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pathology Flashcards

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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)
1
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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
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

Study These Flashcards
A

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

mainly affects:
sacro-iliac joints / spine

22
Q

psoriac arthritis

Study These Flashcards
A

predominantly affects joints of hands and feet

> 10% of patients have psoriasis

23
Q

infectious arthritis

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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
crystal arthropathy
gout - deposition of urate crystals -hyperuriceamia is necessary but not sufficient pseudo gout - calcium pyrophosphate >common 1 1
25
MoA of hyperuriceamia
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
MoA of hyperuriceamia
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
how do crystals end up in the joints ?
unclear - trauma happens in joints with lower temperatures precipitation of crystals - alcohol /drugs /obesity
28
clinical manifestation of crystals arthritis
secondary degenerative changes deposition in soft tissues - gouty trophy renal disease - stones and direct deposition in tubules and interstitium
29
pathological findings of gout / hypercalceamic arthropathy
cytology = needle shaped crystals histology (typhous) = amorphous eosinophilic
30
pseudo gout clinical findings
usually asymptomatic incidental finding on X-ray range in joint pain rhomboidal crystals and not as strongly 'fluorescent"
31
what is the most common arthritis
OA
32
pathogenesis of citrullinated proteins in RA
33
what is osteoporosis
-decreased bone mass -associated with significant risk of fracture -can be localised or generalised
34
localised osteoporosis cause
disuse
35
generalised osteoporosis cause
primary = idiopathic , post-menopausal , senile secondary = endocrine - cushings GI disorders, drugs, misc.
36
when do we have peak bone mass
young adulthood factors affecting = hereditary, diet, physical activity, muscle strength, hormonal
37
factors for osteoporosis
genetic age related changes reduced physical activity hormonal effects calcium
38
what is osteomalacia
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
vitamin D function
stimulates absorption of calcium osteoblasts stimulated to release osteocalcin
40
what is avascular necrosis (AVN)
necrosis of bone and marrow the result of loss of effective vascular supply - can result from fractures
41
predisposing conditions for avascular necrosis
alcohol corticosteroids connective tissue disorders decompression (the bends) sickle cell disease infection, pregnancy
42
what would AVN in the femoral head look like
wedge shape infarct and is often subchondral -essentially looks like another border
43
what is creeping substitution
when new bones grows over dead bone
44
hyperparathyroidism - how does it come about
elevated calcium signals to stop PTH release but not in HPPT
45
normal function and MoA of PTH
-
46
what happens to bones in HPPT
cont. osteoclasis osteoporosis brown tumours - osteitis fibrosa cystic
47
what is a brown tumour
>osteitis is late stage
48
what is renal osteodystrophy
49
Paget's disease
abnormality of bone turnover occurs in late adulthood often asymptomatic osteitis deformas
49
Paget's disease causes
uncertain genetic = SQSTM1/p62 RANKL viral infection ie measles
50
the three stages of Pagets
osteolytic - reabsorption pits with large osteoclasts mixed - osteoclasis and osteoblastic activity osteosclerotic net result = mosaic pattern = thick excess bone with abnormal reversal lines
51
what bones are most commonly affected in Pagets and what happens
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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