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Blood and Lymph: Unit 3 > Rheum > Flashcards

Rheum Flashcards

1
Q
  • What does rheumatology mean? Only study joints? What is very important?
  • Inflammatory disease: AM stiffness? Fatigue? Activity? Sleep? Corticosteroids?
  • Mechanical disease: AM stiffness? Fatigue? Activity? Sleep?
  • OA: Inflammatory? Which joints? Nodes? (2) ESR? CRP?
  • RA: Inflammatory? Which joints? What effected? ESR? CRP? May be related to historically?
  • Gout: High levels of? Diagnosed by this? How?
A
  • Study of flow; no; good H and P
  • > 1 hr; yes; helps; worsens; help
  • Short; no; does not help; does help
  • No; weight bearing joints; Heberdens and Bouchards; negative for both
  • Yes; small joints; synnovitis; positive for both; industrial revolution
  • Uric acid; no; look at synovial fluid
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2
Q
  • Pseudogout: Synovial fluid has what in it?
  • Spondyloarthropathies: Joints? Common HLA?
  • SLE: Which systems? ANA? Low compliment?
  • Sjorgens: Autoimmune of?
  • Systemic sclerosis: Fibrosis of?
  • Vasculutis: Vessel inflamm. with?
  • Management? (5)
A
  • Calcium pyrophosphate crystals
  • Spine; HLA-B27
  • Multiple; Positive; 3 and 4 low
  • Exocrine gland
  • Skin
  • Hemmorrhaging
  • NSAIDs, Gluco., DMARDS, anti TNF, MAB’s
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3
Q
  1. ) OA: Degeneration of? Hypertrophy of?
    - Often due to? Risk factors? (3)
    - Joints effected? (5) Symmetrical?
    - Improves with rest? Activity? Systemic?
    - Bone abnormalities? (4)
    - Fluid?
    - 5 parts of cartilage?
    - Vascular?
    - Cytokines promoting damage? (3)
A
  • articular cartilage; contiguous bone
  • wear and tear; age, obesity, trauma
  • Hip, lower lumbar, knee, DIP, PIP; no
  • Yes; No; No
  • Enlargement; H and B nodules, genu varus, osteophytes
  • Type 1 (200-2k WBC’s) (25% PMN’s
  • T2 collagen, chondrocytes, proteoglycans/hyluranic acid, MMP’s, Water
  • No
  • IL1 = More MMPs; TNFa=More MMPs; Complement activated
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4
Q
  1. ) OA: Culture joints for? What to expect?
    - Expected X-ray findings? (4)
    - Pathogenesis: Chondrocytes can synthesize what to build? To destroy? Lower proteoglycans leads to? (3) Chondrocytes then release? (4) Causing? Adipokines? Genetics?
A
  • Cell count (WBC), Crystals, Culture (gram); Type 1
  • Decreased joint space, loss of cartilage, bone cysts, osteophytes
  • Collagen/proteoglycans; MMP’s; Decreased hydrophiliity, loss of collagen, chondrocytes dying; IL1, TNFa, NO, PG’s = more MMP’s; Also may play a role; Possible abnormal T2 collagen
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5
Q
  1. ) RA: Systemic? Autoimmune? Predominately in what joints? What leads to cartilage/bone destruction? Also leads to? Which is?
    - Genetics associated? AM stiffness? Activity? What is often spared?
    - Can lead to what systemically? (3)
    - Test for what? Which is?
    - Anemia?
    - CRP? ESR? Synovial fluid? Mostly what cells?
    - Treatment? (2)
A
  • Yes; yes; peripheral, symmetric; Inflamm synovitis; Pannus (inflamed gran. tissue which then contracts)
  • HLA-DR4; Yes; Helps; DIP’s
  • Rheum nodules; Pleural effusions; lung fibrosis
  • RF = IgM anti IgG (Fc portion)
  • yes
  • Both positive; inflammatory >2k; Neutro’s
  • NSAIDs, DMARDS (inhibit lympho/macs)
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6
Q
  1. ) RA: Synovial fluid compartment contains? Underinfluence of? (2) Release? (3)
    - Synovial tissue: Contain? (3) Release? (3) More important in disease progression? T cells?
    - Pathology: Ag+APC leads T cells to release? (2) Leads to activation of B cells which release? (2) And Macs which release? (4) Importance of RANK protein? Macs on chondrocytes?
    - Anti CCP is an AB against? Specific enzyme test?
    - Genetics: Which class MHC? Shared epitope? Where on ab?
A
  • Neutros; IL8/TGFb; NO/PG’s/LT’s
  • Macs/Lymphos/fibros; IL1/IL6/TNFa; Synovial tissue; May also play role
  • IL6/IL17; RF/anti-CCP; TNFa, IL1, IL6, RANK proteins; change onsteocytes to osteoclasts; degrad enzymes
  • cintrinulated (arginine) proteins; PAD
  • Class 2; QKRAA; 3rd hypervariable region
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7
Q
  1. ) Spondyloarthropathies: RF in serum? Often effects? Genetic involvement? Ligaments?
    - Ankylosing Spondylitis: Often involves? Effects who most? How many months? AM? Activity? Chest expansion? Hips/shoulders?
    - Labs: ESR? RF? ANA?
    - X ray: Marginal? 10% have? Joint space?
    - Extra acrticular involvement? (4)
    - Reactive arthritis causes? Other 2 sub types?
    - What did rat study show with AS?
    - Treatment? (5)
A
  • No; Axial skeloton; HLA-B27; enthestisis (lig inflamation)
