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PHAR 255 - Therapeutics (3) > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Colloid Cell role?

A

-Store building blocks (Tyrosine, Iodide, Thyroglobulin).

-Hormonal assembly & storage.

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2
Q

Follicular Cell role?

A

-Transport cells… Pump building blocks into the Colloid & aid in T3 / T4 secretion into circulation.

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3
Q

Parafollicular Cell role?

A

-Calcitonin release (blood / bone Ca2+ balance).

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4
Q

What are the three building blocks required for MIT / DIT synthesis?

A

1) Iodide
2) Thyroglobulin
3) Tyrosine

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5
Q

Physiologic ratio of T4 : T3?

A

13 : 1

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6
Q

How much more potent is T3 (versus T4)?

A

4x

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7
Q

What do T3 & T4 do to the Heart? Adipose Tissue? Muscle?

A

Heart: Increase HR & force of contraction.

Adipose Tissue: Catabolic (fat breakdown).

Muscle: Catabolic (muscle breakdown).

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8
Q

What do T3 & T4 do to Bone? Nervous System? Gut?

A

Bone: Developmental.

Nervous System: Developmental.

Gut: Metabolic.

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9
Q

What percentage of T3 in circulation is derived from peripheral T4 to T3 conversion?

A

80% (20% comes directly from the Thyroid Gland).

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10
Q

What triggers TSH release?

A

Low circulating T3 / T4 levels.

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11
Q

Chronically low serum Iodide levels cause an ______ (increase or decrease) in Thyroid Hormone production?

A

Decrease; Initially, it increases (compensatory mechanism causing upregulation of receptors & transporters at level of the Thyroid), but chronically depleted Iodide levels cause reduced T3 / T4 production.

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12
Q

An initial excess of Iodide causes an ______ (increase or decrease) in Thyroid Hormone production.

A

Decrease; Chronic elevations (beyond 7d in length) cause increased T3 / T4 production & secretion as we’re escaping the negative feedback loop.

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13
Q

What percentage of total T3 / T4 is protein bound (& therefore physiologically inactive)? What percentage is free & able to invoke physiological effects?

A

Protein Bound: 99.66%
Free: 0.33%

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14
Q

Out of every ten patients with Thyroid Disease, _____ are women.

A

eight

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15
Q

At what age do we see hypothyroidism rates at and above 25%?

A

65yrs+

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16
Q

Most common form of Hyperthyroidism?

A

Toxic Diffuse Goiter (aka Graves Disease)

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17
Q

What are the four types of Hyperthyroidism?

A

1) Toxic Diffuse Goiter

2) Toxic Multi-Nodular Goiter

3) Acute Phase of Thyroiditis

4) Toxic Adenoma

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18
Q

Other name for Toxic Multi-Nodular Goiter?

A

Plummers Disease

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19
Q

Goiter is defined as what?

A

Generalized Thyroid Enlargement.

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20
Q

Describe Graves Disease.

A

-Young females (20-50yrs).

-Autoimmune in nature… ABs against TSH Receptor.

-Most common hyperthyroidism form!

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21
Q

Why does Graves Disease induce Hyperthyroidism?

A

AB binding to TSH Receptors means that negative feedback loop can’t work… Leads to loss of TSH production!

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22
Q

Describe Plummers Disease.

A

-Old females (> 50yrs).

-2nd most common form of hyperthyroidism.

-Iodine deficiency most common trigger for nodular growth.

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23
Q

How does Iodine deficiency in Plummers Disease invoke hyperthyroidism?

A

-Less T4, Thyroid Cells enlarge & mutate, become constitutively active!

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24
Q

T or F: Toxic Multi-Nodular Goiter develops rapidly (over course of a few months).

A

False… Several years to develop (slow process).

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25
Q

How is hyperthyroidism invoked in those with Acute Thyroiditis?

