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Therapeutics Y2 Sem 2 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What is the difference between T3 and T4

A

It is the # iodine groups Tri vs Tetra

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2
Q

What is the colloid cells funcitons?

A

Storage or the thyroid, Iodine, Tyrosine, Thyrogobulin (These are stored in the thyroid)

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3
Q

What are follicular cells?

A

Responsible for pumping T3/T4 into circulation

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4
Q

What are parafollicular cells?

A

Calcitonin release, which is responsible for blood serum.

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5
Q

How is T3/T4 made

A

Combination of mono or di-iodotyrosine (MIT +DIT= T3), DIT + DIT= T4

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6
Q

What is the physiological ration of T4:T3?

A

13:1 ish, population average that is

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7
Q

Why would the thyroid produce two different thyroid hormones?

A

Enables more mechanisms for homeostasis. Because T3 is more potent then T4,

Helps with homeostasis generally.

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8
Q

What is the synthesis and secretion of T3 and T4 controlled by

A

TSH which is controlled by thyrotropin-releasing hormone

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9
Q

Where T4 converted to T3?

A

Kidney and liver generally

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10
Q

What is the actions of T3/T4 in the Heart

A

Chronotropic and inotropic

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11
Q

What is the actions of T3/T4 in the Adipose tissue

A

Catabolic

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12
Q

What is the actions of T3/T4 in the muscle

A

Catabolic

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13
Q

What is the actions of T3/T4 in the Bone?

A

Developmental

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14
Q

What is the actions of T3/T4 in the Nervous system

A

Developmental

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15
Q

What is the actions of T3/T4 in the GUt

A

Metabolic

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16
Q

What is the actions of T3/T4 in the Other tissues

A

Calorigenic

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17
Q

What hormone is involved in the production of T3/T4 and is the main drug target?

A

Thyroid peroxidase

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18
Q

All T4 in circulation is produced in?

A

Thyroid

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19
Q

How much T3 is produced in thyroid?

A

Only about 20% as the remainder is converted from T4

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20
Q

How much more potent is T3 then T4?

A

approx 4x

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21
Q

How much of T4 is converted in the inactive rT3?

A

45%

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22
Q

What use to be an issue with old T3/T4 tests?

A

They use to test for all levels (Protein bound and unbound), where protein bound is inactive

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23
Q

How is thyroid hormone production regulated?

A

Negative feedback loop

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24
Q

How is TSH stimualted?

A

Low circulating T3/T4 levels and low serum iodide levels

Low serum iodide leads to a state of hypothyroidism

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25
Q

What is hormone release inhibited by?

A

High circulating T3/T4 levels
Lithium (Because its a molecule that mimics Iodide)
Iodide

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26
Q

What happens if you flood the thyroid with iodine?

A

Inhibits a process in the thyroid where it decreases T3/T4 production. It will escape that inhibition

It will lead to a temporary inhibition

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27
Q

What percentage of individuals is estimated to live with Hypo/hyperthroidism>?

A

10%, 50% indiagnosed

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28
Q

Hypothyroidism usually affects ___ more

A

women 8 out of 10

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29
Q

What is common during pregnancy with thyroid

A

Hypothyroidism

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30
Q

What are the 4 common causes of hyperthyroidism?

A

I. Toxic diffuse goiter (Graves disease)
II. Toxic multi-nodular goiter (Plummers disease)
III. Acute phase of thyroiditis
IV. Toxic adenoma

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31
Q

What is a goiter?

A

Just an enlargement

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32
Q

What is Toxic diffuse goiter

A

Graves disease

Generally an autoimmune disorder that leads to antibody development of the TSH receptor and secrete t3/t4 unchecked

Because we have antibody binding here too our thyroid negative feedback loop will cause our TSH levels to drop.

This will not do anything because of the antibodies

Leads to enlargement of the cells

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33
Q

What is Toxic multi-nodular goiter

A

Plummer disease, where the TSH receptors mutate and escapes the negative feedback loop

Iodine deficiency is the most common trigger

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34
Q

What is the general flow chart of Hyperthyroidism as it relates to plummer disease

A

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

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35
Q

What is Acute phase of thyroiditis

A

Generally trauma, or pregnancy during delivery, only the acute phase would lead to hyperthyroidism

Cells beocme highly permeable and T3/T3 leaks out of colloid.Passive diffusion during this acute phase. and eventually T3/T4 stores depelte and leads to hypothyroidism

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36
Q

Which hyperthyroidism disease can cause hypothyroidism? How?

