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Terms
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- Hypersensitivity or Allergy
-
* A state of increased or excessive response to the presence of an antigen (foreign protein or allergen) to which the patient has been previously exposed.
* Symptoms range from uncomfortable feelings (sneezing) to life threatening reactions (anaphylaxis) - IMMUNITY
-
- IS COMPOSED OF MANY CELL FUNCTIONS THAT PROTECT PEOPLE AGAINST THE EFFECTS OF INJURY OR MICROSCOPIC INVASION
- AS LONG AS MICROORGANISMS DO NOT ENTER THE BODYÂ’S INTERNAL ENVIORMENT, THEY POSE NO THREAT TO HEALTH - DEFENSE- FOUR SYSTEMS
-
- SKIN AND MUCOUS MEMBRANES
- INFLAMMATORY RESPONSE
- MONONUCLEAR PHAGOCYTE
- IMMUNE SYSTEM - INFLAMMATORY RESPONSE
-
- VASCULAR RESPONSE-PHASE 1 AND PHASE 2
- CELLULAR RESPONSE
- FORMATION OF EXUDATE AND HEALING - INFLAMMATION IS ALWAYS PRESENT WITH INFECTION
- BUT INFECTION IS NOT ALWAYS PRESENT WITH INFLAMMATION
- VASCULAR RESPONSE PHASE 1
-
- IMMEDIATE SHORT TERM CONSTRICTION OF ARTERIOLES AND VENULES AS A DIRECT RESULT OF TRAUMA
- LASTING SECONDS TO MINUTES - VASCULAR- PHASE 2
-
- INCREASED BLOOD FLOW TO THE AREA
- SWELLING (EDEMA FORMATION)
- INJURED TISSUES AND LEUKOCYTES IN THIS AREA SECRETE VASOACTIVE CHEMICALS (HISTAMINES, SEROTONIN, KININS) - VASCULAR –PHASE 2
-
- THESE VASOACTIVE CHEMICALS CAUSE CONSTRICTION OF THE SMALL VEINS AND DILATION OF THE ARTERIOLES IN THE IMMEDIATE AREA, LEADING TO REDNESS AND INCREASE WARMTH
- INCREASING THE SUPPLY OF NUTRIENTS TO THE AREA BY INCREASING BLOOD FLOW
VASCULAR PHASE 2
- PAIN INCREASES THE PERSONS AWARENESS THAT A PROBLEM EXISTS AND ENCOURAGES FURTHER ACTION
- SWELLING CREATES A CUSHION OF FLUID AND DILUTES THE CONCENTRATION OF TOXINS - CELLULAR RESPONSE- NEUTROPHILS
-
- NEUTROPHILS ARE THE FIRST LEUKOCYTES TO ARRIVE (6-12 HOURS) THEY ENGULF BACTERIA, FOREIGN MATERIAL AND DAMAGED CELLS
- DEAD NEUTROPHILS, DIGESTED BACTERIA, AND OTHER CELL DEBRIS ACCUMULATE FORMING PUS - CELLULAR RESPONSE
-
- TO KEEP UP WITH THE DEMAND FOR NEUTROPHILS, THE BONE MARROW WILL INCREASE MORE NEUTROPHILS INTO CIRCULATION, RESULTING IN AN ELEVATED WHITE COUNT
- SOMETIMES THE DEMAND FOR NEUTROPHILS INCREASES SO MUCH THAT THE BONE MARROW RELEASES IMMATURE FORMS INTO CIRCULATION (SHIFT TO THE LEFT) - CELLULAR RESPONSE - MONOCYTES
-
- SECOND TYPE OF PHAGOCYTIC CELLS THAT MIGRATE (3-7 DAYS)
- TRANSFORM INTO MACROPHAGES
- CLEAN THE AREA SO HEALING CAN BEGIN
