1. SYSTEMIC LUPUS ERYTHEMATOSIS

2. INTRODUCTION

3. DEFINITION
 SLE is a chronic multisystem inflammatory disease
of autoimmune in origin

4. INCIDENCE
 More women are affected than men

5. ETIOLOGY
 Viral infection
 Genetic factors
 bacterial infection
 drugs, (Sulpha drugs hydralazine procainamide)
 Purperium
 Exposure to sunlight, sun burns
 Hormones

6. PATHOPHYSIOLOGY

7. CLINICAL MANIFESTATIONS
 Skin
 Butterfly-shaped rash
 Discoid lesions are ring-shaped
 Discoid lesions may also result in
erythematous, scaly plaques

8. ARTHRITIS:
 Generally bilateral and symmetric,.
 Can resemble RA
 Unlike RA, the arthritis is non erosive;.
 Tendon involvement is common

9. CARDIAC
 Pericarditis.
 Pleural effusion.
 Myocarditis.
 Endocarditis.
 Coronary arteritis—less common.

10. PULMONARY:
 Pleuritis.
 Pleural effusion.
 Lupus pneumonitis.
 Pulmonary hemorrhage.
 Pulmonary embolism.

11. GASTROINTESTINAL.
 Oral ulcers.
 Acute or sub acute abdominal pain.
 Pancreatitis.
 Spontaneous bacterial peritonitis.
 Bowel infarction.

12. RENAL:
 Nephritis.
 Focal segmental glomerulonephritis
 Proliferative
 Membranous nephritis

13. CENTRAL NERVOUS SYSTEM:
 Neuropsychiatric disorders.
 Depression
 Psychosis.
 Transient ischemic attacks/stroke.
 Epilepsy.
 Migraine headache.
 Myleopathy.
 Guillain-Barre syndrome.
 Chorea and other movement disorders.

14. HEMATOLOGIC:
 Hemolytic anemia.
 Leucopenia.
 Thrombocytopenia

15. CONSTITUTIONAL:
 Fever.
 Weight loss.
 Fatigue.

16. DIAGNOSTIC EVALUATION
 CBC
 ESR
 Complement levels
 Urinalysis
 24-hour urine for protein and creatinine clearance.
 Chest x-ray
 Computed tomography (CT) scan or MRI.

17. MANAGEMENT
 Pharmacologic
 NSAIDs—to reduce pain and inflammation.
 Antimalarials—to decrease disease activity.
 Corticosteroids—to reduce inflammatory process.
 Immunosuppressive—to suppress immune process

18. NON PHARMACOLOGIC
 Avoid direct exposure to sunlight to reduce the
chance of exacerbation.
 Behavior modification to prevent exacerbations and
to reduce symptoms.
 Joint protection and energy conservation.

19. OTHER MANAGEMENT
 Close follow-up for evaluation of
cardiac, neurologic, renal, and other body systems.
 Referral to specialists for systemic manifestations.

20. NURSING ASSESSMENT
 Obtain clinical history, review systems, and perform
physical examination for characteristic findings.
 Assess for signs and symptoms of infection and
other side effects to medications.
 Assess patient's and family's ability to cope with
impact of prolonged disease.

21. NURSING DIAGNOSES
 Fatigue related to chronic inflammation and altered
immunity as evidenced by lack of energy inability to
maintain usual routine
 Acute pain related to inflammatory process and
inadequate comfort measures as evidenced by
complaints of joint pain lack of relief from pain
relieving measures ,reduction of activity to avoid
exacerbation of pain

22.  Impaired skin integrity related to photosensitivity
,skin rash ,and alopecia as evidenced by rash
anywhere on body butterfly rash on face hairless
areas of ulceration on fingertips, complaints of
urticaria and photosensitivity
 Knowledge deficit related to lack of exposure to and
unfamiliarity with information resources as
evidenced by questions about SLE
misinterpretation of information and inaccurate
follow -through of instruction

23. NURSING INTERVENTIONS REDUCING PAIN
 Administer and teach self-administration of
medications
 use of hot or cold applications, relaxation
techniques

24. INCREASING CONTROL OVER DISEASE
PROCESS
 Instruct patient to avoid factors that may exacerbate
disease.
 Avoid exposure to sunlight and ultraviolet light.
 Use sunscreen with sun protection factor (SPF)of 15 or
greater. Avoid prolonged sun exposure.
 Wear protective, lightweight clothing, long sleeves, hats.
 Avoid use of tanning beds.
 Avoid exposure to drugs and chemicals.
 Avoid exposure to hair spray
 Avoid exposure to hair-coloring agents.

