THYROID NOTES

Outline:

TERMS: Euthyroid, Goiter, Thyrotoxicosis, Exophthalmos, Myxedema, Graves' Disease, Hashimoto's disease, Thyroid Storm, Cretinism

1. HYPERTHYROIDISM: (Review Patho, Thyroid Storm, Etiologies, Labs)

A. GOALS OF THERAPY

(1) Blocking the effects of excessive hormone stimulation

(2) Establishing normal thyroid function (euthyroid)

(3) Treating troublesome symptoms of the patient

B. HEAD TO TOE ASSESSMENT:

(1) General Survey

(2) Integumentary

(3) Head and Neck

(4) Neurologic

(5) Pulmonary, C-V

(6) G.I.

(7) Extremities

(8) Pt. Complaints

2. Results of Diagnostic Testing?

3. Nursing Diagnoses

4. Management & Nursing Care:

(1) Drug Therapy:

a. Antithyroid drugs: (p. 1839)--Thionamides(PTU, Tapazole) block thyroid hormone synthesis; Iodine decreases synthesis and release; beta blockers such as Inderal relieve symptoms of sympathetic stimulation such as tachycardia, palpitations, diaphoresis, and anxiety

(2) Radioactive Iodine(RAI):

a. Usually one treatment, followed by suppression of hormone output several weeks later

b. Complications: hypothyroidism--may have to take hormone replacement therapy

(3) Surgery:

a. Done when drug therapy or RAI fail or cannot be tolerated or when excessive tissue(goiter) is unsightly or is compressing vital structures

b. Types: Subtotal and Total Thyroidectomy

c. Pre-op care: clients should be euthyroid before surgery; this is achieved with antithyroid drugs; iodine preparations are also given to reduce size and vascularity of gland; cardiac problems must be stabilized and pt. must be in good nutritional state; teaching centers around preventing strain on suture line and addressing concerns about scarring in neck area

d. Post-op care:

• a. Airway
• b. Vital Signs
• c. Positioning
• d. Controlling pain
• e. Assessing for complications: respiratory distress, hemorrhage, hypocalcemia, laryngeal nerve damage
• f. Teaching: signs of hypothyroidism and adverse effects of drug therapy, wound care, limitations, follow-up care

2. HYPOTHYROIDISM: (Review patho, Myxedema Coma, Etiologies, Labs)

A. ELDERLY CONSIDERATIONS:

B. SYSTEMIC EFFECTS: Abnormalities in Lipid Metabolism, Increase in Interstitial Fluid, Anemia

C. HEAD TO TOE ASSESSMENT:

(1) General Survey

(2) Head and Neck

(3) Neurologic

(4) Pulmonary, C-V

(5) G.I., G.U.

(6) Extremities

(7) Pt. complaints

C. Diagnostic Testing

D. Nursing Diagnosis:

E. Management and Nursing Care:

(1) Drug Therapy--Hormone replacement generally with Levothyroxine(Synthroid), Cytomel or Thyrolar

a. Elderly, cardiac and myxedematous patients are extremely sensitive to thyroid hormones--initial dosage should be markedly reduced

b. Interactions with many other drugs--may alter effectiveness of Coumadin, cause an increase in requirement for insulin or oral hypoglycemics in diabetics or have additive effect with drugs that stimulate the heart or decrease the response to beta blockers

c. Patient teaching:

1. Treatment is lifelong

2. Take before breakfast to prevent insomnia

3. Check pulse--if >100, notify health care provider

4. Do not change brands or go to generics

5. Consult health care provider before taking other drugs

6. Teach S&S of hyper and hypothyroidism

7. Follow up with TSH blood tests as ordered after starting therapy and once a year for maintenance

 For more information on Thyroid Disease and Treatment:

American Thyroid Association:

http://www.thyroid.org

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3. Adrenal Crisis: Case Study:

Adam Walker, a 40 yr. old man, with a five year history of Addison's Disease, was admitted to the hospital for a cholecystectomy. Two days after the surgery, he developed hypotension and electrolyte imbalances. Blood was obtained for CBC, electrolytes, and plasma cortisol level, and I.V. fluids were started. He was transferred to the ICU, where the following data were obtained:

Vital Signs: B/P= 80/48, Pulse =126, R=18, Temp= 100.8

Labs: Na=123, K=6.6, Cl=88, CO2=19, Glucose=60, BUN=30, Cr=1.0, Hgb=15

Upon physical assessment, he was lethargic but oriented x3, moved all extremities to command, but was unable to lift his legs off the bed against resistance. He denied incisional pain, but complained of acute abdominal pain and nausea. His cardiac monitor showed sinus tachycardia without ectopy but with tall "T" waves. No murmurs, rubs or gallops were auscultated. Peripheral pulses were present but diminished. Bilateral breath sounds were audible and clear. His urine output was 15 to 20 ml/hr and was dark yellow without visible sediment. His skin was pale and cool, with hyperpigmented areas on his inner arms and genitalia and bluish black spots visible on his lips.

