MSK Flashcards

1
Q

What is the function of type A and type B cells in the sunovium?

A

Type A clear debris

Type B produce synovial fluid components

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2
Q

Describe osteoarthritis

A

Progressive loss of articular cartilage

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3
Q

Give the components of the extracellular matrix of a chondrocyte

A

Type II collagen

Proteoglycans

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4
Q

Give 6 risk factors for osteoarthritis

A
Age
Inflammation
Joint injury
Mechanical stress and obesity 
Neurologic disorders
Genetics
Medications
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5
Q

How can articular damage to the chondrocytes cause a loss of elasticity and an inflammatory response?

A

Loss of polteoglycans and increase in type I collagen leads to loss of elasticity
Chondrocytes can undergo apoptosis and flake off into the synovial space
Type A cells bring in macrophages and lymphocytes which produce pro-inflammatory cytokines, causing synovitis

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6
Q

Give 3 bone changes as a result of osteoarthritis

A

Fibrillations: cracks on articular surface
Bone-bone contact: eburnation (looks like polished ivory)
Osteophytes: bone grows outwards, joints look wider

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7
Q

Where are Heberden nodes found?

A

Distal interphalangeal joints

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8
Q

Where are Bouchard nodes found?

A

Proximal interphalangeal joints

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9
Q

Describe the pattern of pain and stiffness in osteoarthritis

A

Stiffness: less than an hour in the morning, worsens at the end of the day
Pain: sharp ache/ burning, worse with activity

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10
Q

How would you treat osteoarthritis?

A
Losing weight
Exercise
Physical therapy
Pharmacological: reduce pain/ inflammation
Hyaluronic acid injections
Surgery
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11
Q

Which human leukocyte antigens are genetic risk factors for rheumatoid arthritis?

A

HLA-DR1 and HLA-DR4

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12
Q

What is the role of environmental factors in rheumatoid arthritis?

A

Cigarette smoke/ pathogens can modify our own antigens

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13
Q

Give 3 proteins which can be modified through citrullination in rheumatoid arthritis

A

IgG antibodies
Type II collagen
Vimentin

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14
Q

What is the result of citrullination in rheumatoid arthritis?

A

Antigens are no longer recognised by immune cells and are taken to a lymph node and presented to CD4+ helper cells which present to B cells which proliferate and differentiate into plasma cells producing autoantibodies

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15
Q

What is a panus?

A

Thick, swollen synovial membrane with granulation tissue containing fibroblasts, myofibroblasts and inflammatory cells

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16
Q

Over time, what damage can the panus cause?

A

Damages other soft tissue, cartilage and can erode bone

Activated synovial cells release proteases which break down cartilage so exposed bone can rub against each other

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17
Q

What effect can inflammatory cytokines have on T-cels presenting RANK-L in rheumatoid arthritis?

A

T-cells present RANK L which binds to RANK on osteoclasts which are activated to break down bone

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18
Q

Give 2 antibodies produced in rheumatoid arthritis and state what they bind to

A
Rheumatoid factor (IgM) binds to Fc of altered IgG
Anti-CCP binds to citrullinated proteins and forms immune complexes which activate the compliment system and cause inflammation
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19
Q

What is the result of immune complexes depositing in:
The brain
Skin nodules
Blood vessels

A

Brain: IL-1 or 6 causes pyrogens (fever)
Skin nodules: filled with macrophages and lymphocytes + with central necrosis
Blood vessels: Inflammation, so prone to atheromatous plaques

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20
Q

What is the result of immune complexes depositing in:
The lungs
Skeletal muscle
Liver

A

Lungs: pleural cavities fill with fluid: pleural effusion
fibroblasts form scar tissue in the interstitium
Skeletal muscle: Protein breakdown
Liver: Increased hepcidin, decreases iron by inhibiting absorption and trapping iron in macrophages/ liver cells

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21
Q

How many joints are typically affected in rheumatoid arthritis?

A

> 5

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22
Q

It there a symmetrical or asymmetrical pattern of join inflammation in rheumatoid arthritis?