A

Inflammation leads to increased permeability of Colloid Cells… Become leakier, leads to T3 / T4 seepage into circulation via Passive Diffusion mechanisms!

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26
Q

T or F: Acute Thyroiditis will eventually lead to hypothyroidism.

A

True… T3 / T4 stores eventually will become depleted with increased leakage into circulation!

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27
Q

How do benign tumors on the Thyroid invoke hyperthyroidism?

A

Tumors become active & secrete T3 / T4, but DO NOT respond to the Negative Feedback Loop (constitutively active similar to Plummers Disease).

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28
Q

Clinical presentation of hyperthyroidism?

A

-Hand Tremors
-Diarrhea
-Heat Intolerance
-Weight Loss
-Weakness
-Tachycardia
-Amenorrhea
-Sweaty
-HTN
-Insomnia

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29
Q

Unique symptoms to Graves Disease?

A

-Exophthalmos (“Bug Eyes”)
-Periorbital Edema
-Diplopia (Double Vision)
-Pre-Tibial Myxedema (Purpley / Orangeish rash on shins)

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30
Q

Jane has the following clinical values:

Serum TSH = 0.09mIU / L
Free T3 = 5.8pmol / L
Free T4 = 13pmol / L

What type of Hyperthyroidism does she potentially have?

A

Toxic Diffuse (Graves)…

-Very depleted Serum TSH
-Elevated Free T3
-Normal Free T4

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31
Q

Gladys has the following clinical values:

Serum TSH = 0.09mIU / L
Free T3 = 5.8pmol / L
Free T4 = 100pmol / L

What type of hyperthyroidism might she have?

A

Toxic Diffuse (Graves)…

-Very depleted Serum TSH
-Elevated Free T3
-Extremely elevated Free T4

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32
Q

Cassandra has the following lab values:

Serum TSH = 0.09mIU / L
Free T3 = 5.8pmol / L
Free T4 = 25pmol / L

What type of hyperthyroidism might she have?

A

Toxic Multi-Nodular (Plummers)…

-Very depleted Serum TSH
-Elevated Free T3
-Slightly elevated Free T4

**Toxic Diffuse possible though (Free T4 ranges from normal to greatly elevated)! **

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33
Q

Why is Amiodarone a clinically significant interaction as it pertains to T3 / T4 synthesis and release?

A

Can invoke both Hyper and Hypothyroidism (typically increases synthesis / release of T3 & T4).

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34
Q

What are our three options for treating hyperthyroidism?

A

1) Drugs (Thioamides & Beta Blockers)

2) Radioactive Iodine

3) Thyroidectomy

35
Q

What are the Thioamide drugs used for treating hyperthyroidism?

A

Methimazole
Propylthiouracil

36
Q

Why is pre-treatment with Thioamides necessary before Radioactive Iodine therapy?

A

RAI can initially exacerbate hyperthyroidism!

37
Q

Of the three hyperthyroid treatment options (Thioamides / RAI / Thyroidectomy), which ones are more typically curative?

A

RAI & Thyroidectomy… Thioamides are most often a temporary fix, but curative options should be considered if disease state isn’t controlled on just Thioamides.

38
Q

Why is PTU considered to be a more potent drug than MMI?

A

-PTU inhibits Thyroid Peroxidase-mediated T3 & T4 production, as well as peripheral tissue conversion of T4 to T3.

-MMI only acts within the Thyroid… No effects on peripheral tissue conversions!

39
Q

How do Beta Blockers work in hyperthyroidism?

A

-Block peripheral tissue conversion of T4 to T3 (similar to PTU).

-To be used for symptomatic relief (Palpitations, Tachycardia, Anxiety, Tremors, Heat Intolerance).

40
Q

In terms of dose titration trends, how do we see PTU & MMI dosed?

A

ID: High
MD: Low

-Trends is in reverse of usually seen dosing… Thyroid should start to shrink when one receives high initial doses (necessitating dose reduction).

