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Rheumatology -IM plat Flashcards

1
Q

Etiopathogenesis of Osteoarthritis

A

Most common joint disease and a leading cause of disability in the elderly

Sine qua non is hyaline cartilage loss

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2
Q

Risk Factors for OA

A
  • Age (most important)
  • Obesity
  • repeated joint use
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3
Q

Manifestations of OA

A

Activity-related

starting as episodic and progressing continuously with accompanying brief morning stiffness (<30 min) that gradually resolves

Commonly affected Joints

  • Cervical
  • spine
  • lumbosacral
  • spine
  • Hip
  • Knee
  • 1st MTP
  • distal
  • proximal IPs
  • base of the thumb

Buckling of the knees may occur due to weakness of muscles crossing the joint

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4
Q

Diagnostics for OA

A

No blood tests is indicated

Synovial fluid analysis

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5
Q

Management of OA

A

NON-PHARMACOLOGIC

  • Exercise with brief periods of rest
  • Weight management (wt loss to 5kg = 50% pain reduction)
  • Correction of possible misalignment
  • Acupuncture
  • Oral standardized
  • ginger preparation
  • Surgery
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6
Q

Pharmacologic Management for OA

A
  • Non-opiod analgesics
  • Opiod-like analgesics
  • Traditional NSAIDs
  • Oral COX-2 inhibitors
  • Intraarticular injections
  • Hexosaminases
  • Capsaicin
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7
Q

NON-opiod analgesics

A

Paracetamol 500 mg up to QID

  • Initial treatment

Modulates the endogenous cannabinoid system in the brain

Can prolong half life of warfarin

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8
Q

Opiod Analgesics

A

Tramadol 50-100 mg q4-q6

Binds to the u-opiod receptor

SE: Dizziness, sedation, nasuea/vomiting, Urinary retention, constipation, dry mouth

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9
Q

Traditional NSAIDs

A

Suppress inflammation by ihibiting both COX-1 and COX-2 activity

Naproxen 375-500 mg BID, taken with food

SE: GI ulceration and bleeding, edema, renal insufficiency

Diclofenac gel 1% gel, 4 g QID Should be rubbed onto joint

  • Skin irritation common
  • Avoid if with renal disease
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10
Q

Oral COX-2 inhibitors

A

Inhibits COX-2 activity only

  • Celecoxib 100-200mg QD-BID
  • Eterocoxib

SE: Increased risk for stroke and MI

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11
Q

Capsaicin

A

Bind to the vanilloid receptor sybtype 1 (TRPV1) thereby modulating pain sensations.

0.025%-0.075% cream 3-4x day

Can irritatemucous membrane

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12
Q

Etiopathogenesis of Gouty Arthritis

A

Metabolic disease that usually affects men (30s onwards) and postmenopausal women

  • Increased body urate pool with hyperuricemia
  • Urate overproduction
  • Urate Underexcretion
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13
Q

Precipitants of Hyperuricemia (Gouty)

A
  • Dietary excess
  • Trauma,
  • surgery
  • Excessive ethanol ingestion
  • Hypouricemic therapy
  • Serious comorbid illnesses such as stroke and MI
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14
Q

Manifestations of Gouty Arthritis

A
  • Acute arthritis usually initially affecting MTP of the first toe (PODAGRA) or ankle or knee, followed by episodes of acute mono-or oligoarthritis and finally chronic nonsymmetric synovitis with topaceous deposits
  • Inflamed Heberden’s and Bouchard’s nodes
  • Initial attacks mimic cellulitis, subside spontaneously over 3-10 days, and have varying asymptomatic periods until the next attack
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15
Q

Asymptomatic hyperuricemia

A

Hyperuricemia in the absence of gouty arthritis and uric acid nephrolithiasis

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16
Q

Hyperuricemia

A
  • Men: >7 mg/dL
  • Female: >6 mg/dL
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17
Q

Acute Gouty Arthritis

A

Urate crystal in the joint fluid, and/or

Presence of six of the 12 clinical laboratory, and Xray phenomenon

  • Max. Inflammation developed within 1 day
  • More than 1 attack of acute arthriitis
  • Monoarticular arthritis
  • Redness over joints 1st MTP joint pain or swelling
  • Unilateral first MTP joint attack
  • Unilateral tarsal joint attack
  • Suspected Tophus
  • Hyperuricemia
  • Asymmetric swelling within a joint on X-ray
  • Subcortical cysts without erosions on x-ray
  • Negative organisms on culture of joint fluid during attack
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18
Q

Intercritical (interval) Gout

A

Asymptomatic periods between gouty attacks

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19
Q

Chronic Tophaceous gout

A
  • occurs in untreated gouty arthritis
  • Low grade inflammation of joints with sporadic flares
  • Joint deformities occur due to deposition of urate crystals, forming visible tophi
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20
Q

24-h uric acid urine collection

A
  • >800mg/24h (over producers)
  • <600 mg/24 h (under excretors)
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21
Q

Treament goal for gout:

A

Uric acid <6mg/dL

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22
Q

Medical management of Acute Attacks

A

Recommended first-line options

  • Colchicine
  • NSAIDs
  • Oral Costicosteroid
  • Articular aspiration and injection of steroids
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23
Q

Colchicine

A

1 mg LD within 12 hours of flare onset followed 1 hour later by 0.5 mg; or TID unil flare subsides.

