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Musculoskeletal, Skin > 090514 gout, rheumatold arth, osteoarth > Flashcards

090514 gout, rheumatold arth, osteoarth Flashcards

1
Q

synovial membrane is not present over what?

A

articular cartilage

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2
Q

patterns of arthritis

A

inflam or non-inflam

monoarthritis or polyarthritis

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3
Q

what are some causes of inflammatory monoarthritis?

A

trauma
crystals (monosodium urate, calcium pyrophosphate)
septic joint
other

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4
Q

how can you tell if the arthritis is inflammatory (vs non inflammatory)?

A

morning stiffness of longer than 1 hr

PE: erythema and warmth, synovitis (thickening of synovium around joints, tenderness upon palpation)

lab: ESR and CRP, peripheral blood leukocytosis, joint fluid analysis
radiography: XR (erosions of bone at joint margins)

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5
Q

WBCs would be elevated in synovial fluid for what types of arthritis?

A

inflammatory (septic would have an extraoridinarily high WBC count)

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6
Q

90% of gout occurs due to?

A

underexcretion

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7
Q

where does uric acid in gout come from?

A

1/3 from dietary nucleotides and nucleoproteins

2/3 from cellular nucleotides and nucleoproteins

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8
Q

how is uric acid usually excreted?

A

1/3 through the gut (bacterial degradation)

2/3 through renal excretion

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9
Q

how much is usually excreted of uric acid of the filtered load?

A

10%

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10
Q

how would does overproduction-induced hyperuricemia occur?

A

enzymatic abnormalities
increased cell turnover
diet
ethanol

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11
Q

how would underexcretion-induced hyperuricemia occur?

A

metabolic syndrome
renal disease
drugs like diuretics, cyclosporine
ethanol

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12
Q

what is the onset of gout in men related to?

A

uric acid level

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13
Q

what test supports gout?

A

yellow, parallel crystals of monosodium urate (mneunomic is yellow, parallel, allopurinol–all double L’s)

uric acid level–if higher, higher chance of gout happening

swelling, warmth, tenderness

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14
Q

tophaceous gout

A

large deposits of uric acid crystals

can get secondary calcification of tophi

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15
Q

what can precipitate a gout attack?

A

elevation of uric acid

reduction of uric acid (see third point here)

release of crystals from pre-formed deposits

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16
Q

inflammatory cascade of gout

A

MSU crystals are phagocytosed by monocyte, you get inflammasome activation, then monocyte release IL-1, which then activates the endothelium, get pro-inflammatory mediators and neutrophil recruitment

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17
Q

CPPD deposition disease occurs in whom?

A

12% of elderly

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18
Q

what is the cause of CPPD deposition disease

A

unknown but most cases are related to overproduction of PPi

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19
Q

what is CPPD

A

calcium pyrophosphate dihydrate, formed from pyrophosphate and calcium coming together to make the crystal

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20
Q

in pts less than 60, CPPD can occur how?

A

secondary to problems like hemochromatosis, hypophosphatasia, hypomagnesemia, hyperparathyroidism

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21
Q

how is psuedogout diff from gout

A

acute arthritis like gout, but in usually larger joints (knee, wrist, shoulder)

Diagnosed from thromboidal shaped, positively birefringent cyrstals in joint fluid

XR: diagnosis may be supported by chondrocalcinosis but not seen always

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22
Q

CPPD arthritis signs

A

commonly asymptomatic

or pseudogout - acute inflam of 1 or 2 joints

or osteoarthritis (but may be associated with osteoarthritis in atypical joints)

or like rheumatoid arthritis (MCP involvement)

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23
Q

how should NSAIDs be used to treat gout

A

within first 24 hrs

indomethacin, naproxen

never use aspirin (aspirin inhibits uric acid secretion)

for the inflammation in gout

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24
Q

how are steroids used to treat gout

A

symptomatic relief for pts that can’t take NSAIDs

used short term

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25
Q

MOA of colchicine in treating gout

A

antimitotic

interferes with microtubule formation, inhibits neutrophil activation and migration

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26
Q

route of administration of colchicine for gout

A

oral

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27
Q

what is notable about colchicine for gout

A

CYP450 metabolism

substrate for P-glycoprotein

significant adverse effects (narrow therpeutic toxicity window, GI) —therefore use is limited

contraindicated for hepatic or renal disease pts, elderly, CYP3A4 and P glyprotein drug taking pts

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28
Q

for multiple acute gout attacks, drug therapies to prevent gout flare and destruction on joint snad kidneys?