TISSUE REPAIR AND REPLACEMENT
- BEGINS AT THE TIME OF INJURY
- LEUKOCYTES INDUCE THE REMAINING HEALTHY TISSUE TO DIVIDE
- REPAIR- PRIMARY, SECONDARY AND TERTIARY INTENTION - NORMAL IMMUNE RESPONSE
- - IMMUNITY IS A STATE OF RESPONSIVENESS TO FOREIGN SUBSTANCES SUCH AS MICROORGANISM AND TUMOR PROTIENS
- THREE FUNCTIONS OF THE IMMUNE RESPONSE
-
- DEFENSE- PROTECTS AGAINST INVASIONS BY ATTACKING FOREIGN ANTIGENS AND PATHOGENS
- HOMEOSTASIS- DAMAGED CELLULAR SUBSTANCES ARE DIGESTED AND REMOVED
- SURVEILLANCE- MUTATIONS ARE RECOGNIZED AS FOREIGN AND DESTROYED - TYPES OF IMMUNITY
-
- INNATE- EXISTS IN A PERSON WITHOUT PRIOR CONTACT WITH AN ANTIGEN
- AQUIRED- THE DEVELOPMENT OF IMMUNITY EITHER ACTIVE OR PASSIVE - ACTIVE AQUIRED IMMUNITY
- - ACTIVE- RESULTS FROM THE INVASION OF THE BODY BY FOREIGN SUBSTANCES AND DEVELOPMENT OF ANTIBODIES AND SESITIZED LYMPHOCYTES, MAY RESULT NATURALLY OR ARTIFICIALLY
- PASSIVE AQUIRED IMMUNITY
- - THE HOST RECIEVES ANTIBODIES TO AN ANTIGEN RATHER THEN SYNTHESIZING THEM- MOTHER TO FETUS- ARTIFICIAL OCCURS THROUGH INJECTION WITH SERUM ANTIBODIES, IMMEDIATE EFFECT THOUGH SHORT LIVED
- ANTIGEN
- - A SUBSTANCE THAT ILLICITS AN IMMUNE RESPONSE, MOST ARE COMPOSED OF PROTIENS. ALL OF THE BODYÂ’S CELLS HAVE ANTIGENS ON THEIR SURFACE THAT ARE UNIQUE TO THAT PERSON AND ENABLE THE BODY TO RECOGNIZE SELF
- LYMPHOID ORGANS
-
- CENTRAL LYMPHOID- THYMUS GLAND AND BONE MARROW
- PERIPHERAL- TONSILS, GUT, GENITAL, BRONCHIAL AND SKIN ASSOCIATED LYMPHOID TISSUE, LYMPH NODES AND SPLEEN
CELLS INVOLVED IN THE IMMUNE RESPONSE - - MONONUCLEAR PHAGOCYTES-
- MONOCYTES IN THE BLOOD AND MACROPHAGES FOUND THROUGHOUT THE BODY. MONONUCLEAR PHAGOCYTES HAVE A CRUCIAL ROLE, RESPONSIBLE FOR CAPTURING, PROCESSING, AND PRESENTING THE ANTIGEN TO THE LYMPHOCYTE
-
CELLS INVOLVED IN THE IMMUNE RESPONSE
- MONONUCLEAR PHAGOCYTES- -
MONOCYTES IN THE BLOOD AND MACROPHAGES FOUND THROUGHOUT THE BODY. MONONUCLEAR PHAGOCYTES HAVE A CRUCIAL ROLE, RESPONSIBLE FOR CAPTURING, PROCESSING, AND PRESENTING THE ANTIGEN TO THE LYMPHOCYTE
- THIS STIMULATES A HUMORAL OR CELL MEDIATED IMMUNE RESPONSE. CAPTURING IS ACCOMPLISHED THROUGH PHAGOCYTOSIS, THE MACROPHAGE BOUND ANTIGEN WHICH IS HIGHLY IMMUNOGENIC, IS PRESENTED TO CIRCULATING T OR B LYMPHOCYTES AND THUS TRIGGERS AN IMMUNE RESPONSE
LYMPHOCYTES
- PRODUCED IN THE BONE MARROW, THEY DIFFERENTIATE INTO B AND T LYMPHOCYTES
