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1. Rheum RC > RA > Flashcards

RA Flashcards

1
Q

RA Etiology:
- Genetic
- Enviro
- Antibodies

A

Genetic: MHC region for HLA-DR genes, SNPs of STAT4, PTPN22, TRAF1

Enviro: smoking, silica, pollution, viruses, bacteria

Antibodies to citrullinated/ carbamylated proteins –> immune complex, complement activation, inflammation, NETosis, osteoclast-genesis/activation, adaptive immune system

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2
Q

RA Classification Criteria

A

2010: ACR/EULAR: 6 or more

  1. Swollen/tender joint
    * One medium to large joint (shoulders, elbows, hips, knees, ankles) = 0
    * 2–10 medium to large joints = 1
    * 1–3 small joints (MCP, PIP, 2–5 MTP, or wrist with or without large joint involvement) = 2
    * 4–10 small joints (with or without large joint involvement) = 4
    * >10 joints (at least one small joint involved) = 5
  2. Serology
    * -RF and -ACPA = 0
    * Low +RF or low +ACPA (<=3 x ULN) = 2
    * High +RF or high +ACPA (>3 x ULN) = 3
  3. Acute-phase reactants
    * Normal CRP and normal ESR = 0
    * Abnormal CRP or abnormal ESR = 1
  4. Duration of self-reported symptoms
    * <6 weeks = 0
    * ≥6 weeks = 1
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3
Q

DDx RA

A
  • Seroneg (PEAR)
  • Crystal (CPPD, polyarticular gout)
  • CTD (SLE, SSc, PM, Vasc, MCTD, PMR)
  • Infectious (EBV, HIV, Parvo, rubella, Hep C)
  • FM, OA

Uncommon:
- Infectious: endocarditis, rheumatic fever, Lyme
- Metabolic: hypothyroid, hemochromatosis, hyperlipoproteinemias (types II, IV), amyloid arthropathy
- Infiltrative: sarcoidosis,
- Vascular: hemoglobinopathies (sickle cell disease)
- Malignant: malignancy, paraneoplastic syndrome, hypertrophic osteoarthropathy,
- Inflamm: Behçet’s disease, Relapsing polychondritis, R3SPE, FMF, SAPHO

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4
Q

RA Epidemiology (race, age, prevalence)

A

All races (higher in Native Americans)
Age: 40-60 in F, older in M
1% of US

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5
Q

RA Patterns

A
  • Insidious (55%–65%): Arthritis over weeks to months.
  • Subacute (15%–20%): Similar to insidious onset but more systemic symptoms.
  • Acute (10%): Severe onset, some have fever.

b) Variant patterns of onset (10% of patients)
* Palindromic (episodic) pattern: Usually <5 joints and resolves within several days.- Tx: HCQ may decrease frequency of attacks and progression to RA.
* Insidious onset of elderly (>65 years): Pain/stiffness of limb girdle joints often with swelling of UE (difficult to differentiate from PMR & RS3PE)
* Arthritis robustus: Typically seen in men: bulky, proliferative synovitis –> erosions/ deformities with little pain or disability.
* Rheumatoid nodulosis: recurrent joint pain/swelling in, subcutaneous nodules, and subchondral bone cysts on XR.

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6
Q

RA Hand/Wrist deformities

A

Wrist:
- Volar subluxation (due to articular cartilage degradation and ligamentous laxity)
- Radial deviation (extensor carpi ulnaris tendon weakness = unopposed radial)
- Piano key ulnar head (radioulnar ligament damage –> floating ulnar styloid)
-Vaughan-Jackson deformity

MCPs:
- Subluxation (metacarpal head dorsally, prox phalanx head volar)
- Ulnar deviation

Fingers
- Ulnar drift (with wrist radial deviation, finger tendons pull fingers ulnarly)
- Fusiform swelling—PIP synovitis (spindle-shaped)
- Boutonnière
- Swan-neck
- Hitchhiker thumb (Z thumb)

Opera glass hands - bone resorption/shortening

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7
Q

RA XR findings

A

A—Alignment, abnormal; no ankylosis
B—Bones—periarticular (juxtaarticular) osteopenia; no periostitis or osteophytes
C—Cartilage—uniform (symmetric) joint space loss in weight-bearing joints; no cartilage or soft tissue
calcification
D—Deformities (swan neck, ulnar deviation, boutonnière) with symmetrical distribution
E—Erosions, marginal
S—Soft-tissue swelling; nodules without calcification.

