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msk > pathology > Flashcards

pathology Flashcards

1
Q

what are the main types of arthritis

A

osteoarthritis

rheumatoid arthritis

psoriatic arthritis

fibromyalgia

gout / pseudo-gout (crystal arthropathy)

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2
Q

osteoarthritis

A

degenerative changes in articular joints

aging and biochemical stress:
>primary - insidious, no overt cause, age related
>secondary - predisposing cause, excess inappropriate weight bearing/deformity/injury/systemic conditions

an important cause for joint replacement surgery

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3
Q

when do primary forms of OA present

A

> 50yrs

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4
Q

when do secondary forms of OA present

A

earlier in life

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5
Q

pathogenesis of OA

A

degeneration of cartilage and disordered repair

injury to chondrocytes leading to remodelling of bone, due to active chondrocyte response in the articular cartilage and the inflammatory cells in surrounding tissues

> chondrocyte inflammation > can only get worse > stimulate changes in synovial and subchondral bone

repetitive injury

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6
Q

early changes of OA

A

damage to cartilage
clusters of chondrocytes
1
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7
Q

eburnation

A

loss of articulate cartilage
/ subchondral sclerosis

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8
Q

later changes

A
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9
Q

osteophyte

A

projection of the cartilage
/ disorganised bone remodelling

> can irritate nerves

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10
Q

subchondral cysts

A

accumulation of cartilage fluid

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11
Q

RA

A

autoimmune, symmetrical

chronic inflammatory disorder
presents more in women 3f:1m
relatively young people can get it ie presents commonly in 2nd and 4th generations

presents with features of arthritis:
occurs in - synovium, peripheral joints, PIPs, MCPs, and can take systemic effects

a systemic disorder

extra-articular disease can be seen:
rheumatoid nodules over pressure points/ can be seen over internal organs as well

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12
Q

RA symptoms

A

symmetrical
malaise, fever
generalised MSK apin
joint involvement becomes apparent :
-symmetrical : swollen warm painful joints

worse in the morning and get better with movement

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13
Q

RA progression

A

> joint swelling, decreased range of movement, joint fusion (ankylosis)
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14
Q

RA - genetic factors

A

HLA DRB1
HLA DR4

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15
Q

RA - environmental factors

A

infection and smoking

citrillunation of proteins ie collagen, filaggrin and fibronectin

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16
Q

RA - immunology mechanism of action ie what cytokines etc

A

IFNG
IL-17
1
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17
Q

acute phase of RA

A

pannus formation - hyperplastic and reactive synovium

cartilage is destroyed - loss of joint space

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18
Q

chronic phase of RA

A
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19
Q

what is the rheumatoid nodule

A

essential area is necrotic tissue and surrounding that are histiocytic cells (darker) ie granulation

it is a necrotising granuloma

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20
Q

what are the other extra articular manifestations of RA

A

there’s just too many

Resp:
pneumonitis - from methotrexate use
pul. fibrosis
pleural effusions

CV:
raynauds
valvulitis
endocarditis
pericarditis
LVF

renal:
glomerulonephritis

eyes:
scleritis
dry eyes
anterior uveitis

mucocutaneous:
alopecia
oral/nasal ulceration
malar rash
photosensitivity
systemic sclerosis

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21
Q

seronegative sponfyloarthritides features

A

HLA B27

ie ankylosing spondylitis , reactive and enteritis associated arthritis

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21
Q

ankylosing spondylitis

A

presents in 2nd to 3rd generations of life
males more affected

mainly affects:
sacro-iliac joints / spine

22
Q

psoriac arthritis

A

predominantly affects joints of hands and feet

> 10% of patients have psoriasis

23
Q

infectious arthritis

A

potentially destructive

suppurative - haematogenous spread of organisms

involves a single joint - usually a knee joint

acutely painful and swollen joint - would aspirant purulent fluid

ie mycobacterial ,Lyme, viral, Staph A

24
Q

crystal arthropathy

A

gout - deposition of urate crystals
-hyperuriceamia is necessary but not sufficient

pseudo gout - calcium pyrophosphate
>common
1
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25
Q

