N304 Exam 1

Front 1

What is lupus erythematosus?

Back 1

1. A chronic, progressive, connective tissue disorder characterized by immune dysregulation resulting in the production of ANA and generation of immune complexes

2. Characterized by spontaneous remissions and exacerbations

3. Potentially fatal

Front 2

Which group is primarily affected by lupus?

Back 2

Women of child-bearing age (15-40 years)

Front 3

What are the classifications of lupus?

Back 3

1. Discoid lupus erythematosus (DLE)
2. Cutaneous lupus erythematosus
3. Systemic lupus erythematosus (SLE)

Front 4

What is discoid lupus erythematosus (DLE)?

Back 4

1. Characterized by skin rash only—patchy, crusty, sharply defined skin plaques that may scar, usually seen on the face or other sun-exposed areas

2. Usually unaccompanied by ANA or other autoantibodies

3. DLE only rarely progresses to SLE (approx. 10%)

Front 5

What % of DLE progresses to SLE?

Back 5

10%

Front 6

What is a main clinical manifestation of SLE?

Back 6

Butterfly rash on the face

Front 7

What are other symptoms of SLE?

Back 7

1. Pleural effusions
2. Heart problems
3. Arthritis
4. Lupus nephritis
5. Raynaud's phenomenon

*symptoms may vary widely among individuals

Front 8

What is Raynaud's phenomenon?

Back 8

The characteristic red, white, and blue color changes and severe pain in the digits that are caused by arteriolar vasospasm

Front 9

What is the etiology of SLE?

Back 9

Immune system dysfunction — suppressor T-cells are unable to suppress the production of lymphocytes against self-antigens; number of autoantibodies are allowed to proliferate, attacking its own

Front 10

What is the genetic factor of SLE?

Back 10

Genetics-increased prevalence of SLE among identical twins and first and second degree relatives

Front 11

What is the hormone factor of SLE?

Back 11

Hormones — more prevalent in women during reproductive years (15-40 years)

Front 12

Which ethnic groups are more commonly affected by SLE?

Back 12

Three times more common in African American blacks; also more common among Asians

Front 13

What environmental factors influence SLE?

Back 13

1. Sunlight
2. Stress
3. Chemical Substances
4. Viruses

Front 14

What is the effect of sunlight on SLE?

Back 14

Exposure to UVB light causes certain cellular proteins to accumulate in abnormally large amounts on the cell’s surface and react with autoantibodies, leading to a local or systemic inflammatory response

Front 15

What is the effect of stress on SLE?

Back 15

1. Unclear

2. Patients ascribe first symptoms to a stressful event. Need to examine role of stress hormones (adrenaline, cortisone).

Front 16

What is the effect of chemical substances on SLE?

Back 16

Produces symptoms similar to SLE — Chlorpromazine, Hydralazine, Isoniazid, Methyldopa, Procainamide. Proven association.

Front 17

Which chemical substances have been proven to produce similar symptoms to SLE?

Back 17

1. Chlorpromazine
2. Hydralazine
3. Isoniazid
4. Methyldopa
5. Procainamide

Front 18

What is the effect of viruses on SLE?

Back 18

May possibly infect B cells and produce autoantibodies

Front 19

What is the pathophysiology of SLE?

Back 19

1. Abnormal suppressor T cell functions

2. Increased production of autoantibodies against nucleic acid, single-stranded and double-stranded DNA

3. As a result, immune complexes form in the serum and organ tissues which cause inflammation and damage

4. These complexes invade organs directly or cause vasculitis which deprives organs/tissues of blood and oxygen

Front 20

What are the integumentary clinical manifestations of SLE?

Back 20

1. Characteristic butterfly-shaped rash across the bridge of the nose and cheeks (dry, scaly, raised rash), or discoid lesions.

2. Alopecia

Front 21

What are the musculo-skeletal clinical manifestations of SLE?

Back 21

1. Polyarthritis in 90% of patients similar to those seen in RA

2. Muscle atrophy from disuse or from skeletal invasion by immune complexes (myositis)

3. Myalgia (muscle pain)

4. Avascular necrosis often seen on clients on long term steroid therapy. Chronic steroid use cause constriction of small blood vessels supplying the joint which causes the tissue to die.

Front 22

What causes avascular necrosis?

