Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y2 - BRS - MSK > How to Treat MSK Conditions Tutorial > Flashcards

How to Treat MSK Conditions Tutorial Flashcards

1
Q

What is Greek for bone?

A

Osteo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 4 types of bone cells?

A

Osteogenic cell = precursor, bone ‘stem cell’
Osteogenic cells give rise to:
Osteoblasts =
‘Bone forming’
Secretes ‘osteoid’
Catalyse mineralisation of osteoid
Osteocyte =
‘Mature’ bone cell
Formed when an osteoblast becomes imbedded in its secretions
Sense mechanical strain to direct osteoclast and osteoblast activity
Osteoclast =
‘Bone breaking’
Dissolve and resorb bone by phagocytosis
Derived from bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The balance between which 2 types of bone cells is responsible for the turnover of bone?

A

Osteoblast and osteoclast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the organisation of the cortical (compact) bone?

A

Cortical bone = outer shell of the bone

Made up of osteons and osteoblasts and osteoclasts which sit ont he lining of the bone on the outside (periosteum) or inside (endosteum)

Central canal = Haversian canal
And concentrically around the central canal are the osteocytes - sitting within the mineralised bone matrix
Volkmann’s canals = transverse system communicating between the osteocytes and the Haversian canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is an osteon?

A

Repeated structural units

Concentric ‘Lamellae’ (made up of osteocytes) around a central ‘Haversian Canal’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the structure of a cross section of long bones?

A

Periosteum – Connective tissue covering
Outer Cortex – compact (cortical) bone
Cancellous bone
Medullary cavity - central part of the bone, contains yellow bone marrow and cancellous bone
Nutrient Artery
Articular cartilage: on surface of bone at a joint only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do bones grow in children?

What is the structure of the long bone?

A

Growth plate proximally AND distally in long bones - known as the physis

Above the physis (closest to the joint) is the epiphysis and below is the metaphysis
Main body of the bone = diaphysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 3 mechanisms of fracture?

A
  1. Trauma - low energy or high energy
  2. Stress - abnormal stresses on normal bone
  3. Pathological - normal stresses on abnormal bone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why might the bone be abnormal pathologically?

A

Pathological causes of abnormal bone =
Osteoporosis - low bone mineral density
Low bone mineralisation e.g. Vit D deficiency, osteomalacia / rickets
Malignancy - primary bone cancer or bone metastases
Infection e.g. osteomyelitis
Osteogenesis imperfecta
Pagets - degenerative turnover of bone that leads to abnormal bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the difference between pathological VS insufficiency fractures?

A 
Pathological = all abnormal bone
Insufficiency = subgroup of pathological, usually applies to abnormalities due to metabolic diseases e.g. age related osteoporosis, or abonrmal mineralisation due to vitamin d deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are fracture patterns described?

A
  1. Soft tissue integrity - open (breached) VS closed
  2. Bony fragments - greenstick, simple, or multifragmentary (comminuted)
  3. Movement - displaced or undisplaced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 3 phases of fracture healing?

A
  1. Inflammation - bone bleeds, blood brings swelling but also cells and cytokines that eventually produce new blood vessels and osteoblasts gradually start producing collagen
  2. Repair - soft callus formation (type II collagen - cartilage) initially, that then turns into type I collagen forming a hard callus (bone)
  3. Remodelling - overtime, osteoclasts and osteoblasts remodel bone according to the stresses placed on it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is Wolff’s law?

A

Bone grows and remodels in response to the forces that are placed on it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical signs of a fracture?

A

Pain
Swelling
Crepitus - abnormal popping or cracking of a joint
Deformity
Adjacent structural injury e.g. nerves, vessels, ligaments, tendons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the investigations of fracture?

A

X-ray = first line investigation for suspected fractured bone
CT scan = used to assess exact architecture of a fracture as they only tell you about bones
MRI = mainly for soft tissue information
Bone scan = rarely used, but used for multiple fragments OR spread of infection so they are not performed without very good reason due to dye injection, exposure of radiation etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are fractures described on radiographs?

A 
Location - which bone and which part of the bone? (use thirds or diaphysis/metaphysis/epiphysis)
Pieces -  simple or multifragmentary?
Pattern - transverse, oblique or spiral?
Displacement - displaced or undisplaced?
Translated or angulated?
Plane - X, Y or Z plane?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 2 types of displacement?

A
  1. Translation - lateral (along a straight line)

2. Angulation - fracture is angled (no longer in a straight line)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the different types of translation?

A

Up or down = proximal / distal
Side to side = medial or lateral
Forward or backward = anterior / posterior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the different types of angulation?