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8
Q

RA C spine involvement
- subluxation
- impaction
- which joints
- neurologic manifestations

A
  • C1–C2 atlantoaxial subluxation (60%–65%) –> anterior: C1 arch and C2 odontoid gap >3mm 2/2 synovial proliferation around odontoid –> stretch/rupture of transverse/alar ligaments; >9mm anterior atlantodontoid interval or <14mm posterior atlantodontoid interval risks spinal cord compression
  • C1–C2 impaction: superior migration of odontoid from destroyed occipitoatlantal and atlantoaxial joint articulations between C1 and C2 –> impinge brainstem if moves into foramen magnum (worst neuro prognosis = odontoid ≥5 mm above Ranawat’s line)
  • Subaxial involvement: involves C2–C3 and C3–C4 facets and intervertebral disks –> “stair-stepping” vertebrae (important if >3.5mm)

Manifestations:
-neck pain to occiput
-painless sensory loss (hands/feet)
- syncope/death
- cerebral ischemia w vertebral insufficiency

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9
Q

Rheumatoid Nodules
- Histology / Layers

A
  • Inner: Central area of fibrinoid necrosis
  • Middle: Palisading macrophages and histiocytes
  • Outer: Monocytes and cellular connective tissue
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10
Q

RA Ocular Manifestations

A
  • MOST COMMON: Sicca
  • Episcleritis (painless)
  • Scleritis –> scleromalacia perforans
  • Choroid and retinal nodules,
  • Ulcerative keratitis (corneal melt)
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11
Q

RA Pulmonary Manifestations

A
  • Pleura: thickening, pleuritis, exudative effusion
  • Interstitium: IPF/UIP >NSIP, COP, nodules, pneumoconiosis (Caplan’s syndrome), apical fibrobullous dz, lymphocytic interstitial PNA (LIP)
  • Airway: criocoarytenoid arthritis, dysphagia, hoarseness, stridor, bronchiolitis (proliferative and obstructive), bronchiectasis
  • Vascular: PH, vasculitis
  • Other: infection, drug related, amyloid
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12
Q

RA Cardiac Manifestations

A
  • Pericarditis: constriction, effusion, tamponade
  • Myocarditis: CHF, afib
  • Coronary: CAD, arteritis, vasculitis
  • Nodules on valves: valvulopathy, conduction, endocarditis
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13
Q

RA Neuro Manifestations

A
  • Entrapment neuropathy: median nerve (carpal tunnel), posterior tibial nerve (tarsal tunnel), ulnar nerve (cubital tunnel), and posterior interosseous branch of the radial nerve
  • Peripheral neuropathy
  • Mononeuritis multiplex
  • CNS vasculitis
  • C1/C2 subluxation or impaction
  • Subaxial subluxation (C2/C3 and C3/C4)
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14
Q

RA Heme Manifestations

A
  • Felty’s syndrome (leukopenia, splenomegaly, RA)
  • Lymphomas
  • Large granular lymphocyte syndrome: neutropenia, splenomegaly, susceptibility to infections
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15
Q

RA Other manifestations

A
  • Sjögren’s syndrome
  • Amyloidosis
  • Osteoporosis
  • Ossicles of ear: tinnitus and decreased hearing.
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16
Q

RA Derm Manifestations

A
  • Palmar erythema,
  • Subcutaneous nodules,
  • Vasculitis
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17
Q

Tx of Felty

A
  • If RA and infxn: MTX –> +Ritux –> +Steroids as needed (unless infxn). TNF not effective.
  • G-CSF if severe infxn (risk of arthritis/vasculitis)
  • Splenectomy (for severe infxns and nonhealing ulcers)
  • Others: LEF, CNI, CYC, Abatacept > TNF

DC SSZ (neutropenia)

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18
Q

RA Disease activity measures

A

DAS28
SDAI
CDAI
RAPID3

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19
Q

RA Markers of poor prognosis

A
  • Poor functional status (HAQ >1) at presentation
  • Long dz duration prior to tx
  • Low education level (<gr 11)
  • Male
  • Smokers
  • Polyarthritis (small and large) >13
  • Erosions within 2 years of onset
  • Extraarticular dz: nodules, vasculitis
  • HLA-DR4 genetic marker
  • RF & CCP +
  • ANA + (if also RF+)
  • Persistently elevated ESR or CRP
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20
Q

RA Treatment targets
-how soon treatment
-activity level

A

Therapy within 3-6 mo of synovitis
Aim for LDAS or remission

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21
Q

SDAI calculation

A

Simplified disease activity index: TJC (0–28) + SJC (0–28) + PtGA (0–10) + PhGA (0–10) + CRP (mg/dL)
i.e. CDAI + CRP

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22
Q

CDAI calculation

A

Clinical disease activity index: TJC (0–28) + SJC (0–28) + PtGA (0–10) + PhGA (0–10)

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23
Q

RAPID calculation and cutoffs

A

Routine assessment of patient index data: MDHAQ (0–10) + patient pain (0–10) + PtGA (0–10)

Cutoff: <1, 1.3-2, 2.3-4, 4.3-10

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24
Q

RA Mortality causes

A

CV
Infection: PNA
Cancer: lymphoma, leukemia, lung, melanoma
Renal: amyloid
GI bleed: NSAID

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25
Q

RA synovium histology

A

Hyperplasia (1-2 –> 6-10 cells thick
Hypercellularity (T-lymph and macrophages mainly, but also plasma cells, activated fibroblasts, dendritic cells)
Neovascularization/angiogenesis

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26
Q

RA synovium cytokines elevated
Which responsible for systemic fx

A

TNF, IFNg
IL-1, 2, 6

IL6 - fatigue, cognitive dysfunction, and altered HPAA function

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27
Q

** RA: adhesion molecules in synovium**

A

M6- leukocyte activation antigen, is a potent inducer of enzymes for degrading cartilage and bone in RA

RANKL (Receptor Activator of Nuclear Factor-kappaB ligand) expressed on activated T cells and synovial fibroblasts and on bone lining cells for osteoclast activation

VCAM, ICAM

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28
Q

MTX lung:

-Manifestations
- Imaging findings
- BAL
- Biopsy
- Tx

A
  • SOB, fever, cough over weeks after starting drug
  • CXR - bilateral interstitial opacities or mixed interstitial/alveolar pattern; NSIP
  • CT - GGO
  • BAL: lymphocytosis w low CD4/8, +/-eos
  • Biopsy - Interstitial pneumonitis w granuloma, occasional eos and bronchiolitis
  • Tx: stop MTX, give steroids
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29
Q

RA effusion features

A
  • Subclinical: small-mod size, unilateral, asymptomatic
  • Exudative (high prot and LDH, low gluc and pH <7.2)
  • RF positive
  • Cell count <5000, mostly lymh but PMN and eos initially
  • Cholesterol > 5.2 (chol crystals)
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30
Q

4-5 clinical manifestations that help to differentiate amyloidosis from RA on physical exam

and biopsy results

A
  • Macroglossia
  • Shoulder pad sign
  • Enlarged liver
  • CHF, periph edema (also from nephrotic syndrome and prot losing enteropathy)
  • Arthropathy similar to RA: symmetric, shoulders, knees, wrists, MTP and PIP’s, lesser degree elbows and hips, tender w AM stiffness
  • Amyloid nodules ( biopsy positive for Congo red birefringemnt
  • Periorbital purpura
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31
Q

RA Pregnancy
- When remit vs flare

A

2/3 remit from T1-T3 –> 2/3 flare in 1st 6mo
1/3 flare during pregnancy (mostly T1)

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32
Q

RA Ulnar deviation pathogenesis
3 reasons

A
  • Extensor carpi ulnaris weakness from laxity and erosion –> radial deviation of the wrist and compensatory ulnar pull of finger tendons
  • Failure of radial collateral ligament from MCP synovitis causing stretching/thinning –> imbalance favouring ulnar collateral ligaments
  • Weakened radial collateral ligament –> unopposed abductor digiti minimi muscle –> drift of little finger
  • MCP synovitis and subluxation
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33
Q

Boutonnière
Pathogenesis and DDx

A

PIP synovitis –> extensor tendon elongation and rupture dorsally –> lateral and volar displacement of lateral bands ie shortens –> flexes PIP and hyperextends DIP

DDx: RA, trauma (blunt/laceration), burns.

