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GNRS 515 Advanced Pathology For Nurse Practitioners: Alterations In Muscular Development + DMD

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GNRS 515 Advanced Pathology For Nurse Practitioners: Alterations In Muscular Development + DMD

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GNRS 515 Advanced Pathology For Nurse
Practitioners: Alterations In Muscular Development
+ DMD

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Terms in this set (31)


TERM DEFINITION LOCATION

Duchenne's Muscular dystrophy deficiency; it is the gene that
Dystrophy causes muscles to attach themselves to
surrounding structures




Classic Inflammatory joint disease can Infectious (by invasion of pathogens) or
be: Noninfectious
-By deposition of crystals (gout)
-Immune reactions (rheumatoid arthritis)


Historically called arthritis. Characterized by damage
to synovial membrane or articular cartilage and
systemic signs of inflammation: fever, leukocytes,
malaise, anorexia, & hyperfibrinogenemia.


rheumatoid arthritis (RA) chronic, systemic, inflammatory autoimmune disease


It particularly affects the joints and involves:
-Synovial inflammation
-Joint swelling, and ankylosis
-Destruction of articular cartilage


It affects the synovial membrane first


Many cytokines and inflammatory enzymes
contribute to the joint damage, and development of
an exaggerated immune response, including:
Interleukins, T & B cells, and collagenase

,RA Patho Quick Leukocytes infiltrate into the synovium leading to
synovitis and eventual joint damage


[May spread to surrounding capsules]


Joints most commonly affected include:
Fingers (first), wrist, elbow, shoulder
Feet, ankles, knees
Hip and cervical spine
Tissues of the lungs, heart, kidneys and skin can be
affected as well


RA Genetic RF Genetic RF:
Most significant, are variations in HLA genes, genes
of the major histocompatibility complex
Particularly the HLA-DRB1 gene, an MHC class II
gene expressed in antigen presenting cells
Proteins produced from HLA genes assist the
immune system in distinguishing self proteins from
non-self proteins (bacteria and viruses)


Epigenetic factors can confer the effects of
environmental triggers, such as smoking or diet
T cell abnormalities appear in individuals with RA,
indicating a defect in telomere repair (results in faster
aging and loss of immune function)
Those with a genetic predisposition to RA have an
increased risk when they smoke
-Or repeated bronchial stress
-Or infections (Epstein-Barr virus, E. coli)
-This results in repeated activation of innate immunity
which occurs over many years
Autoimmunity increases gradually until some
unknown process tips the balance toward clinically
apparent disease
Once the inflammatory process is established, the
synovium in RA organizes itself into an invasive
tissue that can degrade cartilage and bone

, RA Environmental RF: RF:
Age (highest among adults in their sixties)
Gender (two to three times higher in women)
Nulliparity
Women who breast-feed have a decreased risk of
developing RA
Low socioeconomic status, obesity
Early life exposures (children whose mothers smoked
have double the risk)

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