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HLA and Autoimmune Disorders Overview

This document summarizes information about two autoimmune disorders: systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). SLE is a chronic multi-system autoimmune disease characterized by abnormal T cell function and exaggerated autoantibody production that can cause multiorgan failure. RA is a chronic systemic inflammatory disease that affects peripheral joints and surrounding tissues, causing pain, stiffness, and progressive joint deformities. Both disorders involve genetic and environmental risk factors and are treated primarily through rest, activity modification, medications like NSAIDs and corticosteroids, and occasionally more aggressive therapies like splenectomy or chemotherapy.

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0% found this document useful (0 votes)
220 views7 pages

HLA and Autoimmune Disorders Overview

This document summarizes information about two autoimmune disorders: systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). SLE is a chronic multi-system autoimmune disease characterized by abnormal T cell function and exaggerated autoantibody production that can cause multiorgan failure. RA is a chronic systemic inflammatory disease that affects peripheral joints and surrounding tissues, causing pain, stiffness, and progressive joint deformities. Both disorders involve genetic and environmental risk factors and are treated primarily through rest, activity modification, medications like NSAIDs and corticosteroids, and occasionally more aggressive therapies like splenectomy or chemotherapy.

Uploaded by

febie pacheco
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd

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

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