- B LYMPHOCYTES- PRODUCED IN THE BONE MARROW THEY DIFFERENTIATE INTO PLASMA CELLS WHEN ACTIVATED, PLASMA CELLS PRODUCE ANTIBODIES (IMMUNOGLOBULINS)
LYMPHOCYTES (CONT)
- T LYMPHOCYTES- CELLS THAT MIGRATE FROM THE BONE MARROW TO THE THYMUS DIFFENTIATE IN TO T LYMPHOCYTES (THYMUS-DEPENDENT) THE THYMUS SECRETES HORMONES, INCLUDING THYMOSIN, THAT STIMULATES THE MATURATION OF T LYMPHOCYTES,COMPOSING 70 TO 80% OF THE CIRCULATING LYMPHOCYTES AND ARE RESPONSIBLE FOR IMMUNITY TO INTRACELLULAR VIRUSES, TUMOR CELLS, AND FUNGI. THEY LIVE FROM A FEW MONTHS TO LIFETIME AND ACCOUNT FOR LONG TERM IMMUNITY - T CELLS
-
T CYTOXIC
T HELPER (CD4)
T SUPPRESSOR (CD8) - T CYTOXIC
- INVOLVED IN ATTACKING ANTIGENS ON THE CELL MEMBRANE OF FOREIGN PATHOGENS AND RELEASING CYTOLYTIC SUBSTANCES THAT DESTROY THE PATHOGEN. THESE CELLS HAVE ANTIGEN SPECIFITY AND ARE SENSITIZED BY EXPOSURE TO THE ANTIGEN
- T HELPER (CD4) AND T SUPPRESSOR (CD8)
- ARE INVOLVED IN THE REGULATION OF CELL MEDIATED IMMUNITY AND THE HUMORAL ANTIBODY RESPONSE. WITH MANY AUTOIMMUNE DISEASES THE NUMBER OF T SUPPRESOR CELLS DECREASES IN PROPORTION TO THE NUMBER OF T HELPER CELLS, THUS RESULTING IN AN OVERAGGRESSIVE IMMUNE RESPONSE. HIV INVADES T HELPER CELLS, THUS DECREASING THE NUMBER AND FUNCTION. THEREFOR PEOPLE LIVING WITH HIV DO NOT MOUNT AN AGGRESSIVE IMMUNE RESPONSE AND ARE AT AN INCREASED RISK FOR OPPORTUNISTIC INFECTIONS
- NATURAL KILLER CELLS
- - THESE CELLS ARE NOT T OR B CELLS, BUT ARE LARGE LYMPHOCYTES WITH NUMEROUS GRANULES IN THE CYTOPLASM, THEY DO NOT REQUIRE PRIOR SENSITIZATION FOR THEIR GENERATION. INVOLVED IN RECOGNITION AND KILLING OF VIRUS INFECTED CELLS, TUMOR CELLS, AND TRANSPLANTED GRAFTS
- CYTOKINES (Messenger Cells)
- - THE IMMUNE RESPONSE IS A COMPLEX INTERACTION OF T, B CELLS, MONOCYTES, AND NEUTROPHILS. THESE INTERACTIONS DEPEND ON CYTOKINES (SOLUBLE FACTORS SECRETED BY WBCÂ’S AND A VARIETY OF OTHER CELLS IN THE BODY) THAT ACT AS MESSENGERS BETWEEN THE CELL TYPES. CYTOKINES INSTRUCT CELLS TO ALTER THEIR PROLIFERATION, DIFFERENTIATION, SECRETION OR ACTIVITY
- HUMORAL IMMUNITY - CELLS INVOLVED
-
- B LYMPHOCYTES
- PRODUCTS- ANTIBODIES
- MEMORY CELLS- PRESENT
- PROTECTION- BACTERIA, VIRUSES (EXTRACELLULAR), RESP AND GI PATHOGENS
- EXAMPLES- ANAPHYLACTIC SHOCK, TRANSFUSION REACTIONS, BACTERIAL INFECTIONS, ATOPIC DISEASES -
CELL-MEDIATED IMMUNITY
- CELLS INVOLVED -
- T LYMPHOCYTES, MACROPHAGES
- PRODUCTS- SENSITIZED T CELLS, LYMPHOKINES
- MEMORY CELLS- PRESENT
