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Pathopharm 326 > Musculoskeletal (OA, RA, SLE) > Flashcards

Musculoskeletal (OA, RA, SLE) Flashcards

1
Q

4 major parts of a joint

A

subchondral bone plate

articular cartilage

synovium

joint capsule

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2
Q

synovial or diarthrodial joint is any joint that allows __________.

A

movement

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3
Q

three phases of bone healing

A
  • inflammatory
  • reparative
  • remodeling
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4
Q

inflammatory phase of bone healing

A

hematoma forms at fx site
provides stability
aseptic inflammation occurs

duration
1-3 days for hematoma
3 days - 2 weeks for early repair

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5
Q

reparative phase of bone healing

A
  • fibrous cartilage → formation of granular tissue containing blood vessels, fibroblasts, osteoblasts
  • formation of callus → when granular tissue has matured
  • ossification → space in bone is bridged and fx ends are united; callus replaced by trabecular bone

duration → 6 weeks

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6
Q

remodeling phase of bone healing

A

bone consolidation with final remodeling

healing complete

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7
Q

osteoarthritis (oa)

A

degeneration of joints cause by aging and stresses
most common cause of disability in US
obesity and aging are ↑ oa in U.S.

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8
Q

commonly affected joints of oa

A 
cervical spine
lumbosacral spine
hip
knee
hand 
first metatarsal phalangeal joint (big toe)
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9
Q

spared joints of oa

A

wrist
elbow
ankle

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10
Q

etiology of oa

A

stresses applied to joints (weight bearing)
degeneration of cartilage (begins in articular cartilage)
chronic disease

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11
Q

osteophytes

A
  • small bony projections that develop along the rim of bone adjacent to cartilage loss
  • important hallmark of OA
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12
Q

sxs of oa

A
  • deep aching joint pain, esp. after exercise, relieved with rest
  • joint pain during cold weather
  • stiffness in the morning
  • crepitus of joint during motion
  • joint swelling
  • altered gait
  • limited range of motion (thickening of synovial fluid)
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13
Q

OA physical exam

A

joint
deformity
tenderness
↓ ROM

fingers often involved
distal interphalangeal joint (DIP) - Herbeden’s nodes
proximal (PIP) - Bouchard’s nodes

both caused by osteophytes

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14
Q

dietary supplement for oa

both also naturally occur in the body

A

glucosamine sulfate - maintains cartilage health

chondroitin sulfate - might slow cartilage breakdown

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15
Q

s/s of DDD in lumbar spine

A
  • pain in low back that radiates down back of leg (sciatica)
  • pain in buttocks or thighs
  • pain that worsens when sitting, bending, lifting, or twisting
  • pain that’s minimized when walking, changing positions or lying down
  • numbness, tingling, or weakness in the legs
  • foot drop
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16
Q

s/s of DDD in cervical spine

A
  • chronic neck pain that can radiate to the shoulders and down arms
  • numbness or tingling in the arm or hand
  • weakness of the arm or hand
17
Q

rheumatoid arthritis

A

type III hypersensitivity

systemic, autoimmune disease of the synovium

18
Q

RA etiology & risk factors

A

not fully understood
environmental and genetic factors

40s-60s
women (2.5x higher risk than men)
tends to show up after pregnancy
tobacco use

19
Q

RA patho

A

autoimmune attack against the synovial tissue
Immune cells activated
-lymphocytes
-macrophages
-produce rheumatoid factor (RF) → auto-antibody against IgG
-formation of immune complexes & activates complement

measure RF in serum and that’s how RA’s diagnosed

20
Q

progression of RA

A
  • cartilage is destroyed by osteoclasts
  • pannus develops → type of scar tissue that’s vascularized so it’s able to get nutrients but also contains inflammatory cells
  • pannus very destructive
  • causes: bone erosion, bone cysts, fissure development
21
Q

RA clinical manifestations

A
  • early → vague sxs of fatigue, malaise, wt loss, generalized stiffness
  • joint manifestations → symmetrical (different from OA); pain, stiffness, motion limitation; inflammation: heat, swelling, tenderness

advanced disease → deformity & disability; joint subluxation

RA nodes feel spongy, soft
OA hard bc it’s bone
Swan neck deformity - common; joint has lost structure so it bends down (tip of finger)

22
Q

RA can also be systemic

A

important to assess other systems

rheumatoid nodules - occur in about 25% of RA pts

  • immune-mediated granulomas
  • develop around inflamed joints & lungs
  • subcut and firm, sometimes painful
23
Q

systemic lupus erythematous (SLE)

A 
type III hypersensitivity
autoimmune inflammatory disease
   -multiple organ systems
   -acute flare-ups
   -unpredictable

attacks body’s dna

two forms

  • discoid - targets skin
  • systemic - internal organs
24
Q

SLE predisposing factors

A 
genetic factors
female
20-40
blacks
sun exposure/uv rays
allergy to abx
prolonged exposure to estrogen
tobacco use
25
Q

SLE patho

A
  • beta lymphocytes are hyperactive & produce autoantibodies (antinuclear antibody)
  • activated against DNA
  • formation of immune complexes
  • can impact all major organ systems
  • inflammatory response destroys tissue
  • kidneys often affected
26
Q

SLE manifestations (early?)

A 
extreme fatigue
photosensitivity (butterfly rash)
fever
wt changes
unusual hair loss
edema
raynaud's phenomenon - capillary constriction in distal extremities, often triggered by cold
27
Q

SLE manifestations

A

CNS: HA, dizziness, seizures, stroke

Lungs: pleuritis, pleural effusions

heart: myocarditis & endocarditis
kidneys: nephritis (50% develop kidney damage)

blood vessels: vasculitis

blood: anemia, leukopenia, thrombocytopenia, blood clots
joints: arthritis

28
Q

SLE flares

A

warning sign: fatigue, pain, HA

prevention → recognize warning signs and avoid triggers

triggers: sunlight exposure, infection, abruptly stopping a med (steroids), stress (try to manage)

29
Q

Sjogren syndrome (seen in RA & SLE)

A

autoimmune destruction of any moisture producing gland
enlarged glands with decreased functioning

lacrimal: ↓tearing, burning, itchy dry eye
salivary: dry reddened deeply fissured tongue; loses its papilla; ↑ risk for candida infections

30
Q

methotrexate

A

classification: antineoplastic (folic-acid antimetabolite)
DMARD (disease modifying anti-rheumatic drug)

moa: immunosuppressive

administered weekly via PO or SQ/IV route

31
Q

methotrexate SEs

A

GI: N/V, anorexia, liver toxicity
bone marrow suppression
shortened life expectancy

Pt teaching: watch for signs of infection; expect GI effects

32
Q

methotrexate nursing implications

A

11 black box warnings

folic acid supplementation is necessary

NO ETOH

Teratogenic

Contact HCP if s/s of infection develop

33
Q

hydroxychloroquine

A

DMARD
antimalarial, antirheumatic

MOA: unknown, antiinflammatory properties

slows progression of RA when used with another DMARD

SE: retinopathy (rare)

Pathopharm 326 (16 decks)

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