NCLEX: Immunologic disorders

Nursing diagnoses

When caring for patients with immunologic disorders, you’ll find that several nursing diagnoses can be used over and over. Commonly used diagnoses appear here, along with appropriate nursing interventions and rationales.

 

Risk for infection

Related to external or internal factors, Risk for infection may be associated with AIDS, SCID, pernicious anemia, and other immune disorders.

Expected outcomes
• Patient remains free from signs and symptoms of infection.
• Patient maintains adequate respiratory function.
• Patient states ways to prevent infection, including proper hand washing and good personal hygiene.

Nursing interventions and rationales
• Practice strict hand hygiene before and after patient contact to avoid spreading pathogens.
• Monitor the patient closely for signs and symptoms of infection, such as fever and chills. Check vital signs every 4 hours. Close monitoring allows for timely intervention.
• Maintain skin and mucous membrane integrity to help prevent infection. Encourage ambulation, and help turn the patient every 2 hours. Don’t give an enema or a suppository or take the patient’s rectal temperature. Encourage mouth care with sodium bicarbonate and natural saline rinse (1 teaspoonful per 8 oz) to inhibit microbial growth. Perform daily hygiene and oral assessment.

• Help the patient perform coughing and deep-breathing exercises to prevent pulmonary stasis. Removal of secretions helps prevent respiratory tract infections.
• Make sure visitors and staff members with upper respiratory tract infections wear masks when with the patient to protect him from pathogens.
• Teach the patient measures to minimize the risk of infection. Participating in his care encourages his compliance with therapy and lifestyle modifications.

Ineffective coping

Related to perceived or impending personal loss, Ineffective coping may be associated with life-threatening immunodeficiency disorders.

Expected outcomes
• Patient identifies mechanisms for coping effectively.
• Patient demonstrates an active role in self-care activities.
• Patient identifies appropriate resources to maximize his status.

Nursing interventions and rationales
• Encourage the patient and his family to discuss past coping mechanisms and their effectiveness. Doing this reinforces successful coping behaviors and fosters a sense of control.
• Urge the patient and his family to participate in care and ongoing decision making, to increase their sense of self-worth and mastery over the current situation and allow the patient to progress at his own pace.
• Refer the patient and his family to appropriate community resources as needed for continued support to restore and maintain psychological equilibrium and prevent future crisis.

Common immunologic disorders

Immunologic disorders range from mild ailments (such as hypersensitivity vasculitis) to life-threatening ones (such as anaphylaxis). Some are congenital, whereas others are acquired.
Immunologic disorders may result from:
• hyperreactivity, as in allergic rhinitis
• autoimmunity, as in SLE
• immunodeficiency, as in AIDS.

Acquired immunodeficiency syndrome

Marked by progressive weakening of cell-mediated immunity, AIDS increases susceptibility to opportunistic infections and unusual cancers. Diagnosis comes from careful correlation of the patient’s history and clinical features with counts of certain types of T cells.

Time and mortality

The time between probable exposure to the human immunodeficiency virus (HIV, the agent that causes AIDS) and diagnosis of AIDS averages 8 to 10 years. Children seem to have a shorter incubation time, with a mean of 8 months. Worldwide, more than 75% of AIDS patients die within 2 years of diagnosis. Patients may be HIV-positive and asymptomatic for varying periods.

What causes it
AIDS is caused by infection with HIV, a retrovirus present in body fluids, such as blood and semen. Modes of HIV transmission include:
• sexual contact, especially associated with trauma to the rectal or vaginal mucosa

• transfusion of contaminated blood or blood products
• use of contaminated needles
• placental transmission from an infected mother to a fetus through cervical or blood contact at delivery
• breast milk from an infected woman.

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Compromising circumstances

Risk factors for AIDS include:
• sexual contact with someone who has AIDS or is at risk for it
• present or past abuse of I.V. drugs
• transfusion of blood or blood products.
Prenatal and perinatal exposure to AIDS increases the risk of AIDS in infants, as does breast-feeding if the mother has AIDS or is at risk for it.

Pathophysiology
HIV attaches to helper T cells having an antigen called CD4+ on their surface. CD4+ serves as a receptor for the virus, allowing it to enter the cell. After invading the cell, HIV either replicates, leading to cell death, or the virus becomes latent.

