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xB12W2 > PATHOPHYSIOLOGY OF JOINT DISEASE > Flashcards

PATHOPHYSIOLOGY OF JOINT DISEASE Flashcards

1
Q

What is the typical age and gender of rheumatoid arthritis?

A

female (3:1) and any age

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2
Q

describe the pattern of joint involvement in rheumatoid arthritis?

A

polyarticular and symmetrical - mostly MCP, MTP, PIP and wrists but can also affect larger joints

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3
Q

what does polyarticular mean?

A

many joints are affected

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4
Q

what are the signs and symptoms of rheumatoid arthritis?

A 
joitn swelling, redness, warmth
early morning stiffness >30 minutes
ulnar deviation
boutonniere deformity
swan neck deformity
baker cysts 
fever, malaise, low appetite, muscle weakness
pain in mCP and MTP joints on squeezing
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5
Q

whats the aetiology of rheumatoid arthritis?

A

a combination of genetic predisposition and environmental factors which cause modifiction of our own antigens

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6
Q

what are some genes that predispose us to rheumatoid arthritis?

A

variations in HLA-DRB1 and HLA-DR4

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7
Q

what are some envrionemntal factors that can cause rheumatoid arthritis?

A

smoking
alcohol
specific pathogens

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8
Q

briefly outline the pathogenesis of rheumatoid arthritis?

A

the trigger event causes modification of our own antigens through citrulinnation. Antigens activate immune response leading to autoantibodies being produced
inflammatory cytokines lead to activation of fibroblast-like synoviocytes which cause synovial cell proliferation = pannus which damages bone, cartilage, soft tissue over time due to release of proteases, RANKL and antibodies forming immune complexes in joint spaces

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9
Q

why can rheumatoid arthritis cause systemic symptoms

A

because the inflamatory cytokines can escape through the bloodstream and reach multiple organ systems

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10
Q

how can rheumatoid arthritis cause a fever?

A

IL-1 escapes into the bloodstream and acts as a pyrogen in the brain

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11
Q

why can rheumatoid arthritis make atherosclerosis more common?

A

because it causes vasculitis

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12
Q

why can rheumatoid arthritis cause anaemia?

A

inflammatory cytokines can make the liver produce hepcidin in high amounts which decreases iron levels by inhibiting absorption and trapping iron in macrophages or liver cells

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13
Q

how can rheumatoid arthritis cause problems within the lungs?

A

inflammatory cytokines can activate fibroblasts in the lungs causing scar tissue and decreasing gas exchange

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14
Q

why is rheumatoid arthritis symmetrical?

A

the fibroblast-like synoviocytes can migrate between joints

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15
Q

how do we diagnose rheumatoid arthritis?

A

blood tests for erythrocyte sedimentation rate, C-reactive protein, rheumatoid factor and anti-CCP
X-rays and MRI scans
assessing physical ability

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16
Q

why do we do an erythrocyte sedimentation rate test for rheumatoid arthritis?

A

The proteins that indicate inflammation cause the red blood cells to stick together and tumble to the bottom of the tube. A faster sedimentation rate indicates greater inflammation.

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17
Q

what does a C-reactive protein test do?

A

tells us about inflammation as C-reactive protein is sent into the blood stream from the liver when there is inflammation

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18
Q

what are rheumatoid factors?

A

autoantibodies against IgG

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19
Q

how do we assess physical ability when diagnosing rheumatoid arthritis?

A

using a health assessment questionnaire

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20
Q

why do we do scans to diagnose rheumatoid arthritis?

A

they can show decreased bone density, bony erosions, soft tissue swellings and narrowing of the joint spaces

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21
Q

what are some consequences of chronic systemic inflammation because of rheumatoid arthritis?

A 
CVD causing reduced life expectancy
insulin resistance
felty syndrome
increase osteoporosisi risk
increased dementia risk
pain sensitisation
hypercholesterolaemia
sarcopenia
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22
Q

why can rheumatoid arthritis lead to premature ischaemic heart disease?

A

because the inflammatory cytokines can cause vasculitis = increased atherosclerosis risk = increased CVD risk

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23
Q

what is felty syndrome?

