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CMPP > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

what kind of crystals is gout caused by?

A

monosodium urate monohydrate cyrstals

NEGATIVE BIREFRINGENT CRYSTALS

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2
Q

what causes gout’s inflammatory reaction

A

urate crystal deposition

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3
Q

where do urate crystals deposit in gout

A

in the blood, joint, bursae, and tendon

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4
Q

how is uric acid formed?

A

end-stage by-product of purine metabolism

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5
Q

how is uric acid excreted

A

renally

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6
Q

hyperuricemia = uric acid above

A

6.8 mg/dL

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7
Q

why does uric acid accumulate

A

overproduction (increased consumption or endogenously)

underexcretion

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8
Q

causes of underexcretion of uric acid

A 
idiopathic
inability to excrete
meds
kidney disease
chronic ETHOH use
dehydration
starvation
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9
Q

causes of overproducers of uric acid

A 
ETOH use
myeloproliferative disorders
psoriasis
hemolytic anemais
cell-lysis chemo
excessive exercise
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10
Q

foods associated with higher incidence of gout

A 
seafood
meats
fructose
soft drinks
wine
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11
Q

causes of gout flares

A

acute increases or decreases in urate levels –> production, exposure, or shedding of crystals.

alchohol, high purine foods, rapid weight loss, dehydration

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12
Q

is gout genetic?

A

it can be.
heritability 62%
3 associated genes

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13
Q

gender and age predominance of gout

A

male

30-60

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14
Q

when is it least likely for women to get gout

A

before menopause

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15
Q

how dose gout start

A

monoarticularly

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16
Q

how soon does gout reach maximum intensity

A

12-24h

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17
Q

when dose gout improve?

A

in days to weeks

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18
Q

symptoms of an acute gout attach

A 
severe pain
redness
warmth
swelling of joint (most common MTP)
\+/- fever
arthritis in other sites (fingers, instep, ankle, knee)
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19
Q

gout of the 1st MTP

A

podagra

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20
Q

progression of gout

A

attacks more severe and slower to resolve if go untreated

more severe and polyarticular with time

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21
Q

what happens after 20 or so years of untreated urate deposition

A

chronic tophaceous gout

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22
Q

urate crystal masses surrounded by inflammtory cells and fibrosis which are firm, moveable, and yellowish. tend to ulcerate with a chalky material

A

chronic tophaceous gout

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23
Q

where do tophi usually appear in chronic tophaceous gout

A 
pinna of ear
other involved joints
extensor surfaces of forearm
olecranon
infrapatellar tendon
achilles tendon
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24
Q

use of serum uric acid elevation in gout

A

not sufficient

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25
Q

how to diagnose an acute attack of gout

A

arthrocentesis- rule out septic joint
negatively birefringent crystals (get sample to lab quickly before they dissolve)
high WBC count in synovial fluid
on plain radiograph: erosions with overhanging edges

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26
Q

WBC count in synovial fluid of gout

A

> 15,000 but usually

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27
Q

gout on plain film

A

overhanging edges with erosions

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28
Q

3 steps of managing gout

A

treat acute attack
provide prophylais
lower excess stores of urate to prevent flares and tissue deposition

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29
Q

NSAIDs for how long in acute gout attack

A

7 days

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30
Q

NSAIDs used for gout

A

indomethacin

naproxin

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31
Q

precautions with indomethacin

A

GI upset

give pepcid and take with food

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32
Q

contraindications to indomethacin and naproxin

A

CKD with Cr clearance

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33
Q

med used for pts with gout who have NSAID intolerance or contraindication

A

colchicine

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34
Q

MOA of colchicine

A

inhibits neutrophil chemotaxis and inflammatory mediator release

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35
Q

how does colchicine help gout

A

only helps inflammation so need something else for pain

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36
Q

3rd line treatment of gout

A

glucocorticoids
prednisone (oral)
triamcinolone (intrarticular)

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37
Q

risk reduction of recurrence for gout

A

weight loss
reduce ETOH
discontinue diuretics
discontinue ASA

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38
Q

period between gout attacks

A

intercritical period

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39
Q

when should urate lowering therapy be started

A

at least 2 weeks after a flare has resolved.

otherwise can precipitate a gout attack

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40
Q

should we start prophylaxis tx for gout if there is a known cause

A

nope!

