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Pathology > MSK > Flashcards

MSK Flashcards

1
Q

What affects bone remodelling osteoclasts and osteoblasts

A
  • Parathormone
  • PDGF
  • IL1
  • TNF
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2
Q

Describe the steps involved in fracture healing

A
  1. Haematoma and acute inflam
  2. Organisation of haematoma (granulation tissue forms)
  3. Primary callus response- oestoprogenitor cells become bone forming cells
  4. External bridging callus- bone formation bridging the gap where the fracture is
  5. Remodelling months later

Treatment for fracture: Complete immobilisation and good blood and 02 supply

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3
Q

What are the complications of a fracture

A

Early
-infection -Blood loss from haemorrhage -skin loss and soft tissue injury -damage to nerves and vessels -dislocation of joint

Delayed
-damage to epiphyseal plates -delayed union -non-union -secondary osteoarthritis -avascular necrosis of bone

Systemic

  • Cardiac shock and circulatory failure (blood loss) -Sepsis -pneumonia -bed sores
  • DIC -Fat embolus -DVT and PE -Resp distress syndrome (fractured ribs)
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4
Q

What factors impair bone healing

A

-Age -Malnutrition -Diabetes -Cancer -Radiotherapy -Soft tissue injury -Compound fracture -Large fracture gap -Poor immobilisation -Infection -Ischaemia

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5
Q

Describe the features of acute osteomyelitis

A
  • Septic presentation
  • Increased WCC, pyrexia and toxaemia (blood poisoning)
  • X-rays no use in early stages - X-ray changes take 10 days dont wait on these
  • Crying children in babies
  • Haematogenous spread from a minor infection
  • Staph aureus most common , Haemoglobin influenzae in children under 4 with no Hib vaccine , salmonella type in sickle cell anaemia

Changes on X-ray will show
-Full around periosteum and thickened bone-
Histology - Necrotic bone and neutrophils

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6
Q

How do we prevent bone infection

A
  • Urgent and thorough debridement of open fractures and same day treatment
  • Strict aseptic technique in ortho surgery
  • Appropriate prophylactic antibiotics in open fractures
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7
Q

Describe the features of chronic osteomyelitis

A
  • Very different to acute
  • Complication of poorly treated acute
  • Adults usually
  • Continued infection causes bone necrosis and new bone formation
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8
Q

What are the complications of osteomyelitis

A
  • Septicaemia -Bone deformity -Secondary arthritis -Formation of skin sinus -Squamous carcinoma
  • Systejmic amyloid
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9
Q

What is bone/ joint tuberculosis

A
  • Never primary in bone disease always secondary to biliary TB or pulmonary TB or reactivation of secondary infection
  • Affects spine, long bones, hips, knees and small bones of hands and feet
  • TB osteomyelitis= insidious chronic infection and very destructive
  • Has caseating granulomata, spinal involvement can lead to scoliosis and kyphosis
  • Can cross disc space involving multiple,e vertebrae, psoas abscess and ankylosing of jointsand systemic amyloid- renal and liver failure
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10
Q

What is osteoporosis and what are the causes

A

-Reduction in amount of bone and loss of micro-architecture leading to weakened bone and pathological fracture

  • Normal mineralisation*
  • Normal bone just not enough of it- no increase in osteoblasts or osteoclasts

Causes
-Idiopathic, senilinity, post menopausal, cushing’s disease, steroids, thyrotoxicosis, hypogonadism (lack of sex hormones), hyperparathyroidism, alcohol abuse, scurvy

Peak bone mass is 20-30 flattens out at 40 then starts to drop - females loose bone mass quicker than males at menopausal stage - HRT helps prevent this

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11
Q

What are the main osteoporosis risk factors

A
  • Female -Caucasian/ asian -Early menopause -Sedentary -Slim build -Nulliparity -Amenorrhoea
  • Fam history -Smoking -Alcohol -Steroids -Previous fractures -Low calcium intake
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12
Q

