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HYMS Block 12 > MSK conditions > Flashcards

MSK conditions Flashcards

1
Q
  1. What is a soft tissue injury?
  2. Give two examples of soft tissue injuries
  3. What needs to be considered and excluded with any open wound?
A
  1. an acute connective tissue injury, that may involve skin, subcutaenous tissues, muscles, ligaments, tendons, nerves, blood vessels or cartilaginous structures
  2. bruises and sprains
  3. nerve injury
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2
Q
  1. At what age are bruises and fractures uncommon and could be indicative of child abuse?
  2. Name other injuries that could indicate child abuse (4)
A
  1. under the age of 1
  2. extensive or unusual pattern of bruising - back, buttocks, arms, abdomen
    suspicious burns
    multiple injury sites
    atypical fracture patterns
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3
Q

Name risk factors for soft tissue injuries in older people (4)

A
  1. increased risk of falls
  2. living in long term institutionalised care - proxy for frailty
  3. age related changes in skin and soft tissues
  4. medication - may impact ability to clot
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4
Q

Describe the pathology and functional impairment in the following grades of soft tissue injury:

  1. first
  2. second
  3. third
A
  1. minor contusion with bleeding. minimal functional impairment
  2. moderate contusion. Overall structure intact. Pain, some loss of muscle power/range
  3. structural disruption; instability and/or loss of function
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5
Q
  1. Using the PRICE pneumonic, describe the immediate management of soft tissue injuries
  2. Name 6 instances when you would consider surgical repair
A 
1. P - protection
   R - rest
   I - ice
   C - compression
   E - elevation
2. heavy contamination
    suspected nerve damage
    suspected vascular damage
    loss of tendon function
    communication with the joint cavity
    when there is an underlying fracture
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6
Q

Name three key physical signs of fractures

A
  1. local bone tenderness
  2. crepitus
  3. deformity and/or swelling and/or loss of function
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7
Q

Describe the following types of fracture:

  1. closed/simple
  2. colles fracture
  3. smiths fracture
  4. open fracture
  5. undisplaced fracture
  6. displaced fracture
  7. spiral fracture
  8. comminuted fracture
  9. avulsion
  10. stress fracture
A
  1. skin intact; fracture uncontaminated
  2. distal radial fracture caused by falling on outstretched hand. Posterior displacement
  3. distal radial fracture caused by falling onto flexed wrists; anterior displacement
  4. fracture in which there is a break in the skin. Soft tissue or fracture are contaminated, and nerves may be damaged
  5. bone maintains its proper alignment
  6. bones get displaced from original position
  7. result of twisting of limb
  8. bone is broken into multiple pieces
  9. piece of bone is displaced due to muscle/ligament attachment
  10. fatigue induced fracture of the bone caused by repeated stress over time
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8
Q

Describe the following consequences of femoral head fractures:

  1. Blood loss
  2. Compartment Syndrome
  3. Avascular Necrosis
A
  1. the femur is very vascular therefore fractures can result in significant blood loss
  2. increase in pressure within a confined compartmental space decreases perfusion to that compartment; this leads to ischemia and necrosis
  3. disruption of blood supply due to fracture/surgical repair causes death of bone tissue
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9
Q
  1. What is a pathological fracture?

2. Name 4 causes of pathological fractures

A
  1. a bone fracture caused by disease that lead to weakness of the bone structure
  2. osteoporosis
    Paget’s disease/osteitis deformans
    Tumour deposits
    Bone cysts
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10
Q

Describe the 4 stages of fracture management

A
  1. primary survey - ABCDE
  2. recusitation
  3. Secondary survey - complete evaluation, including diagnostic tests
  4. Definitive care
    - open wound management
    - reduction and stabilisation
    - rehabilitation
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11
Q
  1. What is the function of articular cartilage? (2)
  2. What 2 layers form the joint capsule?
  3. What is the function of synovial fluid? (3)
A
  1. minimise friction. shock absorption
  2. synovial layer, and fibrous layer. Synovial layer forms synovial fluid
  3. lubrication. shock absorption. nutrient distribution
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12
Q

