Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1 STEP UW sclerodermos > RA, osteoarthritis, ankylo > Flashcards

RA, osteoarthritis, ankylo Flashcards

1
Q

In gout - depositions of what component?

A

Monosodium urate crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a risk factor for hyperuricemia?

A

increased purine metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is a risk factor for gout?

A

elevated uric acid levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is important enzyme in purine synthesis?

A

phosphoribosyl pyrophosphate (PRPP) synthetase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What produces PRPP synthetase?

A

activated ribose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What component is needed for de novo synthesis of purine and pyrimidine nucleotides?

A

activated ribose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

activated ribose is used in ………….. and ………… synthesis.

A

de novo purine and pyrimidine synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What mutation in what structure leads to increased production and degradation of purines?

A

Activating mutation involving PRPP synthetase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

activating mutation in PRPP synthetase cause …………….. activation of purine synthesis pathway.

A

feed-forward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is result of feed-forward activation of the purine synthesis pathway?

A

More purine molecules will undergo degradation, resulting in hyperuricemia and increase risk of gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What joints most commonly in acute gouty arthritis?

A

First metatarsophalangeal joint or knee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

acute gouty arthritis symptoms develops within ………..

A

rapidly over 24h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

manifestation (3) of acute gouty arthritis?

A

swelling, erythema and exquisite tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What method is used for diagnosis of acute gouty arthritis?

A

Joint aspiration –> needle-shaped, negatively birefringent crystals under polarized lamp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are primary immuno cells in acute gouty arthritis?

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pathophysio of acute gouty arthritis?

A

Neutrophils –> phagocytosis of urate crystals –> release of various cytokines and inflammatory mediators –> further neutrophils activation and chemotaxis –> positive feedback loop that amplifies the inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is first therapy in acute gouty arthritis?

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why NSAIDs used in acute gouty arthritis as primary agent?

A

inhibit prostanoid biosynthesis (prostaglandins, prostacyclin, thromboxane) –> broad ant-inflammatory effect that includes INHIBITION OF NEUTROPHILS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why patients may be contraindicated for NSAIDs?

A

peptic ulcers, renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What use in acute gouty arthritis if patient cannot use NSAIDs?

A

Colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is effect of colchicine on neutrophils?

A

impairs migration and phagocytosis by interfering with microtubule formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What mechanism by colchicine decrease neutrophils activation?

A

Colchicine decreases tyrosine phosphorylation in response to monosodium urate crystals, resulting in decreased neutrophil activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What cells are targeted in therapy of acute gouty arthritis?

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a central mechanism involved in precipitating an acute gouty attack?

A

NEUTROPILS!!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are other 2 types of cells play role in acute gouty arthritis?

A

synovial cells and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Depositions of what in pseudogout?

A

calcium pyrophosphate dihydrate crystals (in synovial fluid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is second line treatment for acute gouty arthritis?

A

colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What 2 primarily involved joints in gout and pseudogout?

A

pseudo - knee (50proc)

gout - first metatarsophalangeal joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What cells count is increased in synovial fluid in pseudogout and what cell predominance?

A

incr. WBC with neutrophils predominance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is seen under polarized light in pseudogout?

A

rhomboid-shaped calcium pyrophosphate dihydrate crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Birefringent crystals in pseudogout?

A

Positively birefringent (IN GOUT NEGATIVE!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Pseudogout crystals are blue when aligned …………

A

parallel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Pseudogout crystals are yellow when aligned ……….

A

perpendicular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Calcific tendonitis results from the deposition of …………..

A

calcium hydroxyapatite crystals in periarticular soft tissues (esp. tendons)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the most commonly affected structure in calcific tendonitis?

A

The rotator cuff tendons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What colour of gout crystals in parallel?

A

yellow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What colour of gout crystals when perpendicular?

A

blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What immunity is involved in RA?

A

Both humoral and cell-mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is humoral immunity in RA?

A

autoantibodies against citrullinated polypeptides (anti-CCP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What T cells are activated in RA?

A

CD4 = Th1 and Th17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What cells play a role in early disease process in RA?

A

Th1 and Th17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What cells activation leads to progressive articular destruction?

A

macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Activation of macrophages in RA leads to ……………..

A

development and progressive articular destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What cytokines release macrophages in RA?

A

IL-1 and TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What cytokines leads to progressive articular destruction in RA?

A

IL-1 and TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What enzymes contribute to cartilage destruction in RA?

A

proteases - collagenase, metalloproteinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Why occurs bony erosions in RA?

A

due to effect of cytokines - TNF-alpha and IL-1 –> both activate osteoclasts –> bony erosions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Monoclonal antibodies that are used in RA are targeted to ………………

A

inhibits TNF-alpha and IL-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are rheumatoid antigens that activate …………..

A

citrullinated peptides, type II collagen; activates T lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What leads to synovial hyperplasia?

A

activated T cells release cytokines –> synovial hyperplasia + recruitment of additional mononuclear cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Why needed synovial angiogenesis in RA?

A

due to accelerated metabolic rate of inflamed synovial tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Accelerated metabolic rate of inflamed synovial tissue leads to ……………..

A

local hypoxia + increased hypoxia-inducible factor 1 + VEGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What cells produce hypoxia-induced factor 1 and VEGF in RA?

A

Local macrophages and fibroblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hypoxia-induced factor 1 and VEGF leads to ………..

A

synovial angiogenesis (neovascularization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

new blood vessels in RA due to neoangiogenesis provide ………….. and facilitate ……………

A

provide nutrients that facilitate expansion of inflammed synovium into a rheumatoid pannus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is rheumatoid pannus?

A

Invasive mass in RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Rheumatoid pannus consists of ……………

A

fibroblast-like synovial cells + granulation tissue + inflammattory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what can do rheumatoid pannus over the time?

A

it encroaches into the joint space and can destroy the articular cartilage and erode the underlying subchondrial bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What can lead to fusion of the bones across the affected joint (bony ankylosis)?

A

ossification of the panus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Ossification of the pannus can lead to …………………..

A

fusion of the bones across the affected joint (bony ankylosis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What arthritis is in RA?

A

chronic, symetrical, polyarticular with swelling and stiffness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Late-stage RA is characterized by …………….

A

widespread joint deformities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Late stage RA deformities include ……………………….. (3)

A

ulnar deviation at the MCP joints, swan-neck deformities in the digits, and additional deformities (eg, volar subluxation of the carpus, radial drift) at the wrists.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

eventually in RA joint space is replaced by ……………

A

rheumatoid pannus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What joints are primarily involved in RA?

A

Small joints of hands (MCP and PIP) and wrists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are affected joints in RA?

A

PIP, MCP, wrist, elbow; knee, ankle metatarsophalangeal joints in feet

67
Q

What joints are usually spared in RA?

A

lumbosacral and hips

68
Q

What causes swelling, warmth and tenderness in RA?

A

overt synovitis

69
Q

overt synovitis in RA leads to …………..

A

swelling, warmth and tenderness

70
Q

X ray findings in RA?

A

joint space narrowing and marginal joint erosions

71
Q

What 2 cytokines are likely protective against joint destruction in RA?

A

TGF-beta and IL-10

72
Q

What T lymphocyte and interferon play a role in RA?

A

Th1 and INF-gama

73
Q

histopathologic findings of subcutaneous RA nodules include ……….

A

necrotic center surrounded by palisading macrophages and lymphocytes

74
Q

Cutaneous manifestation of RA? (2)

A

subcutaneous nodules and leg ulcers

75
Q

histology of RA?

A

Synovial hyperplasia

76
Q

What cervical pathology seen in advanced RA?

A

antlantoaxial subluctation (displacement of C1 and C2 vertebrae)

77
Q

Atlantoaxial subluxation (ie, displacement of C1 on C2 vertebrae) is caused by ……………………

A

ligamentous deterioration in the cervical spine

78
Q

What can lead to dislocation and spinal cord injury in RA atlantoaxial subluxation?

A

significant neck extension (eg during intubation)

79
Q

What is the most common form of arthritis?

A

osteoarthritis

80
Q

What joints affects osteoarthritis?

A

knee, lumbar spine, hips and distal joints of hand

81
Q

In osteoarthritis pain typically ……………………………… and is relieved by …………….

A

Pain typically worsens with activity and is relieved by rest

82
Q

What accelerates the progression of osteoarthritis?

A

age, joint trauma, excessive mechanical stress (eg obesity, joint deformities) + repetitive stress

83
Q

Osteoarthritis is characterized by …………. (2)

A

progressive fibrillation + erosion of articular cartilage

84
Q

Fibrillation in osteoarthritis include (3)

A

fissuring, fracturing, flaking

85
Q

What is a major contributor to cartilage destruction in osteoarthritis?

A

increased intraarticular metalloproteinase activity

86
Q

How strongly manifest synovitis in osteorthritis?

A

symptoms such redness or warmth is less prominent than in classic inflammatory arthritis disorders

87
Q

What proinflammatory mediators have been linked to osteoarthritis? (3)

A

IL-6, macrophage chemotactic protein-1

88
Q

What is the level of effusion in osteoarthritis?

A

if it occurs, then effusions are small

89
Q

what 2 changes include the periarticular area in osteoarthritis? why they occur?

