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Clinical 2 (Part B) > 5 - Thyroid > Flashcards

5 - Thyroid Flashcards

1
Q

What gender is more affected?

A

women

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2
Q

Describe the negative feedback loop of the endocrine system

A
  • Hypothalamus secretes TRH
  • Stimulates pituitary gland to secrete TSH
  • Thyroid secretes T4 and T3
  • T4 and T3 send a message to the hypothalamus to stop secreting the stimulating hormones

*negative feedback loop

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3
Q

What do thyroid hormones do in children?

A

Important for normal growth and development

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4
Q

What do thyroid hormones do in adults?

A

Maintain metabolic stability

  • regulate normal growth and maturation
  • thermoregulation (T4 increases in cold environments)
  • cognitive and peripheral nervous function
  • cardiac function (high level of T4 increase cardiac output and HR)
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5
Q

Is T4 or T3 produced exclusively by the thyroid gland?

A

T4

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6
Q

Where else is T3 produced?

A

by deiodination of T4 (I think this happens in liver ???)

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7
Q

The thyroid gland manufactures and stores T3 and T4 in _________ - a protein that both synthesizes and stores the hormone

A

thyroglobulin

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8
Q

You need ____ for the synthesis of thyroid hormones and the source is from your diet (seafood, diary, iodinated salt).

A

iodine

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9
Q

How much T4 is produced per day?

A

80-100 mcg

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10
Q

How much T3 is produced per day?

A

30-40 mcg

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11
Q

____ T4 and T3 determine hormone biologic activity

A

Free

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12
Q

Most T4–>T3 happens in the periphery by _________

A

5’-deiodinase

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13
Q

What are some binding proteins that are ensuring the serum T3 and T4 remain within normal limits?

A
  • TBG (thyroxine-binding globulin)
  • TTR (transthyretin)
  • albumin
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14
Q

T4 or T3:

Longer half life and less potent?

A

T4

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15
Q

T4 or T3:

Shorter half life and more potent?

A

T3

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16
Q

List the 4 types of general thyroid disorders

A

1) Hypothyroidism
- Primary
- Central
2) Subclinical hypothyroidism
3) Hyperthyroidism
4) Subclinical hyperthyroidism

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17
Q

What are some causes of primary hypothyroidism?

A
  • Autoimmune thyroiditis (Hashimoto’s)
  • Congenital
  • Iodine deficiency
  • Intrafiltrative disease (viral or bacterial)
  • Latrogenic (thyroid surgery, radioiodine, neck irradiation)
  • Drugs (lithium, amiodarone, interferon, tyrosine kinase inhibitors)
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18
Q

What are some causes of central hypothyroidism?

A

Problem with the hypothalamus and/or pituitary

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19
Q

Briefly list a few hypothyroidism symptoms

A

Think about metabolic rate slowing down:

  • weight gain
  • bradycardia
  • fatigue and weakness (in hyper too)
  • dry skin
  • cold extremities
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20
Q

Briefly list a few hyperthyroidism symptoms

A

Think about metabolic rate speeding up:

  • weight loss
  • tachycardia
  • hyperactivity, irritability
  • fatigue and weakness (in hypo too)
  • diarrhea
  • warm skin
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21
Q

What lab results would you see for primary hypothyroidism?

A 
TSH = high
T4 = low
T3 = low (or normal)
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22
Q

What lab results would you see for subclinical hypothyroidism?

A 
TSH = high
T4 = normal
T3 = normal
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23
Q

What lab results would you see for hyperthyroidism?

A 
TSH = low
T4 = high
T3 = high
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24
Q

What lab results would you see for subclinical hyperthyroidism?

A 
TSH = low
T4 = normal
T3 = normal
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25
Q

Goals of therapy for thyroid conditions ?

A
  • Achieve euthyroid state and manage symptoms
  • Recognize which patients with loiter or thyroid nodules require treatment
  • Ensure appropriate management of thyroid conditions in pregnancy
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26
Q

What are risk factors for thyroid disease?

A
  • Personal or strong family Hx of thyroid disease
  • Diagnosis of autoimmune disease
  • Past history of neck irradiation
  • Drug therapies such as lithium and amiodarone
  • Women over age 50
  • Elderly
  • Women who are pregnant or post partum
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27
Q

What does hyperthyroidism refer to ?

A

overproduction of thyroid hormone by the thyroid gland

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28
Q

What is the most common cause of hyperthyroidism in adults?

A

Graves’ disease

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29
Q

What is Grave’s disease?

