Endocrine Notes RNpedia PDF

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ADDISON’S DISEASE

Definition

Hyposecretion of adrenocortical hormones leading to:  Metabolic disturbances (sugar)  Fluid and electrolyte imbalances (salt)  Deficiency of neuromuscular function (salt and sex)

CUSHING’S DISEASE

Hypersecretion of adrenocortical hormone Hyperplasia of Adrenal gland 2. Tubercular infection (MILIARY – TB to adjacent organs) 1.

Predisposin g Factors

1. 2.

Atrophy of the Adrenal gland Fungal infections

1.

2. 1.

2.

3.

4.

5. 6. 7.

hypoglycemia (TIRED)  Tremors and tachycardia  Irritability  Restlessness  Extreme fatigue  Diaphoresis and depression Decreased tolerance to stress (d/t decreased cortisol) à Addisonian Crisis Hyponatremia  Hypotension  Signs of dehydration  Weight loss Hyperkalemia  Irritability and agitation  Diarrhea  Arrhythmias Decreased Libido Loss of pubic and axillary hair Bronze-like skin pigmentation d/t

3.

4.

5.

6. 7. 8.

Hyperglycemia à can lead to DM 1. Polyuria 2. Polydipsia 3. Polyphagia 4. Wt. Gain 5. Glucosuria Increased susceptibility to infection (Reverse isolation!) Hypernatremia 1. HPN 2. Edema 3. Wt. gain Moon face appearance, buffalo hump, obese trunk, pendulous abdomen, thin extremities Hypokalemia 1. Weakness and fatigue 2. Constipation 3. U wave on ECG tracing Hirsutism Easy bruising Acne and Striae

Addison’s Disease vs Cushing’s Disease

Diabetes Insipidus Nursing Care Plan & Management NOTES



Description Diabetes insipidus is hyposecretion of ADH caused by strokes, trauma, or idiopathic causes.  Kidney tubules fail to reabsorb water. 

Assessment           

Polyuria of 4 to 24 L per day Polydipsia Dehydration Decreased skin turgor, dry mucous membranes Inability to concentrate urine A low urinary specific gravity: 1.006 or less Fatigue Muscle pain and weakness Headache Postural hypotension that may progress to vascular collapse without rehydration Tachycardia

Medical Management

Objectives of therapy are to ensure adequate fluid replacement, to replace vasopressin, and to search for and correct the underlying intracranial pathology. Treatment for diabetes insipidus of nephrogenic origin involves using thiazide, diuretics, mild salt depletion, and prostaglandin inhibitors (eg., ibuprofen, indomethacin, and aspirin).

Vasopressin Replacement Desmopressin (DDAVP), administered intranasally, 1 or 2 administrations daily to control symptoms  Lypressin (Diapid), absorbed through nasal mucosa into blood; duration may be short for patients with severe disease  Intramuscular administration of ADH (vasopressin tannate in oil) every 24 to 96 hours to reduce urinary volume (shake vigorously or warm; administer in the evening; rotate injection sites to prevent lipodystrophy) 

Fluid Conservation Clofibrate, a hypolipidemic agent, has an antidiuretic effect on patients who have some residual hypothalamic vasopressin.  Chlorpropamide (Diabinese) and thiazide diuretics are used in mild forms to potentiate the action of vasopressin; may cause hypoglycemic reactions. 

Nursing Interventions       

Monitor vital signs and neurological and cardiovascular status. Provide a safe environment, particularly for the client with a change in level of consciousness or mental status. Monitor electrolyte values and for signs of dehydration. Monitor intake and output, weight, and specific gravity of urine. Maintain the intake of adequate fluids, and monitor for signs of dehydration. Instruct the client to avoid foods or liquids that produce diuresis. Administer chlorpropamide (Diabinese) if prescribed for mild diabetes insipidus.

Administer vasopressin tannate (Pitressin) or desmopressin acetate (DDAVP, Stimate) as prescribed; these are used when the ADH deficiency is severe or chronic.  Instruct the client in the administration of medications as prescribed (DDAVP may be administered by injection, intranasally, or orally).  Instruct the client to wear a Medic-Alert bracelet. 

Hyperthyroidism Nursing Care Plan and Management Graves

Description 1. Hyperthyroidism is a hyperthyroid state resulting from hypersecretion of thyroid hormones (T3 and T4). 2. Hyperthyroidism is characterized by an increased rate of body metabolism. 3. A common cause is Graves’ disease, also known as toxic diffuse goiter. 4. Clinical manifestations are referred to as thyrotoxicosis.

