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Medicine Phase 2A (OWN) > MSK > Flashcards

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
Q

Describe the 3 specific deformities found with rheumatoid arthritis

A

Ulnar deviation
Boutonniere deformity: PIP flexion, DIP hyper-extension
Swan neck: PIP hyper-extension, DIP flexion

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26
Q

How can a Baker (popliteal) cyst form as a result of rheumatoid arthritis?

A

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

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27
Q

Give 4 extra-articular symptoms of rheumatoid arthritis

A

Fever
Low appetite
Malaise
Weakness

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28
Q

Give the 3 conditions that make up Felty syndrome

A

Rheumatoid arthritis
Splenomegaly
Granulocytopoenia

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29
Q

How would you diagnose rheumatoid arthritis?

A

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

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30
Q

How would you treat rheumatoid arthritis?

A

Disease modifying anti-rheumatic drugs (DMARDs):
Methotrexate
Hydroxychloroquine
Sulfasalazine

Biologic response modifiers:
Abatacept (suppress T cells)
Rituximab (suppress B cells)

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31
Q

Describe gout

A

Monosodium urate crystals deposit in the joints which then become red, hot, swollen and tender

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32
Q

What is the cause of gout?

A

Hyperuricemia

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33
Q

What are purines and what are they converted to in the body?

A

N-containing, key components of DNA and RNA, covered to uric acid which has limited solubility in body fluid

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34
Q

What happens when uric acid levels are greater than 6.8mg/dL

A

Urate ion binds to sodium and forms monosodium urate crystals

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35
Q

Give 3 generic causes of monosodium rate crystal formation

A

Increased purine consumption
Decreased clearance of uric acid
Increased production of purines

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36
Q

Give 4 foods which are high in purines

A

Shellfish
Anchovies
Red meat
Organ meat

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37
Q

What may cause a decrease in clearance of uric acid?

A

Dehydration

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38
Q

What may cause an increase in the production of purines?

A

High-fructose corn syrup beverages

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39
Q

Give 6 risk factors of gout

A 
Obesity
Diabetes
Chemo
Genetic predisposition
CKD
Meds: thiazide diuretics and aspirin
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40
Q

What is the most commonly affected joint with gout?

A

First metatarsal joint of the big toe: podogra

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41
Q

What is the cause of inflammation in gout?

A

Leukocyte migration to site in order to eliminate uric acid

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42
Q

How would you treat gout?

A 
Decrease pain and swelling:
NSAIDs, corticosteroids and colchicine (inhibits WBC migration)
Treat underlying cause:
Diet modification
Decrease uric acid levels:
Xanthine oxidase inhibitors:
Allopurinol
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43
Q

What causes chronic gout and what are the risks with this?

A 
Repeated gouty attacks
Risk of:
Arthritis
Tissue destruction
Kidney stones and urate neuropathy
Tophi (permanent nodules)
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44
Q

Describe pseudogout

A

Calcium pyrophosphate deposition

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45
Q

Describe the pattern of acute pseudogout

A

Monoarthropathy of larger joints in the elderly

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46
Q

Describe the pattern of chronic pseudogout

A

Inflammatory, symmetrical polyarthritis and synovitis

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47
Q

Give 3 potential causes of acute pseudogout

A

Illness
Surgery
Trauma

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48
Q

Give 4 risk factors of pseudogout

A

Old age
Hyperparathyroidism
Haemochromatosis
Hypophosphataemia

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49
Q

How would you diagnose pseudogout?

A

Polarised light microscopy of synovial fluid

X-Ray: soft tissue calcium deposition

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50
Q

How would you manage pseudogout?

A

Acute: cool packs, rest, aspiration, intra-articular steroids
Prophylaxis: NSAIDs and colchicine
Chronic: Methotrexate and hydrochloroquine

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51
Q

Describe osteoporosis

A

Age-related disorder causing gradual loss of bone density and strength

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52
Q

Give 5 modifiable risk factors for osteoporosis

A 
Excess alcohol
Vitamin D deficiency
Smoking
Malnutrition
Underweight
Heavy metals
PPIs
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53
Q

Give 5 non-modifiable risk factors for osteoporosis

A 
Female
Age
Menopause
Ethnicity
FHx
Build
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54
Q

How would you diagnose osteoporosis?

A

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
Q

How would you treat osteoporosis?

A

Weight-bearing/ resistance exercises
Fall prevention
Medications: bisphosphonates

56
Q

Which human leukocyte antigen is associated with spondyloarthropathies?

A

HLA B27 (class I surface antigen)

57
Q

What does SPINE ACHE stand for, in relation to spondyloarthropathies?

A 
Sausage digits (dactylitis)
Psoriasis 
Inflammatory back pain
NSAIDs good response
Enthesis

Arthritis
Chrons/ colitis
HLA B27
Eye (uveitis)

58
Q

Describe ankylosing spondylitis

A

Inflammatory arthritis of the spine and rib cage, eventually leading to new bone formation and fusion of the joints

59
Q

Give 5 factors which reflect a poor prognosis in ankylosing spondylitis

A 
Male
Smokers
B27 +ve
Syndesmophytes at presentation
High CRP
60
Q

Describe the signs and symptoms of ankylosing spondylitis

A

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
Q

How would you manage ankylosing spondylitis?

A 
Hip replacement
Exercise
NSAIDs
TNF-alpha blockers
Local steroid injections
62
Q

Give the 5 types of psoriatic arthritis

A 
Symmetrical polyarthritis
DIP joints
Spinal 
Asymmetrical oligoarthritis
Psoriatic arthritis mutilans
63
Q

What percentage of psoriasis cases also have psoriatic arthritis?

A

10-40%

64
Q

What X-Ray changes would you see with psoriatic arthritis?

A

Erosive X-Ray changes “pencil in cup” appearance

65
Q

How would you manage psoriatic arthritis?

A

NSAIDs, sulfasalazine, methotrexate

Anti-TNF

66
Q

Describe reactive arthritis

A

Sterile inflammation of the synovial membrane, tendons and fascia, triggered by an infection at a distal site

67
Q

Give 3 gut-associated causes of reactive arthritis

A

Salmonella
Shigella
Yersinia

68
Q

Give 2 STIs which can cause reactive arthritis

A

Chlamydia

Ureaplasma urealyticum

69
Q

Give 6 signs and symptoms of reactive arthritis

A

Arthritis
Conjunctivitis
Sterile urethritis
Circinate balanitis (painless penile ulceration)
Iritis
Keratoderma blenorrhagica (brown plaques on soles and palms)

70
Q

How would you diagnose reactive arthritis?

A

High ESR, high CRP
Aspirate joint to exclude infection/ crystals
Urethral swab/ stool culture

71
Q

How would you treat reactive arthritis?

A

Steroids (local injections)
NSAIDs
If symptoms >6moths: consider sulfasalazine/ methotrexate

72
Q

What is the typical clinical presentation of septic arthritis?

A

Fever
Inflammation (warmth, red, effusion, pain)
Loss of function and range of movement

73
Q

Give 3 causes of septic arthritis

A

Staphylococcus aureus
Group A streptococcus
Neisseriae Gonorrhoea

74
Q

How might an infection be introduced into the synovium, causing septic arthritis?

A

URTI, LRTI, STI travels in blood
Osteomyelitis
Directly through procedures/ surgery
Skin infection

75
Q

How would you diagnose septic arthritis?

A 
FBC, CRP, ESR
Joint aspiration with a microscopy culture sensitivity
Blood cultures
Electrolyte, urea, creatitnine 
US/X-Ray (joint space widening)
76
Q

How would you treat septic arthritis?

A 
Joint drainage: needle aspiration
Broad spectrum IV Abx
Once cultures come back: specific Abx
IV: 2 weeks
Oral: 4 weeks
77
Q

How can osteomyelitis occur and what does it cause?

A

Bacterial infection of the bone, causing bone cell necrosis, pus formation and weak bones

78
Q

What type of bone does osteomyelitis usually affect?

A

Long bones

79
Q

Give 4 risk factors of osteomyelitis

A

Diabetes
IVDU
Prior splenectomy
Trauma

80
Q

Give 4 symptoms of osteomyelitis

A

Pain
Redness
Fever
Weakness

81
Q

How would you diagnose osteomyelitis?

A

FBC (Inflammation/ infection)

MRI

82
Q

How would you treat osteomyelitis?

A

Prolonged antibiotic treatment

PICC line/ central venous catheter for long-term IV abx

83
Q

In SLE, what is the role of susceptibility genes?

A

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
Q

What is the consequence of a buildup of nuclear antigens in SLE?

A

They form antigen-antibody complexes with antinuclear antibodies

85
Q

Where do antigen-antibody complexes deposit in SLE and what is the result of this?

A

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
Q

Give 5 tigers/ risk factors for SLE

A 
Smoking
Viruses
Bacteria
Sex hormones (oestrogen)
Medications:
Isoniazid
Hydralazine 
Procainamide
87
Q

Describe the type II hypersensitivity reaction in SLE

A

Antinuclear antibodies bind to RBCs, WBCs and phospholipids, marking them for phagocytosis and destruction

88
Q

How many of the criteria must the patient meet to be diagnosed with SLE?

A

> 4

89
Q

Give the 11 criteria for SLE

A

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
Q

How would you prevent/ limit severity of SLE flare ups?

A

Avoid sunlight
Corticosteroids
Immunosuppressants

91
Q

Describe an osteoid osteoma

A

Benign, bone-forming lesion in young patients causing localised pain

92
Q

How would you diagnose and manage an osteoid osteoma?

A

CT/ X-Ray

NSAIDs, radiofrequency ablation

93
Q

Describe an osteoblastoma

A

Bone producing tumour, causing pain

94
Q

What would an X-Ray of an osteoblastoma show?

A

Bone destruction, surrounded by reactive new bone

95
Q

Describe an osteochondroma

A

Metaphyseal lesion, covered by cartilage cap, grows away from growth plate- stops after puberty (painless lump)

96
Q

Describe an osteosarcoma

A

spindle cell neoplasms that produce osteoid

97
Q

Which mutation is associated with an osteosarcoma?

A

P53

98
Q

Why does osteosarcoma have a poor prognosis?

A

Aggressive local growth
Rapid haematological spread
Poor response to chemo

99
Q

Describe a Ewings sarcoma

A

Small round cell tumour that arises from neural crest cells characterised by a translocation mutation t(11;22)

100
Q

What is the name of the neurotransmitter released by the cell body of an axon in response to nociceptor stimulation?

A

Substance P

101
Q

Give the neurotransmitters released by the inhibitory neuron

A

Serotonin

Norepinephrine

102
Q

What is the role of nearby epithelial cells in fibromyalgia?

A

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
Q

Give 3 causes of fibromyalgia

A

Low levels of serotonin
High levels of substance P
High levels of nerve growth factor

104
Q

Give the 3 factors taken into account for the diagnosis of fibromyalgia

A

Pain location
Symptom severity score (fatigue, poor sleep, headache)
Duration

105
Q

How would you treat fibromyalgia?

A

Exercise
Relaxation techniques
Meds:
Amitriptyline
Serotonin-Norepinephrine reuptake inhibitors (SNRIs)
Anticonvulsants: pregabalin and gabapentin

106
Q

Describe the character of mechanical back pain

A

Better/ worse depending on position
Typically worse when moving
May be due to minor injury (sprain or strain)
Can be associated with stress

107
Q

Give 5 symptoms of prolapsed/ herniated disc

A 
Lower back pain
Numbness/ tingling
Neck pain
Problems straightening your back
Muscle weakness
108
Q

Describe spondylolisthesis

A

A bone in the spine slips out of position

109
Q

Give 5 symptoms of spondylolisthesis

A 
Lower back pain: worse with activity/ standing
Sciatica
Tight hamstring muscles
Stiffness/ back tenderness
Kyphosis
110
Q

Give 5 causes of mechanical back pain

A 
Birth defect
Repetitive spinal trauma
Vertebral joints becoming worn and arthritic
Sudden trauma/ spinal injury
Bone abnormality
111
Q

How would you treat mechanical back pain?