A

Distal fragment moving away from the midline = valgus
Distal fragment moving towards the midline = varus
Backwards = volar
Front = Dorsal
Look at patient feet up - Internal (towards midline) / External (away from midline) rotation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the general principles of fracture management?

A

Reduce - open or closed
Hold - metal or no metal
Rehabilitate - move, physiotherapy, use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How can fractures be reduced?

A

Closed:
Manipulation
OR
Traction - pulling the skin or place pins in the bone (skeletal)

Open:
Mini-incision
OR
Full exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How can fractures be held?

A

Closed:
Plaster
OR
Traction (skin or skeletal)

Open:
Fixation (using metal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the different types of fixation?

A

Fixation uses metal and there are two methods: internal VS external

Internal (metal underneath the skin) =
Intramedullary = through the central canal of the bone using pins or nails
OR
Extramedullary = surface of the bone using plate/screws or pins

External (through the skin) =
Monoplanar
OR
Multiplanar

24
Q

How can patients be rehabilitated?

A

Using the limb - use pain relief and retrain the
Move
Strengthen the muscles around the limb
Weight bear - put stresses along the limb to remodel the bone in the right fashion

25
Q

What are some possible fracture complications?

A

General (complications affecting the whole body) - can be early or late:
Fat embolus - fat globules from bone marrow can enter the blood from the fracture, usually occurs within a few hours
DVT (deep venous thrombosis) - blood clot in the vein, that can become a thromboembolus
PE (pulmonary embolism) - fat embolus travelling to the lungs
Systemic sepsis from an infection that is spreading
Prolonged immoblity can increase risk of UTI, chest infection, pressure sores on the area of the body you are sitting on

OR

Local (complications just affecting the area around the fracture):
Can be divided into urgent, less urgent and late

26
Q

What are some urgent local complications of fractures?

A 
Local visceral injury
Vascular injury
Nerve injury
Compartment syndrome
Haemarthrosis 
Infection
Gas gangrene - infection caused by clostridium
27
Q

What are some less urgent, local complications of fractures?

A 
Fracture blisters
Plaster sores
Pressure sores
Nerve entrapment
Myositis ossificans - inflammation of the muscles, which causes calcium depositions on the muscles forming bone = stiff and painful muscles 
Ligament injury
Tendon lesions
Joint stiffness
Algodystrophy
28
Q

What are some late local complications of fractures?

A 
Delayed union - the bone hasnt healed in the time it normaly takes 
Malunion
Non-union
Avascular necrosis
Muscle contracture
Joint instability 
Osteoarthritis
29
Q

What is important to note in the history of a patient with a fracture?

A

Age
Comorbidityrespiratory/cardiovascular/diabetes/cancer
Preinjury mobilityindependent/shopping/walking/sports
Social hx: relatives, stairs, etoh

30
Q

What are the causes of a fracture? (esp. a neck of femur fracture)?

A

Insifficiency fracture - often in older age from osteoporosis

Requires trauma in younger population

OR combination of both

31
Q

What is the anatomy of the neck of a femur (NoF)?

A 
Articular cartilage on the femoral head
Femoral head attached to neck
Neck attached to shaft
2 lumps - greater and lesser trochanters
Inter-trochanteric line inbetween
32
Q

How do you classify an intra VS extra capsular NoF fracture?

A

In front or behind trochanteric line:
Above the intertrochanteric line = intracapsular
Below the intertrochanteric line = extracapsular

33
Q

How do you decide whether to fix or replace a NoF fracture?

A

Based on location / displacement and age:
Location = if extracapsular, usually try to fix it as there is minimal risk to the blood supply and avascular necrosis (AVN), so can be fixed using plates and screws (dynamic hip screw)
If intracapsular: if undisplaced, less risk to blood supply so fix with screws, if displaced, 25-30% risk AVN so replace in older patients, and fix in younger patients (<55)

34
Q

If the patient has a displaced intracapsular fracture and they are over 65, how do you decide whether they need a total or partial hip replacement?

A

Total hip replacement =
Walks >mile a day
Independent
Minimal co-morbidities

Heiarthroplasty (half hip replacement) - metal rubs on socket =
Lower morbidity
Multiple comorbidities

35
Q

What are the 3 classifications of joints?

A
  1. Fibrous = e.g. skulls, contain sutures, syndesmosis and interroseous membranes
  2. Cartilaginous = synchondroses e.g. sppone, symphyses e.g. pubic
  3. Synovial = calssified in how the move: plane, hinge, condyloid, pivot, saddle, ball and socket
36
Q

How are synovial joints stabilised?

A

The proportions of the 3 components:
Bone surface congruity
Ligaments
Muscles / tendons

37
Q

What are the components of the synovial joint?

A

2 bones encases in a capsule
Synovial membrane lines the capsule - this secreted synovial fluid that nourishes and lubricates the joint
Both heads of the bone have hyaline articular cartilage

38
Q

What is the hyaline articular cartilage composed of?

A

Composed of:

1) specialized cells (chondrocytes)
2) extracellular matrix: water, collagen and proteoglycans (mainly aggrecan)

Cartilage is avascular – it has no blood supply

Surface = horizontal collagen arrangement with horizontal cellular arrangement

39
Q

What is aggrecan?

A

A proteoglycan that possesses many chondroitin sulfate and keratin sulfate chains

Characterised by its ability to interact with hyaluronan (HA) to form large proteoglycan aggregates

40
Q

What is arthritis and what are the 2 major divisions?

A

Osteoarthritis (OA) = wear and tear of articular cartilage
Inflammatory arthritis = inflammation of the synovial membrane

Each can lead to each other

41
Q

How can OA lead to inflammatory arthritis as well?

A

Articular cartilage becomes eroded and worn
So the bones begin to produce more bone leading to sunchondral sclerosis and osteocytes
This then creates some inflammation as a by-product

42
Q

What is the WHO definition of OA?

A

A long-term chronic disease characterized by the deterioration of cartilage in joints which results in bones rubbing together and creating stiffness, pain, and impaired movement

43
Q

What are the risk factors of OA?

A 
Age
Excess weight / obesity
Mechanical constraints (e.g. intense sport)
Hereditary
Female, menopause
Osteonecrosis
Leg bone malalignment 
Oestrogen deficiency
Metabolic Syndrome 
Secondary to spondylarthritis or RA
Injury e.g. to cruciate ligament, meniscectomy
Metabolic diseases
Infectious diseases involving the bone
RA sequellae
44
Q

How does OA present clinically?

A

Pain (exertional / rest / night
Diability - walking distance / stairs / giving way
Deformity
Previous history - trauma, infection etc.
Treatments given - physio, injections, operations, etc.
Other joints affected

45
Q

How do you assess for OA?

A

Look
Feel
Move
Special tests

46
Q

What is seen on a radiograph (x-ray) showing OA?

A

Osteophyte
Loss of joint space
Subchondral cysts
Sclerosis

47
Q

How is OA managed conservatively and operatively?

A 
Conservative:
Analgesics
Physiotherapy
Walking aids
Avoidance of exacerbating activity
Injections (steroid, viscosupplementation)
Operative / surgical:
Replace knee / hip
Realign knee / hip
Excise - toe
Fuse - big toe
Synovectomy - RA
Denervate - wrist
48
Q

What are the 2 main types of bone infection?

A

Osteomyelitis - infection in the shaft of the bone

Septic arthrtiis - if the infection is in the joint

49
Q

How are osteomyelitis and septic arthritis differentiated?

A

Mainly location

Can be localised / confirmed using an X-ray or an MRI

50
Q

How does osteomyelitis present clinically?

A 
Refer to pathology lectures
Acute or chronic
Primary or secondary
Pain/swelling/discharge
Systemic signs:
Fevers, sweats wt loss
51
Q

How does septic arthritis present clinically?

A

Pain
Joint swelling/stiffness
Fevers, sweats, wt loss
Usually one joint affected - a painful, red, hot, swollen joint with fever

52
Q

What causes septic arthritis?

A

Bacterial infection of a joint (usually caused by spread from the blood) - e.g. Staphylococcus aureus, Streptococci, Gonococcus

53
Q

What are the risk factors for septic arthritis?

A

Immunosuppressed
Pre-existing joint damage
Intravenous drug use (IVDU)

54
Q

Why is septic arthritis a medical emergency?

A

Untreated, septic arthritis can rapidly destroy a joint

55
Q

How is septic arthritis diagnosed?

A

Joint aspiration - fluid sent out to lab for urgent gram stain and culture

56
Q

What are other investigations can help diagnose septic arthritis?

A 
Radiology:
Plain films
MRI scans: bony architecture/collections
CT if MRI not available
Bone scans: multifocal disease
Labelled White cell scans
Bloods = usually non-specific but sitll tell you if there is an infection:
CRP: acute marker
ESR slower response
WCC
TB culture/PCR
57
Q

What is the treatment for osteomyelitis VS septic arthritis?

A

Osteomyelitis:
Antibiotics: iv weeks
Surgical drainage: especially collections/sequestrum
Chronic: antibiotic suppression/dressings
Worst case scenario: amputation

Septic Arthritis:
Surgery: joint washout and drainage (repeated if required)
Iv antibiotics (days/weeks)
Immobilise joint in acute phase
Physiotherapy once over acute phase

Y2 - BRS - MSK (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions