autoimmune disorders Flashcards
Normal immune response
- recognition phase: body recongizes something is not suppose to be there
- amplification phase: start fighting off the antigen
- effector phase: getting rid of antigen
- terminator phase: going back to normal
- memory
Dysfunction of the immune system
- genetic alterations: mutations that inactivate receptors (immunodeficiencies)
- signaling molecules; conditions with inflammatory components
T
types of autoimmune disease
- organ specific
- systemic
organ specific autoimmune
- addisons disease
- chron disease
- diabetes
- graves disease
- affects a specific organ
Systemic
autoimmune diseases
- Amyloidosis
- MS
- Myasthenia gravis
- psoriasis
- lupus
- affects the body
Etiology ad risk factors for developing an autoimmune disease
- genetic
- hormonal
- enviromental influences
Immunologic tolerance
what is it and types
- unresponsiveness of the immune system to it’s own tissue
- self tolerance
- central
- peripheral
self tolerance (immunologic tolerance)
- The ability of the immune system to be unreactive to self/ones tissue
- therefore t-cells recognize and react against self antigens if this is lost
the immune system’s ability to recognize what is ‘self’
Central immunologic tolerance
- loss of self reactive t cells and b cells
- produces immature lymphocytes
- lymphocytes that do not get survivial signals = apoptosis
Peripheral immunologic tolerance
- mature lymphocytes recognition becomes inactive or supressed by T-cells
Pathogenesis
of autoimmune disorders
- disruption of immunoregulatory mechanism
- change in cell mediated or humoral immune response
- results in self-destruction of tissues
Gene susceptibility in autoimmune
- gene maping
- candidate for Loci for susceptibility: identifiable regions of a chromosome that are inherited with the illness in families,
- Epigenetic (internal/external factors)
- HLA locus
Infections, tissue injury and autoimmunity
How are infections and tissue injury related to autoimmunity
- bacteria
- myocoplasma
- viruses
- can precipitate autoimmunity esp. if left untreated
- there is also a genetic component
Medical management of autoimmune disorders
- DX: lab tests, and presentation
- Treatment: meds ie. corticosteriods, saliclates (apsirin), other
Systemic lupus
- Discoid and SLE
- inflammatory disease
- more common in women of child bearing age
- african american more likely
- first degress relatives having it puts you at risk
Etiology of SLE
- interrelated immunologic, environmental, hormonal, genetic
- periods of intermittent exacerbations and flareups
- theory of latent virus infection
- physical or mental stress
- strep/viral infections
- sun expoure (unable to protect dermal layer)
- immunizations
- pregnancy
- abnormal estrogen metabolism
Pathogeneis of
systemic lupus
- autoantibodies
- vascular abnormalities
- infammatory mediators
DX of systemic lupus
- clinical findings
- lab tests (ANA, anti-double-stranded DNA antibody, anti-sm, antiphospholidpid antibody and low complements)
Impairments/symptoms of SLE
- MSK
- neuromusuclar
- Cardiovascular/pulmonary
- other
- MSK: arthralgias, polyarthritis
- neuromusuclar: neuropsychiatric manifestations, cognitive impairments
- Cardiovascular/pulmonary: vasculitis, pericarditis, dyspnea, myocarditis, endocarditis, tachycardia, pneumonitis, CHF, pulmonary HTN, leg ulcers, raynauds
- other: fever, wt gain, malaise, fatigue, skin rashs, alepecia, leg ulcers gangrene, renal disease, anemia
Medical management of SLE
- prevent flare ups with lifestyle changes and support groups
- meds
- treat symptoms
- cannot push them during flare ups
Medications for SLE
- NSAIDs
- corticosteriod-sparing agents
- anticoagulants
- antimalarial agents flare ups
- immunomodulating drugs
- cyclophosphamide
- corticosteriods
- cytotoxic drugs
Special implications for PT with lupus
- skin inspection and care (watch for infection)
- pacing activities
- strengthening to tolerance
- education: awareness of triggers
- monitor for medication reactions
- monitor changes in systems
Fibromylagia: incidence
- 90% of cases in women
- age 20-55
- 1st degress femal relatives
Risk factor for fibromyalgia
- prolonged stress
- anxiety
- trauma
- rapid steriod withdrawal
- hypothyroidism
- infections
Etiological factors for fibromyalgia
- under investigation
- diet
- viral
- sleep disorders
- occupations
- seasonal
- enviornmental influences
Pathogenesis of firbomyalgia
- CNA malfunction related to pain transmission and inhibition ??
Diagnosis
of fibromyalgia
Clinical finding criteria:
1. widespread (4 quadrant pain) both above and below the waist present for at least 3 months
2. subjective report of pain when pressure is applied to 11/18 comon FMS tender points
FMS: tender points
- Low cervical (C5-C7)
- Second rib costochondral junctions
- Lateral epicondyle
- knees (medial condyle/fatt pad)
- occiput (bilateral)
- trapezius,
- supraspinatus (above medial border of scapula)
- gluteal
- Greater trochanter
System involvemetn with
Fibromyalgia
- MSK:
- neuromuscular
- Cardiovascular/pulmonary
- Other:
- MSK: myalgias, arthralgias, muscule pain, tender points, morning stiffness >30 minutes
- neuromuscular: hyperactive sympathetic/hypoactive parasympathetic, global anxiety, cognitive problems
- Cardiovascular/pulmonary: Mitral valve prolapase
- Other: visual problems, mental and physical fatigue, IBS, headahces, dry eyes and mouth, hypersensitivity to noise odors heat or cold,
`
Medical management
fibromyalgia
Treatment
- treatment
- pharmaceuticals: antidepressants, muscule relaxants, analgesics, anticonvulsants
Sepcial implications for PT
fibromyalgia
- screening- composite autonomic symptoms scale (COMPASS)
- nail bed blanching with pain
- monitor for response for meds
- monitor vitals
- US
- education to recognize triggers and learn to pace
- low to moderate intensity aerobic exercise and strengthening
- aquatic therapy
Isoimmune disease
- organ and tissue transplantation
- prescreening for HLA match
- immunosuppressants post transplant (selective immunosuppressants)
cyclosporine and tacrolimus
- FK, CYA< and rapa
- affects specalized T cells turning into T help cells or T suppressor cells cytotoxic
Immunosupressant med
Azathioprine and mycophenolate mofetil
- act on bone marrow and thymus
- affects B-cells, T-cells, lympohid tissue
Prednisone
what does it affect
- acts on monocytes and immature lymphocytes
- affects macrophages, lympthocytes (bone marrow, thymus, B-cells, T-cells and lymphoid tissue)
