MSK wk4 Flashcards

1
Q

What does an osteoblast do?

A

Builds bone

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2
Q

What does an osteoclast do?

A

Deconstructs bone

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3
Q

What is pagets bone disease?

A

A localised disorder of bone turnover
Increased bone resorption followed by increased by increased bone formation
However, disorganised placement
Bigger, less compact, more vascular and more susceptible to deformity and fracture
Deep pulsating pain

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4
Q

What is the genetic component of Paget’s disease?

A

SQSTMI gene

15-30% cases are familial

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5
Q

What is the suspected environmental trigger of pagets disease?

A

Possible chronic viral ingection within osteoclast

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6
Q

What are the symptoms of paget’s disease?

A
Over 40
Bone pain
Bone deformity
Excessive hear over pagetic bone
Neurological problems such as nerve deafness
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7
Q

What is the presentation of paget’s disease?

A
Isolated elevation of serum alkaline phospjatase
Bone pain + local heat
Bone deformity/fracture
Hearing loss
Rarely osteosarcoma in bone
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8
Q

How do you treat Paget’s disease?

A

Nothing if asymptomatic
Do not treat on raised alkaline phosphatase alone
IV bisphosphonate therapy
One off therapy of zoledronic acid

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9
Q

What is rickets/osteomalacia?

A

Severe nutritional Vit D/calcium deficiency results in insuficient mineralisation
Rikets in children; osteomalacia in adults

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10
Q

What are the symptoms of rickets?

A
Stunted growth
Fontanelles in skull don't fuse so enlarged head
Enlarged abdomen
Bent legs
Growth plates enlarged - abnormal joints
More common in darker skin
Failure to thrive
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11
Q

What are the symptoms of osteomalacia?

A

Microfractures
Never get through cortex

Bone pain
Muscle weakness
Increased fall risk

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12
Q

What is osteogeneis imperfecta?

A

Connective dissue genetic disorder
Characterised by fragile bones - fracture in acts of daily life
Other non-bone features as defect in type 1 collagen
Large clinical range (even within families)

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13
Q

How many types of osteogensis imperfecta?

A

8, although only 4 common
Type 1 - milder form - when child starts to walk
Type 2 - lethal by age 1
Type 3 - progressive deforming with severe bone dysplasia and poor growth
Type 4 - similar to type 1 but more severe

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14
Q

What are the other features of osteogensis imperfecta?

A
Growth deficincy
Defective bone formation
Hearing loss
Blue sclera (eyes etc very obvious)
Scoliosis/barrel chest
Ligamentous laxity
Easy bruising
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15
Q

How do you manage osteogenesis imperfecta?

A

Treat all fractures
Medical - IV bisphosophates
Social - educational and social adations
Genetic counselling

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16
Q

What is osteoporosis?

A

Metabolic bone characterised by low bone mass and micro architectural deterioation of bone tissue leading to enhanced fragility + fracture risk

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17
Q

What is Q fracture?

A

Program with variables to predict risk of fracture within age 30-85 in men and women

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18
Q

What is a DXA scan?

A

Scan that calculates bone density

Along with a T score - standard deviations against the norm

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19
Q

What are the endocrine causes of osteoporosis? (secondary osteoporosis)

A
Thyrotoxicosis
Hyper/hypo parathyroidism
Cushings
Hyperprolactinaemia
Hypopituitarism
Low sex hormone levels
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20
Q

What are the rheumatic causes of secondary osteoporosis?

A

Rheumatoid arthritis
Ankylosing spondylitis
Polymyalgia rhuematica

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21
Q

What are the gastroenterologycauses of secondary osteoporosis?

A

Inflammatory diseaes (UC/crohns)
Liver diseaes - PBC, CAH, alcoholic/viral cirrhosis
Malabsorption

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22
Q

What medications cause osteoporosis?

A
Steroirds
PPI
Enzyme inducting antiepipleptic medications
Aromatase inhibitrs
GnRH inhibitors
Warfarin
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23
Q

How do you prevent osteoporotic fractures?

A

Minimise risk factors
Ensure good calcium and vitamin D
Fall prevention strategies
Medications

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24
Q

What medications are used for osteoporosis?

A

HRT (best before early 60s/late 50s)
Selective oestrogen modulator (raloxifene)
Bisphosponates! Normal first line
Denosumab

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25
Q

What are the side effects of HRT?

A

Increased risk of blood clots
Increased risk of breast cancer of breast cancer with extended use into late 50s/early 60s
Increased heart disease risk/stroke if used after large gap from menopause

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26
Q

What are the side effects of selective osestrogen receptor modulator (raloxifene)?

A

Endometrium cancer. Therefore limited to 5 yr use

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27
Q

What are the negative effects of SERMs?

A

Hot flushes if taken close to menopause
Increased clotting
Lack of protection at hip site

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28
Q

What are the limitations of bisphosponates?