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34
Q

Pathogenesis: Swan-neck

A

Lateral and DORSAL displacement of lateral bands –> shortening –> flexes DIP and hyperextends PIP

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35
Q

Felty Triad and other features

A
  • RA, leukopenia, splenomegaly,
  • RA assoc’d: erosions, wt loss, sicca, episcleritis, eye lid necrosis, pleuritis, vasculitis, neuropathy, nonhealing ulcers, hyperpigmentation
  • Leukopenia assoc’d: Infection, NHL risk
  • Splenomegaly assoc’d: LN, hepatomegaly/cirrhosis, portal HTN, varices
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36
Q

LGL (pseudo Felty) vs Felty

A
  • LGL: lymphocytosis in periph blood and BM.
  • FS: hypocellular BM
  • LGL leukemia - Monoclonal T-cell
  • FS: Polyclonal T cell
  • LGL CD2, 3, 8, 16, and 57 surface phenotypes in the peripheral blood smear (BM bx required to confirm)
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37
Q

Vaughan-Jackson deformity
- Features
- Mx

A

Extensor tendon rupture (D3-D5) from chronic wrist tenosynovitis + damaged ulnar styloid –> rupture (surgical emergency)
- Scallop sign

  • Prevention via screening for extensor tendon weakness or restriction
  • Tenosynovectomy +/- ulnar head surgery if high risk.
  • After rupture: surgical repair
38
Q

RA Vasculitis Types and manifestations

A
  • Leukocytoclastic - papable purpura. Vasculitis of post capillary venules
  • Small arteriolar - infarcts of digital pulp and nailfolds (rarely gangrene), distal sensory neuropathy (due to vasculitis of vasa nervorum)
  • Medium vessel - resembles PAN (visceral arteritis), mononeuritis multiplex, livedo reticularis
  • Pyoderma gangrenosum
39
Q

Pathogenesis: Z thumb

A

1st MCP synovitis weakens capsule/ ligament → stretching EPB allowing EPL to sublux volarly → flexing MCP and hyperextending IP

40
Q

Rheumatoid Nodules DDx

A

Nodule + arthritis:
- MTX-induced accelerated rheumatoid nodulosis (–> multinucleated giant cell formation via a1 adenosine R)
- RA,
- Xanthoma,
- Gout (tophi),
- SLE (rare), IIm, SSc (calcinosis)
-Amyloidosis, Sarcoid
- Rheumatic fever (rare), Leprosy
- Multicentric reticulohistiocytosis,

No arthritis: Granuloma annulare

41
Q

**IL6 role RA **

A
  • Autoimunity: Induce B cell maturation and TH17 differentiation
  • Systemic fx: acute phase rxn and anemia via hepcidin, fatigue via HPAA
  • Bones: Recruits osteoclasts and induces MMPs for erosions
  • Blood vessels: Induce vascular permeability via VEGF production; Activate neutrophil migration to tissue
42
Q

MTX-induced accelerated rheumatoid nodulosis Tx

A
  • DC MTX and switch DMARD/biologic
  • Continue MTX if cosmetic only
  • If pain, mass effect: steroid injxn
  • Case series: IL6, JAKi, RTX
43
Q

** How to calculate HAQ**

A

41 total items:
-20 four‐point Likert‐scale Qs for specific ADL in 8 functional categories (each category scored based on highest sub-question)
-13 Qs for use of assistive devices
- 8 Qs assessing help received

Responses options/scale.
0 = without difficulty,
1 = some difficulty,
2 = much difficulty
3 = unable to do.

Scoring.
1) Use highest subcategory score for category. If used aids/help, increase score from 0/1 to 2 (no change if alrdy 2 or 3)
2) sum category scores;
3) divide final sum by the number of categories for final HAQ score rounded to the nearest value evenly divisible by 0.125.
**Requires a minimum of 6 categories answered; if less, do not score.

Score interpretation.
Total score is between 0–3.0, in 0.125 increments. Increasing scores indicate worse functioning with 0 indicating no functional impairment and 3 indicating complete impairment.