Causes Graves’ disease has an autoimmune derivation and is caused by circulating anti-TSH autoantibodies that displace TSH from the thyroid receptors and mimic TSH by activating the TSH receptor to release additional thyroid hormones. Graves’ disease is also associated with Hashimoto’s disease, a chronic inflammation of the thyroid gland that usually causes hypothyroidism but can also cause symptoms similar to those of Graves’ disease. Thyrotoxicosis has several different pathophysiological causes, including autoimmune disease, functioning thyroid adenoma, and infection.

Assessment

1. Enlarged thyroid gland (goiter) 2. Palpitations, cardiac dysrhythmias, such as tachycardia or atrial fibrillation 3. Protruding eyeballs (exophthalmos) possibly present 4. Hypertension 5. Heat intolerance 6. Diaphoresis

7. Weight loss 8. Diarrhea 9. Smooth, soft skin and hair 10.

Nervousness and fine tremors of hands

11.

Personality changes

12.

Irritability and agitation

13.

Mood swings

14.

Oligomenorrhea (Irregular menstrual periods in women)

Complications Thyroid crisis (storm), also called thyrotoxicosis, is a sudden worsening of hyperthyroidism symptoms that may occur with infection or stress. Fever, decreased mental alertness, and abdominal pain may occur. Immediate hospitalization is needed. Other complications related to hyperthyroidism include:  Heart-related complications including:  Rapid heart rate  Congestive heart failure  Atrial fibrillation  Increased risk for osteoporosis, if hyperthyroidism is present for a long time  Surgery-related complications, including:  Scarring of the neck

 Hoarseness due to nerve damage to the voice box  Low calcium level due to damage to the parathyroid glands (located near the thyroid gland)  Treatments for hypothyroidism, such as radioactive iodine, surgery, and medications to replace thyroid hormones can have complications.

Primary Nursing Diagnosis  Activity intolerance related to exhaustion and fatigue

Diagnostic Evaluation  Thyroid-stimulating hormone (TSH) assay reveals a decrease in result (normal TSH: 0.5– 1.5 mU/L). Elevation of thyroid hormones decreased TSH secretion by negative feedback.  Elevated Thyroxine (T4) radioimmunoassay (normal values: 5.0–12.0 μg/dL). Elevation reflects overproduction of thyroid hormones; monitors response to therapy.  Elevated Tri-iodothyronine (T3) radioimmunoassay (normal values: 80–230 ng/dL). Elevation reflects overproduction of thyroid hormones.  Other Tests: 24-hr radioactive iodine uptake; thyroid autoantibodies; antithyroglobulin; electrocardiogram (ECG)

Medical Management Treatment is directed toward reducing thyroid hyperactivity for symptomatic relief and removing the cause of complications. Three forms of treatment are available:  Irradiation involving the administration of 131I or 123I for destructive effects on the thyroid gland

 Pharmacotherapy with antithyroid medications  Surgery with the removal of most of the thyroid gland Radioactive Iodine (131I) 131



I is given to destroy the overactive thyroid cells (most common treatment in the elderly).



131

I is contraindicated in pregnancy and nursing mothers because radioiodine crosses the placenta and is secreted in breast milk.

Pharmacotherapy  The objective of pharmacotherapy is to inhibit hormone synthesis or release and reduce the amount of thyroid tissue.  The most commonly used medications are propylthiouracil and methimazole (Tapazole) until patient is euthyroid.  Maintenance dose is established, followed by gradual withdrawal of the medication over the next several months.  Antithyroid drugs are contraindicated in late pregnancy because of a risk for goiter and cretinism in the fetus.  Thyroid hormone may be administered to put the thyroid to rest.

Adjunctive Therapy  Potassium iodide, Lugol’s solution, and saturated solution of potassium iodide (SSKI) may be added.

 Beta- adrenergic agents may be used to control the sympathetic nervous system, effects that occur in hyperthyroidism; for example, propranolol is used for nervousness, tachycardia, tremor, anxiety, and heat intolerance.

Surgery  Surgical treatment with thyroidectomy is no longer the preferred choice of therapy for Graves’ disease but is an alternative therapeutic approach in some situations. In particular, it is used for patients who cannot tolerate antithyroid drugs, have significant ophthalmopathy, have large goiters, or cannot undergo radioiodine therapy.

Pharmacologic Highlights  Propylthiouracil (PTU) an antithyroid agent is given to return the patient to the euthyroid (normal) state. PTU inhibits use of iodine by thyroid gland; blocks oxidation of iodine and inhibits thyroid hormone synthesis  Methimazole (Tapazole) an antithyroid agent is given to return the patient to the euthyroid (normal) state by inhibiting use of iodine by thyroid gland.  Other Drugs: Beta-adrenergic blockers, corticosteroids, radioactive iodine

Nursing Interventions 1. Provide adequate rest. 2. Administer sedatives as prescribed. 3. Provide a cool and quiet environment. 4. Obtain weight daily. 5. Provide a high-calorie diet.

6. Avoid the administration of stimulants. 7. Administer antithyroid medications (propylthiouracil [PTU]) that block thyroid synthesis, as prescribed. 8. Administer iodine preparations that inhibit the release of thyroid hormone as prescribed. 9. Administer propranolol (Inderal) for tachycardia as prescribed. 10. Prepare the client for radioactive iodine therapy, as prescribed, to destroy thyroid cells. 11.

Prepare the client for thyroidectomy if prescribed.

Documentation Guidelines  Physical findings: Cardiovascular status (resting pulse, blood pressure, presence of angina or palpitations), bowel activity, edema, condition of skin, and activity tolerance  Physical findings: Hypermetabolism, eye status, heat intolerance, activity level  Response to medications, skin care regimen, nutrition, body weight, comfort  Psychosocial response to changes in bodily function, including mental acuity, behavioral patterns, emotional stability

Discharge and Home Healthcare Guidelines  DISEASE PROCESS. Provide a clear explanation of the role of the thyroid gland, the disease process, and the treatment plan. Explain possible side effects of the treatment.  MEDICATIONS. Be sure that the patient understands all medications, including the dosage, route, action, adverse effects, and the need for any laboratory monitoring of thyroid medications. If patients are taking propylthiouracil or methimazole, encourage

them to take the medications with meals to limit gastric irritation. If the patient is taking an iodine solution, mix it with milk or juice to limit gastric irritation and have the patient use a straw to limit the risk of teeth discoloration.  COMPLICATIONS. Have the patient report any signs and symptoms of thyrotoxicosis immediately: rapid heart rate, palpitations, perspiration, shakiness, tremors, difficulty breathing, nausea, vomiting. Teach the patient to report increased neck swelling, difficulty swallowing, or weight loss.

Thyrotoxicosis (Thyroid Storm) Description Thyroid storm is a life-threatening condition in which patients with underling thyroid dysfunction inhibit exaggerated signs and symptoms of hyperthyroidism. Thyroid storm is precipitated by stressors such as infection, trauma, DKA, surgery, heart failure, or stroke. The condition can result from discontinuation of antithyroid medication or as a result of untreated or inadequate treatment of hyperthyroidism. The excess thyroid hormones increase metabolism and affect the sympathetic nervous system, thus increasing oxygen consumption and heat production and altering fluid and electrolyte levels.

image by: http://hyperthyroidismsymptomsx.com/

Signs And Symptoms             

Sudden onset of fever Tremors Flushing Profuse palm sweating Tachydysrhythmias Extreme restlessness Nausea Vomiting Diarrhea Weight loss Fatigue Muscle weakness Atrophy

Physical Examination Vital signs

   

Systolic hypertension or hypotension HR: tachycardia disproportionate to the degree of fever RR: >20 breaths/ min Temperature >102.2 °F can be higher

Neurologic   

Agitated Tremulous Delirious coma

Cardiovascular    

Bounding pulses Systolic murmur Widening pulse Weak thready pulses

Pulmonary  

Tachycardia Crackles may be present

Gastrointestinal 

Increased bowel sounds

Endocrine 

Thyroid may be enlarged or nodular

Acute Care Patient Management Nursing Diagnosis: Decreased cardiac output related to increased cardiac work secondary to increased adrenergic activity; Deficient fluid volume secondary to increased metabolism and diaphoresis.

Outcome Criteria

    

Patient alert and oriented Peripheral pulses palpable Lung clear to auscultation Urine output 30 ml/hr Absence of life-threatening dysrhythmias

Patient Monitoring 1.

Continuously monitor ECG for dysrhythmias or HR ? 140 beats/min that can adversely affect cardiac output and monitor for ST segment changes indicative of myocardial ischemia. 2. Continuously monitor oxygen saturation with pulse oximetry. 3. Continuously monitor pulmonary artery pressure. 4. Monitor fluid volume status; measure urine output hourly and determine fluid balance every 8 hours.

Patient Assessment 1.

Assess cardiovascular status; extra heart sounds, complaints of orthopnea or dyspnea on exertion. 2. Assess hydration status because dehydration can further decrease circulating volume and compromise cardiac output. 3. Assess for pressure ulcer development secondary to hypoperfusion.

Diagnostic Assessment 1. 2.