A

Adequate renal function needed
Adequate calcium/vit D levels
Good dental health advised
ONLY work in osteoporosis

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29
Q

What is the MOA of bisphosponates?

A

Bind to calcium
Inert until osteoclast comes up
Poisons osteoclast - and dies

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30
Q

What are the side effects of bisphosponates?

A
Oesophagitis
Iritis/uveitis
Not same in eGFR less than 30
Atypical demorla shaft fractures
Osteonecrosis Jaw
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31
Q

What is denosumab?

A

Monoclonal antibodiy against RANKL

Reduces osteclatic bone resoprtion

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32
Q

What are teh side effects of denosumab?

A

Allergy/rash

Symptomatic hypogylcaemia if given when vit D deplete

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33
Q

What is teriparatide?

A

An analogue of parathyroid hormone

Only anabolic treatment for bone

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34
Q

What are the side effects of teriparatide?

A

Injection site irritation
Rarely - hypercalcaemia
Allergy
Only one treatment course otherwise osteosarcoma

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35
Q

What are the different connective tissue diseases?

A
Systemic Lupus Erythematous (SLE) 
Scleroderma 
Sjogren's Syndrome 
Auto-Immune Myositis 
Mixed Connective Tissue Disease
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36
Q

What are the types of systemic vasculitis?

A

Giant Cell Arteritis
ANCA associated vasculitis:
Granulomatosis Polyangiitis (Wegner’s Granulomatosis)
Microscopic Polyangiitis
Eosinophilic Granulomatosis Polyangiitis (Churg-Strauss Granulomatosis)

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37
Q

What are the types of multi-system autoimmune conditions?

A

Connetive tissue diseases

Systemic vasculitis

38
Q

What is the process for diagnosing multi-system autoimmune conditions?

A
Cardinal features in history/exam
Immunology
Imaging
Tissue
Exclusion of differentials
39
Q

What are the mimics of multi-system autoimmune conditions (something that presents with multiple systems at once)?

A

Drugs (cocaine, minocycline
Infection (HIV, Endocarditis, Hep, TB)
Malignancy (lymphoma)

Cardiac myxoma
Cholesterol emboli
Scurvey

40
Q

What are the common patterns of SLE (lupus)?

A
4+ of:
Malar rash (butterfly rash)
Discoid rash
Photosensitivty
Oral ulcers
Arthritis
Serositis
Renal
Neurological
Haematological
Immunological
ANA
41
Q

Who is affected by SLE (Lupus)?

A

Young females
Women 9:1 compared to men
Young (20% before 16, 65% before 16-55)
Afro-caribbeans >asian > caucasian

42
Q

What is the difference on X-ray between lupus arthritis and rheumatoid arthritis?

A

In rheumatoid arthritis damage seen on x-ray

Lupus - only ligaments softened (reversible)

43
Q

What are the kidney involvement signs of lupus ?

A

Blood + protein in urine dipstick

44
Q

What is scleroderma?

A

Thickening of skin - top layer of skin 5x thicker than it should be

45
Q

Who is affected by scleroderma?

A
Girls 3:1
Middle aged (30-50)
46
Q

What are the groups of scleroderma?

A

Morphea
Limited
Diffuse

47
Q

What is the morpea group of scleroderma?

A

No complications beyond cosmetic

48
Q

What s the limited group of scleroderma?

A

Skin thickening limited to hands and forearms (does not travel above elbow)
AKA crest syndrome

49
Q

What does crest stand for?

A

C - calsidosis
R- Ranodes (poor circulation in fingers)
E - Oesphageal dismobility (heartburn, GORD)
S - scleradactialy (sausage fingers)
T - Teljectasia (small blood vessel visible on face/chest)

Don’t need all to diagnose

50
Q

What is diffuse scleroderma?

A

Thickening of skin can be across whole body

51
Q

What are the complciations ofl imited scleroderma?

A

Pulmonary hypertension

52
Q

What are the complications of diffuse scleroderma?

A

Pulmonary fibrosis
Renal crisis
Small bowel bacterial overgrowth

53
Q

Who gets sjorgens syndrome?

A

Women (9:1)
Onset 40-50 yrs
More common than others, less severe

54
Q

What is sjogren’s syndrome?

A

Syndrome that affects salivary glands + tear glands
Dryness in eyes + mouth
Parotid enlargement

55
Q

What are the complications of sjogren’s syndrome?

A
Lymphoma
Neuropathy
Pupura
Intestitial lung disease
Renal tubular acidosis
56
Q

What is autoimmune myositis?

A

Immune system affects muscles, often proximal (upper limb, thigh)
Weakness not pain

57
Q

What are the types of auto-immune myositis?

A

Polymyositis - younger patietns
Dermatomyositis - elderly people (skin lesiojns
Gottron’s papules
Helitrope rash

58
Q

What is a heliotrope rash?

A

Scaly lesion on knucles

59
Q

What is a gottron’s papule?

