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Y1 Medicine - Body in Motion (Semester 1) > MSK - Ageing > Flashcards

MSK - Ageing Flashcards

1
Q

What are the two main categories of metabolic bone disease?

A
  1. Disorders of Bone Remodelling
  2. Disorders of Mineralisation
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2
Q

What is osteoporosis?

A

Osteoporosis is disorder of bone quantity, not quality - decreased bone mass and bone mineral density

Results in…
Deterioration of microarchitecture
Compromised bone strength
Increased risk of fractures

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3
Q

What is paget’s disease? What the associated clinical features?

A

Characterised as abnormal localised bone remodelling

Primarily increased OC resorption - resulting in increased but disorganised bone formation

Polyostotic disease – multiple bones are diseased

2nd most common metabolic bone disease

Clinical features…
1. Enlarged skull
2. Bowing of long bones
3. Large joint OA
4. Fractures
5. Nerve compression (e.g. due to thickening of the skull) - Deafness

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4
Q

What is Paget’s sarcoma?

A

Pagets disease turns into a malignant bone cancer

Makes up less than 1% of Paget’s cases

Most commonly osteosarcoma
Osteo = osteoblastic differentiation and malignant osteoid production
Sarcoma = malignancy from mesenchymal cells

Metastatic disease has poor prognosis

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5
Q

Outline the pathogenesis behind paget’s disease.

A

Most cases are spontaneous but with a significant genetic component - appears to be a genetic predisposition, that requires an environmental trigger

Pathology - Abnormal osteoclasts/precursors
Greater in number, unusually large and hypersensitive to stimulation

3 phases which can co-exist in the same bone
1. Lytic – Intense osteoclastic resorption
2. Mixed – resorption and compensatory formation (OB activity)
3. Sclerotic – predominant osteoblastic formation

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6
Q

What investigations and treatments are used for paget’s disease?

A
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7
Q

What is osteopetrosis?

A
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8
Q

Summary of osteoporosis, paget’s disease and osteopetrosis.

A
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9
Q

What are the two disorders of mineralization?

A

Disorders of Mineralisation
1. Hyperparathyroidism
2. Vitamin D-related disorders (osteomalacia, rickets)

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10
Q

What is hyperparathyroidism?

A
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11
Q

What are the consequences of having elevated PTH?

A

All resulting in increased bone breakdown

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12
Q

How does hyperparathyroidism present itself clinically?

A

Symptoms and signs

‘Bones, stones, abdominal groans. Thrones and psychic moans’
Bones - arthiritis, osteoporosis, gout, pseudo-gout.
Stones - Kidney stones - elevated Ca2+
Abdominal groains - constipation, GI Ulcers and acute pancreatitis, polyuria
Psychic moans (most common presentation) - fatigue, depression, confusion

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13
Q

What are the treatments for hyperparathyroidism?

A

Depends on whether it is primary or secondary

Primary
Parathyroidectomy = 97% cure - surgical removal of gland/tumour

Secondary
Tackle the underlying cause
Vit D deficiency most common
Renal disease - complex

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14
Q

Recap what are the sources of Vitamin D, how is it metabolized and what effects does it have on the body (Calcium and Phosphate)?

A
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15
Q

What is rickets?

A

Rickets – disease of childhood

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16
Q

How does rickets appear clinically?

A
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17
Q

What are the treatments used for rickets?

A
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18
Q

What is Osteomalacia?

A
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19
Q

How does osteomalacia present itself clinically? What treatment is required?

A
  • Bone and muscle pain
  • Atypical fractures - ‘Looser zones’
  • Femur/femoral neck fractures
  • Proximal muscle weakness
  • Fatigue
  • Hip arthritis with ‘protrusio’ - head of the femur pushes into the acetabulum – left hand side

Treatment = Large doses of vitamin D

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20
Q

What does the epidemiology of osteoporosis look like?

A
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21
Q

How does bone mass/density change as we age?

A
  1. Increase in bone mass - Men – higher peak bone mass – more muscle mass – greater pull – greater bone density - peaks at late 20’s - Men start at a higher peak bone density relative to women
  2. Consolidation period
  3. Decline – age related bone loss – after the age of 40

Quicker drop off in females - drop in oestrogen after menopause which is protective - inhibits Rank-L

Eventually people’s bone density decreases to a point where it is below the fracture threshold – in terms of bone density – at this point their at a high risk of low energy fractures

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22
Q

How does bone mass/density change as we age?

