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AGPC 4!!!!!! > Joint Disorders > Flashcards

Joint Disorders Flashcards

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1
Q

Synovial fluid

A

Cartilage is most commonly the problem in a presenting patient. It does not have any blood supply and wears and tear with time and increased body mass. Synovium secretes nutrients (synovial fliuids) provides nutrients to cartilage and lubrication

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2
Q

Ligaments

A

connect bone to bone. Issue = lack of stability. Main purpose of ligament is stability.

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3
Q

Tendon

A

Tendons connect bone to the muscle. This main purpose is mobility. Tendon tear = lack of mobility, weakness.

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4
Q

Nerve (referred pain)

A

active and passive is normal, Poorly localized, “ burning”, parasthesia, numb, loss of sensation

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5
Q

Tendon, bursa

A

active is limited, passive is normal, localized pain

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6
Q

Muscle

A

active limited, passive is normal, Bilateral and proximal, Myalgia muscle pain is usually bilateral and proximal (shoulders, thighs) never localized

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7
Q

Joint

A

active and passive are limited, localized

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8
Q

Diagnostic approach to joint pain

A 
History and physical: 
Distribution?  
Timing (acute vs. chronic)? 
Inflammatory pain?
Distribution?  
Extra-articular manifestation?
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9
Q

Arthragia

A

pain

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10
Q

Arthritis

A

true joint inflammation

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11
Q

RA and Lupus

A

Same joints inflammed on both sides. Symmetrical small joints (wrists, hands) These are both chronic. > 6 weeks. Polyarticular

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12
Q

Viral (Hepatitis B&C, Epstein Barr, HIV, Parvovirus B19)–

A

symmetric, smaller joints more common Polyarticular

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13
Q

Polyarticular

A

> 4 joints. RA. Lupus. Viral.

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14
Q

Mono/ Olygoarticular

A

1-3 joints

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15
Q

Osteoarthritis

A

weight bearing joints (hips, knees, low spine)

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16
Q

Septic arthritis

A

monoarticular

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17
Q

Crystal arthritis (Gout/ pseudo-gout)

A

monoarticular, most common 1st metatarsophalangeal

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18
Q

Ankylosing spondylitis

A

(severe back pain in young patients < 40, more common in men)- spine joints

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19
Q

Other monoarticular causes

A

Lyme arthritis
Psoriatic arthritis (<10% of patients w/ psoriasis)
Arthritis w/ IBD ( in 20-30% )
Reactive arthritis ass with immune response to bacterial infections (usually 3 weeks after GI or GU infections)

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20
Q

Inflammation

A

Erythema
Warmth
Swelling
Stiffness (“gelling”) during period of inactivity > 1 h (better with exercise, hot shower, movement)

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21
Q

Examples of inflammation

A

RA, SLE, Ankylosing spondylitis, Gout, septic

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22
Q

No inflammation in this condition

A

OA

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23
Q

History of inflammation

A

Prolonged morning stiffness (> 1 hour), stiffness/ pain improves with activity

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24
Q

OA symptoms

A

No or minimal morning stiffness (< 30 min), pain worse with activity, Bony crepitus , mild tenderness, hard bony joint enlargement
NO redness, NO warmth, NO soft effusion, ESR, CRP normal

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25
Q

RA, SLE, Ankylosing spondylitis, Gout, septic inflammation s/s

A

Joint effusion (soft joint swelling, “bogginess”), tenderness, redness, warmth, ESR , CRP elevated

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26
Q

SLE extra articular symptoms

A

SLE – multiple extra-articular symptoms (arthritis is one of the manifestations). Skin lesions are common. Renal involvement is common

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27
Q

RA extra articular symptoms

A

few extra-articular symptoms (predominantly arthritis). Skin lesions are unusual and limited to subcutaneous nodules

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28
Q

OA extra articular symptoms

A

none

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29
Q

Psoriatic arthritis

A

skin (plaques), nails (pitting)

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30
Q

HIV, Hepatitis extra articular symptoms

A

asymptomatic or multiple systemic symptoms

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31
Q

A 67 y/o presents with a red and swollen Rt. knee for one day. He is unable to bear weight today. There is a limited passive and active ROM. Right knee joint appears swollen, red and tender

A

Both passive and active = joint
Acute = 1 day
Red, tender joint

Septic arthritis
Gout
Presents similarly

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32
Q

A 67 y/o obese female presents with Rt. knee pain for one year. She denies morning stiffness but reports that pain is worsen when a day goes by.
On exam- Rt. Knee- no swelling, or redness

A

Chronic, monoarticular
No morning stiffness = no inflammation
Pain worsens as the day goes by = degenerative bone problem
Joint problem = both active and passive are limited

