N302 Final

Front 1

Hyperthyroid Disease

Back 1

1. T3 &/or T4 are ↑

2. TSH will ↓ to slow release of T3/T4

Front 2

Hypothyroid Disease

Back 2

1. T3 &/or T4 are ↓

2. TSH will ↑ to stimulate release of T3/T4

Front 3

Testing for hyperthyroidism

Back 3

Includes measurement of the following blood values: triiodothyronine (T3), thyroxine (T4), T3 resin uptake (T3RU), and thyroid-stimulating hormone (TSH). Antibodies to TSH (TSH-RAb) are measured to determine the presence of Graves' disease.

Front 4

Hyperthyroidism

Back 4

1. Thyrotoxicosis

2. Excessive thyroid hormone secretion
-- ↑ Circulating free thyroxine (T4)
-- ↑ Free triiodothyronine (T3)

3. Excessive thyroid hormone secretion leads to hyperthyroidism. The manifestations of hyperthyroidism are called thyrotoxicosis

Front 5

Causes of Hyperthyroidism

Back 5

1. Graves' disease (the most common etiology with 70-80%)

2. Toxic thyroid adenoma

3. Toxic multinodular goiter

Front 6

Dx of Hyperthyroidism

Back 6

1. Thyroid hormones -- TSH, T3, T4, T3 Resin uptake, Free thyroxin index, T4 RIA, Thyroid Calcitonin

2. Thyroid antibodies

3. Thyroid Radioactive Iodine Uptake (RAIU)

4. Thyroid Ultrasonography Scan

5. EKG

Front 7

HYPERTHYROIDISM TREATMENT

Back 7

1. Nonsurgical Intervention
a. Rx--suppress thyroid hormones propylthiouracil (PTU), methimazole (Tapazole), and carbimazole (Neo-Mercazole)
b. Iodine-- ↓ blood flow to thyroid gland
c. Beta-adrenergic blocking drugs: propranolol (Inderal, Detensol)
d. Relieves diaphoresis, anxiety, tachycardia, and palpitations
e. RAI Therapy: Oral I-131
f. Diet -- ↑ Calories, carbohydrates & proteins

Front 8

RAI Therapy: Oral I-131

Back 8

The client with hyperthyroidism may receive RAI in the form of oral 131I. The dosage depends on the thyroid gland's size and sensitivity to radiation. The thyroid gland picks up the RAI, and some of the cells that produce thyroid hormone are destroyed by the local radiation. Because the thyroid gland stores thyroid hormones to some degree, the client may not have complete symptom relief until 6 to 8 weeks after RAI therapy.

Front 9

Radioactive iodine therapy (RAI)

Back 9

1. Not used in pregnant women

2. Additional drug therapy may be needed.

3. Implement radiation precautions.

4. Monitor regularly for changes in thyroid function.

Front 10

RAI Therapy

Back 10

RAI therapy is performed on an outpatient basis. One dose may be sufficient, although some clients need a second or third dose. The radiation dose is low enough that radiation precautions are not needed. Reassure the client that the radioactivity is quickly eliminated. The degree of thyroid destruction is variable. Some clients become hypothyroid as a result of treatment. This problem may occur within a few weeks, or it may take several years to develop. The client then needs lifelong thyroid hormone replacement. All clients who have undergone RAI therapy should be monitored regularly for changes in thyroid function.

Front 11

Surgical Interventions for Hyperthyroidism

Back 11

1. Thyroidectomy (Total or partial)

2. Must be euthyroid before

3. Post Op Complications
a. Hemorrhage
b. Resp. distress
c. Hypocalcemia &/or Tetany (Parathyroid gland injury)
d. Laryngeal damage
e. Thyroid storm

Front 12

Tetany

Back 12

Ask the client about any tingling around the mouth or of the toes and fingers. Assess for muscle twitching as signs of calcium deficiency. Calcium gluconate or calcium chloride for intravenous (IV) use must be available in an emergency situation

Front 13

Post Op Care for Hyperthyroidism

Back 13

1. Semi Fowlers
2. Support head & neck (sandbags/pillows)
3. Humidify air
4. Suction PRN
5. Inspect drsg & behind neck for bleeding
6. Assess for laryngeal stridor
7. Loosen drsg if constricting airway
8. Trach set at bedside

