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MSPA4023 - Clinical medical & public heath > Musculoskeletal topic 1 > Flashcards

Musculoskeletal topic 1 Flashcards

About arthritis and rheumatological conditions (83 cards)

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1
Q

What is rheumatoid arthritis?

A

an autoimmune condition that causes chronic inflammation in the synovial lining of the joints, tendon sheaths and bursa. It is a type of inflammatory arthritis.
- tends to affect multiple small joints symmetrically across both sides of the body

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2
Q

What are the causes of Rheumatoid arthritis?

A

autoimmune system
genetic –> Human leukocyte antigen HLA-DR1 & HLA-DR4
environment –> smoke, pathogen (gut bacteria)

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3
Q

Explain how rheumatoid arthritis forms and affects the joints.

A
  • citrullination, which arginine –> citrulline
  • causes the immune cells not to recognise the cells and lead to produce specific autoantibodies and attack own cells in the joints
  • synovial cells proliferate and cause pannus
  • pannus can cause damage to the cartilage and other soft tissues and erode bone
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4
Q

Clinical features of RA

A
  • muscle weakness
  • malaise
    -fever
  • rheumatoid nodules at the elbow, arms and wrists
  • stiffness usually lasts more than 45min in the morning
  • anaemia
  • Baker (popliteal) cyst at the knee joint
  • Ulnar deviation
  • Boutonniere deformity
  • Swan neck deformity
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5
Q

Where does RA usually occur in?

A

Affects multiple joints:
* Metacarpophalangeal (MCP)
* Proximal inter-phalangeal (PIP)
* Metatarsophalangeal (MTP)
if it further worsens:
* Shoulders
* Elbows
* Knees
* Ankles

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6
Q

What are the symptoms for a flare of RA

A
  • Swollen
  • Warm
  • Red
  • Painful
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7
Q

What is Felty syndrome?
And what triad does it consist of ?

A

Complication of RA, life-threatening infection
- Rheumatoid arthritis
- Splenomegaly
- Granulocytopenia

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8
Q

What investigation would you do on RA?

A

Blood tests such as:
- Rheumatoid factor
- anticitrullinated peptide (anti-CCP) antibody
- CRP & ESR
- X-ray
- Ultrasound / MRI to detect any synovitis

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9
Q

How would you manage RA?

A
  • Disease-modifying anti-rheumatic medications (DMARDs)
     Methotrexate
     Leflunomide
     Sulfasalazine
  • Biologic therapies
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10
Q

What examples of biologics can you give when managing RA?

A

adalimumab
infliximab
etanercept
Rituximab

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11
Q

Rheumatoid arthritis often/rarely________ affects the distal interphalangeal joints

A

Rheumatoid arthritis very rarely affects the distal interphalangeal joints.
Enlarged and painful distal interphalangeal joints are more likely to represent Heberden’s nodes due to osteoarthritis.

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12
Q

When will you recommend an urgent rheumatology referral?

A

When patient experiences persistent synovitis along with their RA

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13
Q

what tools are used to monitor disease activity and response to treatment of RA?

A

Disease Activity Score 28 Joints (DAS28) score

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14
Q

Give some side effect for the following:
Methotrexate
Leflunomide
Sulfasalazine
Hydroxychloroquine
Anti-TNF medications
Rituximab

A

Methotrexate: Bone marrow suppression and leukopenia, and highly teratogenic
Leflunomide: Hypertension and peripheral neuropathy
Sulfasalazine: Orange urine and male infertility (reduces sperm count)
Hydroxychloroquine: Retinal toxicity, blue-grey skin pigmentation and hair bleaching
Anti-TNF medications: Reactivation of tuberculosis
Rituximab: Night sweats and thrombocytopenia

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15
Q

What is Osteoarthritis?

A

Result from an imbalance between cartilage damage and the chondrocyte response, leading to structural issues in the joint.

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16
Q

What is the synovial joint made of?

A

articular cartilage and synovium

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17
Q

What cells maintain the articular cartilage? And what’s its job

A

Chondrocyte
they produce extracellular matrix-like
type II collagen–> structural support
proteoglycan –> elasticity

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18
Q

Where are the common affected area of osteoarthritis?

