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Abbey MSII Unit 1 pt 2 > Lange 24. > Flashcards

Lange 24. Flashcards

1
Q

What is the initiating force of an acute disease usually?

A

exogenous

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2
Q

What activates regional blood vessel endothelium?

A

proinflammatory cytokines (TNF, IL1)

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3
Q

IL-12

A

produced by infected monocyte-macrophages skew lymphocyte toward TH1

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4
Q

TH1 cell cytokine production

A

IL-2, interferon-gamma, TNF (Tcells)

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5
Q

IL-4

A

TH2 lymphocyte creation

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6
Q

TH2 cell cytokine production

A

IL-4, 5, 6, 10 (B-cells)

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7
Q

Classical complement pathway is activated when?

A

when antibody binds to its specific antigen (induces inflammatory cell recruitment and activation)

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8
Q

myelomonocytic cells

A

neutrophils and macrophages

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9
Q

proinflammatory mediators

A

TNF, IL-1, IL-6, prostaglandins, leukotrienes

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10
Q

Autoimmune diseases are characterically driven by what?

A

antigen

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11
Q

T cells induce apoptosis in which ways?

A

Fas-Fas-ligand pathway, perforin, granzymes

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12
Q

SLE autoantibody

A

Ro

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13
Q

Gout

A

crystal-induced inflammation of synovial joints

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14
Q

What is the most frequent cause of decreased excretion of uric acid?

A

decreased glomerular filtrating rate

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15
Q

What are primary causes of hyperuricemia through overproduction?

A

primary defects in the prime salvage pathway leading to an increase in de novo purine synthesis and high flux through the purine breakdown pathway

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16
Q

What are secondary causes of hyperuricemia through overproduction?

A

increased cell turnover and DNA degradation

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17
Q

What is formation of crystals markedly influenced by?

A

physical factors (temperature and blood flow)

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18
Q

What makes monosodium crystals NOT biologically inert?

A

negatively charged surface function as efficient initiators of the acute inflammatory response - activating the classic complement pathway (making C3a and C5a) - chemoattractants for neutrophil influx - also activate kinin system (local vasodilation, pain, swelling)

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19
Q

What is the mechanism that the acute inflammatory response is able to down modulate itself in gout?

A
  1. efficient phagocytosis 2. increased heat and fluid influx (crystal solubilization) 3. coating of crystals with serum proteins (make less inflammatory) 4. recreation of anti-inflammatory cytokines 5. phagocytosis of previously activated apoptotic neutrophils
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20
Q

podagra

A

severe inflammatory arthritis at the first metatarsophalangeal joint (most frequent manifestation of gout)

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21
Q

How does podagra typically present?

A

patient describes waking in middle of night with dramatic pain, redness, swelling, warmth of the area

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22
Q

Common sites of gout flares

A

toes, midfoot, ankles, knees

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23
Q

Which drugs, and how, reduce duration of a gouty flare?

A

NSAIDs (reduce prostaglandin synthesis), Colchicine (reduce neutrophil migration), corticosteroids (decrease activation of myelomonocytic drugs

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24
Q

How is gout diagnosed?

A

examination of synovial fluid under polarizing microscope. MSU crystals = negatively birefringent needle-like structures - engulfed by polymorphonuclear neutrophils

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25
Q

Chronic gout

A

formation of tophi - firm, irregular subcutaneous deposits of MSU crystals

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26
Q

Where do tophi most often form?

A

along tendinous tissues on the extensor surfaces of joints and tendons

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27
Q

How do tophi appear on examination?

A

extruding chalky material containing urate crystals onto skin surface

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28
Q

Chronic erosive polyarthritis

A

uric acid increases over the years, deposits occur in multiple joints resulting in a persistent but more indolent inflammatory arthritis associated with remodeling of the thin synovial membrane into a thickened inflammatory tissue - can also result in renal tubular injury and nephrolithiasis

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29
Q

Treatment of acute gouty arthritis

A

agents that decrease inflammatory cell recruitment and activation to the involved joints

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30
Q

Treatment of chronic gouty arthritis

A

chronic therapy to decrease serum uric acid levels into normal range - uricosuric agnets (probenecid), allopurinol and febuxostat (impede uric acid synthesis by inhibition of xanthine oxidase, pegloticase (converts uric acid to allantoin)

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31
Q

Which drugs are most appropriate for treatment of uric acid overproduction?

