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Rheumatolgy > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

Septic Arthritis: 5

A
  1. Septic arthritis is a medical emergency!
  2. Immediate referral for joint aspiration.
  3. Treatment is an aggressive and prolonged course of IV and oral antibiotics.
  4. Complications include irreversible joint damage and death.
  5. Morbidity and mortality are high in patients with RA, prosthetic joints, severe and multiple co-morbidities and the elderly.
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2
Q

Septic Arthritis:

Epidemiology/Etiology:

A

Higher in pts with RA, DM or those with prostheses.

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3
Q

Triggers of septic arthritis:

A

Hematogenous spread to the joint – most common

Direct inoculation after joint aspiration, injection… etc.

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4
Q

septic arthritis Risk Factors: 8

A
  • > 80 years old
  • Presence of diabetes mellitus
  • Presence rheumatoid arthritis
  • Presence of prosthetic joint (especially hip/knee)
  • Recent joint surgery
  • Recent skin infection
  • Recent intraarticular injections (steroids)
  • IV drug use and alcoholism
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5
Q

septic arthritis Clinical Features: 8

A
  • Acute onset of pain (1 day – 2 weeks), redness, swelling and decreased motion in one joint
  • Affects one joint (<20% of cases have more than one joint involved)
  • Large joints are affected more commonly than small joints
  • Knee (50%) > Hip > shoulder > elbow
  • Fever (30 – 60%)
  • Malaise and poor appetite
  • Joint is warm and tender to touch
  • History of RA, injections, trauma, DM or recent infection.
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6
Q

Septic arthritis mortality:

A

Note: Mortality is high in those with RA because incidence in those with RA is higher and it is difficult to distinguish septic arthritis from an acute flare.

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7
Q

Septic arthritis

Diagnostic Testing: 7

A
  • Joint Aspiration (STAT)
  • Purulent synovial fluid
  • Elevated leukocyte count (>100,000 WBC/mm3)
  • Gram stain and/or culture positive
  • Crystal analysis negative
  • Blood cultures – run if bacterial infection suspected even w/o fever
  • Positive in 40-50% of cases
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8
Q

Septic arthritis Treatment:

DO NOT delay treatment. Delay in treatment can mean death or permanent damage to the joint.

A
  1. Antibiotic Therapy (1 – 6 weeks)
  2. Joint aspiration and drainage – generally done before ABX given
  3. Surgical drainage
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9
Q

Septic arthritis Naturopathic Support: 4

A

Vitamin C:
Vitamin A:
Glutamine:
EFAs: (EPA + DHA)

(CAGE)

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10
Q

GOUT Intro: 6

A
  • Purine loading and insulin resistance are two key mediating mechanisms for gout.
  • Individuals with hyperuricemia should be screened for hypertension, coronary artery disease, diabetes, obesity and alcoholism.
  • Joints most affected: first metatarsal phalangeal (MTP) joint.
  • Joint aspiration is the preferred method of diagnosis.
  • Affects men more than women.
  • Diet and lifestyle have a huge impact on treatment outcome.
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11
Q

GOUT Etiology: 4

A
  • Uric acid is a byproduct of human purine metabolism
  • Urate excretion occurs via the gut and the kidneys
  • Underexcretion from renal insufficiency, systemic illnesses, dehydration, drug reactions, toxins
  • Hyperuricemia drives precipitation of crystals which triggers an inflammatory response
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12
Q

GOUT Diet and Hyperuricemia: 3

Diet increases serum urate by?

A
  • Increasing dietary purines
  • Increasing metabolic production
  • Decreasing renal excretion
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13
Q

GOUT Diet and Hyperuricemia:

Important Points:3

A
  • Protein consumption DOES NOT increase the risk of hyperuricemia
  • Not all purine rich foods increase serum urate
  • Non-purine foods that increase urate: fructose and alcohol
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14
Q

GOUT Risk Factor: 8

A
  • Obesity and weight gain
  • Purine rich food (meat, seafood)
  • Alcohol
  • Fructose
  • Medications (salicylates, diuretics, HTN meds)
  • Toxicity (lead)
  • Co-morbidities (HTN, psoriasis, diabetes)
  • Insulin Resistance
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15
Q

GOUT Clinical Feature:

  1. Asymptomatic hyperuricemia- 1
  2. Acute (recurrent) gouty arthritis- 3
  3. Chronic gouty arthritis (tophaceous)- 3
A

1.Asymptomatic hyperuricemia – not a disease in the absence of Sx
2.Acute (recurrent) gouty arthritis
•Single joint involved (first MTP joint, midfoot, ankles, knees)
•Explosive pain, usually starting in the evening or early morning
•Within hours (24), joint is hot, dusky red, swollen and tender
3.Chronic gouty arthritis (tophaceous)
•No pain-free periods
•Tophaceous deposits (usually painless)
•Marked limitations in joint movement