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41
Q

3 prophylactic meds for gout

A

probenecid
allopurinol
febuxostat

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42
Q

MOA of probenecid

A

promotes renal clearance of uric acid.

inhibits urate-anion exchangers in proximal tubule that mediates urate reabsorption.

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43
Q

contraindication of probenecid

A

nephrolithiasis (never restart if they get a kidney stone)

impaired renal function

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44
Q

how is probenecid dosed

A

multiple doses per day

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45
Q

MOA of allopurinol

A

xanthine oxidase inhibitor (inhibits production of uric acid)

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46
Q

allopurinol side effects

A 
mild rash may disappear 
GI distress/diarrhea
hypersensitivity syndrome (eospinophilia, fever, hepatitis, poor renal function, erythematous desquamative rash)
SJS, TEN
ampicillin + allopurinol --> rash in 20%
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47
Q

what other med in conjunction with allopurinol causes a rash

A

ampicillin

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48
Q

the “new xanthine oxidase inhibitor”

A

febuxostat (Uloric)

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49
Q

which med is more effective for hyperuriciemia: uloric or allopurinol

A

uloric and doesn’t have any hypersensitivity side effects but is super expensive

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50
Q

CPPD

A

pseudogout

calcium pyrophosphate deposition disease

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51
Q

presentation of CPPD

A

monoarticular or polyarticular.
involves the knee as the initial joint in 50% of the time.
slower onset than gout

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52
Q

joint fluid in CPPD

A

rhomboid crystals

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53
Q

tx for CPPD

A

aspiration and NSAIDs

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54
Q

does CPPD recur?

A

yes, but not typically like gout

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55
Q

three major types of inflammatory myopathies

A

polymyositis
dermatomyositis
inclusion body myositis

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56
Q

general features of inflammatory myopathies

A

progressive and symmetric muscle weakness
proximal muscle weakness
facial muscles unaffected
dysphagia or headrop

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57
Q

describe polymyositis

A

subacute inflammatory myoapthy affecting adults

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58
Q

is polymyositis associated with other autoimmune/connective tissue disease

A

commonly, yes

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59
Q

where does weakness start in polymyositis

A

distally

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60
Q

how soon does polymyositis progress?

A

weeks to months

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61
Q

elevated levels of ____ in polymyositis

A

CK

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62
Q

characteristic rash with associated muscle weakness

A

dermatomyositis

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63
Q

3 signs of dermatomyositis

A

heliotripic discoloration of upper eyelids and edema
gottron’s sign (flat red rash on face and knuckle scales)
V sign

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64
Q

does dermatomyositis occur with other autoimmune/inflammatory disorders?

A

not usually but sometimes scleroderma or mixed connective tissue disease

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65
Q

pathophys of dermatomyositis

A

unknown but WBC spontaneously invade muscles

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66
Q

positive diagnostic workup dermatomyositis

A

+CK
+ jo-1 Ab
MRI –> inflammation
muscle biopsy (CONFIRMATION)

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67
Q

confirmatory test for dermatomyositis

A

muscle biopsy

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68
Q

treatment of dermatomyositis

A

oral corticosteroids (months to years)
immunosuppressive drugs
IVIG
PT

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69
Q

how does death occur usually in dermatomyositis

A

pulmonary, cardiac, or other systemic complications

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70
Q

scleroderma aka

A

systemic sclerosis

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71
Q

gender and age predominance of scleroderma

A

female

30-50

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72
Q

two types of scleroderma

A

diffuse cutaneous SSc

limited cutaneous SSc

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73
Q

3 cardinal features of the disease

A

vasculopathy
cellular and humoral autoimmunity
progressive visceral and vascular fibrosis

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74
Q

explain vasculopathy in scleroderma

A

intimal proliferation in the small and medium sized arteries resulting in luminal narrowing and an obliterative vasculopathy

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75
Q

explain cellular and humoral autoimmunity in scleroderma

A

activated T cells and macrophages accumulate in the affected organs. they have an enhaced ability to bind to the epithelium and fibroplasts and promote collagen synthesis

76
Q

explain progressive visceral and vascular fibrosis in scleroderma

A

follows vasculopathy and cellular and humoral autoimmunity. it’s a replacement of normal tissue architecture with dense connective tissue which results in irreversible accumulation of scar tissue.