  • Sacroilliac; young males; 3 mo; Stiff; helps; may be decreased; may also be involved
  • Increased; Negative; Negative
  • Syndesmophytes; spinal fusion; good
  • Uveitis, colitis, Cauda equana, dactilitis (sausage fingers)
  • Salmonella, shigella, chlamydia, yersinella; psoriatic, colitic
  • Environmental trigger is critical
  • No smoking; no pillows, NSAIds, cortico, anti TNF
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8
Q
  1. ) Spondylo:
    - 4 AS theories?
    - Genetics: What plays role? General pop effected? With B27? B27 plus 1 deg rel? MZ twins? 90 caucasians with disease? Genetics account for? B27? reactive arthritis?
    - Reiters triad with? (3)
A
  1. ) Molec mimicry: B27 with same epitope leading to immune response or overlooking ag 2.) Arthrithrogenic peptide: Gut flora leaks 3.) Heavy chain thoery: Stable homodimers with no B2 microglobbulin 4.) Protein unfold: Misfolded ER leads to stress
    - Class 1 B-27; 0.1-0.2; 1-2; 10-20; 60%; B27+; 60-90% HLA-B27
    - With reactive arthritis: Conjuctivitis, arthritis, urethritis
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9
Q
  1. ) SLE: Systemic disease? Common presentations? (4)
    - ANA? Common ab’s? (3)
    - Type 2? Type 3?
    - Effects seen by type 2? (4)
    - Effects seen by type 3?
    - Organ specific diseases? (4)
    - Epi: Men or women? Races?
    - Enviromental? (2)
    - Genetics? (2)
A
  • Yes; Malar rash, photosensitivity, renal issues, hematologic problems
  • Positive; To smith, DNA, cardiolipins
  • Ab mediated, complexes
  • Hemolytic anemia, anti phospholipid abs –> block clotting cascade (Higher PTT); ANA ab’s against DNA, histone, non histone; CNS involved
  • Nephritis from complexes lodged
  • Diabetes, good pasture, Myo gravis, Hoshimoto
  • Women, AA and hispanic
  • Sex hormones, Sun (dead keatinocytes)
  • c4a null alleles; HLA-DR3
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10
Q
  1. ) SLE: Patho: Misdirected?
    - 6 theories?
    - Treatment? (4)
    - Innate involved? TLR7? TLR9? How are PMN’s implicated?
A
  • Recognition of self as antigen
    1. ) Loss of T cell tolerance: T cells allow self Ab’s to be switched to IgM
    2. ) Polyclonal activation: LPS fires up B cells
    3. ) Molec mimicry cross rxn 4.) Illicit help = foreign+ self presented 5.) Sequestered ag: Tissue damage has self exposed 6.) Immuno def.
  • Less sun exposure; NSAIDs/steroids; anti malarials lower humerol response; IVIG
  • DNA immune complexes; RNA protein complexes from N’s Netosis (releasing DNA when dead)
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11
Q
  1. ) Crystal Arthropathies:
    - Gout: Deposition of what to urate crystals? Due to? What inflammation due to crystals? (2)
    - Purine Metabolism: AMP/GMP broken down to? Then broken down to? Then? By what? Build up due to?
    - 4 stages of gout and their presentation?
    - Risk factors? (4)
    - Active PRPP synthase or deficient HGPRT? Complete loss in?
A
  • MSU (monosodium urate); hyperuricemia; articular and periarticular
  • Hypoxanthine and guanine; xanthine; uric acid; xanthine oxidase; over production or lowered excretion (FAR more common)
    1. ) Asymptomatic = MSU > 7mg/dl
    2. ) Acute: Podagra MTP flare up
    3. ) Intercritical: Asymptomatic intervals
    4. ) Chronic: Tophi = crytals in soft tissue/joints; often in digits, olecranon bursa and achilles
  • obesity, insulin reisistance, htx, dehydration
  • Increased Uric acid/ Lesch-Nyhan
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12
Q
  1. ) Crystal arthropathies:
    - Gout mechanism: Triggers? (4) Crytals interact with synovial lining leading to? Picked up by which TLR’s? Leads to release of? (3) NLRP3 in cell cleaves? Leads to?
    - Secondary hyperurucemia due to? What is activated? Which is?
    - Gout: Inflammatory fluid? Crytals? (2)
    - Pseudogout: Inflammatory? Crystals? (2) Due to overabundance of? Via what gene? Crystals released by? Not in what like gout? First MTP?
A
  • Low temp, trauma, low Ph, dehydration; activation of mono/macs; TLR2/4; TNFa, IL6, IL8; IL1B; bringing in more macs
  • Drugs lower renal excretion; URAT1; urate organic anion exchanger in proximal tubules
  • Yes; needle shaped; neg. byfringence
  • Yes; rhomboid + byfringence; PPi; ANKH gene; CPPD crystals released by shedding; not formed in synovial fluid; rarely effected
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13
Q
  1. ) Vasculitis:
    - Large vessel: a.) Giant Cell: Where? (2) Effects? Common genetic?
    b. ) Takayasu’s: Effects? Upper? Granulomatous?
  2. ) Medium Vessel: a.) PN effects? (3)
    b. ) Kawasaki: Effect who? Damage by?
  3. ) Small Vessel: ANCA positives? (3) Distinct feature? Feature to all three?
    b. ) ANCA negatives? Unique feature?
A

