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MSK 3 Flashcards

1
Q

what is a synovial joint

A

two (or more) articulating bones

ARTICULATING surfaces covered by HYALINE cartilage

enclosed fibrous capsule

NON-ARTICULATING surfaces lined by SYNOVIUM (synovial membrane)

joint space filled with synovial fluid

formed from condensing mesenchymal tissue–> interzonal mesenchyme (menisci, cruciate ligaments, synovium)

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2
Q

describe the structure of articular cartilage

A
  1. no perichondrium–> makes healing and nutrition difficult
  2. not innervated
  3. negligible friction
  4. chondrocytes make ALL the proteins–> type II collagen and proteoglycans
  5. formed by ARCHES–> the arches confer structural stability and ability to be compressed (weight bearing)
  6. mechanism of walking circulates and renews water content–> supplies nutrients and removes waste from joint
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3
Q

what are the two basic layers of the synovium

A
  1. superficial (cellular lamina) inner border

2. deep (subcellular intima)

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4
Q

what is found in the superficial/cellular lamina layer of the synovium

A

consists of SYNOVIOCYTES (which gives the impression of a cell membrane)

  • lines inner surface of the synovium
  • variable shapes
  • 1-3 cell layers thick
  • no intracellular junctions or basement membrane (therefore not true epithelium)

**there are two types of synoviocytes: A and B

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5
Q

what are the two types of synoviocytes and how do they differ

A

found in the superficial/cellular lamina layer of the synovium

A–> 20-30%; MONOCYTE derived–> phagocytose particles within the joint space, produce lytic enzymes; become macrophage-like synovial presenting (dendritic) cell in rheumatoid arthritis

B–> predominant; MESENCHYME derived–> synthesize and secrete lubricating molecules like hyaluronic acid and lubricin

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6
Q

what is found in the deep/subcellular intima layer of the synovium

A

vascular connective tissue (may be loose, fibrous or adipose)

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7
Q

what is the source of synovial fluid

A

2 sources: transudate of serum and secretion from type B synoviocytes

transudate is from fenestrated capillaries in the connective tissue of the synovium (excludes molecules > 100 nm)

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8
Q

what happens to the transudate portion of the synovial fluid during inflammation

A

during inflammation, capillaries become leaky and cell counts increase from 100/ml to >50 000/ml and EXUDATE

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9
Q

what is the meniscus composed of

A

fibrocartilage

mixture of dense regular CT and cartilage

type I collagen fibres in parallel

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10
Q

what is the purpose of the structure of the synovial joint? (i.e what function does it serve)

A

the presence of lubricating fluid and the capsule around the joint allow for a greater range of motion without friction

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11
Q

how do the synovial joint structures relate to one another during expansion (i.e not weight bearing)

A
  1. negative GAG side chains repel each other
  2. side chains attract water
  3. cartilage matrix volume increases
  4. matrix expansion is limited by the collagen arcade
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12
Q

how do the synovial joint structures relate to one another during compression (i.e weight bearing)

A
  1. weight bearing pushes GAG side chains together
  2. side chains release water
  3. reduces cartilage matrix volume
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13
Q

describe the consistency of synovial fluid

A

viscous

non-newtonian fluid with egg white consistency

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14
Q

what is the principle role of synovial fluid

A

reduce friction between articular cartilage during movement

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15
Q

what secretes synovial fluid

A

(some is transudate from fenestrated capillaries)

synovial membrane secretes synovial fluid in the joint cavity

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16
Q

what does synovial fluid contain

A
  1. hyaluronan–> secreted by fibroblast-like cells (type B synoviocytes)
  2. lubricin–> secreted by chondrocytes of the articular cartilage and type B synoviocytes
  3. interstitial fluid filtered from the blood plasma
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17
Q

in addition to reducing friction, what is another role of synovial fluid

A

also participates in nutrient and waste transportation

fluid supplies oxygen and nutrients and removes CO2

protects cartilage and other joint structures from stresses during loading

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18
Q

how does synovial fluid protect joint structures/cartilage during loading

A

it is a non-compressable fluid film trapped between articular surfaces during loading–> this is called molecular sieving

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19
Q

list the different types of synovial fluid

A

type 0–> normal

type 1–> non-inflammatory

type 2–> inflammatory

type 3–> septic

type 4–> hemorrhagic

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20
Q

describe the following attributes of type 0 (normal) synovial fluid

  1. volume
  2. viscosity
  3. clarity
  4. color
  5. WBC count
  6. polys (%)
  7. gram stain
  8. glucose
  9. protein
  10. crystals
A

for type 0 (normal)

  1. less than 3.5 ml
  2. high
  3. clear
  4. colorless/straw
  5. less than 200
  6. less than 25%
  7. negative
  8. normal
  9. normal (1/3 serum)
  10. none
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21
Q

describe the following attributes of type 1 (non-inflammatory) synovial fluid

  1. volume
  2. viscosity
  3. clarity
  4. color
  5. WBC count
  6. polys (%)
  7. gram stain
  8. glucose
  9. protein
  10. crystals
A

for type 1 (non-inflammatory)

  1. > 3.5 ml
  2. high viscosity
  3. clear
  4. straw/yellow color
  5. 200-2000 WBC/mm3 (mostly mononuclear)
  6. less than 25%
  7. negative
  8. normal
  9. normal (1/3 serum)
  10. none
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22
Q

describe the following attributes of type 2 (inflammatory) synovial fluid

  1. volume
  2. viscosity
  3. clarity
  4. color
  5. WBC count
  6. polys (%)
  7. gram stain
  8. glucose
  9. protein
  10. crystals
A

for type 2 (inflammatory)

  1. > 3.5 ml
  2. low viscosity
  3. cloudy
  4. yellow color
  5. 2000-75000 WBC/mm3 (mostly polyonuclear)
  6. > 50% polys
  7. gram stain negative
  8. decreased glucose
  9. increased protein
  10. positive for crystals if in the setting of gout; negative for crystals if in the setting of rheumatoid arthritis
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23
Q

describe the following attributes of type 3 (septic) synovial fluid

  1. volume
  2. viscosity
  3. clarity
  4. color
  5. WBC count
  6. polys (%)
  7. gram stain
  8. glucose
  9. protein
  10. crystals
A

for type 3 (septic)

