Module 3: Thyroid and Adrenal Disorders Flashcards

1
Q

Thyroid Hormone Production

A

Pathway:

  1. Hypothalamus secretes TRH
  2. TRH stimulates anterior pituitary to secrete TSH
  3. TSH stimulates the thyroid gland to produce thyroid hormones T3 and T4
  4. Biologic effects

Thyroid hormones three main actions:

  1. Stimulate energy use
  2. Stimulate the heart
  3. Promote growth and development

T4 elevation inhibits the secretion of TSH (feedback loop)

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2
Q

Thyroid Disorder: Hypothyroidism

A

S/S (Decreased metabolism):

  1. Face is pale, puffy, and expressionless
  2. Skin is cold & dry
  3. HR and temp. lowered
  4. Goiter may be present
  5. Altered MS
  6. Lethargy/fatigue

Laboratory values:

  1. TSH elevated
  2. Total T4, free T4 lowered

Tx: Thyroid replacement therapy (i.e. synthetic T3 or T4)

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3
Q

Thyroid Disorder: Hyperthyroidism

A

S/S (Increased metabolism):

  1. Skin warm & moist
  2. Increased appetite
  3. Rapid/strong heartbeat
  4. Anxiety
  5. Skin warm & moist
  6. Exophthalmos (protrusion of the eyeballs) — wrt antibodies (Grave’s)

Laboratory values:

  1. TSH lowered
  2. Total T4, free T4 elevated

Tx: Thyroid removal, radioactive iodine (destroys tissue to stop over-production of thyroid hormones), and antithyroid meds.

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4
Q

Thyroid Hormone Preparations

A

Prototype: Levothyroxine

MOA: Synthetic form of T4 that mimics T4 functions

Therapeutic use: All forms of hypothyroidism (usually Hashimoto’s autoimmune disorder)

Dosage form:

  1. IV dose 50% lower than oral dose — used for severe, life-threatening hypothyroidism (myxedema coma)
  2. Oral — FDA allows interchangeability, but AACE does not (due to discrepancy of bioequivalence)

PK: Half-life = 7 days

DDIs:

  1. Drugs that reduce levothyroxine absorption — i.e. vitamin supplements, acid suppressors
  2. Drugs that increase levothyroxine metabolism (strong inducers) — i.e. phenytoin, carbamazepine, rifampin
  3. Warfarin simultaneously depletes vitamin K dependent clotting factors

AEs (Narrow therapeutic index dosing that is very pt-sepcific, overall well tolerated, and requires monitoring):

  1. Thyroid storm
  2. Atrial fibrillation
  3. Bone loss

RN implications:

  1. Assess pt for S/S of hypothyroidism, and thyroid storm (tachycardia, angina, tremor, nervousness, insomnia, hyperthermia, heat tolerance, sweating)
  2. Monitor pt’s T4 and TSH levels for effectiveness

Pt education:

  1. Admin. meds. on empty stomach (at least 30-60 min. before breakfast)
  2. Consult with pharmacist or provider before switching levothyroxine preparation — potential for a varied response from different products
  3. Continue for life, even if feeling better
  4. Warn pts about DDI risk, especially absorption
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5
Q

Anti-Thyroid Drugs

A

Prototype: Methimazole

MOA:

  1. Suppresses synthesis of thyroid hormone
  2. Prevents oxidation of iodine and from being incorporated into tyrosine, but does not destroy thyroid hormone stores

PK: Half-life = 6-13 hours; takes 3-12 weeks to reach euthyroid state

Therapeutic use:

  1. Hyperthyroidism (generally Grave’s)
  2. Thyrotoxic crisis (thyroid storm)

Individual variation:

  1. Pregnancy — fetus in first trimester does not produce thyroid
  2. Pt at risk for liver failure
  3. Immunosuppression — can cause agranulocytosis

AEs (Generally well tolerated):

  1. Agranulocytosis: dramatic reduction in circulating granulocytes (increased risk of infection) — Early S/S: Sore throat, fatigue, and fever (within 2 mos. of therapy)
  2. Hypothyroidism

RN implications:

  1. Admin.: follow hazardous precautions (some teratogenic effects)
  2. Monitor: S/S of hypo/hyperglycemia and agranulocytosis; TSH levels and WBC counts (at baseline and periodically)

Pt education:

  1. Take med. at the same time daily
  2. Refrain from abrupt discontinuation
  3. Maintain consistent diet and notify physician of any diet changes that increase consumption of iodine-containing foods (i.e. seafood, salt-containing products)
  4. Be aware of S/S of hypothyroidism and agranulocytosis
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6
Q

Adrenal Hormones

A

Glucocorticoids:

  1. Promote glucose availability
  2. Promote fat and protein breakdown
  3. Maintains the vascular system
  4. Promote CNS excitability
  5. Support muscle function
  6. Respiration function in neonates

Mineralocorticoids:

  1. Promote sodium and potassium balance (RAAS)
  2. Maintains the CV homeostasis
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7
Q

HPA Axis:

A

Pathway:

  1. Circadian rhythms and stress
  2. Stimulates the hypothalamus to release CRH
  3. CRH stimulates the anterior pituitary to release ACTH
  4. ACTH stimulates the adrenal cortex to release cortisol
  5. Biologic effects

Functions:

  1. Stress response
  2. Regulates glucose release and metabolism
  3. Fluid and electrolyte balance
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8
Q

Adrenal Disorder: Addison’s Disease

A

S/S (Adrenal insufficiency):

  1. Anorexia, N/V, weight loss
  2. Hypotension
  3. Electrolyte imbalances

Tx: Physiologic replacement with meds. (lifelong) — physiologic vs. stress dosing

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9
Q

Adrenal Disorder: Cushing’s Syndrome

A

S/S (Glucocorticoid excess):

  1. Hyperglycemia
  2. HTN
  3. Fat redistribution

Tx:

  1. Surgical removal followed by physiologic replacement
  2. Little to no role of drug therapy
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10
Q

Glucocorticoids

A

Prototype: Hydrocortisone (-sone, -solone)

MOA: Mimics effect of natural steroid hormone

Therapeutic use:

  1. Acute and chronic replacement therapy for adrenal insufficiency (physiologic dose)
  2. Non-endocrine disorders (lower dose) — i.e. CA, inflammation, and allergic reactions (pharmacologic doses)

Dosage forms:

  1. IV — extreme stressors, trauma (i.e. surgery)
  2. PO (lifelong)

AEs (Overall well tolerated):

  1. Adrenal suppression
  2. GI discomfort
  3. Infection
  4. Cushing’s syndrome
  5. Osteoporosis

RN implications:

  1. Monitor pt’s baseline electrolytes, weight, and HR
  2. Monitor for S/S of infection
  3. Monitor pt’s stool and signs of GI discomfort (bloody or tarry stools, abdominal pain, or blood-tinged emesis)

Pt education:

  1. Pt to follow prescribed dosing schedule
  2. Do not stop abruptly
  3. Lifelong therapy
  4. Warn pt’s that dose may increase at times of stress

Emergency preparedness:

  1. Dosage may be increased at times of stress
  2. For mild or febrile illness, follow the “3 times usual dose x 3 days” rule
  3. Advise pt to carry an emergency supply of oral and IV products at all times
  4. Wear medic alert bracelet
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11
Q

Acute Adrenal Insufficiency: Adrenal Crisis

A

S/S:

  1. Hypotension
  2. Dehydration
  3. Weakness
  4. Lethargy
  5. GI symptoms

Triggered by adrenal failure, pituitary failure, failure to receive adequate replacement during stress, and/or abrupt discontinuation of high dose glucocorticoid therapy

Tx:

  1. IV hydrocortisone as IV bolus followed by IV NS with dextrose
  2. Additional IV hydrocortisone admin. q8h
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12
Q

Mineralocorticoid

A

Prototype: Fludrocortisone

MOA: Mimics effect of natural steroid hormones

Therapeutic use: Acute and chronic replacement therapy for adrenocortical insufficiency (with glucocorticoid)

AEs (Overall well tolerated):

  1. HTN
  2. Edema
  3. HF
  4. Hypokalemia
  5. Cardiac enlargement

RN implications:

  1. Monitor pts for excessive weight gain
  2. Educate pt’s on manifestations of sodium and water retention
  3. Monitor breath sounds, BP, and serum potassium
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