41
Q

How long does it take the Thyroid & its negative feedback loop to establish new homeostatic setpoints (upon PTU / MMI dose administration)?

A

4 to 6 wks

42
Q

Common therapeutic duration of PTU / MMI use?

A

12 - 18mths

43
Q

Is it true that experienced side effects of Propylthiouracil are dose-related?

A

False… Dose-related for MMI (but NOT for PTU).

44
Q

What are the commonly experienced side effects of the Thioamide drugs?

A

-GI Upset
-Rash
-Abnormal Taste & Smell
-Joint Pain

RATES TYPICALLY HIGHER WITH PTU

45
Q

Important counseling point to stress to patients initiating Thioamides?

A

-“Push through side effects as best as you can!”

-Tolerance develops over course of 4wks, & pharmacological alternatives for hyperthyroidism are sparce!

46
Q

Transient decreases in neutrophil count are generally okay in those initiating Thioamides. However, a reduction >/= ___ - ___ % is troublesome.

A

20 - 30% (can progress into Agranulocytosis)

47
Q

Important counseling point upon Thioamide initiation (as it pertains to illness)?

A

-“If you ever feel something beyond minor illness lasting past a couple days, go get bloodwork done!”

-Want to establish that patients aren’t neutropenic, or else minor illness can progress into something potentially fatal (body is less able to fight infection off)!

48
Q

What other important counseling point should you mention to someone starting PTU specifically?

A

“Here’s what to look out for in terms of Liver issues… Tired, Darkened or intensively yellowed urine, Jaundice, Upper Right Quadrant Pains”.

49
Q

When do Liver panels become concerning to someone initiating PTU or MMI?

A

-AST / ALTs > 3x upper limit of normal!

-Assess those who are Alcoholics closely as well.

50
Q

In 1st Trimester, which Thioamide is safest? 2nd & 3rd Trimester?

A

1st: PTU
2nd / 3rd: MMI

51
Q

Which Thioamide demonstrates quicker euthyroid onset: PTU or MMI?

A

MMI (8wks versus 12wks for PTU)

52
Q

What is the preferred Beta Blocker in hyperthyroidism (due to its short DOA & ability to withdraw or titrate quickly)?

A

Propranolol

53
Q

What are the compelling indications for Radioactive Iodine usage?

A

-Mild Hyperthyroidism

-Normal / Slightly Enlarged Gland

-No Exophthalmos

54
Q

When is Radioactive Iodine outright a contraindication?

A

-Pregnancy / Lactation

-Severe Hyper / Exophthalmos

55
Q

What patient groups are the only ones we won’t pre-treat with Thioamides?

A

-Allergy
-Severe Hepatotoxicity or Agranulocytosis incident

56
Q

If one is to pre-treat with Thioamides prior to RAI administration, how should we do it?

A

1) Initiate 4-6wks prior to RAI.

2) Stop 3d prior to RAI.

3) Restart 3d after RAI.

4) Taper & d/c once thyroid levels decline.

57
Q

Important counseling point for those on RAI?

A

First five days: No exchanging eating utensils or sharing food, avoidance of close contact with pregnant women or young children.

58
Q

What are some preceding events that can trigger Thyroid Storm / Thyrotoxicosis?

A

-RAI / Thyroidectomy
-Direct Trauma
-Infection
-Birthing

59
Q

What drug measures must be initiated for someone experiencing Thyroid Storm?

A

-Beta Blockers (Sx Relief)

-High Dose Anti-Thyroid Meds (PTU preferred due to increased potency)

-Iodine 1hr post Anti-Thyroid

-Steroids (block T4 — T3 conversion)

60
Q

Most common form of hypothyroidism?

A

Hashimoto’s (aka Chronic Autoimmune Thyroiditis)

61
Q

How does Hashimoto’s work?

A

ABs bind to TSH Receptors, directly destroys Thyroid Cells.

62
Q

Two most common drug-induced causes of hypothyroidism?

