Musculoskeletal Flashcards
1
Q
When one foot is midstance, what will the other one be?
A
Toe off.
2
Q
For what proportion of the gait cycle is the foot on and off the ground?
A
Stance phase = 60%
Swing phase = 40%
3
Q
What is the difference between a step and a stride?
A
A step is the distance between the heel strike of one foot and the heel strike of the other, a stride is the length between the heel strike of one foot and that foot’s next heel strike.
4
Q
What is the difference between walking and running?
A
In walking you always keep one foot on the ground, in running there are periods where neither foot is on the ground.
5
Q
What are synergistic muscles?
A
Muscles that facilitate the motion of an agonist muscle.
6
Q
What is the difference between agonist and antagonist muscles?
A
Agonist muscles cause a movement by contracting, antagonist muscles oppose a movement.
7
Q
What is the difference between concentric and eccentric muscle contraction?
A
Concentric = muscle shortens when it contracts Eccentric = muscle lengthens when it contracts
8
Q
What is the difference between the action of ankle dorsiflexors and the action of ankle plantarflexors?
A
Ankle dorsiflexors make the toes point up, ankle plantarflexors make the toes point down.
9
Q
What are the four stages of stance phase?
A
Heel strike- foot dorsiflexed, hip extensive contract, intrinsic foot muscles reserve arch
Flat foot - knee extensors make knee stiff, hip abductors stabilise pelvis, preserve longitudinal arch of foot with intrinsic muscles
Midstance
Propulsion - contract plantarflexors, hip abductors stabilise pelvis, intrinsic foot muscles preserve arch
10
Q
What are the three stages of swing phase?
A
Toe off - eccentric contraction of hip flexors decelerates hip
Initial swing - concentric contraction of hip flexors accelerates mass, dorsiflexors clear foot of ground and prepare for heel strike
Terminal swing - hip extensors decelerate thigh, eccentric contraction of knee flexors decelerates leg, ankle dorsiflexed, knee extensors extend knee to place foot
11
Q
What are 5 conditions that can alter the gait cycle?
A
Ageing - decrease in muscle bulk and flexibility reduces stride length so increases number of steps
Structural damage to nerves, blood supply, tendons, bones
Arthritis, and other inflammatory and degenerative conditions
Neurological conditions e.g Parkinson’s
Footwear
12
Q
What do you call the gait where it hurts to weight bear on the affected limb so the stance phase is reduced?
A
Antalgic gait
13
Q
What do you call the gait that is unsteady and uncoordinated, so there is a wide base with feet thrown out and the trunk may sway?
A
Cerebellar/ataxic gait
14
Q
What do you call the shuffling gait with short steps and trunk flexed forward?
A
Parkinsonian
15
Q
What do you call the gait where the hip abductors are weakened so the pelvis drops to the side of the non weight bearing leg, like a waddle?
A
Myopathic/Trendelenburg gait
16
Q
What do you call the gait where the ankle dorsiflexors are weak so the limb has to be lifted higher for the foot to clear the ground?
A
Neuropathic/ high-stepping gait
17
Q
What is moment/torque?
A
The perpendicular distance between a joint and the muscles line of action.
18
Q
What should the lengths of the inlever and outlever be when you want strength and when you want speed?
A
If you want strength of force, you need a relatively long inlever and relatively short outlever.
If you want speed you need a relatively short inlever and relatively long outlever.
19
Q
What is the normal human gait cycle?
A
The period from heel strike of one limb to the next time that heel hits the ground.
20
Q
Where is the CoM in humans standing upright?
A
In the midline of the pelvis, anterior to S2.
21
Q
Which muscle groups allow us to sway slightly forwards and backwards to keep our CoM inside our base of support and ourselves balanced?
A
Plantarflexors if the CoM has moved just anterior to base of support.
Dorsiflexors if the CoM has moved just posterior to the base of support.
22
Q
What 5 adaptations do humans have for efficient bipedalism?