By hook or by crook

HIV infection results in profound pathology—either directly or indirectly. Direct pathologic effects come about through destruction of CD4+ cells, other immune cells, and neuroglial cells. Indirect pathologic consequences occur through the secondary effects of CD4+ T-cell dysfunction and the resulting immunosuppression.

What to look for
After initial exposure, an infected person may have no signs or symptoms—or may have a flulike illness (seroconversion illness) and then remain asymptomatic for years.

Cunning contagion

However, as the syndrome progresses, he may have neurologic signs and symptoms caused by HIV encephalopathy or signs and symptoms of an opportunistic infection or disease, such as Pneumocystis jiroveci pneumonia, cytomegalovirus, or cancer. Eventually, repeated opportunistic infections overwhelm his weakened immune defenses, invading every body system.

What tests tell you
• The Centers for Disease Control and Prevention defines AIDS as a CD4+ cell count below 200 cells/μl or when a patient has an opportunistic infection in the setting of HIV infection.

• Enzyme-linked immunosorbent assay and a confirmatory Western blot assay detect HIV antibodies to diagnose HIV infection.
• Levels of circulating HIV (“viral load”) are measured regularly to assess the risk of disease progression and the patient’s response to therapy.

How it’s treated
Although no cure exists for AIDS, signs and symptoms can be managed with treatment. Primary therapy for HIV infection includes four categories of antiretroviral drugs:
• Reverse transcriptase inhibitors include nucleoside and non nucleoside reverse transcriptase inhibitors. Drugs in this category include abacavir (Ziagen), delavirdine (Rescriptor), didanosine, lamivudine, nevirapine (Viramune), tenofovir (Viread), and zido vudine (Retrovir).
• Protease inhibitors include fosamprenavir (Lexiva), i ndinavir (Crixivan), ritonavir (Norvir), saquinavir (Invirase), and tipranavir ( Aptivus).
• Fusion inhibitors include enfuvirtide (Fuzeon).
• Integrase inhibitors include raltegravir (Isentress). Used in various combinations, these drugs are designed to inhibit HIV viral replication.

Slowing things down

Treatment with zidovudine effectively slows the progression of HIV infection, decreasing the number of opportunistic infections, prolonging survival, and slowing the progress of associated dementia. However, the drug can cause severe adverse and toxic reactions.

Tweaking the immune system

Other drug therapies used in AIDS include immunomodulatory drugs, designed to boost the weakened immune system, and antiinfective and antineoplastic agents, used to combat opportunistic infections and associated cancers. HIV and AIDS drugs are the subject of a great deal of research. New drugs are constantly being developed, and many studies are under way to determine the optimal treatment regimens.

What to do
• Monitor the patient for fever, noting its pattern.
• Assess for tender, swollen lymph nodes, and check laboratory values regularly.
• Watch for signs and symptoms of infection, such as skin breakdown, cough, sore throat, and diarrhea.
• Watch for signs of oral candida infection (thrush).

• Follow standard precautions as directed by your facility, depending on the patient’s disease stage and condition.
• Offer support in coping with the social impact and discouraging prognosis of AIDS.
• Evaluate the patient. After counseling and treatment, he should be able to state the early signs and symptoms of infection, explain how HIV is transmitted, and describe the limitations AIDS may impose on his lifestyle. He also should be able to maintain an optimal nutritional status.

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Anaphylaxis

Anaphylaxis is an exaggerated hypersensitivity reaction to a previously encountered antigen. A severe anaphylactic reaction may induce vascular collapse, leading to systemic shock and, in some cases, death.

What causes it
An anaphylactic reaction results from systemic exposure to a sensitizing drug or other antigen, such as:
• penicillin (the most common cause) or other antibiotics
• serums
• vaccines
• allergen extracts
• enzymes
• hormones
• sulfonamides
• local anesthetics
• salicylates
• polysaccharides.

Toxic triggers

Anaphylaxis may also result from diagnostic chemicals (including radiographic contrast media containing iodine), foods, sulfites, insect venom (such as from a bee sting) and, rarely, a ruptured hydatid cyst (a liver cyst containing tapeworm larvae).

