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PBL Y2 S3 > Case 9 - Stress fractures > Flashcards

Case 9 - Stress fractures Flashcards

1
Q

What is the role of the menisci?

A
  • Deepen articular surface of tibia (increases stability of knee joint)
  • Act as shock absorbers by increasing the surface area
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2
Q

What is the patellar ligament a continuation of? Where does it attach?

A

Quadriceps femoris tendon, attaches to the tibial tuberosity

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3
Q

What is the role of the collateral ligaments?

A

Stabilise the knee by preventing excessive medial or lateral movements

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4
Q

Where do the 2 collateral ligaments attach?

A

Tibial (medial) collateral: from medial epicondyle of femur to medial condyle of tibia
Fibular (lateral) collateral: from lateral epicondyle of femur to fibular head

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5
Q

Where do the ACL and PCL attach?

A

ACL: anterior intercondylar region of tibia to femur intercondylar fossa
PCL: posterior intercondylar region of tibia to anteromedial femoral condyle

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6
Q

What are transverse tubules?

A

Invaginations of the sarcolemma

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7
Q

How is skeletal muscle derived embryologically?

A

Paraxial mesoderm > somite > myotome > skeletal muscle

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8
Q

What is a myofibril composed of?

A

Thin filaments = actin, bounded with troponin and tropomyosin
Thick filaments = myosin (chain, 2 globular heads)

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9
Q

What is epimysium, endomysium and perimysium?

A

Epimysium = Membrane surrounding muscle
Endomysium = Membrane surrounding individual muscle fibres
Perimysium = membrane surrounding a fasicle (group of muscle fibres)

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10
Q

What are I bands?

A

Light bands, only contain actin (and Z discs).

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11
Q

What are A bands?

A

Dark bands, contain myosin and actin (where actin overlaps myosin)

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12
Q

What are H bands?

A

Zone of thick filaments with no actin.

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13
Q

Which band disappears with contraction?

A

I bands, as actin overlaps myosin

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14
Q

What is the sarcoplasm comprised of?

A

It is intracellular fluid:
- Lots of myoglobin (oxygen-carrying molecule)
- Potassium, magnesium and phosphate ions
- Sarcoplasmic reticulum
- Protein enzymes

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15
Q

What is the role of titin and where does it attach?

A

Has an elastic end attaching to the Z disc (acts as a spring and changes length as the sarcomere contracts/ relaxes), and the other part attaches to myosin.
Role = provides strength to sarcomere

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16
Q

Describe the structure of actin

A

1 molecule of ADP = active site. Tropomyosin is wrapped around the active helix; at rest this covers the active sites. Troponin (I, T, C) is attached intermittently, forming a complex.

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17
Q

What are the 3 types of troponin and what do they have strong affinity for?

A

Troponin I: strong affinity for actin
Troponin T: strong affinity for tropomyosin
Troponin C: strong affinity for calcium

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18
Q

How many troponin complexes are there per actin filaments (roughly)? What is the significance of this?

A

1 complex per 7 actin
Allows for cooperativity, i.e. when troponin C binds to calcium, the signal is relayed and not every troponin complex requires calcium to switch actin ‘on’

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19
Q

What is a motor unit?

A

Muscle unit plus its motor neurone (axon)

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20
Q

What is a muscle unit?

A

Muscle fibres innervated by a single motor neurone

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21
Q

What is a motor neurone pool?

A

Collection of neurones innervating a single muscle

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22
Q

What is an innervation ratio?

A

The number of fibres innervated by a motor unit

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23
Q

What is the resting membrane potential of skeletal fibres?

A

around -80 to -90mV

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24
Q

Which neurone transmits the impulse to a motor neurone of the muscle?

A

Alpha motor neurone

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25
Q

Explain how the arrival of an impulses causes an end-plate potential

A

Impulse at muscle = opens voltage-gated Ca2+ channels, leading to calcium ion influx. Vesicle exocytosis of ACh into cleft
Opens ligand-gated ACh channels = Na+ in and K+ out
End-plate membrane depolarises, leading to an end plate potential

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26
Q

What enzyme breaks down ACh?

A

Acetylcholinesterase

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27
Q

How does an end plate potential lead to intracellular calcium release?

A

1: Depolarisation wave moves along the sarcolemma to the transverse tubules (close tot the sarcoplasmic reticulum)
2: Opens voltage-gated Ca2+ channels within the SR, leading to release of Ca2+ into sarcoplasm
3: Ca2+ influx activates ryanodine receptors in the SR (an intracellular Ca2+ store)
4: Increased intracellular Ca2+

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28
Q

Explain the process of a power stroke

A

1: Ca2+ binds to troponin C, which shifts tropomyosin and exposes the binding site for myosin
2: myosin can form a cross bridge with actin
3: ATPase in myosin head splits ATP into ADP + Pi + energy (power stroke)
4: ATP is used to break the bridge, so myosin can move further down
5: Ca2+ channels in SR close, Ca2+ active transport pumps (SERCA) use ATP to restore low levels of Ca2+ in sarcoplasm
6: troponin-tropomyosin rebinds to actin

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29
Q

What is hypertrophy and what is it caused by?

A

When muscle cells increase in size, due to satellite cells fusing and increased protein synthesis

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30
Q

What are satellite cells? What do they prevent?

A

Known as ‘skeletal stem cells’, which stay asleep until needed. They are post-mitotic so cannot proliferate, but self-renew and differentiate into new muscle.
They prevent nuclear dilution

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31
Q

Describe type 1 muscle fibres

A

Oxidative fibres: contracts slowly but never really fatigue due to its myoglobin store, which captures O2 and releases it when haemoglobin is insufficient

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32
Q

Describe the following characteristics for type 1 muscle fibres:
- Myosin
- Ca2+ pump rate
- Diameter
- Oxidative capacity
- Glycolytic capacity
- Fatigue

A
  • Slow myosin
  • Moderate Ca2+ pump rate
  • Moderate diameter
  • High oxidative capacity
  • Moderate glycolytic capacity
  • Resistant to fatigue
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33
Q

Describe type 2A muscle fibres

A

These are fast oxidative fibres, which are glycolytic. They don’t have as fast a contraction as type 2B but are fairly resistant to fatigue. Have a very high oxidative capacity too

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34
Q

Describe the following characteristics for type 2A muscle fibres:
- Myosin
- Ca2+ pump rate
- Diameter
- Oxidative capacity
- Glycolytic capacity
- Fatigue

A
  • Fast myosin
  • High Ca2+ pump rate
  • Small diameter
  • very high oxidative capacity
  • High glycolytic capacity
  • resistant to fatigue
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35
Q

Describe type 2B muscle fibres

A

Fastest muscle fibre, all glycolytic as they cannot deliver efficient oxygen in time. Produces lactic acid and fatigues fairly quickly

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36
Q

Describe the following characteristics for type 2B muscle fibres:
- Myosin
- Ca2+ pump rate
- Diameter
- Oxidative capacity
- Glycolytic capacity
- Fatigue

A
  • Fastest myosin
  • High Ca2+ pump rate
  • Large diameter
  • Low oxidative capacity
  • high glycolytic capacity
  • Non-resistant to fatigue
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37
Q

Which type fibres have a faster nerve conduction and why?

A

Type 2 = have a thicker myelin sheath

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38
Q

What is the effect of high-intensity aerobic training on:
- Alpha motor neurones
- Hypertrophy
- Mitochondria
- Muscle fibres
- Activation of muscle fibres

A
  • Increased alpha-motor neurone firing frequency and conduction velocity
  • increased hypertrophy so increased force
  • More mitochondria = increased oxidative capacity
  • Increased muscle fibres activated by each alpha neurone
  • Preferential activation of type 2A
  • Increased number of type 2a fibres
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39
Q

What is the effect of resistance training on:
- Motor unit recruitment
- Hypertrophy
- Mitochondria
- Myofibrils

A
  • Can recruit motor units not in consecutive order, i.e. can recruit larger ones first for a more powerful contraction (Hennemans size principle)
  • Hypertrophy of muscle fibres, preferentially fast-twitch (type 2)
  • Usually no change in mitochondria
  • Increased formation of myofibrils, thus increased number of actin and myosin
40
Q

What is the effect of aerobic training on:
- Muscle fibres
- Hypertrophy
- Mitochondria
- Capillaries
- Myoglobin
- Recruitment of muscle fibres

A
  • Transition of fibres to type 1 (slow twitch)
  • Usually no to little muscle hypertrophy
  • More mitochondria for more ATP
  • Capillarisation = increases O2 and substrate supply
  • More myoglobin = increased O2 storage supply
  • Decreased recruitment of type 2 fibres
41
Q

What are the 2 main phases of the gait cycle? What steps and proportion of the whole cycle do they account for?

A

1- Stance phase; 60% of cycle, including heel strike, support and toe-off phases
2- Swing phase; 40% of cycle, including leg lift and swing phase

42
Q

What are the steps in the gait cycle?

A

1- Heel strike
2- Support / mid-stance
3- Heel-off
4- Toe-off
5- Leg lift
6- Swing

43
Q

What muscles are active during the heel strike phase? What is their action?

A

Gluteus maximus: acts on hip to decelerate forward motion of the lower limb
Quadriceps femoris: keeps leg extended at knee, thigh flexed at hip
Anterior compartment of leg: maintains ankle dorsiflexion

44
Q

What muscles are active during support (mid-stance) phase of the gait cycle? What is their action?

A
  • Quadriceps femoris: stabilises knee in extension, supports body weight
  • Foot invertors and evertors: stabilises foot
  • Gluteus minimus and medius, tensor fascia lata: abduct the lower limb to keep the pelvis level and counter imbalance
45
Q

What muscles are active during toe off phase of the gait cycle? What is their action?

A
  • Hamstring muscles: extends thigh at hip
  • Quadriceps femoris: maintains extended position of knee
  • Posterior compartment of leg (mainly gastrocnemius, soleus and tibialis posterior): plantar flexes ankle
46
Q

What muscles are active during leg lift phase of the gait cycle? What is their action?

A
  • Iliopsoas and rectus femoris: keeps thigh flexed at hip, resisting gravity
  • Quadriceps femoris: extends leg at knee, positions foot for landing
  • Anterior compartment of leg: maintains ankle dorsiflexion so heel is in place for landing
47
Q

What are the 3 causes of ataxia?

A

Cerebellar ataxia, i.e. cerebellar stroke, MS
Vestibular ataxia, i.e. Meneires disease
Sensory ataxia, i.e. loss of proprioception (i.e. diabetes mellitus)

48
Q

How might an apraxic gait present and what are some potential causes?

A

Problem with cortical integration (i.e, frontal lobe), can be caused by hydrocephalus or a stroke.
“Marche a petit pas” (shuffling): patient takes small steps and a broad based gait (seems as if they’ve forgotten how to walk)

49
Q

How might an antalgic gait present and what are some potential causes?

A

Results from pain on weightbearing. Commonly seen in patients with chronic musculoskeletal pain or lower limb injuries.
Shortened stance phase and decreased cadence (limping)

50
Q

How might a myopathic (Trendelenburg) gait present and what are some potential causes?

A

Occurs when a patient has malfunctioning hip abductors, so pelvis drops towards the side of the raised limb during swing phase. Can be caused by systemic disease (hyperthyroidism, Cushing’s) or muscular dystrophies.
Patients have a waddling gait and circumducting leg

51
Q

How might a neuropathic (high-steppage) gait present and what are some potential causes?

A

This is gait caused from foot drop, i.e. weakness of muscles that dorsiflex the ankle (tibialis anterior), supplied by common fibular nerve [L4, L5, S1]. During swing phase, the foot drops and toes drag so the patient has to flex knees and hips excessively to prevent dragging.
Causes: L5 radiculopathy, common fibular nerve palsy

52
Q

How might cerebellar ataxia present?

A

Broad-based gait, patient may sway from side to side and could fall. Appears as if they’re drunk

53
Q

How might hemiplegic gait present and what are some potential causes?

A

Caused by a unilateral UMN lesion - i.e. stroke or MS. Classically the patient has a flexed upper limb and extended lower limb on the affected side.
As the leg is held stiffly, the patient has to circumduct the leg around in swing phase. This is an asymmetrical gait

54
Q

What is the Q angle?