A 
Splenomegaly
Arthritis rheumatoid
Neutropenia 
Thrombocytopenia
Anaemia
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24
Q

why can rheumatoid arthritis increase the risk for osteoporosis?

A

it can cause bony erosions but also the inactivity of limbs further increases the risk

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25
Q

how can rheumatoid arthritis be a risk factor for dementia?

A

as the increased atherosclerosis risk may lead to reductions in cerebral blood flow = increased dementia risk

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26
Q

what are the 3 main pharmacological ways tpo treat rheumatoid arthritis?

A

disease-modifying antirheumatic drugs
biological treatments
JAK inhibitors

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27
Q

Other than pharmacological methods, what are some ways in which we can treat rheumatoid arthritis?

A

painkillers/steroids
supportive treatments e.g. physio
surgery

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28
Q

whats the main example of DMARD taken for rheumatoid arthritis?

A

methotrexate

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29
Q

what are common side effects of methotrexate?

A 
nausea
loss of appetite
sore mouth
diarrhoea
headaches
hair loss
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30
Q

why may you need blood tests during methotrexate treatment?

A

to assess blood cells and liver function as these can be affected

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31
Q

why may you sometimes have a chest x-ray and breathing test when you begin taking methotrexate?

A

because it can affect the lungs so these can be used as a comparison for if it does

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32
Q

what are 3 examples of DMARDs other than methotrexate?

A

leflunomide
hydroxychloroquine
sulfasalazine

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33
Q

what are some examples of biologicals used to treat rheumatoid arthritis?

A 
adalimumab
rituximab
etanercept
infliximab
toxilizumab
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34
Q

when are biologicals offered as treatment for rheumatoid arthritis?

A

if DMARDs are not effective alone then they will be taken with biologicals

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35
Q

when are JAK inhibitors offered to treat rheumatoid arthritis?

A

for those who cannot take DMARDs/biologicals or do not find them effective (they will usually be taken with methotrexate)

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36
Q

what are side effects of steroids?

A

weight gain, osteoporosis, easy bruising, muscle weakness, thinning of skin

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37
Q

what types of surgery are there for rheumatoid arthritis?

A

arthroscopy
joint replacement
synovectomy

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38
Q

what is a synovectomy?

A

the destruction or surgical removal of the synovium

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39
Q

what is an arthroscopy?

A

a keyhole surgery for joints - can remove inflamed joint tissue

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40
Q

what is the early arthritis clinic?

A

a specific clinic set up to facilitate prompt diagnosis and specific targeted treatment. this encourages early referral, makes a definitive diagnosis which allows for early treatment. Also focusses on educating the patient

41
Q

what is the most common joint disorder?

A

osteoarthritis

42
Q

how many over 75s have osteoarthritis?

A

80%

43
Q

whats the typical gender and age of onset for osteoarthritis?

A

females is more common

>45

44
Q

whats the pattern of joint involvement in osteoarthritis?

A

polyarticular with hands (DIP, PIP, CMC), knees, hip and feet (MTP) being most common
can be symmetrical or not

45
Q

whats the difference between primary and secondary osteoarthritis?

A

primary - idiopathic, no preceding injuries

secondary - caused by congenital abnormality, trauma, etc

46
Q

what are the signs and symptoms of osteoarthritis?

A 
stiffness that worsens with activity so worse at the end of the day (can get early morning stiffness but its usually <30 mins)
genu varum or valgum
muscle waisting
tenderness on joint palpation
crepitations and a grating sensation
reduced joint movement
bone spurs
47
Q

what are some risk factors for osteoarthritis?

A 
age
female 
genetics
obesity
oestrogen deficiency
bone mineral density
occupation that requires lifting
pre-existing joint abnormality
past trauma
48
Q

whats the cause of osteoarthritis?

A

cartilage on ends of bones breaks down and isnt reapired - caused by risk factors e.g. joint injury

49
Q

whats on the surface of the synovium?

A

type A cells - clear cellular debris

type B cells - produce components of synovial fluid

50
Q

outline the pathology of osteoarthritis?

