MSK/Rheumatology Flashcards

(119 cards)

1
Q

Define crystal arthropathies and name 2

A

Gout and Psuedogout

Describes acute intermittent episodes of joint inflammation caused by accumulation of urate crystals within synovial joints.

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2
Q

What type of crystals are found in gout and describe their structure and appearance (3)

A

Monosodium Urate Crystals

Needle-shaped

Negatively Bifringent under polarized light

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3
Q

What type of crystals are found in pseudogout and describe their structure and appearance (3)

A

Calcium pyrophosphate crystals

Small rhomboid brick shaped

Positively bifringent under polarized light.

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4
Q

Where does gout most commonly affect? (2)

A

1st metatarsophalangeal joint (big toe = podagra)

Osteoarthritic joints (ankle, foot, hand, wrist, elbow or knee)

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5
Q

What is the principle driver of gout?

A

Hyperuricaemia (high uric acid levels)

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6
Q

Describe the pathophysiology of gout (3)

A

Purines > Hypoxanthine > Xanthine > Uric acid

Uric acid precipitates, forming monosodium urate crystals.

Urate crystals trigger acute inflammatory response (recruitment of neutrophils) causing neutrophilic synovitis.

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7
Q

What enzyme catalyses the conversion of xanthine to uric acid?

A

Xanthine oxidase

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8
Q

What foods/drinks contain purines? (3)

A

Fizzy drinks

Alcohol

Red meats

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9
Q

Name 1 xanthine oxidase inhibitor

A

Allopurinol

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10
Q

Where is uric acid predominantly excreted from?

A

Kidneys

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11
Q

Give 5 risk factors for gout that result from reduced urate excretion

A

Elderly

Male

Impaired renal function

Post-menopausal women

Drugs (Aspirin, Indapamide, Tacrolimus, Pyrazinamide)

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12
Q

What drug is it important to stop in patients with hypertension presenting with gout? What should be given instead?

A

STOP Diuretics (indapamide)

Switch to ARB (losartan) as promotes uric acid excretion

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13
Q

Name 4 drugs associated with gout

A

Aspirin (high dose)

Indapamide (diuretic)

Tacrolimus (for severe eczema)

Pyrazinamide (TB)

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14
Q

Give 4 clinical features of gout

A

Acute monoarthritis (rapid onset - severe pain - big toe)

Urate deposits (tophi in pinna, tendons or extensor surfaces)

Joint stiffness, swelling, effusion

Renal disease (hyperuricaemia > CDK = radiolucent stones/interstitial nephritis)

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15
Q

Give 4 differentials for gout

A

Septic arthritis (consider in any monoarthropathy)

Pseudogout

Reactive arthritis

Haemarthrosis (bleeding into joints - haemophilia)

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16
Q

What investigation is used to definitively diagnose gout?

A

Joint aspiration (arthrocentesis) with synovial fluid analysis.

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17
Q

What additional investigations is it important to conduct when investigating ? gout(4)

A

Synovial Fluid Culture - To exclude septic arthritis

WBC - High neutrophils

Serum urate - Raised

X-ray (shows punched out erosions in juxta-articular bone and joint space narrowing)

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18
Q

What drugs can be used to manage acute gout? (4)

A

NSAIDs - Naproxen/Ibuprofen (contraindicated in CKD)

Corticosteroids - Prednisolone

Colchicine

IL-1 inhibitors - Anakinra or Canakinumab

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19
Q

What drugs are used to treat recurrent episodes of gout? (2-3 weeks post acute episode) (3)

A

Allopurinol (xanthine oxidase inhibitor)

Probenecid (inhibits uric acid reabsorption = increased uric acid excfretion in urine)

Rasburicase (recombinant urate oxidase)

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20
Q

Give 3 side effects of Colchicine

A

Diarrhoea

Nausea

Abdominal pain

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21
Q

What dietary change can help reduce the risk of developing gout in the future?

A

Switching to a high dairy diet

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22
Q

Define pseudogout

A

Crystal arthropathy characterised by the deposition of calcium pyrophosphate crystals within joints.

Can be acute or chronic

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23
Q

How may acute pseudogout present?(2)

A

Presents with acute monoarthropathy (usually of larger joints in the elderly).

Usually occurs spontaneously and can be provoked by illness, trauma or surgery.

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24
Q

How may chronic pseudogout present?