a. ) Temporal, eyes; internal elastic lamini; HLA-DR4
b. ) Aortic arch; no, lower; yes
a. ) skin, bifurcation, kidneys
b. ) Kids; cytokine mediated
1. ) GPA = C-ANCA
2. ) Churg Strauss: Eisinophil involvement
3. ) MPA = P-ANCA
* ENT, Lungs, Kidneys
1. ) HSP = IgA
2. ) ECV = Cyroglobins (hep c)
3. ) CLA = Immune complexes

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14
Q
  1. ) Vasculitis:
    - Clinical features? (2)
    - ESR? CRP? Compliment? Albumin?
    - Mechanisms: IC? ANCA? Antiendothelial via? (2) T cell endothelial injury via? Endothelial infection?
    - Types of ANCA’s? Where? Bind? Effect?
    - Treatment? (2)
    - Mechanism? (6)
    - Cause immune complexes? (4)
A
  • Palpable purpura, systemic symptoms
  • High; High; Low; Low
  • Yes; Yes; ADCC and compliment; HLA-DR4; MHC Class 2
  • C = cytoplasmic = PR3 on neutrophils primary granules
  • P = perinuclear; binds MPO
  • Both amplify immune response
  • Glucocoticoids, Ritixumab
  • Inflamation –> PAF –> Incr. vasc perm –> IC deposition –> Complement –> PP
  • Bugs, drugs, malignancy, connective tissue disorders
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15
Q
  1. ) PS/DS:
    - Type: 1? 2? 3? 4? 5?
    - Clinical findings? (7)
    - Most important extra muscular finding?
    - Markers of disease: Anti-JO-1 and? Leads to? (4)
    - Labs: CPK? Myoglobin? AST? ALT? ESR? ANA?
    - EMG: Distinct how? (3)
A
  1. ) PM 2.) DM 3.) PM/DM with neoplasia 4.) Childhood DM 5.) PM/DM with another connective tissue disorder
    - proximal muscle weakness; Gottmans papules; heliotrope rash; V sign, Shawl sign, mechanics hands, preiungal erythema
    - Lung disease
    - Anti-histatydyl tRNA; fever, arthritis, lung, vasculitis
    - High, high, high, high, high, ANA positive
    - Low amplitude, fibrillations, irreg spiking
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16
Q
  1. ) PS/DS:
    - Find what on MRI of kids?
    - DM: Cell type? Where? Compliment?
    - PM: Cell type? Where? Compliment? Cytokines? (3) Assoc with heart disease? ER synthesis?
    - May be viral (Flu, COX, HIV, exho) why? (3)
    - Treatment? (3)
A
  • Calcinoisis
  • CD4, B, Macs, DCs, perivascular/around fassicle, yes
  • CD8, within fassicles; no; INF, TNFa, IL1; yes; problem leading to stress
  • viral particles found, spring ususally, INF found via microarray
  • PT, prednisone, Ritiuximab
17
Q