A
1) Iliofemoral ligament twisted around the head of the femur which prevents backward movement, allows flexion but prevents extension
2) Cervical, thoracic and lumbar curvatures of spine, so weight borne by spine s over the base of support and cancelled out
3) Human pelvis is wider, shorter and has more antero-posteriorly orientated ilium than chimpanzee
4) Sacroiliac joint is closer to acetabulum (because ilium is wider than it is tall) so weight is transferred from spinal column to hip joint without putting too much stress on ilium
5) Chimpanzees only have extensors because the muscles only at the back, humans have hip abductors as well as extensors so the Trendelenburg gait is prevented
23
Q
Weakness in which muscles causes Trandelenburg gait?
A
Gluteus medius and gluteus minimis muscles. Gait causes a lot of energy expenditure.
24
Q
What is the difference between the human femur and chimpanzee femur?
A
The human femur has a larger head because each bone bears more weight.
The human femur is angled inwards (bicondylar angle) so when one leg is lifted the base of support is still directly below the trunk.
25
What is coxa vara?
The femoral neck have a decreased angle of below 120 degrees. This mildly shortens the leg leading to a waddling gait.
26
What is coxa valga?
An increased angle of the femoral neck of above 140 degrees. Caused by weakness in abductor muscles and lack of normal weight bearing.
27
What is the normal angle if the femoral neck?
125 degrees
28
What is the difference between the human femur and chimpanzee femur?
The human femur has a larger head because each bone bears more weight.
The human femur is angled inwards (bicondylar angle) so when one leg is lifted the base of support is still directly below the trunk.
29
What is coxa vara?
The femoral neck have a decreased angle of below 120 degrees. This mildly shortens the leg leading to a waddling gait.
30
What is coxa valga?
An increased angle of the femoral neck of above 140 degrees. Caused by weakness in abductor muscles and lack of normal weight bearing.
31
What is the normal angle if the femoral neck?
125 degrees
32
Name two adaptations of the human knee to bipedalism.
The anterior and posterior cruciate ligaments, and the lateral (fibular) and medial (tibia) collateral ligaments which bind the knee together and stop the femur sliding over the tibia.
The knee-locking mechanism - when quadriceps fully extend the knee, the femoral and tibial condyle said pack closely together and are held tight by ligaments.
33
How is the human foot adapted for bipedalism?
There are lateral and medial longitudinal arches as well as transverse arches so that body weight is distributed across the foot when standing and it acts as a shock absorber.
34
What are some functions of the skeletal system?
Support soft tissues
Provide attachment points for the tendons of skeletal muscle
Protect important internal organs e.g brain, spinal cord, lungs
Assist movements
Storage and release of minerals e.g calcium and phosphorus
Maintain homeostasis
Haematopoiesis
Triglyceride storage in yellow bone marrow
35
What are the five parts of a long bone?
Proximal epiphysis, physis, metaphysis, diaphysis [the shaft], (then distal metaphysis, distal physis, distal epiphysis).
There is also articular cartilage on the epiphysis, which reduces friction and absorbs shock.
36
How do osteoclasts carry out bone resorption?
They secrete HCl and lysosomal enzymes to digest protein and minerals of ECM.
37
What are the 4 situations where bone ossification occurs?
1) Initial bone formation in an embryo and foetus
2) Bone growth to reach adult size
3) Remodeling of bone throughout life
4) Repair of bone fractures
38
What are the two types of bone formation in the embryo and foetus?
```
Intramembranous ossification (gives rise to dermal bones).
Endochondral ossification (replaces cartilage with bone).
```
39
What bones are formed by intramembranous ossification?
Flat bones of skull, ossification of fontanelles in infant skull, facial bones, mandible, medial clavicle.
40
What are the 4 stages of bone formation by intremembranous ossification?
1) Development of ossification centre - mesenchymal cells clustering together an developing into osteogenic cells then osteoblasts which secrete ECM
2) Calcification- Calcium and minerals deposited and crystallised to hydroxyapatite in collagen fibre framework, hardening the bone and trapping mature osteocytes in lacunae
3) Formation of trabeculae - ECM develops into trabeculae which fuse into spongy bone around blood vessels, connective tissue differentiated int red bone marrow
4) Formation of periosteum - mesenchyme condenses around bone to form periosteum, thin layer of compact bone develops around spongy bone
41
What are the six stages on endochondral ossification?
1) Development of cartilage model - mesenchymal cells cluster at site where bone will develop and differentiate into chondroblasts, a cartilage model of hyaline cartilage covered in perichondrium is produced
2) Growth of cartilage model - chondroblasts embedded in ECM form chondrocytes, there is interstitial growth due to cell division of chondrocytes, ECM begins to calcify
3) Primary ossification centre develops - nutrient artery penetrates perichondrium, osteogenic cells in perichondrium develop into osteoblasts, so perichondrium becomes periosteum and starts to form bone, osteoblasts form spongy bone trabeculae by depositing bone ECM over remains of calcified cartilage
4) Development of medullary cavity - osteclasts break down spongy bone trabeculae to form medullary cavity in diaphysis
5) Secondary ossification centres develop - epiphyseal arteries enter epiphysis and stimulate bone formation
6) Formation of articular cartilage and epiphyseal growth plate - hyaline cartilage on outside of epiphysis becomes articular cartilage, hyaline cartilage between epiphysis and metaphysis is epiphyseal growth plate responsible for lengthwise growth of long bones.
42
What is the difference between primary ossification and secondary ossification in endochondral bone formation?
Primary ossification is from the outside in, secondary ossification is outwards from the centre to the periosteum.
43
What are the four layers of the epiphyseal growth plate?
1) Zone of resting cartilage - nearest to epiphysis, small scattered chondrocytes a choring growth plate to epiphysis
2) Zone of proliferating cartilage - chondrocytes replicate and secrete ECM to replace chondrocytes dying at diaphyseal side
3) Zone of hypertrophic cartilage - large maturing chondrocytes
4) Zone of calcified cartilage - a few cells thick, dead chondrocytes in calcified ECM, osteoclasts clear calcified cartilage and osteoblasts secrete ECM (endochondral ossification to increase length of diaphysis)
44
When adulthood is reached, what structure remains of the epiphyseal plate?
Epiphyseal plate.
45
What type of growth allows bone to increase in width?
Appositional growth.
46
What is bone remodelling?
The ongoing replacement of old bone tissue by new bone tissue.
47
What are the stages of bone resorption?
Osteoclast attaches tightly to bone, with ruffled border on endosteum or periosteum.
Under tight seal of ruffled border, osteoclast releases HCl and lysosomal enzymes to digest protein.
The enzymes digest collagen and other proteins, HCl dissolves the bone minerals.
Several osteoblasts together carve a tunnel into old bone.
The degraded bone proteins and extracellular minerals enter the osteoclast in vesicles by endocytosis, then exit into the interstitial fluid by exocytosis and diffuse into blood capillaries.
When an area of bone has been cleared, osteoclasts move away and osteoblasts step up to form new bone.
48
What factors affect bone remodelling?
Minerals (e.g calcium and phosphorus) being taken in in the diet.
Vitamin A stimulates osteoblast activity, vitamin C is needed for collagen synthesis, vitamin D increases calcium absorption from the intestine, vitamins K and B12 are needed for synthesis of bone proteins.
Hormones like oestrogen, androgens, parathyroid hormone, calcitonin, growth factors.
49
What is the difference between the signals affecting formation of the skeleton earlier on and later on?
Earlier on it is genetic signals, later on it is functional signals like where the bone is stressed and bearing load.
50
Which type of bone formation starts with neural crest cells?
Intramembranous ossification.
51
Why does cartilage have a slow metabolic rate?
It is avascular and relies on diffusion.
52
On an X-ray how can you tell the difference between a physis and a bone fracture?
Growth plate - bone goes dark, light. dark, light, dark
Fracture - bone goes dark, dark, dark
This is because on an X-ray spongy bone appears darker than compact bone and periosteum.
53
What happens if bone is constantly bearing tension instead of load?
It becomes a ligament.
54
What are the three structural types of joints?
Fibrous e.g suture
Cartilaginous e.g physis
Synovial e.g ball and socket
55
What are the three functional types of joints?
Synarthrosis - immovable
Amphiarthrosis - slightly moveable
Diarthrosis - freely moveable
56
What are the three types of fibrous joints?
1) Sutures - between bones of skull (synarthrosis)
2) Syndesmoses - dense irregular connective tissue forms ligament between bones allowing some movement (amphiarthrosis)
3) Interosseous membranes - sheet of dense irregular connective tissue between two neighbouring long bones allowing some movement (amphiarthrosis)
57
What are the two types of cartilaginous joints?
1) Primary - Synchrondroses (hyaline cartilage, synarthrosis)
2) Secondary - Symphysis (fibrocartilage, amphiarthrosis)
58
What are the characteristics of a synovial joint?
Diarthrosis
Articular cartilage - hyaline cartilage covering epiphysis
Articular capsule enclosing synovial cavity
59
What are the functions of the articular cartilage?
Reduce friction
| Shock absorber
60
What are the two layers of the articular capsule?
Outer fibrous membrane - dense irregular connective tissue
| Inner synovial membrane - areolar connective tissue with elastic fibres and articular fat pads
61
What are the 5 stages of fracture repair?
1) Haematoma - blood leaking from broken blood vessels, clot restricts circulation so phagocytes and osteoclasts clear dead bone cells
2) Sub-periosteal and endosteal cell proliferation - fibroblasts from periosteum produce collagen fibres, chondroblasts produce a fibrocartilage soft callus
3) Callus of woven bone - osteogenic cells produce osteoblasts which produce lamellae to convert fibrocartilage callus to spongy bone
4) Consolidation of woven bone to lamellar bone - bone is load bearing so compact bone can replace spongy bone
5) Remodeling - osteoclasts resorb fragments of broken bone and compact bone replaces spongy bone
62
What are 7 things that influence bone remodelling?
```
Calcitonin
Parathyroid hormone
1,25-(OH)2 vitamin D3
Growth hormone
Growth factors
Oestrogen
Cytokines (e.g pro inflammatory cytokines like interleukin 1 and interferon gamma)
```
63
What functions does calcium have?
Intracellular signalling
Blood coagulation
Contraction-excitation coupling
Synaptic transmission
64
In what three ways is calcium transported in the blood?
50% as ionised calcium (Ca2+)
40% bound to albumin
10% complexed mostly to citrate and phosphate
65
What three ways is phosphate carried in the blood?
55% ionised phosphate (HPO4)2-
10% bound to protein
35% complexed to sodium, calcium, or magnesium
66
What is the amount of calcium in the body, and what is the recommended daily intake?
1000g of calcium in the body
| Recommended daily intake = 1000mg
67
How much phosphorus is there in the body?
600g
68
How is 1,25-(OH)2 vitamin D3 produced?
1) UV light converts 7-dehydrocholesterol in the skin into cholecalciferol (vitamin D3)
2) In the liver there is 25-hydroxylation to produce 25-(OH) vitamin D3
3) In the kidneys there is 1-hydroxylation to produce 1,25-(OH)2 vitamin D3
69
How is 1,25-(OH)2 vitamin D3 broken down?
1,25-(OH)2 vitamin D3 induces 24 hydroxylase in the liver to produce 1,24,25-(OH)3 vitamin D3 which is the first step in the catabolism of vitamin D3.
Vitamin D toxicity won't occur because high vitamin D3 levels induce 24 hydroxylase to catabolise vitamin D3.
70
What is synostosis?
Converting cartilage to bone.
71
Which cells in the parathyroid glands secrete parathyroid hormone?
