Exam 1 Flashcards
causes of immunosenecence
Thymic involution causes decrease in production of T-cells, with memory T-cell proliferation increasing to compensate. Decreased IL-2 production and decreased expression of IL-2 receptors
what does IL-2 do
tells the T-cells to proliferate
what accounts for increase in autoimmunity in the elderly?
decreased regulation of CD8 T-cells, so they attack “self”
definition of sarcopenia
loss of skeletal muscle and function due to a variety of causes
what assesses for sarcopenia
DEXA scan
DEXA aka
dual-energy x-ray absorptiometry
prevalence of sarcopenia ages 60-69
15%
prevalence of sarcopenia over age 80
> 40%
muscle mass loss after age 65
5% per year
pathophysiology of IBM
MAC triggers cytokines amyloid deposits
CK levels in IBM
normal
Muscle biopsy IBM
CD8 MHC1 lesion
IBM distribution
distal
poly distribution
proximal
dermato distribution
everywhere
treatment for inflammatory myopathies
steroids, methotrexate, IVIG
long term treatment for dermato
methotrexate
short term treatment for dermato flare-ups
steroids
dermatomyositis presentation
transient weakness with hand, foot, face rash
muscle effects of statins
rhabdomyolysis, increased CK, myalgias, myoglobinuria
muscle effects of glucocorticoids
atrophy with proximal weakness
muscle effects of alcohol
muscle breakdown, rhabdo, myoglobinuria
muscle effects of local drug injections
necrosis, skin induration, limb contractures
PR presentation
bilateral shoulder and pelvic girdle pain “belt area” with upper limbs more painful, weight loss, night sweats, fever
PR tests
no muscle biopsy, elevated CRP/ESR, low CK
PR treatment
prednisone (long-term) 100 mg
what tests to monitor PR/GCA treatment
CRP, ESR
PR/GCA treatment
prednisone 200 mg
GCA presentation
headache, jaw claudication, temporal artery tenderness, transient unilateral vision loss, fever, anemia
GCA management
refer to ophthalmology for biopsy (not evident on ophthalmic exam)
GCA treatment for vision loss
IV steroids
GCA treatment, if no vision loss
oral steroids
ESR CRP for GCA
elevated
common locations for GCA
temporal artery, aortic arch
how to distinguish GCA from takayasu
Takayasu more common in young females
amaurosis fugax aka
transient monocular vision loss
if GCA biopsy is negative…
treat anyway
presentation of OA
monoarticular, goes away after 30 minutes
RA joints affected
MCP, (ulnar deviation)
OA joints affected
DIP (herberden) and PIP (bouchard)
inflammatory markers for RA/OA
positive for RA, negative for OA
presentation of RA
“malar rash” polyarticular pain and stiffness, unchanging
pathophys of RA
immune cells complex within the synovium of a joint leading to pannus formation and joint destruction
peak incidence of RA
60s to 80s
possible etiologies of RA
genetic, infectious, hormonal, environmental
diagnosis of RA
RF, anti-CCP antibodies
RA management
non-pharmacologic: education, support, OT/PT, psych. Pharmacologic: DMARDs (methotrexate), NSAIDs, biological DMARDs (eternacept - expensive, leflunomide), antimalarials
what to do before starting immunosuppressants
test for TB, renal, LFTs, vaccinate, examine comorbidities (HIV)
SLE presentation in elderly
malar rash, glomerulonephritis, cytopenia
SLE most affected population
young females, elderly people
SLE delay in diagnosis causes
must have 4/11 diagnostic criteria; they don’t always present all at once
early SLE symptoms
malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis