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NR566 Chapter 41 complete study guide

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 Clinical signs & symptoms, risk factors, associated symptoms, and diagnosis o HYPERTHYROIDISM (Thyrotoxicosis)  Grave’s disease- common etiology of hyperthyroidism  Autoimmune disease characterized by generation of abnormal IgG autoantibodies to thyroid peroxidase and thyroglobin -> binds to the TSH receptors -> activating excessive glandular growth and hormone production.  S/Sx:  heat intolerance  heightened sensitivity to SNS stimulation  nervousness  irritability  palpitations  tremors  increased heart rate  low TSH and TRH, increased iodine reuptake  goiter- enlargement of thyroid gland  disproportionate increased T3 production- HALLMARK of long-term overstimulation of the gland.  Risk Factors:  DM  Pernicious anemia  Primary adrenal insufficiency  Vitiligo  Leukotrichia (prematurely gray hair)  Vitiligo  Drug compounds that contain iodine or affect iodine metabolism  Viruses and pregnancy (can trigger thyroiditis)  Diagnosis:  Low TSH, High T3 and T4 = primary hyperthyroidism  Low TSH, normal T3 and T4 = subclinical hyperthyroidism o HYPOTHYROIDISM  Primary:  defective hormone synthesis resulting from autoimmune thyroiditis, endemic iron deficiency, or antithyroid drugs that were used to treat hyperthyroidism  congenital defects or loss of tissue after treatment for hyperthyroidism  decreased thyroid hormone level -> hypothalamus -> increased TRH -> increased TSH -> stimulates thyroid gland enlargement  Hashimoto’s thyroiditis- immune related disorder in which all components of thyroid gland are injured, but especially the TSH receptors.  Subacute thyroiditis- an inflammation of the thyroid often preceded by a viral infection.  Congenital hypothyroidism- occurs in infants as a result of absent thyroid tissue and hereditary defects in thyroid hormone synthesis  Secondary (less common):  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.  S/Sx:  Low basal metabolic rate  Cold intolerance  Lethargy  Slightly lowered body temperature  Myxedema (occurs in long-standing untreated hypothyroidism, sign of severe hypothyroidism)  Pitting, boggy edema  Around the eyes  Hands  Shins  Supraclavicular fossae  Thickening of the tongue  Thickening of the laryngeal-pharyngeal membranes (thick, slurred speech, hoarseness)  Risk Factors:  Primarily occurs in women older than 50yo  Family hx of thyroid disease or autoimmune disease  Type 1 DM  Rheumatoid arthritis  Currently taking anti-thyroid medications  Treated with radioactive iodine for thyroid cancer  Thyroid surgery  Radiation exposure to neck or upper chest area  Diagnosis:  High TSH, low T3 and T4  Time anticipated for total reversal of hyperthyroid symptoms with methimazole o Treatment is for 6-18 months, with most patients being treated for 1yr.  Monitor TSH and free T4 every 3-4wks o Methimazole vs. propylthiouracil (PTU)  Methimazole works faster than PTU  PTU is associated with hepatotoxicity- not indicated for children  Methimazole has once daily dosing- adherence is significantly better  Methimazole crosses the placenta; PTU less likely (80%-90% protein bound and ionized by physiological pH)- preferred tx for pregnancy with hyperthyroidism  Other drugs used to provide symptomatic relief o Beta-blockers  address the symptoms of hyperthyroidism by decreasing the response to sympathetic stimulation  adjunct therapy to control uncomfortable or unhealthy tachycardia  Routine testing with drug therapy o HYPERTHYROIDISM:  Monitoring therapy includes attention to clinical status and thyroid function test results.  Clinical Status: weight, degree of heat tolerance, appetite, anxiety level, energy level, resting HR, skin texture, temperature  Monitor TSH and free T4 every 3-4wks after initiating antithyroid agent (e.g. methimazole) o HYPOTHYROIDISM:  Monitoring thyroid replacement therapy has 3 parameters: clinical symptoms, TSH, and free T4  Clinical symptoms- alone, are generally not an effective monitoring  TSH evaluaton every 6-8 wks (normalized and stable TSH levels often take 6-12months to achieve)  Free T4- measurement can help determine how excessive the dose is. More reliable once the patient is stable (after 12mos)

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Chapter 41: HYPERTHYROIDISM and HYPOTHYROIDISM




 Clinical signs & symptoms, risk factors, associated symptoms, and diagnosis
o HYPERTHYROIDISM (Thyrotoxicosis)
 Grave’s disease- common etiology of hyperthyroidism
 Autoimmune disease characterized by generation of abnormal IgG
autoantibodies to thyroid peroxidase and thyroglobin -> binds to the
TSH receptors -> activating excessive glandular growth and hormone
production.
 S/Sx:
 heat intolerance
 heightened sensitivity to SNS stimulation
 nervousness
 irritability
 palpitations
 tremors
 increased heart rate
 low TSH and TRH, increased iodine reuptake
 goiter- enlargement of thyroid gland
 disproportionate increased T3 production- HALLMARK of long-term
overstimulation of the gland.
 Risk Factors:
 DM
 Pernicious anemia
 Primary adrenal insufficiency
 Vitiligo
 Leukotrichia (prematurely gray hair)
 Vitiligo
 Drug compounds that contain iodine or affect iodine metabolism
 Viruses and pregnancy (can trigger thyroiditis)
 Diagnosis:
 Low TSH, High T3 and T4 = primary hyperthyroidism
 Low TSH, normal T3 and T4 = subclinical hyperthyroidism

, o HYPOTHYROIDISM
 Primary:
 defective hormone synthesis resulting from autoimmune thyroiditis,
endemic iron deficiency, or antithyroid drugs that were used to treat
hyperthyroidism
 congenital defects or loss of tissue after treatment for hyperthyroidism
 decreased thyroid hormone level -> hypothalamus -> increased TRH ->
increased TSH -> stimulates thyroid gland enlargement
 Hashimoto’s thyroiditis- immune related disorder in which all
components of thyroid gland are injured, but especially the TSH
receptors.
 Subacute thyroiditis- an inflammation of the thyroid often preceded by
a viral infection.
 Congenital hypothyroidism- occurs in infants as a result of absent
thyroid tissue and hereditary defects in thyroid hormone synthesis

 Secondary (less common):
 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.

 S/Sx:
 Low basal metabolic rate
 Cold intolerance
 Lethargy
 Slightly lowered body temperature
 Myxedema (occurs in long-standing untreated hypothyroidism, sign of
severe hypothyroidism)
 Pitting, boggy edema
 Around the eyes
 Hands
 Shins
 Supraclavicular fossae
 Thickening of the tongue
 Thickening of the laryngeal-pharyngeal membranes (thick,
slurred speech, hoarseness)
 Risk Factors:
 Primarily occurs in women older than 50yo
 Family hx of thyroid disease or autoimmune disease
 Type 1 DM
 Rheumatoid arthritis
 Currently taking anti-thyroid medications
 Treated with radioactive iodine for thyroid cancer
 Thyroid surgery
 Radiation exposure to neck or upper chest area

 Diagnosis:
 High TSH, low T3 and T4

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