A

articular cartilage damage (for many reasons) activates chondrocytes for repair but eventually chondrocytes become exhausted and undergo apoptosis and we just got progressive articular cartilage damage.
Type A cells try to remove the mice debris and this causes inflammatory cells to be recruited which release cytokines and cause synovitis

Bone eventually rubs on bone = friction = inflammation = pain

51
Q

what are joint mice and what clears them?

A

fragments of bone/cartilage etc

tyep A cells

52
Q

what are osteophytes?

A

bony spurs/lumps

53
Q

why is age a huge factor for osteoarthritis?

A

as we age we get thinning of cartilage and brittling of bones = increased risk of cartilage destruction

54
Q

what is eburnation?

A

specific type of bone sclerosis consisting of a marbled appearance of weight-bearing joints with complete cartilaginous erosion, leaving polished, sclerotic bone as the new articular surface bone

55
Q

what are heberden nodes?

A

small, pea-sized bony growths that occur on the distal interphalangeal joint of fingers

56
Q

what are bouchard nodes?

A

small, pea-sized bony growths that occur on the proximal interphalangeal joint of fingers

57
Q

how do we diagnose osteoarthritis?

A

arthrocentesis/joint aspiration of synovial fluid
x-ray and MRI
blood test for ESR, RH and anti-CCP to rule out RA

58
Q

how do we manage osteoarthritis?

A

strenghtening exercises, weight loss if overweight, pain killers, NSAIDs, supports/braces, TENS, manual therapy, joint arthoplasty
- no cure so its focussed on symptom management to optimise function and slow progression

59
Q

what type of arthritis is septic arthritis

A
60
Q

what are the signs and symptoms of septic arthritis?

A

acute joint pain and swelling in a singular joint for <2 weeks - most likely to affect large joints
systemic symptoms e.g. fever, sweats, rigors, confusion
skin lesions, inability to move the joint

61
Q

what are some predisposing factors for rheumatoid arthritis?

A

trauma
recent local infection or septicaemia
IV drug abuse
recent invasive procedure
pre-existing joint disease
immunosuppression (conditions and drugs e.g. steroids)
antibiotic use where sepsis may have only been partially treated

62
Q

what organism can cause septic arthritis in infants?

A

streptococcus

hemophilus if unvaccinated

63
Q

what organism can cause septic arthritis in adults?

A

staphylococcus

64
Q

what organism can cause septic arthritis in those who are sexually active?

A

gonoccocus

65
Q

what organism can cause septic arthritis in those with sickle cell?

A

salmonella

66
Q

what organism can cause septic arthritis in those who use Iv drugs?

A

staphylococcus

pseudomonas

67
Q

what investigations are done to check for septic arthritis?

A

joint aspiration of synovial fluid with immediate microscopy and culture
blood work - FBC, ESR, CRP, U&E and LFT (to monitor inflammation)
bloodcultures/swabs/MSU/sputum testing
X-ray/MRI (to check for joint damage_

68
Q

how do we treat septic arthritis?

A

empirical antibiotics - IV for 2 weeks min and then oral for 4 weeks
aspirate joints to dryness as often as required

69
Q

what antibiotic is first line choice for septic arthritis?

A

flucloxacillin
if penicillin reistsant then clindamycin
if staph aureus then vancomycin
if gonococcal or gram neg then cefotaxime

70
Q

what are the 2 most common types of crystal arthritis?

A

gout and calcium phosphate disease (aka pseudo gout)

71
Q

what crystals are present in gout?

A

monosodium urate

72
Q

what crystals are present in calcium phosphate disease/pseudogout?

A

calcium pyrophosphate dyhydrate crystals

73
Q

what age and gender is gout most likely in?

A 
men 
older ages (women post menopause)
74
Q

what comorbidities is gout associated with?

A

hypertension, cardiovascular disease, renal impairment, diabetes, obesity, hyperlipidaemia

75
Q

what are risk factors for gout?

A 
older age
men 
genetics
impaired renal function
hyperuricaemia
high purine diet (red meat and seafood)
lots of sugary drinks
alcohol consumption particularly beer
obesity
certain meds
76
Q

why is gout more common in men?