REVIEW THYROID STUDIES AS AVAILABLE. Review serial serum electrolytes, serum glucose, and serum calcium levels to evaluate the patient’s response to therapy. 3. Review serial ABGs for hypoxemia and acid-base imbalance, which can adversely affect cardiac function. 4. Review serial chest radiographs for cardiac enlargement and pulmonary congestion.

Patient Management

1. 2. 3. 4. 5. 6. 7. 8. 9.

Administer dextrose-containing intravenous fluids as ordered to correct fluid and glucose deficits. Carefully assess the patient for heart failure or pulmonary edema. Dopamine may be used to support blood pressure. Provide supplemental oxygen as ordered to help meet increased metabolic demands. Once the patient is hemodynamically stable, provide pulmonary hygiene to reduce pulmonary complications. If the patient is in heart failure, typical pharmacologic agents for treatment of heart failure may also be indicated. Reduce oxygen demands by decreasing anxiety, reduce fever, decrease pain, and limit visitors if necessary. Anticipate aggressive treatment of precipitating factor. Institute pressure ulcer strategies.

Hypothyroidism (myxedema) Description 1.

Hypothyroidism is a hypothyroid state resulting from a hyposecretion of the thyroid hormones T4 and T3. 2. Hypothyroidism is characterized by decreased rate of body metabolism.

Causes Hypothyroidism can be a primary disorder that results from disease in the thyroid gland itself or a secondary or tertiary disorder. In most cases, hypothyroidism occurs as a primary disorder and results from the loss of thyroid tissue, which leads to inadequate production of thyroid hormones (primary hypothyroidism). It is most frequently autoimmune in origin but can also be related to iodine deficiency.  Secondary hypothyroidism, which occurs in only 5% of cases, is caused by a failure of the pituitary gland to stimulate the thyroid gland or a failure of the target tissues to respond to the thyroid hormones. Tertiary hypothyroidism is caused by failure of the hypothalamus to produce thyroid-releasing factor.  The most common cause of goitrous hypothyroidism in North America is Hashimoto’s disease, which causes defective iodine binding and defective thyroid hormone production. Hashimoto’s disease is common in the same family and is considered an autoimmune disorder leading to chronic inflammation of the thyroid gland and hypothyroidism but can also lead to hyperthyroidism. 

Risk Factors  

Age over 50 years Being female

Assessment 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Lethargy and fatigue Weakness, muscle aches, paresthesias Intolerance to cold Weight gain Dry skin and hair Loss of body hair Bradycardia Constipation Generalized puffiness and edema around the eyes and face. Forgetfulness and loss of memory Menstrual disturbances

12. Cardiac enlargement, tendency to develop congestive heart failure.

Complications Myxedema coma, the most severe form of hypothyroidism, is rare. It may be caused by an infection, illness, exposure to cold, or certain medications in people with untreated hypothyroidism. Symptoms and signs of myxedema coma include:     

Below normal temperature Decreased breathing Low blood pressure Low blood sugar Unresponsiveness

Primary Nursing Diagnosis 

Activity intolerance related to weakness and apathy

Diagnostic Evaluation     

Thyroid-stimulating hormone (TSH) assay result is >4.0 mU/L ( normal values: 0.5–1.5 mU/L). Normal value excludes primary hypothyroidism and a markedly elevated value confirms the diagnosis. Thyroxine (T4) radioimmunoassay decreased (normal values: 5.0–12.0 μg/dL). Reflects underproduction of thyroid hormones; monitors response to therapy. Tri-iodothyronine (T3) radioimmunoassay decreased (normal values: 80–230 ng/dL). Reflects underproduction of thyroid hormones. Electrocardiogram (ECG) reveals low voltage, T wave abnormalities. Other Tests: 24-hr radioactive iodine uptake; thyroid autoantibodies; antithyroglobulin

Medical Management Most patients are diagnosed and treated on an outpatient basis. The goal of treatment is to return the patient to the euthyroid (normal) state and to prevent complications. The treatment of choice is to provide thyroid hormone supplements to correct hormonal deficiencies.  Treatment of the elderly patient is approached more cautiously because of higher risk for cardiac complications and toxic effects. The medication should not be given if the pulse rate is greater than 100. The treatment is considered to be life-long, requiring ongoing medical assessment of thyroid function.  Polypharmacy is a significant concern for the hypothyroid patient. Several classifications of drugs are affected by the addition of thyroid supplements, including beta blockers, oral anticoagulants, bronchodilators, digitalis preparations, tricyclic antidepressants, and cholesterol lowering agents.  Because significant cardiovascular disease often accompanies hypothyroidism, the patient is at risk for cardiac complications if the metabolic rate is increased too quickly. Therefore, the patient needs to be mo...