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16
Q

GOUT Diagnostic Testing: 5

A
  • Joint aspiration
  • Urate crystals in the synovial fluid
  • Serum uric acid
  • Does not confirm or exclude acute gout
  • During acute attacks, levels may be normal
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17
Q

GOUT ACR Diagnostic Criteria: 2

A
  • The presence of urate crystals in synovial fluid (definitive Dx)
  • Urate crystals identified in tophi
18
Q

GOUT Treatment – Acute Attack: 7

A
  • Treatment should begin AS SOON as the attack begins if possible (or at least within several hours).
  • Treatment can stop within 2-3 days of complete cessation of symptoms.
  • Joint should be rested and elevated; ice packs may help to reduce pain and swelling.
  • NSAIDs – for mild to moderate pain prn
  • Naproxen 500mg BID
  • Colchicine – for mild/moderate pain when NSAIDs are contraindicated
  • Most effective if administered within 12 – 24 hours of Sx onset
19
Q

GOUT Preventative Therapies: 3

A
  • Urate lowering therapies will only help lower acute attacks if taken for > 1 year.
  • Allopurinol: titrate up 100mg/day to reach 200 – 600mg po qd (Max daily dose: 800mg po qd)
  • Serum urate should be measured every 3 months during the first year, then annually
20
Q

GOUT Dietary Modifications: 8

A 
•Eliminate alcohol consumption
•Reduce purine intake
    1. Meats: organ meats, seafood, red meats, poultry
    2. Yeast (brewer’s and baker’s)
•Reduce body weight
•Reduce refined carbohydrates
•Low fat intake
•Increase fluid intake
21
Q

GOUT Supplementation and Herbs: 5

A
  • Fish Oils: 3000mg EPA + DHA/day
  • Folic Acid: 10 – 40mg/day2
  • Quercitin: 200 – 400mg TID between meals3
  • High Anthocyanidin/Proanthocyanidin’s:
  • Note: High doses of vitamin C may increase uric acid levels
22
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Intro 7

A
  • Mostly idiopathic but can be a genetic mutation.
  • Joints most involved: metacarpophalangeal, wrist, elbow, knees, hips.
  • Primary metabolic or familial disorders and hyperparathyroidism should always be considered.
  • It predominantly affects those over 55.
  • Disease of the elderly.
  • Strong overlap with osteoarthritis (OA).
  • 3 syndromes fall into CPPD: Pseudogout, chrondrocalcinosis, pyrophosphate arthropathy.
23
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Etiology:
Risk factors: 4

A
  • Previous joint trauma
  • Presence of osteoarthritis (knee)
  • Hemochromatosis (MCP joints)
  • Hyperparathyroidism, hypomagnesemia, hypophosphatasia
24
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Clinical features:
Asymptomatic CPPD- 2
Acute CPP crystal arthritis (Pseudogout)- 4
Chronic CPP crystal inflammatory arthritis (Pseudo-RA)- 3

A

Asymptomatic CPPD
•Most common presentation
•Crystal deposition present on x-ray, but no symptoms.

Acute CPP crystal arthritis (Pseudogout)
•Large joints: knee most common
•Generally only one joint
•Excruciating pain, sudden onset, erythema, warmth and swelling
•Fever and chills may be present

Chronic CPP crystal inflammatory arthritis (Pseudo-RA)
•MCP, wrists, elbows (joints spared by OA)
•Generally multiple joints involved
•Non-erosive, inflammatory arthritis with CPPD crystals

25
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Diagnostic Testing: 6

A
  • Joint aspiration!
  • Acute CPPD will have turbid synovial fluid with neutrophils
  • CPP crystals present
  • Radiographic imaging or ultrasound
  • Chondrocalcinosis is a common finding in the elderly and does NOT necessarily indicate clinical CPPD disease.
  • Degenerative changes – can also occur with OA
26
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Acute conventional tx: 6

A
  • Removal of crystals through joint aspiration
  • Intra-articular corticosteroids
  • Ice or cool pack application (acute flares)
  • NSAIDs – acute flares for continued pain
  • Colchicine – acute flares for continued pain
  • Most effective when given within the first 24 hours of acute flare
27
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Medications for prevention:
-1st & 2nd line txs

A

First line treatment:
•low-dose colchicine: (NSAID)

Second line treatment:
•Methotrexate:
•Hydroxychloroquine:

28
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Naturopathic tx: 5

A
  • Anti-inflammatory diet
  • Fish Oils: 3000mg EPA + DHA/day
  • Harpagophytum procumbens/Devil’s claw
  • Boswellia serrata
  • High Anthocyanidin/Proanthocyanidin’s:
29
Q