Front 14

Grave's Disease

Back 14

1. Most common cause of hyperthyroidism.

2. Autoimmune disease

3. TSI’s (thyroid stimulating immunoglobulins)

4. Thyroid receptor antibodies (TRAb)

5. TSI/TRAb binds to the receptor for TSH on the thyroid gland

6. Acts just like TSH (DECREASED TSH release)

7. Creates enlargement of the gland

8. Stimulates release of thyroid hormones (INCREASED T3, T4)

Front 15

Grave's Disease

Back 15

With hyperthyroidism, both the T3 and T4 blood levels are elevated, causing the hypermetabolism. In Graves’ disease, the autoantibodies bind to the TSH receptor and activate it, causing an overproduction of thyroid hormones. The increased metabolic rate negatively feeds back and suppresses hypothalamic secretion of thyrotropic hormone, which in turn suppresses thyroid-stimulating hormone (TSH). When the TSH levels are elevated, causing an increased synthesis of thyroid hormones, the hyperthyroidism is not a result of Graves’ disease.

Front 16

Grave's Disease

Back 16

1. Hyperthyroidism

2. Goiter

3. Exopthalmos - Abnormal protrusion of the eyeball

4. Pretibial Edema - dry waxy swelling on anterior surface of lower legs

5. Infiltrative Opthalmopathy
↑ Thyroid Autoantibodies (to TSH) (95%)

6. Familial, occurs most often in women <40

7. Complications -- Thyroid Storm (Thyroid Crisis)

Front 17

Grave's Disease and Eyes

Back 17

1. Ask the client about changes in vision, such as blurring or double vision and tiring of the eyes.

2. Infiltrative ophthalmopathy, which leads to exophthalmos, is common in clients with Graves' diseaseThe wide-eyed or "startled" look is due to edema in the extraocular muscles and increased fatty tissue behind the eye, which pushes the eyeball forward. Pressure on the optic nerve may impair vision. Swelling and shortening of the muscles may cause problems with focusing. If the eyelid fails to close completely and the eye is unprotected, the eye may become overdry and develop corneal ulcers or infection. Observe the client's eyes for excessive tearing and a bloodshot appearance, and ask about sensitivity to light (photophobia).

Front 18

INFILTRATIVE OPTHALMOPATHY

Back 18

1. Provide symptomatic treatment.

2. Treatment of hyperthyroidism does not correct eye and vision problems of Graves’ disease.

3. Elevate the head of bed at night.

4. Instill artificial tears.

5. Treat photophobia with dark glasses.

6. Give steroid therapy.

7. Provide diuretics

Front 19

Thyroid Storm

Back 19

1. Cause—sudden, excessive thyroid hormone release

2. Spontaneous
a. Related to:
Major stressor( surgery, death of a friend)
Infection
Extreme emotional stress
Abrupt withdrawal of antithyroid meds
DKA
Pulmonary Thromboembolism
Vigorous palpation of a large goiter
Salicylates (INCREASED free thyroid hormones to critical levels)

Front 20

Thyroid Storm

Back 20

The manifestations of thyroid storm are caused by excessive thyroid hormone release, which dramatically increases metabolic rate
a crisis of uncontrolled thyrotoxicosis caused by the release into the bloodstream of increased amounts of thyroid hormone. Thyroid storm may occur spontaneously or be precipitated by infection, stress, or a thyroidectomy performed on a patient who is inadequately prepared with antithyroid drugs.

Front 21

Thyroid Storm

Back 21

1. Dramatic ↑ in metabolic rate

2. Life-threatening event

3. Mortality rate—25% (even with treatment)

Front 22

Sx of Thyroid Storm

Back 22

Signs and symptoms develop quickly
1. Main—sudden high fever (106°), tachycardia, systol.
2. Hypertension, acute resp. distress
3. Minor—N/V, diarrhea, anxiety, tremors
4. As crisis progresses—restlessness, confusion, psychosis, seizures, coma

Front 23

Thyroid Storm Sx

Back 23

Characteristic signs are fever that may reach 106° F, a rapid pulse, acute respiratory distress, apprehension, restlessness, irritability, and prostration. The patient may become delirious, lapse into a coma, and die of heart failure. Also called thyroid crisis.

Key manifestations include fever, tachycardia, and systolic hypertension. The client may have gastrointestinal problems such as abdominal pain, nausea, vomiting, and diarrhea. Often the client with thyroid storm is very anxious and has tremors. As the crisis progresses, he or she may become restless, confused, psychotic, and may have seizures, leading to coma.

