IMMUNOLOGIC (AUTOIMMUNE) DISORDERS Genetic predisposition
Hormonal as evident by usual onset during
AUTOIMMUNITY childbearing years
“self” as a threat, abnormal response Environmental factors triggered by sunlight,
Human Leukocyte Antigen (HLAs) – genetic thermal changes and burns
marker Possibility of drug-induced SLE by taking
hydralazine, isoniazid and procainamide
Risk Factors Diagnostic Tests
Hereditary ANA (antinuclear antibody) titer
Women o Not definitive
African American Inc. ESR and C reactive protein
High levels of estrogen, suppresses T cells o Distinctive of inflammation
Dec. C3 and C4
Mechanism of Actions o Utilized in immune response
Cell mediated CBC
o abnormal T cells, abundance of T o Anemia, thrombocytopenia,
cytotoxic cells, deficiency of T leukopenia, and positive ANA
suppressor helper cells Coomb’s test
Antibody mediated o Detect of chances of hemolytic disease
o development of auto antibodies where autoantibodies would attack the
Immune complex diseases RBC
o deposition of immune complexes or
serum levels Signs and Symptoms
Arthritis
Diagnostic Tests o Most common manifestation, morning
Autoantibody assays sickness
Complement fixation Butterfly/malar rash
Complement assays o Most common symptom, drug-induced
HLAs Pleuritis and pleural effusion
Hematologic depression
Management Renal failure
Pharmacologic Immunosuppressive agents, o Lupus nephritis
corticosteroids, anti-inflammatory Cardiac & CNS involvement
o Lessen the action o Depression and psychosis
Plasmapheresis Pericarditis
o Filtration of plasma to remove o Leading cause of death
circulating immune complexes and Pancytopenia
remove antibodies Oral ulcers
Splenectomy and chemotherapy o During exacerbation
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
- Multisystem autoimmune disease that is
characterized by fluctuating chronic hoarse and
causes multiorgan failure
- Abnormal T cell function and exaggerated
production of auto antibodies
Types
1. Systemic
o Systemic reaction
Categories of Treatment
2. Discoid
1. Conservative
o Skin rashes without systemic response
Rest and pharmacotherapy
o Chronic rash with erythematous
2. Aggressive
papules or plaques and scaling and
Splenectomy and chemotherapy
cause scarring and pigmentation
changes
Management
o Skin manifestations are provoked by
Palliative care:
sunlight or artificial ultraviolet light
Recognize flare-ups
o Apparent on scalp and neck
Schedule rest & activity
Maintain integrity of immune system
Etiology
Lessen stress
Presence of HLA, C2 & C4 complement
Avoid environmental triggers
complexes
Stop drugs that induces attacks
Estrogen inhibits suppressor T cells
Plasmapheresis
Women of childbearing age
Risk factors
Pharmacologic Management
NSAIDS
Aspirin – anti-inflammatory
Hydroxychloroquine
o Treat skin lesions
Glucocorticosteroids
Anti-hypertensive drugs
Dietary changes
o Minimize the effect of renal
involvement
Dialysis or kidney transplant
o Renal failure STAGES OF RHEUMATOID ARTHRITIS
Immunosuppressive therapy 1. Synovitis
(cyclophosphamide) Congestion and edema of synovial
o Diffused proliferative membrane
glomerulonephritis Infiltration by lymphocytes,
Gamma globulin macrophages, and neutrophils local
Systemic corticosteroids inflammatory response
o To reduce systemic symptoms of SLE for These cells including fibroblasts
acute generalized exacerbation or for (synovial cells) – help to degrade bone
serious disease related to vital organ and cartilage
systems such as pleuritis, pericarditis, 2. Pannus
lupus nephritis, vasculitis, and CNS Thickened layer of granulation tissue,
involvement covers and invades cartilage
Intralesional corticosteroids Eventually destroys capsules and bone
o Antimalarials – to treat refractory skin 3. Fibrous ankylosis
lesions Fibrous invasion of pannus and scar
Topical corticosteroid creams formation which occludes the joint
o Skin lesion space
Bone atrophy and misalignment causing
RHEUMATOID ARTHRITIS visible deformities and disrupting the
Chronic systemic inflammatory disease articulation of opposing bones results in
Affects peripheral joints and surrounding muscle atrophy and imbalance and
muscles, tendons, ligaments, and blood vessels possibly partial dislocation
Partial remission and unpredictable 4. Bony ankylosis
exacerbations Fibrous tissue calcifies
Prevalence increases with age Total immobility
Etiology
Unknown
Theories: infection (Epsteinn- Barr), lifestyle
factors, rheumatoid factor (IgM antibodies
against IgG aggregate into complexes and
generate inflammation causing eventual
triggering damage and autoimmune responses)
Predisposed by SLE SWAN NECK
- Joint swelling and edema of joint space
Complications
Pain
Joint deformities
Fibrosis ankylosis
Signs and symptoms
Persistent low-grade fever
Joint pain and tenderness
Gradual appearance of rheumatoid nodules
Diminished joint functions & deformities
(morning stiffness)
o
Bilateral and symmetrical articular symptoms ULNAR DRIFT
o Fingers to wrist, knees, elbows - Flexion deformities or hyperextension of
o Stiffening after destruction of synovium metacarpal phalangeal joints
Boutenniere deformity - Subluxation of the wrist and stretching of
Ulnar drift tendons pulling the fingers to the ulnar side
Fatigue, malaise and anorexia
Nursing Management
Assess all joints carefully.