Pathophysiology
Here’s how an anaphylactic reaction occurs:

On initial exposure to an antigen, the immune system responds by producing IgE antibodies in the lymph nodes. Helper T cells enhance this process.

Antibodies bind to membrane receptors located on mast cells in connective tissues and on basophils.

The next time the person encounters this antigen, the IgE antibodies, or cross-linked IgE receptors, recognize it as foreign and activate the release of powerful chemical mediators.

What to look for
An anaphylactic reaction usually produces sudden distress within seconds or minutes after exposure to an allergen. (A delayed or persistent reaction may occur up to 24 hours later.) Severity of signs and symptoms depends on the original sensitizing dose of antigen, amount and distribution of antibodies, and the antigen’s entry route and dose.

Right out of the gate…

Initial signs and symptoms of anaphylaxis include:
• a feeling of impending doom or fright
• weakness
• sweating
• sneezing
• pruritus (itching)
• urticaria (an itchy skin eruption causing wheals) and angioedema (acute swelling of the face, neck, lips, larynx, hands, feet, genitalia, or internal organs)
• cardiovascular changes, such as hypotension, shock, and arrhythmias

• respiratory signs and symptoms, including swelling of the nasal mucosa, profuse runny nose, nasal congestion, sudden sneezing attacks, and hoarseness, stridor, and dyspnea (early signs of acute respiratory failure)
• GI and genitourinary signs and symptoms (severe stomach cramps, nausea, diarrhea, and urinary urgency and incontinence).

How it’s treated
Anaphylaxis is always an emergency. It requires an immediate injection of epinephrine 1:1,000 aqueous solution, repeated every 5 to 20 minutes as necessary.

Epi to the rescue

In the early stages of anaphylaxis, when the patient still has normal blood pressure and is conscious, give epinephrine I.M. or subcutaneously. Massage the injection site to help the drug move into circulation faster.
With severe reactions, when the patient has lost consciousness and is hypotensive, give epinephrine I.V.

What to do
• Maintain a patent airway. Observe the patient for early signs of laryngeal edema (stridor, hoarseness, and dyspnea), which typically necessitate endotracheal intubation or a tracheotomy and oxygen therapy. If he’s in cardiac arrest, begin cardiopulmonary resuscitation (CPR) at once.
• Watch for hypotension and shock, and maintain circulatory volume with volume expanders (plasma, saline solution, and albumin), as needed and ordered.
• After the initial emergency, give other medications as ordered: epinephrine solution or suspension subcutaneously, corticosteroids and diphenhydramine I.V. for long-term management, and aminophylline I.V. over 10 to 20 minutes for bronchospasm. Keep in mind that rapid aminophylline (Truphylline) infusion may cause or aggravate severe hypotension.
• If a patient must receive a drug to which he’s allergic, help prevent
a severe reaction by making sure he’s carefully desensitized beforehand with gradually increasing doses of the antigen or advance steroid administration.
• Evaluate the patient. On recovery, his blood pressure should be within normal limits and his respirations should be regular and unlabored.

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Asthma

A chronic reactive airway disorder, asthma causes episodic, reversible airway restriction with bronchospasm, increased mucus secretion, and mucosal edema. Although this common condition can strike at any age, children under age 10 account for 50% of the cases.

From within or without

Asthma can be intrinsic or extrinsic. Extrinsic asthma results from sensitivity to specific external allergens. In intrinsic asthma, the symptoms aren’t associated with an allergic reaction, and the immune system isn’t involved in the reaction.

All in the family?

About one-third of all asthmatics share the condition with at least one member of their immediate family, and roughly three-fourths of children with two asthmatic parents also have asthma.

What causes it
Extrinsic asthma follows exposure to pollen, animal dander, house dust or mold, pillows containing feathers or a silky material called kapok, food additives containing sulfites, or other sensitizing substances. Intrinsic asthma may be triggered by irritants, anxiety, fatigue, endocrine changes, temperature and humidity changes, or viruses.

Cataloging causes

Other causes of asthma include aspirin, various non steroidal antiinflammatory drugs (NSAIDs, such as indomethacin [Indocin] and mefenamic acid [Ponstel]), tartrazine (a yellow food dye), exercise, and occupational exposure to an allergenic factor (such as platinum).

