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Osteoporosis and Metabolic Disease Flashcards

1
Q

Definition of osteoporosis

A

a metabolic bone disease characterised by low bone mass and micro architectural deterioration of bone tissue, leading to enhanced bone frailty and a consequent increase in fracture risk

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2
Q

Causes of osteoporosis

A 
thyrotoxicosis
hyper/hypo parathyroidism 
cushings
hyperprolactinaemia
hypopituitarism 
low sex hormone levels 
RA
ankylosing spondylitis 
polymyalgia rheumatica 
UC/chrones
liver diseases
- PBC, CAH, alcoholic cirrhosis, viral cirrhosis (Hep C)
malabsorption 
- CF
- Chronic pancreatitis 
- coeliac disease 
- whipples disease
- short gut syndrome
- ischaemic bowel 
medications
- steroids
- PPI
- enzymes inducing antiepileptic medications
- aromatase inhibitors (used in breast cancer)
- GnRH inhibitors
- Warfarin
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3
Q

Risk of fractures in osteoporosis

A

age
BMD
Falls
Bone turnover

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4
Q

What assessment in done to indicate whether someone is at risk of osteoporosis?

A

FRAX - fracture risk assessment tools

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5
Q

What is considered as a significant risk of fracture in osteoporosis?

A

> 10 % risk of osteoporotic fracture over 10 days

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6
Q

What should be done if a patient has significant risk of fracture?

A

Be referred for a DXA scan (dual energy X ray absorptiometry)

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7
Q

Who should be sent for a DXA scan in osteoporosis regardless of their %?

A

Oral steroids

suffer a low trauma fracture

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8
Q

Prevention of osteoporotic fractures

A

minimise risk factors
ensure good calcium and vit D status
falls prevention strategies
medications

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9
Q

Treatment of osteoporosis

A 
HRT
SORMR (selective oestrogen receptor modulator) - raloxifene
bisphosphonates - MAIN TREATMENT
Denosumab 
Teriparatide
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10
Q

Side effects of HRT

A

Increased risk of

  • blood clots
  • breast cancer with extended use into 50s/60s
  • heart disease and stroke if used after a large age gap from menopause
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11
Q

Side effects of SERMS

A

Hot flushes if close to menopause
increased clotting risks
lack of protection at hipsite

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12
Q

First line of treatment for osteoporosis

A

Oral biphosphonates

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13
Q

Side effects of biphosphonates

A

oesophagitis
iritis/uveitis
ONJ
atypical femoral shaft fractures

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14
Q

What needs to be done In long term use of bisphosphonates?

A

drug holiday for 1 - 2 years

usually after 10 years oral biphosphonates

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15
Q

What does denosumab do?

A

reduces osteoclast bone resorption

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16
Q

How is denosumab taken?

A

SC injection every 6 months

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17
Q

Side effects of denosumab

A

allergy/rash

symptomatic hypocalcaemia if given when vit D deplete

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18
Q

What is teriparatide?

A

intermittent human parathyroid hormone

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19
Q

side effects of teriparatide

A

injection site irritation
rarely hypercalcaemia
allergy
cost

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20
Q

What do osteoblasts do?

A

Fill in pit produced by the osteoclasts

controlling cell

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21
Q

What do osteoclasts do?

A

secretes acid into bone environment to dissolve it and produces a pit in the bone

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22
Q

Bone remodelling time; adult vs child

A

adult - very slow

child - really fast

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23
Q

What controls osteoblasts?

A

Parathyroid hormone

Vitamin D

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24
Q

What are the bone active hormones?

A

parathyroid hormone

vitamin D

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25
When does accelerated loss of bone mass begin?
menopause
26
What is the difference between rickets and osteomalacia?
They are both the same condition, just occur at different times
27
When does osteomalacia occur?
After the epiphyseal plates fuse
28
When does rickets occur?
Before the epiphyseal plates fuse
29
What casues rickets/osteomalacia?
severe nutritional vit D or calcium deficiency
30
Presentation of rickets
``` Stunted growth odd curve to spine or back large forehead odd shaped ribs and breast bones large abdomen wide bones wide ankles odd shaped legs failure to thrive ```
31
Osteomalacia symptoms
``` bone pain muscle weakness increased falls risk dont get deformities you can visualise microfractures of the bone ```
32
Definition of osteogenesis imperfecta
Genetic disorder of connective tissue characterised by fragile bones from mild trauma and even acts of daily life
33
Pathology of osteogenesis imperfecta
Defects in type I collagen Defective osteoid formation due to congenital inability to produce adequate intercellular substances like osteoid, collagen and dentine Failure of maturation of collagen in all of the connective tissues
34
Presentation of osteogenesis imperfecta
``` early osteoporosis growth deficiency defective tooth formation - dentigenesis imperfecta hearing loss blue sclera scoliosis/barrel chest ligamentous laxity easy bruising ```
35
Treatment of osteogenesis imperfecta
surgical - to treat fractures medical - to prevent fractures - IV bisphosphonates educational and social adaptations
36
Paget's disease of bone definition
Localised disorder of increased and uncontrolled bone turnover
37
Pathology of Paget's disease of bone
Excessive osteoclastic resorption followed by increased osteoblastic activity increased bone resorption by increased bone formation not occurring in a structured fashion Leads to disorganised bone - bigger - less compact - more vascular - more susceptible to deformity and fracture leading to pulsating pain
38
Causes of paget's disease of bone
``` Strong genetic component (15-30%) Restricted geographical distribution - those of Anglo-Saxon origins Environmental trigger - possibly of chronic viral infection with osteoclast ```
39
Symptoms of pagets disease of bone
> 40 y/o Bone pain occasionally bone deformity excessive heat over pagetic bone neurological complications e.g. nerve deafness ISOLATED ELEVATION OF SERUM ALKALINE PHOSPHATE (ALP) Calcium and phosphate typically normal bowed bone tibia broad forehead rarely the development of osteosarcoma in affected bone
40
Where can you get pagets disease of bone?
can be localised i.e. in one bone or can be widespread i.e. in bits all over the body never affects the WHOLE skeleton
41
Who with pagets is treated?
Bone pain Skull or long bone deformity Fracture Periarticular pagets
42
Most common areas to get pagets
Skull Spine Pelvis Long bones of the lower extremities
43
Predisposing factors to pagets
Increasing age Male Northern latitude FH
44
What % of patients with pagets disease are symptomatic?
5%
45
Other markers of bone turnover
PINP CTx NTx Urinary hydroxyproline
46
Is pagets easy to treat?
Yes
47
Treatment of pagets disease
IV biphopshonates
48
How do bisphosphonates work?
Analogues of pyrophosphate - inhibit osteoclasts by reducing recruitment and promoting apoptosis
49
Management of patients at risk of corticosteroid induced osteoporosis - the two groups
1. Patients > 65 y/o or those who have previously had a fragility fracture SHOULD be offered bone protection 2. Patients < 65 y/o should be offered a BONE DENSITY SCAN with further management dependent on this
50
Results of the bone density scan in the < 65s and their treatment
T > 0 = Reassure T 0 to -1.5 = Repeat bone density scan in 1 - 3 years T < - 1.5 = Offer bone protection
51
Subtypes of osteogenesis imperfecta
Type I - Type 4
52
Type I osteogenesis imperfecta
Collagen normal quality but insufficient quality
53
Type II osteogenesis imperfecta
Poor collagen quality and quantity
54
Type III osteogenesis imperfecta
Collagen poorly formed | Normal quantity
55
Type IV osteogenesis imperfecta
Sufficient collagen quantity but poor quality
56
What is osteopetrosis?
Bones become harder and more dense which can lead to pathological fractures
57
Who gets osteopetrosis?
Young adults
58
Inheritance of osteopetrosis
AR
59
What does radiology of osteopetrosis show?
Lack of differentiation between the cortex and the medulla described as - MARBLE BONE
60
What blood tests is osteoporosis associated with?
NORMAL blood tests (Ca, P, PTH, ALP)
61
What is the Z score of DEXA scans adjusted for?
Age Gender Ethnic factors
62
What do the T and Z scores of the DEXA scan look at?
T - bone density compared to a healthy 30 year old | Z - compares your bone density to someone your age and body size

MSK (25 decks)

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