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Year 2 > MSK Diseases 2 > Flashcards

MSK Diseases 2 Flashcards

1
Q

Bone and soft tissue tumours

Hx

O/E

A

Hx

  • Bone pain
  • Night pain
  • Previous history of Cancer
  • Red flags: worsening pain, weight loss, night sweats

O/E

  • Lump/ soft tissue mass
  • Skin may be stuck to mass
  • Lymph nodes
  • nothing
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2
Q

Bone and soft tissue tumours

Ix

A
  • Bloods: FBC, U&E, CRP, ESR
  • Bone profile: Ca, Phosphate, albumin, ALP
  • LFTs, LDH (lactate dehydrogenases)

Markers of bone tumours: LDH, ALP

-X-ray (rule of 2)

Whole bone, 2 views, 2 joints (above and below)

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3
Q

Bone and soft tissue tumours

Diagnosis?

A
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4
Q

Bone and soft tissue tumours

Benign more common in children

TRUE OR FALSE

A

TRUE

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5
Q

What is the malignant bone and soft tissue tumour in children

A

Ewing’s sarcoma most common

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6
Q

Compare and contrast well defined, ill defines and sclerotic bone and soft tissue tumours

A
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7
Q

Examples of benign tumours

A

Osteoma

Osteochondroma

Giant cell tumours

Bone cysts

endochrondromas

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8
Q

What is Osteoma?

A
  • benign overgrowth of bone most typically occurring on the skull
  • more common in children
  • resolve by itself in about 18 months
  • night pain relieved by NSAIDs
  • associated with Gardner’s syndrome (a variant of familial adenomatous polyposis, FAP)
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9
Q

What is Osteochondroma?

A

exotosis

most common benign bone tumour

more in males, usually diagnosed in patients ages <20 years

cartilage-capped bony porkection on the external surface of a bone

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10
Q

WHat is a giant cell tumour?

A
  • tumour of multinucleated giant cells within a fibrous stroma
  • peak incidence 20-40 years
  • occus most frequently in th epiphyses of long bones
  • X-ray shows a “double bubble” or “soap bubble” appearance
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11
Q

Examples on malignant bone tumours

A
  • Metastasis
  • Multiple myelomas

Primary

  • Osteosarcoma
  • Chondrosarcoma
  • fibrosarcoma

Haematological

  • Leukaemia
  • Lymphoma
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12
Q

Features of malignant bone tumours

A

More common in older (>40yr)

Hypercalcemia

Fractures

Cauda equina

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13
Q

Multiple myelomas are neoplastic plasma cells

TRUE OR FALSE

A

TRUE

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14
Q

How do you identify multiple myelomas

A
  • Bence-jones proteins in urine
  • Presentation: CRAB

HyperCalcaemia

Renal failure

Anaemia

Punced out Bony lesions

Pathological fractures

  • Histology: round plasma cells, eccentric nucleus, clock face chromatin
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15
Q

Examples of primary bone tumours (malignant)

A

Osteosarcoma

Ewing’s sarcoma

Fibrosarcoma

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16
Q

Features of Osteosarcoma?

A
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17
Q

Features of Ewing’s sarcoma

A
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18
Q

Features of Fibrosarcoma

A
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19
Q

Which one is Sun burst appearance and which one is Codman’s triangle

A
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20
Q

Muscle and ligamentous injuries

A
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21
Q
A
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22
Q

How do you grade in muscle injuries

A
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23
Q

What is grading for ligamentous injuries like?

A
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24
Q

What is the healing potential for Ligaments

A

— Depends upon grade of injury and ligament injured.

— 3 phases - same as bone.

  • Inflammation.
  • Repair - Type III collagen
  • Remodelling - Type I collagen
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25
Q

What is the healing potential for Tendon

A
  • Depend upon Grade of injury.
  • Repairs weakest at 7 - 10 days.
  • Regain most of original strength at 21 - 28 days.
  • Maximum strength at 6 months
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26
Q

What is the importance of physio?

