hyperthyroidism and hypothyroidism Flashcards

1
Q

Thyrotropin-releasing hormone (TRH)

A
  • Secreted by hypothalamus occurs in response to cold, stress, and decreased levels of thyroxine (T4)
  • Secretion stimulates the synthesis of thyroid-stimulating hormone (TSH) by the anterior pituitary
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2
Q

thyroid stimulating hormone (TSH)

A

Stimulates the thyroid gland to produce thyroid hormones

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3
Q

thyroid hormones

A

T4 and triiodothyronine (T3)
- Synthesized from iodine and tyrosine molecules by follicular cells in the thyroid gland

The thyroid gland synthesizes and releases about 20% of T3 with the remainder of T4 converted to T3 peripherally when additional thyroid hormone is needed
- Such as during stress and cold temperatures

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4
Q

T4 and T3 are only clinically active when they are free

A

The amount of active thyroid hormone in the plasma produces a feedback loop that inhibits or further stimulates TRH and TSH secretion to decrease or increase thyroid hormone production

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5
Q

thyroid function tests

A

The provider should consider ordering a TSH and free T4 in the primary care office to assess thyroid function
- Serum TSH results are most sensitive for diagnosing common forms of hypothyroidism and hyperthyroidism

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6
Q

goiter

A

Excess growth could be from an autoimmune process or abnormal cellular function

Size does not correlate with function!!
May be:
- Euthyroid (normal functioning)
- Collections of subfunctioning tissue
- Focal cellular growths (nodules) that might produce excess amounts of thyroid hormones

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7
Q

hyperthyroidism

A

Also called thyrotoxicosis
- Occurs when the feedback loop fails, and excessive levels of thyroid hormone are circulating

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8
Q

causes of hyperthyroidism

A

o Hyperfunctioning thyroid nodule
o Toxic diffuse goiter (Graves disease)
o Thyroiditis
o Anterior pituitary disorders
o Toxic multinodular goiter
o Excess thyroid supplementation
o Iodine-induced disease, including amiodarone therapy

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9
Q

graves disease

A

An autoimmune disorder characterized by generation of abnormal immunoglobulin G (IgG) autoantibodies to thyroid peroxidase and thyroglobulin
- These antibodies bind to the TSH receptors -> activate excessive glandular growth and hormone production
- Alters the feedback system such that the hyperfunction of the thyroid gland does not trigger suppression of TSH and TRH as it normally would

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10
Q

what does graves disease cause?

A

Causes hyperfunction of the thyroid gland with increased iodine uptake and subsequent systemic metabolism
- Causes the thyroid gland to become more vascular, enlarged, and form a goiter
- A disproportionate increase in T3 production is a result of long-term overstimulation of the gland
- Leads to decreased concentration of thyroxine-binding globulin and increased circulating levels of free hormone

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11
Q

s/s graves disease

A

 palpitations
 tremor
 anxiety
 possible weight loss
 heat intolerance
 heightened sensitivity to sympathetic nervous system stimulation

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12
Q

hyperthyroidism - medications

A

antithyroid drugs (ATDs) that inhibit the synthesis of new thyroid hormone by thyroid gland, but do not treat the underlying pathophysiology of hyperthyroidism

  1. propylthiouracil
    - also inhibits the peripheral conversion of T4 to T3
  2. methimazole
    - typically preferred d/t longer half life -> allows for once daily dosing
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13
Q

low-dose beta blockers for hyperthyroidism

A

may be prescribed as adjunct therapy to control symptomatic tachycardia from hyperthyroidism
1. propranolol
2. atenolol
- allows for once daily dosing
- better choice for patients with hx of reactive airway disease or DM b/c atenolol is cardioselective

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14
Q

preoperative preparation for hyperthyroidism

A
  1. ATDs to prevent postoperative thyroid storm
  2. Potassium iodide
    - Should be prescribed TID for 10 days before surgery
  3. Beta blocker
    - to improve preoperative control of tachycardia
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15
Q

potassium iodide for hyperthyroidism

A

might be considered before preoperative preparation for thyroid surgery
- blocks peripheral conversion of T4 to T3
- inhibits hormone release
- decreases the vascularity of the tissue

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16
Q

initial drug of choice for hyperthyroidism

A

methimazole
 Once daily dosing
 Reduced interference with RAI
 Decreased risk of hepatic side effects

17
Q

methimazole dosing severe disease or large goiter

A

20-40mg/day

18
Q

methimazole dosing mild disease or small goiter

A

10-15mg/day

19
Q

methimazole pediatric dosing

A

0.25-1mg/kg/day

20
Q

propylthiouracil dosing

A

 Initial dose: 50-100 mg TID
 Typical maintenance dose: 100-150mg/day
 If severe disease or large goiter: up to 400mg/day

21
Q

patients should consider radioactive iodine therapy if they

A

 Are unable to achieve symptom control
 Relapse after completion of treatment
 Are unable to take ATDs

22
Q

surgery for hyperthyroidism

A

recommended for goiters larger than 80 grams
 Considered the fastest intervention for treatment
 Total removal of the gland decreases the risk for relapse seen with a partial gland removal

23
Q

adverse reactions with ATDs

A

o Agranulocytosis (rare but potentially fatal complication)

o The hepatic concerns with propylthiouracil makes methimazole a safer alternative for all age groups

24
Q

monitoring for ATDs

A

Monitor changes in TSH and free T4 levels
- Monitor every 3-4 weeks until a euthyroid state is achieved
- TSH might remain decreased for several weeks even after there is an euthyroid state
- Once TSH level is WNL -> monitoring is decreased to every 3-6 months, then annually based on symptom relief

25
primary hypothyroidism disorders
* autoimmune thyroiditis * endemic iodine deficiency * ATDs used to treat hyperthyroidism
26
secondary causes of hypothyroidism
Conditions that cause either pituitary or hypothalamic failure - TSH response is inadequate so that the gland is normal or reduced in size, with both T3 and T4 synthesis equally reduced
27
primary hypothyroidism is based on the hypothalamic-pituitary-thyroid gland feedback system
Occurs when the hypothalamus response to a decreased thyroid hormone level with an increase in TRH -> resulting in increased TSH secretion -- This stimulates thyroid gland enlargement, goiter formation, and preferential synthesis of T3 and T4
28
Hashimoto thyroiditis
an immune-mediated disorder in which all components of the thyroid gland are injured, especially the TSH receptors Antibodies generated to attack glandular antigens impair: - TSH response - Hormone synthesis - Hormone release
29
subacute thyroiditis
an inflammation of the thyroid often preceded by a viral infection - Elevated levels of thyroid hormones are d/t the release of stored thyroglobulin related to the inflammatory process - NSAIDs: used to address inflammation - Beta blockers: used to reduce tachycardia Usually spontaneous remission of this disorder - Can become chronic
30
congenital hypothyroidism
occurs in infants because of absent thyroid tissue and hereditary defects in thyroid hormone synthesis An infant with no T4 during fetal life will be mentally impaired - Can be modulated with administration of T4 immediately after birth
31
secondary hypothyroidism can result from
1. Administration of drugs that reduce thyroid hormone production and treat hyperthyroidism 2. Pituitary disorders  Cushing syndrome  Acromegaly  Pituitary adenomas
32
net result of secondary hypothyroidism
inadequate TSH production that results in poor production of both T3 and T4
33
the clinical features of hypothyroidism are attributed to the metabolic effects of decreased circulating levels of thyroid hormone
Pt develops a low basal metabolic rate  Cold intolerance  Lethargy  Slightly lower body temp
34
severe hypothyrodism
can cause a medical emergency of myxedema coma s/s  hypoventilation  hypotension  hypoglycemia  lactic acidosis
35
treatment of hypothyroidism
patients should be prescribed a replacement therapy with the administration of synthetic thyroid hormones o levothyroxine (T4) o liothyronine (T3) o liotrix (4:1 or 3:1 mixture of T4 and T3)
36
levothyroxine dosing
patients with a TSH > 10mlU/L o initial dose: levothyroxine 50-75 mcg daily patients with a TSH > 20 mlU/L o weight based approach o 0.6mcg/kg daily
37
if there is a need to rapidly correct a hypothyroid state
liothyronine is preferable because of its rapid onset and dissipation of action - advantages must be weight against the wide swings in T3 levels and possible cardiotoxicity
38
monitoring for hypothyroid tx
TSH level to be evaluated at the initiation of therapy and every 4-8 weeks until the patient achieves a stable euthyroid state - Prescribed TSH levels to be repeated 6-8 weeks after any dose adjustment - Normalized and stable TSH levels often take 6-12 months to achieve Once euthyroid -> stable TSH monitoring occurs every 12 months depending on symptoms and stability