A

Angle between force vector (angle) of quadriceps tendon and force vector of the patella tendon

55
Q

Give the average Q angle for males and females

A

Females = 13 to 18 degrees
Men = 12 to 15 degrees

56
Q

How can excessive pronation affect Q angle and position of the tibia?

A

Increases Q angle stress and causes excessive internal rotation of the tibia. You then put more weight on the medial side of the tibia (can develop into shin splints)

57
Q

What is the effect of a weak gluteus medius on the femur and Q angle?

A

Results in internal rotation of the femur, which can exacerbate the effect of a greater Q angle

58
Q

What is periosteum?

A

Covers surface of bone, similar to fascia but contains bone stem cells and nerve endings. It blends with fascia on the tibia

59
Q

What is patellar femoral pain caused by? How can it be treated?

A

The knee cap is normally aligned in trochlear groove, but it can be shifted out causing pain. This worsens with intense activity or prolonged sitting.
Treated w physiotherapy (stretch and strengthen quadriceps, main knee stabilisers), RICE, NSAIDs and orthotics

60
Q

What is medial tibial stress syndrome? What can predispose someone to this?

A

Overuse injury of the shin area, causing a stress reaction of the tibia and surrounding musculature as the body’s unable to heal properly with repetitive contractions and strain (‘shin splints’).
> Increasing loads, volume and high impact exercises can predispose

61
Q

What are the 2 main theories of the pathophysiology for medial tibial stress syndrome?

A

1: Periostitis: inflammation and agitation of periosteum, i.e. fascia of leg muscle pulls on periosteum, which could irritate nerve endings and cause pain
2: Stress reaction: for bones to get stronger they have to temporarily get weaker, so during this weakening = stress reaction and pain

62
Q

What are some intrinsic risk factors to MTSS?

A
  • Female
  • previous history of MTSS
  • High BMI
  • Navicular drop (measure of arch height and pronation)
  • Ankle plantar flexion ROM
  • Vitamin D deficiency
63
Q

What complaints do patients with MTSS normally present with?

A
  • Exercise induced pain along distal 2/3 of border
  • Pain provoked by exercise and reduced with rest
  • No cramping or burning pain in posterior compartment
64
Q

What would a physical exam reveal if a patient had MTSS?

A

Pain when palpating posteromedial tibial border
Absence of severe swelling, erythema, loss of distal pulses etc.

65
Q

How would MTSS be treated?

A

Analgesia for pain - ibuprofen, paracetamol
Rest !
Massage therapy - relieve muscle tension

66
Q

What is a stress fracture?

A

Hairline fracture caused by overuse or repetitive stress, leading to pain of aching or burning along the bone

67
Q

What process can lead to a stress fracture?

A

Disruption to the balance between accumulation of microdamage and bone repair processes, i.e. when microdamage > repair = stress response, which can lead to stress fractures

68
Q

What are some intrinsic risk factors for stress fractures?

A
  • Low bone mineral density
  • Menstrual patterns: late menarche, amenorrhea
  • BMI < 19 (low)
  • Low energy or eating disorders
  • History of stress fractures
69
Q

What are some extrinsic factors for stress fractures?

A

Training regimen, diet, equipment (surfaces, shoe type)

70
Q

Where is the risk of a stress fracture the highest?

A

Areas that are poorly vascularised, i.e. anterior tibia, navicular, 5th metatarsal

71
Q

What is the first-line for diagnosing a stress fracture? Give one disadvantage

A

X-ray: findings can be subtle but later would show thickening and sclerosis of endosteum, and periosteal new bone formation.
Lags behind clinical picture by several weeks - may need to repeat 2wks later

72
Q

When might a bone scan be performed?

A

If worried about multiple non-contiguous stress fractures, i.e. 2nd or 5th metatarsal fracture in combination with a tibial fracture. Shows areas of high cell turnover (sensitive but not specific)

73
Q

What may be done upon a physical examination for a suspected stress fracture?

A

Palpate fracture site = tenderness
Percussion of bone away from fracture site - may produce pain
If pain isn’t too bad, hopping on 1 foot (functional stressing of bone)

74
Q

How are stress fractures treated?

A
  • Rest
  • Immobilisation and protected weight-bearing
  • Avoid NSAIDs, such as ibuprofen – may slow bone healing
  • Get patient on-board with management plan
  • Treat underlying conditions
75
Q

What is the theory behind pulsed ultrasound therapy for stress fractures?

A

up-regulate chondrocytes, increasing endochondral ossification

76
Q

What is the theory behind extracorpeal shock wave therapy? How does it work?

A

Applies strong energy pulses to affected area for short periods. This stimulates cells responsible for bone healing, i.e. osteoblast stimulation.
Also thought to induce perosteal detachment and micro trabecular fracture, which stimulates fracture healing

77
Q

Which stress fracture is most concerning and why?

A

Anterior tibial (‘dreaded black line’) stress fractures - indication for surgery as its unlikely to heal

78
Q

How does tibial nail with drilling work to treat stress fractures?

A

Tibial intramedullary nail inserted down canal of tibia, drilling increases bleeding in the area and stimulates healing.

79
Q

What can cause an ACL tear and how might it present?

A

Non-contact twisting injuries
- Pain, swelling, ‘pop’ sound
- Swelling is secondary to heme arthrosis (ACL torn so bleeds into knee)
- Knee can buckle; instability of knee as ACL usually stops tibia sliding forwards in relation to femur

80
Q

What is the female:male ratio for ACL tears and why is this the case?

A

4.5 to 1 (F:M): females have a wider pelvis size, so vastus lateralis develops more than vastus medialis, which pulls the patella laterally and can lead to a tear

81
Q

What 2 tests may be performed for diagnosis of ACL tears, after acute pain and swelling have settled?

A

Lachmann’s test
Anterior drawer test

82
Q

What scan is first-line for diagnosing an ACL tear?

A

MRI scan

83
Q

What may be used to visualise the torn cruciate ligament?

A

Athroscopy (gold-standard)

84
Q

Following an ACL tear injury, what is the management?

A
  • Urgent referral to A&E or fracture clinic
  • RICE
  • NSAIDs
  • Crutches and knee braces
  • Athroscopic surgery: ACL reconstruction
85
Q

How does ACL reconstruction work? How long might recovery take?

A

New ligament is formed using a graft of ligament from another location, the graft acts as a scaffolding for the new ligament to grow on.
Recovery is around 6 months

86
Q

What tendons may be used for ACL reconstruction?

A

hamstring tendon
Quadriceps tendon
Patella tendon

87
Q

What is the main indication for ACL reconstructive surgery?

A

Symptomatic instability of the knee

88
Q

How do ACL tears repair?

A

Full tears cannot repair as there is no blood supply to the ligament. It can be reconstructed by attaching a new graft / tissue to it.

89
Q

What does the female athlete triad include?

A

Bone mineral density
Energy availability
Menstrual function/ dysfunction

90
Q

How do orthotic devices help gait?

A

Stop us pronating, decreases a high Q angle and lowers biomechanical stress on the knee joint.

91
Q

What is the placebo effect?

A

Any favourable psychological or psychophysiological effect produced by placebos. The change in symptom(s) is not directly attributable to drug or treatment under investigations.

91
Q

What is the placebo effect?

A

Any favourable psychological or psychophysiological effect produced by placebos. The change in symptom(s) is not directly attributable to drug or treatment under investigations.

92
Q

What is the name given to adverse physiological or psychophysiological effects caused by a placebo?

A

Nocebo effect

93
Q

How does the placebo effect work?

A

Based on expectancies - the idea that we can make ourselves better through beliefs and expectations

94
Q

What is conditioning?

A

Associating previous health care experiences with positive outcomes

95
Q

What are conventional medicines?

A

CAM’s are therapies/ interventions that are:
- Non-standard/ unconventional
- Non-prescription
- Non-surgical
(Can be pharmacological or non-pharmacological)

96
Q

Whats the difference between complementary and alternative medicines?

A

Complementary = as well conventional treatment
Alternative = instead of conventional treatment

PBL Y2 S3 (10 decks)

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