Name 5 signs and symptoms of rheumatoid arthritis

A
  1. slow onset
  2. joint swelling
  3. symmetrical polyarthritis, mainly affects small joints in hands and wrists
  4. early morning stiffness
  5. dramatic NSAID response
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13
Q
  1. Where is the primary site of inflammation in RA?
  2. What are central to inflammation in RA?
  3. Which cells are involved, which leads to immune amplification?
  4. What is the result of inflammation of (1)? (2)
  5. How are fibroblasts involved?
A
  1. synovial membrane
  2. cytokines, particularly TNF-alpha
  3. T cells
  4. becomes hyperplastic and thickened
    this blocks the normal route of nutrition for the hyaline cartilage, therefore it thins and exposes underlying bone
  5. fibroblasts from the proliferating synovium erode bone
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14
Q

Name 7 consequences of chronic systemic inflammation in RA

A
  1. early ischaemic heart disease
  2. sarcopenia (loss of skeletal muscle mass)
  3. hypercholesterolaemia
  4. pain sensitisation
  5. osteoporosis
  6. insulin resistance
  7. dementia
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15
Q

How can smoking increase the risk of RA

A

citrullinates protein - conversion of arginine to citrulline

autoantibodies often attack citrullinated proteins

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16
Q

Name 4 biochemical tests for RA

A
  1. CRP - not very specific
  2. ESR - not very specific
  3. Rheumatoid Factor
  4. CCP - most specific test for RA
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17
Q
  1. Which joints are affected in OA?

2. Name 9 risk factors associated with OA

A
  1. hand joints, axial skeleton, large weight bearing joints
2. age
female
fam hx
obesity
oestrogen deficiency
low bone mineral density
occupation
pre-exisiting joint abnormality
past trauma
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18
Q
  1. What type of arthritis is gout?
  2. Name three co-morbidities associated with gout
  3. Name risk factors associated with gout
A
  1. crystal arthritis
  2. renal impairment
    coronary artery dusease
    metabolic syndrome
  3. age, male, gender, impaired renal function
    hyperuricaemia, high purine diet, high alcohol consumption, obesity, low dose aspirin, thiazides
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19
Q
  1. What is gout caused by?

2. describe the formation of urate

A
  1. hyperuricaemia - too much uric acid in the blood. results in formation of uric acid crystals
  2. adenosine > inosine > hypoxanthine > xanthine > urate
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20
Q
  1. What happens under conditions of uricaemia?
  2. Name three causes of hyperuricaemia
  3. Where is the common site of a gouty attack?
  4. What is tophaceous gout?
  5. How is gout treated?
A
  1. urate becomes ionised and combines with Na to form urate crystals
  2. increased purine consumption - red meat, seafood
    increased purine production - lymphoma, leukaemoa, haemolytic anaemia, chemotherapy
    decreased urate clearance
  3. big toe
  4. recurrent gouty attacks cause inflammation and permanent damage to the affected joint
  5. Allopurinol - decreases uric acid production
21
Q
  1. What is septic arthritis?
  2. Name 4 bacteria that can cause septic arthritis
  3. Name 3 ways in which septic arthritis can occur
A
  1. infection of a joint
  2. S aureus. strep spp. N. gonorrhoea. salmonella
  3. can seed the joint from bacteraemia, direct inoculation or spread from adjacent osteomyelitis
22
Q
  1. What three investigations should be performed for septic arthritis?
  2. How should septic arthritis be treated?
A 
1. routine bloods
blood cultures (particularly those with pyrexia)
joint aspiration
  1. IV antibiotics for 2 weeks
    aspiration of joint
    further treatment with oral antibiotics until signs and symptoms resolve and ESR/CRP are returning to normal
23
Q

Name some risk factors for falls

A
  1. gait deficit
  2. balance deficit
  3. parkinson’s disease
  4. epilepsy
  5. dementia
  6. stroke
  7. peripheral neuropathy
  8. visual deficit
  9. anti-arrythmic drugs
  10. psychotropic drugs
24
Q
  1. Name 4 common fracture sites following a fall

2. Other than fractures, name 2 other serious consequences of falls

A
  1. distal radius (colles fracture)
    vertebra
    proximal femur
    proximal humerus
  2. multiple minor injuries
    long lie > hypothermia, pressure sores etc
25
Q
  1. What is the characteristic deformity following a hip fracture?
  2. What is avascular necrosis?
  3. How is it treated?
  4. How are hip fractures managed? (3 step process)
A
  1. shortened and externally rotated leg
  2. vascular occlusion of the femoral head, leading to ischaemic death of bone. Bone structures then collapse, resulting in pain, loss of joint function and long-term joint damage
  3. Total hip replacement
  4. admit quickly
    operate within 36 hours
    mobilise within 24 hours
26
Q
  1. What is osteoporosis?

