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msk & rheum Flashcards

1
Q

articular cartilage properties

A

white
smooth
tough
resistant (deforms but bounces back)

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2
Q

stain for chondrocytes

A

toludine blue
chondrocytes and proteoglycans

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3
Q

deep hyaline

A

bone like
stacked chondrocytes
high proteoglycan

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4
Q

intermediate hyaline

A

spaced chondrocytes
lacunae

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5
Q

superficial hyaline

A

flat chondrocytes - parallel to surface

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6
Q

cartilage ECM 3 components

A

proteoglycan (aggrecan = -ive => pull in H2O => swelling pressure + resist compression)

type 2 collagen (long = tensile strength)

water

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7
Q

only cartilage cells

A

chondrocytes (only 5%)

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8
Q

functions of chondrocytes

A

make + degrade cartilage matrix

interact with matrix via GF + mechano-transductor signals

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9
Q

properties of chondrocytes

A

exist in hypoxia - no BV/innervation
no division after adolescence

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10
Q

break down of collagen 2
(+where)

A

metalloproteinases 1 + 8 + 13

break 3/4 from N terminal

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11
Q

mmp 3

A

breakdown other matrix proteins + other collagens like stromelysin

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12
Q

non-specific collagenase

A

cathepsin K

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13
Q

parts of aggrecan

A

hyaluronan
link
G1, G2, G3
keratin sulfate
chondroitin sulfate

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14
Q

aggrecanase (where + examples)

A

breaks down aggrecan

NITEG-ARGSV

e.g.: ADAMTS 4+5

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15
Q

matrix metalloproteinases (where + examples)

A

breaks down aggrecan

DIPEN-FFGV

e.g. MMP 3

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16
Q

intrinsic maintenance of cartilage

A

(anabolic + anti-catabolic effects)

tissue inhibitor of metalloproteinases (TIMPS) 1-4

growth factors (FGF2, IGF, TGF, activin A)

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17
Q

extrinsic maintenance of cartilage

A

(anabolic + anti-catabolic effects)

hormones (test/oes)
some drugs e.g FGF 18

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18
Q

why no exercise = bad for joints

A

cartilage/chondrocytes need mechanical load to maintain cartilage thickness + turnover

no exercise = atrophy

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19
Q

molecular changes in OA

A

aggrecanases = break down aggrecan
collagenases = breakdown collagen
loss of water after initial swelling

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20
Q

pathological changes in early OA

A

loss of proteoglycan
fibrillation of surface = loss of integrity at surface

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21
Q

pathological changes in late OA

A

fissuring = loss of integrity all the way down
partial/whole loss of joint space
osteophytes
bone cysts
synovial inflammation

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22
Q

OA risk factors

A

age
obesity
family

chondrodysplasia
medical conditions - haemochromatosis

secondary joint damage due to inflammatory arthropathies e.g rheumatoid

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23
Q

what defect causes chondrodysplasias

A

defects in type 2 collagen
e.g stickler syndrome

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24
Q

general OA cause

A

normal joint + abnormal force
abnormal joint + normal force

Mechanical tissue injury

damage / inadequate repair

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25
Q

clinical signs of OA

A

joint pain
stiffness
loss of function

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26
Q

presentation of OA

A

crepitus (popping/clicking sounds)
stiffness after immobility - gelling
bone deformity
joint line tenderness
loss of normal range

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27
Q

x-ray OA (order of severity)

A

joint space narrowing
osteophytes (bony projections due to cartilage degeneration)
subchondral sclerosis
bone (subchondral) cysts

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28
Q

blood tests for OA

A

normal

(but sometimes low inflamm response testing for rheumatoid, secondary causes - iron, calcium , PTH, glucose)

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29
Q

hand OA

A

heberdens nodes:

distal + proximal interphalangeal + base of thumb

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30
Q

surgery OA options

A

athroplasty - surgical total replacement
uni-compartmental replacement of knee
trapeziectomy = removal of base of thumb

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31
Q

nervous control of skeletal muscle

A

somatic nervous system - voluntary movement
lower motor neurone

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32
Q

types of muscles

A

parallel - like strap muscles
fusiform - like bicep
triangular - like pec major

uni/bi/multi penate

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33
Q

connective tissue in muscle fibres
(smallest unit => largest)

A

myofibre = endomysin
fascicle = perimysin
whole muscle = epimysin

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34
Q

fibril structure

A

fused myocytes - multinucleated

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35
Q

sarcomere parts
(shorten when contracted)