Osteoarthritis: 8

Intro

A
  • The most common form of arthritis.
  • Strongly associated with aging.
  • Injury to the joint often precipitates formation of OA over time.
  • Affects big and small joints: Hip, knee, spine, feet, hands
  • Defined mostly by degeneration, loss of cartilage and osteophyte formation, inflammation is generally a secondary component.
  • Physical activity may aggravate symptoms temporarily but has a significant impact on improving joint function over time.
  • Pharmaceutical medications are only used for acute pain as needed.
  • Also called degenerative joint disease (DJD) or degenerative arthritis
30
Q

Osteoarthritis:

Etiology: 4

A
  • Initiating mechanism is usually damage or stress to the normal articular cartilage
  • Cytokines promote cartilage degradation:
  • Basic calcium crystals influence cartilage calcification
  • Inflammation is present, but is not the initial precipitating factor
31
Q

Osteoarthritis:

Risk factors:

A
  • Age >55
  • Female
  • Obesity – mostly associated with knee/hip OA
  • Previous injury/trauma or overuse of the joint
  • Genetics – possibly HLA-A1 and HLA-B8
  • CPPD
32
Q

Osteoarthritis:

Clinical Features: 8

A
  • Insidious onset
  • Joint pain worse with activity, better with rest
  • Morning stiffness, relieved 30 min after waking
  • Affects large and small joints: knee, fingers (IP), hip, spine (lower cervical/lumbar)
  • Tenderness to palpation of the joints
  • Joint swelling may be present
  • Crepitus is the most common finding
  • Osteophytes may be palpable
33
Q

Osteoarthritis:

Areas Affected: 5

A
  • Knee – osteophytes, effusion, crepitus, decreased ROM
  • Hands – debilitating pain, decreased ROM, bony enlargements in DIPs (Heberden’s) and PIPs (Bouchard’s).
  • Feet – 1st MTP, decreased ROM
  • Hips – Pain in the hip or referred to the knee (rule out bursitis)
  • Spine – usually C5, T8, L3, osteophytes may lead to spinal stenosis
34
Q

Osteoarthritis:

Diagnostic Testing: 7

A
  • Lab testing is rarely needed
  • Only to rule out of RA or other inflammatory joint problems.
  • Radiographic imaging – correlates poorly with symptoms
  • Joint space narrowing
  • Subchondral sclerosis and cysts
  • Osteophytes
  • Joint aspiration – leukocyte level low, calcium crystals may be seen
35
Q

Osteoarthritis:

Conventional Medications: 6
These are implemented when nonpharmacologic measures fail;

A

NSAIDs (oral and topical) – Naproxen 375mg po qd - bid
•Topical NSAIDs should be used before oral
•May increase the rate of degeneration of the cartilage
•Lowest dose for the shortest amount of time if using oral.
•Do not use oral NSAIDs in those with gastrointestinal, cardiovascular or renal complications

Glucocorticoids
•Intraarticular injections – only if NSAIDs are ineffective or contraindicated.
•Duration of efficacy is limited to 4 weeks

36
Q

Osteoarthritis:

Exercise: 4

  • Exercise is crucial for improving physical function and reducing pain7-11
  • Consistent exercise is as effective for pain and function as NSAIDs
A
  • Helps control weight
  • Increases muscle strength
  • Range of motion and strengthening exercises – symptom relief
  • Low load exercises
37
Q

Osteoarthritis:

Nutritional supplementation: 11

A
  • Glucosamine Sulfate: 1500mg/day12,13
  • Chondroitin Sulfate
  • Hyaluronic Acid:
  • Niacinamide:
  • SAMe:
  • Avocado soybean unsaponifiables (ASU):
  • Vitamin C:
  • Vitamin D:
  • Vitamin K:
  • Antioxidants:
  • Proteolytic Enzymes
38
Q

Osteoarthritis:

Botanical Medicine: 4

A
  • Boswellia serrata:
  • Zingiber officionalis (Ginger)
  • Harpagophytum procumbens: (Devil’s claw)
  • Salix alba (willow bark)
39
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Clinical features:

Acute CPP crystal arthritis (Pseudogout)- 4

A 
Acute CPP crystal arthritis (Pseudogout)
•Large joints: knee most common
•Generally only one joint
•Excruciating pain, sudden onset, erythema, warmth and swelling
•Fever and chills may be present
40
Q

Calcium Pyrophosphate Dihydrate Deposition (CPPD): “Psedogout”:

Clinical features:

Chronic CPP crystal inflammatory arthritis (Pseudo-RA)- 3

A

Chronic CPP crystal inflammatory arthritis (Pseudo-RA)
•MCP, wrists, elbows (joints spared by OA)
•Generally multiple joints involved
•Non-erosive, inflammatory arthritis with CPPD crystals

Rheumatolgy (14 decks)

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