77
Q

what puts scleroderma patients at risk for visceral organ involvement

A

diffuse cutaneous Ssc

78
Q

is the interval between raynad’s and other manifestations brief or prolonged in DSSc

A

brief

79
Q

symptoms of diffuse cutaneous DSSc

A

arthralgias
muscle weakness
decreased joint mobility
stiffness

80
Q

how does diffuse SSc present

A

progressive skin induration starting in the fingers and ascending from distal to proximal extremities, face, and trunk

81
Q

does diffuse or limited cutaneous SSc have a better prognosis

A

limited

82
Q

what is CREST syndrome associated with?

A

limited cutaneous SSc

83
Q

where does limited cutaneous SSc manifest

A

fingers, distal extremities, and face NOT trunk

84
Q

is the interval between raynad’s and other manifestations brief or prolonged in limited cutaneous SSc

A

years

85
Q

CREST syndrome

A 
Calcinosis
Raynaud's phenomenon
Esophageal dysmotility
Sclerodactyly
Telangectasias
(need 3)
86
Q

explain raynaud’s

A

episodic vasoconstriction in the fingers and toes triggered by exposure to cold, change in temperature, emotional stress, or vibration. pallor followed by cyanosis.

87
Q

is raynaud’s painful?

A

yes

88
Q

what causes raynaud’s

A

vasoconstriction, ischemia, reperfusion

89
Q

explain esophageal dysmotility in scleroderma

A

lower esophagus has prominent atrophy in the muscular layer, diminished peristaltic activity

90
Q

three results of esophageal dysmotility in scleroderma

A

GERD
dysmotility
SBO

91
Q

explain sclerodactyly in scleroderma

A

thickening of skin which is bl and symmetric

fixed flexion contractures of fingers with reduced hand motility. Skin looks tight and taught.

92
Q

describe telangiectasias in scleroderma

A

dilated skin capillaries which are prominent on the face, lips, hands, or oral mucosa

93
Q

organ involvement in diffuse scleroderma

A 
skin features
pulmonary features
GI involvement
renal involvement 
cardiac involvement
94
Q

lab features of scleroderma

A

normochromic normocytic
+ ANA but not specific
+ anticentromere Ab in some

95
Q

how to you absolutely diagnose scleroderma

A

skin biopsy

96
Q

is scleroderma diagnosed clinically

A

mostly

97
Q

treatment for scleroderma

A

there is none :(

treat the secondary problems

98
Q

leading cause of disability in the elderly

A

osteoarthritis

99
Q

the most common type or arthritis

A

osteoarthritis

100
Q

age and gender predominance of osteoarthris

A

females over 60

101
Q

definition of OA

A

articular cartilage loss
increasing thickness and sclerosis of the subchondral bony plate
outgrowth of osteophytes at the joint margin
mild synovitis
weakness of the muscle briding the joint

102
Q

pathophysiology of OA

A

articular cartilage loss
mild synovitis
bone adcacent to the joint reinforces itself with subchondral scerlosis and cartilage loss

103
Q

explain the changes of cartilage in OA

A

in OA cartilage is metabolically ative, this causes an unfurling of the tightly woven collagen matrix which causes increased vulnerability of cartilate- looses its compressive stiffness

104
Q

is healthy cartilage metabolically fast or slow

A

slow

105
Q

commonly affected joints in OA

A 
cervical spine
lumbosacral spine
hip
knee
MTP
DIP
PIP
base of thumb
106
Q

OA risk factors

A

age, genetics, obesity
past injury to a joint
malalignment of joint
repetitive joint use

107
Q

is OA genetic

A

50% of the hand and hip OA is

108
Q

clinical features of OA

A

joint pain that is activity related

joint stiffness

109
Q

physical exam findings of OA

A

joint margin tendernses
hip restricted internal rotation/adduction
painful ROM in large joints
crepitus when joint is ROM
joints cool and bony hard, synovium normal
bony joint enlargement from osteophytes

110
Q

can osteophytes cause radicular symptoms

A

sure thang

111
Q

blood tests for OA

A

nonezo

112
Q

xray findings in OA

A 
joint space narrowing 
asymmetric
subchondral sclerosis
marginal osteophytes
subcondral cysts
113
Q

treatment of OA

A

allieviate pain

minimize loss of physical function

114
Q

what treatment for mild disease or intermittent symptoms of OA

A

reassurance or nonpharmacologic

115
Q

nonpharmacologic treatment of OA

A

avoid aggrevating activities
improve strength and conditioning of muscles that bridge the joint (PT)
use splints, braces, or canes with weight bearing
weight loss
exercise