25. MEDICATIONS
 Teach self-administration of pharmacologic agents to
reduce disease activity.
 Encourage good nutrition, sleep
habits, exercise, rest, and relaxation to improve general
health and to help prevent infection.
 Encourage ventilation of feelings, counseling, or
referrals to social work, occupational therapy, as
needed.

26. MAINTAINING SKIN AND MUCOUS MEMBRANE
INTEGRITY
 Apply topical corticosteroids to skin lesions as
ordered.
 Suggest alternative hairstyles, scarves, and wigs to
cover significant areas of alopecia.
 Encourage good oral hygiene and inspect mouth for
oral ulcers.
 Avoid hot or spicy foods that may irritate oral ulcers.
 Apply topical agents or analgesics to reduce pain
and
to promote eating.

27. REDUCING FATIGUE
 Advise patient that fatigue level will fluctuate with
disease activity.
 Encourage patient to modify schedule to include
several rest periods during the day, pace activity
and exercise according to body's tolerance, use
energy conservation techniques in daily activities.
 Teach relaxation techniques, such as deep
breathing, progressive muscle relaxation, and
imagery to reduce emotional stress that causes
fatigue.

28. PRESERVING URINARY ELIMINATION
 Assist with monitoring of urinary status as indicated
by degree of renal involvement.
 Monitor intake and output and urine specific gravity.
 Measure urine protein, micro albumin, or obtain24-
hour creatinine clearance, as ordered.
 Check test results of serum blood urea nitrogen
(BUN) and creatinine.

29. PATIENT EDUCATION AND HEALTH
MAINTENANCE
 Stress that close follow-up is mandatory, even in
times of remission, to detect early progression of
organ involvement and to alter drug therapy.
 Advise on the use of special cosmetics to cover
skin lesions.Advise about reproduction.
 Avoid pregnancy during time of severe disease
activity.
 Immunomodulators may have teratogenic effects.
 Use of some drugs for treatment of SLE can result
instability.

30. COMPLICATIONS
 Renal failure.
 Permanent neurologic impairment.
 Infection.

31. GOUT

32. INTRODUCTION

33. DEFINITION
 Gout is a disorder of purine metabolism
characterized by elevated uric acid levels and
deposition of urate in joints and other tissues

34. INCIDENCE
 more commonly in men, middle aged men are more
affected

35. ETIOLOGY
 Common causes
 Under excretion of uric acid
 Medications and chemicals

36. COMMON CAUSES
 Inherited enzyme defects.
 Certain disease conditions:
 Myelo proliferative disorders.
 Lymphoproliferative disorders.
 Cancer chemotherapy.
 Hemolytic anemias.
 Psoriasis.

37. UNDER EXCRETION OF URIC ACID (90% OF
CASES)
 Renal disease.
 Endocrine disorders

38. MEDICATIONS AND CHEMICALS:
 Diuretics.
 Ethanol (alcohol).
 Low-dose aspirin.
 Pyrazinamide— anti tuberculosis agent.
 Lead.
 Volume depletion states—nephrogenic diabetes
insipidus.

39. PATHOPHYSIOLOGY
 Uric acid is the major end product of purine
catabolism and is primarily excreted by the kidneys
hyperuricemia may be result of of increased purine
synthesis decreased renal excretion or both, Gout
results from an overabundant accumulation and
subsequent deposition of uric acid in the body.