A
  • Autoimmune disease
  • Thyroid stimulating antibodies (TSAb) –> thyrotropin receptor on the surface of thyroid cell
  • Immunoglobulins activate the enzyme adenylate cyclase in the same manner as TSH
  • Results in hormone synthesis/release
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30
Q

look at slide 22

A

prob won’t but okay dude

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31
Q

Goals of therapy for hyperthyroidism?

A

1) Minimize or eliminate symptoms, improve quality of life
2) Minimize long term damage to organs (heart disease, arrhythmias, sudden cardiac death, bone demineralization, fractures)
3) Normalize fT4 and TSH concentrations

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32
Q

What are treatment options for hyperthyroidism?

A

1) Ablation with radioactive iodine or surgery
2) Thionamides
3) Non-selective Beta blocker
4) Iodine

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33
Q

What is Ablation?

A
  • Often the treatment of choice for Grave’s disease, toxic nodule, multinode goiter
  • Ablative therapy often leads to HYPOthyroidism
  • Note patients will be asked to stop their medications weeks before radioactive ablation therapy
34
Q

What will cause a higher uptake of radioactive iodine?

A

Higher TSH level

35
Q

List 2 thionamides

A

Methimazole (MMZ)

Prophylthiouracil (PTU)

36
Q

What is the MOA of Methimazole ?

A

Inhibits the synthesis of thyroid hormones by blocking the oxidation of iodine in the thyroid gland: blocks the synthesis of thyroxine and T3; does not inactivate the circulating T3 and T4

37
Q

When would you use methimazole?

A

Preferred agent for Grave’s disease

38
Q

If pregnant do you use methimazole?

A

Use PTU in the first trimester, switch to MMZ in second trimester (risk of embryopathy)

39
Q

SE of methimazole?

A

rash, arthralgias, lupus-like symptoms, fever, agranulocytosis early in therapy

40
Q

What should we monitor while on methimazole?

A

baseline CBC, and then may repeat if patient becomes febrile or develops pharyngitis

41
Q

When will you see an effect with methimazole?

A

Slow onset in reducing symptoms (weeks). Maximal effect may take 4-6 months

42
Q

MOA of prophylthiouracil

A

Inhibits the synthesis of thyroid hormones by blocking conversion of thyroxine to T3 in peripheral tissues; does not inactivate circulating T3 and T4

43
Q

When do we use PTU ?

A
  • If tolerant to MMZ, cannot have had agranulocytosis

- If pregnant use PTU in first trimester

44
Q

SE of PTU

A

rash, arthralgias, lupus-like symptoms, fever, agranulocytosis early in therapy

*HEPATOTOXICITY

45
Q

Monitoring of PTU

A

baseline CBC, and then may repeat if patient becomes febrile or develops pharyngitis

46
Q

Efficacy of PTU

A

Slow onset in reducing symptoms (weeks). Maximal effect may take 4-6 months.

47
Q

PTU may cause severe ____ injury

A

liver

*this is idiosyncratic

48
Q

What 4 things are part of monitoring thionamide (MMZ or PTU) therapy ?

A

1) TSH
- Every 4-6 weeks until stable
- Can remain suppressed for months. May use fT4 initially

2) fT4
- Every 4-6 weeks until stable
- In 4-12 weeks most are euthyroid

3) Symptom improvement
- should improve in a few days-weeks
- adjust to maintenance dose once euthyroid

4) Toxicity
- Baseline CBC
- Educate patients to report pharyngitis
- Baseline LFT
- Patients should be monitoring for signs of hepatotoxicity (pruritic rash, jaundice, light stools, dark urine, tiredness, nausea, anorexia, joint point or abdominal pain or feel ill)

49
Q

MOA of Beta blockers

A

Beta blockade to mitigate the beta-adrenergic manifestation of hyperthyroidism

50
Q

What is the role of BB in hyperthyroidism?

A

used for severe symptoms while awaiting onset of thiourias (palpitation, anxiety, tremor, heat intolerance)

51
Q

What type of BB do we choose for hyperthyroidism and why?

A

Non-selective (non ISA)
-easier to titrate and withdraw

Choose: Propranolol

52
Q

AE of BB?

A

fatigue, lethargy, peripheral coldness, dizziness, vertigo, bradycardia

53
Q

MOA of iodines and iodides ?

A

Inhibits the release of stored thyroid hormone. Minimal effect on the hormone synthesis. Helps to decrease the vascularity and the size of the gland before surgery.

54
Q

What is the iodine solution called ?

A

Lugols suolution (6.3-8mg iodide per drop)

55
Q

SE of Lugols solution (iodine)?

