• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/100

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

100 Cards in this Set

  • Front
  • Back
what is the female to male ratio with RA
2:1 to 4:1
what is RA
autoimmune disease of unknown origin
where does the autoimmune reaction in RA occur
synovial tissue
what does pannus in RA do
erodes bone and destroys cartilage
what happens with RA
- phagocytosis w/ enzyme production in joint
what do enzymes in RA breakdown (4)
collagen and cause
- edema
- proliferation synovial membrane
- pannus formation
where do degenerative changes occur with RA
muscle fibers
result of RA
- loss tendon and ligament elasicity and contractile power
S&S of RA (6)
- joint pain
-swelling
-warmth
- erythema
- lack of function
- deformity
what does deformity in RA depend on
disease stage and severity
where does Ra usually begin
small joints (hands, wrist, feet)
progression of RA goes where (7)
- knees
-shoulders
- hips
-elbows
- ankles
- cervical spine
-TMJ
what are the Sx like during onset of RA
bilateral and symmetric
when is RA the worst
AM (joint stiffness)----classic sign
common with RA
deformities of hands and feet
what type of disease is RA
systemic
what are the common S&S of RA (10)
- fever
-wt loss
- fatigue
- anemia
- lymph node enlargement
- raynauds phenonmenon
- arteritis
- neuropathy
-pericarditis
- splenomegaly
- sjogren syndrome
what is sjorgens syndrome
dryness of eyes and mucus membranes
what are rheumatoid nodules
- non tender, movable nodules in SQ tissue
rheumatoid nodules are associated with what
rapid progression/destructive disease
DX for RA (7)
- Px exam
- xray
- rheumatoid factor (75%)
- elevated ESR
- decreased RBC and C4 complement
- positive CRP
-positive antinuclear antibody
mgnt for RA early disease (5)
- education (balancing rest and exercise)
- salicylates or NSAIDS, COX2
- DMARDS
- methotrexate
- biologic response modifiers
what are the DMARDS (4)
- antimalarial
-gold
- penicillamine
- sulfasalazine
successful in preventing joint destruction and long term disability
methotrexate
what are the biologic response modifiers (5)
- etanercept ( enbrel)
- infliximab (remicade)
- adalimumab (humira)
- golimumab (simponi)
- anakinra (kineret)
what do the BRM do with RA
inhibit cytokines
mgnt for moderate erosive RA (3)
- OT/PT
- cyclosporine
-immunosuppressants
what are the cyclosporins (3)
- neoral
-sandimmune
- gengraf
can help enhance methotrexate
immunosuppresants
mgnt for persistent erosive RA (2)
- recontructive surg
- corticosteriods
used when pain is not controlled and it interferes with independence
reconstructive surg (synovectomy, tenorrhaphy, arthrodesis, arthroplasty)
low dose while slower acting meds take effect
corticosteriods
mgnt for advanced unremitting RA
- immunosuppressive agents
affec antibody production at cellular level
- immunosuppressive agents
what are the - immunosuppressive agents (4)
- rhematrex
- cytoxan
- imuran
- arava
what can result with use of immunosuppressive agents (4)
-bone marrow suppression
-anemia
-GI disturbance
-rashes
what should be done if RA is unresponsive to DMARDS
apheresis (filters out IgG )
inborn errors of immune function
primary immunodeficiencies
when are primary immunodeficiencies typically diagnosed
infancy in the 4-6 mth period
S&S of phagcytic dysfunction (6)
- bacterial inf
- fungal inf
- viral inf
- recurring abscesses
- sinusitis
- bronchitis
tx for phagcytic dysfunction (4)
- abx
- antifungal/antivirals
- GM-CSF
- G-CSF
Dx for phagcytic dysfunction (2)
- S&S
- prolonged infection with no response to tx
used cautiously with phagcytic dysfunction
prophylactic medication
considered a curative option for phagcytic dysfunction
hematopoietic stem cell transplantation (HSCT)
replaces abnormal production with normal functioning cells
HSCT
lack plasma cells and antibody production
agammaglobulinemia (brutons disease)
decreased production with decreased immunity
B cell def
diminished antibody production from lack of differentiation into plasma cells
hypogammaglobulinemia
hypogammaglobulinemia AKA
CVID
risks with CVID (4)
- autoimmune diseases
- granulomatous
- malignancy
- pernicious anemia
Tx for B cell def (3)
- IVIG
- cyroprecipitate
- plasma
what can t cell def lead to
opportunisitc infections