116
Q

pharmacotherapy of OA

A 
NSAIDs
acetaminophen
COX2 inhibitors
intraarticular injections (glucocorticoid and hyaluronic acid)
opiates
117
Q

MOA of NSAIDs

A

decrease prostaglandins, COX1 and 2 inhibitors

118
Q

how to dose NSAIDs in OA

A

initially prn then daily if ineffective, with food and possibly a PPI

119
Q

side effects of NSAIDs

A

nausea
dyspepsia
GI bleeds
ulcer dz

120
Q

why are some hesitant about COX2 inhibitors

A

risk of cardiovascular events, prothrombic

121
Q

COX2 is FDA approved for…

A

RA and OA

122
Q

contraindications of celebrex

A

aspirin or sulfa allergy

third trimester of pregnancy

123
Q

glucocorticoid injections good for what in OA

A

temporary effectiveness

acute flairs

124
Q

intraarticular injections good for what in OA

A

still pretty short term in effectiveness

viscoelastic and lubricating properties

125
Q

surgical tx for OA

A

arthroplasty

126
Q

inflammatory disorder of unknown cause that affects the axial skeleton

A

ankylosing spondylitis

127
Q

age and gender predominance in AS

A

males 10-30

128
Q

antigen correlated to AS

A

HLA-B27

129
Q

pathogenesis of AS

A

immune related
begins where articular cartilage, ligaments, and other structures attach to bones. Inflamed joint infiltrated with CD4, CD8, and macrophages and TNFa

130
Q

what is AS triggered by

A

absolutely nuttin

131
Q

clinical manifestations of AS

A 
bony tenderness
systemic illness
SI joint/spine inflammation
persistent low back pain
spinal ligament inflammation/dysmotility
intercostal ligament inflammation
minor back trauma --> fractures
extraskeletal features
132
Q

where is bony tenderness in AS

A

spinous processes
illiac crests
greater trochanter
costosternal junctions

133
Q

systemic illnesses associated with AS

A

fatigue
anemia
weight loss

134
Q

is inflammation limited to the axial skeleton in AS

A

peripheral oligoarthritis in 30%

135
Q

does back pain improve or worsen with exercise in AS

A

improve

136
Q

is spinal mobility and chest expansion affected in AS

A

YAS

137
Q

signs of AS on xray

A 
bamboo spine (syndesmophytes)
squaring of anterior vertebrae
138
Q

what causes chest expansion to be limited in AS

A

intercostal ligament inflammation

139
Q

where is most of the osteoporosis and rigidity in AS

A

cervical spine

140
Q

extraskeletal features of AS

A

fatigue
weight loss
anterior uveitis (pain, redness, photophobia, lacrimation)
aortic root and valve thickening and inflammation
AV conduction deficits and aortic insufficiency
upper lobe pulmonary fibrosis
radicular symptoms from cauda equina fibrosis
colon or ileum inflammation

141
Q

physical exam findings of AS

A 
limitation of anterior and lateral flexion and extension of L spine and chest expainsion
SI joint pain
paraspinous muscle spasm
lumbar lordosis is lost
fixed forward flexion and hip and neck
142
Q

AS lab findings

A 
none are diagnostic
CRP and SED elevated
mild anemia
synovial fluid non-specific inflammatory
PFTs- dereased VC and increased residual capacity
143
Q

criteria for chronic inflammatory back pain of AS

A

more than three months

age of onset

144
Q

schober test

A

for AS
mark L5 and measure 10cm above L5
patient flexes forward. look for an increase in space from mark to L5 by atleast 5cm

145
Q

chest expansion test for AS

A

at fourth intercostal space look for

146
Q

AS tx

A 
stop smoking
protect spine
spinal extention exercises
hard mattress (prevent spinal flexion)
treat coexisting diagnoses
147
Q

coexisting diagnoses of AS and their tx

A

uveitis-steroids

cardiac dz-pacemaker

148
Q

mainstay of therapy (first line) for AS

A

NSAIDs

reduce pain and increase mobility

149
Q

Anti-TNF for AS

A

cause dramatic radiologic and clinical benefits and reverse significantly
need a definitive dx before you start
need to test for TB first

150
Q

three anti-TNF drugs for AS

A

infliximab (Remicade)
etanercept (enbrel)
adalimumab (humira)

151
Q

toxicity of anti-TNF agents

A 
serious infection
pancytopenia
demyelinating disorders
exacerbation of CHF
SLE-like illness
hypersensitivity at infusion or injection site
severe liver dz
152
Q

acute nonpurulent arthritis complicating an infection elsewhere in the body

A

reactive arthritis

153
Q

do all reactive arthritis pts have a preceeding clinical infection?