Front 24

Typical Vital Signs of Thyroid Storm

Back 24

1. Fever, may be > 102°-106°

2. Sinus tachycardia 160

3. Systolic hypertension BP 210/120

4. Resp 32

5. O2 Sat 88%

Front 25

Typical Labs of Thyroid Storm

Back 25

1. TSH—undetectable

2. T4 & T3—elevated

3. Hypercalcemia

4. INCREASED Alk Phosphatase

5. Hyperglycemia

6. INCREASED circulating catecholamines

Front 26

Priority Nursing Actions/ Interventions for Thyroid Storm

Back 26

1. Maintain Airway - Oxygen, ventilator; Check resp. frequently; Auscultate for crackles; O2 Sat; ABG’s

2. Thyroid crisis is a life-threatening emergency that has a 25% mortality rate, even with intervention. Maintaining a patent airway and providing adequate ventilation are the primary concerns for clients in thyroid crisis

3. Decrease HR & BP -- Cardiac monitor HR/rhythm; Freq. BP; Beta Blockers--Inderal IV for tachycardia

4. Decrease body temp -- Tylenol (No ASPIRIN; Cooling blanket

5. Prevent adrenal insuficiency -- Corticosteroids

6. Prevent Thyroid Hormone Release
a. Lugol’s Solution (Iodine) PO or IV
b. Propylthyouracil
c. Lithium
d. Iodinated contrast

Front 27

Lithium

Back 27

Lithium antagonizes antidiuretic hormone and can cause symptoms of diabetes insipidus

Front 28

Other Actions/Interventions for Thyroid Storm

Back 28

1. IV D5W 100 cc’s/hr to replace fluids lost through diaphoresis, possible nausea and vomiting

2. Hydrocortisone 100mg IV every 8 hours to prevent adrenal insufficiency

3. ABSOLUTE BEDREST!

Front 29

Refractory Cases of Thyroid Storm

Back 29

1. Removal of circulating thyroid hormones
a. Plasmapheresis
b. Plasma Exchange
c. Peritoneal hemodialysis

Front 30

Hypothyroidism

Back 30

Failure of thyroid hormone secretion
a. ↓ Circulating free thyroxine (T4)
b. ↓ Free triiodothyronine (T3)

Front 31

Primary causes of Hypothyroidism

Back 31

1. Thyroiditis
2. Toxins
3. Auto antibodies
4. Lack of Iodine/tyrosine injest.
5. Thyroid surgery
6. RAI Tx

Front 32

Secondary causes of Hypothyroidism

Back 32

1. Pituitary/hypothalmic

2. Tumors/infections

Front 33

Results of Hypothyroidism

Back 33

1. Myxedema - Generally non-pitting edema

2. Thickened tongue

3. Edema in larynx—husky voice

4. ↓ gen. function

5. Rare—can lead to coma --> ↓ cardiac function/perfusion

Front 34

Myxedema

Back 34

Most tissues and organs are affected by the low metabolic rate caused by hypothyroidism. Cellular energy is decreased, and metabolites build up. The metabolites are compounds of proteins and sugars called glycosaminoglycans. These compounds build up inside cells, which increases the mucous and water, forms cellular edema, and changes organ texture. The edema is mucinous (called myxedema) rather than edema caused by water alone. This edema changes the client's appearance. Nonpitting edema forms everywhere, especially around the eyes, in the hands and feet, and between the shoulder blades. The tongue thickens and edema forms in the larynx, making the voice husky. General physiologic function is decreased.

Front 35

Hypothyroidism

Back 35

1. Thyroiditis
a. Acute—bacterial
b. Subacute--viral
c. Chronic--Hashimoto’s—auto antibodies
d. Dysphagia
e. Painless gland swelling (goiter)

2. Thyroid Cancer

Front 36

Hypothyroidism Treatments

Back 36

1. Thyroid hormone replacement
a. Synthroid (T4)
b. Cytomel (T3)
c. Thyrolar (T3/T4 combination 4:1)

Front 37

MYXEDEMA COMA

Back 37

1. Critical hypothyroidism

2. Mortality rate—60%

3. Uncommon

4. Occurs in winter (when thermoregulatory sensors are high)

5. Occurs mostly in women over 60 yo who have had longstanding hypothyroidism

Front 38

Sx of Myxedema coma

Back 38

1. Profound DECREASED metabolic activity

2. Hypothermia

3. Hypotension

4. Bradycardia

5. Mental status depression--Progresses to stupor and coma

6. Hyponatremia -- INCREASED release of Antidiuretic hormone

7. Hypoglycemia

Front 39

Labs for Myxedema coma

Back 39

1. TSH INCREASED

2. T3 & T4 undetectable

Front 40

Treatment for Myxedema coma

Back 40

1. High-dose Thyroxine IV
a. Bolus—300-500 mcg
b. 50-100 mcg daily

2. Watch for cardiovascular complications

3. Ventilator

4. Warming blanket

5. Correct electrolyte abnormalities