: the TSH guidelines are more strict during pregnancy

A

T- more strict and vary based on trimester

1st trimester: 0.1-2.5 mIU/L
2nd + 3rd trimester: 0.2-3.0mIU/L

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24
Q

T or F: some clinicians treat pregnant patients for hypothyroidism when they have high TSH levels (>2.5) with normal FT4

A

T - this is subclinical hypothyroidism
— some clinicians treat these patients even though their FT4 is normal with close monitoring

Factors to consider: have they had multiple miscarriages before, do they have postive Abs, or preeclampsia

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25
Q

Instead of universal screening of asymptomatic women in 1st trimester for hypothyroidism, what are some targeted factors we can use to target our screening?

A

1) Patients who live in area with moderate to severe Iodine insufficiency
2) symptoms of hypothyroidism
3) Family history of thyroid disease
4) Goiter, age >30, T1DM , recurrent miscarriages, BMI> 40, infertility, prior thyroid surgery

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26
Q

T or F: High cholesterol is associated with hypothyroidism

A

T - people with hypothyroidism may have a more difficult time clearing cholesterol from their bodies

  • not making more of it, just can’t clear it
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27
Q

T or F: IM levothyroxine is preferred to IV levothyroxine

A

F: prefer IV
- IM: greater variation in absorption

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28
Q

T or F: If a patient is taking triiodothyronine, we would expect their T4 to be low

A

T - Triiodothyronine is synthetic T3
- T4 turns into T3 but since we are giving straight T3 — would expect their to be low T4 in the blood

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29
Q

What are the approximate dosage equivalents for levothyroxine and triiodothyronine

A

60mcg of levothyroxine approximately = 25 to 37.5 mcg of triiodothyronine

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30
Q

What is the main structural difference between T3 and T4?

A

The number of iodine molecules
- T3: has once less iodine (3 iodines)
T4: 4 iodines

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31
Q

T or F: the thyroid gland produces mainly T3 and only some T4

A

F: it produces mostly T4 + just some T3

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32
Q

What enzyme converts T4 to T3

A

5’-deiodinase enzymes

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33
Q

In the thyroid gland, what is the Iodide incorporated with to make DIT/MIT?

A

Thyroglobulin - organic compound

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34
Q

T or F: higher order brain areas or stimuli can impact the hypothalamus-pituitary- thyroid gland

A

T-
cold, acute psychosis and circadian rhythm can increase hypothalamus release of TRH

stress- decrease TRH release

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35
Q

T or F: Thyroid hormone receptor is a intracellular receptor

A

T
intracellular receptor with two different subtypes (alpha and beta)

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36
Q

What doe thyroid hormone do in the body?

A

Increase metabolic rate/increase catabolism of fuels + oxygen consumption by tissues
- increase respiratory rate , HR and body temp

37
Q

T or F: there are different deiodinase enzymes in different tissues

A

Yes - D1, D2, D3 found in different tissues
- all convert T4 to T3

38
Q

What are the other ways to metabolize thyroid hormone

A

1) Further de-iodine to T2 and T1
2) Conjugate via phase II reactions
3) Decarboxylate via P1 reactions

39
Q

T or F: Thyroid hormone in the blood is mostly free and unbound

A

F- it is 99+% bound by TBG + other proteins

= only the free hormone can diffuse into target tissues

40
Q

T or F: T4 has higher binding affinity to the thyroid receptor and is responsible for most of the effects of thyroid hormone

A

F - T3 has higher binding affinity

41
Q

MoA of thyroid hormone receptor

A

intracellular nuclear receptor
- sits on thyroid response elements in the promoter/regulatory regions of target genes

  • when hormone binds: it can either attract transcription machinery to enhance or block transcription of target genes

** either way: binding ends up causing movement to hyperbolic state/increase energy consumption

42
Q

Levothyroxine causes a stable pool of ——— in the blood

A

T4: increases T4 storage in the blood bound to plasma protein

43
Q

Drug interactions with levothyroxine

A

1) Estrogen : increase TBG (plasma protein)— more protein binding to T4 causing reduction in free T4

2) Other agents that impact absorption : cholesterol lowering meds, phosphates, iron, calcium, agents the decrease HCl secretion

44
Q

T or F: Liothyronine/synthetic T3 is easier to monitor compared to levothyroxine

A

F - it is harder to monitor and there are more adverse effects
- hard to get right dose because more fluctuation in levels/ shorter half life
-

45
Q

What are the main strategies that can be used to treat hyperthyroidism?

A

1) Interfere with thyroid hormone production
2) Blockage of thyroid hormone release
3) Destruction of thyroid gland
4) Blockage of thyroid hormone effects on target tissues
5) Supportive care for symptom management

46
Q

MoA of Thioamides for hyperthyroidism

A
  • accumulates in the thyroid gland

-Inhibit thyroid peroxidase: prevents the addition of iodine to thyroglobulin in the thyroid (prevent thyroid hormone production)

  • doesn’t impact thyroid hormone storage so may take 3-4 weeks for effects to be seen
  • eventually is metabolized to glucuronide conjugate and excreted
47
Q

What are the types of thioamides used for hyperthyroidism and what are the differences between them?