A

Hypersensitivity, metallic taste, soreness or burning in the mouth or tongue

*May reduce uptake of radioactive iodine therapy - do not take on the days prior to ablation

56
Q

Describe the efficacy of Lugols solution (iodine)

A
  • Effective for 7-14 days
  • Usual role is 7-10 days prior to surgery
  • Can be used after ablative therapy x 3-7 days
  • Role in stopping thyroiditis mediated release of stored hormone
  • Acute role in thyroid storm
57
Q

What is a thyroid storm?

A

-Severe and life-threatening decompensated thyrotoxicosis. Mortality rate may be as high as 20%

58
Q

What are some precipitating causes of a thyroid storm?

A

Trauma, infection, antithyroid agent withdrawal, severe thyroiditis, post ablative therapy (especially if inadequate pretreatment).

59
Q

Describe the presentation of a thyroid storm

A

Fever, tachycardia, vomiting, dehydration, coma, tachypnea, delirium

60
Q

What is the treatment for a thyroid storm?

A 
PTU or MMZ
Idide
Beta blocker
Steroid
Antipyretic (want to use tylenol over NSAIDs because NSAIDs can cause a displacement of protein bound thyroid)
61
Q

What treatment options are available for hypothyroidism?

A

1) Desiccated thyroid (T3/T4)
- Porcine source

2) Liothyronine (T3)
- Cytomel

3) Levothyroxine (T4)
- Eltroxin
- Synthroid

62
Q

MOA of levothyroxine

A

Synthetic T4 supplement

63
Q

Why is levothyroxine the drug of choice for hypothyroidism ?

A

Easier to titrate that desiccated thyroid or liothyronine - allows for body to fine tune itself by converting exogenous Lt$ to the more biologically active T3 or inert rT3 in target tissues

64
Q

List some AE from levothyroxine that usually occur from overtreatment

A
  • palpitations
  • alopecia, sweating, excessive
  • weight loss
  • diarrhea
  • insomnia
  • anxiety, nervousness
  • fatigue
65
Q

When should levothyroxine be taken?

A

Best absorption on an empty stomach - so take it 30-60 mins prior to breakfast or at bedtime (4h after meal)

66
Q

Describe Liothyronine (T3) for treating hypothyroidism.

A
  • Essentially no role in thyroid replacement
  • Short t1/2, need multiple doses
  • Rapid absorption causes high Cpeak immediately after dosing
  • Increased incidence of CV side effects
  • More difficult dose titration
  • Increased cost
  • Only plays a role in patients who insist or lack of response to T4 ?
67
Q

Describe desiccated thyroid (T3/T4) for treating hypothyroidism.

A

Natural product with varying potencies depending on batch/lot#

  • Allergic reactions
  • Rapid absorption causes high Cpeak immediately after dosing
  • More difficult dose titration
68
Q

When and what are we monitoring after initiating thyroid therapy?

A

monitor TSH q4-8 weeks until normal, then q6-12 months

69
Q

When and what are we monitoring after changing thyroid therapy?

A

monitor TSH q6-8 weeks

70
Q

In pregnancy, requirements ______

A

increase

71
Q

What is the most accurate indication of thyroid status in pregnancy?

A

TSH (total T4 recommended also)

72
Q

How often do we monitor TSH in pregnancy?

A

every 4 weeks during 1st half of pregnancy, then 1 additional time between week 26-32

73
Q

How do we adjust LT4 (levothyroxine) dose in pregnancy?

A

by 25-50 mpg to achieve TSH target

74
Q

When should therapy be considered for pregnant women?

A

if TSH is greater than the upper limits of TSH ranges for each trimester

75
Q

After delivery, what dose of levothyroxine do we give?

A

Pre-conception dose, and then test TSH again in 6-8 weeks

76
Q

Who do we treat for subclinical hypothyroidism?

A
  • Elevated THS with normal T4. Often the result of early Hashimoto’s disease
  • Treatment is controversial as risk reduction has been seen only in the elderly

Treat for TSH between 4.5-10 AND:

  • symptoms of hypothyroid
  • antithyroid peroxidase antibodies present
  • Hx CVD, HF or risk factors
77
Q

What is a Myxedema coma?

A

-Severe and life-threatening decompensated hypothyroidism

78
Q

What are some precipitating causes of Myxedema coma?

A

Trauma, infections, heart failure, medications (sedatives, narcotics, anesthesia, lithium, amiodarone)

79
Q

What is the presentation of a Myxedema coma?

A

Coma is not required and is uncommon despite terminology; altered mental state (very common); diastolic hypertension, hypothermia, hypoventilation

80
Q

What is the treatment for Myxedema coma?

A
  • Thyroid hormone replacement IV
  • Antibiotic therapy
  • Steroid

Clinical 2 (Part B) (30 decks)

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