Brainscape's Knowledge GenomeTM

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


See full index

Neurological, neuromuscular and musculoskeletal disease > Pathophysiology of joint disease > Flashcards

Pathophysiology of joint disease Flashcards

1
Q

What is rheumatoid arthritis?

A

An auto-immune disease where you have inflammation of the lining layer of joints = synovium
- Combination of genetic predisposition and environmental trigger

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

Which joints are primarily affected in RA?

A

MCPs, MTPs and wrists
Wrist joints
Elbow joints

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

At what age are you more susceptible to RA, if any?

A

It may begin at any time in life

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

Symptoms of RA

A
  • Insidious onset
  • Joint swelling
  • Early morning stiffness >30mins
  • MCPs, MTPs and wrists
  • Dramatic NSAID response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathophysiology of RA?

A
  • The trigger event (smoking etc) sets off a cascade of immune system activation, primarily delivered by T-cells. The T-cells will either:
    1. Directly activate cytokines through the activation of macrophages and fibroblasts, this will activate both activating and inhibiting cytokines, where the activating cytokine effects predominate in RA, these are TNF-alpha, IL-1 and IL-6. These cytokines potentiate the process of cell activation, they will also increase enzyme formation which perpetuates the inflammatory activity inside the synovium ultimately leading to tissue damage.
    2. Activate B-cells which are important for antibody production such as rheumatoid factor, which we can measure in the clinic as a marker for positive RA, they lead to ongoing inflammation and tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is pannus in RA?

A

A type of extra growth in joints that can cause pain, swelling, and damage to your bones, cartilage and other tissue

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

What happens at the joint level in RA?

A
  1. The synovial membrane thickens
  2. A new network of blood vessels is formed - bringing in T cells, B cells and neutrophils
  3. Synovial membrane invades cartilage in early RA
  4. In established RA, we get pannus which destroys the cartilage and bone, leading to irreversible damage, bone and joint damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the S factor for RA?

A
  1. Stiffness: early morning and >30mins
  2. Swelling: persistent swelling of one joint or more, especially hand joints
  3. Squeezing: squeezing the joints is painful in RA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors for RA

A
  • Age
  • Sex
  • FHx
  • Smoking
  • Obesity
  • Prev. joint injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is RA diagnosed?

A
  1. Blood tests: rheumatoid factor, anti-ccp antibodies, CRP, ESR
  2. X-rays
  3. Examination of joint fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of RA?

A
  1. DMARDs: methotrexate, hydroxychloroquine
  2. Cytokine targeting drugs : adalimumab, infliximab = TNFa blockers
  3. NSAIDs
  4. Corticosteroids: prednisone, dexamethasone, betamethasone, beclamethasone, fluticasone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is osteoarthritis?

A

Osteoarthritis (OA) is the most common form of arthritis.

- A degenerative joint disease or “wear and tear” arthritis.

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

Which joints are primarily affected in OA?

A
  • DIP, PIP, CMC, MTP1
  • Large weight bearing joints
  • Axial skeleton: spine (particularly cervical and lumbar spine), the neck
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Signs and symptoms of OA?

A
  • Nodular, boney, hard swelling affecting smaller joints of hands (DIP and PIP), knees, hips and lower back.
  • Symptoms worse after activity
  • Early morning stiffness <30 minutes
  • LESS inflammation than RA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Risk factors for OA? General and biomechanical

A
  • Depend on the site
  • General:
    1. Older age
    2. Female sex
    3. Genetic - FHx
    4. Obesity
    5. Oestrogen deficiency
    6. BMD
  • Local/biomechanical:
    1. Occupation
    2. Pre-existing joint abnormality
    3. Past trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Diagnosis of OA

A
  • X-ray - look for 4 features:
    1. Loss of joint space
    2. Subchondral cysts
    3. Subchondral sclerosis
    4. Osteophyte formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of pain in OA?

A
  • Prostaglandins
  • Synovitis
  • Cytokines
  • Subchondral fractures
  • Periosteal elevation
  • Muscle spasm - atrophy, sarcopenia etc
  • Venous congestion
  • Biomechanical effects: favouring one leg over another etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the management objectives for OA?

A

THERE IS NO CURE

  • Pain relief
  • Patient education and information access
  • Optimisation of function
  • Exercise and strengthening
  • Weight loss
  • Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the two types of crystal arthritis?

A
  1. Gout

2. Calcium phosphate disease

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

What is the difference between gout and calcium phosphate disease?

A

The crystals which form as part of the disease process are: uric acid for gout, and calcium pyrophosphate dihydrate crystals for calcium phosphate disease

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

What is the consequence of crystal presence in crystal arthritis?

A

They provoke an acute inflammatory reaction in and around the joint which can cause chronic joint damage with recurrent episodes of inflammation over time

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

Epidemiology of gout - Age?

A

Incidence increases with age

23
Q

Comorbidities common in gout patients?

A
  • Renal impairment
  • Coronary heart disease
  • Metabolic syndrome
  • Obesity
  • Dyslipidaemia
  • Hypertension
  • Type 2 diabetes
24
Q

Risk factors for gout: modifiable vs non-modifiable

A
  • Modifiable:
    1. HYPERURICAEMIA - MAIN CAUSE
    2. High-purine diet
    3. Alcohol consumption
    4. Obesity
    5. Certain medications e.g. diuretics
  • Non-modifiable:
    1. Age
    2. Male gender
    3. Race
    4. Genetic factors
    5. Impaired renal function
25
Q

Which medications act as modifiable risk factors for gout?

A
  1. Low dose aspirin
  2. Thiazides
  3. Furosemide
  4. Cyclosporin and other cytotoxic/cytostatic drugs
  5. Ethambutol
  6. Levdopa
  7. Nicotinic acid
26
Q

Pathophysiology of gout

A
  • Gout occurs when urate crystals (monosodium urate) precipitate either on articular cartilage or on tendons in and around soft tissues
  • They provoke an acute inflammatory reaction
27
Q

Where does urate come from?

A

End product of purine metabolism

  • Normal urate level is close to the limit of solubility, so it is more likely to form into crystals when there is hyperuricaemia
  • YOU CAN HAVE HYPERURICAEMIA AND NOT HAVE GOUT
28
Q

Which enzyme is responsible for the breakdown of hypoxanthine and xanthine into uric acid?

A

Xanthine oxidase

29
Q

What are the two mechanisms for hyperuricaemia?

A
  1. Overproduction of urate/uric acid

2. Underexcretion of urate/uric acid

30
Q

Explain how an overproduction of urate can take place?

A
  1. Increased nuclear protein turnover in certain haematological diseases such as lymphoma, leukaemia, haemolytic anaemia where you have an increased risk of breakdown products HIGH IN PURINE resulting in hyperuricaemia
  2. Conditions where there are increased rates of cellular proliferation and cell death e.g. psoriasis, chemotherapy, radiotherapy
31
Q

Explain how an underexcretion of urate can take place? This is the most common cause of hyperuricaemia

A
  1. Hereditary
  2. Patients taking diuretic drugs
  3. Patients with diseases affecting GFR
  4. Alcohol use
  5. Cyclosporin use
32
Q

How can alcohol use cause an underexcretion of urate?

A

increases purine catabolism in liver which increases lactic acid formation that blocks urate secretion by renal tubules

33
Q

Triggers of ‘gouty attacks’

A

Presence of crystals followed by mobilisation of urate due to changes in serum water level followed by either:

  1. Direct trauma
  2. Intercurrent illness/surgery that triggers acute phase response
  3. Dehydration/acidosis (incl. alcohol binge)
  4. Medications (including initiation of urate lowering drugs)
  5. Rapid weight loss
34
Q

Give an example of a medication used to lower urate levels

A

Allopurinol

35
Q

Clinical manifestation/picture of gout?