A

Presents as an inflammatory RA-like (symmetrical) polyarthritis and synovitis (>5 joints)

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25
What triad of pathology is typically seen in osteoarthritis?
Cartilage erosion and thickening of subchondral bone Disordered bone repair (formation of osteophytes) Synovial inflammation
26
Define osteoarthritis
Describes a degenerative joint disorder characterised by the progressive loss of hyaline cartilage, particularly of synovial joints.
27
Give 5 risk factors for pseudogout
Hyperparathyroidism Haemochromatosis Hypothyroidism Age Hypophosphataemia (may be 2nd to hyperparathyroidism)
28
Describe the clinical presentation of pseudogout
Osteoarthritis/RA live involvement of joints (wrists, shoulders, knee ect) Symptoms of gout (swelling, effusion, pain ect)
29
What may be seen on an x-ray of a patient with pseudogout?
Chondrocalcinosis (soft tissue Ca deposits)
30
Other than joint aspiration (atherocentesis) what additional investigations are important to conduct in a patient with pseudogout? (2)
Serum calcium levels (to exclude hyperparathyroidism - low) Serum parathyroid hormone (to exclude hyperparathyroidism - low)
31
How does osteoarthritis typically present (4)
Joint pain, Stiffness, Deformity and loss off function.
32
Where anatomically is the most common presentation of osteoarthritis?
OA of the knee
33
What cells produce cartilage? And from what substance makes cartilage resistant to compression?
Chondrocytes Chondroitin sulfate
34
Name 3 types of cartilage and give examples of where they are found.
Hyaline cartilage (most widespread types - articular surfaces of long bones, rib tips, rings of trachea) Fibrous cartilage (pubic symphysis, intervertebral discs, menisci) Elastic cartilage (Epiglottis and pinnae of ear)
35
What are the main components of fibrous cartilage?
Type I and Type II collagen
36
What are the main components of elastic cartilage?
Elastin and Type II collagen
37
What type of cartilage is found in the pubic symphysis, intervertebral discs and menisci?
Fibrous cartilage
38
What type of cartilage is the most widespread cartilage found on the articular surfaces of long bones, rib tips and rings of the trachea?
Hyaline cartilage
39
What ultimately drives the progression of osteoarthritis? name 3 factors that influence this.
Reduced formation and increased breakdown of articular hyaline cartilage; Metalloproteinase over production (enzymes catalyse collagen) Production of IL-1 and TNF-a (stimulates chondrocytes to produce metalloproteinases) Production of NO (NO activates metalloproteinases)
40
Give 3 clinical features of osteoarthritis
Pain (Worse with prolonged activity) Joint stiffness (<30mins morning stiffness - improves through the day) Bouchard's (PIP) and Heberden's (DIP) Nodes
41
What is the primary investigation for osteoarthritis? What would it likely show?
X-Ray of affected joint LOSS; - Loss of joint space (joint space narrowing) - Osteophyte formation - Subchondral sclerosis - Subchondral cysts
42
What blood tests would be conducted when investigating osteoarthritis? (4)
CRP (Normal) ESR (Normal) Rheumatoid Factor (Negative) Anti-CCP (Negative)
43
What investigation can be used to assess osteoarthritic damage to the knee?
Arthroscopy
44
How is osteoarthritis managed? (3)
Exercise (improve muscle strength) (weight loss if overweight) Patient Education Analgesia (Oral/Topical)
45
Describe the 1th to 4th line analgesic treatments for osteoarthritis (5)
1st - Topical analgesia (Diclofenac/Ibuprofen gel/Capsaicin) 2nd - Paracetamol + Topical Analgesia 3rd - NSAID + Paracetamol + Topical Analgesia 4th - Opioid (codeine) + Paracetamol + Topical Analgesia Adjunct - Intra-articular steroid injections (Methylprednisolone acetate)
46
Describe 3 surgical methods of treating osteoarthritis
Arthroscopy Osteotomy (removing bone) Arthroplasty (joint replacement)
47
Give 3 indications for conducting an arthroplasty in a case of osteoarthritis
Uncontrolled pain (particularly at night) Significant limitation of function Patient age
48
Define Rheumatoid Arthritis and describe how it is characterised.
Describes a chronic systemic inflammatory disease primarily affecting synovial joints of the hands and feet. Characterised by symmetrical, deforming peripheral polyarthritis (>5 joints).
49
What is Rheumatoid Arthritis associated with and why?
An increased risk of cardiovascular and cerebrovascular disease as atherosclerosis is accelerated
50
Give 3 risk factors for rheumatoid arthritis
Smoking Genetics - HLA-DR1/DR4 Female
51
What is the main driver of rheumatoid arthritis? What factors drive this? (3)
Synovial inflammation (synovitis) Driven by; TNF, IL-1 and IL-6
52
What 4 processes occur during the development of Rheumatoid Arthritis?
Recruitment of inflammatory Cells (T-cells, B-cells, Macrophages) Synovial Hyperplasia Increased angiogenesis Joint effusion (swelling from excess synovial fluid)
53
What joints are primarily affected in Rheumatoid Arthritis? How does this differ to Osteoarthritis?
RA = MCP and PIP Joints of the hands and feet OA = PIP and DIP joints (not MCP)
54
Give 3 clinical features of rheumatoid arthritis
Symmetrical Arthritic of MCP and POP joints lasting >6 weeks Pain/stiffness worse in the morning (relieved with exercise) Systemic illness (fatigue, weightloss, carpal tunnel syndrome)
55
Give 5 systemic, extra articular symptoms of rheumatoid arthritis
Carpal Tunnel Syndrome/Frozen Shoulder/Quervains tenosynovitis Fatigue/Weight loss Heart - Pericarditis/Pericardial effusion Eyes - Sceleritis/Uveitis Lungs - Pleural effusions/Fibrosing alveolitis
56
Name and describe 1 rare complication of rheumatoid arthritis
Felty's syndrome SANTA; - Splenomegaly - Anaemia - Neutropenia - Thrombocytopenia - Arthritis (rheumatoid)
57
What clinical signs may be seen in rheumatoid arthritis? (4)
Boutonniere's/Swan Neck Deformities Ulnar deviation and subluxation Raynauds Signs of inflammation (hot, red, swelling, pain, loss of function)
58
What blood tests may be ordered to investigate rheumatoid arthritis?
ESR/CRP (Raised) Rheumatoid Factor (Positive) Anti-CCP (Positive - Useful if RF is negative)
59
What imaging investigation is useful to use to investigate rheumatoid arthritis? What may it show?
X-ray Shows periarticular erosions at joint margins. May later progress to joint space narrowing.
60
Describe the management of rheumatoid arthritis
1st line; DMARDs - Methotrexate/Sulfasalazine (Pregnancy) Analgesia - NSAIDs/Aspirin Corticosteroids - Prednisolone 2nd line Anti-TNF medications - Infliximab (if unresponsive to DMARD) 3rd line Rituximab (If unresponsive to Anti-TNF)
61
Give 4 possible side effects of methotrexate
Hepatotoxicity Anaemia (Macrocytic) Pulmonary fibrosis Pancytopenia
62
Describe spondyloarthropathies
A group of chronic inflammatory conditions affecting the spine and peripheral joints
63
Spondyloarthropathies are associated with what allele?
HLA-B27
64
Name 4 types of seronegative spondyloarthropathies
Ankylosing spondylitis Psoriatic arthritis Reactive arthritis Enteric arthropathy
65
What common clinical features are seen in seronegative spondyloarthropathies? (SPINEACHE)
S - Sausage Digit (Dactylitis) P - Psoriasis I - Inflammatory back pain N - NSAID good response E - Enthesitis (achilies tendon, costochondritis) A - Arthritis (axial - spine/sacroiliac joints) C - Crohn's /Colitis/Raised CRP H - HLA-B27 E - Eye (Uveitis)
66
How do spondyloarthropathies tend to present? (3)
Asymmetrical Large joint oligoarthritis (<5 joints) or monoarthritis Seronegative (RF negative)
67
Define ankylosing spondylitis
Chronic inflammatory disease characterized by stiffening and inflammation of the spine and sacroiliac joints
68
How does ankylosing spondylitis differ to rheumatoid arthritis?
In contrast to RA, where inflammation and erosion are the only pathological processes present, AS also involves subsequent repair (ossification). Inflammation in AS patients is dominated by inflammatory cells and an increased number of osteoclasts.
69
Give 3 epidemiological features of ankylosing spondylitis
More common in men Early presentation (late teens/early 20s) Gradual onset lower back pain
70
Describe the typical presentation of ankylosing spondylitis. (5)
Typical presentation is a man <30 yrs with gradual onset of lower back pain, worse in the morning relieved with exercise. Asymmetrical involvement Morning stiffness/pain relieved by exercise Iritisis/uveitis Enthesitis Kyphosis/Lumbar lordosis