A

allopurinol
febuxostat
probenecid
pegloticase

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29
Q

allopurinol MOA

A

blocks xanthine oxidase, inhibiting terminal steps in uric acid biosynthesis

converted to oxypurinol, which is the active compound (hypoxanthine normally is converted to xantine; allonpurinol is a structural analog of hypoxanthine)

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30
Q

adverse effects of allopurinol

A

hypersensitivity

acute gout attack (give drug w/ colchicine or NSAID)

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31
Q

use of allopurinol

A

prevention of primary hyperurecemia of chronic gout

prophylactic treatment in secondary forms of hyperurecemia

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32
Q

febuxostat MOA

A

non-purine xanthine oxidase inhibitor (not a structural analog for binding to xanthine oxidase)

forms stable complex with both reduced and oxidized xanthine oxidase and inhibits catalytic fxn in both states

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33
Q

compare fubuxostat vs allopurinol in treating gout

A

febuxostat is more potent
incidence of adverse events like dizziness, diarrhea, headache and nausea was similar in both drugs

incidence of CV side effects higher in febuxostat

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34
Q

MOA of pegloticase

A

PEGylated-polyethylene glycol covalently linked to the molecule

the molecule is a recombinant form of urate oxidase enzyme (uricase, an enzyme usually not in humans)

uricase will convert uric acid to allantoin

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35
Q

side effects of pegloticase

A

infusion site rxns (must be given IV)
gout flare
immune response (at PEG portion of molecule)

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36
Q

uses of colchicine

A

acute gout attacks (within hours)

prophylactically in pts with chronic gout

37
Q

use of pegloticase

A

refractory chronic gout

38
Q

probenecid MOA

A

increases uric acid exretion by competing with renal tubular acid transcrporter (OAT/URAT1) so that less urate is reabsorbed

39
Q

route of administration of probenecid

A

oral

40
Q

what is notable about probenecid

A

dose-dependent half life (second order kinetics)

plasma protein binding

41
Q

side effects of probenecid

A

GI
ineffective in pts with renal insufficiency
contraindicated in pt with uric acid kidney stones

42
Q

Rheumatoid arthritis involves what cells of immune system

A

T cell disease with significant B cell contribution

43
Q

what factors predispose someone to getting rheumatoid arthritis

A 
genetic (HLA-DR)
hormonal (females more than males)
environmental (smoking)
infections
stress
44
Q

what do you see in rheumatoid arthritis with regards to the synovrium

A

invasion by immune lineage cells with recruitment of local cells (synovial fibroblasts)

get proliferation of synovium (synovitis) with characteristics of a benign locally invasive tumor

45
Q

pathology of rheumatoid arthritis

A

chronic papillary synovitis:

chronic inflammation of synovium (frequently formed lymphoid follicles)

accompanied by synovial cell hyperplasia–resulting in papillary like pattern on surface of synovium

hyperplastic inflammed synovium extends over articular surface forming pannus which fills joint space (gradually, articular cartilage is destroyed; increased osteoclast activity in underlying bone; end result may be joint fusion (ankylosis) due to fibrosis and ossification)

46
Q

diff btwn rheumatoid arthritis and osteoarthritis

A

ostephytes and new bone formation are not prominent in RA

47
Q

rheumatoid nodules

A

occur in 25% (usually in severe disease)

central zone of fibrinoid necrosis surrounded by rim of epithelioid histiocytes and then lymphocytes and plasma cells

caused by necrosis secondary to vascular damage possibly secondary to vasculitis

develop commonly on skin subcutaneously in areas exposed to pressure (extensor surfaces of forearm and elbow)

48
Q

Hx of RA

A

gradual onset of joint pain, swelling, inflammation

inflam present for greater than 6 weeks in 3 or more joints

symmetrical in nature

morning stiffness lasting more than 1 hour for >6 wks

difficulty opening jars, etc, pain in the ball of foot upon arising from bed

49
Q

what is RF?

A

IgM binding to IgG

however, not positive in all RA pts

50
Q

anti-cyclic citrullinated peptide (CCP)

A

may be seen in early RA
positive in some cases of RF negative RA
same sensitivity as RF; more specific than RF
correlates with overall disease activity

51
Q

clinical presentation of RA

A

affects usually small joints of hands and feet

usually not DIPs; PIPs and MCPs are common

tends to be in rows

can see swan neck deformity (hyperflexion of DIP, hyperextension of PIP); Boutiniere deformity (PIP flexion, DIP hyperextension)

52
Q

criteria for classification of RA

A

4 out of the 7 below for greater than 6 weeks:

AM stiffness greater than 1 hr
symmetrical arthritis
at least three swollen joints
wrist, MCP, PIP involvement
rheumatoid nodules
positive RF
XR change typical of RA in hand
53
Q

how is RA systemic?