A

osteophyte formation and subchondrial sclerosis;

due to excessive bone remodeling

90
Q

RA vs OA periarticular changes?

A

RA - periarticular bone erosions;

OA - osteophyte formation and subchondral sclerosis

91
Q

clinical manifestation of osteoarthritis?

A

chronic knee pain + crepitus

92
Q

If there is arthritis in thoracic spine - what 2 probable pathologies maybe it is?

A

osteoarthritis or spondyloarthritis

93
Q

musculoskeletal manifestation in hereditary hemochromatosis? (2)

A

Arthritis

Chondrocalcinosis

94
Q

What joints are affected in hereditary hemochromatosis?

A

2nd and 3rd MCP joints

95
Q

HH-associated arthritis is thought to be caused by ………………..

A

iron deposition

96
Q

Where are iron depositions in HH-assoc arthritis?

A

Iron deposition in the articular cartilage and synovium.

97
Q

Iron deposition in the articular cartilage and synovium leads to ………………….. (2)

A

free radical damage and crystal deposition

98
Q

HH-assoc arthritis resembles …………….

A

osteoarthritis

99
Q

X ray of HH-assoc arthritis

A

characteristic deformities (hook like osteophytes) and chondrocalcinosis (depositions of calcium pyrophosphate dihydrate in the articular cartilage)

100
Q

what is relation of erosion in gouty arthritis and cartilage?

A

Bony erosion are commonly near the articular surface

101
Q

What induces patho of ankylosing spondylitis?

A

Altered gut biome/defective mucosal barrier

102
Q

What cytokines increased in ankylosing spondylitis? (3)

A

IL-17, TNF-alpha, prostaglandins

103
Q

What genes increase risk for ankylosing spondylitis?

A

HLA-B27

104
Q

Exercise increase or reduce pain in ankylosing spondylitis?

A

Relieved with exercise but not with rest. Rest at night therefore induces nocturnal pain

105
Q

Age of onset of ankylosing spondylitis?

A

<40 y/o

106
Q

Where is pain in ankylosing spondylitis?

A

chronic inflammatory back and buttock pain

107
Q

X ray in ankylosing spondylitis? 2 main

A

sacroiliitis, bridging syndesmophytes

108
Q

What relieves pain in ankylosing spondylitis?

A

activity and warm shower

109
Q

What are inflammations in fingers and tendons in ankylosing spondylitis?

A

dactylitis and enthesis

110
Q

Changes in ankylosing spondylitis in chest region?

A

Decreased chest expansion

111
Q

inflammatory markers in ankylosing spondylitis?

A

CRP and ESR

112
Q

What means seronegative spondyloarthropathies?

A

absence of serum rheumatoid factor

113
Q

AS vs RA?

A

AS - simultaneous erosion of bone and new bone formation.

RA – only erosions are seen.

114
Q

Changes in gut microbiome/intestinal mucosal barrier leads to …………………..

A

enhanced IL-17-mediated inflammatory response.

115
Q

IL-17–mediates inflammatory response via ……………. and …………….

A

Innate lymphoid cells and T helper cells (eg, Th1, Th17)

116
Q

IL-17 stimulates production of additional inflammatory factors …………… (2)

A

primarily TNF-alpha and prostaglandins

117
Q

Cytokines in ankyl. spond. activates ………… and leads to ……………….

A

Cause activation of osteoclast precursor cells –> bony erosions

118
Q

Bony erosions occurs primarily in ……………..

It results in ……………. and increases risk for ……………..

A

Vertebral bodies –> results in destruction of the microarchitecture, increasing the risk for secondary osteoporosis and compression fractures.

119
Q

When starts bone formation (reparation) in ankyl. spond?

A

Once the inflammation subsides

120
Q

Excessive bone formation especially occurs in …..(what areas)…………….. in ankyl.spond.

A

in areas where fat metaplasia fills previously eroded sites.

121
Q

bone formation occurs primarily at the ……………

It manifests as …………

A

periosteum-cartilage junction and manifests as bridging syndesmophytes in the vertebral column

122
Q

bridging syndesmophytes in the vertebral column leads to ……………. (manifestation)

A

Spinal rigidity, postural alterations and increased risk of fracture.

123
Q

in what bones are seen bridging syndesmophytes?

A

in vertebral column

124
Q

Where occurs ankylosis?

A

bony fusion of the apophyseal and sacroiliac joint).

125
Q

What is ankylosis?

A

bony fusion

126
Q

Skeletal manifestations of AS occur primarily at sites of ……….. likely due to …………

A

mechanical stress, such as the entheses, likely due to the migration of activated immune cells to these areas

127
Q

What 3 medications in ankyl. spondyl?

