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Year 1 - Semester 2 > Locomotor > Flashcards

Locomotor Flashcards

1
Q

What is aggrecan

A

Main proteoglycan in cartilage

Negative

Resists compressive force

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2
Q

What are the three types of cartilage

A

Hyaline
Articular on movable joints to cushion, reduce friction (along with synovial fluid)
Spread load and resist compressive forces
Collagen II forms an irregular basketweave pattern in ECM
In joints, larynx, trachea, bronchi, ribs

Fibro-cartilage
Connects hyaline cartilage to tendon/ligament
Parallel bundle of collagen I fibres to resist tensile strength
Intervertebral discs and meniscus of knee

Elastic - allows flexibility rather than support
External ear, epiglottis

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3
Q

What is an osteon

A

Concentric layers of bone with a central haversian canal carrying blood vessels and nerves along the long axis of the bone

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4
Q

What are Volkmann’s canals

A

Channels for blood which are s perpendicular to the Haversian canals which supply them from the periosteum

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5
Q

What is the difference between lamellar bone and woven bone

A

Woven bone is not arranged regularly and is weaker, being produced when bone is laid down rapidly

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6
Q

How is bone formed

A

Collagen matrix laid down then calcium apatite then hydroxyapatite
Vitamin D dependent

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7
Q

What are the different parts of a bone called

A

Ends are epiphysis

Middle is diaphysis

Between them is the metaphysis

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8
Q

What are osteoprogenitor cells

A

Precursors to osteoblasts

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9
Q

Osteoblasts

A

Lay down new bone matrix

Regulate osteoclast differentiation and action

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10
Q

Osteoclast

A

Resorbs bone by secreting acid and proteases.

RANK ligand increases formation and activity but can be mopped up by osteoprotegrin

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11
Q

Osteocyte

A

Mature osteoblasts entombed in bone matrix lacunae

Regulate bone remodeling when signalled mechanically or via hormones.

Long processes connect to other cells

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12
Q

What are bone resorption signals

A

RANKL

Sclerostin - inhibited by mechanical loading

Parathyroid hormone - stimulated when blood Ca is low to release from bone

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13
Q

What is the apophysis

A

Where bone attaches to tendon

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14
Q

What is ossification

A

Deposition of osteoid

Intramembranous - deposition on mesenchymal cells within a fibrous membrane to increase bone thickness. This matrix is mineralised as usual and osteoblasts are embedded to form osteocytes - repairs fractures

Endochondral - deposition in cartilage framework to lengthen bones - produces most of the skeleton

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15
Q

Secondary ossification

A

Endochondral ossification of epiphysis

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16
Q

Achondroplasia

A

Mutated FGF3 receptor leads to reduced chondrocyte growth –> short stature

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17
Q

What influences remodelling

A

Mechanical load, biological hormones, calcium and cytokines

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18
Q

What are the stages of remodelling

A

Activation - lining cells expose bone and secrete collegenase. Ocytes make RANKL to recruit osteoclasts

Resorption - osteoclasts borders become ruffled and secrete acid and proteases, then die by apoptosis

Formation - osteoblasts differentiate and lay down down osteoid in cavity then become osteocytes

Mineralisation - calcium laid down (promoted by high Pi/PPi ratio - phosphate - pyrophosphate)
Inhibited by osteopontin

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19
Q

Protective factors

A

Oestrogen inhibits osteoclast activity, recruits osteoblasts and is a RANKL antagonist

Calcitonin opposes PTH by inhibiting osteoclasts to decrease serum calcium

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20
Q

Describe fracture healing

A 
Macrophages remove debris
Fibrin clot
Inflammation and granulation tissue
Callus formation ( collar of cartilage and bone surrounding fracture to stabilise outer edges of bone)
Ossified to woven bone
Remodelling

Direct fracture repair - no callus formation but healing is simply an extension of remodelling giving rigid fixation
Pins may be necessary to immobilise bone for healing

Mechanotransduction - the conversion of mechanical stimulus into a biological response

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21
Q

Describe synovial joints

A

Capable of wide range of movement
Held in a fibrous synovial joint capsule with an inner membrane lining (synovium)
Ligaments may be internal or external to this
Bone ends covered in hyaline cartilage and between them is synovial fluid - capillary exudate and glycoproteins

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22
Q

Connective tissue disorders

A

Marfan - autosomal dominant - mutated fibrillin 1- long extremities,joint hypermobility, aortic rupture

Scurvy- vit c deficiency - fragile blood vessels, haemorrage, tooth/gum damage, poor health

Osteogenesis imperfecta I - reduced collagen I

Osteogenesis imperfecta II - abnormal collagen I

Ehlers-danlos syndrome IV - autosomal dominant, reduced collagen III, complicates pregnancy

Other ehlers-danlos - disrupted stages of collagen synthesis

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23
Q

Describe osteoarthritis

A

Multifactorial chronic degeneration of articular hyaline cartilage

Pain that worsens on joint use, loss of movement range, bone/soft tissue swelling, tenderness and creaking joints

Loss of collagen through chondrocyte matrix metalloproteases is irreversible to need to prevent this

Collagen II matrix damage leads to increase cartilage hydration which makes it weak.

