inflammation Flashcards
RA: Early pathologic change is
rheumatoid synovitis. Synovium becomes inflamed. Lymphocytes and plasma cells increase.
RA: Over time, ____________ occurs, and ______________ grows across the cartilage surface (pannus) from the edges of the joint. Joint surface shows loss of _______ beneath the extending pannus, most marked at joint margins.
articular cartilage destruction
vascular granulation tissue
cartilage
RA: Inflammatory pannus causes focal destruction of _______. Osteolytic destruction of ______ occurs at joint edges, causing erosions seen on x-rays. This phase is associated with _________.
bone
bone
joint deformity
RA onset
young/middle age
RA is more common in _____ than _____
women
RA weight is
lost or maintained
RA is a ________ disease with exacerbations and remissions.
systemic
RA affected joints
Small joints typically affected first (PIPs, MCPs, MTPs), wrists, elbows, shoulders, knees. Usually bilateral, symmetric joint involvement.
RA pain characteristics
Stiffness lasts 1 h to all day and may ↓ with joint use. Pain is variable, may disrupt sleep.
RA effusions are _______
common (loss of fluid)
RA Nodules are present, especially on _____ surfaces
extensor
RA synovial fluid WBC count
5000–60,000/μL (could be high) with mostly neutrophils; decreased viscosity.
RA x rays show
Joint space narrowing and erosion with bony overgrowths, subluxation with advanced disease. Osteoporosis related to decreased activity, corticosteroid use.
most likely lab findings for RA
RH (Rheumatoid factor) positive
increased ANAs (antinuclear antibodies)
positive anti-CCP (anti-citrullinated peptide)
increased ESR (Erythrocyte Sedimentation Rate) /CRP (C-Reactive Protein)
typical RA deformities
(A) Ulnar drift. (fingers bend toward pinky)
(B) Boutonnière deformity. (middle joint bends down, distal joint extends up)
(C) Hallux valgus. (big toe deviates toward other toes)
(D) Swan neck deformity. (distal joint bent toward palm, proximal joint bent away from palm)
RA can affect nearly every ____________
body system
Atherosclerosis (narrow, hard arteries) can result from
chronic inflammation that damages endothelial cells within blood vessels. More cholesterol plaques may be formed. When plaques break loose, they can lead to heart attack or stroke.
Sjögren syndrome
dried up
Felty syndrome
enlarged spleen and low white blood cell (WBC) count
increased risk of lymphoma
RA stages
1) no destruction
2) slight destruction, no deformities
3) joint deformity without joint fusion
4) joint fusion
A RA patient-specific treatment plan considers
disease activity, joint function, age, sex, family and social roles, and response to previous treatment
DMARDs stands for
disease-modifying antirheumatic drugs
BRMs - Biologic response modifiers (also called biologics or immunotherapy) are used to
slow disease progression
BRMs can be used to treat patients with moderate to severe RA who have not responded to DMARD
synovectomy
removal of joint lining
arthroplasty
total joint replacement
Gout is a type of arthritis characterized by
elevation of uric acid (hyperuricemia) and the deposit of uric acid crystals in 1 or more joints.
marked by painful flares lasting days to weeks followed by long periods without symptoms.
Uric acid is the major end product of purine catabolism. It is excreted by the ______
kidneys
Gout occurs when either the kidneys cannot excrete enough ______ or there is too much being made for the kidneys to handle effectively.
uric acid
Primary hyperuricemia
genetic. Accumulation of uric acid may be due to a lack of uricase.
Uricase breaks down ______ into water-soluble products for elimination in urine. A lack of uricase then leads to __________
uric acid
uric acid retention
Secondary hyperuricemia may be caused by
conditions that increase uric acid production or decrease uric acid excretion or drugs that inhibit uric acid excretion
Persons with other forms of inflammatory arthritis (e.g., RA, PsA) are more likely to develop
gout
Not everyone with high uric acid levels develops gout. Two processes are essential for a person to develop gout:
crystallization (excess urate coalesces into crystals) triggering inflammation
The gold standard for diagnosis of gout is
synovial fluid aspiration
Acute gout is treated with
oral colchicine (Colcrys, Mitigare, antiinflamatory but not analgesic) and NSAIDs (for pain)
Systemic lupus erythematosus (SLE) is a
multisystem inflammatory autoimmune disease
lupus clinical manifestations
butterfly rash
skin lesions
erurythmia
kidney, renal, cardiac, psychological, nervous system problems
oral ulcers
siezures
photosensitivity
arthritis
lupus treatment
NSAIDs and Antimalarial agents, such as hydroxychloroquine and chloroquine
Also
Steroid sparing Methotrexate as well as
Corticosteroids, anticoagulants, immunosuppressive drugs
Fibromyalgia (FMS) is a
chronic central pain syndrome marked by widespread, nonarticular musculoskeletal pain and fatigue with multiple tender points. It is a common musculoskeletal disorder and a major cause of disability
FMS involves abnormal central processing of _________________ in the CNS
nociceptive pain input
FMS clinical manifestations
widespread burning pain that fluctuates through the course of a day
may have pain in response to a stimulus that does not typically cause pain (allodynia)
neurological manifestations of SLE
stroke, siezures, psychosis
Articulation
Joint
Or
Being able to pronounce things clearly
Swelling, pain, heat, redness, loss of mobility
Local manifestations of inflammation
Fever, leukocytosis (increases WBC), malaise, fatigue
Systematic manifestations of inflammation
Allopurinol (a xanthine oxidase inhibitor) treats for _____ but not ______
Treats for gout flare-ups (by reducing uric acid) but not pain
Diet education for gout requires refraining from foods high in _____
Purine (liver, beer, anchovies, wine)
Lupus patients should limit their ______ exposure
Sun
Use cold for _____ and heat for ______
Cold for gout, heat for lupus
FMS can be treated with ____ and _____
Anticonvulsants and antidepressants