What is osteomalacia and what are the causes and the signs

A

-Disease characterised by reduced mineralisation of bone- poor mineralisation involving low serum
calcium and phosphate mainly

Causes

  • Deficient diet -Lack of sun exposure- vit D needed for calcium absorption
  • Malabsoprtionb -Chronic liver disease -Phenytoin therapy -Chronic renal disease -Hypophosphatemia

Signs
-Abnormal blood chemistry -Bone pain -Proximal myopathy -Osteopenia on x-ray -Pathological fracture

Bone biopsy needed for diagnosis

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13
Q

What is Paget’s disease and how does it present

A

Increased rate of bone remodelling - increased bone resorption and bone formation

  • More resorption than formation usually then osteoblasts have to work much harder
  • Very rare under 40
  • Affects long and flat bones- vertebrae, pelvis, skull
  • Increased bone markings - may see coxa vara in femur (looks like a walking stick) - loss of angle between hip joint and femur
  • Bone pain
  • Pathological fracture
  • Skeletal derfomity - enlarged skull, bowing of limbs
  • Many patients asymptomatic
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14
Q

What are the complications of pagets disease

A

-Pathological fracture -Secondary osteoarthritis -Nerve compression- cranial and spinal - if skull 8th CN -Sarcoma development - reason for bone tumour in an older person Wh

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15
Q

What is the basis for osteoarthritis

What is secondary osteoarthritis

A
  • Articular cartilage in joins distributes force and is made of chondrocytes that do not regenerate- wear and tear , change in composition of GACs, fibrillating and splitting or cartilage with eventual loss
  • A degenerative arthropathy increased frequency with age- affects weight bearing joints and DIP joints

Secondary osteoarthritis
-Previous joint fractures -Osteonecrosis (ischaemis ect) -Metabolic bone disease -Joint infection (septic arthritis) -Congenital hip dislocation -RA -Perthe’s disease

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16
Q

What are the radiological features of osteoarthritis

A

LOSS

  • Loss of joint space
  • Osteophytes
  • Sub chondral sclerosis- increased bone formation around joint margins- bright white line
  • Subchondral cysts - osteocartilagenous growths

Also

  • Eburnation of bone surface (shiny)
  • Secondary synovitis (inflam)
17
Q

Describe the features of rheumatoid arthritis and what it presents with

A
  • Inflammatory arthropathy
  • Auto-immune disease- RA IgM which reacting with part of sensitised IgG (Immunoglobulin+ immunoglobulin = activation of complement)
  • Immune complex formed activated IL1, IL6 and TNF a - inflam mediators leading to marked inflammation and destruction of cartilage
  • Increased incidence with HLA- Dr4

Presentation

  • Symmetrical synovitis with systemic manifestations
  • More common in females
  • 20-50 yrs
  • Seropositive arthropathy
  • Starts as synovitis and then becomes arthritis
18
Q

Describe the pathology behind rheumatoid arthritis

A
  • Synovial hyperplasia - finger like folds
  • Chronic inflammation
  • Lymphocytic aggregates and lymphoid follicles
  • Synovial features are not specific for RA but indicate inflammatory arthropathy
  • Subcutaneous rheumatoid nodules
19
Q

What systemic diseases are associated with RA

A
  • Vasculitis
  • Pericarditis
  • Lung fibrosis
  • Increased infection risk
  • Systemic amyloid
20
Q

Describe the features of gout

A
  • Crystal arthropathy
  • Precipitation of sodium rate into soft tissues
  • Presents like septic arthritis in acute attacks - red hot painful joint
  • Chronic tophaceous gout- giant cell response to deposition of urea
  • Increased rate in dehydrated patients or in increased cell death - cell mediated hypersensitivity reaction to crystals precipitating out
21
Q

What are the causes of gout

A
  • Congenital purine metabolism error
  • Chronic renal failure - renal tubules dont secrete rate so too much absorption increases serum urate
  • Thiazide diuretics
  • Increased cell turnover - leukaemia, lymphoma treatment or myeloproliferative disorders
  • Allopurinol given with chemo to prevent this*
22
Q

Describe the features of seronegative arthropathy

A
  • No rhematoid factor found in blood
  • ALL HAVE SOME SPINAL INVOLVEMENT
  • Ankylosing spondylitis, psoriatic arthropathy, Reiter’s disease and arthritis with IBD
  • ENTHESITIS not synovitis- inflammation where a tendon/ ligament is attached to a bone leading to secondary ossification and spondylitis
  • Spondyloarthropathy
  • Syndesomophytes seen in spine
23
Q

What are the features of an osteoma

A

-Benign bone forming tumour
-4th and 6th decades more common in males
-Craniofacial skeleton- frontal and ethmoid sinuses, jaw bones and cranium
-Incidental finding
Treated: Observation or simple excision

24
Q

Describe the features of osteoid osteoma

A 
Benign bone forming tumour 
-Small size and severe pain 
-Young adults more common in males 
Treated: Radiofrequency ablation 
-Most common in proximal femur
25
Q

What are the features of an osteoblastoma

A

-Benign bone forming tumour
-Young adults more common in males
-Pain and swelling with neuro symptoms - numb ect
-Vertebral column and sacrum
Treatment: Curette or en bloc resection very good prognosis

26
Q

What are the features of osteosarcoma

A
  • High grade malignant tumour with neoplastic cells producing bone
  • Most common primary malignant tumour
  • Young patients 10-20 and second peak in 50s
  • Male most common
  • Enlarging painful mass
  • Idiopathic or due to diseased bone eg pagets
  • Knee region or humerus

Treatment: Preoperative chemo - complete necrosis = associated with enhanced survival

  • Surgery- limb salvage or amuputation
  • Radio for unresectable tumours
27
Q

What are the features of an osteochondroma

A
  • Benign cartilage capped tumour that comes from metaphysics (growth plate)
  • Mutations in EXT genes
  • Most common primary bone tumour
  • Second decade of life and asymptomatic
  • Solitary lesion or multiple lesions
  • Mostly in knee
  • Grow slowly but growth stops at puberty
  • Treated by excision and unlikely to become malignant
28
Q

What are the features of an endochondroma

A
  • Benign primary tumour made of chondrocytes producing cartilage matrix that arises within the medullary cavity
  • 3rd and 4th decades
  • Mostly bones of hands and feet
  • Occasionally femur tibia and humerus
  • Slow growth
  • No treatment if asymptomatic or curette if painful with bone graft and cement packing
  • Can get multiple lesions in Ollier disease and Mffuci syndrome
29
Q

What are the features of Chondrosarcoma

A
  • Malignant cartilaginous matrix producing tumour
  • Idiopathic
  • Higher risk in oilier and maffuci syndrome
  • 5th to 7th decades
  • Pain and enlarging mass
  • Pelvis and proximal femur
  • Treatment: Surgical- aggressive curettage at grade 1 or wide surgical resection grade 2 or 3
  • Radiotherpay if unresectable
30
Q

Describe the features of fibrous dysplasia

A

-Common monastic 1 bone or polyostotic many bones benign fibre-osseous neoplasm of bone
-Mutation in cell surface g protein causing production of cyclic AMP and hyperactivity of cells
-Bone lesions in childhood that grow with skeleton
-Pain
-Usually monostotic
-Affects ribs, femur, tibia, jawbone, skull, humerus
Treatment: Observation or surgery
Prognosis: Depends on severity and extent but can undergo malignant transformation

31
Q

Describe the features of a giant cell bone tumour

A
  • Benign but locally aggressive
  • Skeletally nature patients 3rd to 5th decades
  • Pain and swelling
  • Knee region
  • An osteoclast giant cells express receptor RANK

Treatment: Surgery: curettage or en bloc resection
Drugs- RANK ligand inhibitors
Radiation

Pathology (12 decks)

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