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EOP 1 > MSK - Phase 1 > Flashcards

MSK - Phase 1 Flashcards

1
Q

Gross anatomy + types of bone

A

Features of bone include:

  • diaphysis/shaft
  • epiphyses at ends
  • metaphysis between, contains epiphyseal plate or growth plate
  • rich blood supply
  • marrow fills hollow interior
  • surrounding layer of periosteum on the outside with endosteum lining the interior
  • Woven bone* – common initial stage with randomly arranged collagen fibres found in foetuses, post-fracture and other pathological states, much weaker
  • Lamellar bone* – much stronger layered form of bone remodelled from woven bone
  • compact: layers of Haversian systems on the outside of bone
  • spongy: branches of trabeculae that form along lines of mechanical stress
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2
Q

Mechanisms of bone growth

A
  • intramembranous ossification* – for flat bones, layers of mesenchymal cells form a template for growth with spongy bone forming first before peripheral remodelling to create compact bone
  • Endochondral ossification* – all other bones develop in this way e.g. long bones
  1. chondrocytes form a template of hyaline cartilage in the rough shape of the bone
  2. calcification causes chondrocytes to die
  3. osteoblasts invade cartilage scaffolding to form an ossification centre (primary centre in diaphysis and secondary centres in epiphyses)
  4. cartilage persists in the epiphyseal plate until adolescence when fusion prevents further growth
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3
Q

Overview of bone remodelling

A

Bone is a dynamic tissue with constant turnover and remodelling involving three cell types:

  • osteoblasts – mesenchymal cells that produce osteoid, the collagen matrix that acts as a scaffold for bone and becomes mineralised through positive feedback + seed crystals
  • osteocytes – trapped osteoblasts that reside in lacunae of Haversian systems, connected to each other by canaliculi, act as stress transducers
  • osteoclasts – haematopoietic cells that produce enzymes and HCl to degrade bone and resorb the mineral components

Turnover of bone is regulated by a number of physical and chemical factors including hormones, mechanical stress, drugs, temperature, inflammation

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4
Q

Hormones + processes of calcium and phosphate metabolism

A
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5
Q

RANK/RANK-L/OPG signalling pathway in osteoporosis

A
  1. RANK-L produced by osteoblasts binds to RANK expressed on osteoclast to promote their recruitment and activity
  2. OPG also produced by osteoblasts binds to RANK-L to prevent it activating RANK, thereby suppressing osteoclasts from being overactivated
  3. Oestrogen normally limits RANK-L production, following menopause there is an increase in RANK-L which overwhelms OPG resulting in excess bone resorption
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6
Q

Pathophysiology of osteoporosis

A

Osteoporosis is a disease of ageing in which there is excessive osteoclast activity causing net resorption, factors contributing to this include:

  • relative vitamin D deficiency, prompting osteoclasts to access Ca2+ by resorbing bone
  • decline in recruitment and activity of osteoblasts
  • further increase in osteoclast activity due to reduced circulating oestrogen via RANK-L

The result of these changes is net resorption of bone leading to a brittle skeleton that is easily fractured, further confounded by – vision loss, cognitive deficits etc.

Most common fractures: neck of femur, humerus, scaphoid (wrist), vertebrae

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7
Q

Pharmacological management of osteoporosis

A
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8
Q

Definitions of osteoporosis

A

osteopaenia = 1–2.5 SDs below the mean in young people

osteoporosis = >2.5 SDs below the mean in young people

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9
Q

Overview of osteomalacia

A

Osteomalacia = disease of bone mineralisation rather than resorption, osteoid is being produced at a normal rate however mineral deposition is not occurring to create strong bone, results in weakness and growth defects in children (bowed legs, skull thinning)

Causes include:

  • vitamin D deficiency
  • gastric surgeries
  • coeliac disease
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10
Q

Classification of fractures

A

Open: skin or other external surface (includes GIT) is pierced by broken bone

Closed: all surfaces remain intact and broken bone is contained

Further classification based on morphology of break

  • bone – which bone is involved
  • site – where in the bone is the fracture
  • appearance – transverse, oblique, spiral, comminuted, segmented etc.
  • relationship of bone parts – displacement, angulation, translation
  • relationship to joints – intraarticular vs. extraarticular
  • relationship to skin – tenting, open/compound, closed
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11
Q

Types of joints with examples of each

A
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12
Q

Components of a synovial joint

A

Articular cartilage – thin plates of hyaline cartilage that transition from spongy bone to cover the articular surfaces of bone to provide smooth movement, avascular/aneural/alymphatic

Fibrous capsule – surrounds the ends of both bones and contains the joint, stabilises and limits movement in all directions equally

Synovial membrane – thin vascular inner lining of joint capsule that produces synovial fluid

Synovial fluid – plasma filtrate containing hyaluronic acid, lubricin, proteinase, collagenase that forms a thing layer at the surface of cartilage to nourish and absorb shock

may also have bursa, meniscus, fat pads etc. depending on joint

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13
Q

Types of muscle fibres

A
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14
Q

Connective tissue in muscles

A

epimysium – surrounding muscles

perimysium – surrounding muscle fibre fascicles

endomysium – surrounding individual muscle fibres

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15
Q

Acute vs. chronic muscle injuries

A

Acute

  • strain: over-elongation or excess force causing a tear, often at muscle/tendon junction
  • contusion: direct impact to muscle which causes bruising

Chronic

  • overuse: repeated small amounts of force → microtrauma → tissue failure
  • tendinopathy: damage to tendon resulting in thickening/nodules
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16
Q

Models of postural control

A

Feedback = balance is disturbed, muscle programs are activated to restore it

  • ankle strategy used in younger people
  • hip strategy used by the elderly

Feedforward = awareness of a balance disturbance before it occurs, allows for internal prediction and anticipatory postural adjustment to minimise disturbance

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17
Q

Components of the extracellular matrix

A
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18
Q

Disorders associated with connective tissue + ECM

A
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19
Q

Phases of wound healing

A

First intentions: thin, clean surgical wound that is sutured resulting in minimal scarring

Second intentions: complicated with inflammation + scarification

  1. inflammation – blood clotting, immune response
  2. proliferation – granulation tissue forms, angiogenesis occurs, macrophages/fibroblasts multiply
  3. maturation – formation of a fibrous scar, wound contraction, tissue remodelling
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20
Q

Overview of osteomyelitis

A

Osteomyelitis = inflammation of bone due to microbial infection, most commonly occurs at extremes of age and can be either acute or chronic

Two major routes of infection:

  • direct spread (80%) – from adjacent sites including soft tissue, prosthetics, ulcers, penetrating wounds – typically S. aureus, can be polymicrobial
  • haematogenous spread (20%) – typically caused by a single organism such as Staphylococcus, H. influenzae, E. coli, P. aeruginosa, GAS, GBS

Can result in abscess formation, ischaemic necrosis of bone, septicaemia, cellulitis, failure to thrive

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21
Q

Pathophysiology of rheumatoid arthritis

A

rheumatoid arthritis = peripheral, symmetrical, deforming polyarthropathy

  1. Citrullination = arginine → citrulline within some proteins (e.g. collagen, vimentin), this process can be accelerated due to smoking and results in self-antigens being seen as foreign by some HLA alleles (DR1/DR2)
  2. Immune response is initiated against citrullinated proteins
    1. autoantibodies produced: anti-CCP + rheumatoid factor, these initiate the complement cascade and promote inflammation
    2. immune cell infiltrate and production of cytokines
    3. proliferation of synovial membrane → fibrous pannus which damages joint
    4. T cells express RANK-L which promotes osteoclast activity
  3. Ongoing immune response spreads systemically resulting in extra-articular manifestations
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22
Q

Extra-articular manifestations of RA

A

Mneumonic : A Pulmonary CVRS

Most common systemic signs include:

  • Rheumatoid nodules = foci of central fibrinoid necrosis within skin
  • Anaemia of chronic disease
  • Pulmonary: fibrosis, pleural effusion
  • Cardiovascular: atherosclerosis, myocardial infarction, pericarditis + effusion
  • Sjogren’s syndrome
  • Vasculitis
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23
Q

X-ray signs of RA

A

Mneumonic: JOMS

  • marginal erosions
  • joint space narrowing
  • osteoporosis
  • soft tissue swelling
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24
Q