A

oestrogens are uricosuric (promote excretion of uric acid)

77
Q

why can sugary drink consumption lead to gout?

A

frucostose corn syrup can cause hyperuricaemia

78
Q

why can high beer consumption lead to gout?

A

beer is rich in purines

79
Q

which meds are risk factors for gout?

A 
thiazide diuretics (lots of elderly population have these)
low dose aspirin (not hugh dose!)
furosemide
cyclosporine
ethambutamol
levodopa
nicotinic acid
80
Q

why can low dose aspirin cause gout?

A

as it can cause uric acid retention

high dose aspirin is actually uricosuric

81
Q

why are humans predisposed to gout compared to other mammals?

A

as most mammals have uricase which converts urate to a more soluble, excretable product but we do not have this enzyme

82
Q

where does urate come from in our bodies?

A

metabolism of endogenous (typically DNA and RNA) and exogenous (food-derived) purines.

83
Q

outline the pathophysiology of gout?

A

hyperuricaemia causes urate to form crystals, particularly over joints where blood is moving more slowly, which accumulate in joints = inflammation = pain
repeated gouty attacks can cause destruction of joint tissue, resulting in arthritis

84
Q

what are the 2 main mechanisms for hyperuricaemia?

A

overproduction of urate

underecretion of urate (most common)

85
Q

what are the main mechanisms of overproduction of urate?

A

increased nuclear protein turnover e.g. lymphoma, leukaemia and haemolytic anaemia
increased rate of cellular porliferation and death
hereditary abnormalities e.g. enzyme deficiencies
certain food and beverages e.g. shellfish, red meat, high fructose corn syrup drinks, beer

86
Q

what are the main mechanisms for underexcretion of urate?

A 
herediatry reasons
taking thiazide diuretics
diseases that reduce GFR e..g CKD
dehydration (allows precipitation)
high alcohol levels
immunosuppressants damaging renal tubes, lead poisoning, cyclosporin etc
87
Q

what are the signs and symptoms of gout?

A

excrutiating pain with sudden onset - often begins at night (particulat MTP joint of first toe, midfoot, ankle, knee, wrist, finger joints, olecranon bursa)
usually monoarticular
inflammation
low grade fever

88
Q

what is podagra?

A

gout of the big toe

89
Q

what is chronic gout?

A

repeated gouty attacks causing tissue destruction and leading to deformity
can leave trophi which are permenant deposits of urate crystals just beneath the skin

90
Q

what do trophi look like?

A

visible under the skin and tend to look like swollen nodule

The material may be in a liquid, pasty, or chalky state.

91
Q

how is gout diagnosed?

A

aspiration of synovial fluid / collection of fluid from trophi
(under microscope you would see long, needle shaped crystals which, under a polarising filter, would be yellow and/or blue)

92
Q

why does gout increase the risk of kidney stones?

A

higher level of uric acid being excreted by the kidneys, and they have more acidic urine, which makes the uric acid more likely to form stones

93
Q

if you have gout, how should you avoid kidney stones?

A

increase fluid intake
decrease salt and purine consumption
urine alkalinization with potassium citrate

94
Q

what are the 3 stages of gout?

A

asymptomatic hyperuricaemia
a period of acute attacks followed by variable intervals with no symptoms
a final period of chronic tophaceous gout, where people have nodules affecting joints.

95
Q

how are acute attacks of gout treated?

A

colchicine or high doses of an NSAID with a PPI (excluding aspirin)
A short course of oral corticosteroid or a single injection of intramuscular corticosteroid are effective alternatives

96
Q

what does colchicine do?

A

inhibits WBC migration - decreases pain and swelling

97
Q

how should you treat acute attacks of gout if they are very frequent (3 in 12 months)?

A

An interleukin-1 inhibitor, such as canakinumab

98
Q

how should you treat long term gout?

A

treat the underlying cause

urate lowering therapy e.g. xanthine oxidase inhibitors (allopurinol) or uricosuric drugs

xB12W2 (6 decks)

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