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33
Q

A 36 y/o presents w/ symmetric wrist joints pain and swelling for 6 months. She reports 2 hours morning stiffness and improvement in symptoms when the day goes by. She is chronically tired. On exam – wrist joints are “boggy”, tender and warm

A 
Symmetrical = polyaricular
Wrist – small joint
Chronic
Morning stiffness = inflammation
Boggy, tender, warm
Lupus, Rhematoid
Limited acitve and passive == joint pain
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34
Q

A 36 y/o presents w/ symmetric wrist joints pain and swelling for 3 weeks. She reports 2 hours morning stiffness and improvement in symptoms when the day goes by. She is chronically tired. There is no rashes reported. On exam – wrist joints are “boggy”, tender and warm

A

3 weeks
Multiple joints
Morning stiffness = inflammation

Need 6 weeks until you can dx lupus

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35
Q

describe RA

A

Chronic autoimmune inflammatory disorder that predominantly affects joints
PROGRESSIVE disease (progress to joint destruction) if untreated
More common in women
Peak age of onset 25-50
Chronic PROLIFERATIVE SYNOVYTIS (inflammation of synovium) Joint EROSION joint deformities (advanced stage)

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36
Q

Clinical presentation of RA

A

SYMMETRIC SMALL joint involvement (wrists , hands, but NOT DIP) for at least 6 WEEKS Morning stiffness (> 1 h), IMPROVES w/ ACTIVITY On PE joints are swollen ( “bogginess”), tender, sometimes warm and erythematous, limited active and passive ROM. Deformities (advanced disease)
Extra-articular manifestations: rheumatoid nodules on exterior surfaces (20%), anemia of chronic disease, fatigue, osteoporosis. Pleural effusion and pericarditis are rare
RA is associated with an increased CV risk !!!

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37
Q

Diagnosis of RA

A

Diagnosis is CLINICAL (polyarticular arthritis > 6 week duration not attributed to viral arthritis or SLE). Tests to support clinical diagnosis (should never be used as the sole criteria for diagnosis) :

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38
Q

Tests to support clinical diagnosis of RA

A

Elevated ESR or CRP
(+) Rheumatoid factor in 70-80% (fairly sensitive) and poor specificity. High titers in patient with classic symptoms predict RA
(+) Anti-CCP (antibodies to cyclic citrulinated peptide) is more specific (95%) and slightly more sensitive (80-85%)
-Presence of both RA and anti-CCP makes a diagnosis is more likely
(+) abnormalities on x-rays

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39
Q

Anti CCP +

A

Severe RA

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40
Q

Abnormalities on x-ray in RA

A

Soft tissue swelling, bone erosions, joint narrowing

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41
Q

RA treatment goals

A 
Stop progression of the disease !!! (RA is not curable)
Improve symptoms (minimize pain, improve mobility)
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42
Q

Medications that improve symptoms of RA

A

NSAIDS, +/- steroids
Symptomatic control (breakthrough pain)
Work fast

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43
Q

Disease modifying antirheumatic drugs (DMARD)

A

Methotrexate, TNF inhibitors

44
Q

Methotrexate

A

initial oral , weekly dosage, well tolerated, inexpensive. Supplement daily folate

45
Q

TNF inhibitors

A

(Adalimubab- Humira®, Infliximab- Ramicade® )- IV or SubQ injections, well tolerated, expensive. Can be used in combination with MTX (more effective than alone)
70% achieve clinical remission
Do not work immediately (6 weeks)
Should start EARLY rather than later ( EARLY aggressive approach) Check for TB.

46
Q

Major s/e methotrexate

A

liver dysfunction and suppression of bone marrow. Monitor CBC and liver enzymes. Excreted in the kidneys. If renal dysfunction toxicity. Also given in ectopic pregnancy, will stop DNA synthesis.

47
Q

Systemic lupus erythematous (SLE)

A

Autoimmune disease with multi-organ involvement
More common in women ( 90%)
The disease is more common and more severe among women of African American and Hispanic backgrounds
Relapsing and remitting course (unpredictable flares)

48
Q

Clinical presentation of SLE Skin manifestations

A

in 70% of patients:
acute malar rash (butterfly rash), alopecia, painless oral ulcers
chronic discoid rash (raised edges, leaves scars)
subacute photosensitivity rash (sun exposed areas,” sunburn” that lasts months)

49
Q

Arthritis in SLE

A

in 40% (small joints, non-erosive deformities unusual)

50
Q

Lupus nephritis

A

in 70%: glomerulonephritis of varies degrees of histologic and pathologic abnormalities

51
Q

Cardiac and pulmonary in SLE

A

in 30-50% of patients :pericarditis, pericardial effusion, pulmonary effusion

52
Q

SLE CNS abnormalities

A

in 70%: headaches, cognitive/behavioral dysfunction, depression, seizures

53
Q

Hematologic SLE

A

anemia, thrombocytopenia, leukopenia

54
Q

Constitutional SLE

A

fatigue, weight loss, low grade fever, myalgia

55
Q

Discoid rash

A

This is chronic skin infection. Annular, raised, scaly borders. Tinea is itchy because it is fungal. This is not itchy. Is chronic.