A
  1. Increase in bone mass - Men – higher peak bone mass – more muscle mass – greater pull – greater bone density - peaks at late 20’s - Men start at a higher peak bone density relative to women
  2. Consolidation period
  3. Decline – age related bone loss – after the age of 40

Quicker drop off in females - drop in oestrogen after menopause which is protective - inhibits Rank-L

Eventually people’s bone density decreases to a point where it is below the fracture threshold – in terms of bone density – at this point their at a high risk of low energy fractures

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23
Q

What are insufficiency and fragility fractures?

A

Insufficiency - like a stress fracture -repeated loading

Fragility - normal force, abnromal bone - fracture

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24
Q

What is a common spinal fracture observed in older patients?

A

Forms a vicious cycle – compression – more forward lean – increased compression

Osteoporosis - risk factor

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25
What is a common fracture observed in the arm in older patients?
Proximal Humerus Fracture
26
What is a common fracture seen in the forearm in older patients?
Wrist fractures - associated with displacement of wrist reltaive to radius Most common MSK injury 17.5% of all fractures 3:1 female:male Eponymous terms Smith’s = volar extra-articular (forward) Colles’ = dorsal extra-articular (backwards)
27
How are wrist fractures managed?
Reduction and immbolization - cast is normally sufficient Sometimes surgery is required - plate and screws **Outcomes** - Usually very good if adequate rehab - Residual stiffness quite common - Complex regional pain syndrome Increased risk for future fracture - Most people over 55 need DEXA scan
28
How do fractures in the pelvis normally present? How are they normally treated/managed?
Pelvis can be divided into multiple rings - usually have two fractures in a single ring structure Conservative management - bedrest, NSAIDs, physio
29
What is important to remember with hip fractures?
Very high morbidity/mortality - 1/3 will return to previous function - 1/3 will loose independence - 1/3 will die within a year Hence, quick surgery to fix or replace the hip and allow immediate mobilisation is important
30
What is the current treatment/management plan for hip fractures?
Historically was bedrest - associated with a whole host of morbidities - wasting, infection, etc. All hip fractures treated with surgery now (almost)
31
What are the different form surgery used for hip fractures?
Important consideration - Blood supply of the femoral head – retinacular vessels – fractures that are before the neck, the vessels are not effected but if its higher up --> bone may lose blood supply – necrosis – replacement – usually hemi-arthroplasty Intracapsular & extracapsular refer to the location of the fracture
32
What is an important consideration when deciding whether to fix or replace a fractured hip?
Blood supply of the femoral head – retinacular vessels – fractures that are located before the neck, the vessels are not effected But if its higher up – bone may lose blood supply – necrosis – replacement – usually hemi-arthroplasty
33
What are atypical femor fractures?
Atypical femoral fracture is an uncommon complication of long-term use of bisphosphonates Features... 1. Insufficiency fracture - No trauma 2. Subtrochanteric - within 5cm below lesser trochanter 3. mainly transverse 4. Involve lateral cortex 5. Endosteal or periosteal thickening 6. Cortical beaking - little bump Why? Osteoclast remodelling inhibited Unable to heal micro-trauma Goal - Aim to prevent complete fracture - Biphosphonate holiday and surgery (intramedullary nail)
34
What is arthritis?
Refers to any disorder which affects joints Symptoms of pain and stiffness Characterized by the destruction/degeneration of joint cartilage Over 100 different types but osteoarthritis (most common) and rheumatoid arthritis are most prevelant
35
What is hyaline cartilage?
Hyaline cartilage - found at the ends of articulating joints - flexible, resilient and has a very low friction co-efficient Found at the ends of long bone and at the costal cartilage of ribs
36
What are the different components that make up hyaline cartilage?
37
How is hyaline cartilage structured?
38
When looking at the overarching arragnment of collagen fibres in hyaline cartilage, what do we observe?
Organization of fibers – loop structure
39
How does the healing of superficial and deep lacerations differ in hyaline cartilage?
Superficial laceration – low levels of healing + some cell proliferation – common in arthritis
40
How do the following factors change with age and in OA - Water content, elasticity/stiffness, chrondrocytes, proteoglycans and collagen?
41
How does NICE define OA?
OA - a syndrome of joint pain accompanied by varying degrees of functional limitation and reduced quality of life Reduced quality of life - important aspect
42
How does bossman Gavin define OA and what are the primary & secondary causes?
43
What is a more appropriate way of viewing OA - instead of simply wear and tear?
Wear, Flare and Repair 1. Overuse, obesity, malalignment 2. Inflammation 3. Repair processes suboptimal
44
What are the four cardinal signs of OA on a radiograph?
45
What are the defining features that characterize OA
Missing from diagram - primarily effects larger joints
46
How is OA normally diagnosed?
47
What are the treatment options for OA?
Conservative should be considered first... - Patient education - Physiotherapy and exercise - Lifestyle changes and adaptations a) Lose weight b) Simple Analgesia c) Walking aids If conservative means are exhausted or in the presence of disabling symptoms, joint replacement should be considered
48
Are the outcomes for joint athroplasty normally succesful?
49
What is rheumatoid arthritis (RA)?
- Chronic systemic autoimmune disease - Cell-mediated immune response against soft tissue and bone - Affects almost every body system
50
How does fully developed RA present itself clinically?
Inflammatory polyarthritis - Symmetrical - Peripheral (small and large joints) - Morning joint stiffness - Erosive and deforming - Progressive hand deformities - Subcutaneous nodules - +ve RF and anti-CCP Uncommon to see patient's with very severe RA these days - improved management
51
What is the underlying pathophysiology behind RA?
Increased levels of protein citrullination (arginine converted to citruline) - these modified protein are immunogenic, in turn and triggering an autoimmune response Results in a T-cell mediated immune reponse - B-cells receive antigen - processed - Presents antigen to T-cell - T-cell activates presenting B-cell - B-cell population amplify and produce auto-antibodies (RF and anti-CCP) RF - antibody that recongizes the Fc portion of IgG antibodies Anti-CCP - antibodies that target citrulinated proteins/peptides
52
Why is anti-CCP important for disease diagnosis?
People that are asymptomatic still produce anti-CCP This is ideal, as it allows us to detect the presence of RA and begin treatment early
53
How does RA present itself clinically?
Deformities also possible but less common
54
What are the extra-articular and systemic symptoms in RA patients?
Average of 10 year reduction in life expectancy
55
How does RA differ to OA in terms of their presentation and symtpoms?
RA - smaller joints progressing to larger ones OA - primarily effects larger joints
56
How is RA diagnosed?
Basically perform a blood test looking at levels of RF and anti-CCP (Better sensitivity - present in 96-98% of RA patients) Possibility of also performing an x-ray
57
What does the X-ray of RA patients look like?
Erosive arthritis - Joint space narrowing - Subchondral erosions - “Gull-wing" appearance - Joint ankylosis - stiff joints - Subluxations/dislocations - less common
58
What are the four overarching principles for RA management?
1. Treatment shared between patient and rheumatologist 2. Maximise long term HRQL through control of symptoms, prevention of structural damage, normalisation of function and social participation. 3. Abrogation of inflammation is the most important 4. Treatment to disease activity optimises outcome
59
What drugs are the first line treatment for RA?
Early initiation of DMARDs is important - improves symptoms and delays progression Monotherapy with **methotrexate** as first line DMARD - alternatives: sulfasalazine, leflunomide, hydroxychloroquine Combined with short term glucocorticoids use Following first line DMARDs - disease activity needs to be monitored a) Gradual reduction/stopping drugs b) Step-up strategy - Add further cDMARDs in combination or consider biological DMARDs, eg TNF inhibitors, rituximab
60
Apart from DMARDs, what other ways is RA managed?
61
If we have an acute episode of monoarthritis, what is the differential diagnosis? How to approach?
Acute monoarthritis - Inflammation of a single joint that has been present for 2-52 hours Differential diagnosis - GRASP 1. Gout 2. Reactive arthritis - arthritis that develops following an infection where the organism cannot be recovered from the joint. 3. Autoimmune/arthritic 4. Septic arthritis 5. Pseudogout - deposition of calcium pyrophosphate dihydrate crystals in the synovium Septic Arthritis until proven otherwise - Time is vital: leads to cartilage injury, septic shock and death
62
How does septic arthritis normally present?
63
What investigations should be conducted on patients that are suspected of having septic arthritis?

Y1 Medicine - Body in Motion (Semester 1) (11 decks)

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