A 
Rest
NSAIDs
Physio
Corticosteroid injections
Surgery
112
Q

How does the parathyroid gland respond to low calcium?

A

Releases parathyroid hormone which causes osteoclasts to release HCl leading to bond breakdown and release of phosphate and calcium in the blood

113
Q

Why does ionised calcium level not increase much with increased bone resorption in osteomalacia?

A

Phosphate and calcium ions bond to form calcium phosphate

114
Q

Give 2 causes of excess loss of phosphate leading to osteomalacia

A

Primary hyperparathyroidism: excess phosphate lost in urine

Facing syndrome: PCT losing capacity to reabsorb a number of solutes

115
Q

Give 5 causes of phosphate malabsorption in the GI tract leading to osteomalacia

A

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
Q

Give 2 causes of insufficient calcium absorption leading to osteomalacia

A

Lack of dietary calcium

Resistance to action of vitamin D

117
Q

Give 6 primary causes of osteomalacia

A 
Renal tubular acidosis
Malnutrition
Malabsorption syndrome
Chronic kidney failure
Oncotic osteomalacia
Coeliac disease
118
Q

Describe degenerative disc disease

A

Natural breakdown of an intervertebral disc of the spine due to daily stresses

119
Q

How does degenerative disc disease occur?

A

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
Q

Describe the symptoms of degenerative disc disease

A

Pain in the neck, hips, buttocks/ thighs

Commonly worse on movement

121
Q

How would you diagnose degenerative disc disease?

A

Physical exam: muscle weakness, tenderness, poor range of motion
MRI: degenerative fibrocartilage and clusters of chondrocytes

122
Q

How would you treat degenerative disc disease?

A 
Physio
Anti-inflammatories: NSAIDs
Traction
Steroid injection
Surgery
123
Q

Give 3 general symptoms of vasculitis

A

Fever
Weight loss
Fatigue

124
Q

Who is most commonly affected by giant cell arteritis and which artery is affected?

A

> 50 y/o
Women > men
Affects carotid artery

125
Q

What lab results would you see with giant cell arteritis?

A

High ESR

Granulomas in tunica intima

126
Q

Which arteries are generally affected with medium vessel vasculitis?

A

Muscular arteries supplying the organs

127
Q

How would you treat giant cell arteritis or medium vessel vasculitis?

A

Corticosteroids

128
Q

Give a key complication of giant cell arteritis

A

Blindness

129
Q

Give an example of medium vessel vasculitis and how it causes damage

A

Polyarteritis nodosa:

Immune cells attack endothelium and cause damage/ fibrosis, leading to organ ischaemia

130
Q

Describe the mechanism of small vessel vasculitis

A

B-cells produce anti-neutrophilic cytoplasmic antibodies attack neutrophils in arterioles, capillaries and venuoles

131
Q

Describe Paget’s disease

A

Disrupts normal cycle of bone renewal causing bones to become weakened and possibly deformed

132
Q

Give 4 symptoms of Paget’s disease

A

Travelling shooting pain
Numbness and tingling
Joint pain, stiffness and swelling
Constant dull bone pain

133
Q

How would you treat Paget’s disease?

A

Bisphosphonate medication/ vit D/ calcium supplements
Painkillers
Physio
Surgery

134
Q

Give 6 potential complications of Paget’s disease

A 
Bone cancer
Breaks
Enlarged/ misshapen bone
Hearing loss
Hypercalcaemia
Heart problems

Medicine Phase 2A (OWN) (10 decks)

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