Inhibits microtubule polymerization and neutrophil activity/motility, giving its anti-inflammatory effect

Avoid in patients with severe renal impairment and those receiving CYP3A4 inhibitors

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24
Q

NSAIDs in acute flares of GA

A
  • Celcoxib 400 mg BID
  • Diclofenac 50 mg TID
  • Etoricoxib 120 mg OD
  • Indomethacin 25-50 mg TID
  • Naproxen 500mg BID
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25
Q

Steroids

A

Prednisolone 30-35 mg/day (or its equivalent for 3-5 days)`

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26
Q

Anakinra

A

100 mcg/day SC for 3-5 days

IL-1 Blocker

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27
Q

Indications for Therapeutic Arthrocentesis

A
  • Unable to take oral medications
  • Have only 1-2 actively inflamed joints
  • Ready access to a clinician with expertise in arthrocentesis
  • Can be performed immediately prior to injecting intraarticular medications
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28
Q

Flare Prophylaxis for Gouty Arthritis

A

Recommended during the first 6 months of ULT or until serum uric acid is <6 mg/dL

Colchicine 0.5-1 mg/day

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29
Q

Urate lowering therapy

A

Indicated in all patients with

  • recurrent flares (>2/year),
  • tophi
  • urate arthropathy,
  • and/or nephrolithiasis

Should be started close to time of first diagnosis in

  • patients <40 years old
  • SUA >8 mg/dL with commorbidities

Target lifelong SUA: <6 mg/dL

Lower target: <5 mg/dL

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30
Q

Allopurinol

A

Inhibits xanthine oxidase blockng uric acid production

Initial low dose: 100 mg/day and increased at 100 mg increments every 2-4 weeks

Usual dose: 300 mg/day

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31
Q

Febuxostat

A

Inhibits xanthine oxidase blocking uric acid production

40-80 mg/day

Indicated if SUA target cannot be reached by Allopurinol or if allopurinol is not tolerated

32
Q

Benzbromarone

A

Increases uric acid excretion

50-200 mg/day

Potent inhibitor of CYPC29

33
Q

Pegloticase

A

Pegylated recombinant porcine uricase

8 mg IV q2 weeks

Indication:

  • patients with crystal proven
  • severe debilitating chronic tophaceous gout

Contraindicated in G6PD deficient patients

34
Q

Etiopathogenesis of Rheumatoid Arthritis

A

Chronic inflammatory disease of unknown etiology marked by symmetric, peripheral polyarthritis

may result in a variety of extraarticular manifestions, lung ivolvement, pericarditis, peripheral neuropathy, vasculitis, and hematologic abnormalities

35
Q

Joint Involvement in RA

A
  • small joints of hands and feet
  • Early morning stiffness> 1 hour easing with physical activity
  • wrist
  • MCP
  • PIO
  • Swan neck deformity
  • Boutonniere deformity
  • Z-line deformity
  • Flexor tendor tensosynovitis
36
Q

Swan neck deformity

A

hyperextension of the PIP with flexion of the DIP joint

37
Q

Boutonniere deformity

A

Flexion of the PIP with hyperextension of the DIP joint

38
Q

Z-line deformity

A

Subluxation of the first MCP with hyperextension of the 1st IP joint

39
Q

Hallmark of RA

A

flexor tenosynovitis

40
Q

Subcutaneous nodules in RA

A

benigh, firm,nontender and adherent to periosteum, tendons, or bursae

41
Q

Pleuritis and pericarditis in RA

A

most frequent site of cardiac involvment in RA is the pericardium

42
Q

Vasculitis in RA

A

Fever of >39.3 during the clinical course should raise suspicion of systemic vascultis

43
Q

Constitutional symptoms in RA

A

weight loss, fever, fatigue, malaise, depression, and cachexia in more severe cases

44
Q

Diagnostic tests for RA

A

Serum Markers:

  • RF
  • anti-CCP

Acute phase reactants

CBC

  • normocytic normochromic anemia

Synovial fluid Analysis

  • Consistent with inflammatory arthritis

Joint imaging

  • Juxtaarticular osteopenia (initial finding)
  • soft tissue swelling
  • Joint effusions
  • symmetric joint space narrowing
  • Joint subluxation and collapse
45
Q

Monitoring for RA

A

every 1-3 months in active disease,

with treatment adjusted if no improvement seen by 3 months or target not reached by 6 months

46
Q

Remission

A

defined as having all of the following:

  • Tender joint <1 swollen
  • joint count <1
  • CRP <1 mg/dl
  • patient global assessment scale <1
  • must have a clinical disease activity index score of <2.8
47
Q

NSAIDs for RA

A

adjunctive therapy

48
Q

Glucocorticoids for RA

A

low to moderate dose for rapid disease control before the onset of fully effective DMARD therapy

1 to 2 week burst of glucocorticoids for acute disease flares

49
Q

csDAMRDs

A

Slow or prevent structural progression of RA

Cornerstone of therapy which should be started as soon as diagnosis of RA is made