A

Acute phase of thyroiditis, depletes stores of T3/T4

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37
Q

What is Toxic adenoma?

A

Benign tumours growing on thyroid gland and the tumors secretion of T3/T4 but not responding negative feedback loop

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38
Q

What are some side effects related to hyperthyroidism? (The main ones 7)

A
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39
Q

What is an issue with hyperthyroidism diagnosis?

A

It is difficult to detect if it is not screened for

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40
Q

If someone have toxic diffuse goiter>

A
  • Exophthalmos (or proptosis)
  • Peri-orbital edema- Eye buldging
  • Diplopia
  • Diffuse Goiter
  • Pre-tibial myxedema
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41
Q

What is the toxic nodular goiter specific symptoms?

A
  • Same general hyperthyroidism symptoms
  • Individual thyroid nodules may be palpable
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42
Q

What are the general lab values thyroid issues (Sub-clinical hyperthyroidism)

A

TSH decreased <0.3
Free T3 Normal
Free T4 Normal

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43
Q

What are the general lab values thyroid issues (Toxic Diffuse)

A

TSH decreased alot <0.1
Free T3 Increased
Free T4 Normal to extremely increased

44
Q

What are the general lab values thyroid issues (Toxic multi-nodular)

A

TSH decreased <0.1
Free T3 Increased
Free T4 Increased

45
Q

What is the issue with toxic diffuse and toxic multi-nodular

A

They are incredibly hard to differentiate between

46
Q

Which drug can have a high effect on the thyroid levels?

A

Amiodarone

47
Q

When someone starts amiodarone what is typically more common (Hypo or Hyper

A

Hyper>hypo

48
Q

What are the main treatment drug classes for hyperthyroidism/

A

Thioamides
Beta blockers

49
Q

What are the two anti-thyroid drugs?

A

Methimazole and Propylthiouracil

50
Q

What are the indicatiosn for the thioamides?

A

Toxic diffuse goiter
Toxic multi nodular goiter
Pre-treatment before RAI

51
Q

What ist he goal of therapy when using a thioamide?

A

Achieve remission, but know that 30% remain in remission after 1-2 years of therapy (Relpase common)

52
Q

What is the MOA the thioamides?

A

Interferes with thyroid peroxidase mediated processes in the production of T3/T4

53
Q

What does propulthiouracil inhibit that methimazole doesnt”

A

Conversion of T4 to T3

54
Q

What is the dosing and administration of thioamides?

A

We are going to START HIGH!!! (Very different form oridinary meds) and then we are going to lower maintenance doses

55
Q

When do we decrease dose of thioamides?

A

Once euthryoid is achieved

56
Q

When do we titrate the dose of thioamides?

A

If the TSH and T4 does not imporve in 4-6 weeks

57
Q

What are the special dosing/administration instructions of thioamides?

A

None really can take with or without food

58
Q

What is the onset of effect of thioamides?

A

Symptom improvement within 1-4 weeks

Euthyroid in 2-3 months

59
Q

What is Euthyroid?

A

normal thyroid function that occurs with normal serum levels of TSH and T4.

60
Q

What is the duration of therapy for thioamides and hyperthyroidism?

A

12-18 months common, but may taper to D/C and see if relapse eoccurs

61
Q

What are the common side effects of thioamides?

A

Gi-upset, rash. arthralgia, abnormal taste/smell

62
Q

What thioamide is dose dependant with side effects?

A

MMI (Methimazole) not PTU (Propylthiouracil)

63
Q

What are some serious side effects of thioamides?

A

Neutropenia
Hepatotoxicity
Vasculitis

64
Q

What are some key things patients should watch out for while on this thioamides?

A

Watch for flu like symptoms and for liver related issues

65
Q

What are the main drug interactiosn of thioamides?

A

Warfarin (Decrease in INR), Digoxin (Increase DIG)

66
Q

What are the monitor parameters usually for thioamide discontinuation?

A

TSH at 3,6,12, annualy

Within the first 3 months we may see suppressed TSH and normal T4/T3 hence relapse likely

67
Q

What should be monitored at baseline and 1 week later with thioamide treatment?