A
  • Hips
  • Knees
  • Distal interphalangeal (DIP) joints in the hands
  • The carpometacarpal (CMC) joint at the base of the thumb
  • Lumbar spine
  • Cervical spine (cervical spondylosis)
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19
Q

What clinical features would you see in osteoarthritis?

A
  • joint pain and stiffness
  • worsen with activity & end of the day
  • deformity
  • instability
  • Restricted range of motion
  • Crepitus on movement (cracking sounds)
  • Effusions (fluid) around the joint
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20
Q

In what condition where you can make a diagnosis without any investigation into Osteoarthritis

A
  • patient over 45
  • has typical pain associated with activity
  • no morning stiffness / stiffness that lasts under 30 minutes
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21
Q

What are the mnemonics used to monitor X-rays in Osteoarthritis?

A

Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts

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22
Q

What are the non-pharmacological management methods for osteoarthritis?

A

Therapeutic exercise
weight loss
occupational therapy

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23
Q

What are the pharmacological management methods for osteoarthritis?

A

topical NSAIDs
oral NSAIDs w PPI
joint replacement (standard in hips and knees)
Intra-articular steroid injections

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24
Q

differences between osteoarthritis and rheumatoid arthritis

A

Osteoarthritis:
- degenerative disease
- cartilage loss
- morning stiffness - less than 30min
- asymmetrical
- only affects the distal phalangeal & thumb bones
_____________________________________
Rheumatoid arthritis:
- autoimmune disease
- inflamed synovium
- morning stiffness - more than 30min
- symmetrical
- extra-articular involment