Characteristic deformities of RA

A
  • Ulnar deviation of MCP joints
  • Boutonniere: PIP flexion, DIP extension
  • Swan-neck: PIP extension, DIP flexion
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25
Q

Pharmacological management of RA

A
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26
Q

Pathophysiology of osteoarthritis

A

Osteoarthritis is a degenerative joint disease resulting from wear and tear of joint structures, poor vascular supply → poor capacity for healing

Contributing factors may include:

  • obesity
  • traumatic damage
  • occupation or sport
  • connective tissue disorders or other diseases of cartilage
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27
Q

X-ray signs of osteoarthritis

A
  1. reduced joint space
  2. osteophytes
  3. subchondral cysts
  4. subchondral sclerosis
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28
Q

Other types of arthritis/arthropathies

A

Seronegative spondyloarthropathies: spectrum of inflammatory joint diseases that primarily affect entheses

  • ankylosing spondylitis – inflammation of the sacroiliac joint + lumbar spine
  • psoriatic arthritis – associated with psoriasis
  • reactive arthritis – associated with infection e.g. gastroenteritis, UTI, Chlamydia
  • enteropathic arthritis – associated with IBD

Crystal arthropathies: result from deposition of precipitated crystals within the joint space

  • gout – uric acid
  • pseudogout – calcium pyrophosphate

septic arthritis: active infection within joint from direct or haematogenous spread most commonly due to S. aureus infection

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29
Q

Types of pain

A

(three N’s)

nociceptive → activation of nociceptors reflective of tissue damage

neuropathic → damage to sensory nerves

neuroplastic → issues with peripheral or central pain processing

30
Q

Pain receptors + fibres

A
31
Q

Radiculopathy overview

A

Radiculopathy = damage to spinal nerves resulting in pain/numbness and muscle weakness in dermatome and myotome distribution, usually due to compression in IV foramen

  • disc herniation
    • lumbar: central herniation will impinge on cauda equina (SN below) while far lateral herniation will impinge on the exiting spinal nerve (SN above) e.g. L4/5 disc: central L5 radiculopathy, lateral L4 radiculopathy
    • cervical will impinge on the nerve root leaving at that level
  • osteoarthritis of facet joints or ligament pathology
32
Q

Spectrum of peripheral nerve injuries

A

neuropraxia → stretching or nerve that damages sheath

axonotmesis → severance of axons while sheath remains intact

neurotmesis → complete transection of nerve including axon + sheath

33
Q

Intervertebral disc structure + pathology

A

IV-disc structure consists of:

  • annulus fibrosis – fibrous laminar rings, poorly-localised pain innervation
  • nucleus pulposus – hydrated gel distributes force and resists compression
  • herniation* → results when unbalanced mechanical pressures deform the annulus fibrosis allowing the nucleus pulposus to protrude, usually central or lateral
  • discitis* → inflammation, linked to vertebral osteomyelitis
34
Q

Spondylolysis vs. spondylolisthesis

A

Spondylolysis = vertebral stress fracture

Spondylolisthesis = shifting of vertebrae out of alignment due to weakening by stress fractures

35
Q

Types of hypersensitivity reaction

A
36
Q

Brief outline of SLE, scleroderma, Sjogren’s syndrome

A

systemic lupus erythematosus = autoimmune reaction against nuclear antigens such as DNA and histones resulting in production of anti-nuclear antibodies which form immune complexes that deposit throughout the body causing systemic effects

  • specific organ manifestations: pleuritis, pericarditis, arthritis, renal disease, seizures

scleroderma = group of autoimmune diseases characterised by increased collagen production, results in skin thickening, Raynaud’s phenomenon other systemic effects e.g. GORD

Sjogren’s syndrome = autoimmune disease affecting exocrine glands resulting in dry eyes and mouth, progresses to systemic effects and often associated with SLE and RA

37
Q

Stages of anaesthesia

A

Different drugs and adjuvants can be used at each stage, with different pros/cons