A
  1. Promote early function.
  2. Increase ROM.
  3. Encourage weight bearing.
  4. Improve muscular strength/endurance and control.
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27
Q

Bone structure

  • Outer= inner=
  • ECM=
  • Bone is layer down in lamellae
  • Osteon-=
  • Volkmann’s cannal=
  • Woven bone=
A
  • Outer= cortex, inner=trabecular
  • ECM= osteoclasts, osteoblasts and osteocytes
  • Bone is layer down in lamellae
  • Osteon-= concentric lamellae with central haversian canal
  • Volkmann’s cannal= in between osteons
  • Woven bone= immature bone
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28
Q
A
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29
Q

Normal function of bone

A
  • Support
  • Movement
  • Protects organs
  • Hematopoiesis
  • Mineral homeostasis
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30
Q

Bone remodelling

A

RANKL-RANK-OPG:

RANK binds to osteoclast precursor

RANKL binds to RANK->stimulates NFkB-> activates osteoclast formation

OPG inhibits RANK/RANKL binding-> inhibiting osteoclast formation

31
Q

WHat is Reverse RANK-RANKL signaling

A

RANK binds to extracellular vesicle-> attaches to RANKL on osteoblast-> stimulates RUNX2-> osteogenesis

Sclerostin inhibits Wnt-> inhibiting osteogenesis

32
Q

Bone mineralisation is associated with?

A

calcium and phosphate

33
Q

Ca2+ regulated by ____ cells of the Parathyroid gland

A

Ca2+ regulated by chief cells of the Parathyroid gland

34
Q

What happens if there is a decrease in calcium?

A

If decrease in Ca2+-> PTH-> decrease PO4 & increase Ca2+

35
Q

What happens next after increase in calcium and decrease in phosphate

A

binds to osteoblasts-> promotes osteoclastogenesis via RANKL upregulation-> excess Ca2+ ( CKD -> 2dary hyperparathyroidism)

stimulates production of calcitriol-> promotes synthesis of calbindin in intestinal epithelial cells-> increased absoprtion of Ca2+ in GI tract

promotes Ca2+ reabsorption in kidneys

36
Q

What does oestrogen inhibit

A

sclerostin

37
Q

inhibition of sclerostin allows?

A

osteoblastogenesis

+ inhibits RANKL-> no osteoclastogenesis

38
Q

What happens when there is oestrogen deficiency?

A

Oestrogen deficiency-> osteoclastogenesis, no inhibition of sclerostin-> inhibited osteoblastogenesis

Perimenopause/Childbearing-> estrogen-> osteoblastogenesis

Postmenopausal-> problems start – osteoporosis/ osteopenia

39
Q

What is osteoporosis?

A
  • Porous bones- reduced trabecular bone à increased risk of fracture (50 y/o female = 50% lifetime risk of fragility fractures)
  • resorption>formation
  • Most common metabolic bone disease
40
Q

Osteoporosis RF

A
  • Affects women more after menopause à less oestrogen àosteoclastogeneis + uninhibited sclerostin à deceased osteoblastogenesis
  • Affects old people more (senile osteoporosis) à impaired osteoblast function à more resorption
  • Older age
  • Female
  • Reduced mobility and activity
  • Low BMI (<18.5 kg/m2)
  • Rheumatoid arthritis
  • Alcohol and smoking
  • Long term corticosteroids. NICE suggest the risk increases significantly with the equivalent of more than 7.5mg of prednisolone per day for more than 3 months)
  • Other medications such as SSRIs, PPIs, anti-epileptics and anti-oestrogens
41
Q

What is the determinant of osteoporosis

A

•Determinants of peak bone mass: genetics, body weight, sex hormones, diet, exercise

Determinants of bone loss: sex hormone deficiency, genetics, diet, immobility, diseases, drugs (corticosteroids, aromatase inhibitors, glitazones

42
Q

CF of osteoporosis

A
  • height loss
  • thoracic kyphosis or lumbar lordosis
  • protuberant abdomen
  • decreased lung capacity
  • early satiety, weight loss, oesophageal reflux
43
Q

Ix for osteoperosis?

A

-DEXA scan

  • Compares pts bone density to that of a normal adult
  • Produces a T-score = 2.5 è osteoporosis
  • X ray
  • PTH, TFTs, vit D, urinary calcium (24hr), bone turnover markers- CTX & P1NP
44
Q

Treatments for osteoporosis

A

Antiresorptive:

  • Bisphosphonates eg alendronic acid
  • Anti-RANKL ab eg Denosumab

Anabolic:

  • recombinant PTH eg teriparatide
  • Anti-sclerostin Ab eg Romosozumab
45
Q

What is pagets disease

A
  • Disorder of bone remodelling – focally increased and disorganised bone turnover
  • driven by abnormal osteoclasts à increased and haphazard osteoblast activity à formation of poor quality woven bone

Paget’s disease of bone refers to a disorder of bone turnover. There is excessive bone turnover (formation and reabsorption) due to excessive activity of both osteoblasts and osteoclasts. This excessive turnover is not coordinated, leading to patchy areas of high density (sclerosis) and low density (lysis). This results in enlarged and misshapen bones with structural problems that increase the risk of pathological fractures. It particularly affects the axial skeleton (the bones of the head and spine).

46
Q

Causes for pagets disease

A

Genetics

  • Fx
  • Mutations- SQSTM1 most common
  • Ethnicity

Environmental

  • Involvement of paramyxovirus
  • Mechanical loading of affected bone
  • Poor nutrition in childhood
47
Q

CF of pagets disease

A
  • Early – asymptomatic
  • Bone Pain= bone impinges on nerves
  • Overgrowth of bone
  • Facial deformity- leontiasis
  • Hearing loss- impingement on auditory nerve
  • Vision loss – impingement on optic nerve
  • Osteosarcoma à pagets sarcoma
  • Kyphosis
  • Lower limb muscle weakness
  • Pelvic asymmetry
  • Bow legs
  • Arthritis
  • Fractures
  • Bone deformity
  • Fractures
  • Hearing loss can occur if it affects the bones of the ear
48
Q

Ix for pagets disease

A
  • Elevated ALP (isolated)
  • Elevated bone turnover markers à P1NP and CTX
  • X ray- osteolysis, osteosclerosis, chaotic bone architecture, bone expansion and deformity
  • Radionucleotide bone scan- increase in tracer uptake in affects bones
49
Q

Pagets disease treatment

A

•Bisphosphonates eg Zoledronate and risedronate – they cause osteoclast dysfunction/death

Other measures include:

  • NSAIDs for bone pain
  • Calcium and vitamin D supplementation, particularly whilst on bisphosphonates
  • Surgery is rarely required for fractures, severe deformity or arthritis
50
Q

What is rickets

A
  • decreased serum calcium/phosphate à widening and delay of mineralisation of growth plates in bones
  • Associated with osteomalacia
51
Q

Causes for Rickets

A

•Causes bowing deformity of bones, rachitic rosary, Harrison sulcus, widened wrist

52
Q

Rickets

other features

A
  • Widening gair/ delay in walking
  • Bone pain, fatigue
  • Fractures
  • Short stature
  • Tetany/ seizures
  • Cardiomyopathy
53
Q

What can you see radiologically with rickets

A
54
Q

What other types of rickets

A

Vitamin d dependent rickets

Hypophosphatemic rickets

55
Q

Vitamin d dependent rickets

Causes?

Types?

A

Caused by

  • Deficiency in 1 alpha hydroxylase
  • Inactivating mutations in the vit D receptor

VDDR type I:

  • Deficiency in 1-alpha hydroxylase ( converts into calcitriol)
  • 25(OH) will be normal/high but 1,25(OH) will be low

VDDR type II:

  • Inactivating mutations in Vit D receptor- VDR
  • Both 25(OH), 1,25(OH) will be normal or high
56
Q

Hypophosphatemic rickets

WHat is it

subtypes?

A
  • Excessive renal phosphate losses
  • Low serum phosphate for normal bone mineralisation
  • Excess in FGF23 expressed by osteocytes
  • PHEX, DMP1 normally inhibit FGF23-> mutations increase FGF23
  • Subtypes:
  • XLH: X-linked, PHEX- more common
  • ADHR:AD, FGF23
  • ARHR:AR, DMP1
57
Q

What is osteomalacia?

causes

A
  • Softening of bones dues to defective mineralisation of newly formed bones
  • Mainly caused by vit D deficiency, Hypophosphatemia, inhibitors of mineralisation
58
Q

CF for osteomalacia

A
  • Bone pain
  • Bone tenderness
  • Fractures
  • Muscular weakness
  • Malaise
  • Tetany
  • Fatigue

Looser zones are fragility fractures that go partially through the bone.

59
Q

Ix for osteomalacia?

A
60
Q

Treatment for Rickets and osteomalacia

A
  • Vitamin D and calcium
  • Active vit D metabolites (+/- calcium infusions) for VDDR
  • Phosphate supplements for hypophosphataemic rickets, plus active vitamin D metabolites
  • Burosumab (anti FGF23 ab) for children with XLH
61
Q
A
62
Q

What is FRAX Tool

A

The FRAX tool gives a prediction of the risk of a fragility fracture over the next 10 years. This is usually the first step in assessing someone’s risk of osteoporosis.