- PROTECTION- FUNGUS, VIRUSES(INTRACELLULAR), CHRONIC INFECTIOUS AGENTS, TUMOR CELLS
- EXAMPLES- TB, FUNCAL INFECTIOUS, CONTACT DERMATITIS, GRAFT REJECTION, CA CELLS - Transmission of HIV
-
- Fragile virus transmitted only through contact with bodily fluids
– Blood, semen, vaginal secretions, and breast milk
– Sex with infected partner, exposure to infected blood or blood products, pregnancy, and breast feeding - Pathophysiology of HIV
- - HIV causes immune dysfunction by destroying CD4+ T cells (T helper cells)
- - Immune problems start when CD4+T cell counts drop below
- 500 cells/ìl
- HIV destroys CD4+ cells 3 ways
- – Antibodies against HIV bind to the infected cells and activate the complement system, which destroy the infected cells
- CLINICAL CATAGORIES
-
A
B
C - CLNICAL CATAGORIES A
- - HIV POSITIVE AND IS EITHER ASYMPTOMATIC, HAS PERSISTANT LYMPHADENOPATHY, OR ACUTE HIV INFECTION. DISEASE CLASSIFICATION OF A1, A2, OR A3 DEPENDING ON THEIR CD4 + T LYMPHOCYTE COUNT
- CLNICAL CATAGORIES B
- B1, B2, OR B3
- CLINICAL CATAGORIES C
- CLASSIFICATIONS OF C1,C2 OR C3 DEPENDING ON THEIR CD4 + T LYMPHOCYTE COUNT
- TO BE DIAGNOSED AS HAVING AIDS A PERSON MUST BE INFECTED WITH HIV AND HAVE A CLINICAL DISEASE THAT INDICATES CELLULAR IMMUNODEFICIENCY, A CD4 + T-LYMPHCYTE COUNT BELOW
- 200 MM3 OR A CD4 + T- LYMPHOCYTE TOTAL PERCENTAGE BELOW 14
-
ETIOLOGY
- A SPECIAL TYPE OF VIRUSES KNOWN AS RETROVIRUSES, WHICH DIFFER FROM OTHER VIRUSES - IN THEIR EFFICENCY OF CELLULAR FUNCTION. RETROVIRUSES HAVE ONLY RNA AS THEIR GENETIC MATERIAL THE MOST IMPORTANT DIFFERENCE IS A SPECIAL COMPLEX OF ENZYMES WITHIN THE RETROVIRUS CALLED REVERSE TRANSCRIPTASE. THIS ENZYME INCREASES THE EFFICIENCY OF VIRAL REPLICATION ONCE IT ENTERS THE HUMAN CELL (FIGURE 367)
- Clinical Manifestations and Complications
-
- Acute infection
– Flu-like syndrome
- Acute retroviral syndrome
- Chronic HIV infection
– Is generally asymptomatic early on
– When CD 4+ counts drops to 200-500 cells/ìl, symptoms occur
- Oral hairy leukoplakia
- Candida infection
- Fever, sweats, diarrhea, headaches - Diagnostic Studies
-
- Screening tests detect HIV-specific antibodies
– May take up to 2 months before antibodies can be detected (window period) - Progression monitored by
- CD4+ T cell counts
- Lab tests measuring
- viral activity
- Collaborative Care
-
- Monitoring HIV disease progression and immune function
- Initiating and monitoring antiretroviral therapy (ART) - Bactrim used ?