A

no!

154
Q

antigen that reactive arthritis is associated with

A

HLA-B27

155
Q

triad of reactive arthritis

A

arthritis
conjunctivitis
urethritis

156
Q

reactive arthritis pathophys

A

AA sequences in microorganisms mimic those of human proteins

antibodies create autoimmune dz in those genetically predisposed

157
Q

most common infections associated with reactive arthritis

A

GU: chlamydia
GI: salmonella, yersinia, campylobacter

158
Q

when does arthritis start in reactive arthritis

A

1-3 weeks after infection

159
Q

is reactive arthritis symmetrical or asymmetrical

A

asymmetrical of large lower extremity joints

160
Q

what other two manifestations are associated with reactive arthritis

A

dactylitis (sausage digit)
sacroiliitis
oral ulcers
keratoderma blenorrhagica (vesicular skin lesions that become hyperkeratotic on hands and soles)
circinate balanitis (painless vesicles –> erosions on the penis)

161
Q

how long does reactive arthritis last

A

3-5 months but up to a year

162
Q

urogenital symptoms of reactive arthritis

A

cervicitis salpingitis prostatitis

163
Q

are the GU sx of reactive arthritis significant

A

either marked or asymptomatic

164
Q

lab findings in reactive arthritis

A 
ESR and CRP
mild anemia
HLA-B27 in 1/2
elevation of Ab to bacteria
PCR for chlamydia
165
Q

how to dx reactive arhritis

A

no definitive way

166
Q

tx for reactive arthritis

A

NSAIDs

no benefit in tx infection if it’s at this point

167
Q

age and gender predominance of psoriatic arthritis

A

men = women

4th-5th decade

168
Q

location of psoriatic arthritis

A

DIP and SI joints

169
Q

pathyphys of psoriatic arthritis

A

synovium infiltrates with T cells, B cells, and macrophages

170
Q

clinical manifestations of psoriatic arthritis

A 
assymetric oligoarthritis
symmetric polyarthritis
axial arthritis
arthritis DIP
nail pitting
dactylitis
enthesitis
171
Q

enthesitis

A

inflammation of the ligaments or tendons where they insert on the bone

172
Q

lab findings of psoriatic arthritis

A

no diagnostic tests
ESR and CRP elevated
HLA-B27 in most with axial dz

173
Q

xray findings of psoriatic arthritis

A

pencil in cup deformity

telescoping digits

174
Q

treatment of psoriatic arthritis

A

anti-TNF agents

175
Q

enteropathic arthritis

A

IBD and arthritis

arthritis precedes onset of IBD by months to years

176
Q

associated symptoms of enteropathic arthritis

A

dactylitis and enthesopathy
uveitis
erthyma noosum

177
Q

what is erythema nodosum

A

red bumps on the shins

178
Q

treatment for enteropathic arthritis

A

anti-TNF apha agents
infliximab (remicade)
etanercept (enbrel)
adalimumab (humira)

179
Q

lab elevations in enteropathic arthritis

A

HLA
CRP
SED

180
Q

fibromyalgia

A

chronic widespread musculoskeltal pain and fatigue often accompanied by cognitive and psychatric probs

181
Q

PE of fibromyalgia

A

TTP in 11/18

182
Q

symptoms of fibromyalgia

A 
widespread musclar pain
fatigue
fibro fog (attention deficit, difficulty completing tasks)
headache in some
paresthesias
abdominal pain
chest wall pain
183
Q

criteria for fibromyalgia dx

A

TTP in 11/18 for >3 months
normal PE except TTP
normal lab tests (CBC, SED rate, TSH)

184
Q

tx of fibromyalgia

A

challenging but…
TCAs –> SSRIs –> SNRIs
anticonvulsants

185
Q

TCAs for fibromyalgia

A

amitriptyline (elavil) low and slow, QHS,

CMPP (17 decks)

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