o Look for deformities, immobility,
contractures
Administer analgesics
Monitor vital signs, weight changes
Meticulous skin care – nodules, pressure ulcers
Urge patient to perform ADLs
Instruct patient to pace daily activities and
schedule rest periods
RHEUMATOID NODULES
Encourage to take hot showers at bedtimes or
- Subcutaneous, round, and oval nontender
morning to reduce the need for medication
masses usually on the elbows, hand or Achilles
Apply splints as ordered – monitor pressure
tendons resulting from disruption of the
ulcers
synovial
Explain the nature of disease – requires major
changes in lifestyle
Diagnostic Tests
Encourage balanced diet – weight control
X-ray: bone demineralization and soft tissue
Provide emotional support
swelling (early stage), cartilage loss, narrowed
Avoid joint stress:
joint spaces, cartilage and bone destruction and
o Use largest joint available for a given
erosion, subluxation, and deformities (later
task.
stages).
o Slide (do not lift) objects whenever
RF Titer: Positive 75-80% of patients
possible.
Synovial fluid: increased volume and turbidity,
o Always use hands toward the center of
decreased viscosity, elevated WBC count
the body.
Serum protein electrophoresis: elevated serum
globulin level Post-replacement of joint:
o Instruct to maintain exercise regimen or
ESR and C- reactive Protein: elevated in 85-90%
of patients – parallels disease activity prescribed by PT.
o Review prescribed limitations on
CBC- moderate anemia, slight leukocytosis, and
slight thrombocytosis activity.
o Teach S/S of joint incision infection
Management
Synovectomy ACUTE GLOMERULONEPHRITIS
o Removal of disruptive proliferating Bilateral inflammation of glomeruli which
synovium (wrist, knees, fingers) to halt follows streptococcal infection
or delay the disease Acute poststreptococcal glomerulonephritis
Osteotomy Common among boys, 3-7 y.o.
o Removal of bone to realign joint Recovery 95% - children, 70% adults
surfaces and redistribute stress Develops when antigen-antibody complexes
Arthroplasty lodge in glomerular capillaries, causing injury.
o Tendon transfers to prevent deformities Leads to activation complement, leukocyte and
or relieve contractures fibrin release of lysosomal enzymes that
o Joint reconstructions or total joint damage glomerular cell walls.
arthroplasty Leads to platelet aggregation, platelet
o Metatarsal heads and distal ulnar degranulation and increased cell wall
permeability.
resection arthroplasty
Diminishes renal blood flow and GFR.
o Insertion of a stylistic protases in
metacarpal phalangeal joints and
severe diseases
Pharmacologic Treatment
Salicylates
o Aspirin – dec inflammation and relieve
joint pain
NSAIDs
Antimalarials
o Reduce acute and chronic inflammation
Corticosteroid
o Prednisone: low doses for anti-
inflammatory effect
o High doses for immunosuppressive
effects on T cells - Entrapment of antigen-antibody complexes in
Azathiprine, Cyclosporine& Mehtotrexate the glomerular capillary membrane after
o In early disease for suppression of T and endogenous or exogenous infection with GABS
B lymphocyte proliferation causing - Circulating antigen-antibody complexes in the
destruction of the synovium glomerular capillaries causing glomerular injury
and the release of immunologic substances that MULTIPLESCLEROSIS
lyse cells and increase membrane permeability Involves sporadic patches of axon demyelination
and nerve fiber loss throughout the CNS.
Etiology Results in varied neurologic dysfunction
Strep infection of respiratory tract 20-50 yo
Impetigo Characterized by exacerbations and remissions
IgA nephropathy (Berger’s disease) May progress rapidly
Lipid nephrosis May cause death within months of onset
Signs and Symptoms Risk Factors
Oliguria – smoky or coffee-colored to Emotional stress
hematuria, decreased GFR Fatigue
Proteinuria Pregnancy
o Increased permeability of glomerular Acute respiratory infections
membrane
Bibasilar crackles Etiology
o Hypervolemia or heart failure Unknown
Dyspnea and orthopnea Autoimmune response
o Pulmonary edema secondary to Latent viral infection
hypervolemia, periorbital edema Environmental and genetic factors
Hypertension
o Mild to severe Signs and Symptoms
o Due to decreased GFR, sodium or water Sensory impairment: burning, pins and needles
retention Weakness and paralysis
Diplopia, blurred vision, and nystagmus
Diagnostic Tests Gait ataxia
Blood testing: elevated antistreptolysin-O titers, Constipation
electrolytes, BUN and creatinine, low serum Dysphagia
protein and hemoglobin level, elevated anti- Depression, euphoria, apathy, forgetfulness
Dnase B titers Urinary incontinence
Streptozyme analysis Impaired motor function
o Test strep antigen, elevated antibody Optic neuritis
Kidney biopsy – most definitive
Urinalysis: presence of RBC, WBC, mixed cell
casts & protein
o Renal failure
KUB Xrays
o Enlarged bilateral kidney enlargement
Xrays
o Symmetric contraction with normal
pelvis and calyces
Culture – GABS
Management
Treatment of primary disease to alter
immunologic cascade would depend on the
process of destruction of the kidney
Antibiotics, anticoagulants, vasodilators,
corticosteroids
Fluid restrictions
Dialysis
Plasmapheresis
Dietary restrictions
Loop diuretics
Nursing Management
Check V/S and electrolyte values.
Monitor I/O and weigh OD
Assess serum creatinine, BUN and urine
creatinine clearance levels daily.
Report signs of ARF.
Monitor for ascites and edema. Diagnostic tests
Provide a high-caloric diet that’s low in protein, MRI: multifocal white matter lesions
sodium, potassium and fluids Lumbar puncture: normal total CSF protein,
Provide good skin care and oral hygiene elevated IgG, elevated CSF WBC
Take diuretics in the morning Evoked potential studies: slowed conduction of
Prevent secondary infection nerve impulses.
Management
Immune system therapy - Interferon
Stretching & ROM exercises
Frequent rest periods
Treatment of associated bowel & bladder
problems
Adaptive devices
Physical & speech therapy
Vision therapy & adaptive lenses
Pharmacologic Treatment
ABC-R Drugs
o Avonex
o Betaseron
o Copaxone
o Rebif Diagnostic tests
IV Methylprednisolone Fasting plasma glucose level: 130mg/dl or more
Azathioprine, (Imuran), Methotrexate on at least two occasions
(Rheumatrex) & Cyclophosphamide (Cytoxan) HbA1c level
Baclofen (Lioresal) and Tizanidine (Zanaflex)
Management
Botulinum toxin injections
Individualized meal planning
TCA, Phenytoin (Dilantin) or Carbamazepine
(Tegretol) Regular exercise
Insulin replacement
Nursing Management Pancreas transplantation
Educate patient and family about the disease. Dialysis
Emphasize the need to avoid stress, infections, Renal transplantation
and fatigue and to maintain independence.
Stress importance of eating a nutritious, well- Nursing Management
balanced diet that contains roughage and Stress the importance of complying with
adequate fluids. prescribed treatment program
Promote emotional stability. Teach patient and family about possible adverse
o Establish daily routine. effects of medications
o Encourage regular rest periods. Watch for hypoglycemia and ketoacidosis and
o Encourage daily physical exercise. teach patient and family on how to recognize
and respond to these complications
Monitor blood glucose, HbA1c, lipid level and
DIABETES MELLITUS TYPE 1 (DMTYPE 1)
BP regularly
Characterized by hyperglycemia, lipolysis and
protein catabolism resulting from lack of insulin
production in pancreas
Etiology
Autoimmune
Idiopathic
Signs and Symptoms
Polyuria and polydipsia
Fatigue and lethargy
Vision changes
Numbness and tingling
Slow-healing skin infections or wounds
Complications
Microvascular
o Retinopathy
o Nephropathy
o Neuropathy
Macrovascular
o Coronary disease
o Peripheral disease
o Cerebral artery disease
Watch for adverse effects of corticosteroid
therapy.