- to prevent pneumonia
- Preventing and detecting
- opportunistic infections
- Greatest work risk is through
- puncture wounds
-
Antiretroviral Therapy
Adherence to drug regimens is critical to -
– prevent disease progression
– opportunistic disease
– viral drug resistance - Common opportunistic infections
-
– Pneumocysits carinii pneumonia
– Cryptococcal meningitis
– Cytomegalovirus retinitis
– Mycobacterium avium complex - Osteoarthritis
-
* Before age 50, men are more often affected than women
* Incidence of OA after 50 is twice as great in women - Etiology of Osteoarthritis
-
* Age is the strongest risk factor
* Estrogen reduction at menopause
* Genetic factors
* Modifiable risk factors have also been identified- obesity, regular moderate exercise has shown to decrease development, although strenuous exercise has shown to increase risk - Pathophysiology of Osteoarthritis
-
* Central cartilage becomes thinner
* Cartilage and bony growth (osteophytes) increase at the joint margins - Pathophysiology of Osteoarthritis Incongruent joint surfaces create -
-
- Uneven distribution of stress across the joint
- Reduction in motion -
Pathophysiology of Osteoarthritis
* Secondary synovitis -
- Inflammatory changes
- early pain and stiffness -
Clinical Manifestations of Osteoarthritis
* No systemic manifestations
* Joint pain- stiffness... -
- Predominant symptom
- Relieved by rest in early stages -
Clinical Manifestations of Osteoarthritis
* Joint pain ... -
- Affects joints asymmetrically
- Early morning stiffness
* Resolves within 30 minutes -
Clinical Manifestations of Osteoarthritis
* Joint pain
- May be referred to -
* Groin
* Buttock
* Medial side of thigh or knee -
Clinical Manifestations of Osteoarthritis
* Joint pain
- Crepitation ... - Grating sensation caused by loose particles of cartilage in the joint cavity
-
Clinical Manifestations of Osteoarthritis
* Most commonly involved joints -
- Weight-bearing joints (hips, knees)
- Metatarsophalangeal (MTP)
- Cervical and lower lumbar vertebrae - Early morning stiffness of osteoarthritis may be helped by...
- Warm showers
-
Clinical Manifestations of Osteoarthritis
* Deformity -
- HeberdenÂ’s nodes- hard nodules
Distal intephalangeal joints of the fingers
* Indication of osteophyte (a bony out growth) formation -
Clinical Manifestations of Osteoarthritis
* Deformity -
- BouchardÂ’s nodes- bony enlargements
* Proximal interphalangeal joints
- Nodes often red, swollen, tender - Diagnostic Studies for Osteoarthritis
-
* Bone scan
* CT
* MRI
* X-ray
* No lab tests - Collaborative Care for Osteoarthritis
-
* Heat and cold applications
- May help reduce pain and stiffness
- Ice is not used as often as heat -
Collaborative Care for Osteoarthritis
* Rest and joint protection ... -
- Rest during any periods of acute inflammation
- Immobilization not to exceed 1 week -
Collaborative Care for Osteoarthritis
* Heat and cold applications
- Ice when?
- Heat when? -
Ice - Acute inflammation
Heat - Stiffness -
Collaborative Care for Osteoarthritis
* Nutritional therapy and exercise ... - - Weight-reduction plan
-
Collaborative Care for Osteoarthritis
* Complementary and alternative therapies -
- Acupuncture
- Yoga -
Collaborative Care for Osteoarthritis
* Drug Therapy -
- Opioid analgesics
- Corticosteroids
- DMARDs-disease modifying antirheumatic drugs
- Immunosuppressants- alters the immune response suppressing synovitis of active RA - Nursing Assessment of Osteoarthritis
-
* Type, location, severity, frequency, and duration of joint pain and stiffness
* Pain-relieving practices - Nursing Diagnoses for Osteoarthritis
-
* Acute and chronic pain
* Disturbed sleep pattern
* Impaired physical mobility
* Self-care deficits
* Imbalanced nutrition: less than body requirements
* Chronic low self-esteem -
Nursing Management of Osteoarthritis
Planning - Overall goals -
* Maintain or improve joint function
* Use joint protection measures
* Achieve independence of self-care
* Use pharmacologic strategies to manage pain -
Nursing Implementation r/t Osteoarthritis
Health Promotion - * Elimination of modifiable risk factors
-
Nursing Management r/t Osteoarthritis
Nursing Implementation - Acute Intervention -
* Pain management
* Patient and family teaching -
Rheumatoid Arthritis (RA)
* A chronic, progressive, _____ disease characterized by inflammation of connective tissue in the diarthrodial (synovial) joints - systemic
- Does Rheumatoid Arthritis have periods of remission and exacerbation
- Yes
- Is cause of Rheumatoid Arthritis (RA)?
- No
- Has there been an infectious agent cultured from blood and synovial tissue or fluid in pateints with Rheumatoid Arthritis?
