Musculoskeletal topic 1 Flashcards

About arthritis and rheumatological conditions

You may prefer our related Brainscape-certified flashcards:
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
Q

What is polymyalgia rheumatica

A

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)

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26
Q

What are the potential causes of Polymyalgia rheumatica (PMR)

A

HLA-DR4 genes
adenovirus
Parvovirus B19
long term glucocorticoid uses

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27
Q

typical features of polymyalgia rheumatica

A
  • Women
  • over 50 years old
  • Caucasians (white)
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28
Q

Clinical features of Polymyalgia rheumatica

A
  • 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
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29
Q

What investigations would you do to diagnose Polymyalgia rheumatica?

A

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

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30
Q

What is the first-line treatment for Polymyalgia rheumatica?

A

Prednisone 15mg with follow-up after 1 week

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31
Q

What is the management of patients on long-term steroids?
(there’s a mnemonic for it)

A

“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)

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32
Q

What is GOUT?

A

Inflammatory disease where uric acid precipitates into crystals that deposit in various joints around the body

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33
Q

where are the commonly found area of gout?

A

The base of the big toe - metatarsophalangeal joint (MTP joint)
The base of the thumb - carpometacarpal joint (CMC joint)
Wrist

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34
Q

How’s GOUT usually presented as?

A

Single, acute, hot, swollen and painful joint

35
Q

On top of GOUT, what other differential diagnosis can be related to GOUT?

A

septic arthritis

36
Q

Risk factors of GOUT

A
  • Male
  • Obese
  • High purine diet
  • Alcohol
  • Diuretics
  • Cardiovascular / kidney disease
  • Family history of Gout
37
Q

What is the clinical presentation of GOUT?

A
  • 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
Q

What investigation would you do to confirm the diagnosis of GOUT?

A

Aspirate fluid from the joint - examine any septic arthritis.
X-ray

39
Q

How will you treat GOUT?

A

First-line –> NSAIDs
Second-line –> Colchicine
Third-line –> steroids (prednisolone)

Prophylaxis:
- Allopurinol
- Lifestyle changes

40
Q

What are the side effects and caution when taking Colchicine?

A

gastrointestinal discomfort: diarrhoea (dose-dependent)
not suitable for renal impairment/heart disease

41
Q

It is advised to give allopurinol when the patient is diagnosed with acute flare-gout
TRUE or FALSE? WHY?

A

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
Q

In the joint fluid examination after the joint aspiration, what is the different of:
- monosodium urate crystals of gout
&
- calcium pyrophosphate crystals of pseudogout

A

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
Q

What is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis. It can vary from mild stiffening and soreness in the joints to complete joint destruction in arthritis mutilans.

44
Q

What are the key factors to identify psoriatic arthritis?

A
  • 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
Q

How do you differentiate between Psoriatic Arthritis and rheumatoid arthritis?

A

Psoriatic arthritis affects the distal interphalangeal (DIP) joint (which is similar to osteoarthritis) while rheumatoid arthritis rarely affects DIP joints,

46
Q

What clinical presentation can you find in Psoriatic Arthritis?

A
  • Check the skin - for psoriasis
  • Pitting of the nails
  • Onycholysis
  • Dactylitis – inflammation of the full finger
  • Enthesitis - inflammation of the entheses
47
Q

What investigation would you get for Psoriatic Arthritis?

A

Psoriasis epidemiological screening tool (PEST)
X-Ray

48
Q

What procedure must you do if you get a high Psoriasis epidemiological screening tool (PEST) score?

A

required to refer to the rheumatologist

49
Q

Treatment and management for Psoriatic Arthritis?

A

–> NSAIDs
–> DMARDs
- Methotrexate
- Leflunomide
- Sulfasalazine
–> Anti-TNF
- Etanercept
- Infliximab
- Adalimumab

–> Ustekinumab - monoclonal antibody

50
Q

What is osteoporosis

A

involves a significant reduction in bone density which makes the bones weaker and prone to fractures

51
Q

risk factor of osteoporosis

A
  • 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
Q

what investigation would you do to diagnose osteoporosis?

A

DEXA scan to find the bone mineral density
Qfracture tool (10yrs risk of major osteoporotic fracture score)
FRAX tool

53
Q

What management would you do for osteoporosis?

A

increase physical activity
maintain a healthy weight
stop smoking
reduce alcohol consumption
calcium 1000mg
vitamin d 400-800IU

54
Q

What is the first-line treatment for osteoporosis?

A

Bisphosphonates

55
Q

What are the side effects of taking bisphosphonates?

A
  • 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
Q

What other treatment can you use for osteoporosis other than bisphonates?

A
  • Alendronate 70 mg once weekly (oral)
  • Risedronate 35 mg once weekly (oral)
  • Zoledronic acid 5 mg once yearly (intravenous)
57
Q

What is bursitis?

A

acute/chronic inflammation of a bursa

58
Q

What is a bursa?

A

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
Q

Risk factors of bursitis

A
  • Occupation
  • Rheumatoid arthritis
  • Gout/pseudogout
  • Penetrating injury
60
Q

Types of bursitis

A

Prepatellar – patella
Olecranon – elbow
Trochanteric – Hips
Retrocalcaneal – heals
Subacromial - shoulder

61
Q

Clinical presentation of bursitis

A
  • 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
Q

investigations of bursitis

A
  • Gram stain and culture of fluid aspirate
  • X-ray
  • MRI
  • physical examination
63
Q

What will sepsis bursitis present with?

A

Low-grade fever
Erthyma

64
Q

Give me treatment for bursitis

A

first-line - conservation management & analgesia
second-line - corticosteroid injection
third-line - surgery

65
Q

what is the management and treatment for septic bursitis?

A

1st-line - antibiotic therapy + aspiration + conserve management + analgesia
2nd-line - surgical debridement and levage + antibiotic therapy + conserve management + analgesia

66
Q

What is Paget’s disease?

A

A disorder with a lot of bone remodelling of excessive bone resorption & growth which leads to deformities & potential fractures.

67
Q

cause of paget’s disease

A

infections –> measles virus
genetic mutation –> SQSTM1 gene

68
Q

Where does Paget’s disease primarily affect?

A

skull
lumbar vertebrae
pelvis
femur

69
Q

What are the phases of Paget’s disease?

A

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
Q

Clinical features of Paget’s disease

A

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
Q

Investigation on Paget’s disease

A
  • X-ray – check lytic lesion & thickened bone cortex
  • Bone biopsy – excludes malignancies
  • Blood test  INCREASE Alkaline Phosphatase; normal calcium; normal phosphate
72
Q

treatment of Paget’s disease

A

Bisphosphonates
pain reliever
surgery

73
Q

What is an alternative drug used if bisphosphonates is not available in Paget’s disease?

A

calcitonin

74
Q

What are the cells that demineralise the bones?

A

Osteoclast

75
Q

What is the cell that forms new bone?

A

osteoblast

76
Q

What are the mechanisms of bone remodelling?

A
  • 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
Q

What is Gian cell arteritis (GCA)

A

aka temporal arteritis

type of systemic vasculitis that’s affecting the medium and large arteries

78
Q

Which alternative disease is GCS strongly associate with?

A

Polymyalgia rheumatica

79
Q

what is a key complication of GCA and what group of people are commonly affected?

A

complication
- vision loss
- stroke
- weight gain, diabetes & osteoporosis

common in older white patients

80
Q

Presentation of Giant Cell arteritis

A

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
Q

What investigation will be used to diagnose Giant Cell Arteritis?

A

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
Q

First line treatment for GCA?

A

40-60mg prednisolone daily with no visual symptoms / jaw claudication
500mg-100mg methylprednisolone daily with visual symptoms / jaw claudication

83
Q

What other medication can be used to treat GCA after first-line treatment?

A

Aspirin - 75mg decreases vision loss and strokes
proton pump inhibitor - omeprazole
bisphosphonates and calcium and vitamin D - bone protection while on steroids