His plasma cortisol level returned as a 3mg/dl. Intravenous fluids of D5NS were started and a pulmonary artery catheter was inserted with a CVP of 5 and a PAWP of 6. Twenty-five units of synthetic adrenocorticotropic hormone (ACTH) were given I.V. and an ACTH stimulation test was ordered.

Please answer the following questions related to the case study:

1. What hormones are normally released by the adrenal cortex?

Aldosterone(mineralocorticoid), Androgens, Cortisol and corticosterone(glucocorticoids)* 

*Remember: Salt, Sex and Sugar!

2. Describe the normal mechanisms that control the secretion of glucocorticoids and mineralocorticoids.

Secretion of cortisol is controlled by ACTH, which is released from the anterior pituitary. The release of ACTH is regulated by corticotropin-releasing factor(CRF) from the hypothalamus.

Three factors affect the release of CRF and in turn ACTH: plasma cortisol levels, wake-sleep patterns, and psychological and physical stress. When plasma cortisol levels drop, the hypothalamus releases CRF, which stimulates ACTH. The ACTH causes the adrenal cortex to make more cortisol. When the cortisol level rises, the hypothalamus stops releasing CRF. In people with regular sleep patterns, the maximum ACTH release is in the early morning.

Aldosterone release is stimulated by increases in serum potassium, activation of the renin-angiotensin system, and ACTH in a minor way. The renin-angiotensin system(and thus aldosterone release) is stimulated by hypovolemia, hyperkalemia, and B-adrenergic sympathetic stimulation. Aldosterone release is inhibited by decreases in serum potassium, angiotension II, and ACTH.

3. What are the physiological effects of cortisol and aldosterone?

Cortisol:

Aldosterone:

4. What hormones are normally released by the adrenal medulla?

Catecholamines: Epinephrine and Norepinephrine

5. What hormones are deficient in Addison's Disease/Adrenal Crisis?

Glucocorticoids and Mineralocorticoids

6. What are the causes of Adrenal Crisis?

Primary: Idiopathic atrophy (probably due to an autoimmune response), infection, hemorrhage, metastatic disease

Secondary: Hypopituitarism and suppression of the hypothalamic-pituitary axis by exogenous steroids(long term steroid use)

7. What are the possible causes of Mr. Walker's Adrenal Crisis?

 Mr. Walker had primary adrenal insufficiency and the stress of surgery triggered the adrenal crisis. The hyperpigmentation on his arms is due to melanocyte stimulation by an increased level of ACTH. If the ACTH level is increased, the pituitary must be functioning, so the adrenal glands themselves must be at fault(primary cause).

8. How long after receiving steroids should a patient be presumed to have some adrenal suppression?

Any patient who has received steroid replacement for > 1 week is presumed to have some pituitary-adrenal suppression.

If a patient has received chronic steroid therapy, it takes up to 9 months for the pituitary/adrenal glands to recover.

9. What are the clinical indicators of Addison's Disease?

1. Abdominal Pain

2. Nausea/vomiting/diarrhea

3. Hypovolemia/Hypotension

4. Hyponatremia

5. Hypoglycemia

6. Hyperkalemia

7. Hyperpigmentation

8. Weakness/ Fatigue

9. Total eosinophil count(TEC) > 300

10. Mild metabolic acidosis

 11. Weight loss

12. Salt Craving

10. Why does hypotension occur in Adrenal Crisis?

 The vascular response to catecholamines is decreased, as is the vascular tone in the periphery. Vasodilation is the result. In primary causes, aldosterone secretion is decreased, causing severe sodium and water loss from the kidneys. Hypovolemia is the result.

11. List factors that predispose a patient to an acute Adrenal Crisis.

Infection, Trauma, Surgery, Pregnancy, Physical Stress, Exogenous Steroid Use with inadequate length of time for withdrawal

12. Mr. Walker's Na was 123 mEq/liter. What are the clinical indicators of hyponatremia?

13. What is an ACTH stimulation test?

 This is used to determine if the pituitary(Secondary cause) or the adrenals(Primary cause) is at fault.

ACTH is given, and serum cortisol levels are checked. If the level increases, a diagnosis of Secondary adrenal insufficiency is made, meaning that the adrenal glands are functioning and the problem lies with the pituitary.

If no increase in serum cortisol is seen , the problem is Primary adrenal disease.

14. What other diagnostic tests might be done?

 1. Plasma cortisol levels at 8:00 a.m. and 4:00 p.m.--Normal: 7-18mg/dl in a.m., 2-10mg/dl in p.m.

 2. 24 hour urine for 17-hydroxycorticoids--Normal: 2-10mg/24 hrs.

15. What is the usual medical treatment for Adrenal Crisis(an acute emergency)?

1. Rapid fluid replacement, using D5NS (up to 500 ml/ hr.)

2. Steroid replacement, using 100mg. Hydrocortisone I.V. q 6 hrs.

3. Sodium Bicarbonate is ph is < 7.20

4. Recheck Labs in 2 hours

 For chronic adrenal insufficiency(like removal of pituitary or adrenals), patient will need steroid replacement for life!

16. What is Addison's Disease?

Addison's disease is the chronic form of adrenal cortical insufficiency . Adrenal crisis is also referred to as Addisonian crisis.

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