- No
- Onset of rheumatoid arthritis is characterized by _____ (inflammation of the synovial tissue in joints)
- synovitis
-
Etiology and Pathophysiology of Rheumatoid Arthritis (RA)
* Autoimmunity
- Changes begin when a susceptible host experiences an initial immune response to an _____ - antigen
- In rheumatoid arthritis an antigen triggers the formation of an abnormal immunoglobulin ...
- G (IgG) or immunogloulin M (IgM) type (rheumatoid factor) develop against IgG antigenic determinants to form complexes that lodge in synovium and other connective tissues
- RA is characterized by the presence of autoantibodies ...
-
(rheumatoid factor [RF])
- RF and IgG form immune complexes that initially deposit on synovial membranes or superficial articular cartilage in the joints -
Etiology and Pathophysiology of Rheumatoid Arthritis (RA)
* Autoimmunity
- Joint changes from chronic inflammation begin when the hypertrophied synovial membrane invades the surrounding ... -
* Cartilage
* Ligaments
* Tendons
* Joint capsule -
Etiology and Pathophysiology of Rheumatoid Arthritis (RA)
* Autoimmunity
- _____ forms within the joint
- Eventually covers and erodes the entire surface of the articular cartilage
- Inflammatory _____ further contribute to ca -
Pannus
Cytokines -
Etiology and Pathophysiology of Rheumatoid Arthritis (RA)
* Autoimmunity
- Pannus scars and _____ supporting structures - what structures? -
Shortens
- Tendons
- Ligaments -
Etiology and Pathophysiology of Rheumatoid Arthritis (RA)
* Genetic factors
- Genetic predisposition appears to be important in the development of RA
- Strongest evidence for a familial influence is the ª occurrence of certain ... - human leukocyte antigens (HLA)
-
Anatomic Stages of RA
* Stage I – Early - - No destructive changes on x-ray, possible x-ray evidence of osteoporosis
-
Anatomic Stages of RA
* Stage II – Moderate ... -
- X-ray evidence of osteoporosis, with or without slight bone or cartilage destruction
- No joint deformities
- Adjacent muscle atrophy
- Possible presence of extraarticular soft tissue lesions -
Anatomic Stages of RA
* Stage III – Severe ... -
- X-ray evidence of cartilage and bone destruction in addition to osteoporosis
- Joint deformity
- Extensive muscle atrophy
- Possible presence of extraarticular soft tissue lesions -
Anatomic Stages of RA
* Stage IV – Terminal ... -
- Fibrous or bony ankylosis
- Criteria of stage III -
Clinical Manifestations
Joints ... -
* Onset of RA is typically insidious
* Nonspecific manifestations may precede the onset of arthritic complaints
- Fatigue
- Anorexia
- Weight loss
- Generalized stiffness
* Stiffness becomes more localized in the following weeks to months
* Some patients report a history of precipitating stressful events
- Research has been unable to correlate such events directly with the onset of RA
* Specific articular involvement
- Pain
- Stiffness
- Limitation of motion
- Signs of inflammation
* Heat
* Swelling
* Tenderness
* Joint symptoms occur symmetrically and frequently
- Small joints of the hands and feet
- Larger peripheral joints
* Wrists, elbows, shoulders, knees, hips, ankles, and jaw
- Cervical spine
* Often experience joint stiffness after periods of inactivity
* Morning stiffness may last from 60 minutes to several hours or more
* Joints become tender, painful, and warm to the touch
* Joint pain
- ª with motion
- Varies in intensity
- May not be proportional to the degree of inflammation
- Tenosynovitis-inflammation of the tendon sheath
* Difficult for patients to grasp objects
* Inflammation and fibrosis of the joint capsule and supporting structures may lead to deformity and disability
* Subluxation-a partial or incomplete dislocation
- Atrophy of muscles and destruction of tendons around the joint cause one surface to slip past the other -
Clinical Manifestations
Extraarticular Manifestations ...