40. CLINICAL MANIFESTATIONS ACUTE GOUTY
ARTHRITIS
 Generally affects one joint—often first
metatarso-phalangeal joint
 Other joints can be affected, such as ankle, knee;
upper extremities are less commonly involved.
 Pain, warmth, erythema, and swelling of tissue
surrounding the affected joint.
 Fever may occur.
 Onset of symptoms is sudden; intensity is severe.
 Duration of symptoms is self-limiting; lasts
approxi-mately 3 to 10 days without treatment

41. CHRONIC TOPHACEOUS GOUT
 Occurs if acute gout is inadequately treated or if it
goes untreated.
 Characterized by development of tophi or deposits
of uric acid in and around joints, cartilage, and soft
tissues.
 Arthritis is more prolonged in nature with discrete
attacks less common.

42. RENAL DISEASE
 Caused by hyperuricemia (persistent elevation of
uric acid in the blood).
 Kidney stones are composed of uric acid.
 Deposition of uric acid in kidney tissue.

43. DIAGNOSTIC EVALUATION
 Synovial fluid analysis.
 Identification of monosodium urate crystals under
polarized microscopy.
 Synovial WBC count can range from 2,000 to
100,000/mm3.
 Culture of synovial fluid to rule out infection.
 24-hour urine for uric acid to determine
overproduction of uric acid versus under excretion.
 ESR—elevated.
 X-rays of affected joints show changes consistent
with diagnosis of gout.

44. PHARMACOLOGIC MANAGEMENT
 NSAIDs—for acute attacks to relieve pain and
swelling.
 Colchicines—for prevention of acute attacks and
their treatment.
 Oral at onset of an attack, taken hourly until pain
relief or first signs of toxicity (nausea, vomiting
,cramping, diarrhea

45. CORTICOSTEROIDS.
 Intra-articular if attack confined to one joint.
 Oral—in short tapering course if other treatments
are contraindicated or if attack involves many joints.

46. URATE-LOWERING AGENTS
 Uricosuric drugs, such as probenecid
(Benamid), inter-fere with
 tubular reabsorption of uric acid.
 Allopurinol (Zyloprim)—interferes with conversion of
hypoxanthine and xanthine to uric acid.

47. NONPHARMACOLOGIC
 Avoidance of obesity.
 Avoidance of alcohol.
 Low-purine diet gives only a minor decrease in
serum uric acid levels.

48. NURSING ASSESSMENT
 Obtain history for factors predisposing to gout.
 Perform physical examination.
 Inspect involved joint.
 Observe for tophi:
a) Pinna of ear.
b) Olecranon bursa
c) Achilles tendon.
 Assess pain and pain relief pattern if attack is acute

49. NURSING INTERVENTIONS RELIEVING PAIN
 Administer and teach self-administration of pain
relieving medications as prescribed.
 Encourage adequate fluid intake to assist with
excretion of uric acid and to decrease likelihood of
stone formation.
 Instruct patient to take prescribed medications
consis-tently because interruptions in therapy can
precipitate acute attacks.

50. FACILITATING MOBILITY
 Elevate and protect affected joint during acute
attack.
 Assist with activities of daily living.
 Encourage exercise and maintenance of routine
activity in chronic gout, except during acute attacks.
 Protect draining tophi by covering and applying
anti-biotic ointment as needed.

51. PATIENT EDUCATION
 Instruct patient and family about nature of disease.
 Encourage to avoid alcohol.
 Avoid rapid weight loss by fasting or crash
 Avoid medications known to increase uric acid
levels.
 Advise prompt treatment of acute attack
 Instruct in signs and symptoms of allopurinol
hyper-sensitivity
 Review foods containing purine

52. COMPLICATIONS
 Uric acid kidney stone.
 Urate nephropathy.
 deforming arthritis

53. SIDE EFFECTS OF TREATMENT
 Include skin rash
 hypersensitivity syndrome
 renal failure
 bone marrow depression

54. EVIDENCE BASED RESEARCH

55. CONCLUSION

56. BIBLIOGRAPHY

57. Thank you