Chief cells
72
What is parathyroid hormone secreted in response to?
Low plasma Ca2+ concentration
73
What effects do high parathyroid hormone levels have?
Stimulate osteoclasts to carry it bone resorption (effect mediated through osteoblasts which then communicate directly with osteoclasts).
Decrease renal calcium excretion
Increase renal production of 1,25-(OH)2 vitamin D3
74
What effects do low parathyroid hormone levels have?
Stimulate osteoblastic bone formation
75
What is the effect of parathyroid hormone-related protein?
Required for endochondral ossification, so maintains the epiphysial growth plate at a constant width.
Binds to PTH Type 1 receptor so enhances effect of PTH in stimulating osteoclasts, except doesn't increase 1,25-(OH)2 vitamin D3 production.
Predominantly acts locally not systemically.
PTHrP major mediator of hypercalcaemia caused by cancer because it is secreted by malignant cells.
76
Which cells in the thyroid secrete calcitonin!
Parafollicular cells
77
What is calcitonin secreted in response to?
High plasma Ca2+ levels.
78
What is the effect of calcitonin?
Activates calcitonin receptors on osteoclasts and reduces bone resorption.
Decreases 1,25-(OH)2 vitamin D3 synthesis.
79
Which way is calcium moving as a result of parathyroid hormone?
From bone to blood
From intestine to blood
From kidney to blood
80
Which way is calcium moving as a result of calcitonin?
From blood to bone.
81
What are the three effects of 1,25-(OH)2 vitamin D3 which increase blood calcium level?
1) increases absorption of calcium and phosphate (Ca2+ and (HPO4)2-) from the intestine
2) Mobilise calcium and phosphate from reservoirs in the bone
3) Induce marrow monocytes to differentiate into osteoclasts to stimulate bone resorption
82
What effect do oestrogens and androgens have on bone resorption?
Oestrogens inhibit osteoclastogenesis, and bone resorption by osteoclasts. Both osteoblasts and osteoclasts express oestrogen receptors.
Androgens directly target osteoclasts to inhibit bone resorption.
83
What 4 things cause hypercalcaemia?
1) Primary hyperparathyroidism (excess secretion of parathyroid hormone)
2) Malignancy (osteolytic bone metastases, PTHrP secretion)
2) Hyperthyroidism
3) Immobilisation
4) Vitamin D toxicity
84
What three things cause hypocalcaemia?
1) Vitamin D deficiency
2) Renal failure
3) Immature parathyroid gland/immature vitamin D metabolism (Prematurity)
85
What is secondary hyperparathyroidism?
A physiological response to hypocalcaemia producing symptoms similar to primary hyperparathyroidism.
86
What are the symptoms of primary and secondary hyperparathyroidism?
```
Osteitis fibrosa cystica (bone replaced by fibrous tissue, mostly in the skull and phalanges)
Kidney stones
Fractures
Bone pain
Deformity
Periosteal erosions
```
87
What four things can cause osteomalacia/rickets?
Vitamin D deficiency
Institutionalisation
Renal disease
Malabsorption (due to coeliac's disease, or following gastric surgery)
88
What are the two types of inherited rickets?
Vitamin D Dependent Rickets Type 1 - Deficiency of 1-hydroxylase in the kidney
Vitamin D Dependent Rickets Type 2 - resistnace to 1,25-(OH)2 vitamin D3
89
What are the symptoms of osteomalacia and rickets?
Diffuse bone pain or bone pain localised around the hips
Muscle weakness
Elevated alkaline phosphatase levels
Decreased mineralisation
Bowing of weight-bearing long bones (especially in children)
90
What is the prevalence of osteoporosis in women and men over 50?
1 in 2 women, and 1 in 5 men over 50 have osteoporosis.
91
What are the two things that decrease in osteoporosis?
Loss in bone mass, and decrease in mineralisation which leads to a decrease in bone mineral density (BMD).
92
What are the two effects ageing has on bones?
1) Loss of bone mass due to demineralisation (loss of calcium and other minerals from bone ECM)
2) Increased brittleness of bone due to decreased protein synthesis decreasing the collagen fibres in the ECM (so decreasing tensile strength of bone)
93
What 4 things increase bone loss?
Secretion of parathyroid hormone
Menopause
Insufficient vitamin D and calcium
Sedentary lifestyle
94
What 5 things decrease bone loss?
```
Sufficient vitamin D and calcium in the diet
Physical activity
Oestrogens
Androgens
Growth hormone
```
95
What are 5 things used to treat osteoporosis?
Calcium supplements
Hormone replacement therapy (HRT)
Bisphosphonates (inhibit bone resorption)
Calcitonin
Selective Oestrogen Receptor Modulators (SERMs) [only bind to oestrogen receptors in bone]
96
What are the three types of movement?
Reflex - involves reflex arc (e.g stretch reflex)
Voluntary
Rhythmic - due to central pattern generators e.g walking
97
What are motor programs?
Circuitry in the spinal cord for coordinating and executing automatic or repetitive movements They can be initiated or modified by descending pathways from the brain.
98
Which five places do alpha motor neurones receive input?
Muscle spindles (1a afferents) - important for proprioception.
Golgi tendon organs (1b afferents).
Spinal interneurones (can be inhibitory).
Upper motor neurones.
Cutaneous receptors.
99
What is amyotrophic lateral sclerosis (ALS) and what are the symptoms?
Motor neurone disease, where there is progressive degeneration of upper motor neurones from the brain and alpha motor neurones.
Symptoms: muscle atrophy, muscle weakness, difficulty breathing and swallowing, abnormal reflexes, cognitive abilities and sensory neurones generally unaffected. Eye movements relatively preserved (which is characteristic of upper motor neurone lesions).
100
How is riluzole thought to work in treating MS?
It blocks glutamatergic transmission, as MS is thought to be caused by an excess of glutamate.
101
What is the integration centre for reflexes?
CNS - primarily spinal cord
102
What are the two types of reflexes depending on whether an interneurone is involved, and what is the difference between them?
Monosynaptic (e.g stretch reflex) or polysynaptic (reciprocal inhibition). Monosynaptic reflex is faster.
103
What is a reflex?
An involuntary movement resulting from sensory stimulation and involving nerve impulses travelling along a reflex arc.
104
Why do we have reflexes?
To protect ourselves (e.g from overstretching tendons or hot stimuli)
To allow us to coordinate movement so we can carry out daily activity like walking automatically.
105
What is a golgi tendon organ?
A mesh of collagen fibres with a 1b sensory afferent wrapped around them, that is in series with the extrafusal muscle fibres of the muscle belly and prevents muscle overload.
106
Why is the flexor withdrawal/crossed extensor reflex slower than the myotatic stretch reflex?
The myotatic stretch reflex is monosynaptic so is very fast, the flexor withdrawal/crossed extensor reflex is polysynaptic because there are interneurones between the cutaneous nociceptor and alpha motor neurone, so it is slower.
107
How do motor programs in the spinal cord produce complex rhythmic movements like walking or running?
Using spinal central pattern generators.
108
What are central pattern generators?
Neural networks that produce rhythmic patterned outputs without sensory feedback. They generate flexion and extension of limbs during locomotion without you having to think about it (which would really slow you down).
109
What are some examples of rhythmic movements produced by central pattern generators?
```
Walking
Running
Chewing
Swallowing
Respiration
Swimming (in aquatic animals e.g fish)
```
110
What is isokinetic muscle contraction?
Muscle contraction where the resulting movement is at a constant speed.
111
What is the MRC scale of muscle power?
```
5 = full power
4 = reduced power against resistance
3 = active movement against gravity but not against resistance
2 = active movement with gravity eliminated
1 = muscle contractions visible but no movement (fasciculations)
0 = no muscle contraction
```