A

Nsaids –> prostaglandins
anti-TNFalpha
anti-IL-17

128
Q

What 2 cytokines inhibits IL-17?

A

IL-2 and INF-gamma

129
Q

IL-4 may play protective role in ankyl.spondyl how?

A

Limit IL-17 production by Th1 and Th17

130
Q

What are antiinflammatory in ankyl spond?

A

IL-10 and TGF-beta

131
Q

If patient is suspected with ankyl. spond. What method to diagnose?

A

undergo xray of spine and pelvis

132
Q

What shows pelvis xray in akyl.spond?

A

inflammatory arthritis of the sacroiliac joints (ie, sacroiliitis), visible as joint erosions with subchondral sclerosis.

133
Q

Sacroiliitis on xray in ankyl spond is visible as ………..

A

joint erosions with subchondral sclerosis.

134
Q

What shows xray in ankylosis (bony fusion)?

A

heterotropic ossification affecting the margins of the vertebral bodies, which are visible as bridging syndesmophytes

135
Q

How is called continuous syndesmophytes formation in akyl spondyl?

A

bamboo spine

136
Q

do serologic tests are used in ankyl spondyl?

A

no need, because it is seronegative spondyloarthropathy

137
Q

What are conditions related to HLA class II?

A

RA, DM1, celiac disease

138
Q

RA is assoc with what HLA class?

A

II

139
Q

ankyl spondylo. What class of HLA?

A

I

140
Q

what 2 joints are affected in anky spondyl??

A

sacroiliac and apophyseal joints –> leads to restricted spinal mobility

141
Q

what 3 extraskeletal systems are affected in ankyl spondyl?

A

respiratory, cardiovascular, eyes

142
Q

Respiratory involvement in ankyl spondyl?

A

thoracic spine and enthesopathies –> involved costovertebral and costosternal junctions –> limit chest wall expansion –> hypoventilation

143
Q

The most common cardiovascular complication of AS is …………..

A

ascending aortitis, which can lead to dilation of the aortic ring and aortic insufficiency.

144
Q

eye involvement in ankyl spoondyl?

A

Anterior uveitis –> pain, blurred vision, photophobia, and conjunctival erythema.

145
Q

How manifest anterior uveitis in ankyl spondyl?

A

pain, blurred vision, photophobia, and conjunctival erythema.

146
Q

What is normal respiratory variable in ankyl spondyl despite limited chest wall?

A

peak respiratory flow

147
Q

Reactive arthritis classic triad?

A

urethritis + conjuctivitis + asymetric mono/oligoarthritis

148
Q

age of reactive arthritis?

A

20-40

149
Q

What induces reactive arthritis?

A

genitourinary or enteric infection –> autoimmune reaction initiated by the infecting pathogen

150
Q

m/o genitourinary in reactive arthritis?

A

chlamydia ttrachomatis

151
Q

m/os enteritis in reactive arthritis?

A

salmonella, shigella, yersinia, campylobacter, clostridium difficile

152
Q

What is musculoskeletal manifestation of reactive arthritis?

A

asymetric mono/oligoarthritis, enthesitis, dactylitis

153
Q

What extraarticular systems involved in reactive arthritis?

A

ocular, genital, dermal, oral ulcers

154
Q

Dermal manifestation in reactive arthritis? (2)

A

gkeratoderma belnnorrhagicum (yperkeratotic vesicles on the palms and soles) and circinate balanitis (serpiginous annular dermatitis of the glans penis)

155
Q

Genital manifestation in reactive arthritis? (3)

A

urethritis, cervicitis, prostatitis

156
Q

Ocular manifestation in reactive arthritis? (2)

A

conjuctivitis, anterior uveitis

157
Q

What musculoskeletal manifestation occurs in 20proc of reactive arthritis?

A

Axial involvement, including sacroiliitis, may occur in about 20% of cases.

158
Q

treatment of reactive arthritis?

A

Symptoms usually resolve within a few months and would not be chronic

159
Q

dactilits assoc with ….. (3) manifestations

A

ankyl spondyl, reactive artrhritis, enthesitis

160
Q

enthesitis assoc with ….. (3) manifestations

A

ankyl spondyl, reactive artrhritis, psoriasis/psor. arthritis

161
Q

where manifest enthesitis?

A

areas of mechanical stress - insertion of tendons, ligaments, joint capsules on bones

162
Q

3 common clinical syndromes in enthesitis?

A

Achilles tendinitis, plantar fasciitis, and dactylitis (“sausage digits”).

163
Q

Where is pain in achilles tenditinis?

A

posterior heel pain

164
Q

Where is pain in plantar tenditinis?

A

plantar heel pain

1 STEP UW sclerodermos (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions