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Block 12 > The Pathophysiology Of Joint Disease > Flashcards

The Pathophysiology Of Joint Disease Flashcards

1
Q

What is the prevalence of RA in the population

A

1%

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2
Q

Characteristics and distinguishing features of RA

A

Insidious onset
Joint swelling
Early morning stiffness
Dramatic NSAID response is helpful for symptoms

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3
Q

Which joints primarily affected in RA

A

MCPs, PIPs and wrists

Affects small joints in a symmetrical fashion

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4
Q

Where is the primary site of inflammation in RA

A

Synovium

Autoimmune response inflammation drives RA

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5
Q

Activation of T cells in RA leads to what..

A

Cytokines activation via

  • direct activation
  • indirect = activate macrophages/fibroblasts to then activate cytokines
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6
Q

How can T cells also influence B cell activity

A

Activate B cells to generate autoantibodies which will target own tissues —> tissue damage over time

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7
Q

Which 3 cytokines involved in RA

A

TNF alpha

IL-1

IL-6

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8
Q

TNF alpha has paracrine effects, aside from increasing release of other pro-inflammatory mediators how does it affect the following systems:

  • 2 = endothelium
  • 3 = hepatocytes
  • 4 = epidermis
  • 5 = synoviocytes
A

1) increase in adhesion molecules which increases cell infiltration

2) increase in VEGF which results in increased angiogenesis

3) increase in acute phase response which results in increased CRP in serum

4) increased keratinocytes which hyperproliferate leading to skin plaques

5) increased metalloproteinase synthesis which results in articular cartilage degradation

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9
Q

What happens early in disease in RA

A

S.membrane becomes thickened and inflamed with proliferation of new blood vessels thus promoting an in influx of pro-inflammatory cytokines

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10
Q

What is pannus

A

Invading layer of inflammatory tissue formed. Can be painful and damages bones and cartilage

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11
Q

At what point does damage from RA become irreversible

A

Invasion of bone and cartilage into joint space reducing the space and allowing bone erosion to occur

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12
Q

What are effects of chronic systemic inflammation

A

Early IHD

Sarcopenia

Dementia

Hyper cholesterol anemia

Pain sensitisation

Osteoporosis

Insulin resistance

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13
Q

What are the key considerations in treating RA

A

Stopping the inflammation
Preventing the damage
Preserve function

1) early diagnosis (stiffness in morning, swelling, squeezing (painful) —> public health campaigns

2) early intensive treatment such as monoclonal antibodies

3) tight control of inflammation by regular assessment and tweaking meds

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14
Q

What is the most common joint disorder that is considered a normal part of ageing

A

Osteoarthritis

Associated with less inflammation and occurs in weight bearing joints of axial skeleton

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15
Q

What are the risk factors for developing OA

A

Age —> increases with age. 80% of those above 75 affected

Female sex

Genetic - family Hx

Obesity

Oestrogen deficiency

Occupation
Pre-existing joint abnormality
Past trauma

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16
Q

Cause of pain in OA

A

Prostaglandins
Synovitis
Cytokines
Subchondral fractures

Periosteal elevation
Muscle spasm
Venous congestion
Bio mechanical effects

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17
Q

Management of OA

A

Patient education and information access

Pain relief

Optimisation of function

Modification of disease process

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18
Q

Examples of crystal arthritis

A

Gout (contains Uric acid crystals)

Calcium phosphate disease ( contains calcium pyrophosphate dihydrate CPPD crystals)

19
Q

Prevalence of gout

A

1-2% in UK
Men>women
Prevalence increases with age

20
Q

Co-morbidities associated with gout

A

Renal impairment (at double the risk of renal stones)
CHD
Metabolic syndrome:
- obesity
- dyslipidaemia
- hypertension
- T2 DM

21
Q

What are the non-modifiable risk factors for gout

A

Age
Male
Race
Genetic factors
Impaired renal function

22
Q

What are the modifiable risk factors for gout

A

Hyperuricaemia
High purine diet
Alcohol consumption
Obesity
Meds such as diuretics ( increase how much you pee so in blood is more likely to form crystals)

23
Q

Why do uric acid levels need to be below irate solubility level

A

Allows uric acid to dissolve and allow excretion from body

24
Q

What are purine rich foods

A

Red meat
Seafood
Alcohol

25
Q

What drinks should people avoid to control uric acid

A

Soft drinks ( contain fructose and corn syrup—> hyperuricaemia)

Alcohol ( high in purine content)

26
Q

A BMI of 35 increases risk for gout by _____ times

A

3 times

27
Q

Which medications are not good for gout

A

Thiazides
Furosemide
Cyclosporine or other cytotoxic drugs
Levodopa
Nicotinic acid
Low dose aspirin (causes retention)

28
Q

What is urate

A

Product of purine metabolism

Precipitation of uric acid is enhanced when the blood pH is low

29
Q

What is xanthine oxidase

A

Enzyme that converts hypoxanthine to xanthine which is then converted to urate

30
Q

What is the most common drug used to reduce hyperuricaemia

A

Alopurinolol

Xanthine oxidase inhibitor

31
Q

In which conditions do we see an increased production of urate

A

Lymphoma

Leukaemia

Psoriasis

Haemolytic anaemia

32
Q

What renal cause is seen to cause 90% of gout cases

A

Decreased renal excretion of urate/low eGFR conditions

33
Q

Known triggers of a gout attack

A

Direct trauma
Inter current illness
Dehydration/ acidosis ( including alcoholic binge)
Medications
Rapid weight loss

34
Q

What is Podogra

A

Gout affecting big toe, but can also affect foot, ankle, knee, finger, wrist and elbow

Rapid development of sev pain, swelling and tenderness

Often start at night or early morning

Usually monoarticular

35
Q

What can make polyarticular gout attacks more likely

A

Higher risk patients such as
Alcoholics
Post-menopausal women
As disease progresses

36
Q

How is gout diagnosis confirmed

A

Mono sodium urate crystals in microscopic examination

In synovial fluid or tophus aspirates

37
Q

What is septic arthritis

A

Large joints —> pain and swelling

Acute presentation

Systemic presentations such as fever, rigours, confusion and sweats

Joint effusion, heat, erythema, restriction of movement = if all present = sepsis likely

38
Q

Factors pre-disposing to sepsis

A

Trauma
Recent local infection
IV drug abuse
Recent invasive procedure
Pre-existing joint disease

Drugs:
- steroids or immunosuppressants including intracellular-articular joint injections

  • antibiotic treatment (sepsis may been partially treated)
39
Q

What is the investigation of choice for septic Arthritis

A

Joint aspiration - urgent with immediate microscopy and culture

40
Q

How long should IV antibiotics be used for and what should it be followed by

A

2 weeks IV antibiotics and followed by oral for 4 weeks

41
Q

1st line of treatment antibiotic for septic arthritis

A

Flucloxacillin

Or cefuroxime

MRSA related = vancomycin

42
Q

What can B cells produce that can be picked up on diagnostic tests

A

Rheumatoid factor (targets Fc region of IgG)

Anti- CCP (anti-cyclic citrullinated peptide)

Both above are antibodies

43
Q

What are the sepsis 6

A

Give the following three things:

  • high flow oxygen
  • give IV antibiotics
  • give fluids

The following three things should be measured
- blood cultures
- lactate
- urine output

Block 12 (11 decks)

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