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137 Cards in this Set

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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 BODY’S INTERNAL ENVIORMENT, THEY POSE NO THREAT TO HEALTH
DEFENSE- FOUR SYSTEMS
- SKIN AND MUCOUS MEMBRANES
- INFLAMMATORY RESPONSE
- MONONUCLEAR PHAGOCYTE
- IMMUNE SYSTEM
INFLAMMATORY RESPONSE
- SEQUENTIAL REACTION TO CELL INJURY
- NEUTRALIZES AND DILUTES THE INFLAMMATORY AGENT
- REMOVES NECROTIC MATERIAL
- ESTABLISHES AN ENVIORMENT SUITABLE FOR HEALING TO OCCUR
INFLAMMATION IS ALWAYS PRESENT WITH INFECTION
BUT INFECTION IS NOT ALWAYS PRESENT WITH INFLAMMATION
INFLAMMATORY RESPONSE
- VASCULAR RESPONSE-PHASE 1 AND PHASE 2
- CELLULAR RESPONSE
- FORMATION OF EXUDATE AND HEALING
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 BODY’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 WBC’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
- RNA virus
- Virus binds to specific CD4 receptor sites and then enters the cell
- Reverse transcriptase assists to make a single viral DNA and it copies itself to make a double-stranded viral DNA
Pathophysiology of HIV
- Virus enters the cell nucleus
- Using integrase the virus splices itself into genome to become part of the cell’s genetic structure
- Consequences
– All daughter cells from infected cell are infected
– Genetic codes can direct the cell to make HIV
Pathophysiology of HIV
- CD4 cells infected

– Lymphocytes, monocytes/macrophages, astrocytes, and oligodendrocytes
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
– Viral replication leaves holes in cell membranes
– Infected cells fuse with other cells
- Combine to form a syncytium that destroys all affected cells
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
* Noninflammatory disorder of the diarthrodial (synovial) joints
* Progressive deterioration of and loss of cartilage in the joints
* Most common connective tissue disease
* Weight bearing joints, the vertebral column, and hands most affected
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
* May occur as an idiopathic (formally primary) or secondary disorder
* Cause of idiopathic OA is unknown
* Cause of secondary OA is a known event or condition (examples- trauma, repetitive movements, joint instability)
Pathophysiology of Osteoarthritis
* Results from cartilage damage that triggers a metabolic response at the level of the chondrocytes
* Progression causes the normally smooth, white, translucent articular cartilage to become dull, yellow and granular
Pathophysiology of Osteoarthritis
* Affected cartilage gradually becomes softer, less elastic, and less able to resist wear with heavy use.
* Fissures, pitting and ulcerations develop
* Inflammatory enzymes enhance tissue deterioration as a result of altered cartilage metabolism, resulting when phagocytic cells try to rid the joint so small pieces of cartilage torn from the joint surface.
* The repair process is then unable to overcome the rapid process of degeneration
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 ...
- Generally worsens with joint use
- May become worse as barometric pressures fall before inclement weather
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
* Joint pain ...
- Affects joints asymmetrically
- Early morning stiffness
* Resolves within 30 minutes
Clinical Manifestations of Osteoarthritis

* Most commonly involved joints
- Distal interphalangeal (DIP)
- Proximal interphalangeal (PIP)
- Carpometacarpal joint of the thumb
Early morning stiffness of osteoarthritis may be helped by...
Warm showers
Clinical Manifestations of Osteoarthritis

* Most commonly involved joints
- Weight-bearing joints (hips, knees)
- Metatarsophalangeal (MTP)
- Cervical and lower lumbar vertebrae
Clinical Manifestations of Osteoarthritis

* Deformity
- Heberden’s nodes- hard nodules
Distal intephalangeal joints of the fingers
* Indication of osteophyte (a bony out growth) formation
Clinical Manifestations of Osteoarthritis

* Deformity
- Bouchard’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
* No cure
* Pain and inflammation management
* Prevent disability
* Maintain and improve joint function
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
- May help reduce pain and stiffness
- Ice is not used as often as heat
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
- Based on the severity of symptoms
- Salicylates
- NSAIDs
- Nonopioid analgesics
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 cartilage destruction
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 patient’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
- Patient’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 ? minutes at a time)
- Relief of chronic _____
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 patient’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 SLE’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