Decreased PG concentration and chondrocyte death/proliferation indicates damage

Can be abnormal load on normal cartilage or normal load on abnormal cartilage

Loss of joint space is observed, form cysts and osteophytes and subchondral sclerosis.

Large weight bearing joints and distal and proximal inter-pharyngeal joints are most affected

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24
Q

Rheumatoid arthritis

A

Autoimmune disorder attacks synovial membrane

Synovial fluid becomes turbid from neutrophils

Proliferation of the synovium forms a pannus of granulation tissue over articular cartilage which cuts off its nutritional supply

Erosion of cartilage via MMPs

Scar tissue between the bone ends can ossify and immobilise the joint - ankylosis

Ulnar deviation, tendon and ligament rupture, soft tissue swelling. Pain and stiffness recede on use and inflammation tends to be symmetrical and peripheral.
Especially in small joints - not distal inter-pharyngeal joint

Loss of joint space. ESR and CRP are raised

Three times more in females

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25
Q

Osteoporosis

A

Bone resorption exceeds formation - lower bone density

Result of age, reduces exercise, oestrogen deficiency, diet and corticosteroids

Can cause kyphosis

Occurs most frequently in high trabecular content bones - femur head, vertebrae or radius

Dexa scans give a t score for bone density
osteopenia is -1 to -2.5
Below -2.5 is osteoporosis

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26
Q

Pagets disease

A

Increased resorption and formation leading to persisting woven structure and therefore weak bones

Deformities, fractures, pain and nerve compression

Autosomal dominant

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27
Q

Osteomalacia/rickets

A

Vit D deficiency decreases calcium absorption and therefore epiphyseal mineralisation

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28
Q

Osteomyelitis

A

Infection of bone leaving to inflammation which often affects growth plates in children

29
Q

ABCDE

A

Airway - obstruction needing removed, oxygen support needed

Breathing - observation of patient colour, breathing effort, injuries, vital sounds, symmetry and chest sound

Circulation - pulses and capillary refill

Disability - assess neurological function with Glasgow coma scale or AVPU plus temperature and blood glucose

Exposure - keep patient warm and check for any missed injuries

30
Q

Glasgow coma scale

A

Eyes < 4
Verbal < 5
Motor < 6

31
Q

AVPU

A

Alert
Verbal
Pain
Unresponsive

32
Q

Flail chest

A

2+ non-adjacent ribs fractured in two or more places resulting in a section of the ribs which is non functional and moves in and out during breathing

33
Q

Dislocation

A

Complete loss of contact at a joint

34
Q

Subluxation

A

Partial loss of contact at a joint

35
Q

Comminution

A

Fracture producing multiple fragments

36
Q

Greenstick

A

Incomplete breaks with bending

37
Q

Shock

A

Inadequate tissue perfusion leading to end-organ dysfunction

Anaphylactic - give adrenaline
Cardiogenic
Haemorragic/hypovolaemic
neurogenic
Septic

Permissive hypotension is allowing low BP to prevent further blood loss but maintaining cerebral perfusion

38
Q

What are the most vulnerable areas of a childs bone

A

Physis - growth plate

Apophysis - where tendon attached - stress on bone from muscle contraction

Metaphysis - less stable where bone structure changes from solid to weaker

39
Q

Salter harris

A

Where the epiphysis is broken off

40
Q

Osgood schlatters

A

Tibial tuberosity apophysis injury

41
Q

Sever’s disease

A

Chronic apophysitis of the heel in children as their bones are not yet fused

42
Q

Little leaguers elbow

A

Injury to medial chondyle of humerus

43
Q

Varus

A

Bow legged

44
Q

Valgus

A

Knock kneed

45
Q

The ACL

A

Attaches to anterior tibia prevents joint hyperextension, anterior tibial movement, tibial over rotation and varus/valgus angulation

Tears pop and feel unstable as well as swelling and pain

Diagnosed with lachmans test

Surgery for athletes, otherwise RICE and physio

46
Q

Why are girls more prone to ACL injury

A

Higher Q angle gives more knock-kneed stature (valgus on landing)

47
Q

Shin splint

A

Exercise induced pain in the anterior lower leg treated with rest

Can be caused by compartment syndrome where exercise causes increase in blood supply, increasing pressure as the compartment has low compliance. This reduced the blood supply and can cause ischaemia and pain

Can be relieved with fasciectomy

Shin splints can also be caused by dress fractures

48
Q

Female athlete triad

A

Predisposition to stress fractures

Diet, amenorrhea and osteoporosis

High protein limits vit C and D absorption and reduced oestrogen levels increase osteoclast activity

Reduce exercise, diet changes and immobilisation

49
Q

Meniscal tear

A

Can cause knee clicking, locking and chronic pain

The medial collateral ligament is more vulnerable to injury alongside the ACL and medial meniscus known as the unhappy triad