* RA can affect nearly every system of the body
* 3 most common -
- Rheumatoid nodules
- Sjögren syndrome- an autoimmune disorder marked by decreased lacrimal and salivary secretions resulting in dry eyes and mouth
- Felty syndrome-enlarged liver and spleen and neutropenia - Rheumatoid Nodules
-
* Develop in 25% of all patients with RA
* Usually have high titers of RF
* Appear as firm, nontender, granuloma-type masses
* Usually over the extensor surfaces of joints such as fingers and elbows
* Nodules at the base of the spine and back of the head are common in older adults
* Develop insidiously
* Can persist or regress spontaneously
* Usually not removed - Sjögren Syndrome
-
* 10% to 15% of patients with RA
* Can occur as a disease by itself or in conjunction with other arthritic disorders
* Diminished lacrimal and salivary gland secretion
- Burning, gritty, itchy eyes
- « Tearing
- Photosensitivity -
Felty Syndrome
* Occurs most commonly in patients with severe, nodule-forming RA
* Characterized by ... -
- Inflammatory eye disorders
- Splenomegaly
- Lymphadenopathy
- Pulmonary disease
- Blood dyscrasias - Complications r/t Rheumatoid Arthritis
-
* Flexion contractures and hand deformities
- Cause diminished grasp strength
- Affect the patientÂ’s ability to perform self-care tasks
* Nodular myositis and muscle fiber degeneration can lead to pain similar to that of vascular insufficiency
* Cataract development and loss of vision possible from scleral nodules
* Rheumatoid nodules can ulcerate, similar to pressure ulcers
* Hoarseness from nodules on the vocal cords
* Bone destruction from nodules in the vertebral bodies
* Cardiopulmonary effects later in the disease
- Pleurisy, pleural effusion, pericarditis, pericardial effusion, cardiomyopathy
* Carpal tunnel syndrome -
Diagnostic Studies
* Positive Rheumatoid Factor in _____ of patients
* _____ and _____ (CRP) are general indicators of active inflammation
Diagnostic Studies -
80%
ESR
C-reactive protein -
Collaborative Care
* Care of the patient with RA
?
* Physical therapy
?
* Occupational therapy
?
? -
- Drug therapy and education
- Joint motion and muscle strength
- Upper extremity function
- Assistive devices and strategies -
Collaborative Care
_____ therapy is the cornerstone of RA treatment ... -
Drug
* Disease-modifying antirheumatic drugs (DMARDs)
- Potential to lessen the permanent effects of RA -
Collaborative Care of patient with Rheumatoid Arthritis
Drug Therapy
* Choice of drug depends on ... -
- Disease activity
- PatientÂ’s level of function
- Lifestyle considerations -
Collaborative Care
Apheresis -
* Prosorba column is now being used to treat severe RA in patients who do not respond to other treatments
- Prosorba column: a blood filtration device used in apheresis -
Nursing Management of patient with Rheaumtoid Arthritis
* Goals are that patient with RA will -
- Have satisfactory pain relief
- Have minimal loss of functional ability of the affected joints
- Participate in planning and carrying out the therapeutic regimen
- Maintain a positive self-image
- Perform self-care to maximum amount possible -
Ambulatory and Home Care - Pt. with Rheumatoid Arthritis
Rest
* Body alignment
- _____ mattress
- Bed board
* Positions of extension
- Avoid positions of _____
* Lying prone for ... how long? -
Firm
Flexion
half an hour twice daily -
Ambulatory and Home Care - Rheumatoid Arthritis
Heat and Cold Therapy
* Help relieve stiffness, pain, and muscle spasm
* Cold (¡Ü ? to ? minutes at a time)
- Beneficial during periods of disease _____
* Moist heat (¡Ü ? minut -
10 - 15
exacerbation
20
stiffness -
Ambulatory and Home Care
Psychologic Support - Rneumatoid Arthritis
* The patient is constantly threatened by problems ... -
- Limited function and fatigue
- Loss of self-esteem
- Altered body image
- Fear of disability and deformity
- Sexuality - _____ is serious in SLE, because, in part, of the diminshed immune system
- Fever
-
System Lupus Erythematosus
* Most cases occur in women of _____ years - childbearing
-
Etiology and Pathophysiology of SLE
* Onset occurs after onset of _____
* Autoimmune reactions directed against constituents of cell _____, DNA