A

allopurinol and febuxostat

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32
Q

Which drugs is best for the treatment of uric acid underexcretion?

A

probenecid

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33
Q

Which drug is best for rare cases of refractory gout?

A

pegloticase

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34
Q

Immune complex vasculitis

A

acute inflammatory disease of small blood vessels due to ongoing antigen load and an established humoral immune response

35
Q

Which tissues are affected by immune complex vasculitis? Why?

A

skin, joints, kidney - highly enriched in small blood vessels

36
Q

What normally clears immune complexes?

A

reticuloendothelial system

37
Q

When do immune complexes become pathogenic?

A

when circulating immune complexes are deposited in the sub endothelium where they set in motion the complement cascade and activate myelomonocytic cells

38
Q

When does deposition of immune complexes happen?

A

If foreign antigens is in excess as compared to antibody (usually antibody in excess)

39
Q

What is an example of altered pathogenicity of immune complexes?

A

serum sickness - initial antigen load is great, immune response stimulated, immune complexes appear followed by fever, arthritis, rash, glomerulonephritis, antibodies begin to exceed antigen, immune complexes resolve

40
Q

What do acute immune complex glomerulonephritis cause?

A

proteinuria, hematuria, formation of red blood cell casts due to disruption of the glomerular basement membrane

41
Q

What are the “pauci immune” vasculitis processes?

A

granulomatosis with polyangiitis (GPA) and polyarteritis nodosa

42
Q

GPA clinical hallmarks

A

granulomatosis with polyangiitis - granulomatous inflammation of the upper airway (sinusitis) and lower airway (trachea, lungs), as well as a necrotizing vasculitis involving the kidneys and other organs

43
Q

What antibodies are highly specific to granulamatosis with polyangiitis? (GPA)

A

ANCA antibodies (antineutrophil cyotplasmic antibodies) - directed against components situated within neutrophil cytoplasmic granules - can bind and activate neutrophils at the interface of the plasma and vessel wall causing vascular damage

44
Q

Polyarteritis nodosa. What is the hallmark?

A

vasculitis affecting medium-sized muscular arteries and arterioles. Hallmark = intense and destructive myelomonocytic cellular infiltrate in the blood vessel wall (fibrinoid necrosis) leading to vessel occlusion, marked luminal narrowing,and obsolescence

45
Q

What are common manifestations of polyarteritis nodosa?

A

infarction of nerve trunks, bowel ischemia, kidney ischemia, deep cutaneous ulcerations

46
Q

SLE

A

prototypic systemic autoimmune rheumatic disease - chronic inflammatory injury to and damage of multiple organ systems

47
Q

What is a key feature of SLE?

A

unique adaptive immune response driven by antigen contained in self tissues

48
Q

What are tissues frequently affected in SLE?

A

skin, joints, kidneys, blood cell lines, serial surfaces, brain

49
Q

Who is SLE most common in?

A

black women

50
Q

What is a strong risk factor in development of lupus?

A

genetic deficiencies of the proximal components of the classic complement pathway (C1q, C1r, C1s, C4)

51
Q

What is the classic complement pathway required for?

A

efficient noninflammatory clearance of apoptotic cells by macrophages

52
Q

What is the initiation of SLE?

A

unique form of apoptotic cell death that occurs in a promise context

53
Q

What is a critical susceptibility defect for the development and propagation of SLE?

A

impairment of normal clearance of apoptotic cells in tissues

54
Q

How is SLE propagated?