A

Symmetrical

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23
Q

Which joints are commonly affected in rheumatoid arthritis?

A

MCP, PIP, MTP

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24
Q

Give 4 symptoms of rheumatoid flares

A

Swollen
Warm
Red
Painful

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25
Describe the 3 specific deformities found with rheumatoid arthritis
Ulnar deviation Boutonniere deformity: PIP flexion, DIP hyper-extension Swan neck: PIP hyper-extension, DIP flexion
26
How can a Baker (popliteal) cyst form as a result of rheumatoid arthritis?
One way valve forms in the knee joint, causing fluid to fill the semi-membranous bursa Synovial sack can bulge posteriorly into the popliteal fossa
27
Give 4 extra-articular symptoms of rheumatoid arthritis
Fever Low appetite Malaise Weakness
28
Give the 3 conditions that make up Felty syndrome
Rheumatoid arthritis Splenomegaly Granulocytopoenia
29
How would you diagnose rheumatoid arthritis?
Blood tests: Rheumatic factor and anti-citrullinated peptide antibody (anti-CCP) X-Ray: loss of bone density, bony erosions, soft tissue swelling, narrowing of joint space
30
How would you treat rheumatoid arthritis?
Disease modifying anti-rheumatic drugs (DMARDs): Methotrexate Hydroxychloroquine Sulfasalazine Biologic response modifiers: Abatacept (suppress T cells) Rituximab (suppress B cells)
31
Describe gout
Monosodium urate crystals deposit in the joints which then become red, hot, swollen and tender
32
What is the cause of gout?
Hyperuricemia
33
What are purines and what are they converted to in the body?
N-containing, key components of DNA and RNA, covered to uric acid which has limited solubility in body fluid
34
What happens when uric acid levels are greater than 6.8mg/dL
Urate ion binds to sodium and forms monosodium urate crystals
35
Give 3 generic causes of monosodium rate crystal formation
Increased purine consumption Decreased clearance of uric acid Increased production of purines
36
Give 4 foods which are high in purines
Shellfish Anchovies Red meat Organ meat
37
What may cause a decrease in clearance of uric acid?
Dehydration
38
What may cause an increase in the production of purines?
High-fructose corn syrup beverages
39
Give 6 risk factors of gout
``` Obesity Diabetes Chemo Genetic predisposition CKD Meds: thiazide diuretics and aspirin ```
40
What is the most commonly affected joint with gout?
First metatarsal joint of the big toe: podogra
41
What is the cause of inflammation in gout?
Leukocyte migration to site in order to eliminate uric acid
42
How would you treat gout?
``` Decrease pain and swelling: NSAIDs, corticosteroids and colchicine (inhibits WBC migration) Treat underlying cause: Diet modification Decrease uric acid levels: Xanthine oxidase inhibitors: Allopurinol ```
43
What causes chronic gout and what are the risks with this?
``` Repeated gouty attacks Risk of: Arthritis Tissue destruction Kidney stones and urate neuropathy Tophi (permanent nodules) ```
44
Describe pseudogout
Calcium pyrophosphate deposition
45
Describe the pattern of acute pseudogout
Monoarthropathy of larger joints in the elderly
46
Describe the pattern of chronic pseudogout
Inflammatory, symmetrical polyarthritis and synovitis
47
Give 3 potential causes of acute pseudogout
Illness Surgery Trauma
48
Give 4 risk factors of pseudogout
Old age Hyperparathyroidism Haemochromatosis Hypophosphataemia
49
How would you diagnose pseudogout?
Polarised light microscopy of synovial fluid | X-Ray: soft tissue calcium deposition
50
How would you manage pseudogout?
Acute: cool packs, rest, aspiration, intra-articular steroids Prophylaxis: NSAIDs and colchicine Chronic: Methotrexate and hydrochloroquine
51
Describe osteoporosis
Age-related disorder causing gradual loss of bone density and strength
52
Give 5 modifiable risk factors for osteoporosis