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25
What is polymyalgia rheumatica
It's an immune-mediated disease that causes pain and stiffness in the shoulders, pelvic girdle and neck. - it's known to have a close association with giant cell arteritis (GCA)
26
What are the potential causes of Polymyalgia rheumatica (PMR)
HLA-DR4 genes adenovirus Parvovirus B19 long term glucocorticoid uses
27
typical features of polymyalgia rheumatica
- Women - over 50 years old - Caucasians (white)
28
Clinical features of Polymyalgia rheumatica
- Bilateral shoulder pain & elbow - Bilateral pelvic girdle pain - Interfere with sleeps - Last about 45mins in the morning - Worse after rest or inactivity - Happen more than 2 weeks
29
What investigations would you do to diagnose Polymyalgia rheumatica?
Blood test such as: ESR CRP Creatine kinase FBC U&E LFT Calcium Rheumatoid factor Urine dipstick Anti-cyclic citrullinated peptide (Anti-CCP) Anti-nuclear antibodies (ANA) - Chest X-Ray
30
What is the first-line treatment for Polymyalgia rheumatica?
Prednisone 15mg with follow-up after 1 week
31
What is the management of patients on long-term steroids? (there's a mnemonic for it)
"Don't STOP" Don't - steroid dependence occurs after 3 weeks of treatment, and abruptly stopping risks adrenal crisis Sick day rules - steroid doses may increase if the patient becomes unwell Treatment card - let others know they're steroid-dependent Osteoporosis prevention may require - bisphosphonates & calcium & vitamin D Proton pump inhibitors might considered (omeprazole)
32
What is GOUT?
Inflammatory disease where uric acid precipitates into crystals that deposit in various joints around the body
33
where are the commonly found area of gout?
The base of the big toe - metatarsophalangeal joint (MTP joint) The base of the thumb - carpometacarpal joint (CMC joint) Wrist
34
How's GOUT usually presented as?
Single, acute, hot, swollen and painful joint
35
On top of GOUT, what other differential diagnosis can be related to GOUT?
septic arthritis
36
Risk factors of GOUT
- Male - Obese - High purine diet - Alcohol - Diuretics - Cardiovascular / kidney disease - Family history of Gout
37
What is the clinical presentation of GOUT?
- Subcutaneous uric acid deposits in the DIP, ears and elbows - Single, acute, hot, swollen & painful Affects the: - Metatarsal-phalangeal joint (base of the big toe) & - Capo-metacarpal joint (wrist)
38
What investigation would you do to confirm the diagnosis of GOUT?
Aspirate fluid from the joint - examine any septic arthritis. X-ray
39
How will you treat GOUT?
First-line --> NSAIDs Second-line --> Colchicine Third-line --> steroids (prednisolone) Prophylaxis: - Allopurinol - Lifestyle changes
40
What are the side effects and caution when taking Colchicine?
gastrointestinal discomfort: diarrhoea (dose-dependent) not suitable for renal impairment/heart disease
41
It is advised to give allopurinol when the patient is diagnosed with acute flare-gout TRUE or FALSE? WHY?
FALSE - cos first line is NSAIDs, so like ibuprofen or naproxen and only allopurinol after the acute attack, if started then can continue during an acute attack
42
In the joint fluid examination after the joint aspiration, what is the different of: - monosodium urate crystals of gout & - calcium pyrophosphate crystals of pseudogout
Monosodium urate crystals of gout Needle-shaped and negatively birefringent of polarised light Calcium pyrophosphate crystals of pseudogout rhomboid-shaped and positively birefringent of polarised light
43
What is psoriatic arthritis?
Inflammatory arthritis associated with psoriasis. It can vary from mild stiffening and soreness in the joints to complete joint destruction in arthritis mutilans.
44
What are the key factors to identify psoriatic arthritis?
- Asymmetrical oligoarthritis (1-4 joint affected only 1 side - Symmetrical polyarthritis (more than 4 joints same side) - Distal interphalangeal predominant pattern - Spondylitis - Arthritis mutilans
45
How do you differentiate between Psoriatic Arthritis and rheumatoid arthritis?
Psoriatic arthritis affects the distal interphalangeal (DIP) joint (which is similar to osteoarthritis) while rheumatoid arthritis rarely affects DIP joints,
46
What clinical presentation can you find in Psoriatic Arthritis?
* Check the skin - for psoriasis * Pitting of the nails * Onycholysis * Dactylitis – inflammation of the full finger * Enthesitis - inflammation of the entheses
47
What investigation would you get for Psoriatic Arthritis?
Psoriasis epidemiological screening tool (PEST) X-Ray
48
What procedure must you do if you get a high Psoriasis epidemiological screening tool (PEST) score?
required to refer to the rheumatologist
49
Treatment and management for Psoriatic Arthritis?
--> NSAIDs --> DMARDs - Methotrexate - Leflunomide - Sulfasalazine --> Anti-TNF - Etanercept - Infliximab - Adalimumab --> Ustekinumab - monoclonal antibody
50
What is osteoporosis
involves a significant reduction in bone density which makes the bones weaker and prone to fractures
51
risk factor of osteoporosis
- Older age - Post-menopausal women - Reduced mobility and activity - Low BMI (under 19 kg/m2) - Low calcium or vitamin D intake - Alcohol and smoking - Personal or family history of fractures - Chronic diseases (e.g., chronic kidney disease, hyperthyroidism and rheumatoid arthritis) - Long-term corticosteroids (e.g., 7.5mg or more of prednisolone daily for longer than 3 months) - Certain medications