A

Lithium, Amiodarone

63
Q

How does Lithium induce hypothyroidism?

A

Blocks iodine transport into the Thyroid (thus building block necessary for Thyroid synthesis can’t get in & couple).

64
Q

How does Amiodarone induce hypothyroidism?

A

Increased release of Thyroid Hormone leads to eventual depletion!

65
Q

What are the clinical presentations of hypothyroidism?

A

-Weight Gain
-Fatigue
-Cold Intolerance
-Bradycardia
-Constipation
-Heavy Menstruation

66
Q

How do lab test values differ between Subclinical & Chronic Autoimmune Thyroiditis (ie. Hashimoto’s)?

A

Sub: Slightly elevated TSH (between 4.5 - 10mIU / L), normal Free T3 & T4.

Hash: Greatly elevated TSH (> 10mIU / L), reduced Free T3, greatly reduced Free T4.

67
Q

What drugs reduce TSH levels?

A

Amiodarone, GCs, Metformin

68
Q

What drugs decrease T4 to T3 conversion?

A

Amiodarone, GCs, BBs

69
Q

What drugs increase T3 / T4 metabolism?

A

All the seizure drugs!!!

70
Q

When is Liothyronine add-on appropriate?

A

Patients inadequately controlled on Levothyroxine!

71
Q

Does Liothyronine have effects on just T3?

A

YES! NO T4 EFFECTS!

72
Q

Relative to Levothyroxine, would you expect reduced or heightened rates of adverse cardiac effects for those on Liothyronine?

A

Heightened (due to T3 effects).

73
Q

If I had a Serum TSH level between 4.5 and 10mIU / L (ie. Slightly Elevated), what would be an appropriate empirical Levothyroxine dose?

A

25 - 50mcg

This is the empirical dose for Subclinical Hypothyroidism based upon baseline TSH levels!

74
Q

What is the average replacement dose of Levothyroxine (on a / kg / day basis)?

A

1.6mcg / kg / day

75
Q

Because of its poor bioavailability, when is the best time to take Levothyroxine?

A

1st thing in AM (promotes better adherence), 30mins before breakfast (empty stomach very important).

76
Q

What is the titration plan for Levothyroxine users?

A

12.5 - 25mcg to start, increase by same interval q4-6wks!

77
Q

Side effects of Levothyroxine?

A

Basically anything seen in clinical presentation of hyperthyroidism!

-CV Risk
-BMD Reductions
-All other signs of hyper

78
Q

What drugs reduce absorption of Levothyroxine?

A

-H2 Blockers (Ranitidine)
-Antacids (Tums)
-PPIs (Omeprazole / Pantoprazole / Esomeprazole)
-Ca2+ / Multivitamins
-Bile Acid Sequestrants (Cholestyramine)

79
Q

By how many hours should we space Levothyroxine dosing to avoid DDIs with therapies that reduce absorption?

A

2-4hrs… If Raloxifene specifically, then 12hrs!

80
Q

What types of drugs increase Levothyroxine metabolism?

A

-Ciprofloxacin
-Phenytoin
-Carbamazepine
-Rifampin

Pregnancy does as well!

81
Q

Symptomatic improvements should be seen in how many weeks on Levothyroxine? Max effects?

A

Sx Relief: 2-3wks
Max Effect: 4-6wks

82
Q

Most patients with Subclinical Hypothyroidism don’t require treatment. However, when might we want to consider treatment?

A

-Develop Hypothyroidism symptoms / clinical presentations

-Planning to become pregnant

-Developed heart failure

-Extremely young patient

83
Q

A patient comes in after 6wks complaining of a lack of hypothyroidic relief. What questions should you ask?

A

-Taking at same time of day?

-Other comorbidities (ie. Celiac)?

-Taking with food? Other drugs? Dairy?

-Recently become pregnant?

PHAR 255 - Therapeutics (3) (7 decks)

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