Back 22

Chronic steroid use cause constriction of small blood vessels supplying the joint which causes the tissue to die

Front 23

What are the renal clinical manifestations of SLE?

Back 23

Nephritis– approx. 50% of clients with SLE have some type of nephritis (glomerular changes leading to renal failure)

Front 24

What is the leading cause of death in SLE?

Back 24

Lupus nephritis

Front 25

What symptoms should be assessed is lupus nephritis?

Back 25

1. Changes in urine output
2. Proteinuria
3. Hematuria
4. Fluid retention

Front 26

What are the cardiovascular clinical manifestations of SLE?

Back 26

1. Pericarditis
2. Raynaud’s Phenomenon

Front 27

What is the most common cardiovascular clinical manifestation of SLE?

Back 27

Pericarditis

Front 28

What is the effect of pericarditis on SLE?

Back 28

Causes tachycardia, chest pain and myocardial ischemia

Front 29

What is the prevalence of Raynaud's phenomenon?

Back 29

15% of SLE

Front 30

What are the respiratory clinical manifestations of SLE?

Back 30

Pleural effusions or pneumonia are found in 50% of clients with SLE

Front 31

What are the neural clinical manifestations of SLE?

Back 31

1. Possible pyschoses, paresis, seizures, migraine headaches, cranial nerve palsies

2. Peripheral neuropathy

Front 32

What are the gastrointestinal clinical manifestations of SLE?

Back 32

1. Abdominal pain — maybe due to serositis (peritoneal involvement), mesenteric arteritis, pancreatitis, or colonic ulcers

2. Hepatomegaly

3. Splenomegaly

4. Lymph node enlargement

Front 33

What are the other clinical manifestations of SLE?

Back 33

1. Fever — classic sign of a flare or exacerbation

2. Generalized weakness

3. Fatigue in 90% of patients

4. Anorexia

5. Weight Loss

Front 34

How is SLE diagnosed?

Back 34

Extremely difficult to diagnose because the symptoms affect almost every body systems and because the symptoms tend to come and go (remissions and exacerbations)

Front 35

What laboratory tests are used to diagnose SLE?

Back 35

1. No single laboratory test can definitely prove or disprove SLE

2. The American College of Rheumatology (ACR) developed a set of diagnostic criteria

Front 36

How does the American College of Rheumatology (ACR) set of diagnostic criteria help determine SLE?

Back 36

Presence of at least 4 criteria indicates SLE

Front 37

What are the diagnostic criteria for SLE according to the American College of Rheumatology (ACR)?

Back 37

1. Facial rash confined to the cheeks (malar rash)
2. Discoid rash (raised patches, scaling)
3. Photosensitivity (skin rash developed as a result of exposure to sunlight)
4. Oral or nasopharyngeal ulcers
5. Nonerosive arthritis of at least 2 peripheral joints.
6. Serositis--inflammation of serous membrane such as the pleura and pericardium (pleurisy, pericarditis). One of the cardinal findings in SLE.
7. Renal disorder (proteinuria or cellular casts)
8. Neurologic disorders (seizures or psychoses)
9. Hematologic Disorders (hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia)
10. Immunologic disorders (positive LE cell prep, anti-double-stranded DNA, anti-Smith antigen, false-positive VDRL syphilis test, antiphospholipid antibodies)
11. Presence of AntiNuclear Antibody (ANA)

Front 38

What is one of the cardinal findings in SLE?

Back 38

Serositis

Front 39

What is serositis?

Back 39

Inflammation of serous membrane such as the pleura and pericardium (pleurisy, pericarditis)

Front 40

What laboratory assessments for conducted with SLE?

Back 40

1. ANA
2. Complements
3. C-reactive protein
4. ESR
5. SPE
6. CBC
7. Chemistry, lytes,cardiac and liver enzymes, clotting factors
8. Renal functions
9. Kidney biopsy

Front 41

What does the ANA lab assessment yield with SLE?

Back 41

1. Positive in close to 100% of patients with SLE

2. Anti-Smith antibody (ribonucleoprotein found in cell nucleus) — positive in 30% of SLE patients

3. Anti-nDNA (native or double-stranded DNA) — 60-80 % positive in SLE patients

Front 42

What does the complement lab assessment yield with SLE?

Back 42

C3 and C4 levels are decreased

Front 43

What does the C-reactive protein lab assessment yield with SLE?

Back 43

Elevated levels

Front 44

What is C-reactive protein?

Back 44

CRP (C-Reactive Protein) is a protein produced primarily by the liver during an acute inflammatory process and other diseases. A positive test result indicates the presence, but not the cause of disease. The synthesis of CRP is initiated by antigen-immune complexes, bacteria, fungi, and trauma. CRP is functionally analogous to IgG except that it is not antigen-specific. The CRP test is a more sensitive and rapidly responding indicator than the ESR. In an acute inflammatory change, CRP shows an earlier and more intense increase than ESR; with recovery, the disappearance of CRP precedes the return of ESR to normal. The CRP disappears when the inflammatory process is suppressed by anti-inflammatory agents, salicylates or steroids.

Front 45

What does the ESR lab assessment yield with SLE?

Back 45

Elevated rates of sedimentation (therefore increased clotting time)

Front 46

What does the SPE lab assessment yield with SLE?

Back 46

Increased levels of gammaglobulins

Front 47

What does the CBC lab assessment yield with SLE?

Back 47

May show pancytopenia caused by direct attack of the blood cells or bone marrow by immune response

Front 48

What is the purpose of the chemistry, lytes,cardiac and liver enzymes, clotting factors assessments?

Back 48

Chemistry, lytes,cardiac and liver enzymes, clotting factors to assess body system functioning

Front 49

What tests are conducted to assess renal function?

Back 49

1. Creatinine
2. Creatinine Clearance
3. UA (proteinuria, casts)

Front 50

What is the purpose of the kidney biopsy?

Back 50

Kidney biopsy to determine presence of immune complexes and glomerular inflammation

Front 51

What are the types of pharmacotherapy for SLE?

Back 51

1. ASA

2. NSAIDS

3. Corticosteroids

4. Gold salts

5. Immunosuppressive agents — Imuran, Cytoxan

6. Plaquenil — to decrease inflammatory response

7. Plasmapheresis

8. Renal transplantation

Front 52

What is plasmapheresis?

Back 52

The removal of plasma from previously withdrawn blood by centrifugation, reconstitution of the cellular elements in an isotonic solution (with albumin), and reinfusion of this solution into the donor or another client who needs red cells rather than whole blood. This method removes the antibodies that cause the disease.

Front 53

What are the nursing diagnoses of SLE?

Back 53

1. Fatigue
2. Body image disturbance
3. Pain
4. Altered tissue perfusion
5. Knowledge deficit: Preventing Lupus Flare

Front 54

What are the interventions for fatigue?

Back 54

1. Evaluate for factors that may exacerbate fatigue such as overexertion, insomnia, depression, stress, anemia

2. Adequate rest, healthful diet, exercise, attention to psychosocial factors

Front 55

What are the interventions for body image disturbance?

Back 55

1. 80% of SLE patients have skin manifestations, alopecia, painful skin ulcers, pruritus

2. Minimize direct exposure to UV rays from sun and from fluorescent and halogen light bulbs

3. Use of sunscreen 15-30 SPF

4. Provide info on hypoallergenic make-up

5. Keep warm (pts. with Raynaud’s phenomenon)

Front 56

What are the interventions for pain?

Back 56

1. Arthralgia experienced by 95% of SLE patients

2. Pain management — NSAIDs, heat or cold therapy, splints/braces, ROM exercises

Front 57

What are the interventions for altered tissue perfusion?

Back 57

1. CMST

2. Stress importance of not smoking

3. Avoid cold temperatures, teach s/s vascular impairment

Front 58

What are the warning signs of a lupus flare?

Back 58

1. Increased fatigue
2. A new or higher fever
3. Increased pain
4. Development or worsening of a rash
5. GI upset
6. Headache or dizziness

Front 59

What are the client teachings regarding SLE?

Back 59

1. Avoid prolonged exposure to sunlight or other forms of UV lighting

2. Wear long sleeves and large-brimmed hat when outdoors

3. Use sunscreen with an SPF of 15 or higher

4. Clean skin with mild soap

5. Moisturize/lotion to dry skin areas

6. Use mild shampoo and avoid perms or frostings

7. Delay elective surgery, including dental surgery, until in remission

8. Carefully plan pregnancy until in remission. 25% of lupus pregnancies end in miscarriages or stillbirth; 25 % premature births

9. Pregnancy-induced HTN may occur