44
Q

Claw toe deformity
- Pathogenesis
- DDx

A

Chronic MTP hyperextension leads to unopposed flexion of the DIP and PIP.
Atrophy/weakness of intrinsic muscles overpowered by extrinsinc (EDL, EDB, FDL)

DDx:
Synovitis,
-Trauma
- Delayed/missed compartment syndrome of deep posterior compartment of leg/foot
- Cavus deformity
- Neuromuscular disease

45
Q

Foot pain DDx

A

Synovitis,
MTP subluxation,
Bunion (Hallux valgus),
Stress fracture of MTP,
Toe deformities,
Enthesitis/plantar fasciitis,
Tendonitis,
Bursitis,
Rheumatoid nodules,
Neuropathy (eg Tarsal tunnel, vasculitic, drug-related)

46
Q

Preop Screening

A
  • C-spine XR (flex/extend) if pain
  • Screen cardiac disease
  • Cricoartyenoid joint disease
47
Q

Claw vs Mallet vs Hammer

A

Claw: MTP extended, PIP flexed, DIP flexed
Mallet: DIP flexed, others neutral
Hammer: PIP flexed, others extended or neutral

48
Q

Pregnancy + Breastfeeding (BF) Meds
- NSAIDs
- ACE/ARB
- Pred
- TNFi
- Continue
- Discontinue
- Not compatible

A

NSAIDs - DC in 3rd to prevent premature fetal ductus arteriosus closure (ok 1-2), ibuprofen for BF

ACE6ARB - DC in T2/3 - fetal renal fx

Pred <20mg (if >20mg, hold BFfor 4h)
TNFi: DC in 3rd (ok 1-2), ok for BF

Continue: HCQ, SSZ, colch, AZA, CNI (preterm, low birth weight, NOT for BF)

Discontinue at conception and in preg: anakinra, belimumab, abatacept, anti IL6, anti IL17, JAKi

NOT COMPATIBLE preg and breastfeeding: MTX, MMF, LFN, CYC, Thalidomide, Tofa, apremilast, baricitinib

49
Q

RA ILD:
-Risk factors to DEVELOP
-Poor prognosis

A

Smoking
Age
High anti CCP-RF
Fam Hx RA
Male
MUC5B promoter variant

-Male, older
-Hx of exacerbation
-Low DLCO
-UIP (honeycombing)
- Extent of fibrosis

50
Q

Drugs to avoid in ILD

A

MTX, LFN
Gold
TNFi

51
Q

Felty DDx

A

LGL-L
EBV/HIV
Meds: TNFi, MTX
SLE

52
Q

Pathogenesis:
-Hallux valgus
-Splay foot
- Hindfoot valgus
-Pes planus

A

-Hallux valgus: sznovitis 1st MTP, lax ligament, lateral deviation prox phalanx

-Splay foot: MTP laxity + intrinsic muscle weakness

  • Hindfoot valgus: synovitis midtarsal, subtalar, ankle; tibialis posterior rupture, lax ligament

-Pes planus: synovitis peritalar joints and tib post –> midtarsal, subtalar instability –> navicular pushed anterior/down depressing medial longitudinal arch

53
Q

Tx for
LGL-L
Rheumatoid robustus with amyloid
RA w/ vasculitis
RA w/ nodules on MTX
RA with cricoarytenoid disease

A

LGL-L: MTX, CNi, CYC, +/- pred

Amyloid: MTX, CYC, TNFi, Toci,

Vasculitis: pulse steroids +/- ritux/cyc

Nodules on MTX: DC MTX, can inject nodules w steroids or surgically remove, maybe colchicine, SSZ, HCQ can shrink nodules

Cricoarytenoid: treat RA, inject vocal cords, ENT

54
Q

Indications for C spine fusion in RA

A

-Atlantoaxial subluxation w/ posterior antlantodens interval of <14mm
OR 5mm of basilar invagination

-Subaxial subluxation and sagittal diameter of spinal canal of <14mm

55
Q

RA mech of wrist radial deviation

A

Extensor carpi ulnaris tendon weakness = unopposed radial

56
Q

RA mech of Piano key ulnar head

A

Radioulnar ligament damage –> floating ulnar styloid

57
Q

RA mech of ulnar drift of fingers

A

With wrist radial deviation changes line of pull –> finger tendons pull fingers ulnarly