A

1) Propylthiouracil (PTU)
- along with inhibiting thyroid peroxidase can also inhibit peripheral deiodination (convert T4 to T3)
- better in severe states
- preferred for 1st trimester in pregnant women

2) Methimazole
- drug of choice because has longer half life + less frequent dosing

48
Q

Toxicity of thioamides

A

some people get itchy rash, fever, arthralgia, benign transient leukopenia

Rare SEs: jaundice, agranulocytosis, liver failure (PTU only)

49
Q

Hyperthyroidism therapy: iodides MoA

A

-helps decrease thyroid hormone production via Wolff-Chaikoff effect
—— high doses of iodide result in acute inhibition of Iodine intake into the thyroid gland; therefore decreasing TH synthesis and release

**aka : high doses of iodides inhibits its own transport into the thyroid; thought to be protective mechanism

  • quick onset but effect only lasts 3 weeks (If Jeff’s lecture though - says 10 days ??)
50
Q

What other ions can be used to compete with iodide in hyperthyroidism ?

A
  • perchlorate
  • pertechnetate
  • thiocyanate

** can compete with iodide and prevent transport into thyroid gland

51
Q

MoA: Radioactive iodine (sodium-131 I) for hyperthyroidism

A
  • can be admin orally to destroy thyroid tissue
    —accumulates in thyroid and emits beta and gamma radiation
  • tetratogen and excreted in breast milk

**other iodine isotopes can be used in diagnosis + scanning **

52
Q

What happens if a person is exposed to potassium iodide by accident?

A
  • can be produced via nuclear fission
  • if exposed: normally admin normal iodide to compete with radioactive Iodide to prevent damage
53
Q

Why might you need beta blockers if you have hyperthyroidism?

A
  • high levels of TH can enhance sympathetic activation of CV system causing tachycardia, palpitations, arrhythmia
  • use beta blockers to reduce SNS activation and prevent these symptoms

** can also use non-dihydropyridine type calcium channel blockers as second line to beta blockers

54
Q

Corticosteroid use in hyperthyroidism

A

Blocks conversion of T4 to T3
- use during thyroid storm

55
Q

T or F: Immunosuppressants can be used in Graves’ disease

A

T - can be used in combo to thiamine therapy

56
Q

T or F: thyroid hormone receptor isoforms can be tissue specific

A

T
Beta: found in liver; agonist may lower cholesterol without AEs of levothyroxine
Alpha: found in heart; agonist may be used for heart failure

they are looking at potentially using isoform specific thyroid hormone analogs to target these specific tissues + have set effects

57
Q

T or F: High TSH and high FT4 is normally seen in hyperthyroidism

A

F - low TSH and high FT4

58
Q

What is the first symptom that people with hyperthyroidism “complain” about/notice

A

Atrial fibrillation

59
Q

What are the 3 treatment options for hyperthyroidism

A

1) Thioamides: methimazole (MMI)and propylthiouracil (PTU)

2) Radioactive Iodine (RAI)

3) Surgery

60
Q

T or F: Remission of hyperthyroidism symptoms is possible during use of thioamides

A

T - possible remission due to immune effects but the rate is low (20-40%)

61
Q

When would you use a PTU over MMI to treat hyperthyroidism

A

PTU is preferred option during first trimester of pregnancy and for during a thyroid storm
— because has two effects: impacts TH production and also prevents T4- T3 conversion

62
Q

What treatment options for hyperthyroidism result in permanent hypothyroidism

A

RAI - because destroying tissue with radioactive iodine

surgery

63
Q

What is the best treatment option to treat toxic nodules and toxic multinodular goiter in hyperthyroidism

A

RAI

64
Q

Methimazole: dosing

A

Initial: 10-40mg/day depending on disease severity

Maintenance : 5-15mg daily
- if higher dose: divide to BID-TID to help decrease GI upset

Max: 120mg/day

AE: rash, allergic reaction , agranulocytosis and hepatotoxicity (less risk than PTU)

65
Q

PTU dosing

A

Initial : 50-150mg TID (multiple doses a day)

Maintenance: 50mg BID or TID

Max: 1200mg/day

AEs: rash, allergic reaction, agranulocytosis, severe hepatotoxicity
—- stop if rash, fever, sore throat, or jaundice

66
Q

PTU and MMI : onset + duration of therapy

A

Onset: 3-4 weeks but may see some symptom improvement in 1 week

Euthyroid: 6-8 wks

** effects take long time due to time needed to deplete re-existing Thyroid hormone storage

Duration: by 12-18 mths about 50% achieve remission and can stop use (closely monitored though )

67
Q

Thioamides treatment: monitoring parameters

A

TSH, FT4, WBC with differential

** measure TSH + FT4 (FT3) monthly until euthyroid (6-8wks) than continue to measure q3-6 mths

FT3 is used to look at variant with T3 toxicosis

68
Q

When is RAI the preferred treatment option for people with hyperthyroidism

A

1) they have toxic multinodular goiter
2) Cardiovascular disease/problems
3) fail to respond to thioamides or have AEs from thioamides
4) they have recurrent hyperthyroidism even after surgery

69
Q

T or F: Patients with RAI can set off airport radiation for up to 12 weeks after RAI

A

True

70
Q

T or F: RAI is a good treatment option for those with active opthalmopathy (eye problems?)