Pathophysiology
In asthma, tracheal and bronchial linings overreact to various stimuli, causing episodic smooth-muscle spasms that severely narrow the airways. Mucosal edema and thickened secretions further block the airways.

There’s inflation…and then there’s hyperinflation

During an asthma attack, expiratory airflow decreases, trapping gas in the airways and causing alveoli to hyperinflate. Atelectasis (lung tissue collapse) may occur in some lung regions. Increased airway resistance leads to labored breathing.

What to look for
Usually, extrinsic asthma is accompanied by signs and symptoms of atopy (IgE-mediated allergy), such as eczema and allergic rhinitis. It commonly follows a severe respiratory tract infection, especially in adults.

Drama and distress

An acute asthma attack may begin dramatically, with simultaneous onset of severe multiple symptoms. Sometimes, however, onset is slow, with gradually increasing respiratory distress. Asthma that causes cyanosis, confusion, and lethargy indicates the onset of life-threatening status asthmaticus and respiratory failure.
Signs and symptoms of asthma include:
• sudden dyspnea, wheezing, and tightness in the chest
• coughing that produces thick, clear, or yellow sputum
• tachypnea and use of accessory respiratory muscles.
Other findings may include a rapid pulse, profuse perspiration, hyperresonant lung fields, and diminished breath sounds.

What tests tell you
• Pulmonary function studies reveal signs of obstructive airway disease (decreased flow rates and forced expiratory volume in 1 second), low-normal or diminished vital capacity, and increased total lung and residual capacity.
• Arterial blood gas analysis reveals reduced partial pressure of oxygen and partial pressure of arterial carbon dioxide (PaCO2). With severe asthma, PaCO2 may be normal or elevated, indicating severe bronchial obstruction.
• A chest X-ray may show lung hyperinflation, with areas of local atelectasis.
• Skin testing for specific allergens may be necessary if the patient lacks a history of allergy.
• Inhalation bronchial challenge testing evaluates the significance of allergens identified by skin testing.

How it’s treated
Treatment usually is tailored to each patient and focuses on identifying and avoiding precipitating factors, such as allergens or irritants. Usually, such stimuli can’t be removed entirely. Although desensitization to specific antigens may be helpful, it’s rarely totally effective or persistent.
Drug therapy usually includes a bronchodilator and proves more effective when begun soon after symptom onset. Other drugs used to treat asthma may include:
• rapid-acting epinephrine
• terbutaline
• long-acting beta agonists (Serevent) or short-acting beta agonists ( Maxair)
• theophylline and oral preparations containing theophylline
• oral sympathomimetics
• oral or inhaled corticosteroids
• cromolyn (Intal) to help prevent release of the chemical mediators (histamine and leukotrienes) that cause bronchoconstriction
• leukotriene receptor modifiers (Singulair) to help block inflammatory reactions in the lungs.

What to do
• During an acute asthma attack, take appropriate measures to maintain respiratory function and relieve bronchoconstriction, while allowing mucus plug expulsion.
• If the attack was caused by exertion, have the patient sit down, rest, and sip warm water.

Tempering the terror

• Severe breathing difficulty is terrifying. Reassure the patient that you’ll help him. Place him in semi-Fowler’s position, encourage diaphragmatic breathing, and urge him to relax as much as possible.
• Know that status asthmaticus unrelieved by epinephrine is a medical emergency. Severe hypoxemia may require endotracheal intubation and mechanical ventilation.
• Administer drugs and I.V. fluids as ordered.
• Evaluate the patient. With successful treatment, his respirations should be regular and unlabored, and he should exhibit signs of adequate gas exchange, such as absence of cyanosis and confusion. Also, the patient and his family should be able to identify predisposing factors and state measures to eliminate them.

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Systemic lupus erythematosus

A chronic inflammatory disorder of the connective tissue, SLE affects multiple organ systems (as well as the skin) and can be fatal. It’s marked by recurring remissions and exacerbations, which are especially common during the spring and summer. SLE strikes eight times as many women as men, increasing to 15 times as many during childbearing years. SLE occurs worldwide, and is most prevalent among Asians and blacks.

