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BRS > MSK - general > Flashcards

MSK - general Flashcards

1
Q

5 functions of the skeleton?

A 
Support
Protection
Movement
Mineral storage - Ca & PO4
Produces blood cells
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2
Q

Name the two ways bones develop in utero

A

Intramembranous ossification → flat bones

Endochidnral ossification → long bones

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3
Q

Which cells are involved at the outset of ossification?

A

Mesenchymal cells

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4
Q

Outline intramembranous ossification

A

Mesenchymal cells condense and differentiate into osteoblasts → ossification centre forming

Osteoid is secreted and traps osteoblasts → osteocytes

Trabecular matrix and periosteum form

Compact bones develops
Blood vessels condense to red bone marrow

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5
Q

What cartilage is involved in endochomdral ossification?

A

Hyaline

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6
Q

What are the primary and secondary ossification centre know as?

A

Diaphysis

Epiphysis

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7
Q

What are the functions of osteoblasts?

A

Bone forming
Secrete osteoid
Catalyse minerelisation of osteoid

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8
Q

What is the function of osteocytes?

A

Sense mechanical strain and dissect osteoblast and osteoclast activity

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9
Q

Where are osteoclasts derived from?

A

Bone marrow

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10
Q

What are the 2 components of the organic bone matrix?

A 
Type 1 collagen
Ground substance (proteoglycans, glycoproteins, cytokines and growth factors)
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11
Q

What does the inorganic bone matrix consist of?

A

Calcium hydroxyapatite

Osteocalcium phosphate

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12
Q

What type of bone has osteons?

A

Compact

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13
Q

Explain the structure of osteons and how it supports the function of compact bone?

A

Few spaces → helps compact bone provide protection and supports and resist forces

Osteons are repeated lamellae surrounding a Haversian canal containing blood vessels, nerves and lymphatic

Volkmans canals traverse these canals

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14
Q

What are lacuane and what connect them?

A

Small spaces containing osteocytes connect by canaliculi contains ECF

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15
Q

Where is yellow bone marrow found?

A

Medullary cavity

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16
Q

What is the connective tissue covering of bone?

A

Periosteum

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17
Q

2 types of bone growth?

A

Interstitial - increase length

Appositional - increase thickness

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18
Q

Where does interstitial growth happen?

A

Epiphyseal plate

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19
Q

How does interstitial growth differ between epiphyseal and diaphyseal side?

A

ES - hyaline cartilage is active and dividing to form cartilage matrix

DS - cartilage calcifies and dies , replaced by bone

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20
Q

How does aposotiitional growth occur?

A

Ridges in periosteum create groove for blood vessel
Ridges fuse → endosteum lined tunnel
Osteoblasts build new lamellae toward centre of tunnel > osteon
Bone also grows outward from new lamellae

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21
Q

3 types of fibrous joints?

A

Sutures
Syndesmosis
Interosseous membrane

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22
Q

2 types of cartilaginous joints?

A

Synchondroses

Symphyses

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23
Q

6 types of synovial joints?

A 
Plane
Hinge
Saddle
Pivot
Condyloid 
Ball and socket
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24
Q

Shoulder vs hip stability?

A 
Shoulder:
has shallower socket
weaker joint capsule 
less strong ligaments
rotator cuff dependent
unstable but very mobile
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25
Q

3 types of muscle?

A

Smooth
Cardiac
Skeletal

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26
Q

6 different arrangements of muscle fibres?

A 
Unipennate
Bipennate 
Multipennate
Triangular
Fusiform 
Parallel
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27
Q

Muscle structure from largest to smallest?

A 
Muscle surrounded by epimysium 
Fascicles surrounded by perimysisum 
Myofibres surrounded by endomysium
Myofibrils
Myofilaments
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28
Q

Outline the structure of a myofibre?

A 
Sarcolemma plasma membrane 
T tubules
Sarcoplasm containing myoglobin and mitochondria 
Sarcoplasmic reticulum 
Composed of myofibrils
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29
Q

What are the dark and light banks on myofilaments?

A

Dark - A band of myosin

Light - I band of actin

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30
Q

What separates sarcomeres?

A

Z discs

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31
Q

Structure of actin?

A

Helical
Myosin binding site
Troponinnans tropomyosin

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32
Q

What happens to bands during contraction?

A

I band become shorter
A band the same
H zone narrows/disappearss

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33
Q

Explains the steps in producing an action potential in muscle

A 
VGCCs open in response to AP
Ca2+ enters pre synaptic terminal
→ exocytosis of vesicles contains Ach
Ach diffuses across cleft and binds to Ach receptors 
→ AP in muscle
34
Q

What breaks down Ach and the NMJ?

A

Acetylcholine esterase

35
Q

How is a muscle contraction initiated after the AP reaches muscle?

A

AP propagates along membrane and down T tubules
Dihydorpyridine receptor in t tubule detects change in voltage
This causes a shape change in the protein linked to ryanodine receptor
The ryanodine receptor calcium channel in sarcoplasmic reticulum opens
Ca released from SR into sarcoplasm

36
Q

Which receptor detects voltage change in t tubules?

A

Dihydropyridine receptor

37
Q

What type of receptor does Ach bind to at the NMJ?

A

Nicotinic

38
Q

What happens right after Ach binds to receptor?

A

Sodium ions enter muscle and potassium leaves

Overall Increased positive charge in muscle fibre → depolarisation

39
Q

Where do the released calcium ions bind to and what happens next?

A

Troponin receptors, on actin filaments, change shape
Tropomyosin is moved out the way
Myosin attaches to actin → crossbridges form

40
Q

What happens to the Calcium in the sacrcoplasm while APs continue?

A

It is actively transported into SR using ATP

Rate of uptake is <= to release so contraction continues

41
Q

Explain how the ‘power stroke’ is generated?

A

Calcium causes troponin to move from tropomyosin which exposes myosin binding site
Charged (ADP) myosin binds to actin
ADP is discharged causing myosin head to pivot
Actin is pulled towards M line

42
Q

How is the myosin head released and recharged?

A

ATP binds to myosin causing it to be released

ATP is then hydrolysed in to ADP which provides energy to myosin head and its recharged to its original position

43
Q

Describe the neural control of muscle contraction

A

Primary motor cortex - UMN

Synapse with LMN in brainstem or spinal cord

44
Q

What is a motor unit?

A

A single motor nerve fibre and all the muscle fibres it innervates
Stimulation of one motor unit causes contraction of all muscle fibres in it

45
Q

What are the 3 types of motor units and their differences?

A

Slow (I) - smallest cell bodies, dendritic trees, thinnest axons, slowest conduction velocity | red, high myoglobin, high aerobic, low anaerobic capacity

Fast fatigue resistant (IIA) - high myoglobin, pink, high anaerobic capacity

Fast fatiguable (IIB) - low myoglobin, white, high anaerobic capacity, low aerobic

  • larger cell bodies and dendritic trees, thicker axons, faster conduction velocity
46
Q

How are motor units classsified?

A

Tension generated
Contraction speed
Fatiguability

47
Q

How is muscle force regulated? (2)

A

Recruitment

Rate coding

48
Q

Explain the recruitment process?

A

Smaller motor units are recruited first , normally slow twitch
More force = more units recruited

Allows for fine motor control

49
Q

Explain rate coding.

A

As motor unit firing rate increases , force produced increases
Slow units fire at lower frequencies

50
Q

When does summation happen?

A

When motor units fire at a frequency too high to allow for muscle relaxation between APs

51
Q

What are neurotrophic factors?

A

Growth factor that prevent neuronal death and promote growth after injury

52
Q

What determines motor unit characteristic and how is this known?

A

The nerve that innervates them

If two different types of motor units are cross innervated they swap characteristics

53
Q

What are the 3 types of muscle contraction?

