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PR3152 Finals > Thyroid Disorders > Flashcards

Thyroid Disorders Flashcards

1
Q

What are the tests of autoimmunity? (3)

Which 2 are commonly found in Hashimoto’s disease?

Which are specific and confirmatory for Graves’ disease?

A
  1. ATgA: thyroglobulin Ab
  2. TPO: thyroperoxidase Ab
  3. TRAb: thyrotropin receptor lgG Ab ($$$)

ATgA and TPO found in 95% of Hashimoto’s disease

TRAb is specific and confirmatory for Graves’ disease

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2
Q

Compelling indications for screening of thyroid disorders? (8)

A
  • Presence of autoimmune disease (eg T1DM, cystic fibrosis)
  • First-degree relative with autoimmune thyroid disease
  • Psychiatric disorders
  • Taking amiodarone/ lithium
  • Pts who come in for AFib
  • Hx of head/ neck radiation for malignancies
  • S/sx of hypothyroidism/ hyperthyroidism
  • Pediatric pts and pregnant women
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3
Q

How is T3 and T4 levels affected by estrogen and pregnancy?

In a normal state, how does the body compensate for this change?

A

Estrogen and pregnancy causes elevated Thyroxine Binding Globulin (TBG) levels

In normal individuals: FT3 and FT4 levels will ↓ as more T3 and T4 will bind to extra TBG → TSH released to instruct thyroid gland to release more THs → FT3 and FT4 levels return back to normal

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4
Q

3 primary causes of hypothyroidism?

A
  1. Iodine deficiency (MOST common)
  2. Hashimoto disease (autoimmune)
  3. Iatrogenic (thyroid resection/ radioiodine ablative Tx for hyperthyroidism)
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5
Q

2 secondary causes of hypothyroidism?

A
  • Central hypothyroidism (hypothalamus/ pituitary gland unable to secrete TRH/ TSH respectively)
  • Drug-induced (amiodarone, lithium)
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6
Q

Effects of hypothyroidism on pregnancy?

A
  • Miscarriage, spontaneous abortion
  • Congenital defects, impaired cognitive development
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7
Q

Clinical manifestations of hypothyroidism?** (5)

A
  • ↑ total cholesterol, LDL, TGs
  • ↑ atherosclerosis, MI risk
  • ↑ creatinine phosphokinase (CPK) levels
  • ↑ miscarriage risk
  • Impaired fetal cognitive development
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8
Q

How do we diagnose hypothyroidism?

A

S/sx OR screening

PLUS

Primary hypothyroidism
- ↑ TSH, ↓ T4
- Positive ATgA and TPO Ab

OR

Central hypothyroidism
- ↓ TSH, ↓ T4

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9
Q

Goals of Tx? (4)

A
  1. Minimise or eliminate s/sx
  2. Minimise long-term damage to organs (myxedema coma, heart disease)
  3. Prevent neurologic deficits in newborns and children
  4. Normalise free T4 and TSH concentrations
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10
Q

What is subclinical hypothyroidism?

A

Elevated TSH with normal T4, often the result of early Hashimoto disease

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11
Q

When should we treat subclinical hypothyroidism?

A
  • TSH > 10 mIU/L OR
  • TSH 4.5-10 mIU/L AND
    s/sx of hypothyroidism or
    TPOAb present or
    Hx of CVD, HF, or risk factors
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12
Q

What are the risks when TSH > 7.0 mIU/L and when TSH > 10 mIU/L?

A
  • TSH > 7.0 mIU/L in older adults: ↑ risk of HF
  • TSH > 10 mIU/L: ↑ risk of coronary HD
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13
Q

State the pharmacotherapy for hypothyroidism

A
  1. Levothyroxine (synthetic T4)
  2. Liothyronine (synthetic T3)
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14
Q

Dosing for levothyroxine hypothyroidism?

How about for pregnancy women?

A
  • Young, healthy adults: 1.6 mcg/kg/d
  • 50-60 y/o and no cardiac issues: 50 mcg daily
  • With CVD: 12.5 - 25 mcg/d, titrate up slowly

Pregnancy: May need 30-50% ↑ in dosage to maintain euthyroid status

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15
Q

How should we titrate levothyroxine?

A
  • Depends on response → control of s/sx, normalisation of TSH and T4
  • Can ↑ or ↓ in 12.5 - 25 mcg/d increments, or in 15-20% of weekly dose
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16
Q

Dosing for levothyroxine for subclinical hypothyroidism?

A

Initial daily doses of 25-75 mcg recommended

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17
Q

Counselling for levothyroxine? (4)

A
  • Do not take with food; take 30-60 mins BEFORE breakfast or 4 hours AFTER dinner (empty stomach)
  • Calcium, iron supplements, antacids → space AT LEAST 2h apart
  • Takes 4-8w to observe effects (labs)
  • Takes 2-3w to observe symptomatic relief
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18
Q

ADEs of levothyroxine? (3)

A
  • Cardiac abnormalities (tachyarrhythmias, angina, MI)
  • Risk of fractures
  • Hyperthyroidism s/sx
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19
Q

Clinical use of liothyronine? (synthetic T3)

A
  • Combination with T4 can be considered if normalised TSH but still complains of hypothyroidism s/sx
  • Give IV in myxedema coma since more potent (also can give IV levothyroxine)
20
Q

ADEs of liothyronine? Is this preferred over levothyroxine?

A

ADEs similar to levothyroxin but high incidence (hence generally not recommended)

21
Q

Dosing for liothyronine?

A
  • Starting: 25 mcg
  • Elderly/ CVD: 5 mcg
22
Q

Monitoring for Tx for hypothyroidism? (When to monitor and TSH target?)

A

Monitor 4-8w to assess response after initiating or changing Tx

General target: TSH 0.4-4 mIU/L

23
Q

What lab results could signify non-adherence to hypothyroidism Tx?