A 
can have:
Sjogren's
CV disease (similar to diabetes)
lung involvement
GI (b/c of NSAIDs or other med side effects)
neurology (hand numbness, neuropathy)
54
Q

pulmonary involvement of RA

A

rheumatoid pleuritis with exudate that is low in glucose

interstitial fibrosis

nodules

Caplan’s syndrome (rheumatoid pneumoconiosis)

medication related (unusual chronic infections)

55
Q

for RA, etanercept MOA

A

inhibits the ability of soluble TNF-alpha to bind to its receptor

is a recombinant fusion protein

56
Q

onset of action of etanercept

A

1-2 weeks

57
Q

adverse effects of etanercept

A

injection site rxns
increased risk of infections
lymphomas in children

58
Q

etanercept is used for

A

initially just used for moderate to severe RA, but now used for early stage

59
Q

adalimumab MOA

A

IgG monoclonal antibody

binds to soluble and transmembrane forms of TNF-alpha

60
Q

adverse effects of adalimumab

A

same as for etanercept

61
Q

tocilizumab MOA

A

humanized antibody that binds to soluble and membrane bound IL-6 receptors, inhibiting IL-6 signanling

62
Q

adverse effects of tocilizumab

A

injection site rxns
increased risk of infec
alterations in lipid profile

63
Q

uses of tocilizumab

A

adults pts with moderately to severely active RA who haven’t had a good response to TNF antagonists

64
Q

tofacitinib MOA

A

JAK inhibitor, inhibiting cytokine or growth factor mediated gene expression and intracellular activity of immune cells

65
Q

what is notable about tofacitinib

A

it is administered orally (as opposed to tocilizumab and TNF inhibitors)

CYP3A4 metabolism

66
Q

adverse effects of tofacitinib

A

increased risk of infec

increase in cholesterol

67
Q

uses of tofacitinib

A

moderately to severely active RA in pts who have had inadquate response to methotrexate

68
Q

biologic DMARDs

A

proteins designed mostly to target cyokines and cell-surface molecules

69
Q

osteoarthritis

A

progressive disorder of the joints caused by gradual loss of cartilage

bony spurs and cysts develop at margins of joints

70
Q

risk factors for osteoarthritis

A 
female gender (particularly knee and hand)
increasing age
race or ethnicity
genetics
obesity
trauma
71
Q

pathology of osteoarthritis

A

early changes-superficial layers of cartilage are destroyed (limited chondrocyte proliferation and new matrix formation)

72
Q

eburnation

A

advanced osteoarthritis-you see eburnation, which means polished, in the exposed bone

73
Q

advance osteoarthritis-appearance?

A

EBURNATION

SUBCHONDRAL SCLEROSIS-more dense bone develops underneath the areas where cartilage is gone–in these areas, in addition, you can get micro fractures and then cysts–(called SUBCHONDRAL CYSTS, where you have break in the cartilage and then the bone and then fluid goes in)

OSTEOPHYTE FORMATION

74
Q

osteophyte formation

A

bony outgrowths developed at margins of articular surface - cause increase in joint size

75
Q

pathogenesis of OA?

A

imbalance in cytokine and growth factor activity resulting in matrix loss and degradation

etiology is likely multiple:
wear and tear theory is not sufficient to explain
risk factors

76
Q

which joints are affected in OA

A

for women-small joints in hands (DIPs PIPs NOT MCPs)

hips
knees

bunions in the feet

77
Q

PE findings for OA

A

mild to moderate FIRM swelling around joint line (b/c of formation of chondrophytes or osteophytes at margin)

crepitus

restricted ROM limited by pain

weakness and wasting of muscles acting on joint

periarticular tenderness

deformities

Heberden’s and Bouchard’s nodes

hallux valgus (bunion)

genu varus (bow legs)

genu valgus (knock knees0

78
Q

diagnosis of OA

A

blood tests usually not helpful
imaging
synovial fluid aspiration typically viscous and translucent-non inflam WBC count <2000

79
Q

infliximab MOA

A

chimeric IgG monoclonal antibody that binds to both soluble and transmembrane forms of TNF-alpha

80
Q

abatacept MOA

A

costimulation modulator

inhibits T cell activation by binding to CD80 and CD86 on APC and blocking then the required interaction with CD28

81
Q

adverse effects of abatacept

A

headache
hypersensitivity
increased risk of infec
should NOT be used in combo with anakinra or TNF-inhibitors

82
Q

rituximab MOA

A

monoclonal Ig directed against CD20 antigen on B lymphocytes; this activates complement dependent B-cell cytotoxicity and antibody dependent cellular toxicity

83
Q

side effects of rituximab

A

tumor lysis syndrome leading to acute renal failure

84
Q

anakinra MOA

A

antagonist of IL-1 receptor

85
Q

azathioprine MOA

A

purine antimetabolite that inhibits purine biosynthesis, inhibiting DNA synthesis

86
Q

hydroxychloroquine MOA

A

not understood

useful for early, mild disease in RA

87
Q

side effects of hydroxychloroquine

A

retinal damage

88
Q

lefluonomide MOA

A

immunomodulatory agent in RA; inhibits dihydroorotate dehydrogenase, which is involved in production of uridine monophosphate

89
Q

side effects of lefluonomide

A

diarrhea, rash, alopecia, elevated liver fxn tests

Musculoskeletal, Skin (33 decks)

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