2. Name three ways of reducing fractures in those with osteoporosis

A
  1. a skeletal disorder characterised by compromised bone mineral density (Osteoclast activity > osteoblast activity), predisposing an inidividual to an increased risk of fracture
  2. improve bone density
    exercise and nutrition
    fall prevention
27
Q

What is the mechanism of the following drugs used in the treatment of osteoporosis:

  1. bisphosphonates
  2. teriparatide
  3. Denosumab
  4. HRT
A
  1. kills osteoclasts; specificity comes from affinity to calcium.
    Daily use associated with gastric problems
  2. recombinant PTH. Stimulates osteoblasts
  3. RANK-L antagonist therefore prevents the development of osteoclasts. Contraindicated in people with hypocalcaemia
  4. Increased oestrogen which stimulates osteoblasts
28
Q
  1. Where is cortical bone found?
  2. Where is trabecular bone found?
  3. Which type of bone is more metabolically active?
A
  1. shafts of long bones
  2. vertebrae, epiphyses of long bones and iliac crest
  3. trabecular
29
Q

How do osteoblasts regulate osteoclast maturation?

clue: RANK-L and OPG

A

Osteoblasts produce and release RANK-L and OPG
RANK-L promotes osteoclast maturation by binding to RANK expressed on the osteoclast progenitor
OPG binds and sequesters RANK-:, preventing it from binding to RANK
the ratio of RANK-L to OPG is critical in the formation and activity of mature osteoclasts

30
Q

Name three ways in which osteoclasts break down bone

A
  1. integrins bind to bone cytoskeleton and creates a seal
  2. a proton pump secretes H+ and a Cl channel secretes Cl- - acidic environment
  3. secretion of lysosomal enzymes that break down collagen
31
Q

Describe the two hit explanation of why women are more susceptible to osteoporosis

A
  1. lower peak bone density

2. faster rate of bone loss

32
Q
  1. What confers the specificity of bisphosphonates?
  2. How do non-N containing bisphosphonates work?
  3. How do N-containing bisphosphonates work?
  4. Name a side effect of bisphosphonates
A
  1. high calcium binding enables them to accumulate in bone
  2. inhibits ATP dependent intracellular enzymes, therefore promotes osteoclast apoptosis
  3. inhibits enzymes involved in the post translational modification of GTP binding proteins that are important for the formation of the seal formed by osteoclasts in bone remodelling
  4. osteonecrosis of the jaw
33
Q
  1. How does oestrogen prevent osteoporosis?

2. Name a SERM that has fewer side effects than oestrogen, that can treat osteoporosis

A
  1. inhibits PTH activity (and therefore counteracts PTH mediated stimulation of osteoclasts)
  2. raloxifine
34
Q
  1. under physiological conditions, when is calcitonin released
  2. what is its action?
  3. What is the name of the calcitonin preparation given clinically to treat osteoporosis?
A
  1. hypercalcaemia
  2. increases osteoblast activity
    decreases renal and intestinal calcium absorption
  3. salcatonin
35
Q
  1. What are DMARDS?

2. Name three DMARDS that are used as triple therapy

A
  1. Disease modifying anti-rheumatic drugs. Act to reduce damage to the joints
  2. Methotrexate, sulphasalazine, chloroquine
36
Q
  1. What is the MOA of Methotrexate?
  2. What is Sulphasalazine also used to treat?
  3. What is Chloroquine also used to treat?
  4. What do infliximab, etanercerpt and adulibumab interfere with?
  5. Name two drugs that are drugs of last resort for RA
A
  1. inhibits dihydrofolate reductase therefore dampens immune cell activity and production
  2. Crohn’s disease
  3. malaria
  4. TNF-alpha signalling
  5. Ciclosporin and cyclophosphamide
37
Q
  1. What is nociceptive pain?
  2. What is nociceptive pain associated with?
  3. What does nociceptive pain respond well to?
A
  1. pain arising from the stimulation of nerve cells
  2. associated with tissue damage
  3. conventional analgesia
38
Q
  1. What is neuropathic pain?
  2. What is it associated with?
  3. What is it also common with?
  4. Does neuropathic pain correspond to conventional analgesia?
  5. What is chronic pain?
  6. What is chronic pain often associated with?
A
  1. pain associated with neuronal damage or abnormal processing by these neurons
  2. abnormal sensations (dysthesia) and allodynia
  3. autonomic disturbances
  4. no
  5. unpredictable response of an often abnormal nervous system, where the relationship to tissue damage is unclear
  6. other health problems such as fatigue, sleep disturbance, decreased appetite and mood changes
39
Q
  1. What is neural plasticity?
  2. What is peripheral sensitisation?
  3. Name two mechanisms occurring in peripheral sensitisation?
  4. How are inflammatory mediators implicated in peripheral sensitisation?
A
  1. the ability of the brain to change throughout an individual’s life, that enables the brain to compensate for injury and disease
  2. increased sensitivity to afferent nerve stimuli following injury or cell damage to the area
  3. spontaneous neuronal activation - dysthesia, allodynia
    reduced threshold for activation
  4. stimulate or sensitise neurons
    promote an enzyme cascade that upregulates ion channels and nociceptive channels
40
Q
  1. What is central sensitisation?