  1. induction
  2. maintenance
  3. emergence
38
Q

Common IV and inhaled anaesthetics

A

Intravenous

  • propofol, binds to beta subunit of GABA receptor to increase binding affinity of endogenous GABA
  • benzodiazepines also commonly used e.g. midazolam, these bind to alpha and beta subunits of the GABA receptor to increase affinity

Inhaled

sevoflurane, believed to have actions as a GABA receptor modulator as well as an NMDA receptor antagonist

39
Q

Four major postural problems in childhood orthopaedics

A

Generally these postural problems are physiological and will correct with age, suspect pathological cause if painful, age inappropriate, asymmetrical or affecting function

  • flat feet: painless normal childhood variation
  • intoeing: levels of origin – metatarsus adductus, tibial torsion, femoral anteversion
  • bowlegs/knock-knees: knee alignment varies over time but can be associated with rickets or Blount’s disease
  • scoliosis: idiopathic adolescent scoliosis most common in teenage females
40
Q

Other common presentations in childhood orthopaedics

A

Developmental dysplasia of the hip = shallow acetabulum → congenital dislocation

Talipes equinovarus = club foot from dislocated talonavicular joint

Perthe’s disease = avascular necrosis of femoral head with unknown cause

Osgood-Schlatter’s disease = traction injury of tibial tuberosity → microfractures or avulsion

41
Q

Salter-Harris classification of paediatric fractures

A
42
Q

WHO analgesic ladder

A
  1. non-opioid analgesics + adjuvants
  2. mild opioids + adjuvants
  3. strong opioids + adjuvants
43
Q

Types of muscular dystrophy

A

Muscular dystrophies arise from X-linked genetic mutations in the genes that encode the dystrophin protein which has a role in supporting the sarcolemma of muscle cells

  • Duchenne – dystrophin is completely absent
  • Becker’s – some dystrophin present but not enough for normal function

Result is muscle weakness + fatigue, abnormal gait, pseudohypertrophy and eventual failure of the heart and breathing muscles

44
Q

Overview of Guillain-Barré syndrome

A

Type IV hypersensitivity reaction in which there is an immune response direct towards the Schwann cells that form the myelin sheath of peripheral nerves

  • triggered by infection (URTI or gastroenteritis) or vaccination (rare)
  • presents with progressive numbness, tingling, pain, weakness and ataxia
  • most cases will make a full recovery but some fatalities occur due to breathing failure
45
Q

Tumours of nerves, muscles, cartilage and bone

A

Nerves

  • neurofibroma
  • Schwannoma
  • MPNST = malignant peripheral nerve sheath tumour

Muscle

  • rhabdomyosarcoma

Cartilage

  • benign – enchondroma
  • malignant – chondrosarcoma

Bone

  • benign – osteoblastoma, osteoid osteoma
  • malignant – osteosarcoma, secondary metastases
46
Q

Overview of myasthenia gravis

A

Type II hypersensitivity reaction in which there is a chronic autoimmune response initiated by circulating antibodies against the nicotinic acetylcholine receptor of the NMJ

  • typically affects the muscles of the eyes (ptosis, diplopia) and face
  • prognosis is generally good with effective treatment
47
Q

Components of the cytoskeleton

A
48
Q

Types of motor proteins

A

ATP driven enzymes which migrate along the cytoskeleton to perform essential functions such as muscle contraction, intracellular transport, motility and cell division

  • myosins – bind and move along actin filaments
  • kinesins – move towards plus end of microtubules, generally anterograde to periphery
  • dyneins – move towards minus end of microtubules, generally retrograde to centre
49
Q

Sensory receptors of proprioception

A

Muscle spindle → detects muscle stretch

spindles arranged parallel to fibres within muscle, innervated by gamma motor neurons which contract the spindle to reset its length so that it remains sensitive to stretch

Golgi tendon organ → detects muscle tension

innervated collagen fibres in the musculotendinous junction, will terminate contraction if muscle tension becomes excessive

50
Q

Overview of motor neurone disease

A

MND = progressive neurological disease characterised by degeneration of motor neurons with sensory sparing, results in wasting of voluntary muscles and death due to breathing failure

Classification of MND is based on part of the body affected and pattern of involvement