A

Violet discoleration around eyes

60
Q

What are the complciations of auto-immune myosistis?

A

Elderly - cancer

Younger - interstitial lung disease

61
Q

What is giant cell arteritis?

A

Medical emergency
Elderly age
Can often become blind if not immediately treated
Templar artery often affected

62
Q

What are the main classification criteria for giant cell artertiis?

A
3 or more of following
Over 50
New headache 
Temporal artery tenderness
Raised ESR (above 50)
Abnomrla temporal biopsy
63
Q

What is ANCA?

A

Anti-neutraphil cytoplasmic antibody

Targets neutrophils + burst innapropriately - destroys blood vesse

64
Q

What are the main ANCA associated vasculitises?

A

Granulomatosis with Polyangiitis (Wegner’s Granulomatosis)
Microscopic Polyangiitis
Eosinophilic Granulomatosis Polyangiitis (Churg-Strauss Granulomatosis)

65
Q

What is granulomatosis with polyangitis?

A

NEcrotising granulomatous inflammation
Usually invovled URT/LRT esp sinuses
Glomerulonephritis common
Normally affect small-medium vessels

66
Q

What is Microscoptic polynagintis?

A
Necrotising vasculitis with few/no immune deposits 
Normally affects small blood vessels
Necrotising arteritis may be present
Necrotising glomerulonephritis common
Pulmonary capillaritis often occurs
Granulotomatous infiltration absent
67
Q

What is esionpjilic granulomatosis with polyangitis?

A

Eosinophil rich + necrotising granulotomatomous inflammation
Often affects respiratory tract
Necrotising vascultiis often small-medium vessels
Associated with astham + eosinophillia
ANCA more common when glomerulonephritis present

68
Q

What conditions are likely to have anti-nuclear antibodies?

A
SLE (lupus)
Systemic sclerosis
MCTD
Drug induced lupus
Sjorgens syndrome
Poly/dermatomyositis
69
Q

What is the downside to ANA tests?

A

Very sensitive but not specific

70
Q

What are the specific ANA tests for lupus?

A

dsDNA
Ro
Sm

71
Q

What are teh specific ANA for scleroderma?

A

Scl-70

Centromere

72
Q

What are the specific ANA tests for polymyositis?

A

Jo-1

73
Q

What are the specific ANA tests for sjorgens?

A

Ro

La

74
Q

What lab/radiological investigations are used in auto-immune (multi system) diseases?

A

MRI
Pet-scan
Biopsy!

75
Q

What information abuot a patient should be conveyed when the paramedics hand over a patient?

A
Time of injury
Mechanism of injury
Suspected serious injuries
Vital signs
If any interventions have been carried out
76
Q

What is catastrophic haemorrhage control?

A

Treating catastrophic haemorrhage first

If not derteriation can occur

77
Q

What do you assess in airway?

A

Noises (speech, gurgling, stridor?)

Visual (swelling, vomit/blood debris)

78
Q

When should you assume a spine injury?

A

Dangerous mechanism
Reduced conscious level
Injury above clavicles
Neruolgical signs

79
Q

What is assessed in breathing?

A

Look for visible injuries, resp rate, effort/expansion
Palpate/percuss
Ascultate
Oxygen, analgesia + frain if required

80
Q

What is the clinical assessment of circulation? (ABC)

A
Heart rate
Palpable radial pulse?
CRT
BP
Urine output
Confusion?
Pulse pressure?
81
Q

What are the blood tests taken in circulation assesment?

A

Haemoglobin levels

lactate

82
Q

What imaging is done during circulation assessment?

A

Ultrasound

CT

83
Q

What are the five most common sites for blodd loss?

A
Chest
Abdomen
Pelvis
Long bones
Floor
84
Q

What should be considered when thinking about volume replacement?

A

IV access vs IO (intraosseous) access
Tye of fluid
Amount of fluid
Follow transfusion protocols - no need to get BP up to normal, only enough to perfuse organs

85
Q

When volume replacement is being performed, what should you monitor?

A

Vital signs
Urine output
Lactate

86
Q

What is the lethal triad during blood loss?

A

Coagulopathy (execssive bleeding)
Lactate
Hypothermia (clotting factors don’t work well if cold)

87
Q

What should be assessed in the disability stage?

A
AVPU
GCS
Pupils
Tone + reflexes
Log roll
88
Q

What is the expose stage?

A

Exposure to allow for full examination in case of hidden injuries
Recover to keep warm

89
Q

What does DEFG stand for?

A

Don’t ever forget Glucose!

90
Q

What are the bed side tests?

A

ECG
Arterial blood gas
Urine dipstick

91
Q

What does the secodnary survery entail?

A

A detailed head-toe examination
Although now with minimal handling

Also includes radiology

Plan management of injuries

92
Q

What are the options for further managment?

A

Teahter (operative)
Interventional radiology (control bleeding)
ITU