A

m-line = centre
z-disc = ends - where actin meet

h-zone = only myosin
a-band = actin + myosin overlap + h-zone
i-band = only actin

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36
Q

myosin vs actin structure

A

myosin:
2 alpha helices w/2 globular heads
all point the same way

actin:
actin filament w/tropomyosin surrounding
troponin complex => causes tropomyosin to move and reveal myosin binding site when Ca2+ binds

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37
Q

receptor in t-tubule that detects change in voltage during AP

A

dihydropyridine receptor

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38
Q

motor unit

A

single motor neurone and all the muscle fibres it innervates

stimulation of 1 = stimulation of all

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39
Q

innervation ratio of large vs small muscles

A

large = bigger ratio = no need of fine control

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40
Q

slow type muscle fibres (I)
(structure, conduction, force, respiration)

A

thin axon, small body, small dendritic trees

slowest conduction velocity

lowest force that slowly peaks

oxidative phosphorylation - aerobic

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41
Q

fast fatigue resistant muscle fibres (IIA)
(structure, conduction, force, respiration)

A

thicker axon, larger body, longer dendritic trees

medium conduction velocity

medium force - medium peaks

mainly glycolysis - anaerobic

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42
Q

fast fatiguable muscle fibres (IIX)
(structure, conduction, force, respiration)

A

thickest axon, large body, long dendritic trees

fastest conduction velocity

greatest force - fast peaks

glycolysis - anaerobic

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43
Q

what happens after:
long period of training
severe de-conditioning/spinal injury/astronauts
ageing

A

IIX fatiguable => IIA fatigue resistant

I slow => II fatigue resistant (cannot contract for a long time)

decrease in all but greater ratio of slow:fast

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44
Q

Isometric contration

A

muscle stays same length
no movement
increased force

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45
Q

concentric contraction

A

muscle shortening e.g bicep curl

concentric => muscle makes C shape

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46
Q

eccentric contraction

A

muscle lengthening

47
Q

functions of skeleton

A

support
protection
movement
mineral store
blood cell production

48
Q

difference between long bone and flat bone formation

A

flat bone:
intramembranous ossifiction
(mesenchymal cells => bone)

long bone:
endochrondral ossifiction
(mesenchymal cells => cartilage => bone)

49
Q

primary vs secondary ossification centre

A

primary = diaphysis = forms inside cartilage during long bone formation => thickening + elongation

secondary = epiphysis = forms as diaphysis replaces almost all cartilage => elongation => ends of long bones

50
Q

what are:

osteogenic cell

osteoblast
osteoclast

osteocyte

A

genic: bone stem cell

blast: bone forming cell that secretes and catalyses mineralisation of osteoid

clast: bone breaking cell that dissolves + resorbs bone by phagocytosis (made from marrow)

cyte: mature bone cell - made when osteoblast embedded in own secretions

51
Q

where are:

osteogenic cell

osteoblast
osteoclast

osteocyte

A

genic = deep in periosteum

blasts = growing protions - peri/endosteum

clasts = bone surfaces + sites of injured/old/unneeded bone

cytes = entrapped in matrix

52
Q

structures in osteon

A

haversian canal = blood + lymphatics

lamellae around

lacunae = osteocytes w/ecm containing cananiculi

volkmans canal = perforates into neighbouring osteons

53
Q

interstitial growth

A

at physis (hyaline cartilage)

epiphyseal side = hyaline cartilage matrix => active + dividing

diaphyseal side = cartilage calcifies + dies + replaced by bone

54
Q

growth plate zones
RPMCZ

A

reserve zone = matrix production

proliferative zone = mitosis

maturation + hypertrophy zone = matrix calcifies

calcifies matrix zone => cell death

zone of ossification (metaphysis)

55
Q

appositional growth

A

INCREASE THICKNESS

periosteal ridges form for blood vessel
ridges fuse = endosteum lined tunnel
osteoblasts in endosteum build new lamellae inwards => new osteon
bone grows outwards as new lamellae form + new osteons made by new periosteal ridges

56
Q

how fracture caused by abnormal stress to normal bone

A

overuse
stress on bone > capacity to remodel
weakening
fracture

57
Q

osteoporosis/osteopenia

A

clast activity > blast
disrupts microarchitecture = fractures

58
Q

vit D deficiency in bones

A

osteomalacia = adult
rickets = paeds

low D = low Ca + PO4 = defective matrix mineralisation

59
Q

osteomyelitis

A

infection leading to inflammation of bone marrow

60
Q

osteogenesis imperfecta

A

congenital
defect in type 1 collagen

61
Q

pagets disease

A

increased/decreased osteoclast/blast activity = disorganised remodelling + increased breakdown