58
Q

Cutoffs for DAS28, SDAI, CDAI, RAPID 3

A

DAS28: ≤2.6, ≤3.2, >3.2 to ≤5.1, >5.1
-*change must >0.6 to be meaningful

SDAI: ≤3.3, ≤11, >11 to ≤26, >26

CDAI: ≤2.8, ≤10, >10 to ≤22, >22

RAPID3: ≤1, <6, ≥6 to ≤12, >12

59
Q

List 3 proteases produced by synovial fibroblasts

A
  • MMP (matrix metalloproteinases)
  • Serine proteinases (Granzymes A/B, trypsin, tryptase)
  • Cysteine proteinases (Cathepsins B, D, K, L)
  • Aggrecanases (fibronectin)
60
Q

Define pannus

A
  • Proliferative synovium: mononuclear cells (CD4+ T lymphocytes, activated macrophages, B cells, plasma cells, and dendritic cells)
  • Can invade bone/cartilage to cause destruction via fibroblast like synoviocyte and proteinases
61
Q

5 cells found in pannus/synovium

A

Mononuclear cells:
- CD4+ T lymphocytes
- Activated macrophages,
- B cells,
- Plasma cells
- Dendritic cells
- Osteoclasts
- Mast cells
- Fibroblast like synoviocyte

62
Q

Rheumatoid nodule
- Where (and manifestations)

A
  • Forearm extensor surface, olecranon bursa, over joints, and over pressure points (e.g. sacrum, occiput, and heel)
  • Lung (effusion, PTX, fistula, hemoptysis)
  • Cardiac (valvulopathy, stroke, syncope,
  • CNS (SC compression, stenosis)
63
Q

Cytokine with antiinflamm fx

A

Major anti-inflammatory cytokines include IL-4, IL-10, IL-11, and IL-13

64
Q

TNFa roles in RA

A
  • Blood vessel related
    • Angiogenesis
    • Activate endothelial cell adhesion molecules (VCAM, ICAM)
  • Inflammation related
    • Proinflammatory cytokine release (1,6,23)
    • Hepcidin induction (acute phase response)
    • PGE2 production
  • Erosion related
    • Osteoclast activation
    • Chondrocyte activation —> MMP production and cartilage destruction
65
Q

Draw and describe a rheumatoid factor

A

RF = autoantibody (IgM, G, A, E) against antigenic determinants on Fc fragment of immunoglobulin G forming immune complex

66
Q

Nonrheum causes of positive RF

A

CHRONIC

CH: chronic dz: hepatic (PBC), pulmonary (IPF, silicosis, asbestosis)
R: RA
O: Other CTD: SLE, SSc, MCTD< SS, PM, Sarcoid N: neoplastm
I: infxn - TB, IE, Hep B/C, HIV, Mono, Parasitic (toxo, malaria), syphilis, Leprosy, Parvo, Rubella
C: cryo
Chronic liver and renal disease
Elderly

67
Q

What are anti-citrullinated antibodies (ACPA)

A

Proteins directed against citrullinated peptides (eg fibrinogen, T2collagen, vimentin) –> immune complex to start innate/adaptive response, cytokine production, and activation of fibroblast like synoviocytes

(Citrulline formed by deimination of arginine by peptidylarginine deiminase in mucosal surfaces)

68
Q

**DDX of positive Anti-CCP **

A

CTD: RA, SLE, SS, PsA,
Infection: TB
Lung disease: IPAF, RA-ILD

69
Q

**Anti-CCP significance in RA (new and old)

A

New RA:
- Specific for RA
- More severe disease course
- Erosive disease

Old RA:
- Less likely to achieve drug free remission
- Assoc’d w/ ILD and CVD

70
Q

Why cyclic configuration of Ag in assays that test for antiCCP

A

Peptides in peptide-AB complexes adopt beta-turn conformation
This increases ACPA binding affinity (ie increase sensitivity without sacrificing specificity)

71
Q

1 genetic and 1 environmental factor associated with CCP

A

Genetic:
- HLA-DR4,
- PADI4,
- PTPN22

Environmental:
- Smoking (increases PADI), pollution, silica
- Microbiome,
- Infections
- Perionditis - porphyromonas gingivalis can form citrullinated neo antigen –> ACPA

72
Q

Role of smoking in RA

A

Increases risk of ACPA+ RA
Activates innate immune pathway
Induces PADI expression in airway –> more protein citrullination and stimulation for generating ACPAs