MoA of hyperuriceamia

A

synthesis from purine catabolism

excretion via renal

why for synthesis ?
-usually idiopathic
-HGPRT deficiency (enzyme) Lesch Nyhan syndrome
-increased cell turnover ie cancer , psoriasis

why for excretion ?
1

26
Q

MoA of hyperuriceamia

A

synthesis from purine catabolism

excretion via renal

why for synthesis ?
-usually idiopathic
-HGPRT deficiency (enzyme) Lesch Nyhan syndrome
-increased cell turnover ie cancer , psoriasis

why for excretion ?
1

27
Q

how do crystals end up in the joints ?

A

unclear -

trauma
happens in joints with lower temperatures
precipitation of crystals - alcohol /drugs /obesity

28
Q

clinical manifestation of crystals arthritis

A

secondary degenerative changes

deposition in soft tissues - gouty trophy

renal disease - stones and direct deposition in tubules and interstitium

29
Q

pathological findings of gout / hypercalceamic arthropathy

A

cytology = needle shaped crystals

histology (typhous) = amorphous eosinophilic

30
Q

pseudo gout clinical findings

A

usually asymptomatic
incidental finding on X-ray
range in joint pain

rhomboidal crystals and not as strongly ‘fluorescent”

31
Q

what is the most common arthritis

A

OA

32
Q

pathogenesis of citrullinated proteins in RA

A
33
Q

what is osteoporosis

A

-decreased bone mass
-associated with significant risk of fracture
-can be localised or generalised

34
Q

localised osteoporosis cause

A

disuse

35
Q

generalised osteoporosis cause

A

primary = idiopathic , post-menopausal , senile
secondary =
endocrine - cushings
GI disorders,
drugs,
misc.

36
Q

when do we have peak bone mass

A

young adulthood

factors affecting = hereditary, diet, physical activity, muscle strength, hormonal

37
Q

factors for osteoporosis

A

genetic
age related changes
reduced physical activity
hormonal effects
calcium

38
Q

what is osteomalacia

A

concerned with vit D deficiency - via sun, diet

impaired mineralisation of bone matrix - newly formed osteoid seams, thick
> the bone is weakened and prone to fracture

39
Q

vitamin D function

A

stimulates absorption of calcium
osteoblasts stimulated to release osteocalcin

40
Q

what is avascular necrosis (AVN)

A

necrosis of bone and marrow

the result of loss of effective vascular supply - can result from fractures

41
Q

predisposing conditions for avascular necrosis

A

alcohol
corticosteroids
connective tissue disorders
decompression (the bends)
sickle cell disease
infection, pregnancy

42
Q

what would AVN in the femoral head look like

A

wedge shape infarct and is often subchondral
-essentially looks like another border

43
Q

what is creeping substitution

A

when new bones grows over dead bone

44
Q

hyperparathyroidism - how does it come about

A

elevated calcium signals to stop PTH release but not in HPPT

45
Q

normal function and MoA of PTH

A

-

46
Q

what happens to bones in HPPT

A

cont. osteoclasis

osteoporosis

brown tumours - osteitis fibrosa cystic

47
Q

what is a brown tumour

A

> osteitis is late stage

48
Q

what is renal osteodystrophy

A
49
Q

Paget’s disease

A

abnormality of bone turnover

occurs in late adulthood

often asymptomatic

osteitis deformas

49
Q

Paget’s disease causes

A

uncertain

genetic = SQSTM1/p62

RANKL

viral infection ie measles

50
Q

the three stages of Pagets

A

osteolytic - reabsorption pits with large osteoclasts

mixed - osteoclasis and osteoblastic activity

osteosclerotic

net result = mosaic pattern = thick excess bone with abnormal reversal lines

51
Q

what bones are most commonly affected in Pagets and what happens

A

usually axial, small bones are less affected

enlargement and abnormal shape , platybasia , sabre tibia

increased metabolism - high level of alkaline phosphatase

increase of malignancy - osteosarcoma

msk (24 decks)

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