50
Q

Methotrexate

A

csDMARD of Choice

10-25mg/week PO or SC

Folic acid 1 mg/day given to reduce toxicities

contraindicated in pregnancy

51
Q

Hydroxychloroquine

A

200-400 mg/day PO

If with contraindication or early intolerance to metho

52
Q

Sulfasalazine

A

500-1500 mg BID PO

SE: granulocytopenia, hemolytic anemia in persons with G6PD deficiency, nausea, diarrhea

53
Q

Leflunomide

A

10-20 mg/day

SE: hepatoxicity, myelosuppresion, infection, alopecia, diarrhea Contraindicated in pregnancy

54
Q

[RA] Infliximab

A

Chimeric anti TNF

55
Q

[RA] Adalimumab; Golimumab

A

Fully humanized anti TNF

56
Q

[RA] Cetolizumab pegol

A

Pegylated Fc-free fragment of a humanized monoclonal antibody with binding specificity for TNF

57
Q

[RA] Etanercept

A

Soluble fusion protein compromising the TNF receptor-2 in a covalent linkage with the fc portion of IgG1

58
Q

[RA] Anakinra

A

IL -1 receptor antagonist

59
Q

[RA] Abatacept

A

soluble fusion protein consisting of a domain of human CTLA-4 linked to aportion of human IgG

60
Q

[RA] Rituximab

A

Chimeric monoclonal against CD-20

61
Q

[RA] Tocilizumab

A

Humanized monoclonal antibody against IL-6 receptor

62
Q

[RA] Tofacitinib

A

Small molecule inhibitor that targets JAK1 and JAK3

63
Q

[RA] Baricitinib

A

small molecule inhibitor that targets JAK1 and JAK2

64
Q

[RA] Baricitinib

A

small molecule inhibitor that targets JAK1 and JAK2

65
Q

Etiopathogenesis of Infectious Arthritis

A

Hematogenous route is the most common route in all age groups

Knee is most commonly involved

Acute bacterial infection typically involves a single joint or few

66
Q

Etiologic agents of Infectious arthritis

A
  • Infants: Group B streptococcus, Gram (-) enteric bacilli, Staph. aureus
  • Young adults and adolescents: N. gonorrhea

Staphyloccous aureus accounts for most non-gonoccocal isolates in adults of all ages

67
Q

manifestations of Infectious arthritis

A
  • Fever
  • Moderate severe pain that is uniform around the joint
  • MSK: joint effusion, muscle spasm, decreased range of motion
68
Q

Diagnostics in Infectious arthritis

A
  • Acute Phase reactants
  • CBC
  • Synovial fluid analysis
  • Joint imaging
  • Cultures
69
Q

Non pharma management for Infectious arthritis

A

Repeated arthrocentesis

Surgical Drainage/arthroscopic lavage usually indicated for:

  • Septic hip
  • Concomitant osteomyelitis
  • Prosthetic joint infection
70
Q

Recommended Antibiotics

A

Gram(+) smear, MRSA unlikely

  • Oxacillin 2 g IV q4; or Nafcillin 2g IV

Gram (+) smear MRSA likely

  • Vancomycin 1 g IV q12

Gram (-) smear or no organisms on smear

  • Cefotaxime 1 g IV q8; or Ceftriaxone 1-2 g IV q24

Pseudomonas suspect

  • Add aminoglycoside or 3rd gen cephalosporin anti pseudomonal cephalosporin (Ceftazidime 1g IV q8)
71
Q

Duration of Treatment according to organism

A

S. Aureus - 4 weeks

Pneumococcus/ Penicillin sensitive Strep - 2 weeks PEN G 2M units q4 or cefotaxime

Haemophilus influenzae/ Penicillin-resistant streptococcus - 2 weeks Cefotaxime or Ceftriaxone

Enteric gram (-) bacilli -3-4 weeks 2nd/3rd gen Cephalosporin IV or quinolone IV/PO

Pseudomonas aeruginosa - at least 2 weeks of aminoglycoside plus extended-spectrum penicillin or anti-pseudomonal cephalosporin

72
Q

Etiopathogenesis of plantar fascitis

A

Foot pain originating at or near the site of plantar fascia attachment to the medial tuberosity of the calcaneus

Peak incidence: 40-60 years old

Risk Factors:

  • obesity
  • pes planus
  • pes cavus
  • limited ankle dorsiflexion
  • prolonged standing
  • walking on hard surfaces
  • excessive running
  • faulty shoes
73
Q

manifestations of Plantar fascitis

A

severe pain with the first steps upon arising in the morning or following inactivity during the day Pain

usually lessens with weight bearing activity

Pain worse when walking barefoot or climbing stairs

Maximal tenderness over the inferior heel at the site of attachment of the plantar fascia

symptoms resolve in majority of patients after 1 year

74
Q

Diagnostics for Plantar fascitis

A

Plain Xray : heel spurs

Ultrasound: Fascial thickening, edema

MRI: sensitive method but not usually required for diagnosis

75
Q

Plantar fasciotomy

A

patients who do not improve of conservative treatment

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