``` Excess alcohol Vitamin D deficiency Smoking Malnutrition Underweight Heavy metals PPIs ```
53
Give 5 non-modifiable risk factors for osteoporosis
``` Female Age Menopause Ethnicity FHx Build ```
54
How would you diagnose osteoporosis?
X-Ray: cortical thinning, increased radiolucency, fractures Dual-energy x-ray (DEXA) Bone mineral density compared to that of a healthy (30-40y/o) adult population Normal: > -1.0 Osteopenia -2.5< T score < -1.0 Osteoporosis:
55
How would you treat osteoporosis?
Weight-bearing/ resistance exercises Fall prevention Medications: bisphosphonates
56
Which human leukocyte antigen is associated with spondyloarthropathies?
HLA B27 (class I surface antigen)
57
What does SPINE ACHE stand for, in relation to spondyloarthropathies?
``` Sausage digits (dactylitis) Psoriasis Inflammatory back pain NSAIDs good response Enthesis ``` Arthritis Chrons/ colitis HLA B27 Eye (uveitis)
58
Describe ankylosing spondylitis
Inflammatory arthritis of the spine and rib cage, eventually leading to new bone formation and fusion of the joints
59
Give 5 factors which reflect a poor prognosis in ankylosing spondylitis
``` Male Smokers B27 +ve Syndesmophytes at presentation High CRP ```
60
Describe the signs and symptoms of ankylosing spondylitis
Gradual onset of lower back pain (worse at night) Pain radiates to hip/ buttocks from the scaro-illiac joints Spinal morning stiffness Progressive loss of spinal movement
61
How would you manage ankylosing spondylitis?
``` Hip replacement Exercise NSAIDs TNF-alpha blockers Local steroid injections ```
62
Give the 5 types of psoriatic arthritis
``` Symmetrical polyarthritis DIP joints Spinal Asymmetrical oligoarthritis Psoriatic arthritis mutilans ```
63
What percentage of psoriasis cases also have psoriatic arthritis?
10-40%
64
What X-Ray changes would you see with psoriatic arthritis?
Erosive X-Ray changes "pencil in cup" appearance
65
How would you manage psoriatic arthritis?
NSAIDs, sulfasalazine, methotrexate | Anti-TNF
66
Describe reactive arthritis
Sterile inflammation of the synovial membrane, tendons and fascia, triggered by an infection at a distal site
67
Give 3 gut-associated causes of reactive arthritis
Salmonella Shigella Yersinia
68
Give 2 STIs which can cause reactive arthritis
Chlamydia | Ureaplasma urealyticum
69
Give 6 signs and symptoms of reactive arthritis
Arthritis Conjunctivitis Sterile urethritis Circinate balanitis (painless penile ulceration) Iritis Keratoderma blenorrhagica (brown plaques on soles and palms)
70
How would you diagnose reactive arthritis?
High ESR, high CRP Aspirate joint to exclude infection/ crystals Urethral swab/ stool culture
71
How would you treat reactive arthritis?
Steroids (local injections) NSAIDs If symptoms >6moths: consider sulfasalazine/ methotrexate
72
What is the typical clinical presentation of septic arthritis?
Fever Inflammation (warmth, red, effusion, pain) Loss of function and range of movement
73
Give 3 causes of septic arthritis
Staphylococcus aureus Group A streptococcus Neisseriae Gonorrhoea
74
How might an infection be introduced into the synovium, causing septic arthritis?
URTI, LRTI, STI travels in blood Osteomyelitis Directly through procedures/ surgery Skin infection
75
How would you diagnose septic arthritis?
``` FBC, CRP, ESR Joint aspiration with a microscopy culture sensitivity Blood cultures Electrolyte, urea, creatitnine US/X-Ray (joint space widening) ```
76
How would you treat septic arthritis?
``` Joint drainage: needle aspiration Broad spectrum IV Abx Once cultures come back: specific Abx IV: 2 weeks Oral: 4 weeks ```
77
How can osteomyelitis occur and what does it cause?
Bacterial infection of the bone, causing bone cell necrosis, pus formation and weak bones
78
What type of bone does osteomyelitis usually affect?
Long bones
79
Give 4 risk factors of osteomyelitis
Diabetes IVDU Prior splenectomy Trauma