For patients receiving TPN, assess for
inflammation at insertion site.
Observe for signs of complications, such as
perforated colon and peritonitis.
Bleeding precaution
Perioperative care
ULCERATIVE COLITIS PSORIASIS
Inflamed mucosa of the large intestines leading Marked by abnormal epidermal proliferation
to erosion and formation of ulcers. resulting to shortened skin cell life
Produces abscesses and sloughing. (4days) which doesn’t allow time for cell to
Comes in cycles between exacerbation and mature.
remission. This causes the stratum corneum to become
thick and flaky.
Etiology
Idiopathic
E. Coli Etiology
Mediated immune disorder of T cells of the
Signs and Symptoms dermis
Recurrent bloody diarrhea Environment
Abdominal cramping Koebner’s phenomenon
Weight B-hemolytic strep
Complications Signs and Symptoms
Anemia Itching and occasional pain
Colon cancer Erythematous and well- defined lesions
Perforation Plaques with silver scales that flake off easily
Stricture formation and thicken
Toxic megacolon Localized or general pustular psoriasis
Liver disease
Complications
Diagnostic tests Affecting the fingernails
Sigmoidoscopy Pustule formation
Colonoscopy: extend of disease, stricture areas Erythrodermic psoriasis
and pseudopolyps Arthritis
Colonoscopy with biopsy – confirmatory
Barium enema
Elevated ESR
Management
IV hydration
TPN
Surgery
Proctocolectomy with ileostomy
Pharmacologic Treatment
Corticotropin & adrenal corticosteroids
Sulfasalazine Diagnostic tests
Antidiarrheals Skin biopsy: rules out other disease.
Iron supplements Genetic testing – HLA-CV6, -B13, & Bw57
Nursing Management Management
Monitor fluid & electrolyte status. UVB or natural sunlight
Provide good mouth care for patients on NPO.
Tar preparations before UVB exposure Tacrolimus (Prograf)
(Goeckerman regimen) Cyclosporine (Neoral)
Topical and systemic steroids. Mycophenolate Mofetil (CellCept)
Aspirin 8 local heat – psoriatic arthritis Imuran (Azathioprine)
Rapamune (Rapamycin, Sirolimus)
Pharmacologic Treatment
Steroid cream Nursing Management
Anthralin ointment (Anthra- Derm) (Ingram Prevent infection while ongoing
Technique) immunosuppression therapy.
Calcipotriene ointment (Dovonex) Monitor for S/S of infection.
Psoralens Monitor V/S regularly and I/O
Methotrexate (Mexate) Reinforce life-time treatment to prevent
Acitretin (Soriatane) chronic rejection
Cyclosporine (Neoral)
Low-dose antihistamine
Aspirin
Tar shampoo
Nursing Management
Teach correct application of prescribed
ointments, creams and lotions.
Avoid scrubbing skin vigorously.
Protect eyes from UVA – wear goggles.
Watch for adverse effects of medications.
Assure client that this condition is not
contagious.
Teach effective stress management
TRANSPLANT REJECTION
transplant recipient's immune system attacks
the transplanted organ or tissue.
Types
1. hyperacute rejection
2. acute rejection
3. chronic rejection
Risk Factors
post-organ transplant surgery
blood transfusion
Signs and Symptoms
Decreased organ function
o High blood sugar (pancreas transplant)
o Less urine released (kidney transplant)
o Shortness of breath and less ability to
exercise (heart transplant or
o lung transplant)
o Yellow skin color and easy bleeding
(liver transplant)
Pain or swelling in the area.
Fever
Flu-like symptoms
Diagnostic tests
Biopsy
CT scan
ECG
Kidney arteriography
Management
Immunosuppression therapy
Dialysis (kidney transplant)
Prevention:
o Tissue typing
o Blood typing
Pharmacologic Treatment
Prednisone