Digeorge syndrome
thymic hypoplasia (lask of thymus)
what are the T cell cef (2)
- thymic hypoplasia
Tx for chronic mucotaneous candidiasis (3)
- transplant fetal/ postnatal thymus
- BMT
- IVIG
what does chronic mucotaneous candidiasis effect (5)
- mucous membranes
- skin
-nails
- endocrine abnormalities
- hypofunction parathyroid and adrenal cortex
when does thymic hypoplasia occur and what does it look like (4)
- soon after birth
- cardiac anomaly
- hypocalcemic tetany
- facial abnormailites
huge concern with IVIG and can cause what
-cardiac issues
-wt gain
what is SCID
B and T cell missing
what is wiskott aldrich syndrome
variation of SCID
tx for combined B and T cell def (3)
- IVIG
- thymus gland transplant
- HSCT
what is telangiectasis
development and dilation of extra vessels
now viewed as chronic disease treated as outpt
HIV
more acute condition, and may require hospitalization
AIDS
transmission of body fluids containing free virions and infected CD4+ Tcells
HIV 1
how can HIV 1 be transmitted (5)
- blood
- seminal fluid
- vaginal secretions
- amniotic fluid
-brst milk
most important with HIV and AIDS
prevention
replicates RNA strand and then forms DNA and can divide and form new cells
retrovirus
what type of virus is HIV
retrovirus
what are stages of HIV based on (2)
- clinical condition
- CD4 +T cell ct
when are antibodies usually produced with HIV
within 3-12 wks after infection
test done to confirm HIV
- enzyme immunoassay (EIA) and if positive then western blot confirms it
uses saliva to perform EIA
OraSure
tx for HIV
HARRT
adverse effects of HARRT (4)
- hepatoxicity
- nephrotoxicity
- osteopenia
- increased risk of CVD, MI, DM
is tr of HARRT is disrupted what is the result (3)
viral rebound
immune decompensation
- clinical progression
GI effects with HIV (6)
- wt loss
- progressive tissue wasting
- chronic diarrhea
- loss appetite
- N/v
-oral and esophageal candidiasis
most common (80%) w/o prophylactic tx in HIV
pneumocystis pneumonia (PCP)
what does edema from scleroderma cause
- taut
-smooth
- shiny skin
what happens with scleroderma (2)
- tissues become nonfunctional
- fibrotic changes causing loss of elasticity and movement
where does scleroderma changes occur (3)
- blood vessels
- major organs
- body systems
S&S of scleroderma (13)
- raynauds pheno
-swelling of hands
- hardness and rigidity of skin
- wrinkles/lines obliterated
- stiff extrem (loss of mobility)
- frozen face
-rigid mouth
- L vent heart failure
- esophagus hardens
- lungs become scarred
- hardened intestinal mucosa
- renal failure
- CREST
what is CREST (5)
- calcinosis
- raynauds phenom
-esophageal hardening
-sclerodactyly
-telangiectasia
mgnt for scleroderma (8)
-depends on presentation
- pain mgnt
- limit disability
- exercise to reduce contractures
- avoid extreme temps
- lotion to minimize dryness
-CCBs
- anti inflammatory agents
used to control stiffness, arthralgia, and general discomfort with scleroderma
anti inflammatories
help improve raynauds phenom
CCBs
what is sclerodactyly
loss of use of digits
more at risk for SLE
females
disturbed immune regulation exaggerated production autoantibodies
SLE
cause of SLE (3)
- combo genetics
-hormonal factors
- environmental factors
meds r/t chemical induced SLE (5)
- hydralazine
- procainamide
- isoniazid
- chlorpramazine
- some antisz meds
promote onset of flare ups in SLE
B cells
S&S of SLE (10)
- arthritis
- papulosquamous
-annular lesions
- chronic rash
-erythematous rash bridge of nose and cheeks
-oral lesions
- pericarditis
- early atherosclerosis in women
- renal involvement (HTN)
- neurologic changes
dx for SLe (2)
- hx and px
- blood tests
what can be noted on examination of SLE (7)
- skin rashes
- hyper/depigmentation
- sensitivity to sunlight or ultraviolet light
-alopecia
- oral ulcers
-pleural effusions
- infiltrates
topicals corticosteriods with SLE used for what
cutaneuos
low dose corticosteriods with SLE used for what
minor disease activity
high dose oral or IV corticosteriods with SLE used for what
major disease activity
tx for SLE (5)
- NSAIDS adjunt to corticos
- immunosuppresives
- cytoxan
- imuran
- sanimmune
why are immunosuppresives (cyclosporins) given in the AM
bc it can cause hemorrhagic cystitis so need plenty of fluids to flush it out