Pathology (cortex ones better) Flashcards

1
Q

what are autoimmune conditions characterised by

A

presence of autoantibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what autoantibody is present in rheumatoid arthritis

A

rheumatoid factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is rheumatoid arthritis

A

autoimmune disease, typically causing inflammation of the joints but can have many manifestations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is seen histologically in aute RA

A

pannus formation- inflammatory granulation tissue

hyperplasic/ reactive synovium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is seen in chronic RA

A

cartilage is destroyed by inflammatory process, loss of joint space= fibrosis, deformity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what autoantibodies are seen in SLE

A

ones directed at structural parts of DNA- 95% ANA+ve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are inflammatory arthritides

A

inflammatory diseases that affect the joints and surrounding structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is seen acutely is histology of a inflammatory arthritides

A

oedema, fibrin, reactive features in synovial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is seen chronically is histology of a inflammatory arthritides

A

lymphocytes and plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what autoantibody in scleroderma

A

anti centromere, antitelomere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what autoantibody in dermatositis

A

anti jo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is uric acid and why can it reach high concentrations

A

the end product of purine synthesis. Adenine and guanine and purine based, anything that increases turnover of these is associated with a crystal arthropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the two types of crystal arthropathy

A

gout and psuedo gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what causes gout

A

hyperuricaemia- either increased urate production (e.g. increased cell turnover- psoriasis, cancer or tumour lysis) or reduced excretion (drug side effect- thiazide diuretics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the pathological manifestation of gout

A

precipitation of crystals (due to reduced solubility) usually in joints (due to lower temps) elicit inflammatory reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the clinical implications of gout

A
causes secondary degeneration changes in joint, 
deposition in soft tissue causes gouty trophy. 
renal diseases (stones and direct deposition in tubules and interstitium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is seen in cytology of gout

A

needle shaped crystals seen in cross polarised light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is seen histologically in gout

A

amorphous eosinophillic debris and inflammation (giant cells).

NOT crystals as lost during tissue processing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what crystal causes pseudogout/ chrondrocalciosis

A

calcium phosphate (rhomboid shaped crystals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are features of pseudo gout

A

older patient, larger joint. usually asymptomatic but can cause range of joint pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is pagets disease

A

when there is an abnormailty of bone turnover- increased oestoclastic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the cause of pagets

A

unknown, genetic components, RANKL, viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the three stages of pagets

A

osteolytic, mixed and burnt out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the net result of pagets

A

thick excess bone with abnormal reversal lines- mosaic pattern

pain- microfractures or nerve compression (bone expansile)

enlargement and abnormal shape

increased metabolism- heat, warm skin, AV shunt, high output cardiac failure

secondary malignancy (osteosarcoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is histologically in the initially phases of a fracture

A

haematoma (fibrin mesh), influx of inflammatory cells, cytokine release, recruitment of osteoprogenitor cells from periosteum and medulla cavity (repair cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is seen histologically a week after a fracture

A

callous, organised haematoma, early recruitment and bone remodelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what can cause delay healing of a fracture

A

poor blood supply
poor nutrition
too much movement
too great a distance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is a pathological fracture

A

when bone is not normal before fracture e.g. oestoperosis/ tumours (benign/ malignant)

29
Q

what are cancers that commonly metastasise to bone

A

lung, kidney, breasts prostate

30
Q

what does bone metastasis look like

A

most oestolytic- bone is resorbed and appears radiolucent

prostate appears as osteosclerotic- areas of opacity (more dense)

31
Q

what are myeoma/plasmacytoma

A

malignant proliferation of plasma cells, causes bony lesion

32
Q

what is avascular necrosis

A

bone infarction, causes 10% of hip fractures

33
Q

what causes avascular necrosis

A

trauma, alcohol main causes

steroid injection, dysbarism, sickle cell diseases, infection

34
Q

what does avascular necrosis look like histologically

A

wedge shaped area of discolouration, often subcortical

creeping substitution (new bone grows over old dead bone)

35
Q

what is osteoarthitis

A

a degenerative disease cause by mechanical injury due to abnormal load distribution, previous fracture or anatomical abnormality

36
Q

what are the changes of osteoarthritis

A

damage to cartilage surfaces then later damage to the underlying bone

37
Q

what is seen histologically in osteoarthitis

A

fibrillation, erosion/ eburnation (subchondral sclerosis), subchondral cyst formation (synovial fluid accumulation), osteophyte (disorganised bone formation limits joint movement), loss of joint space

38
Q

what causes osteophytes

A

cortical bone thickens to cope with load, rapid bone remodelling= abnormal outgrowths

39
Q

what is subchondral sclerosis a sign of

A

eburnation

40
Q

describe karotyping

A

culture cells and then arrest during cell division- provides overview of chromosomal structure but will not detect small or subtle lesions

41
Q

what is FISH useful for

A

to find known translocations- if signals move together then translocation

42
Q

what does immunohistochemistry do

A

places a pigment on an antibody to target a protein to see whether it is present

43
Q

describe ganglion cysts

A

lump peripheral and near a joint capsule or tendon sheath, common around the wrist

degenerative change within connective tissue. not a true cyst no epithelial lining

44
Q

what is seen histologically in in a ganglion cyst

A

space with myxoid material, secondary inflammatory changes

45
Q

where are common places for superficial fibromatoses

A

dupuytrens, knuckle pads, plantar, penile (peyronie’s)

46
Q

what causes dupuytrens

A

idiopathic- associated with alcohol and anticonvulsants

47
Q

what is deep fibromatoses

A

mesenteric or pelvic tumours

desmoid tumours- deeper in viscera of body

association with gardner’s syndrome

48
Q

what is pigmented villonodular synovitis

A

giant cell tumour that you get in large joints

49
Q

where do you get giant cell tumours of tendon sheath

A

digits

50
Q

describe angiolipoma

A

usually multiple and peripheral, vascular with fibrin thrombin, painful

51
Q

what is a leiomyoma

A

smooth muscle tumour

52
Q

what are the main proteins in smooth muscles

A

actin, desmin and caldesom

53
Q

who gets cardiac phabdomyomas

A

kids

54
Q

what are the forms of skeletal muscle malignant tumours

A

embryonal rhabdomyosarcoma (children), alveolar (young adults), pleomorphic (young adults)

55
Q

do cartilage sarcomas affect the paediatric population

A

no

56
Q

what is more worrying, a cartilage tumour in the extremities or central body

A

central more likely to be sarcoma

57
Q

what is gardners syndrome

A

multiple bone lesions

58
Q

what is characteristic of osteoid osteoma

A

nidus (focus of infection), associated with tenderness

59
Q

what is an osteoma

A

benign tumour of the bone

60
Q

who and where do you get osteosarcoma

A

usually paediatric age group, long bones

61
Q

what is a pathology diagnostic sign of osteosarcoma

A

any malignant tumour that produces osteoid is oestosarcoma until proven otherwise

62
Q

where do osteosarcomas metastasise to first

A

lung fields

63
Q

who gets ewings sarcoma, what is it like

A

children and adolescents

destructive, rapildy growing and highly malignant

64
Q

what do the ewings family of tumours look like

A

small round blue cell tumours

65
Q

what cancer is commonly missdiagnosed as sarcoma

A

carcinoma

66
Q

what is nodular fascitis

A

reactive lesion, affects any age group, rapid growth, snall

67
Q

what is seen histologically in nodular fascitis

A

chaotic appearance, haemorrhage, pseudocystic spaces, large atypical cells, frequent mitoses, normal mitoses

68
Q

what is myositis ossificans

A

reactive lesion, small, preceeds trauma

69
Q

what are rheumatoid nodules

A

common, elbow, reactive lesion