71
What may an pelvic x-ray show in a patient with ankylosing spondylitis? (3)
Sacroiliitis (erosions, irregularities, sclerosis) Syndesmophytes (bony proliferations) Bamboo spine (fusion of spinal joints)
72
How is ankylosing spondylitis managed? (5)
Exercise Analgesia - NSAIDs/Paracetamol Intra-articular corticosteroid injections - Hydrocortisone (if peripheral joint involvement) DMARDs - Sulfasalazine/Methotrexate Surgery (hip replacement)
73
Describe psoriatic arthritis
Describes an chronic inflammatory joint disease associated with psoriasis.
74
What joint is commonly affected in psoriatic arthritis?
Distal Interphalangeal Joint (DIP)
75
What deformities may be seen on an x-ray of a patient with psoriatic arthritis? (3)
Pencil cup deformity (Erosion of DIP joint) Fluffy periostitis (peri-articular new bone formation) Osteolysis
76
Give 4 clinical features of psoriatic arthritis
Psoriatic skin symptoms (Psoriasic plaques on scalp/legs, onycholysis - detachment of nail from nail bed) Prolonged morning stiffness/pain (>30 mins) that improves with use DIP joint involvement Dactylitis
77
Describe reactive arthritis
Reactive arthritis describes an inflammatory arthritis that occurs after exposure to certain gastrointestinal (dysentery) or genitourinary infections (urethritis).
78
Give 3 gastro-intestinal causes of reactive arthritis
Salmonella Shigella Yersinia enterocolitica
79
Give 1 genitourinary cause of reactive arthritis
Chlamydia
80
Describe Systemic Lupus Erythematosus
Describes a multisystemic autoimmune disease characterized by the generation of antibodies against autoantigens (such as Anti-Nuclear Antibody -ANA) which form immune complexes.
81
What type of hypersensitivity reaction is SLE? and why?
Type 3 hypersensitivity reaction Forms immune complexes
82
Give 3 epidemiological factors of SLE
Female Afro-caribbean/asian Genetics - HLA-B8, DR2 and DR3/Compliment deficiency (C3/C4)
83
Give 5 clinical features of SLE
Malar rash (butterfly rash) Photosensitive rash (after sunlight exposure) Discoid rash (keratotic rash - chronic SLE) Arthralgia/arthritis (presents similar to RA) Organ specific features (kidney, eyes, CS, GI, Heart)
84
What immunological tests should be performed when investigating SLE? (4)
ANA (Most sensitive - useful rule out test) dsDNA antibody (Most specific) Anti-Smith Low Cs and C4
85
Give 3 additional tests (non-immunological) to perform when investigating SLE
ESR/CRP (ESR elevated due to systemic inflammation, CRP normal as condition is chronic) Urinalysis (Assess renal involvement) Coombs test (order if pt has features of anaemia)
86
Describe the management of SLE (3)
Analgesia - NSAIDs Suncream Hydroxychloroquine
87
Give 2 potential musculoskeletal features of SLE
Arthralgia Non-erosive arthritis
88
Give 2 potential cardiovascular features of SLE
Pericarditis (most common cardiac symptom) Myocarditis
89
Give 2 potential respiratory features of SLE
Pleurisy Fibrosing alveolitis
90
Give 2 potential renal features of SLE
Proteinuria Glomerulonephritis (diffuse proliferative glomerulonephritis is most common)
91
How is diffuse proliferative glomerulonephritis (caused by SLE) treated? (2)
Treat hypertension Glucocorticoids (prednisolone) with Mycophenolate/Cyclophosphamide
92
Give 2 potential neuropsychiatric features of SLE
Anxiety/Depression Seizures
93
Describe osteoporosis
Osteoporosis is a systemic skeletal disease characterized by low bone mass and structural deterioration in bone microarchitecture. Making bones more susceptible to fracture
94
What is a fragility fracture?
Describes an osteoporotic fracture that occurs as a result of increased bone fragility due to osteoporosis. Typically occurring from the patient falling from a standing height or less.
95
Name 3 common sites for fragility fractures to occur
Wrist, Hip, Spine
96
What cell type drives bone resorption?
Osteoclasts
97
What cell type drives bone formation?
Osteoblasts
98
How does osteoporosis occur?
Occurs as a consequence of imbalances in bone resorption (osteoclasts) and bone formation (osteoblasts), in which bone resorption is favoured, resulting in a net loss of bone density.
99
Name 3 biochemical factors involved in regulating bone remodelling
Parathyroid hormone (increases blood Ca levels by promoting bone resportion) 1,25 dihydroxy vitamin D (Calcitriol) (increases blood Ca levels by promoting bone resorption and renal phosphate resorption) Calcitonin (opposes PTH) (Acts to decrease blood calcium levels by inhibiting bone resorption)
100
Give risk factors for osteoporosis (SHATTERED)
S - Steroid use (>5mg/d prednisolone) H - Hyperthyroidism, hyperparathyroidism, hypercalciuria A -Alcohol and smoking T - Thin (<18.5 BMI) T - Testosterone reduction E - Early Menopause R - Renal or Liver failure (Chronic Kidney Disease associated w/ tertiary hyperparathyroidism) E -Erosive/inflammatory bone disease (myeloma/RA) D - Dietary (reduced calcium intake, malabsorption, diabetes mellitus type 1)
101
What is the gold standard investigation for osteoporosis?
DEXA bone densitometry (T-score <-2.5 = osteoporosis)
102
What assessment tool is used in osteoporosis? What does it estimate?
FRAX (Fracture risk assessment tool) Estimates 10yr risk of osteoporotic fracture in untreated patients
103
FRAX should be conducted in ALL patients before a DEXA except for? (3)
>50 with hx of fragility fractures <40 with major risk factor for fragility fractors With vertebral or hip fractures
104
What metabolite tests would be useful to perform on a patient with osteoporosis?
Calcium (hypocalcemia) Phosphate (low - osteomalacia) PTH Vitamin D TFTs
105
Describe how T-scores used in a DEXA scan are used to assess severity (4)
>-1.0 = Normal -1.0 to -2.5 = Osteopenia < -2.5 = Osteoporosis < -2.5 + fracture = Severe osteoporosis
106
What does a T score of <-2.5 mean?
This means that the patient’s bone density is >2.5 standard deviations below the young adult mean value
107
What does a Z-score compare your bone density to?
to the average values for a person of the same; age, gender and ethnicity.
108
Give 4 pieces of general management advice for managing osteoporosis
Reduce smoking and alcohol intake Increase dietary intake of calcium and phosphate (dairy) Encourage weight bearing or balancing exercises (Tai Chi) Home based fall prevention
109
Give 3 pharmacological managements for osteoporosis
1st line - Alendronic Acid (bisphosphonates) Calcium + Vitamin D supplementation Strontium Ranelate (stimulates bone formation)
110
Give 4 drugs used in the secondary prevention of osteoporosis
Raloxifene (Selective oestrogen receptor modulator) Teriparatide (PTH analogue) Denosumab (RANK Ligand MAB) HRT (Oestrogen)
111
How is osteomalacia characterised?
Osteomalacia is characterised by a normal amount of bone but it has a decreased mineral content (as there is excess unmineralized osteoid and cartilage).
112
What is the difference between rickets and osteomalacia?
Rickets occurs DURING the period of bone growth (before fusion of the epiphysis),this can result in growth retardation and skeletal deformities. Osteomalacia is when this occurs AFTER fusion of the epiphysis.
113
What is the primary cause of osteomalacia?
Vitamin D deficiency
114
Give 4 causes of vitamin D deficiency
Sub-optimal exposure to UV-B (biggest factor) Insufficient dietary intake Insufficient absorption of vitamin D in the smal intestine Liver/Renal failure
115
What is the primary role of vitamin D and how does it achieve this? (3)
Primary role is to maintain blood calcium and phosphate levels. Does this by; Promoting calcium reabsorption in the distal tubule. Promoting intestinal (duodenal) calcium and phosphate absorption. Stimulating osteoclast activity (stimulates bone reabsorption)
116
Give 3 clinical features of osteomalacia
Bone pain Proximal muscle weakness (myopathy) and tenderness Malabsorption syndromes (coeliac, chronic alcoholism, chronic pancreatitis)
117
Give 4 clinical features of Rickets (children)
Bone pain Growth retardation Developmental delay Bony deformities (pigeon chest, bowed legs)
118
What metabolite levels would be seen in the blood of a patient with osteomalacia? (3)
Low calcium Low Vitamin D Low Phosphate
119
How is osteomalacia treated? (2)
Calcium carbonate/citrate Ergocalciferol (Vitamin D)