A

Normalisation of FT4 with consistently ↑ TSH

24
Q

After euthyroid state achieved with the help of the medicines, how often are thyroid function tests (TFT) still recommended?

A

Every 6m → 1y (non-pregnant pts)

25
Q

Target TSH levels of pregnancy in the first, second and third trimester each?

A
  • 1st trimester: < 2.5 mIU/L
  • 2nd trimester < 3.0 mIU/L
  • 3rd trimester < 3.5 mIU/L
26
Q

Causes of hyperthyroidism?

A
  • Toxic diffuse goiter (Graves’ disease): TRAb mimics TSH binding → stimulates TH production
  • Adenomas: pituitary adenomas, toxic adenoma, toxic multi-nodular goiter
  • Drug-induced → amiodarone, lithium
  • Subacute thyroiditis (release of stored hormones)→ infections, drug-induced, early Hashimoto’s disease
  • Surgical resection (often)
  • Thyroidectomy (definitely)
27
Q

What are the s/sx of hyperthyroidism specifically for pregnant women?

A
  • Failure to gain weight despite good appetite
  • Tachycardia
28
Q

How is hyperthyroidism diagnosed?

A

S/sx

PLUS

  • Elevated free T4 serum conc - - Suppressed TSH conc (except in TSH-secreting adenomas)
  • Radioactive iodine uptake (RAIU) for better etiology: (1) Uptake elevated if gland actively secreting TH → Graves’ disease, TSH-secreting adenoma, toxic adenoma, multinodular goiter, (2) Uptake suppressed if thyroiditis or cancer
  • Positive TRAb, ATgA and TPO Ab
  • Biopsy
29
Q

Goals of Tx for hyperthyroidism?

A
  1. Minimise or eliminate s/sx
  2. Minimise long-term damage to organs (HD, arrhythmias, sudden cardiac death, bone demineralisation, fractures)
  3. Normalise free T4 and TSH conc
30
Q

Pharmacotherapeutic agents used for hyperthyroidism? (4)

Which is the first line? Can pregnant pts undergo this Tx?

A

First line: Radioactive iodine ablation (RAI) Tx. AVOID in pregnant women

Thionamides, iodides, non-selective β-blocker

31
Q

In which type of pts do we initiate Tx for hyperthyroidism? (5)

A
  • For those awaiting ablative Tx/ surgical resection
  • ↓ risk of post-ablation hyperthyroidism caused by thyroiditis
  • For those not ablative or surgical candidates & failed to normalise thyroid
  • Mild disease, small goiter, low or -ve Ab titers, women
  • Limited life expectancy
32
Q

What is subclinical hyperthyroidism?

What are its risks? (2)

A

Low/ undetectable TSH with normal T4

  • Elevated risk of AF in pts > 60 y/o
  • Elevated risk of bone fractures in postmenopausal women
33
Q

How can hyperthyroidism affect pregnancy?

A

If untreated, may result in fetal loss

34
Q

How should we treat subclinical hyperthyroidism?

Can we suggest ablative Tx?

A
  • Initial daily doses of PO therapy 25-75 mcg recommended (do not do ablative Tx for young patients)
  • β-blocker esp if AF
35
Q

Name 2 types of thionamides

MOA of thionamides?
What additional effects does PTU have?

A
  • Inhibits iodination and synthesis of TH by acting as substrate for TPO
  • Additional: PTU can block T4/ T3 conversion in periphery @ high doses

Carbimazole also used to control the disease before surgery

36
Q

Dosing for carbimazole (preferred) in hyperthyroidism?

A

Initial 15-60mg daily in 2-3 divided doses

37
Q

Dosing for PTU in hyperthyroidism?

A

Initial 50 - 150mg PO tds → once euthyroid, can ↓ to 50 mg bd/ tds

38
Q

ADEs of thionamides for hyperthyroidism? (4)

A
  • Hepatotoxicity
  • Rash → risk for SJS
  • Agranulocytosis early in Tx (~3m) (rare)
  • Fever
  • Joint pain (carbimazole)
  • Embryopathy
  • Hypothyroidism (monitor thyroid size and TSH levels, once thyroid size reduced and normal TSH levels achieved, titrate and decrease carbimazole’s dose)
39
Q

Onset of thionamides for hyperthyroidism?

A

Slow onset in reducing s/sx, maximal effect may take 4-6m

40
Q

How should we prescribe thionamides for hyperthyroidism in pregnant pts?

A

1st trimester: use PTU (Carbimazole has higher risk of congenital malformations)

2nd and 3rd trimesters: use Carbimazole as has PTU has higher risk of hepatotoxicity

41
Q

What type of iodide is used for hyperthyroidism?

A

Lugol’s solution

42
Q

MOA of Lugol’s solution for hyperthyroidism? (3)

A
  • Inhibits release of stored THs
  • Minimal effect on hormone synthesis
  • Helps decrease vascularity and gland size
43
Q

When should iodides be used for hyperthyroidism?

After how many days of therapy does it have limited efficacy?

A
  • Before surgery (7-10d) to shrink gland
  • After ablative tx (3-7d) to inhibit thyroiditis-mediated release of stored TH (do NOT use before!)

Limited efficacy after 7-14d of tx as TH release resumes

44
Q

Name the type of non-selective β-blocker used for hyperthyroidism

A

Propranolol

45
Q

What is the place in therapy for β-blockers used for hyperthyroidism?

A
  • For symptomatic relief
  • Bridging Tx for thionamide effects to kick in/ before ablation/ surgery
  • PRN for high risk pts (elderly, CV disease)
  • Tx of thyroiditis

Give for subclinical hyperthyroidism, esp if AF

PR3152 Finals (8 decks)

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