A
  1. generation and deposition of immune complexes (esp kidney, joints, skin) 2. autoantibodies bind to extracellular molecules in the target organs and activate inflammatory effector functions at that site, causing tissue damage 3. autoantibodies directly induce cell death by ligating cell surface molecules or by penetrating into living cells and exerting functional effects
55
Q

Where is antigen derived from in SLE?

A

damaged and dying cells

56
Q

Type I interferons in SLE

A

play a central role in amplification pathways - induce differentiation of monocytes into potent antigen-presenting dendritic cells

57
Q

SLE flares

A

reflect immunologic memory, responding more rapidly and vigorously

58
Q

What is a frequent major cause of morbidity and mortality in SLE?

A

renal disease

59
Q

Sjogren Syndrome

A

slowly progressive autoimmune rheumatic disorder in which the exocrine glands are the primary target - more frequent in women

60
Q

Manifestation of Sjogren Syndrome

A

dryness of eyes and mouth

61
Q

Other problems associated with Sjogren syndrome

A

susceptible to dental problems, skin and vaginal dryness, dryness in respiratory track

62
Q

What do more than half of sjogren syndrome patients also affected with?

A

autoimmune thyroid disease

63
Q

What is the treatment for sjogre syndrome?

A

symptomatic improvement (artificial tears, regular supply of becerages, sugar-free gum)

64
Q

Inflammatory myositis

A

gradual development of progressive motor weakness affecting the arms and legs and trunk with histologi evidence of muscle inflammation

65
Q

What are hallmarks of inflammatory myositis?

A

difficulty rising from seated position, getting out of bed, ascending a flight of stair, brushing hair (weakness predominantly proximal rather than distal in location)

66
Q

Common antibody in inflammatory myositis?

A

anti Jo-1 antibodies or anti-Mi-2 antibodies (specific to dermatomyositis)

67
Q

What are the similarities between polymyositis and dermatomyositis?

A

patchy involvement, presence of inflammatory infiltrates, areas of muscle damage and regeneration

68
Q

Polymyositis

A

inflammation located around individual muscle fibers and infiltrate is T-cell and macrophage predominant

69
Q

Dermatomyositis

A

atrophy at periphery of muscle bundles and predominantly B cell and CD4 T cell infiltrate, also some activation of the complement cascade

70
Q

What are the 4 characteristic criteria for diagnosis of polymyositis?

A
  1. weakness 2. elevated laboratory parameters of muscle tissue (creatine phosphokinase of aldolase) 3. an irritable electromyogram upon electrodiagnostic evaluation 4. an inflammatory infiltrate upon histologic evaluation (5. skin rash for dermatomyositis)
71
Q

What is an additional clinical feature of inflammatory myopathies?

A

finding of association with cancer (either co-occurrence or subsequent development within 1-5 years)

72
Q

What is treatment for inflammatory myositis?

A

corticosteroids - often required in high doses

73
Q

Rheumatoid arthritis

A

chronic systemic inflammatory disease characterized by persistent symmetric inflammation of multiple peripheral joints

74
Q

Where does that majority of inflammatory activity in RA occur?

A

joint synovium

75
Q

What is normal synovium composed of?

A

thin cellular lining (1-3 cells thick) and underlying interstitial

76
Q

What does the synovium normally do?

A

provide nutrients and lubrication to adjacent articular cartilage

77
Q

What genetic factor implicates RA?

A

MHC class II alleles (HLA-DR4)

78
Q

Cytokine elaboration in RA is biased towards what?

A

Th1

79
Q

What is the most important upstream principle in the propagation of RA?

A

TNF

80
Q

Treatment of RA

A

methotrexate and anti-TNF therapy (new)

81
Q

RANK

A

expressed on osteoclasts - osteoblast stimulates osteoclast with RANK-L

82
Q

PTH in bone formation

A

stimulates osteoblasts to release RANK-L, cause bone resorption and release of Ca++

83
Q

What stimulates growth of osteoclasts?

A

macrophage colony stimulating factor

Abbey MSII Unit 1 pt 2 (21 decks)

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