A

CBCs and LFTS

68
Q

With respect to pregnancy and thioamides which trimester is usually safest to take one of the drugs?

A

PTU 1st trimester more safe

MMI 2nd and 3rd trimester more safe

69
Q

What are some other medications that could be used to help in hyperthyroidism?

A

Beta blockers to reduce the symptoms of hyperthyroidism

Where we would choose propranolol because of short acting nature, we would then recommended atenolol because it is more cardio selective in naturer

70
Q

What is a more definitive treatment compared to thioamides?

A

Radioactive Iodine 131 treatement

71
Q

When should Iodine 131 treatment be used?

A

Only given mild hyper, downsides it causes permanent hypo, can trigger thyroid storm, worsen exopthalmous

72
Q

What is Exopthalmous?

A

a bulging or protruding eyeball or eyeballs

73
Q

When is radioactive iodine131 CI?

A

Pregnancy/lactation, severe hyperthyroidism/exopthalmous

74
Q

What are the ae of iodine131 treatment?

A

Initial hyperthyroidism, followed by hypothyroidism

75
Q

While being treated with radioactive iodine what are some special instructions?

A
76
Q

When is thryoidectomy and option?

A
77
Q

What is considered subclinical hyperthyroidusm?

A

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

78
Q

What are the management strategies overall for thyroiditis?

A

Self-limiting
B blockers for symptom
NSAIDS
Course of steroids in some cases

79
Q

What is thyroid storm?

A
80
Q

What is Hashimoto’s disease?

A

Destruction of the thyroid essentially

Antibodies in some circumstances can interfere with T3/T4 production

81
Q

What drugs can induce hypothyroidism?

A

Lithium, amiodarone

82
Q

What are the clinical presentations of hypothryoidism?

A
83
Q

What is the general lab testing results of hypo

A
84
Q

What medications cause decreases in TSH?

A
85
Q

What medications decrease T4 –> T3 conversion

A

Amiodarone, beta-blockers, glucocorticoids

86
Q

What decreases synthesis/release of T3/T4?

A

Amiodarone, lithium, iodine

87
Q

What increases T4/T3 metabolismn

A
88
Q

What are our options for thyroid replacement hormone?

A

Desiccated thyroid
Liothyronine
Levothyroxine
Combined T3/T4

89
Q

What is desiccated thryoid?

A

COntains T3 and T4, but cuases high peaks of T3

90
Q

What is a caveate of desiccated thyroid?

A

Not well standardized batch to batch

91
Q

What is ratio of T4 to T3 in desiccated thyroid?

A

4:1, but in our body it should be around 13:1

92
Q

What is Liothyronine?

A

Contains T3 and has no effect on T4, Low half life, costly, cardiac events.

93
Q

What is levothyroxine?

A

Analogie of T4 and standard 1st line therapy for individuals, this allows our body to convert to T3 which is regulated by the body

94
Q

What is the half life of levothyroxine?

A

7 days

95
Q

What is the dosing/administration we should remember of levothryoxine

A

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

96
Q

What is the average replacement dose of levothyroxine needed?

A

1.6mcg/kg/d

97
Q

What should the starting dose range of levothyroxine?

A

12.5mcg/day to wax wt. based

98
Q

How is levothyroxine usually given at the start?

A

12.5-25mcg and titrate up by 12.5-25mcg every 4-6 weeks

99
Q

What are the potential side effects of levothyroxine?

A

Hyperthyroidism symptoms
Cardiac risk increase
aggravate existing CVD
BMD reduction

100
Q

What side effects should people on levothyroxine feel?

A

None if properly dosed

101
Q

What should be monitored while on levothyroxine?

A

TSH aim for low normal value, may take 4-6 weeks to stabilize with each dose change

Free T4 (Normal or slightly elevated)

Free T3 (Normal)

102
Q

How often should TSH be monitored?

A

Once stable and symptom free monitor every 6-24 months

103
Q

What is subclinical hypothyroidism?

A

TSH of 4.5-10 mIU/L normal T3/T4

Where treatment is controversial

104
Q

What if treatment of levothyroxine fails?

A

Adherence
Increased need due to pregnancy, weight gain, or new medications

(Very rare)
Addison’s disease, altered pituitary, insufficient peripheral conversion of T4 to T3

105
Q
A

Therapeutics Y2 Sem 2 (17 decks)

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