MSK

Question 1

OA risk factors

Answer 1

□ Genetic predisposition (rare mutations in collagen types II, IX, XI; GDF-5) impaired cartilage repair

□ Anatomic factors (varus alignment “bow-legged”, valgus alignment “knocked-knee”) misalignment of knee joints → friction, injury

□ Joint injury (sports, surgery)

□ Obesity

□ Ageing (ECM changes: reduced hydration, increased brittleness…)

□ Gender

□ Occupation

Question 2

Pathophysiology of OA

Answer 2

• cartilage degeneration
• chrondroctes proliferation
• bone remodelling and osteophyte formation
• synovial inflammation

Question 3

cp of OA

Answer 3

pain, swelling, erythematous, morning stiffness<30mins, limited joint movement, instability, asymmetrical sx

Question 4

lab findings of OA

Answer 4

ESR <20mm/h

Question 5

*

pain characteristics of OA

Answer 5

slow progression
worse with joint use
relieved by rest
worse in evening, on exertion

Question 6

clinical diagnosis w/o imagin with:

Answer 6

1. > /= 45 yo
2. activity related joint pain
3. morning stiffness<30mins

Question 7

*

additional testing for OA if :

Answer 7

younger individuals
hist of recent trauma
worsening sx/deformity
infection/malignancy
joint involement

Question 8

*

Got of OA

Answer 8

1. relieve pain and inflammation
2. improve/preserve ROM and joint function
3. improve QoL

Question 9

safety concerns w PO NSAIDs

Answer 9

1. Cross-sensitivity reactions
2. NSAID-exacerbated respiratory disease
3. Non-teratogenic effects/ birth defects
4. Increased risk for GI bleed
5. Renal adverse effects
6. CVS risk

Question 9

NPM of OA

Answer 9

1. exercise(strengthening, low-impact)
2. weight management

Question 10

pharm for OA

Answer 10

Analgesics
1. top NSAID
2. PO NSAID
3. PO paracetamol
4. intra-articular glucocorticoid inj
5. duloxetine
6. top capsaicin

Question 11

cp of RA

Answer 11

pain, swelling, red, early morning stiffness >30mins, symmetrical sx, systemic sx(fever, tired, weight loss, depression)

Question 11

patho of RA

Answer 11

genetic + immunologic trigger –> inflammatory cells and prostaglandins release which leads to destruction of articular cartilage and underlying bone

Question 12

lab findings of RA

Answer 12

1. autoantibodies(RF, anti-CCP)
2. ESR, CRP
3. FBC(decr hg, incr WBC and platelets)
4. x-ray/MRI

Question 13

diagnosis

Answer 13

> 4 of :
1. early morning stiffness >1hr x >6weeks
2. swelling of >joints x >6weeks
3. swelling of wrists/MCP/PIP x >6weeks
4. Rheumatoid nodules
5. +ve RF and/or anti-CCP tests
6. radiographic changes

Question 14

GoT of RA

Answer 14

• achieve remission
• prevent joint damage
• control pain

Question 14

NPM of RA

Answer 14

• physical activity
• PT/OT
• weight management
• dietary (fish oil for anti inflammatory)

Question 15

FU for RA

Answer 15

§ Monitor frequently in active disease (every 1-3months)

Treatment should be adjusted if no improvement by 3rd month/ target not reached by 6th month

Question 16

glucocorticoids for RA
- moa
- dose and indication
- side effects

Answer 16

moa
- reduce endothelial dysfunction and permeability, reducing inflammation
indication
- as low dose bridging when initiating DMARDs
- to control flare ups
- continuous low dose for uncontrolled pts
dose
- PO prednisolone <7.5mg/day when initiating DMARDs

side effects
- infections
- myopathy
- OP
- weight gain
- GI ulcer
- cataract/glaucoma
- incr cv risk

Question 16

RS tx for DMARD-naive patients
- Low disease activity:
- Moderate-high disease activity:

Answer 16

Low disease activity:
* Hydroxychloroquine (better tolerated)
* Sulfasalazine > MTX (less immunosuppressive)
* MTX > leflunomide (greater dosing flexibility, lower cost)

Moderate-high disease activity:
* MTX (1st line)
* Add short-term glucocorticoid to alleviate symptoms prior to DMARD action onset

Question 16

pharm for RA

Answer 16

1. NSAID
2. glucocorticoids
3. DMARDs
   * (cs - mtx,sulfasalazine, hydroxychloroquine, leflunomide
   * (b -
   TNFa(etanercept, infliximan, adalimumab)
   IL-6(tocilizumab)
   anti-CD21 B-cell depleting monoclonal antibody(rituximab
   * (ts - JAK inhibitors(tofacitinib, baricitinib)))

Question 17

how long does tx take with DMARD and when is effect seen

Answer 17

Alters disease progression
* Slow/prevent radiographic joint damage
* Improve physical function
* Lower ESR/CRP

Start soonest
* Maximal joint damage within 1st 2 years
* 30% have radiographic erosions at diagnosis
* 60% by 2 years

Slow onset (weeks-months)

Question 18

dose for csDMARDs

Answer 18

MTX (+ folic acid 5mg/week)
○ 7.5mg once weekly
○ Dose increment: 2.5-5mg/week q4-12 weeks based on response
○ Target dose: 15mg/week within 4-6 weeks of initiation (max 25mg/week)

IF MTX CI:

	○ Sulfasalazine: initiate 500mg OD/BD → increase by 500mg/week → 1g BD maintenance (max 3000mg/day)
	
	○ Leflunomide: 100mg/day x3days (optional loading dose), 20mg/day (maintenance dose_
	
	○ Hydroxychloroquine: 200-400mg in 1-2 divided doses (max 5mg/kg/day)

Can add short-term low-dose GC when starting/changing DMARD for moderate/high RA disease activity

○ ≤7.5mg/day prednisolone up to 3 months or equivalent 
	○ Tapered and discontinued within 3 months 
	Discontinue if bDMARD/tsDMARD started

Question 19

SE, ddi, ci for MTX

Question 20

SE, ddi, ci for sulfasalazine

Question 20

SE, ddi, ci for hydroxychloroquine

Question 21

SE, ddi, ci for leflunomide