A

F - contraindicated for these people

71
Q

T or F: there is a risk of hypothyroidism following RAI

A

T - risk of it followed by period of euthyroid

72
Q

T or F: for those with ischemic heart disease, heart failure, or arrhythmia thioamides are used to get people to euthyroid before RAI

A

T - used to get them euthyroid before starting RAI (stop the thioamides 1 week before RAI though after achieve euthyroid state)

73
Q

T or F: RAI can be used in pregnant or lactating women

A

F - Contraindicated

74
Q

When should surgery be considered a treatment option for people with hyperthyroidism?

A

Any of the following:
- they have a large thyroid gland (>80g) or malignancy
- esophageal obstruction/hard time swallowing
- severe eye symptoms
- lack of remission with thioamides
- CI to thioamide or RAI (ex// allergy to thioamides and pregnant)

75
Q

T or F: If surgery is needed for a pregnant lady with hyperthyroidism, it is preferred that it is done in the first trimester

A

F - preferred use in 2nd trimester if surgery is needed

76
Q

Hyperthyroidism surgery preparation steps

A

1) Use MMi until patient is euthyroid
2) Once euthyroid, use iodides for 10-14 days prior to surgery
3) Propranolol use for several weeks before surgery and for 7-10 days post-op

77
Q

What are the potential complications with surgery

A

recurrent laryngeal nerve damage, hypothyroidism (permanent) , hypoparathyroidism

78
Q

T or F: you can breastfeed when doing RAI

A

F - Ci

79
Q

Iodide/Lugol’s solution use for hyperthyroidism

A

used to provide symptom relief (short term), surgery prep, or during thyroid storm

**don’t use before RAI or chronically during pregnancy

80
Q

How is iodide helpful to treat hyperthyroidism

A

multifactorial inhibitory effect
- Wolff-Chaikoff effect: large amount of iodide prevent the organificaiton process (combining of DIT or MIT to make TH) for short term (10 days)

  • inhibits release of TH when dose is more than 6mg/day
  • Prevents iodide transport into thyroid; decrease TH production
81
Q

Positives and Negatives of Iodide use for hyperthyroidism

A

Advantages: rapid onset (2-7 days), simple, cheap

Disadvantages: only temporary relief (10 days), accentuation of thyrotoxicosis, interferes with RAI , min effective dose is 6mg/day

82
Q

What is the Wolff Chaikoff effect

A

transient suppression to TH synthesis when ingesting a large dose of iodide
- inhibits TH production via inhibiting organification in thyroid gland, TH formation in follicle cell, and TH release
- protective mechanism of the body
- escape phenomenon occurs 10 days later

83
Q

What is the Jod-Basedow Phenomenon

A
  • iodide induced hyperthyroidism 2-12 weeks after taking in iodide (opposite of WC effect)
  • take in iodide and increases TH production
  • not what you expect to happen when intake a lot of iodide (negative feedback loop not working)
84
Q

T or F: Some people can’t escape the Wolff Chaikoff Effect and are pushed to hypothyroidism

A

T - some people don’t only experience transient effects due to high dose of iodide

— take in iodide - suppression of TH production but lasts longer than 10 days ; can’t restart TH production — hypothyroidism

85
Q

Which types of Beta blockers can be used for people with hyperthyroidism and why?

A
  • BB without intrinsic sympathomimetic activity (ISA
    ——- ISA: is the effect that BB works as B agonist at rest and B antagonist when not at rest (WE DON’T WANT THIS WHEN TREATING HYPERTHYROIDISM )
  • used to alleviate nervousness, palpitations, fatigue, weight loss, tremor etc

** PROPANOLOL : can also help inhibit T4-T3 conversion**

86
Q

Which Calcium Channel Blockers are used to treat adjunctively hyperthyroidism and why?

A
  • 2nd line to beta blockers
  • use a non-dihydropyridine CCB for symptom relief (these ones don’t impact BP, just help with HR and rhythm)

Options: Diltiazem and Verapamil

87
Q

Why are corticosteroids used adjunctively to treat hyperthyroidism?

A

help manage opthalmopathy (anti-inflammatory effect), thyroid storm, pretibial myexedema, and pretreatment before RAI

** help prevent T4- T3 conversion + help replace any of the natural steroids lost during thyroid storm/prevent hypoadrenalism

88
Q

What are the 4 steps to treat a person with a thyroid storm

A

1) Block synthesis and release of TH: use PTU followed by iodides 1 hour later

2) Propanolol: help with symptoms and decrease T4 to T3

3) Steroids: decrease T4 to T3 conversion and replace steroids lost

4) Supportive treatment examples —- give oxygen, treat infection if have one etc

89
Q

T or F: hyperthyroidism symptoms may be not present in the elderly

A

T - may not be sensed due to the decrease in SNS activity already seen in the elderly

PHARM 220 (4 decks)

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