Diagnosed with MRI or McMurrays test and cartilage lesions are graded 0-4 where 4 is complete thickness loss

It has no vascular supply so cannot regenerate

50
Q

Carpal tunnel

A

Pressure on median nerve at wrist
More common in white women as they have smaller carpal tunnels

Paraesthesia, reduced sensation, muscle wasting and waking due to symptoms

51
Q

Ulnar nerve dysfunction

A

Compression of UN in elbow flexion

Paraesthesia, numbness, weakness

52
Q

Dupuytren’s disease

A

Contraction of the digital and palmar fascia
Myofibrils cause it to thicken an contract

Risk factors are genes, diabetes, cirrhosis, hand trauma

53
Q

Ulnar collateral thumb ligament rupture

A

Pulling thumb back too far

Inhibits tripod grip

Requires surgery

54
Q

Pain

A 
Physiological
Inflammatory
Vascular
Neuropathic
Psychogenic

Somatic pain is peripheral and well discriminated, usually sharper and often acute

Visceral pain is duller and not well discriminated

55
Q

What can cause pain

A

Bradykinin, lactic acid, serotonin, K, H, histamine, substance P, ATP

Prostaglandins increase pain sensitivity

56
Q

How does pain change

A

Early pain is sharp and transmitted quickly by myelinated A fibres which allow accurate localisation

Later pain is transmitted slowly by unmyelinated C fibres and produces dull, throbbing pain

Glutamate is the main excitatory neurotransmitter and acts at AMPA and NMDA receptors

Inhibitory ligands include opioids, noradrenaline, 5-HT (serotonin), GABA and glycine

57
Q

What is the gate control theory

A

That sensory inputs elsewhere can compete to reduce pain (such as rubbing a sore area)

58
Q

Simple analgesics

A

Paracetamol

Acts centrally to inhibit COX which synthesises prostaglandins from arachidonic acid

Decreases sensitivity to pain signals
Also increases bioavailability of 5-HT, inhibiting pain transmission

Anti pyretic effects

Hepatotoxicity

59
Q

Opioids

A

Act at various levels of the visceral pain pathway via inhibitory opioid receptors

These GPCRs block Ca channels to inhibit NT release and open K channels to hyperpolarise cells

Nausea, vomiting, constipation, resp/cough depression, urinary retention, hypotension, miosis, itching, wheal formation

Receptors are downregulated over time - tolerance

Naloxone is a mu receptor antagonists to treat opioid overdose

60
Q

NSAIDs

A

Aspirin (irreversible)

Ibuprofen

COX inhibitor plus anti-inflammatory

Affects COX-1 and COZ-2

Lower platelet aggregation which can lead to bleeding, peptic ulcers, renal damage, gastrotoxicity

Celecoxib is COX-2 selective

61
Q

How is neuropathic pain treated

A

Anti-epileptics or anti-depressants

62
Q

Triptans

A

5-HT agonists uses to treat migraines by constricting blood vessels

63
Q

Biphosphonates

A

alendronate

Reduce bone resorption by decreasing osteoclast recruitment and stimulating osteoblasts to produce osteoclast inhibitors

Also absorb onto hydroxyapatite crystals to prevent dissolution

Must be given constantly as it becomes incorporated into bone

Must be taken upright in the morning with lots of water 30 mins before food to prevent oesophageal rupture

Jaw pain must be reported due to risk of osteonecrosis

64
Q

Oestrogens and analogues

A

Transcription factor for intracellular receptors which inhibit osteoclasts
Can cause cancer however so not really used

Raloxifene/tamoxifene - osteogenesis receptor agonist at bone and antagonist elsewhere- reduces cancer risk and cholesterol

AE - hot flushes and DVT

65
Q

DMARDs

A

Initial treatment - NSAIDs then DMARDs then short course corticosteroids for flare-ups then biological therapy

Prevent RA progression and reduce pain and disability

May take months to take full effect and allow a reduction in NSAID use

Methotrexate - dihydrofolate reductase inhibitor which blocks DNA synthesis in rapidly proliferating cells ie immune cells
Many side effects such as vomiting, hair loss, rash, mouth ulcers, infections, reduced liver function and pulmonary toxicity

Sulfasalazine - anti-inflammatory immunosuppressant
Rash, GI upset, reduced leukocytes and platelets, photosensitivity

Gold, hydroxychloroquine and penicillamine have been used in the past but had multiple toxic effects

Biological therapies (cytokine inhibitors) - immunosuppressants given when DMARDs so not work
Infliximab is a TNF alpha antagonist given by IV in severe RA
66
Q

Why does OA increase with age

A

Keratan sulphate increased, water decreased, protein/urinate increased, extractability of proteoglycans decreased

67
Q

Major hormonal regulators of osteoclasts

A

positive - PTH

Negative - calcitonin, oestrogen

68
Q

Major hormonal regulators of osteoblasts

A

Positive - PTH, Vit D3, oestrogen, growth hormone

Negative - calcitonin

Year 1 - Semester 2 (3 decks)

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