A

Concentric - muscles shorten

Eccentric - muscles elongate , greatest force generated

Isometric - no movement

54
Q

What causes change from type I to type II fibres? (3)

A

Severe de conditioning
Spinal cord injury
Microgravity

55
Q

What occurs to muscle fibres with aging?

A

Loss of type I and II fibres
Greater proportion of II lost
Slower contraction times

56
Q

Most common fibre type change?

A

IIB to IIA from training

57
Q

Types of bone fractures?

A

Trauma - high/low energy
Stress - abnormal stress on normal bones
Pathological - normal stress on abnormal bone

58
Q

Describe how a stress fracture occurs?

A

Overuse of bone
Stress on bone is greater than its ability to remodel
Bone weakens and stress fracture forms

59
Q

What is the female athlete triad?

A

Links to stress fractures

Disordered eating, amennorhea and osteoporosis

60
Q

Name 6 causes of pathological fractures

A 
Vit D deficiency (osteomalacia or rickets)
Malignancy
Osteoporosis 
Osteomyelitis 
Osteogenesis imperfecta
Pagets
61
Q

Some risk factors for osteoporosis?

A

Female gender
Postmenopausal women
Senility (>70)

62
Q

3 causes of secondary osteoporosis?

A

Alcoholism
Hypogiandisim
Glucocorticoids excess

63
Q

How does vitamin d deficiency affect bone?

A

Reduced calcium, magnesium and phosphate absorption
Leads to defect in osteoid matrix mineralisation
Bone is soft and bends in response to stress

64
Q

Outline osteogenesis imperfecta

A

Autosomal
Less type 1 collagen → reduced secretion and abnormal collagen produced
Insufficient osteoid production

65
Q

Name 3 signs associated with OI

A

Blue sclera
Short stance
Lense dislocation

66
Q

Outline Paget’s disease

A

Excessive bone break down
Disorganised remodelling
Leads to bone deformity → pain, fracture, arthritis

67
Q

What are the 4 stages of Paget’s disease?

A

Osteoclast activity
Mixed osteoclast osteoblasts activity
Osteoblasts activity
Malignant degeneration

68
Q

Name 4 primary bone cancers?

A

Ewing’s sarcoma
Osteosarcoma
Chondrosarcoma
Lymphoma

69
Q

Secondary bone cancer - different sites of origin and type?

A

Blastic- prostate

Lytic- kidney, thyroid, lung

Both - breast

70
Q

What is Wolffs law?

A

Bone grows and remodels in response to forces placed on it

71
Q

What are the 3 steps of bone healing?

A

Bleeding and inflammation
Repair
Remodelling

72
Q

Soft vs hard callus formation?

A

Soft callous forms first from type 2 collagen

Converted to hard callous of type 1 collagen

73
Q

What is primary bone healing and its advantages?

A

Intramembranous healing
Gives most stability
Direct to woven bone

74
Q

What is secondary bone healing?

A

Endochomdral healing
Relative stability
More callous because if endochondral ossification

75
Q

What are the 3 steps to fracture management?

A

Reduce
Hold
Rehabilitate

76
Q

what are the different types of reduction?

A

Open: small incision or full exposure

Closed : manipulation or traction (skin or skeletal)

77
Q

What are the types of hold?

A

Closed with plaster or traction

Fixation

78
Q

What are the different fixation options?

A

Internal - intramedulalry (pins or nails) or extramedullary (plate and screws or pins)

External - mono or multiplanar

79
Q

What are the steps in rehabilitation?

A

Use
Move
Strengthen
Weight bear

80
Q

What is the difference between tenidnosis and tendinitis?

A

Abnormal thickening

Inflammation

81
Q

Outline the 3 grades if ligament injury

A

I : slight tear, no instability

II: more severe incomplete tear, some instability

III : complete tear, very unstable, surgery

82
Q

What are the options for ligaments and tendon repair?

A

Immobilise with plaster or boot/brace

Surgery with sutures

BRS (7 decks)

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