Prognosis: Mixed

The prognosis improves with early detection and treatment but is poor for patients who develop cardiovascular, renal, or neurologic complications or severe bacterial infections. About 1 out of 20 patients with discoid lupus erythematosus, another form of lupus erythematosus, later develops SLE.

What causes it
The cause of SLE remains a mystery, but evidence points to interrelated immunologic abnormalities and environmental, hormonal, and genetic factors as possible causes.

A grab bag of causes

Factors that may increase the risk of SLE exacerbation include:
• genetic predisposition
• stress
• streptococcal or viral infections
• exposure to sunlight or ultraviolet light
• immunization

• pregnancy
• abnormal estrogen metabolism.
Medications that increase the risk of SLE include procainamide, hydralazine, anticonvulsants and, less commonly, penicillins, sulfa drugs, and hormonal contraceptives.

Pathophysiology
Autoimmunity is thought to be the prime mechanism associated with SLE. The body produces antibodies against components of its own cells, resulting in immune complex disease. Patients with SLE may produce antibodies against various tissue components (such as RBCs, neutrophils, platelets, lymphocytes) or virtually any organ or tissue in the body.

What to look for
Characteristic findings in SLE include facial erythema (butterfly rash), nonerosive arthritis, and photosensitivity.

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A rash of reactions

The patient may also experience discoid rash (an itchy, scaly, or flaky round or oval rash most common on the face, scalp, neck and chest after sun exposure), oral or nasopharyngeal ulcers, pleuritis, pericarditis, seizures, patchy alopecia, and even psychoses. The patient also commonly has some combination of these systemic signs and symptoms: aching, malaise, fatigue, low-grade or spiking fever, chills, anorexia, weight loss, lymph node enlargement, abdominal pain, nausea and vomiting, diarrhea or constipation, Raynaud’s phenomenon, and irregular menses or amenorrhea.

What tests tell you
• For most patients with active disease, antinuclear antibody, anti-DNA, and lupus erythematosus cell tests are the most specific SLE tests.
• Complete blood count with differential may show anemia and decreased WBC counts. Platelet count may also be decreased.
• Erythrocyte sedimentation rate may be elevated.
• Serum electrophoresis may show hypergammaglobulinemia (an excess of gamma globulins in the blood).
• Urine studies may show urinary RBCs and WBCs, urine casts and sediment, and significant urine protein loss (more than 3.5 g/24 hours).
• Blood studies showing decreased serum complement (C3 and C4) levels indicate active disease.
• A chest X-ray may show pleurisy or lupus pneumonitis (lung inflammation).

How it’s treated
Patients with mild disease need little or no medication. Aspirin and other NSAIDs may control arthritis symptoms. Skin lesions require topical treatment. For acute lesions, corticosteroid creams are recommended. Refractory skin lesions are treated with intralesional corticosteroids or antimalarial drugs, such as hydroxychloroquine (Plaquenil) and chloroquine (Aralen).

Systemic symptoms? Stick with steroids

Corticosteroids remain the treatment of choice for systemic symptoms of SLE, acute generalized exacerbations, and serious disease related to vital organ systems (such as pleuritis, pericarditis, lupus nephritis, vasculitis, and central nervous system involvement).

What to do
• Watch for such signs and symptoms as joint pain or stiffness, weakness, fever, fatigue, and chills, and provide comfort measures for the patient.
• Observe the patient for dyspnea, chest pain, and edema of the arms and legs.
• Note the size, type, and location of skin lesions.
• Check the urine for blood.
• Inspect the scalp for hair loss, and check skin and mucous membranes for petechiae (tiny purplish spots indicating minute hemorrhages), bleeding, ulcers, pallor, and bruising.
• Provide a balanced diet. A patient with renal involvement may require a low-sodium, low-protein diet.
• Apply heat packs to relieve joint pain and stiffness. Encourage regular exercise to maintain full range of motion and prevent contractures.
• Monitor vital signs, fluid intake and output, weight, and laboratory findings.
• Evaluate the patient. With successful therapy, she should be free from pain and stiffness and her vital signs should be within normal limits.

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