  1. > 3.5 ml
  2. mixed viscosity
  3. opaque
  4. mixed color
  5. > 100 000 WBC/mm3
  6. > 75% polys
  7. gram stain often positive
  8. glucose is very decreased
  9. increased protein
  10. no crystals
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24
Q

describe the following attributes of type 4 (hemorrhagic) synovial fluid

  1. volume
  2. viscosity
  3. clarity
  4. color
  5. WBC count
  6. polys (%)
  7. gram stain
  8. glucose
  9. protein
  10. crystals
A

for type 4 (hemorrhagic)

  1. > 3.5 ml
  2. high viscosity
  3. mixed clarity
  4. red color
  5. > 100 000 WBCs/mm3
  6. > 75% polys
  7. negative gram stain
  8. normal glucose
  9. normal protein (1/3 serum)
  10. no crystals
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25
Q

in what patient might you expect to see crystals in synovial fluid

A

in a patient with gout and inflammatory synovial fluid

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26
Q

would you expect to see crystals in the synovial fluid of a patient with rheumatoid arthritis

A

no

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27
Q

in what type of synovial fluid is viscosity low?

A

inflammatory (type 2)

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28
Q

in what type of synovial fluid is there increased protein?

A

inflammatory (2) and septic (3)

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29
Q

what is the normal volume of synovial fluid

A
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30
Q

how does the synovial fluid change in the setting of osteoarthritis

A
  1. non-inflammatory fluid (type 1)
  2. low WBC
  3. mostly mononuclear
  4. thick and transparent–viscous
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31
Q

how does the synovial fluid change in the setting of rheumatoid arthritis

A
  1. inflammatory fluid (type 2)
  2. high WBC
  3. mostly polynuclear cells
  4. thin, watery, slightly turbid fluid
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32
Q

how does the synovium seem in rheumatoid arthritis (rheumatoid synovium) differ from normal synovium

A

in rheumatoid arthritis (RA), the synovium becomes HYPERTROPHIED–> swells to several cell thickness

thick villous fronts with increased number of type 2 synoviocytes

marked edema and cellular infiltrate, predominantly of LYMPHOCYTES –> lymphocytes infiltrate the synovium and some aggregate into large lymphoid follicles–> lymphoid follicles also contain plasma cells

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33
Q

what is pannus

A

unique to RA–> not seen in other inflammatory synovitis

it is FIBROVASCULAR GRANULATION tissue

denotes the markedly hyperplastic synovium which occurs at the cartilage and bone interface

believed to be responsible for the marginal subchondral erosions characteristic of RA

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34
Q

what elements of a history would suggest inflammatory (RA) arthritis

A
  1. morning stiffness lasting for more than 30 min
  2. pain WORSE at REST
  3. begins slowly and insidiously with malaise, fatigue and generalized musculoskeletal pain
  4. usually begins in the hands followed by wrists, ankles, elbows and knees
  5. progressive joint enlargement, decreased ROM evolving to complete ankylosed
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35
Q

what elements of a history would suggest non-inflammatory arthritis

A
  1. SHORT duration morning stiffness (shorter than in RA)
  2. deep achy pain worsens with activity and is RELIEVED by REST
  3. usually asymptomatic until age 50 or so
  4. limited ROM
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36
Q

what elements of a physical exam would suggest inflammatory arthritis (RA)

A
  1. pattern of joint involvement varies but generally is SYMMETRICAL and small joints are affected before large joints
  2. joints may be large and warm
  3. +/- fever
  4. RADIAL deviation of WRIST
  5. ULNAR deviation of FINGERS (swan neck deformity, boutonniere deformity)
  6. large synovial cysts (baker cysts)
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37
Q

what elements on a physical exam might suggest non-inflammatory arthritis (i.e OA)

A
  1. crepitus on passive ROM
  2. joint line tenderness
  3. bony enlargement of affected joints
  4. usually involves the HIPS, KNEES, lower LUMBAR and CERVICAL vertebrae
  5. involves PIP and DIP joints (i.e heberden nodes, bouchard’s nodes)
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38
Q

in which type of arthritis might you expect to see heberdens or bouchard’s nodes

A

non-inflammatory arthritis (OA)

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39
Q

what synovial fluid WBC count would you expect to see in the setting of non-inflammatory arthritis?

A
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40
Q

what synovial fluid WBC count would you expect to see in the setting of inflammatory arthritis (RA)?

A

> 2000/uL

also see high CRP and/or ESR

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41
Q

how do OA and RA presentations tend to differ in regard to the knees in particular?

A

knee joints tend to be:
VALGUS in RA
VARUS in OA

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42
Q

how do the natural histories of OA and RA differ?

A

RA is a disease of subtraction while OA is a disease of cartilage loss but also of addition (subchondral sclerosis and osteophytes)

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43
Q

list the 4 groupings/classifications of inflammatory arthritis

A
  1. seropositive
  2. seronegative
  3. crystal arthropathies
  4. arthritis associated with infection
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44
Q

what diseases fall under:

seropositive inflammatory arthritis

A
  1. rheumatoid arthritis (+RA factor)
  2. lupus (+ ANA)
  3. arthritis of other collagen vascular diseases (+CCP)
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45
Q

what diseases fall under:

seronegative inflammatory arthritis

A
  1. rheumatoid arthritis (- RA factor… occurs in 15% of RA cases)
  2. ankylosing spondylitis
  3. psoriatic arthritis
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46
Q

what diseases fall under:

crystal arthropathies

A
  1. gout
    (monosodium urate crystals)
  2. CPPD
    (calcium pyrophosphate dehydrate crystals)
  3. HAA
    (calcium hydroxyapatite crystals)
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47
Q

what diseases fall under:

arthritis associated with infection

A
  1. septic arthritis
    (S. aureus, S. epidermis)
  2. viral
    (rubella, parvovirus, HBV)
  3. subacute bacterial endocarditis
  4. TB, fungi
  5. lyme arthritis
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48
Q

what viruses are associated with inflammatory arthritis

A

rubella

parvovirus

HBV

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49
Q

list the classifications/groupings of symmetrical polyarthritis

A
  1. infectious
  2. post-infectious
  3. seronegative
  4. rheumatoid arthritis
  5. systemic arthritis
  6. sarcoidosis
  7. malignancy
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50
Q

what diseases are associated with infectious symmetrical polyarthritis

A
  1. bacterial (IE)
  2. lyme
  3. viral (rubella, hepatitis, parvo)
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51
Q

what diseases are associated with post-infectious symmetrical polyarthritis

A
  1. reactive syndrome

2. rheumatic fever

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52
Q

what diseases are associated with seronegative symmetrical polyarthritis

A

spondylarthropathy (psoriatic, IBD)

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53
Q

what diseases are associated with systemic symmetrical polyarthritis

A
  1. Systemic Lupus Erythematosus (SLE)
  2. vasculitis
  3. Still’s
  4. Bechet’s
  5. RP
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54
Q

what are the features of inflammatory arthritis

A

inflammation is localized in a close proximity to skeletal structures which allows inflammatory tissue to directly engage bone and cartilage in the disease process leading to a change and remodelling of the joint architecture

leads to irreversible damage and an impairment or loss of function of joints

hallmark feature of inflame arthritis is it is persistent and symmetrical

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55
Q

what is the hallmark feature of inflammatory arthritis

A

persistent and symmetrical

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56
Q

what % of those with RA are seropositive

A

80-85%

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57
Q

what are the clinical features of seropositive inflammatory arthritis (RA)

A
  1. often have rheumatic nodules, especially in the olecranon process (must be seropositive to have nodules)
  2. often have erosions on underlying bone to joint (present in advanced stages of disease)
  3. joints often become deformed and smaller, due to cartilage destruction
  4. pannus is usually present, which is hypertrophied synovium (this is usually where the erosions occur)
  5. joints can be subluxed or ankylosed
  6. juxta-articular osteopenia is seen in underlying bone (reduced bone mass)
  7. subchondral cysts are often seen in advanced disease
  8. valgus deformity of the knees (as opposed to varus in OA)
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58
Q

for those with RA (seropositive inflammatory arthritis):

where are rheumatic nodules often found?

A

in the olecranon process (though can have elsewhere)

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59
Q

for those with RA (seropositive inflammatory arthritis):

why do you often see joints becoming deformed or smaller?

A

due to cartilage destruction

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60
Q

for those with RA (seropositive inflammatory arthritis):

where do erosions usually occur (in association with what other deformity)

A

erosions usually occur in areas where pannus is present

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61
Q

what is ankylosis

A

immobility and consolidation of a joint due to disease, injury or surgical procedure

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62
Q

what is a subluxed joint

A

partial dislocation

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63
Q

for those with RA (seropositive inflammatory arthritis):

what type of knee deformity do you often see

A

valgus deformity

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64
Q

for those with RA (seropositive inflammatory arthritis):

what joints are involved?

A
  1. small joints of the hands–> tho NOT DIPs
    - -see ulnar deviation of MCPs
    - -Z deformity of the thumb
    - -swan neck or boutonniere deformities as well
  2. wrists
    - can sometimes see radial deviation
  3. elbows
  4. shoulders
  5. hips
  6. knees
  7. ankles
  8. feet
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65
Q

for those with RA (seropositive inflammatory arthritis):

what joints in particular are NOT involved

A

DIP joints of hands

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66
Q

what is the definition of lupus

A

inflammatory autoimmune disorder affecting multiple organ systems characterized by the production of autoantibodies directed against cell nuclei

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67
Q

characterize the nature of the arthritis that can be associated with lupus

A

seropositive inflammatory arthritis

NON-erosive (different than RA)

transient

symmetrical

affecting small joints

seldom deforming

less severe than RA

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68
Q

there is a list of clinical features/symptoms that are associated with lupus and used in diagnosis…. how many of those features must a person have to be diagnosed

A

4/11

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69
Q

what are the 11 clinical features used in the diagnosis of lupus

A
  1. malar rash (fixed erythema, flat or raised)
  2. discoid rash (erythematous raised patches)
  3. renal disease
  4. immunological abnormalities (positive LE cell; anti-ds-DNA; anti-Sm; any anti-phospholipid)
  5. photosensitivity
  6. arthritis
  7. neurological disease
  8. positive ANA
  9. oral ulcers
  10. serositis
  11. hematological disease (hemolytic anemia; leukopenia; lymphopenia; thrombocytopenia)
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70
Q

what “3 Ds” on history can be useful in the diagnosis of arthritis

A
  1. diurnal variation
    - nights and mornings in inflammatory arthritis; prolonged AM stiffness
  2. distribution
    - DIPs are not involved in RA–think OA in this case or psoriatic arthritis
  3. duration
    - acute vs. chronic (always look for pattern)
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71
Q

list the features of pain that should be asked during a history

A

SOREST-AAA

Site--have patient point to spot
Onset--acute, gradual
R--referral/radiation
E--exacerbating/alleviating
S--severity
T--temporal aspects (diurnal variation)

A–aggravating (position, activity)
A–alleviating (position, meds)
A–associated features (morning stiffness, duration, fever, chills)

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72
Q

DDx for monoarticular inflammatory arthritis (general)

A
  1. seropositive (RA)
  2. serogenative
  3. INFECTIOUS
  4. crystal induced
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73
Q

DDx for polyarticular inflammatory arthritis

A
  1. seropositive
  2. seronegative
  3. infectious (lyme disease, bacterial endocarditis, septicaemia, gonoccocal, viral)
  4. post-infectious (rheumatic fever, reactive arthritis)
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74
Q

DDx for non-articular inflammatory arthritis (pain syndrome)

A

soft tissue–> bursitis, tendonitis

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75
Q

DDx for mono-articular non-inflammatory arthritis

A
  1. hemarthrosis (trauma, coagulopathy)
  2. neoplasm
  3. degenerative (especially OA)
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76
Q

DDx for polyarticular non-inflammatory arthritis

A

degenerative (OA)

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77
Q

DDx for non-articular non-inflammatory arthritis (pain syndrome)

A
  1. neurological involvement (spinal stenosis, degenerative disc)
  2. vascular claudication
  3. fibromyalgia
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78
Q

what is one element of the history that can be useful in distinguishing between inflammatory and non-inflammatory arthritis

A

morning stiffness

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79
Q

describe morning stiffness in inflammatory versus non-inflammatory arthritis

A

inflammatory–> morning stiffness lasts more than 30 min and pain is worse at rest

non-inflammatory–> short duration morning stiffness with pain relieved by rest and worsened with activity

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80
Q

what is the etiology of RA

A

not fully understood

evidence of a genetic predisposition–> HLA-DR4 haplotype and HLA-DRB1 linked to higher risk

some evidence of an infectious agent as the trigger for development of RA in a genetically susceptible host

infectious agents known to cause arthritis: parvovirus, rubella, HBV, bacteria

environmental triggers: CIGARETTES, microbes, chemicals

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81
Q

what genetic markers can indicate predisposition/higher risk to RA

A
  1. HLA-DR4 haplotype

2. HLA-DRB1

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82
Q

what are some proposed environmental triggers for RA

A

CIGARETTES
microbes
chemicals

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83
Q

in what ways do the agents:

mycoplasma
parvovirus
retroviruses

trigger RA

A

through direct synovial infection

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84
Q

in what ways do the agents:

enteric bacteria
mycobacterium
EBV

trigger RA

A

via molecular mimicry

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85
Q

in what ways do the agents:

bacterial cell walls

trigger RA

A

macrophage activation

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86
Q

in what ways do the agents:

periodontal bacteria

trigger RA

A

can citrullinate proteins using endogenously produced PAD enzymes

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87
Q

what is the pathogenesis of RA

A

autoimmunity

  1. an inciting agent, such as a microbe, alters normal self antigens–> creates a neo-antigen which the host immune system then reacts against
  2. alternatively, the infectious organism may have similar protein sequences to the HLA-DRB1 sequence of the susceptible host
    - -> this may trick the CD4+ lymphocytes which have antigen recognition sites to HLA markers to react against self cells in a specific way; an infectious agent may express a CROSS REACTIVE T CELL EPITOPE leading to an immune reaction which induces T helper cells (the molecular mimicry hypothesis)
  3. there is also evidence for polycloncal activation of both B and CD4+ T lymphocytes in RA
  4. the usual mechanism which suppresses autoimmunity in the normal host may be impaired when autoreactive antigen presenting cells such as B lymphocytes present antigen to non-autoreactive CD4+ T lymphocytes
  5. autoreactive antigen-presenting cells may stimulate and thereby gain help from CD4+ lymphocytes which would have normally remained anergic
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88
Q

describe the immune/inflammatory mechanisms implicated in RA

A
  1. type I macrophage-like synoviocytes see the trigger antigen and become antigen presenting cells (APCs) which are dendritic like
  2. they present the antigen to T lymphocytes which migrate into the synovium
  3. the T lymphocytes release cytokines TNF-alpha, IL-6–> these cause damage including the activation of osteoclasts in the rheumatic joint (most drugs available are TNF inhibitors)
  4. adhesion molecules released by the endothelial cells of the synovium play an important role in cell binding and organization of cells within the synovium–> some of the lymphocytes within the synovium are organized into lymphoid follicles–> intercellular interaction between CD T cells and macrophages within the synovium leads to the release of various cell-derived lymphokines and cytokines
  5. neutrophils–> not evident in synovial tissue but are the predominant cell in synovial fluid; RA and chemotaxis of neutrophils–> phagocytose the soluble immune complexes, and release prostablandins and leukotrienes
  6. metalloproteases are the enzymes primarily responsible for the tissue destruction seen in RA
89
Q

which cytokines have been most implicated in the pathogenesis of RA

A

TNF alpha and IL-1 (IL-1 according to lecture slide… it said IL-6 in notes)

most RA drugs available on the market are TNF inhibitors

90
Q

what enzymes are the most responsible for the tissue destruction seen in RA

A

metalloproteases

enzymes can degrade cartilage leading to marginal erosions of the joint followed by progressive joint space loss

synovial fibroblasts and monocytes are main cells responsible for metalloprotease production

91
Q

what is rheumatoid factor (RF)

A

an autoantibody against Fc component of IgG

most are IgM theumatoid factors where IgM is directed against the Fc component of IgG

92
Q

what is the clinical and pathophysiological significance of the RF factor and the fact is most commonly IgM?

A
  • because IgM is pentavalent, it can lead to large immune complexes of IgM directed against the Fc component of IgG
  • however, IgG RFs are more likely to lead to systemic vasculitis
  • RF is therefore an autoantibody-antigen complex where IgM or IgG is the antibody and the Fc fragment of IgG is the antigen (forms an immune complex)

these immune complexes can precipitate and deposit or can circulate in various organs

immune complex mediated activation of complement would lead to inflammatory reaction with participation of polymorphs and release of inflammatory mediators

93
Q

what % of patients with RA become RF+ within 2 years of the disease

A

80%

presence of RF correlates strongly with more severe disease and increased risk of extraarticular features

94
Q

in which patients with RA would you find rheumatoid nodules

A

in those patients that are RF +

nodules typically occur at pressure points where there is recent trauma (elbows, extensor region of forearm)

95
Q

describe the structure of rheumatoid nodules

A

centre of nodule is a fibrinoid necrosis in a blood vessel–> immunological staining will reveal RF factor in the middle

nodule begins essentially as small cell vasculitis

96
Q

what does osteoclast-rich pannus do?

A

destroys bone

97
Q

what do the enzymes secreted by neutrophils/synoviocytes/chondrocytes in RA do?

A

destroys cartilage

98
Q

what is the hallmark structural damage seen in RA and why does this happen

A

bone erosion at the joint surface

this happens because inflammation uncouples the balance between bone resorption and formation by an increase in RANKL and DKK

the synovial membrane faces mass influx of immune cells and the proliferation of resident synovial fibroblasts contributes to mass synovial hyperplasia–> this results in structural remodelling

erosions occur due to increased joint osteoclasts which degrade the PERIARTICULAR bone and the MINERALIZED cartilage

99
Q

why are there increased osteoclasts in RA and how to they exert their action that results in bone erosion at the joint surface

A

osteoclasts form locally in the joint from the influx of mononuclear precursor cells–> they are abundantly available due to influx into the inflamed joint

the molecular increase in osteoclast formation is based on MCSF and RANKL in synovial tissue

both MCSF and RANKL drive differentiation of osteoclasts from monocyte precursors

100
Q

what does MCSF stand for and what is its significance in RA

A

“macrophage colony-stimulating factor”

responsible for the early differentiation of osteocytes (important in RA because causes proliferation of osetoclasts at the joint)

101
Q

what does RANKL stand for and what is its significance in RA

A

“receptor agonist of NF-kB ligand”

responsible for late differentiation of osteocytes and activation (important in RA because causes proliferation of osteoclasts at the joint)

102
Q

what is the major cellular source of MCSF and RANKL

A

synovial fibroblasts and activated T cells (TH17)

103
Q

what factors induce the expression of RANKL

A

TNF/IL-1 induce expression of RANKL leading to increased osteoclast activity

104
Q

outline the pathway by which RANKL activity is induced

A

activated T cells release IL-17–> IL-17 induces TNF and IL-1–> this drives inflammation–> TNF and IL-1 induce expression of RANKL

(also may involve IL-6)

105
Q

list the typical regulators of bone formation

A
  1. parathyroid hormone
  2. prostaglandins
  3. BMPs
  4. Wingless (Wnt)
106
Q

what is DDK

A

Dickkopf-1 (DKK-1) is an inhibitory protein of the Wnt signalling pathway that could be involved in subchondral bone erosions occurring in rheumatoid arthritis (RA)

(DDK inhibits normal Wnt function)

107
Q

what is the hypothesis as to why there is no new bone formation in RA

A

normally, Wnt binds LRP5/6 which goes through GSK3/B-catenin to increase mesenchymal differentiation into osteoblasts

however, DDK blocks Wnt and therefore slows osteoblast formation

TNF and inflammation induce DDK–> therefore, it could be why there is no new bone formation in RA

108
Q

what is cathepsin-K

A

a protease that can degrade collagen (can become activated in RA)

109
Q

in a patient presenting with possible RA or SLE, what routine tests would you perform

A
  1. CBC
  2. acute phase reactants (i.e ESR, CRP)
    - these can be overly sensitive and non-specific; are often looked at and followed in inflammatory diseases such as RA, lupus, polymyalgia rheumatic, temporal arteritis
  3. creatine
  4. urinalysis
    * in SLE/lupus and vasculitis diseases
    * do creatine kinase as a baseline and in setting of muscle weakness
110
Q

after a rheumatology review of systems, if you suspect inflammatory arthritis, what tests would you do?

A

RA factor (rheumatoid factor) and anti-CCP (cyclic citrullinated peptide)

111
Q

after a rheumatology review of systems, if you suspect lupus, what tests would you do?

A

ANA (anti-nuclear antibody)

112
Q

what does the ANA test consist of

A

immunofluorescence test that has 5 patterns

it is non-specific and very sensitive (i.e negative ANA makes lupus very unlikely, however positive have poor positive predictive value)

ANA is done in hemodilutions–> the higher the denominator, the higher the titre of ANA (the “more positive”)

113
Q

what tests might be done if there is a + ANA test

A
  1. ENA panel
  2. DNA Ab
  3. complement levels
114
Q

what is an ENA panel

A

(extractable nuclear antigen antibodies)

SSA (Ro) and SSB (La)–> tests for autoantibodies to these

can occur in lupus and Sjogren’s syndrome (Sjogren’s A and Sjogrens B)

antibody can cross placenta and cause congenital heart block and neonatal lupus

115
Q

why might it be important to do an ENA panel in a pregnant woman with signs of autoimmune disorder

A

because anti-SSA/SSB antibody can cross placenta and cause congenital heart block and neonatal lupus

116
Q

what are you testing for when you order a DNA antibody test

A

specific for lupus (specific, not sensitive)

done in the context of a + ANA

117
Q

why do you test complement levels after a + ANA

A

complement levels are decreased in active lupus

118
Q

what are the characteristic histological features of the synovium (and associated joint) in RA

A
  1. synovial cell hyperplasia and proliferation
  2. dense inflammatory infiltrates of CD4+, B cells, plasma cells, dendritic cells and macrophages
  3. increased vascularity due to angiogenesis
  4. fibropurulent exudate on the synovial and joint surfaces
  5. osteoclastic activity in underlying bone which allows the synovium to penetrate into the bone and cause periarticular erosions and subchondral cysts

overall, the above changes form a PANNUS which is a mass of edematous synovium, inflammatory cells, and granulation tissue that grows over the articular cartilage

in time, after the cartilage is destroyed, the pannus bridges the opposing bones to form a fibrous ankylosis which then ossifies to form a bony ankylosis

119
Q

what is a pannus

A

overall, the above changes form a PANNUS which is a mass of edematous synovium, inflammatory cells, and granulation tissue that grows over the articular cartilage

120
Q

what happens to a pannus over time

A

in time, after the cartilage is destroyed, the pannus bridges the opposing bones to form a fibrous ankylosis which then ossifies to form a bony ankylosis (in RA)

121
Q

what changes does the synovium undergo in RA

A

becomes grossly edematous, thickened and hyperplastic, transforming its smooth contour to one covered by delicate and bulbous villi

122
Q

list the radiological features of RA

A
  1. juxta-articular osteopenia
  2. erosions (bite size/”moth eaten” appearance)
  3. eroding of cartilage
  4. concentric joint space loss–> progressive narrowing of knees in both medial and lateral compartments
  5. LACK of osteophytes, sclerosis
  6. ULNAR deviation of hands
123
Q

what is the most common extra-articular feature of RA

A

nodules (especially on the olecranon process)

124
Q

what is Felty’s syndrome

A

splenomegaly, leukopenia

125
Q

what is Sjogren’s syndrome (what does it entail symptomatically)

A
  1. keratoconjunctivitis siccs (KCS)–> xeropthalmia (dry eyes)
  2. xerostomia (dry mouth)… makes them prone to dental carries
  3. parotid gland enlargement
126
Q

what condition, other than lupus, can be ENA or ANA +

A

Sjogren’s

Sjogren’s disease can be a primary idiopathic condition or it can be secondary to other conditions like RA or lupus

127
Q

list the extra-articular features of RA

A
  1. nodules
  2. lung abnormalities (pleuritis, nodules, interstitial lung disease)
  3. pericarditis
  4. Felty’s syndrome
  5. peripheral neuropathy (mononeuritis, symmetrical peripheral)
  6. vasculitis/leg ulcers (small vessel)
  7. amyloidosis
  8. Sjogren’s
  9. A-a subluxation of C1/C2
128
Q

what is A-a subluxation of C1/C2 (what is the abnormality) and what is its relation to RA

A

Atlantoaxial instability (AAI) is characterized by excessive movement at the junction between the atlas (C1) and axis (C2) as a result of either a bony or ligamentous abnormality. Neurologic symptoms can occur when the spinal cord or adjacent nerve roots are involved.

This instability can originate from congenital conditions, but in adults, it is primarily seen in the setting of acute trauma or degenerative changes due to the inflammatory pannus of rheumatoid arthritis (RA).

RA does not usually involve the spine but can be inflamed in upper part of neck

the back of the atlas and from axis or dens can shift back with inflammation and tearing ligaments–> the whole neck moves back–> can lead to blocking/destruction of spinal cord–> must do xray before intubation of an RA patient

129
Q

why must you do an xray before intubation of an RA patient

A

because of possible A-a subluxation of C1/C2 causing instability in the upper neck

130
Q

what is the 10 year survival rate of RA patients with severe disease (>30 active joint count)

A

comparable to a 3-vessel coronary artery disease

people with RA often die earlier of CV complications related to inflammation–> you reduce this risk by reducing inflammation

131
Q

what are the goals of treatment for RA

A

satisfactory tx for RA should achieve the following 3 goals:

  1. relief of signs and symptoms (joint swelling and tenderness)
  2. improvement in physical function and quality of life
  3. inhibition of progression of joint damage
132
Q

what does DMARD stand for

A

disease modifying anti-rheumatic drugs

133
Q

how would you define mild RA

A
  1. at least 3 simultaneously inflamed joints
  2. arthralgia
  3. negative RF
  4. negative anti-CCP
  5. no erosions or cartilage loss on x-ray
  6. blood tests are essentially normal
134
Q

what is the tx for recent onset (

A

NSAID at full therapeutic dose (i.e naproxen, ibuprofen, or diclofenac)

continue NSAID for two weeks until adequate control of the inflammation is achieved

(note that there is no value to adding one NSAID to another)

additional therapies:
acetaminophen for pain
joint protection counseling
enrolment in physical therapy

135
Q

what is the tx for persistent mild RA disease (>6 weeks)

A
  1. physical/occupational therapy
  2. addition of a DMARD to NSAID therapy (hydroxychloroquine or sulfasalazine or methotrexate)

can consider another NSAID or intra-articular injection of corticosteroids if inflammation is not controlled

136
Q

how would you define moderate RA

A

about 75% of presentations are moderate

  1. between 6 and 20 inflamed joints
  2. usually no extra articular features
  3. elevated ESR or CRP
  4. positive RF or anti-CCP
  5. xray shows osteopenia, periarticular swelling, no erosions initially
137
Q

what is the tx for moderate RA

A

as recommended for mild, plus:

should be started on a DMARD–> choice of DMARD is dependent on the relative activity of the disease

the most used DMARD is methotrexate

prednisone can be added for a short period to minimize disease while the DMARD kicks in–> helpful with patients who have issues with NSAIDS; not to be used long term

138
Q

which is the most used DMARD

A

methotrexate

139
Q

in moderate RA, how often should disease response to therapy be assessed

A

every 3-5 weeks

140
Q

how would you define severe RA

A
  1. more than 20 joints inflamed
  2. rapidly declining functional capacity
  3. elevated ESR and CRP
  4. anemia of chronic disease
  5. hypoalbuminemia
  6. positive RF (high titre), high anti-CCP
141
Q

how would you treat severe RA

A

as recommended for those with moderate, plus:

goal of therapy in this case is to suppress synovitis and other signs and symptoms of active disease

patients must be treated AGGRESSIVELY –> involves an NSAID plus an effective DMARD (methotrexate)

prednisone can be added if systemically ill or rapidly deteriorating–> should be tapered off as soon as possible

142
Q

which is the DMARD of first choice

A

methotrexate

143
Q

what is the normal dosing of methotrexate for tx of RA

A

usually started at 15mg/week and rapidly titrated upwards to 25mg/week by oral or SC route

given once a week only

144
Q

how does methotrexate work?

A

it is a structural analogue of folic acid that can competitively inhibit binding of dihydrofolic acid to the enzyme dihydrofolate reductase

folic acid 8-12 hours after methotrexate can be administered to reduce potential toxicity but may reduce efficacy of drug

145
Q

what do you do if initial therapy of RA with methotrexate is ineffective?

A

consider combination therapy (combination therapy usually preferred over solo therapy)

triple therapy: usually consists of methotrexate plus sulfasalazine and hydroxychloroquine (can also include leflunomide and/or cyclosporine)

(azathioprine and intramuscular gold are less commonly used but IM gold is still effective over some DMARDs)

combination therapy regimens:

  1. methotrexate, sulfasalazine and hydrochloroquine
  2. methotrexate and gold
  3. methotrexate and biologic therapy
146
Q

what is combination therapy for RA and why is it presently favored over single agent therapy for RA

A

favored due to perceived advantages i.e it uses lower doses of individual DMARDS and therefore reduces risk of toxicity, and also covers multiple inflammatory pathways

combination therapy regimens:

  1. methotrexate, sulfasalazine and hydrochloroquine
  2. methotrexate and gold
  3. methotrexate and biologic therapy
147
Q

what are some benefits to biologic therapy for RA

A

thought to be more effective and better tolerated than conventional DMARDS

148
Q

what are some disadvantages to biologic therapy for RA

A

high cost and long term effects are unknown

149
Q

who gets to try biologic therapy for RA in BC?

A

it is only offered to those in BC that have tried at least 4 DMARDs including combination DMARDs

150
Q

list the 6 agents that can be used for biologic therapy for RA

A
  1. etanercept
  2. infliximab
  3. adalimumab
  4. anakinra
  5. abatacept
  6. rituximab
151
Q

MOA of etanercept

A

used as biologic tx for RA

recombinant version of the soluble human TNF receptor–> SC twice a week

152
Q

MOA of infliximab

A

used as biologic tx for RA

chimeric human/mouse anti-TNF monoclonal antibody given via IV every 4-8 weeks

153
Q

MOA of adalimumab

A

used as biologic tx for RA

fully human anti-TNF monoclonal antibody (SC every 2 weeks)

154
Q

MOA of anakinra

A

used as biologic tx for RA

recombinant human IL-1Ra

SC daily

not used frequently

155
Q

MOA of abatecept

A

used as biologic tx for RA

a fusion protein composed of the Fc region of the immunoglobulin IgG1 fused to the extracellular domain of CTLA-4–> prevents T cell activation

156
Q

MOA of rituximab

A

used as biologic tx for RA

chimeric monoclonal antibody against CD20 which results in selective B cell depletion for 6-9 months

157
Q

Out of the following conditions, which affect the DIPs?

OA?
RA?
SLE?
Psoriatic arthritis?

A

OA and psoriatic arthritis

not SLE or RA

158
Q

Out of the following conditions, which display symmetry of symptoms?

OA?
RA?
SLE?
Psoriatic arthritis?

A

sometimes OA
yes RA and SLE

(not PsA)

159
Q

Out of the following conditions, which show stiffness in morning ?

OA?
RA?
SLE?
Psoriatic arthritis?

A

RA
SLE
PsA
(not as much OA… short lived)

160
Q

Out of the following conditions, which show sclerosis of the bone?

OA?
RA?
SLE?
Psoriatic arthritis?

A

OA

PsA

161
Q

Out of the following conditions, which show erosions of the bone?

OA?
RA?
SLE?
Psoriatic arthritis?

A

RA

PsA

162
Q

which of the following are worse in the AM versus the PM?

A

AM:
RA
SLE
PsA

PM:
OA

163
Q 
is the synovial fluid inflamed or not inflamed in the following arthropathies?
OA?
RA?
SLE
PsA?
A

inflamed in RA, SLE, PsA

not inflamed in OA

164
Q

list the seronegative inflammatory arthropathies

A
  1. psoriatic arthritis
  2. seronegative spondylarthropathy
  3. ankylosing spondylitis
  4. reactive arthritis
165
Q

what are the seronegative spondylarthropathies (what are they characterized by)

A

heterogenous group of disorders that are unified by:

  1. pathological changes in the LIGAMENTOUS attachments rather than the synovium
  2. involvement of the SACROILIAC joints with or without other joints
  3. absence of rheumatoid factor
  4. association with HLA-B27
166
Q

if you had a suspected inflammatory arthropathy that displayed pathological changes in the ligamentous attachments (not in the synovium) and involvement of the sacroiliac joints, what disease might you suspect

A

one of the seronegative spondylarthropathies

167
Q

what is psoriasis

A

common skin rash in the general population

168
Q

what % of those with psoriasis also get psoriatic arthritis

A

10-30%

169
Q

how can psoriasis/psoriatic arthritis also present?

A

as oncholysis–> pits in the nails and sausage toes/dactylitis

170
Q

when do the symptoms of psoriatic arthritis manifest (what age)

A

between 30-50

171
Q

how is susceptibility to psoriatic arthritis determined

A

by HLA-B27

172
Q

what joints does psoriatic arthritis affect?

A

the DIPs of the hands and feet are the first affected asymmetrically

the arthritis affects the peripheral and axial joints and entheses

173
Q

what are the 5 forms of psoriatic arthritis

A
  1. asymmetric oligoarthritis ( most common form, lower limb joints
  2. polyarthritis–> usually asymmetric (involves DIPs)
  3. DIP variant–> involves DIPs
  4. arthritis mutilans–> least common but also most destructive (erosions of joints, pencil cup deformity)
  5. spondyloarthropathy
174
Q

what is seronegative spondyloarthropathy

A

inflammatory arthropathy

involves inflammatory axial spine involvement

peripheral joint involvement tends to be oligoarticular (large joints, asymmetric)

entheses is involved

syndesmophytes bridge vertebral bodies–> new bone bridging (ankylosing) of the vertebral bodies

associated with HLA-B27

175
Q

what is the enthesis

A

where ligament/tendon inserts into bone

176
Q

what test is done to check for seronegative spondyloarthropathy? why is this particular test done?

A

SCHROEBER’s test

reflects the lack of movement in the spine resulting from inflammatory arthritis in the spine and resulting syndesmophytes bridging vertebral bodies causing ankylosis (bone bridging)

177
Q

what does seronegative spondyloarthropathy lead to

A

sacroilitis
enthesopathy (heel spurs, whiskering of ischium)
can get bamboo spine

178
Q

what are key features of seronegative spondyloarthropathy

A
  1. syndesmophytes–> bony growths from inside ligaments causing bridging of vertebral bodies
  2. sacroilitis–> fusion of SI joints
  3. enthesopathy–> heel spurs
179
Q

describe cardinal features of inflammatory spine pain

A

insidious onset and chronic pain in patient

180
Q

what is the main symptom you feel with a SSpA

A

lower back pain

181
Q

how do SSpAs differ from other forms of arthritis

A

involve the entheses (sites of insertion of ligaments/tendons)

182
Q

what is another name for SSpA

A

ankylosing spondylitis

183
Q

what is the triad of symptoms/conditions associated with Reactive Arthritis

A
  1. arthritis
  2. conjunctivitis
  3. urethritis (chlamydia?) –> can be associated with dysentery
184
Q

what did reactive arthritis used to be called

A

Reiter’s syndrome

185
Q

how soon do arthritis symptoms develop after a bout of urethritis and diarrhea in a patient with suspected reactive arthritis

A

within several weeks

186
Q

what are common early symptoms of reactive arthritis? what are some other notable symptoms?

A

joint stiffness and low back pain are common early symptoms

other symptoms can include spurs and bony outgrowths and sausage toes

187
Q

which joints are most often affected in reactive arthritis

A

ankles, knees and feet are most commonly affected–> frequently in an asymmetric pattern

188
Q

what is the pattern of timing of symptoms in reactive arthritis

A

episodes of arthritis usually wax and wane over several weeks to 6 months

50% are recurrent

189
Q

what is enteritis associated arthritis

A

caused by GI infection by yersenia, salmonella, shigella, campylobacter

lipoproteins on outside of bacteria elicit a range of immunological responses

arthritis appears abruptly and tends to involve the knees and ankles

sometimes involves wrists, toes and fingers

lasts about a year then clears and is rarely accompanied by ankylosing spondylitis

190
Q

list 3 types of endogenous crystals that are shown to be pathologic

A
  1. monosodium urate (gout)
  2. calcium pyrophosphate dehydrate (pseudogout)
  3. basic calcium phosphate
191
Q

what type of crystals are associated with gout

A

monosodium urate

192
Q

how do endogenous and exogenous crystals produce disease

A

by triggering cytokine mediated cascade that destroys cartilage

193
Q

describe the pathogenesis of crystal arthropathies

A

begins with HYPERURICEMIA which causes the precipitation of urate crystals in the joints

this in turn causes:
1. activation of complement–> neutrophil chemotaxis–> phagocytosis of crystals by neutrophils (release of LTB4, prostaglandins and free radicals causing tissue injury)–> lysis of neutrophils (release of crystals that are re-phagocytosed)–> release of lysosomal enzymes from lysed neutrophils–> tissue injury and inflammation

and

  1. phagocytosis by macrophages–> release of IL-1beta and other cytokines (which increase neutrophil chemotaxis)–> act on cartilage and synovium–> release of proteases from cartilage and synovium–> tissue damage and inflammation
194
Q

what are tophi

A

deposits of uric acid crystals in joints, skin or cartilage that may be present in crystal arthropathies

195
Q

how do crystal arthropathies usually present

A

as acute pain–> usually a red hot joint

196
Q

what type of synovial fluid is associated with crystal arthropathies

A

type 2 (inflammatory)– low viscosity, cloudy, yellow, negative gram stains and crystals

197
Q

is crystal arthritis poly- or monoarthritis

A

can be either

198
Q

what are the most common crystals involved in the crystal arthropathies

A

gout uric acid crystals

199
Q

what are risk factors for crystal arthritis

A
  1. increased BMI
  2. metabolic syndrome
  3. renal sufficiency–> increased risk due to decreased excretion
  4. diuretics (especially hydrochlorothiazide)
  5. low dose ASA
  6. diet–> avoid organ meats, seafood, beer, sweetened pop or fruit drinks, and use low fat milk products
200
Q

how do you treat an acute attack of crystal arthritis

A

with NSAIDs, Indocin or colchicine or prednisone

201
Q

in which patients should you avoid using NSAIDs for their crystal arthritis attack

A

if the patient has GI or renal problems

202
Q

when do you start using allopurinol for crystal arthritis tx

A

only after they have had 3 attacks and do not start allopurinol until most recent acute attack is over

when starting allopurinol, have colchicine low dose or NSAID on board–> mobilization gout

must down dose allopurinol in renal insufficiency (go low, go slow)

203
Q

do you treat asymptomatic hyperuricemia

A

no

204
Q

what may be used to reduce inflammation in crystal arthritis tx

A

intra-articular or oral steroids

205
Q

what does allopurinol do

A

it is a medication used primarily to treat excess uric acid in the blood and its complications, including chronic gout–> It is a xanthine oxidase inhibitor which is administered orally.

Allopurinol is a purine analog; it is a structural isomer of hypoxanthine (a naturally occurring purine in the body) and is an inhibitor of the enzyme xanthine oxidase. Xanthine oxidase is responsible for the successive oxidation of hypoxanthine and xanthine, resulting in the production of uric acid, the product of human purine metabolism

206
Q

when would you think joint infection over non-septic joint arthritis

A

if the patient has monoarthritis, this infection

207
Q

how can you distinguish between joint infection and non-septic joint inflammation

A

tap the joint (artherocentesis) to get synovial fluid to send for cell count and differential/gram stain

RA and infection fluid is usually a bit turbid, watery (unless you have frank pus in the joint) with high WBC and many polys

208
Q

what is the etiology/pathogenesis of septic arthritis

A

most cases result from hematogenous seeding of the synovial membrane (abundant vascular supply of synovium, lack of limiting basement membrane allows organisms to target joints in cases of bacteremia)

less common causes are direct inoculation after joint aspiration or corticosteroid injection of joint, animal bites, puncture wounds etc…

209
Q

what pathogens are commonly associated with inflammatory/septic arthritis

A
  1. bacterial–> staph, strep are most common; gonoccocal arthritis
  2. viral–> rubella, hep B, parvovirus
  3. subacute bacterial endocarditis
  4. TB, fungi
  5. lyme arthritis
210
Q

what are clinical features of septic arthritis

A
  1. most commonly monoarticular (monoarticular means trauma, infection or crystals)
  2. most are febrile, but chills are unusual
  3. disseminated gonococcal infection presents either with fever, shaking chills, lesions and tenosynovitis or purulent arthritis
  4. non-gonococcal septic arthritis:
    - acute onset of pain and swelling in a single joint
    - most common in large joints (knee in >50% of cases)
    - often immunocompromised
211
Q

what are the characteristics of septic synovial fluid

A

the 3 Cs–> cells, culture, crystal

purulent

elevated WBC > 50000 (often PMNs)

stain and culture

212
Q

why do we need to know about temporal arteritis/giant cell arteritis

A

it is a rheumatological emergency

213
Q

what is temporal arteritis

A

large vessel vasculitis

rheumatological emergency–> needs high dose steroids

requires temporal artery biopsy but start prednisone first if you suspect temporal arteritis

214
Q

what are the symptoms and characteristics of temporal arteritis

A

new onset of headaches in an older patient (>55 years)

may or may not have swelling and/or tenderness of temporal artery

jaw claudication can be present

high ESR characteristic–> 1/3 normal ESR

215
Q

do we know what causes temporal arteritis?

A

not really

216
Q

what is fibromyalgia syndrome

A

common form of non-articular rheumatism

soft tissue disorder

widespread musculoskeletal pain

believed to represent an increase in the centralized pain response

patients often have a sleep disorder

patients often have a mood/anxiety disorder

no inflammation–> lab tests are normal

217
Q

what are the criteria for fibromyalgia diagnosis

A

need at least 11 painful tender points distributed in all 4 quadrants of the body

218
Q

non-pharmacological tx for fibromyalgia syndrome

A

education
reassurance
regular aerobic exercise
cognitive behavioural therapy

219
Q

pharmacological tx for fibromyalgia

A

night time meds
anti-depressives
nerve modulating drugs (lyrica, neutonin)

MSK (5 decks)

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