62
Q

how pagets becomes malignant [4]

A

osteoclastic activity
mixed osteoclastic/blastic activity
osteoblastic activity
malignant degeneration

63
Q

stages of fracture healing

A

inflammation (haematoma forms - ck release - tissue + BV granulation)

repair (soft callus forms + converts to hard)

remodelling (excess bone removed)

64
Q

primary bone healing vs secondary

A

pri => intramembranous only => forms woven bone directly => absolute stability

sec => endochondral involving periosteum + soft tissue => relative stability

65
Q

fracture management 3 stages

A

reduction (open/closed)
hold (closed = cast, open = int/ext metal)
rehabilitate

66
Q

ligaments (connection, function, role in)

A

connect bone to bone (flexible fibrous connective tissue)

restricts joint motion

stability and proprioception

67
Q

tendons (connection + function)

A

connect muscle to bone (strong fibrous collagen tissue)

transmits forces

68
Q

grade 1-3 of ligament + tendon tears

A

1 = incomplete/slight => no joint instability

2 = moderate/severe => one ligament fully torn => some instability

3 => complete tearing of a ligament => obvious instability

69
Q

stages of ligament/tendon healing

A

bleeding
inflammation
proliferation
re-modelling

70
Q

mono/oligo/polyarthritis

A

no: joints involved

1= Monoarthritis
2-4 = Oligoarthritis
5+ = Polyarthritis

71
Q

2 types of arthritis

A

osteo = degenerative joint disease
rheum = inflammatory

72
Q

physiological, cellular and molecular changes when inflammation at joint

A

increased blood flow
migration of white blood cells into tissues
activation/differentiation of leukocytes
cytokine production

73
Q

main causes of joint inflammation

A

secondary inflamm in response to noxious insult (infection/crystal arthritis - gout/pseudogout)

primary inflamm (immune mediated - rheumatoid/psoriatic/reactive arthritis or SLE)

74
Q

structural joint classification

A

fibrous = no space between
cartilaginous = connected by cartilage
synovial = space between filled with synovial fluid

75
Q

functional joint classification

A

synarthoses = no movement
amphiarthoses = limited movement
diarthoses = free movement

76
Q

synovial joint components

A

synovium

synovial fluid - hyaluronic acid-rich viscous fluid

articular cartilage - type II collagen + proteoglycan (aggrecan)

77
Q

what is the synovium

A

1-3 cell deep lining containing:
macrophage-like phagocytic cells (type A synoviocyte)
fibroblast-like cells that produce hyaluronic acid (type B synoviocyte)
type I collage

78
Q

onset of OA

A

gradual - slowly progressive disorder

79
Q

joints mainly affected by OA

A

joints of hand
spine
weight baring joints of lower limbs
first metatarsophalangeal joint

80
Q

cause of septic arthritis (+3 risk factors)

A

bacterial infection of a joint (usually caused by spread from the blood)

increased risk when: taking immunosuppressants, pre-existing joint damage, intravenous drug use

81
Q

what is special about gonococcal septic arthritis

A

often affects multiple joints (polyarthritis) → less likely to cause joint destruction

usually only one joint is affected by septic arthritis

82
Q

diagnosis of septic arthritis

A

by joint aspiration
send sample for Gram stain and culture

83
Q

common organisms causing septic arthritis

A

staphylococcus aureus
streptococci
gonococcus

84
Q

treatment for septic arthritis

A

surgical wash-out (‘lavage’) & intravenous antibiotics

85
Q

gout vs pseudogout

A

gout: deposition of urate (uric acid) crystals → inflammation (usually in 1st metatarsophalangeal joint)

pseudo: deposition of calcium pyrophosphate dihydrate (CPPD) crystals → inflammation (usually in knee)

86
Q

gout risk factors

A

high uric acid levels (hyperuricaemia)

due to genetic tendency, high intake of purine-rich foods, reduced excretion (kidney failure)

87
Q

pseudogout risk factors

A

osteoarthritis, elderly, intercurrent infection

88
Q

diagnosis of gout/pseudogout

A

synovial fluid analysis

aspirating fluid from affected joint → examining under a microscope using polarised light

89
Q

polarised light analysis for gout vs pseudogout

A

gout: needle shaped crystals with negative birefringence

pseudogout: rhomboid shaped crystals with positive birefringence

90
Q

x-ray for gout vs pseudogout

A

gout: juxta-articular ‘rat-bite’ erosions

pseudo: chondrocalcinosis (calcification of cartilage)

91
Q

rheumatoid arthritis definition

A

chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis

92
Q

synovitis

A

inflammation of the synovial membrane of synovial (diarthrodial) joints

93
Q

main joints affected by rheumatoid arthritis

A

metacarpophalangeal joints (MCP)
proximal Interphalangeal joints (PIP)
metatarsophalangeal joints (MTP)
wrists, knees, ankles

94
Q

key features of rheumatoid arthritis

A

chronic arthritis
poly (many joints)
symmetrical
early morning stiffness in and around joints
joint erosions may be present on radiographs

95
Q

RA blood

A

rheumatoid ‘factor’ may be detected in blood
autoantibody against IgG

96
Q

extra-articular features of RA

A

common: fever, weight loss, subcutaneous nodules

rheumatoid nodules

others = rare e.g. vasculitis, episcleritis

97
Q

what are subcutaneous nodules

A

central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue

associated with rheumatoid factor

98
Q

why synovium becomes proliferated mass of tissue (pannus) in RA

A

neovascularisation: formation of new blood vessels

lymphangiogenesis: formation of new lymphatics

inflammatory cells: activated B and T cells, plasma cells, mast cells, activated macrophages

99
Q

cytokines in RA

A

excess of pro-inflammatory vs anti-inflammatory cytokines (‘cytokine imbalance’)

dominant pro-inflammatory in the RA synovium: TNF-alpha

100
Q

what do proinflammatory cytokines do in RA

A

inflammation + long term bone destruction

activate osteoclasts → bone erosion

activate chondrocytes → cartilage destruction → joint space narrowing

activate synoviocytes → joint inflammation

101
Q

what 2 antibodies are found in RA specifically
(name, type, target of 1)

A

rheumatoid factor => IgM - recognize the Fc portion of IgG as their target antigen

antibodies to citrullinated protein antigens (ACPA)

102
Q

ACPA - what are they, what do they do, how do they cause RA

A

anti-cyclic citrullinated peptide antibody (anti-CCP antibody)

specific for rheumatoid

citrullination of peptides => peptidyl arginine deiminases (PADs) (convert arginine => citrulline)

release proinflammatory cytokines that lead to bone destruction

103
Q

3 requirements of RA treatment

A

early recognition
prompt initiation (joint destroyed over time)
aggressive treatment to suppress inflammation

104
Q

what type of drugs are used to treat RA

A

disease-modifying anti-rheumatic drugs
control the disease process

105
Q

1st line of RA drug treatment

A

methotrexate
hydroxychloroquine/sulfasalazine

106
Q

2nd line of RA treatment

A

biological therapies that offer potent + targeted treatment strategies

e.g. Janus Kinase inhibitors: Tofacitinib & Baricitinib

107
Q

what is a biological therapy + 4 main therapies for RA

A

proteins (usually ABs) used to specifically target another protein e.g. inflammatory cytokine

inhibition of TNF-a
B-cell depletion
modulation of t-cell co-stimulation
inhibition of IL6 signalling

108
Q

key differences between OA + RA

A

onset => RA rapid, OA slow

joint pattern => RA = symmetric, OA = asymmetric

OA = subchondral sclerosis + osteophytes
RA = osteopenia + bony erosions

109
Q

psoriatic arthritis

A

autoimmune
no rheumatoid factors - seronegative
mainly asymmetrical arthritis affecting IPJs

110
Q

what is reactive arthritis

A

sterile inflammation in joints following infection (urogenito/gastro)

not septic arthritis - sterile, no AB therapy + no joint lavage required

111
Q

extra-articular manifestations of reactive arthritis

A

enthesitis: tendon inflammation
skin inflammation
eye inflammation

112
Q

what is systemic lupus erythematos

A

multi-system autoimmune disease leading to multi-site inflammation (joints, skin, kidneys, haematology, lungs, CNS)

associates with autoantibodies directed against components of the cell nucleus

113
Q

what kind of rash is associated with lupus

A

malar/butterfly rash

114
Q

clinical tests for SLE

A

antinuclear antibodies - highly sensitive to SLE but not specific

anti-double stranded DNA antibodies - high specificity but only in the right clinical settings

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