2. How is it implicated in chronic pain?

A
  1. increased response to stimulation, mediated by amplification of signalling in the CNS
  2. associated with the development and maintenance of chronic pain
41
Q

Name 7 co-morbidities associated with chronic pain

A
  1. poor appetite
  2. anxiety
  3. depression
  4. difficulty concentration
  5. drowsiness
  6. lack of energy
  7. difficulty sleeping
42
Q
  1. Name a behavioural consequence of chronic pain
  2. name 2 cognitive consequences of chronic pain
  3. name an affective consequence of chronic pain
  4. What is a positive gain of chronic pain?
  5. what is a negative loss of chronic pain?
A
  1. fear avoidance - inactivity to avoid pain, which can then make pain worse due to muscle stiffness
  2. somatisation - communicating psychological distress in the form of somatic symptoms
    catastrophising
  3. anxiety and depression
  4. sympathy, support, attentiom
  5. loss of income etc
43
Q

Name 6 assessment tools used to assess pain

A
  1. visual analogue score
  2. verbal rating score
  3. brief pain inventory
  4. HAD score
  5. McGill Pain score
  6. LANSS score
44
Q

Name 4 yellow flags associated with pain

A
  1. fear that pain is harmful or severely disabling
  2. fear avoidance behaviour
  3. low mood and social withdrawal
  4. expectation that passive treatment rather than active participation will help.
45
Q

Describe the following gaits:

  1. antalgic gait
  2. ataxic gait
  3. parkinsonian gait
  4. Myopathic gait
  5. Neuropathic Gait
  6. Trendelenburg Gait
A
  1. gait that reduces loading on an affected extremity. Decreases stance phase
  2. unsteady, unco-ordinated gait, associated with cerebellar diseases and MS
  3. patient moves with short, accelerating steps, often on tiptoe. Trunk is flexed forward. Associated with basal ganglia disorders
  4. waddling gait, associated with weakened proximal girdle muscles
  5. weakened foot dorsiflexors lead to high stepping gait
  6. small gluteals (hip abductors) don’t function effectively. Hip drops and lumbar spine flexes towards paralysed side
46
Q
  1. Where is true leg length measured?
  2. What is any discrepancy in true leg length caused by?
  3. Where is apparent leg length measured?
  4. What is any discrepancy in apparent leg length caused by?
  5. How can one determine whether the tibia is shorter?
  6. How can one determine whether the femur is shorter?
A
  1. anterior superior iliac spine to medial maleolus
  2. affected limb is physically shorter
  3. umbilicus to medial malleolus
  4. flexion or adduction deformity
  5. front is not as high as the other leg
  6. from the side, the top of the knee is further back than the other knee
47
Q
  1. Define centre of mass
  2. Define centre of gravity
  3. What is the base of support?
A
  1. weighted average of the centre of mass of each body segment in 3D space
  2. vertical projection of the centre of mass onto the ground
  3. area demarcated by the body’s point of contact with the ground
48
Q

What is the aim of postural control?

A

to keep the body’s centre of mass over/within the base of support during quiet stance and active movements

49
Q
  1. What is the reflex model of postural support?

2. What is the systems model of postural support?

A
  1. believes that postural responses to peturbations arise by reflex pathway activations
  2. describes how the CNS locates the body’s COG and adaptively organises its response to disequlibrium by centrally pre-programming postural sensorimotor strategies

HYMS Block 12 (12 decks)

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