56
Q

Malar rash

A

This is an acute manifestation, comes and goes. NOT CHRONIC. Strep skin infection is well demarcated and on one side and raised. Impetigo is honey colored crusting.

57
Q

Diagnosis of SLE

A

Clinical dx.
Decreased complement level in SLE flare ( indicates disease activity and flare)
X-ray- negative ( non-erosive arthritis)

58
Q

ANA

A

ANA ( anti-nuclear antibody): very sensitive ( 99%). Almost all SLE patients have ANA. Negative ANA – probably not SLE. Positive ANA – not just SLE. INITIAL test

59
Q

Anti-dsDNA

A

(antibodies against double stranded DNA) : very specific to SLE (90%). Used to CONFIRM the diagnosis if ANA is positive

60
Q

Lupus nephritis

A

Deposition of immune complexes in glomerular capillary membrane damage to the membrane

Histological changes and symptoms are variable

Symptoms from asymptomatic to renal failure

61
Q

Diagnosis of lupus nephritis Initial diagnosis ( and monitoring )

A

Serum for creatinine/GFR
Urinalysis for protein and RBC (dysmorphic)
24-h urine collection for urine protein or spot urine protein-to-creatinine ratio (more accurate to determine proteinuria)

62
Q

Definitive diagnosis of lupus nephritis

A

Renal biopsy (to determine histopathology) to determine therapy

63
Q

Treatment of SLE For acute exacerbations

A

Corticosteroids (IV or PO high dose)

64
Q

For maintenance (prevent exacerbations, treat symptoms)

A

Sun screen: exposure to UV light can exacerbate a flare
Hydroxycholoroquine (Plaquenil ®) for skin rashes, arthritis, prevent flares
Cytotoxic drugs (Cyclophosphamide IV) for severe cases of lupus nephritis

65
Q

MTX s/e

A

GI upset, liver toxicity , marrow suppression (anemia, leukopenia, thrombocytopenia)

66
Q

MTX monitoring

A

CBC, liver function, renal function. Screen for viral hepatitis prior. Contra-indicated pregnancy

67
Q

TNF-inhibitors s/e

A

Reactivation of latent TB, fungal and bacterial inf

68
Q

TNF monitoring

A

Screen for latent TB, HIV, viral hepatitis prior and during the therapy
Repeat TB screening annually . continue in pregnancy

69
Q

Hydroxy-choloroquine side effects

A

Retinal damage (irreversible ) – RARE

70
Q

Hydroxy-choloroquine monitoring

A

Fundoscopic exam by a specialist prior and annually, ok in pregnanacy

71
Q

Osteoarthritis (OA)

A

Degenerative disorder affecting cartilage (“ wear and tear”)
PROGRESSIVE
Incidence increases w/ age
Weight-bearing joint is most commonly affected ( knees, hips, lumbar spine). Can affect both DIP and PIP
Risk factor- obesity

72
Q

Clinical manifestations of OA

A

Monoarticular/ Olygoarticular joint involvement. Pain relieved by rest, worsen w/ activity. May be joint stiffness in AM (not prolonged, < 30 min) .On physical exam: bony enlargement and bony crepitus, no warmth, no redness. Limited active and passive ROM due to bony enlargement of joints (osteophytes) and pain. No systemic symptoms

73
Q

Diagnosis of OA

A

Diagnosis is CLINICAL. Tests to support the diagnosis:
Normal CRP, ESR
Abnormalities on x-ray: Joint space narrowing, osteophytes ( bone overgrowth), subchondral bone damage (sclerosis). NO bone erosions

74
Q

Treatment of OA

A

Dx clinical + xray
Treatment weight loss and exercise
Start w tylenol
Move to NSAID

75
Q

tx OA

A

Weight loss

Regular exercise activity to improve ROM, muscle strength (strong muscles joint protection ).

Acetaminophen ( most guidelines recommend for initial use, < 3g/d) NSAIDS topical or oral

Intra-articular injection (no more than 3-4/ year)

Surgery for serious disability

Nutritional products ( OTC glucosamine and chondrotin sulfate) – no good evidence of benefit

76
Q

OA

A

Mainly weight-bearing joints , non inflammatory. No systemic sx. dx- X-ray ( narrowing, osteophytes) . Tx: Weight loss,
Acetaminophen, Surgery

77
Q

RA

A

Small joints hands, wrists, ankles, symmetric ( no DIP), inflammatory ,erosive. Systemic: Minimal, rheumatoid nodules , anemia. Dx: RF, anti-CCP, X-ray ( narrowing, joint erosion, deformities). Tx: Methotrexate+/- TNF inhibitors

78
Q

SLE

A

Small joints, symmetric, inflammatory , non-erosive, Systemic - Multiple ( skin, renal, cardiac, pulmonary, blood), dx - ANA initially, anti-DS DNA X-ray (may be normal), tx Hydroxycholoroquine, steroids

79
Q

Gout

A

Manifestation of hyperuricemia (increased production or decreased excretion)
Deposition of monosodium urate crystals (MSU) in joints
More prevalent in men, in obese individuals, in patients with chronic renal disease
Peak age 40-60

80
Q

Gout foods

A

Precipitated by alcohol ingestion (beer), red meat, seafood

81
Q

Meds causing gout

A

niacin, thiazides, ASA

82
Q

joints affected in gout

A

1st metatarsophalangeal joint is involved (podagra), knee, ankle

83
Q

pseudogout is a build up of

A

calcium

84
Q

gout patho

A

Super saturation of uric acid crystals –> goes to distal joints where is grows in lower temperatures. Uric acid breaks down to purines/nucleic acids – produces DNA

85
Q

formation of uric acid crystals

A

Food with a lot of cells – increased purines and uric acid – seafood, wine
Cell turover like in cancer – releases dna

86
Q

Clinical manifestations of gouty arthritis

A

Sudden onset of exquisite joint pain, often wakes from the sleep
Most often affects big toe
Redness, warm, swelling, tenderness
In recurrent and poorly controlled gout ( chronic) – tophi

87
Q

Gouty tophi

A

aggregation of urate crystals under the skin (chronic gout)

88
Q

Diagnosis of gout

A 
Uric acid – is non diagnostic
25 percent of the time this is negative
Need synovial fluid aspiration
Septic will destroy a joint very fast
Send to the ER if not near an ortho
Best diagnosis is the fluid aspiration
89
Q

Elevated serum uric acid

A

(may be normal in 25% of gout patients) non-diagnostic

90
Q

X-ray normal during early stages

A

(bone erosions in chronic/recurrent) non-diagnostic

91
Q

Elevated CPR, ESR (non-specific)

A

non-diagnostic

92
Q

Aspiration of synovial fluids

A

(WBC 5,000-50,000 cells, with neutrophils < 75%, needle-shape crystals on polarization microscopic examination) diagnostic

93
Q

Degenerative (OA) Labs

A

wbc <5k, PMN <25%, crystals negative

94
Q

Inflammatory (gout , pseudo-gout ) labs

A

wbc 5-50k PMN >50% crystals Needle shaped crystals –gout, Rhomboid crystals-pseudo gout

95
Q

Septic labs

A

wbc > 50, 000, PMN > 75%, no crystals

96
Q

Clinical diagnosis of gout

A

Strongest clinical predictors of gout (the more factors the more confidence in diagnosis):
Acute onset, with maximal symptoms within one day
Joint erythema
History of chronic kidney disease
Male patient
Previous attack of arthritis or joint pain
First metatarsophalangeal joint involved
Serum uric acid >6 mg/dl

97
Q

f/u gout

A

If aspiration is deferred, vigilant follow-up is warranted. Tight follow up like a hawk, if septic will ruin the joint

98
Q

Treatment of acute gout

A

NSAIDs +/- Colchicine – initial

Steroids – if poor response to initial therapy or for patients with renal insufficiency

99
Q

Colchicine not good if

A

kidney disease
Very good at antiinflammatory
Excreted in the urine, biggest side effect is diarrhea

100
Q

Preventative therapy for gout attacks

A

Reduce alcohol intake, high-purine food (red meat, organ meat, seafood, alcohol beverages esp. beer)
Urate lowering therapy if more than 2 attacks per year
Urate lowering therapy should be initiated between flares, not during the attack
Start slow and titrate to uric acid level < 6 mg/ dl

101
Q

Decrease production of uric acid

A

Allopurinol ( first line)
Febuxostat (Uloric®) – if cannot tolerate Allopurinol. Do not give allopurinol in an acute attack. Given inbetween. If during an attack it is given It will mobilize uric acid and will worsen the attack.

102
Q

increase excretion of uric acid

A

Probenecid

103
Q

Colchicine

A

Anti-inflammatory, for acute flare. s/e: GI: diarrhea ( 80% of pt) Excreted in urine> lower doses or avoid

104
Q

Allopurinol

A

Decrease production of uric acid , for prevention s/e: Mild rash. Severe cutaneous reactions are rare DO NOT USE during acute attack

105
Q

Febuxostat (Uloric)

A

Decrease production of uric acid, for prevention s/e: Mild rash and liver function abnormalities. DO NOT USE during acute attack

106
Q

Probenecid

A

Increase excretion of uric acid. for prevention Contraindicated in renal insufficiency, nephrolithiasis

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