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Pathology eLearning - Y5 > Bone Tumours > Flashcards

Bone Tumours Flashcards

1
Q

What are different classifications of fractures?

A

Complete or Incomplete

Closed (Simple): Clean break with intact soft tissue

Comminuted: Splintered bone with intact soft tissue

Compound: Fracture site communicates with skin surface

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2
Q

What are the stages of fracture repair?

A

Organisation of haematoma at fracture site (pro-callus)

Formation of fibrocartilaginous callus

Mineralisation of fibrocartilaginous callus

Remodelling of bone along weightbearing lines

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3
Q

What is this?

A

Fractured bone

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4
Q

What is this?

A

Repaired fracture

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5
Q

What is this?

A

Fracture callous - can be mistaken for osteosarcoma

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6
Q

What are factors influencing fracture healing?

A

Type of fracture

Presence of infection

Pre-existing systemic condition:

  • Neoplasm
  • Metabolic disorder
  • Drugs
  • Vitamin deficiency

Pseudoarthrosis may result

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7
Q

What are common sites of osteomyelitis?

A

Adults:

  • Vertebrae
  • Jaw (2º to dental abscess)
  • Toe (2º to diabetic skin ulcer) (>3mm)

Children:

  • Long bones (usually metaphysis)
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8
Q

What are clinical features of osteomyelitis?

A

General: Malaise, fever, chills, leucocytosis

Local: Pain, swelling and redness

60% positive blood cultures

X-ray: Mixed picture eventually lytic

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9
Q

What are common causative organisms of osteomyelitis?

A

Almost always bacterial

Rarely fungal

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10
Q

What are routes of infection for osteomyelitis?

A

Haematogenous (blood borne)

Direct extension

Traumatic (inc surgery)

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11
Q

What are the causative bacterial species in adults with osteomyelitis?

A

Staph Aureus(90%)

E. Coli

Klebsiella

Salmonella (associated with sickle cell disease)

Psuedomonas (IVDA)

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12
Q

What are the causative bacterial species in neonates with osteomyelitis?

A

Haemophilus influenzae

Group B Streptococcus

Occasionally enterobacter

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13
Q

What is this?

A

Core biopsy - Osteomyelitis

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14
Q

What are common X-Ray changes of osteomyelitis?

A

Usually appear 10 days or so post onset

Mottled rarefaction and lifting of periosteum

>1week: Irregular sub-periosteal new bone formation called involucrum

Later: Irregular lytic destruction (takes 10-14 days)

Some areas of necrotic cortex may become detached called sequestra (takes 3-6 weeks).

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15
Q

What is the Cierny-Mader staging system for osteomyelitis?

A

Anatomic type:

  • Stage 1: Medullary OM
  • Stage 2: Superficial OM
  • Stage 3: Localised OM
  • Stage 4: Diffuse

Physiologic class:

  • Host A: Normal
  • Host B: Local or systemic compromise
  • Host C: Treatment worse than disease
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16
Q

What is the association between TB and osteomyelitis?

A

Rare cause of OM (3-5% cases of extra-pulmonary TB). Affects immunocompromised patients. More destructive and resistant to control.

Spinal disease (50% cases) may result in psoas abscess and severe skeletal deformity (Pott’s disease).

Systemic amyloidosis may result in protracted cases.

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17
Q

What is the association between of syphillis and osteomyelitis?

A

Another rare cause of OM (Treponema pallidum)

May be congenital or acquired

Congenital skeletal lesions:

  • Osteochondritis
  • Osteoperiostitis
  • Diaphyseal osteomyelitis
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18
Q

What are late skeletal lesions associated with syphillis?

A

Non-gummatous periostitis

Gummatous inflammation of bone and joints

Neuropathic joints (Tabes Dorsalis)

Neuropathic shaft fractures

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19
Q

What is Lyme Disease?

A

Inflammatory arthropathy as part of a complex multisystem illness resulting from tick bite. It is the most prevalent vector bone disease in temperate Northern hemisphere.

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20
Q

What is the organism and tick species causing Lyme Disease?

A

Organism: Borrelia burgdorferi

Tick Species: Ixodes dammini

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21
Q

What is the epidemiology of Lyme Disease?

A

Affects both sexes equally.

Onset between May and November

22
Q

What are the three clinical stages of Lyme Disease?

A

Stage 1: Early localised

Characterised by rash (90%) usually within 7-10 days and between 1 & 50cm diameter. Often thigh, groin, axilla (earlobe in children).

Stage 2: Early Disseminated

Effects many organs, musculoskeletal, heart, nervous system.

Stage 3: Late, persistent

Dominated by arthritis.

23
Q

What is the management of Lyme Disease?

A

Treatment is based on prevention.

Vaccines are available.

Antibiotics for proven disease.

No effective prophylaxis.

Diagnosis is clinical. No specific histological features.

24
Q

What is osteoarthritis?

A

Degenerative joint disease

25
Q

What is primary and secondary osteoarthritis?

A

Primary: Age related

Secondary: Any age, previously damaged or congenitally abnormal joint.

26
Q

What is this?

A

Osteoarthritis - femoral head

27
Q

What is this?

A

Femoral head avascular necrosis

28
Q

What is the aetiology of osteoarthritis?

A

Biomechanical factors

Biochemical factors

Ageing

Genetic

29
Q

What is the result of osteoarthritis?

A

Cartilage degeneration

Fissuring

Abnormal matrix calcification

Osteophytes

30
Q

Where are common sites for osteoarthritis?

A

Main sites vertebrae hips and knees

DIPJ/PIPJ of the hand

Carpometacarpal and metatarsophalangeal joints

31
Q

What is this?

A

Synovium in OA

32
Q

What is rheumatoid arthritis?

A

Severe chronic relapsing synovitis

Unpredictable course

33
Q

What is the epidemiology of rheumatoid arthritis?

A

Incidence 1% world population

(Europeans 0.3-1%; Asians 0.1-1.5%; Native Americans 5-7%)

3F:1M

Age 30-40y

34
Q

What is the aetiology of rheumatoid arthritis?

A

Aetiology: Most likely autoimmune

80% patients RF +ve

RF mostly IgM

RF forms immunocomplexes with IgG

These circulating immune complexes may underlie associated extra-articular disease.

35
Q

What are risk factors for rheumatoid arthritis?

A

Genetic predisposition (risk alleles TNFA1P3, STAT4)

Increased incidence amongst first degree relatives

Associated with HLA DR4 & DR1 (Chr 6p21)

36
Q

What are clinical features of rheumatoid arthritis?

A

Mild anaemia

Raised ESR

RF+ve(80%)

+/- Rheumatoid nodules (25%)

Can be multisystem disease

37
Q

What are characteristic sites for rheumatoid arthritis?

A

Radial deviation of wrist

Ulnar deviation of fingers

‘Swan neck’ & ‘Boutonniere’ deformity of fingers

‘Z’ shaped thumb

38
Q

What are differentiating features between RhA and OA?

A

RhA:

  • Symmetrical
  • Small joints, hands and feet, sparing DIPJ
  • Wrists elbows ankles and knees
39
Q

What is the histology of RhA?

A

Proliferative synovitis with:

  • Thickening of synovial membranes (villous)
  • Hyperplasia of surface synoviocytes
  • Intense inflammatory cell infiltrate
  • Fibrin deposition and necrosis

Pannus is the exuberant inflamed synovium the articular surface

40
Q

What is this?

A

Rheumatoid Arthritis

41
Q

What is the inflammatory features of RhA?

A

Proliferative synovitis

Associated upregulation of CFos /AP1 and osteoporosis, IL1β and TNFα

Intense inflammatory cell infiltrate

Production of IL6, TNFα and CRP by liver

IL1 & IL6 induce MMPs – joint destruction

Circadian rhythm of host disturbed

42
Q

What are these?

A

Grimley-Sokoloff cells

43
Q

What are the 5 stages of RhA?

A
  • Unknown antigen reaches synovial membrane
  • T–cell proliferation associated with increased; B-cells and angiogenesis
  • Chronic inflammation with inflammatory cytokines
  • Pannus formation
  • Cartilage and bone destruction
44
Q

What is this?

A

Gout

45
Q

What is gout?

A

Affects any joint but great toe in 90%

Usually limited to lower extremities

Precipitate of needle shaped crystals into joint

Tophus is the pathognomic lesion

46
Q

What is this?

A

Gouty tophus

47
Q

What is this?

A

Urate crystals

48
Q

What are features of pseudogout?

A

Calcium pyrophosphate: Mainly knees

Calcium phosphates (hydroxyapatite): Knees and shoulders

Usual age > 50y

49
Q

What is this?

A

Ca pyrophosphate crystals

50
Q

What is this?

A

Calcium pyrophosphate crystals

51
Q

What is this?

A

Calcium pyrophosphate crystals

52
Q

What are subsets of pseudogout?

A

Sporadic: 8% pts <75; 22%>85 ?F>M

Metabolic: Haemochromatosis, primary HPT, hypoMg; low PO4

Hereditary (autosomal dominant) ANKH mutn: Transmembrane glygoprotein. Chr 8q, 5p, younger age 18% OA knee; 10% hip)

Traumatic

Pathology eLearning - Y5 (17 decks)

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