80
Give 4 symptoms of osteomyelitis
Pain Redness Fever Weakness
81
How would you diagnose osteomyelitis?
FBC (Inflammation/ infection) | MRI
82
How would you treat osteomyelitis?
Prolonged antibiotic treatment | PICC line/ central venous catheter for long-term IV abx
83
In SLE, what is the role of susceptibility genes?
It is more likely for immune cells to attack nuclear antigens They cause less effective clearance of apoptotic bodies, leading to a buildup of nuclear antigens
84
What is the consequence of a buildup of nuclear antigens in SLE?
They form antigen-antibody complexes with antinuclear antibodies
85
Where do antigen-antibody complexes deposit in SLE and what is the result of this?
Kidneys, skin, joints, heart Type III hypersensitivity reaction Cause a local inflammatory response, activating the complement system and an enzyme cascade, leaving cells with free channels so it bursts and dies
86
Give 5 tigers/ risk factors for SLE
``` Smoking Viruses Bacteria Sex hormones (oestrogen) Medications: Isoniazid Hydralazine Procainamide ```
87
Describe the type II hypersensitivity reaction in SLE
Antinuclear antibodies bind to RBCs, WBCs and phospholipids, marking them for phagocytosis and destruction
88
How many of the criteria must the patient meet to be diagnosed with SLE?
>4
89
Give the 11 criteria for SLE
1: Malar (butterfly) rash 2: Discoid rash 3: Photosensitivity 4: Ulcers 5: Serositis 6: Arthritis 7: Renal disorders 8: Neurologic disorders 9: Haematologic disorders 10: Antinuclear antibodies 11: Other autoantibody
90
How would you prevent/ limit severity of SLE flare ups?
Avoid sunlight Corticosteroids Immunosuppressants
91
Describe an osteoid osteoma
Benign, bone-forming lesion in young patients causing localised pain
92
How would you diagnose and manage an osteoid osteoma?
CT/ X-Ray | NSAIDs, radiofrequency ablation
93
Describe an osteoblastoma
Bone producing tumour, causing pain
94
What would an X-Ray of an osteoblastoma show?
Bone destruction, surrounded by reactive new bone
95
Describe an osteochondroma
Metaphyseal lesion, covered by cartilage cap, grows away from growth plate- stops after puberty (painless lump)
96
Describe an osteosarcoma
spindle cell neoplasms that produce osteoid
97
Which mutation is associated with an osteosarcoma?
P53
98
Why does osteosarcoma have a poor prognosis?
Aggressive local growth Rapid haematological spread Poor response to chemo
99
Describe a Ewings sarcoma
Small round cell tumour that arises from neural crest cells characterised by a translocation mutation t(11;22)
100
What is the name of the neurotransmitter released by the cell body of an axon in response to nociceptor stimulation?
Substance P
101
Give the neurotransmitters released by the inhibitory neuron
Serotonin | Norepinephrine
102
What is the role of nearby epithelial cells in fibromyalgia?
They release nerve growth factor which attracts mast cells which release more nerve growth factors This increases the growth and sensitivity of nociceptors, and therefore substance P
103
Give 3 causes of fibromyalgia
Low levels of serotonin High levels of substance P High levels of nerve growth factor
104
Give the 3 factors taken into account for the diagnosis of fibromyalgia
Pain location Symptom severity score (fatigue, poor sleep, headache) Duration
105
How would you treat fibromyalgia?
Exercise Relaxation techniques Meds: Amitriptyline Serotonin-Norepinephrine reuptake inhibitors (SNRIs) Anticonvulsants: pregabalin and gabapentin
106
Describe the character of mechanical back pain
Better/ worse depending on position Typically worse when moving May be due to minor injury (sprain or strain) Can be associated with stress
107
Give 5 symptoms of prolapsed/ herniated disc
``` Lower back pain Numbness/ tingling Neck pain Problems straightening your back Muscle weakness ```
108
Describe spondylolisthesis
A bone in the spine slips out of position
109
Give 5 symptoms of spondylolisthesis
``` Lower back pain: worse with activity/ standing Sciatica Tight hamstring muscles Stiffness/ back tenderness Kyphosis ```
110
Give 5 causes of mechanical back pain
``` Birth defect Repetitive spinal trauma Vertebral joints becoming worn and arthritic Sudden trauma/ spinal injury Bone abnormality ```
111
How would you treat mechanical back pain?
``` Rest NSAIDs Physio Corticosteroid injections Surgery ```
112
How does the parathyroid gland respond to low calcium?
Releases parathyroid hormone which causes osteoclasts to release HCl leading to bond breakdown and release of phosphate and calcium in the blood
113
Why does ionised calcium level not increase much with increased bone resorption in osteomalacia?
Phosphate and calcium ions bond to form calcium phosphate
114
Give 2 causes of excess loss of phosphate leading to osteomalacia
Primary hyperparathyroidism: excess phosphate lost in urine | Facing syndrome: PCT losing capacity to reabsorb a number of solutes
115
Give 5 causes of phosphate malabsorption in the GI tract leading to osteomalacia
Alcohol Medications (antacids) Not enough in the diet Refeeding syndrome (phosphate moves from blood to cells since insulin draws phosphate into cells) Respiratory alkalosis (increases pH in cell, triggering glycolysis)
116
Give 2 causes of insufficient calcium absorption leading to osteomalacia
Lack of dietary calcium | Resistance to action of vitamin D
117
Give 6 primary causes of osteomalacia
``` Renal tubular acidosis Malnutrition Malabsorption syndrome Chronic kidney failure Oncotic osteomalacia Coeliac disease ```
118
Describe degenerative disc disease
Natural breakdown of an intervertebral disc of the spine due to daily stresses
119
How does degenerative disc disease occur?
Daily stresses cause spinal discs to weaken and lose water as the annulus fibrosis weakens As discs weaken and lose water, they begin to collapse This results in pressure on the spinal nerves
120
Describe the symptoms of degenerative disc disease
Pain in the neck, hips, buttocks/ thighs | Commonly worse on movement
121
How would you diagnose degenerative disc disease?
Physical exam: muscle weakness, tenderness, poor range of motion MRI: degenerative fibrocartilage and clusters of chondrocytes
122
How would you treat degenerative disc disease?
``` Physio Anti-inflammatories: NSAIDs Traction Steroid injection Surgery ```
123
Give 3 general symptoms of vasculitis
Fever Weight loss Fatigue
124
Who is most commonly affected by giant cell arteritis and which artery is affected?
>50 y/o Women > men Affects carotid artery
125
What lab results would you see with giant cell arteritis?
High ESR | Granulomas in tunica intima
126
Which arteries are generally affected with medium vessel vasculitis?
Muscular arteries supplying the organs
127
How would you treat giant cell arteritis or medium vessel vasculitis?
Corticosteroids
128
Give a key complication of giant cell arteritis
Blindness
129
Give an example of medium vessel vasculitis and how it causes damage
Polyarteritis nodosa: | Immune cells attack endothelium and cause damage/ fibrosis, leading to organ ischaemia
130
Describe the mechanism of small vessel vasculitis
B-cells produce anti-neutrophilic cytoplasmic antibodies attack neutrophils in arterioles, capillaries and venuoles
131
Describe Paget's disease
Disrupts normal cycle of bone renewal causing bones to become weakened and possibly deformed
132
Give 4 symptoms of Paget's disease
Travelling shooting pain Numbness and tingling Joint pain, stiffness and swelling Constant dull bone pain
133
How would you treat Paget's disease?
Bisphosphonate medication/ vit D/ calcium supplements Painkillers Physio Surgery
134
Give 6 potential complications of Paget's disease
``` Bone cancer Breaks Enlarged/ misshapen bone Hearing loss Hypercalcaemia Heart problems ```