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2a > msk and rheumatology > Flashcards

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?

A

ESP + CRP

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?

A

Gout

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
Q

What are the symptoms and signs of gout?

A

MONOARTICULAR, typically BIG TOE (metatarsophalangeal joint)
SUDDEN ONSET, SEVERE, SWOLLEN RED TOE
CAN’T PUT WEIGHT ON IT!

26
Q

How should you investigate suspected gout?

A

Gold standard: joint aspirate + polarised light microscopy = -vely BIREFRINGENT NEEDLE SHAPED CRYSTALS

27
Q

How do you treat gout?

A
  • DIET: ↓purines, ↑dairy
  • NSAIDS, then consider COLCHICINE, then consider STEROID INJECTION (-acute gout)
  • PREVENTION: ALLOPURINOL (xanthine oxidase inhibitor, ↓ uric acid production)
28
Q

What is pseudogout?

A

Calcium pyrophosphate crystals deposits along joint capsule

29
Q

Who is most likely to present with pseudogout?

A

Elderly females (70+ yo)

30
Q

What are the risk factors for pseudogout?

A

DIABETES, metabolic diseases, OA

31
Q

What are the symptoms and signs of pseudogout?

A

Often POLYARTICULAR w/ KNEE commonly involved
SWOLLEN HOT RED JOINT

32
Q

How should you investigate suspected pseudogout?

A

Gold standard: Joint aspiration + polarised light microscopy = +vely BIREFRINGENT RHOMBOID SHAPED CRYSTALS
(P for pseudo, P for positive)

2a (4 decks)

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