  • Global type: 90% of all cases, affects UMNs and LMNs
    • ALS – muscle weakness and stiffness later spreading to muscles of speech and swallowing
    • bulbar palsy – begins in muscles of speech and swallowing
  • Progressive muscular atrophy: LMN signs initially which may become ALS with later involvement of UMNs, often called flail arm or flail leg depending on where affected
  • Primary lateral sclerosis: rare form that only affects UMNs
51
Q

Major causes of peripheral neuropathy

A

Pneumonic = “Do Alcoholics Giggle Before Producing _T_heir CV”

Peripheral neuropathy = pathology of the peripheral nerves which may include sensory, motor or autonomic effects

  • Diabetes – microvascular damage from hyperglycaemia results in nerve hypoxia
  • Alcohol – damage due to acetaldehyde + ROS from alcohol
  • B12 deficiency – essential vitamin for neurological function
  • Compression/entrapment e.g. carpal tunnel syndrome
  • Guillain-Barré syndrome – autoimmune damage to nerve sheath
  • Toxins e.g. drugs, heavy metals
  • Vasculitis – may be associated with SLE, Sjogren’s
  • Paraneoplastic effects – usually from SCLC
52
Q

Stages of transmission at the neuromuscular junction

A
  1. Nerve action potential: opening of VGSCs propagates AP along axon towards terminal
  2. Release of acetylcholine: AP reaches axon terminal and causes calcium influx which triggers release of ACh stored in synaptic vesicles, this is then recycled via enzymatic degradation by acetylcholinesterase
  3. End plate depolarisation: ACh acts on nicotinic receptors of the motor endplate which are ion channels that allow sodium influx causing depolarisation
  4. Muscle action potential: depolarising current from endplate travels across sarcolemma and down T-tubules where it induces calcium release from the SR and contraction
53
Q

Major types of muscle relaxants

A
54
Q

Inflammatory myopathies

A

Polymyositis = direct immune destruction of muscle fibres

Dermatomyositis = immune cells attack small blood vessels of the muscles and skin

55
Q

Lumbar Plexus

A
56
Q

Brachial Plexus

A

Mnemonic: READ THAT DAMN CADAVERIC BOOK !!!!

R - root (C5-T1)

T - trunk (sup, mid, inf)

D - division (anterior & posterior)

C - cord (lat, pos, med)

B - branches (musculocutaneous, axillary, radial, ulna, median)

57
Q

Cervical Plexus

A

From Week 6 MSK anatomy lab manual

58
Q

Upper Limb Nerve Pathway

A
59
Q

Lower limb muscles

A
60
Q

Lower leg muscles

A
61
Q

Plantar muscles

A

From https://www.orthobullets.com/foot-and-ankle/7003/layers-of-the-plantar-foot

62
Q

Explain the motor and sensory functions of the branches of the brachial plexus

A

Mnemonic:

3 musketeers (C5-C7)

(gun/2) assassins (C5-C6)

5 rats (C5-T1)

5 mice (C5-T1)

2 unicorns (C8-T1)

63
Q

Myotomes and Motor Peripheral innervation of the upper limb

A
64
Q

Sensory PNS Upper Limb nerves

A
65
Q

Dermatomes of Upper Limb

A
66
Q

Muscles of forearm

A
67
Q

Motor testing of upper limbs

A
68
Q

Myotomes and Motor Peripheral Nerve Innervation of Lower Limb

A
69
Q

Dermatomes and Sensory Peripheral Nerves of Lower Limb

A
70
Q

Radiculopathy Vs Peripheral Neuropathy

A
71
Q

Acute pain Vs Chronic Pain

A
  • acute
    • immediate onset, duration of minutes/hours/days/weeks
    • due to immediate/direct injury or insult to the tissue (AMI/trauma/sprain)
    • specific known cause
    • readily responsive to analgesia
    • will resolve once cause is fixed/treated
  • chronic
    • prolonged duration -> weeks/months/years/lifelong
    • often unclear cause
    • diffuse in nature
    • resistant/unresponsive to analgesia (will require weak-stronger opioid)
    • reliant on opioid in order to carry on with ADLs & maintain QOL
    • potentially psychosomatic (previous trauma/PTSD/transferrance etc)
72
Q

Reflexes and corresponding spinal cord level

A

EOP 1 (16 decks)

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