A
  1. Recurrent attacks of acute, very painful, monoarticular inflammation
  2. Typical rapid development of severe pain, swelling and tenderness
  3. Attacks often start at night or early in the morning
  4. Attacks usually resolve within 7-10 days without specific treatment
36
Q

Common sites of acute gout attacks

A
  • MTP1 (first toe)
  • Midfoot, ankle, knee
  • Wrist
  • Finger joints
  • Olecranon bursae
37
Q

Risk factors for gout

A
  1. Alcohol use
  2. Red meat consumption
  3. Age
  4. Diuretics: THIAZIDES
  5. Hereditary
  6. Diseases affecting GFR
  7. Cyclosporin use
  8. Post-menopausal women
  9. Diabetes
  10. OA
  11. Hypertension
  12. High cholesterol
  13. Conditions with increased nuclear turnover such as lymphoma, leukaemia, haemolytic anaemia which gives increased breakdown products high in purine
  14. Conditions with increased cellular proliferation e.g. psoriasis, chemotherapy, radiotherapy
38
Q

Who is at risk of gout being polyarticular rather than monoarticular?

A

High risk patients: alcoholic, postmenopausal women

39
Q

Gout diagnosis

A
  1. Demonstration of monosodium urate crystals by microscopic examination for negatively birefringent crystals in synovial fluid or tophus aspirates permits a definitive diagnosis of gout
  2. Urate crystals are intra- or extracellular
  3. Crystals examined under a polarising filter will be:
    - Yellow when aligned parallel to the axis of the red compensator
    - Blue when aligned perpendicular to the direction of polarisation
40
Q

Treatment for gout

A

Allopurinol - lowers urate levels
NSAIDs
Steroids
Ice pack

41
Q

Men with gout have a two-fold increase of…

A

Kidney stones

42
Q

What is high CRP evidence of?

A

Acute inflammatory response

43
Q

What is the presence of anti-ccp antibodies indicative of?

A

Auto-immune disease - the immune system attacking healthy tissues, and cells such as joints

44
Q

What is septic arthritis?

A

Joint infection

- A MSK emergency as it causes rapid destruction of cartilage and bone, and systemic sepsis may be life-threatening

45
Q

How can septic arthritis occur?

A
  1. If you have an injury or accident to a joint such as a dog bite or a bad cut, causing the bacteria to get into the joint
  2. If bacteria from somewhere else in the body spread into the blood and then into a joint
  3. As a complication of surgery
46
Q

Clinical presentation of septic arthritis? History

A
  • Joint pain
  • Joint swelling
  • Inability to bear weight or move joint
  • Recent increase/acute presentation (symptoms present for <2 weeks)
  • Systemic symptoms: fever, sweats, rigors, confusion (raised WCC/ESR/CRP)
47
Q

Clinical presentation of septic arthritis? Examination

A
  1. Joint effusion / heat / erythema / restriction of movement = PRISH. If all 4 signs are present then sepsis is likely
48
Q

Which joints are more commonly affected in septic arthritis?

A

Large joints such as hip or knee

49
Q

For each of the following patient groups, which organism is the most likely causative agent of sepsis?

  1. Infant
  2. Adolescent to adult
  3. Sexually active
  4. Sickle cell anaemia
  5. IV drug users
A
  1. Infant
    - Streptococcus
    - Haemophilus (*unvaccinated)
  2. Adolescent to adult
    - Staphylococcus
  3. Sexually active
    - Gonococcus
  4. Sickle cell anaemia
    - Salmonella
  5. IV drug users
    - Staphylococcus
    - Peudonomas
50
Q

Investigations with regards to septic arthritis?

A
  • Joint aspiration
  • ALL SPECIMENS TAKEN PRIOR TO ANTIBIOTIC TREATMENT
  • Blood: FBC, ESR/CRP, U&Es, LFTs
  • Microbiology
  • Imaging: X-ray
51
Q

Antibiotic treatment for septic arthritis: No risk factors for atypical organisms

A

Flucloxacillin

52
Q

Antibiotic treatment for septic arthritis: high risk of gram negative sepsis

A

2nd or 3rd gen cephalosporin

53
Q

Antibiotic treatment for septic arthritis: MRSA risk

A

Vancomycin

54
Q

How can you reduce the risk of permanent cartilage damage in septic arthritis?

A
  • Prolonged treatment

- Recurrent aspiration/washout of infected joints

Neurological, neuromuscular and musculoskeletal disease (36 decks)

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