It involves inputting information such as their age, BMI, co-morbidities, smoking, alcohol and family history. You can enter a result for bone mineral density (from a DEXA scan) for a more accurate result but it can also be performed without the bone mineral density.

It gives results as a percentage 10-year probability of a:

  • Major osteoporotic fracture
  • Hip fracture
63
Q

What does DEXA SCAN show

WHO Classification

A

Bone mineral density (BMD

64
Q

What is FRAX assessment

A

Assessing For Osteoporosis

The first step is to perform a FRAX assessment on patients at risk of osteoporosis:

  • Women aged > 65
  • Men > 75
  • Younger patients with risk factors such as a previous fragility fracture, history of falls, low BMI, long term steroids, endocrine disorders and rheumatoid arthritis.
65
Q

FRAX outcome without a BMD result will suggest one of three outcomes:

FRAX outcome with a BMD result will suggest one of two outcomes:

A

FRAX outcome without a BMD result will suggest one of three outcomes:

  • Low risk – reassure
  • Intermediate risk – offer DEXA scan and recalculate the risk with the results
  • High risk – offer treatment

FRAX outcome with a BMD result will suggest one of two outcomes:

  • Treat
  • Lifestyle advice and reassure
66
Q

Management for osteoporosis

A

Lifestyle Changes:

Vitamin D and Calcium:Calcichew-D3, which contains 1000mg of calcium and 800 units of vitamin D (colecalciferol).

Bisphosphonates are the first-line treatment for osteoporosis.

  • Alendronate 70mg once weekly (oral)
  • Risedronate 35 mg once weekly (oral)
  • Zoledronic acid 5 mg once yearly (intravenous)
67
Q

Simplified Pathophysiology Osteomalacia

A

Patients with darker skin require a longer period of sun exposure to generate the same quantity of vitamin D. A standard diet contains inadequately levels of vitamin D to compensate for a lack of sun exposure. Reduced sun exposure without vitamin D supplementation leads to deficiency. Patients with malabsorption disorders (such as inflammatory bowel disease) are more likely to have vitamin D deficiency. The kidneys are essential in metabolising vitamin D to its active form, therefore vitamin D deficiency is common in chronic kidney disease.

Vitamin D is essential in calcium and phosphate absorption from the intestines and kidneys. Vitamin D is also responsible for regulating bone turnover and promoting bone reabsorption to boost the serum calcium level.

Inadequate vitamin D leads to a lack of calcium and phosphate in the blood. Since calcium and phosphate are required for the construction of bone, low levels result in defective bone mineralisation. Low calcium causes a secondary hyperparathyroidism as the parathyroid gland tries to raise the calcium level by secreting parathyroid hormone. Parathyroid hormone stimulates increased reabsorption from the bones. This causes further problems with bone mineralisation.

68
Q
A
69
Q

Patients with osteomalacia are likely to have risk factors such as darker skin, low exposure to sunlight, live in colder climates and spend the majority of their time indoors.

TRUE OR FALSE

A

TRUE

70
Q

Investigations Osteomalacia

A

Serum 25-hydroxyvitamin D is the laboratory investigation for vitamin D. The interpretation of the results is as follows:

  • <25 nmol/L – vitamin D deficiency
  • 25 – 50 nmol/L – vitamin D insufficiency
  • 75 nmol/L or above is optimal

Other investigation results include:

  • Serum calcium is low
  • Serum phosphate is low
  • Serum alkaline phosphatase may be high
  • Parathyroid hormone may be high (secondary hyperparathyroidism)
  • Xrays may show osteopenia (more radiolucent bones)
  • DEXA scan shows low bone mineral densit
71
Q
A
72
Q

Ix Pagets disease

A

Bone enlargement and deformity

  • “Osteoporosis circumscripta” describes well defined osteolytic lesions that appear less dense compared with normal bone
  • “Cotton wool appearance” of the skull describes poorly defined patchy areas of increased density (sclerosis) and decreased density (lysis)
  • “V-shaped defects” in the long bones are V shaped osteolytic bone lesions within the healthy bone

Biochemistry

  • Raised alkaline phosphatase (and other LFTs are normal)
  • Normal calcium
  • Normal phosphate
73
Q

Complications Paget’s Disease

A
  • Osteogenic sarcoma (osteosarcoma)
  • Spinal stenosis and spinal cord compression
74
Q
A

Year 2 (33 decks)

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