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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
3 types of muscle?
Smooth Cardiac Skeletal
26
6 different arrangements of muscle fibres?
``` Unipennate Bipennate Multipennate Triangular Fusiform Parallel ```
27
Muscle structure from largest to smallest?
``` Muscle surrounded by epimysium Fascicles surrounded by perimysisum Myofibres surrounded by endomysium Myofibrils Myofilaments ```
28
Outline the structure of a myofibre?
``` Sarcolemma plasma membrane T tubules Sarcoplasm containing myoglobin and mitochondria Sarcoplasmic reticulum Composed of myofibrils ```
29
What are the dark and light banks on myofilaments?
Dark - A band of myosin Light - I band of actin
30
What separates sarcomeres?
Z discs
31
Structure of actin?
Helical Myosin binding site Troponinnans tropomyosin
32
What happens to bands during contraction?
I band become shorter A band the same H zone narrows/disappearss
33
Explains the steps in producing an action potential in muscle
``` 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
What breaks down Ach and the NMJ?
Acetylcholine esterase
35
How is a muscle contraction initiated after the AP reaches muscle?
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
Which receptor detects voltage change in t tubules?
Dihydropyridine receptor
37
What type of receptor does Ach bind to at the NMJ?
Nicotinic
38
What happens right after Ach binds to receptor?
Sodium ions enter muscle and potassium leaves | Overall Increased positive charge in muscle fibre → depolarisation
39
Where do the released calcium ions bind to and what happens next?
Troponin receptors, on actin filaments, change shape Tropomyosin is moved out the way Myosin attaches to actin → crossbridges form
40
What happens to the Calcium in the sacrcoplasm while APs continue?
It is actively transported into SR using ATP | Rate of uptake is <= to release so contraction continues
41
Explain how the ‘power stroke’ is generated?
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
How is the myosin head released and recharged?
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
Describe the neural control of muscle contraction
Primary motor cortex - UMN | Synapse with LMN in brainstem or spinal cord
44
What is a motor unit?
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
What are the 3 types of motor units and their differences?
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
How are motor units classsified?
Tension generated Contraction speed Fatiguability
47
How is muscle force regulated? (2)
Recruitment | Rate coding
48
Explain the recruitment process?
Smaller motor units are recruited first , normally slow twitch More force = more units recruited Allows for fine motor control
49
Explain rate coding.
As motor unit firing rate increases , force produced increases Slow units fire at lower frequencies
50
When does summation happen?
When motor units fire at a frequency too high to allow for muscle relaxation between APs
51
What are neurotrophic factors?
Growth factor that prevent neuronal death and promote growth after injury
52
What determines motor unit characteristic and how is this known?
The nerve that innervates them | If two different types of motor units are cross innervated they swap characteristics
53
What are the 3 types of muscle contraction?
Concentric - muscles shorten Eccentric - muscles elongate , greatest force generated Isometric - no movement
54
What causes change from type I to type II fibres? (3)
Severe de conditioning Spinal cord injury Microgravity
55
What occurs to muscle fibres with aging?
Loss of type I and II fibres Greater proportion of II lost Slower contraction times
56
Most common fibre type change?
IIB to IIA from training
57
Types of bone fractures?
Trauma - high/low energy Stress - abnormal stress on normal bones Pathological - normal stress on abnormal bone
58
Describe how a stress fracture occurs?
Overuse of bone Stress on bone is greater than its ability to remodel Bone weakens and stress fracture forms
59
What is the female athlete triad?
Links to stress fractures | Disordered eating, amennorhea and osteoporosis
60
Name 6 causes of pathological fractures
``` Vit D deficiency (osteomalacia or rickets) Malignancy Osteoporosis Osteomyelitis Osteogenesis imperfecta Pagets ```
61
Some risk factors for osteoporosis?
Female gender Postmenopausal women Senility (>70)
62
3 causes of secondary osteoporosis?
Alcoholism Hypogiandisim Glucocorticoids excess
63
How does vitamin d deficiency affect bone?
Reduced calcium, magnesium and phosphate absorption Leads to defect in osteoid matrix mineralisation Bone is soft and bends in response to stress
64
Outline osteogenesis imperfecta
Autosomal Less type 1 collagen → reduced secretion and abnormal collagen produced Insufficient osteoid production
65
Name 3 signs associated with OI
Blue sclera Short stance Lense dislocation
66
Outline Paget’s disease
Excessive bone break down Disorganised remodelling Leads to bone deformity → pain, fracture, arthritis
67
What are the 4 stages of Paget’s disease?
Osteoclast activity Mixed osteoclast osteoblasts activity Osteoblasts activity Malignant degeneration
68
Name 4 primary bone cancers?
Ewing’s sarcoma Osteosarcoma Chondrosarcoma Lymphoma
69
Secondary bone cancer - different sites of origin and type?
Blastic- prostate Lytic- kidney, thyroid, lung Both - breast
70
What is Wolffs law?
Bone grows and remodels in response to forces placed on it
71
What are the 3 steps of bone healing?
Bleeding and inflammation Repair Remodelling
72
Soft vs hard callus formation?
Soft callous forms first from type 2 collagen | Converted to hard callous of type 1 collagen
73
What is primary bone healing and its advantages?
Intramembranous healing Gives most stability Direct to woven bone
74
What is secondary bone healing?
Endochomdral healing Relative stability More callous because if endochondral ossification
75
What are the 3 steps to fracture management?
Reduce Hold Rehabilitate
76
what are the different types of reduction?
Open: small incision or full exposure Closed : manipulation or traction (skin or skeletal)
77
What are the types of hold?
Closed with plaster or traction | Fixation
78
What are the different fixation options?
Internal - intramedulalry (pins or nails) or extramedullary (plate and screws or pins) External - mono or multiplanar
79
What are the steps in rehabilitation?
Use Move Strengthen Weight bear
80
What is the difference between tenidnosis and tendinitis?
Abnormal thickening Inflammation
81
Outline the 3 grades if ligament injury
I : slight tear, no instability II: more severe incomplete tear, some instability III : complete tear, very unstable, surgery
82
What are the options for ligaments and tendon repair?
Immobilise with plaster or boot/brace Surgery with sutures

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