rheumatic disease Flashcards
rheumatic diseases
localized or systemic inflammation
- msk system damage, internal organ damage
endogenous vs exogenous in initiating forces of acute diseases
edo: crystal deposition, uric acid (gout)
exo: new medication of infection
general principels of rheumatic diseases
disease initiation, propagation, flares
chronic disease initiating force
remote and unrecognizable (no longer present with typical acute inflammation symptoms)
disease phenotype is fully established
propagation of rheumatic disease
autoimmune response- self-amplified cycle of damage, self-antigens, can elicit innate and adaptive immune response
self-limited
acute episodes of RD. removal of stimulus that causes the inflammation, re-exposure can cause flares
pathogenesis of inflammation 1) cytokines
upregulation of cytokines
2) endothelial activation
pro-inflammatory cytokines-> promote inflammation-> trigger adhesion-promoting receptors on blood vessel endothelium (Adhesion!)
contributes to atherosclerosis
3) complement pathway
augments, amplifies the inflammatory response.
or upregulation= abnormal response
4) immune complex formation
macrophages and neutrophil complexes- damage healthy tissue if released in large amounts- follows upregulation of complement pathway
might present as a rash
5a) cellular cytotoxicity upregulation
cell mediated: cytotoxic T lymphocytes - capable of destroying target cells
5b) cellular cytotoxicity upregulation
antibody-dependent cellular cytotoxicity: destruction of antibody-coated target cells by natural killer cells
6) host tissue differentiation
inflammatory mediators and t cells stimulate cells unrelated to immune response to change function. (think metaplasia)
gout clinical presentation
crystal-induced inflammation of synovial joints
male 3x more than female
monosodium urate crystals in joint space= sever acute joint pain and swelling
most common locations: great toe, midfoot, ankle and knee
gout flare ups
flares: one week, typically resolve spontaneously (self-limiting)
overtime flares can become more frequent and painful- results in chronic destructive condition (joint deformity)
underexcretion vs overproduction etiology in gout
under: 90% of patients, most often due to impaired renal function or diuretics
over: 10% of patiens diet, medication, defects in pathway leading to increased uric acid production
immune system mechanisms involved in gout
triggers complement pathway- attracts neutrophils
vasodilators- pain and swelling
macrophage destruction of crytsals- increased adhesion molecules and localized endothelium response
gout clinical manifestations
podagra: sever inflammatory arthritis at the first metatarsal joint- most frequent
d/dx episodic oligoarticular arthritis: most common type of juvenile arthritis
tophi formation: chronic gout most often occurs on tendon tissue on extensor side of hand
chronic erosive polyarthritis: over years, destruction of joints
gout treatment
anti-inflammatory medication, activation of involved joints- AROM/PROM
prevention: decrease serum uric acid levels (diet)
immune complex vasculitis clinical presentation
acute inflammatory disease of the small blood vessels, palpable purpura, arthritis, abdominal pain
etiology of immune complex vasulitis
antigen from exogenous source- skin infection, virus, seasonal allergies
antigen from endogenous source- systemic lupus, vascular immunoglobins (proteins)
both result in intense inflammatory response
pathophysiology of ICV
antigens elicit an ongoing humoral response due to abundant quantities- initiators
deposition of immune complexes in vessel endothelium- propagator
typically self limiting
serum sickness
immune system reacts to medicines that contain proteins used to treat immune conditions
clinical presentation of lupus
systemic autoimmune RD- chronic inflammation injury damage to multiple organs
females 9x more than men
lupus etiology
complex- genetic susceptibility and poorly defines environmental factors
inefficient clearance of nonimmune apoptotic cells- upregulation inflammatory response
initiation of lupus
hyperactive autoantibody response to self-antigens (comp pathway)
unique apoptotic cell death stimulates immune response
propagation of lupus
combined result- continued immune response and tissue damage due to response derived from apoptotic cells and damaged cells
auto-amplification: hallmark of lupus
clinical manifestation of lupus
multisystem autoimmune disease, characterized by periodic flares, symptoms are highly varied, universal feature: production of autoantibodies, skin rash, renal disease, hematologic disturbances, inflammation of serosal surfaces, neurologic syndromes.
clincial presentation of rheumatoid arthritis
chronic systemic inflam disease
persistent symmetric inflammattion of multple peripheral joints
characterized by chronic inflam proliferation of synovial lining of diarthrodial joints- aggressive cartilage destruction adn bony erosion **
epidemiology of rheumatoid arthritis
1% of pop
femal 3x more
onset in 60s
etiology of RA
majority of destruction occurs in joint rynovium- lungs, skin and blood vessels can be affected
genetic and environmnetal factors can influence condition
pathophysiology of RA
synovium significantly expansion of cellular lining composed of activated cells, high concentration of b cells, t cells, macrophahes= joint pannus
RA synovium can invade adjacent tissue such as cartlage and bone
decreased ROM
initiaitino of RA
genetic factor
environmental factor: cigarette smoking
autoantibodies: hallmark featur- development of antigen-driven autoantibodies
RA propogation
autoantigen interact with immune cells- amplify disease process
RA clinical manifestation
persistent progressive disease, fatigue and joint inflammation, small and large joints (bilateral) joint deformities, cervical spine can be involved but not lower spine
RA treatment
anti-inflammatories, immunomodulatory
all aim to slow progressive joint erosion