73
Q

2 advantages of antiCCP over RF

A

More specific but equally sensitive
Predicts severity and erosive disease

74
Q

Difference between synovial path in PsA vs RA

A

PsA
- LESS cellular infiltrate (T/B cells) with MORE TH17 cells
- MORE vascular tissue in PsA (increased expression of VEGF, ANG2, BFGF)
- LESS hyperplasia of synovium in PsA
- Proliferation of existing vessels by EXTENSION vs/ in RA vessels show BRANCHING = NEOVASCULARIZATION
- NO antibodies to citrinullated peptides

75
Q

Drug induced pneumonitis vs RA-ILD

A
  • MTX pneumonitis happens in 1st year vs more chronic in RA-ILD
  • NSIP (vs UIP in RA-ILD)
  • BAL: lymphocytic (vs neutrophilic or lymphocytic in RA ILD)
76
Q

Drugs safe to use in RA ILD

A

CYC
Steroids
MMF
AZA
Ritux

77
Q

How to diagnose cricoarytenoid arthritis

A

HRCT
PFT
Laryngoscopy

78
Q

**MC tendon rupture in RA **

A

Ulnar extensor tendons (extensor digiti minimi is first)
Then radial extensor tendons
Flexor policis longis = MC flexor to be ruptured (Mannerfelt lesion)

79
Q

Mechanism of stenosing flexor tenosynovitis

A

Thickening/hypertrophy of A1 pulley
Presence of nodules

80
Q

Windswept deformity of the knee

A

Rare complication of untreated RA
Abnormal valgus deformity in one knee with varus in the other

81
Q

PsA vs RA - clinical/lab manifestations

A

DIP involvement
Asymmetric oligoarticular
No RF or CCP
HLAB27, IL23
Nail pitting/dystrophy
Dactylitis and Enthesitis
Axial involvement
Psoriasis

82
Q

PsA vs RA - XR manifestations

A

RA
- Periarticular osteopenia
- Marginal erosions: MCP, wrists, PIP
- NO acral osteolysis

PsA:
- Periostitis
- Ankylosis
- Erosions: MCPs, PIPs, DIPs,
- Dactylitis
- Acral Osteolysis , Arthritis mutilans
- Pencil in cup
- Axial and SI involvement
- Syndesmophytes

83
Q

2 diseases w/ MCP subluxation but NO erosions

A

SLE - Jaccoud’s
Rheumatic fever
Neurologic: cerebral palsy, post CVA

84
Q

Direct/indirect societal costs of RA

A

Direct
- Treatment costs eg meds
- Hospital costs
- Cost of transport, aids

Indirect
- Lost productivity (to employer)
- Home care
- Intangible costs on self esteem, well being

85
Q

Das 28 components

A

SJC, TJC, ESR, Pt global

86
Q

10 methods used in the literature to measure the response on meds in RA?

A

Das 28, CDAI, SDAI, RAPID 3
EULAR response, ACR response,
ACR 20, ACR 50, ACR70
Patient activity scale

87
Q

3 combination tx w/ MTX that is superior to MTX alone

A

MTX+SSZ+HCQ
MTX+LFN
MTX+IFX
MTX+ADA
MTX+ETN

88
Q

What is rate of radiographic progression in RA when using antiTNF?

A

Total sharp score
- Mean annual progression 2.1/year w/ DMARD and 0.7/year by TNF

89
Q

Fertility vs Obstetric outcomes in RA vs healthy

A

Fertility/preg outcomes worse if active disease

Obstetric outcomes increased: HTN, IUGR, C-section, preterm birth,

90
Q

** Change of child developing RA or SARDs if mother has RA**

A

3x more likely to develop RA
Increased likelihood of thyroid disease

91
Q

Risk factors for RA flare during pregnancy

A

TNFi discontinuation early in pregnancy
High disease activity

92
Q

** Vaughan-Jackson deformity DDX **

A
  • Extensor tendon subluxation at MCP (ie not ruptured, but just dysfunctional)
  • Volar subluxation of metacarpal heads preventing finger extension (active and passive)
  • Ulnar nerve palsy affecting 4th and 5th lumbricals, with unopposed MCP extension and unopposed IP flexion
  • Trigger fingers stuck in flexion

1. Rheum RC (23 decks)

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