* Antibody response related to B and T cell hyperactivity -
menarche
nucleus -
Clinical Manifestations of SLE
* Dermatologic -
- Cutaneous vascular lesions
- Butterfly rash
- Oral/nasopharyngeal ulcers
- Alopecia -
Clinical Manifestations of SLE
Musculoskeletal -
- Polyarthralgia
- Arthritis
* Swan neck fingers
* Ulnar deviation
* Subluxation with hyperlaxity of joints -
Clinical Manifestations of SLE
Cardiopulmonary -
- Tachypnea
- Pleurisy
- Arrhythmias
- Accelerates CAD -
Clinical Manifestations of SLE
Renal -
- Nephritis
* Proteinuria
* Glomerulonephritis
* Minimal lupus nephritis, the glomeruli are slightly irregular
* Focal or mild lupus nephritis, the glomeruli have further glomerular change- patient shows signs of renal impairment
* Diffuse, severe proliferative nephritis, more than 50% of the glomeruli are affected and the patient is in renal failure -
Clinical Manifestations of SLE
Nervous system -
- Generalized/focal seizures
- Peripheral neuropathy
- Organic brain syndrome
* Disorientation
* Memory deficits
* Psychiatric symptoms -
Clinical Manifestations of SLE
Hematologic -
- Formation of antibodies against blood cells
- Anemia
- Leukopenia
- Thrombocytopenia
- Coagulopathy
- Antiphospholipid antibody syndrome- a condition characterized by hypercoagulability associated with high levels IgG antibodies against phospholipids -
Clinical Manifestations of SLE
Infection -
- Increased susceptibility to infections
- Fever should be considered serious - Diagnostic Studies for SLE
-
* No specific test
* SLE is diagnosed primarily on a distinct criteria relating to patient history, physical examination, and laboratory findings -
Collaborative Care r/t SLE
Drug therapy -
- NSAIDs
- Antimalarial drugs
- Steroid-sparing drugs
- Corticosteroids
- Immunosuppressive drugs - Nursing Assessment r/t SLE
-
* Assess patientÂ’s physical, psychologic, and sociocultural problems with long-term management of SLE
* Assess pain and fatigue daily
* Obtain subjective and objective data
* Educate and counsel on expected issues - Nursing Diagnoses r/t SLE
-
* Fatigue
* Acute pain
* Impaired skin integrity
* Activity intolerance
* Ineffective therapeutic regimen management -
Nursing Management r/t SLE
Planning
Overall goals -
- Have satisfactory pain relief
- Comply with therapeutic regimen to achieve maximum symptom management
- Demonstrate awareness of, and avoid activities that cause, disease exacerbation
- Maintain optimal role function and a positive self-image -
Nursing Implementation r/t SLE
Health Promotion -
- Prevention of SLE is not possible
- Promote early diagnosis and treatment -
Nursing Implementation r/t SLE
Acute Intervention -
- Record severity of symptoms and response to therapy
- Observe for
* Fever pattern
* Joint inflammation
* Limitation of motion
* Location and degree of discomfort
* Fatigability
* Signs of bleeding
- Monitor weight and I/O
- Collect 24-hour urine sample
- Assess neurological status
- Explain nature of disease
- Provide support -
Nursing Implementation r/t SLE
Ambulatory and Home Care -
- Emphasize health teaching
- Reiterate adherence to treatment does not necessarily halt progression
- Minimize exposure to precipitating factors -
Nursing Implementation r/t SLE
Lupus and pregnancy -
- Infertility can result from SLEÂ’s regimen
- Women with serious SLE should be counseled against pregnancy
- Neonatal lupus erythematosus (NLE) may occur in infants born of women with SLE -
Nursing Implementation r/t SLE
Psychosocial Issues -
- Counsel patient and family that SLE has good prognosis
- Physical effects can lead to isolation, self-esteem, and body image disturbances
- Assist patient in developing goals -
Nursing Management r/t SLE
Evaluation
Expected Outcomes -
- Completion of priority activities
- Verbalization of having more energy
- Expression of satisfaction with pain relief measures
- Performance of activities of daily living without pain
- Limitation of direct exposure to sun and use of sunscreen
- No open skin lesions
- Expression of satisfaction with activity level
- Pacing of activities to match level of tolerance
- Expression of confidence in ability to manage SLE over time and in home environment