Non-neoplastic pathology Flashcards

(45 cards)

1
Q

What are the different categories of non-neoplastic MSK pathologies?

A

Connective tissue disease
Metabolic disease
Fractures
Degenerative disease

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2
Q

What are some common autoantibodies associated with musclo-skeletal diseases?

A

RA- Rheumatoid factor, anti-CCP
SLE - ANA, anti-double stranded DNA, Anti-Sm
Scleroderma - anti-centromere, antitelomere, Anti-Scl-70
Dermatomyositis, polymyositis - anti-Jo-1
Sjogren’s syndrome - Anti-Ro, Anti-La

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3
Q

What is the antibody against in RA?

A

Auto Ab against Fc IgG

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4
Q

What occurs in the acute phase of RA?

A

Pannus formation - inflammatory granulation tissue
Hyperplastic/ reactive synovium
This results in a loss of cartilage and a loss of joint space

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5
Q

What occurs during the chronic phase of RA?

A

Fibrosis

Deformity

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6
Q

What cells are commonly present in inflammatory arthritides?

A

Lymphocytes and plasma cells

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7
Q

What are the acute features of inflammatory arthritides?

A

Oedema, fibrin, reactive features in synovial cells

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8
Q

What conditions fall under inflammatory arthritides?

A

RA, SLE gout, pseudo-gout, ankylosing spondy`litis (AS), psoriatic arthritis (PsA), gonorrhea, tuberculosis, and osteomyelitis

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9
Q

What are the different types of metabolic diseases?

A

Pagets
Oseomalacia
Crystal arthropathies

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10
Q

What is the basic pathogenesis of gout?

A

Uric acid is the end product of purine synthesis
Adenine and guanine are purine based and therefore DNA replication forms urate
In gout, there is either overproduction of uric acid or inadequate excretion

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11
Q

What can cause a pathogenic hyperuricaemia?

A

Usually idiopathic
HGPRT deficiency - lesch nyhan syndrome
Increased cell turnover - psoriasis, cancer (leukemia or tumour lysis following chemotherapy)

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12
Q

What can cause a reduced excretion of uric acid?

A

Under-excretion of an idiopathic cause

Drug side effect - thiazide diuretics reduce urate excretion

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13
Q

What are the clinical manifestations of hyperuricaemia?

A

Precipitation of crystals in small joints due to a reduced solubility
Small joints are cooler in temp, reducing solubility further

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14
Q

Apart from the primary gout in joints, what else can hyperuricaemia do?

A

Deposits in soft tissue - gouty tophus

Deposits in kidneys causing renal colic and AKI

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15
Q

What are the cytological findings of gout?

A

Joint fluid examined uner a cross-polarized light to detect needle shaped crystals

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16
Q

What are the histological findings or gout?

A

Amorphous eosinophilic debris and inflammation (giant cells)

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17
Q

What is a giant cell?

A

A giant cell is a mass formed by the union of several distinct cells (usually histiocytes), often forming a granuloma

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18
Q

What is pseudogout?

A

A crystal arthropahy characterised by calcium pyrophosphate

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19
Q

What is the difference between gout and pseudogout?

A

Gout in older and younger people commonly in small joint

Pseudogout in elderly in large joints

20
Q

What can cause pseudogout?

A

Idiopathic

Hypercalcaemia (inc. hyperparathyrodism), haemachomatosis, huypomagneisa, ochronsis, hypothyrodism

21
Q

What will pseudogout look like radgiologically?

A

Dense deposits on x-ray

22
Q

What does pseudogout look like histologically?

A

Rhomboid shaped crystals that are thicker and bigger than the needle shaped urate crystals

23
Q

What is paget’s disease?

A

Abnormality of bone turnover due to increased osteoclastic activity resulting abnormal bones

24
Q

What can cause paget’s disease?

A

Genetic elements

Viral infection - paramyxovirus, measles, RSV (measles virus nucleoplasmid protein stimulates osteoclas activity)

25
What are the three stages of paget's disease?
Oseolytic Mixed Burnt out - weak bones prone to fractures
26
What bones does paget's tend to affect?
Axial skeleton
27
What are the symptoms of paget's disease?
Pain due to microfracture or nerve compression Enlargement and abnormal shape of bones (leontiasis ossea, platybasia, sabre tibia) Increased metabolism (heat, warm skin, AV shunt causing CV failure) Secondary malignancy - osteosarcoma
28
What is osetomalacia?
A disease caused by abnormal vitamin D metabolism leading to bowed legs, square heads, pigeon chest and rickety rosary
29
Where does the pain originate form in fractures?
Periosteum
30
What are the initial phases of a fracture?
Haematoma - fibrin mesh Influx of inflammatory cells Cytokine release - recruitment of osteoprogenitor cells from periosteum and medullary cavity
31
What will have formed around a fracture after a week?
A callus, organised haematoma and early recruitment and remodeling at both ends of the bone
32
What will a fracture look like 2-3 weeks after the injury?
Max girth of callus Woven bone deposited perpendicular to cortical bone Cartilage deposition at fracture site which undergoes endochondral ossification Bridging with a bony callus
33
What can cause a pathological fracture?
Oseoporosis Tumours Benign - children and primary Malignant - adults and metastatic
34
What are the common organs that metastasize to the bone?
Bad Boys Pee Through Kidneys | Breast, Bronchus, Prostate, Thyroid, Kidneys
35
What will most bone mets look like?
Oseolytic - bone is reabsorbed and looks radiolucent
36
What will prostate mets look like?
Osteosclerotic - areas of opacity
37
What is avascular necrosis?
Bone infarction | Often asymptomatic
38
What can cause avascular necrosis?
Trauma, alcohol, dysbarism, steroid injections, sickle cell disease, infection
39
What is the morphology of avascular necrosis?
Wedge shaped infarct often sub-cortical
40
What are the histological findings of avascular necrosis?
Creeping substitution | Superimposed secondary osteoarthritis
41
What is the most common degenerative disease?
Osteoarthritis
42
What are the joint changes in osteoarthritis?
Early - small cracks in cartilage (fibrillation) | Cartilage becomes completely worn away (eburnation)
43
What causes subchondral sclerosis?
Eburnation
44
What causes subchondral cysts?
Synovial fluid accumulation
45
What causes osteophytes?
Disorganised bone remodeling