msk and rheumatology Flashcards

1
Q

What is osteoarthritis?

A

NON INFLAMM, DEGENERATIVE MECHANICAL SHEARING

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2
Q

What is the most common type of arthritis?

A

Osteoarthritis

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3
Q

What are the risk factors for osteoarthritis?

A

Age (50+ yo)
FEMALE
Obesity
Occupation / sports
Genetic (COL2A1 = genetic predisposition)

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4
Q

What is the pathophysiology of osteoarthritis?

A
  • Imbalanced cartilage breakdown > repair
  • ↑chondrocyte metalloproteinase secretion, degrades T2 collagen + causes CYSTS
  • Bone attempts to overcome this w/ T1 collagen
  • ABNORMAL BONY GROWTH (OSTEOPHYTES) + remodelling
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5
Q

What are the symptoms and signs of osteoarthritis?

A

TRANSIENT (little < 30min) MORNING PAIN —> WORSE AS DAY GOES ON
BOUCHARD (PIP) + HEBDEREN (DIP) NODES on fingers
- ASYMMETRICAL, HARD NON INFLAMED JOINT
- Typically most stressed joints in body (base of thumb/big toe, hip + knee)
- NO EXTRA ARTICULAR Sx

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6
Q

How should you investigate suspected osteoarthritis? And what do you find?

A

XR = LOSS
- Loss of joint space
- Osteophytes
- Subchondral sclerosis
- Subchondral cysts
Bloods = NORMAL

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7
Q

How do you treat osteoarthritis?

A
  1. Lifestyle change: weight bearing, physio
  2. NSAID pain relief
  3. Last resort, consider surgery (arthroplasty/replacement, v good for knee + hip)”
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8
Q

What is rheumatoid arthritis?

A

INFLAMM AUTOIMMUNE POLYARTHRITIS, SYMMETRICAL

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9
Q

What are the risk factors for rheumatoid arthritis?

A

FEMALE 30-50 yo (3x more female pre-menopause, but equal post!)
Smoking
HLA DR4 / HLA DRb1 genetic link

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10
Q

What is the pathophysiology of rheumatoid arthritis?

A

Arginine —> citrulline mutation in T2 collagen
Anti-CCP (cyclic citrulinated peptide) formation
IFN-ɑ causes further pro inflammatory recruitment to synovial
synovial lining expands and tumour like mass (“pannus”) grows past joint margins
pannus destroys subchondral bone + articular cartilage”

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11
Q

What are the symptoms and signs of rheumatoid arthritis?

A

Often WORSE IN MORNING (~30 min), EASES AS DAY GOES ON
Hand:
- BOUTONNIERE (PIP flexion, opp in DIP)
- SWAN NECK (PIP hyperextension, opp in DIP)
- Z THUMB (IP flex, MP h.ext, CMC flex)
- ULNAR FINGER DEVIATION
- BAKER’S CYST = popliteal synovial sac bulge
SYMMETRICAL, HOT, INFLAMED JOINTS
(DIPs OFTEN SPARED)

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12
Q

Where is rheumatoid arthritis most commonly found?

A

Wrist, hand, feet

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13
Q

What are some of the extra-articular complications of rheumatoid arthritis?

A

Complications outside joints
Lungs: PE, pulmorary fibrosis
Heart: ↑ IHD risk
Eyes: episcleritis, keratoconjunctivitis sicca (DRY EYES)
Spinal cord compression
Kidney: CKD
Rheumatoid skin nodules (often on elbows)

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14
Q

What is Felty syndrome?

A

TRIAD:
1. RA
2. Splenomegaly
3. Neutropenia
Causes lifethreatening risk of infections!

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15
Q

How should you investigate suspected rheumatoid arthritis?

A

Bloods: ↑ESR/CRP, normocytic normochromic anaemia of chronic disease (most common - also can be MICRO - NSAID use —> peptic ulcer disease —> Fe def. anaemia OR MACRO - methotrexate use inhibits FOLATE)
Serology: +ve anti CCP (80% specific), +ve RF (70% non-specific)
XR: LESS
- loss of joint space
- eroded bone
- soft tissue swelling
- soft bones (osteopenia)

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16
Q

How do you treat rheumatoid arthritis?

A

Gold standard = DMARD (disease-modifying anti rheumatic drug) - METHOTREXATE (contra-ind in pregnancy, folate inhibitor ∴ DNA synth affected) + BIOLOGIC
Biologics - v good but EXPENSIVE
1st line = (give w/ methotrexate) TNF-ɑ inhibitor - INFLIXIMAB
2nd line = B cell inhibitor (CD20 target) - RITUXIMAV
NSAID analgesia
Intra-articular steroid injection if v painful

17
Q

How can you monitor the progression of rheumatoid arthritis?

18
Q

What are the main 2 types of crystal arthropathy?

A

Gout + Pseudogout

19
Q

What is gout?

A

Hyperuricaemia
Sodium urate crystal deposition along joints + intra-articularly

20
Q

What is the most common inflammatory arthritis in the UK?

21
Q

Who is most likely to present with gout?

A

Middle aged overweight men

22
Q

What are the risk factors for gout?

A

Purine rich foods —> meat, seafood, BEER
(Dairy can be ANTIGOUT!)
CKD + diuretics
(hyperuricaemia ↑ risk, but doesn’t guarantee)

23
Q

What is the pathophysiology of gout?

A

PURINES —(xanthine oxidase)—> URIC ACID (kidney excretion) <——> MONOSODIUM URATE
↑uric acid/CKD = impaired excretion ∴ ↑monosodium urate!

24
Q

What is the pathophysiology of gout?

A

PURINES —(xanthine oxidase)—> URIC ACID (kidney excretion) <——> MONOSODIUM URATE
↑uric acid/CKD = impaired excretion ∴ ↑monosodium urate!

25
What are the symptoms and signs of gout?
MONOARTICULAR, typically BIG TOE (metatarsophalangeal joint) SUDDEN ONSET, SEVERE, SWOLLEN RED TOE CAN’T PUT WEIGHT ON IT!
26
How should you investigate suspected gout?
Gold standard: joint aspirate + polarised light microscopy = -vely BIREFRINGENT NEEDLE SHAPED CRYSTALS
27
How do you treat gout?
- DIET: ↓purines, ↑dairy - NSAIDS, then consider COLCHICINE, then consider STEROID INJECTION (-acute gout) - PREVENTION: ALLOPURINOL (xanthine oxidase inhibitor, ↓ uric acid production)
28
What is pseudogout?
Calcium pyrophosphate crystals deposits along joint capsule
29
Who is most likely to present with pseudogout?
Elderly females (70+ yo)
30
What are the risk factors for pseudogout?
DIABETES, metabolic diseases, OA
31
What are the symptoms and signs of pseudogout?
Often POLYARTICULAR w/ KNEE commonly involved SWOLLEN HOT RED JOINT
32
How should you investigate suspected pseudogout?
Gold standard: Joint aspiration + polarised light microscopy = +vely BIREFRINGENT RHOMBOID SHAPED CRYSTALS (P for pseudo, P for positive)