52
what investigation would you do to diagnose osteoporosis?
DEXA scan to find the bone mineral density Qfracture tool (10yrs risk of major osteoporotic fracture score) FRAX tool
53
What management would you do for osteoporosis?
increase physical activity maintain a healthy weight stop smoking reduce alcohol consumption calcium 1000mg vitamin d 400-800IU
54
What is the first-line treatment for osteoporosis?
Bisphosphonates
55
What are the side effects of taking bisphosphonates?
* Reflux and oesophageal erosions * Atypical fractures (e.g., atypical femoral fractures) * Osteonecrosis of the jaw (regular dental checkups are recommended before and during treatment) * Osteonecrosis of the external auditory canal
56
What other treatment can you use for osteoporosis other than bisphonates?
* Alendronate 70 mg once weekly (oral) * Risedronate 35 mg once weekly (oral) * Zoledronic acid 5 mg once yearly (intravenous)
57
What is bursitis?
acute/chronic inflammation of a bursa
58
What is a bursa?
A bursa is a sac containing a small amount of synovial fluid that lies between a tendon and either skin or bone to act as a friction buffer
59
Risk factors of bursitis
- Occupation - Rheumatoid arthritis - Gout/pseudogout - Penetrating injury
60
Types of bursitis
Prepatellar – patella Olecranon – elbow Trochanteric – Hips Retrocalcaneal – heals Subacromial - shoulder
61
Clinical presentation of bursitis
- Pain at site of bursa - Tenderness to palpation at the site of the bursa - Decreased active range of motion - Low-grade temperature (septic bursitis) - Swelling - Erythema (septic bursitis)
62
investigations of bursitis
- Gram stain and culture of fluid aspirate - X-ray - MRI - physical examination
63
What will sepsis bursitis present with?
Low-grade fever Erthyma
64
Give me treatment for bursitis
first-line - conservation management & analgesia second-line - corticosteroid injection third-line - surgery
65
what is the management and treatment for septic bursitis?
1st-line - antibiotic therapy + aspiration + conserve management + analgesia 2nd-line - surgical debridement and levage + antibiotic therapy + conserve management + analgesia
66
What is Paget's disease?
A disorder with a lot of bone remodelling of excessive bone resorption & growth which leads to deformities & potential fractures.
67
cause of paget's disease
infections --> measles virus genetic mutation --> SQSTM1 gene
68
Where does Paget's disease primarily affect?
skull lumbar vertebrae pelvis femur
69
What are the phases of Paget's disease?
Phase 1 – osteoclasts aggressively demineralise the bone (x20 times) Phase 2 – mixed phase (lytic + blastic phase) Rapid, disorganized proliferation of new bone tissue by osteoblasts Phase 3 – sclerotic phase, where new bone formation > resorption the collagen is structurally disorganized, which leads to weaker bone and easily fracture
70
Clinical features of Paget's disease
early symptoms - nothing pain hearing & vision loss leontiasis vision loss osteosarcoma (bone cancer) kyphosis (hunchback) lower limb muscle weakness pelvic asymmetry bowlegs arthritis / joint inflammation
71
Investigation on Paget's disease
- X-ray – check lytic lesion & thickened bone cortex - Bone biopsy – excludes malignancies - Blood test  INCREASE Alkaline Phosphatase; normal calcium; normal phosphate
72
treatment of Paget's disease
Bisphosphonates pain reliever surgery
73
What is an alternative drug used if bisphosphonates is not available in Paget's disease?
calcitonin
74
What are the cells that demineralise the bones?
Osteoclast
75
What is the cell that forms new bone?
osteoblast
76
What are the mechanisms of bone remodelling?
- osteoblast release Rank L to activated osteoclast to demineralise the bones - osteoblast can also release OPG to inhibit the osteoclast by binding to the Rank L
77
What is Gian cell arteritis (GCA)
#aka temporal arteritis type of systemic vasculitis that's affecting the medium and large arteries
78
Which alternative disease is GCS strongly associate with?
Polymyalgia rheumatica
79
what is a key complication of GCA and what group of people are commonly affected?
complication - vision loss - stroke - weight gain, diabetes & osteoporosis common in older white patients
80
Presentation of Giant Cell arteritis
Unilateral headache - severe and around the temple and forehead * Scalp tenderness * Jaw claudication * Blurred / double vision * Loss of vision if untreated reduced / absent pulsation on the temporal artery
81
What investigation will be used to diagnose Giant Cell Arteritis?
Clinical presentation (S&S) Raised inflammatory markers (Raise ESR) Temporal artery biopsy (showing multinucleated giant cells) Duplex ultrasound (showing stenosis & hypoechoic sign of temporal artery)
82
First line treatment for GCA?
40-60mg prednisolone daily with no visual symptoms / jaw claudication 500mg-100mg methylprednisolone daily with visual symptoms / jaw claudication
83
What other medication can be used to treat GCA after first-line treatment?
Aspirin - 75mg decreases vision loss and strokes proton pump inhibitor - omeprazole bisphosphonates and calcium and vitamin D - bone protection while on steroids

MSPA4023 - Clinical medical & public heath (16 decks)

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