Derm Review:

  1. ) OA: Degeneration of? Hypertrophy of? X ray findings? (5) May be protective? Early OA? (2) Who wins? Fluid? Inflamm. cytokines? (5)
  2. ) RA: Def? (4) Joints? Shared epitope? RF is? Complexes pathogen? Modified arginine leads to? 100% specificity? Fluid? Pannus cells? (3) Effect?
  3. ) Gout: Deposition of MSU due to? Human lack? Genetics of over production? PRPP? HRPRT? Complete lack of? Diagnosis via? Some drugs inhibit? Innate to crystals? Activate NLRP via? What promotes phagocytosis of PMN’s?
  4. ) Pseudogout: Abnormal PPi gene? PPi precipitiates with? Then? CPPD test?
A
  1. ) Articular cartilage, contiguous bone; Joint space loss, subchondral cysts, sclerosis, osteophytes, H and B nodes; Incr. Chondro, Incr MMP’s; MMP’s; non inflamm; IL1, NO, PGE2, IL6, PG’s
  2. ) Systemic, inflamm, AI, symmetric synovitis; erosions, QKRAA in HLA-DR4/ HLA-DR1; IgM anti IgG (fc); yes; anti cintrinulated peptides; RF and anti CCP; inflamm (neutro’s); CD4, fibros, macs; modulate and amplify local response
  3. ) Hyperuricemia; uricase; x linked; overactive; deficiency; arthrocentesis; xanthine oxidase; TLR2/4; capsase 1; IgG
  4. ) ANKH; Ca; shed into joint space; positive
18
Q

Derm Review:

  1. ) Seronegative SA’s: Have what in common? (2) Gene assoc? RF? ANA? TNFa? Incidence? With gene? Those with disease and gene? 1 deg. relative and gene? Rats? RA: Clinical? (2) Related to? (4) Triad?
  2. ) SLE: Def? Misdirected recognition of? Immune response? (2) Genetics? (2) Environment? (2) ANA: anti dsDNA? anti histone? Type 2 effects? (4) Type 3 effects? (1)
A
  1. ) Sacroillitis, enthesitis; HLA-B27; negative, negative, Increased; 0.1-0.2%; 1-2%; 20%; need environmental trigger; dactylitis, lower extremity arthritis; molec mimcry, arthri peptide, heavy chain (activate NK), ER stress response via misfolded; Reiters
  2. ) Chronic, systemic, AI; self as foreign; T and B cell response; HLA-DR3; C4a null; sex hormones, sun; renal; drug induced; anti RBC, WBC, plt, phospholipid (increased clotting); glomneph
19
Q
  1. ) Vasculitis: Inflammation where? Mechanism? (5) Source of antigen? (4) ANCA C? P? Both part of? Amplify what?
  2. ) PM/DM: Inflammatory what? Related to what disease? Myotoxic ab’s pathologic? PM distribution? Cells? DM distribution? Cells? Live virus cultured yet?
A
  1. ) Within or through vessel wall; Inflamm –> PAF’s –> Incr Vasc perm –> IC deposition –> PP; bugs, drugs, malignancy, CT; C=PR3=GPA; P=MPO=MPA; primary neutro granules; immune response
  2. ) Myopathies; Interstitial lung disease; no; endomysial (CD8); perivascular (CD4, Macs, Compliment); NO

Blood and Lymph: Unit 3 (4 decks)

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