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Rheum Flashcards

1
Q

what is osteoporosis

A

loss of bone density without loss of bone mineralisation

results in increased susceptibility to bone fractures

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2
Q

what are the different types of osteoporosis

A

type 1 = post menopausal
type 2 = senile
secondary = disease process or medical tx

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3
Q

what are the risk factors for type 2 osteoporosis

A 
fhx
alcohol
RA
immobility
untreated menopause
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4
Q

what are the risk factors for secondary osteoporosis

A 
Steroid use 
Hyperthyroidism, hyperparathyroidism 
Alcohol
Thin BMI <18
Testeosterone 
Early menopause 
Renal failure 
Erosive bone disease 
Diet - low vit D or Ca
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5
Q

how do steroids cause osteoporosis

A

cortisol inhibits osteoblasts and activares osteoclasts

bone breaks down, reduced bone density

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6
Q

how does hyperthyroidism cause osteoporosis

A

thyroxine inhibits osteoblasts
increased bone breakdown than formation
also hypercalcaemia

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7
Q

what is the clinical presentation for osteoporosis

A

usually asymptomatic
fragility or pathological fracture

  • compression fracture - back pain, loss of height, loss of spine curve, hunched
  • colles fracture - distal radius
  • NOF fracture
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8
Q

3 cells within bone

A

osteoblasts - build bone secrete collagen and hydroxyapetite

osteoclasts - break down bone by secreting digestive enzymes and HCl breaks down bone -> releasing Ca and phosphate

osteocytes - osteoblasts stuck in bone matrix, act as mechanoreceptors

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9
Q

describe the effects of PTH

A

released from PTG in response to low serum Ca

1) leads to increased osteoclast activity - PTH stimulates RANK-l which stimulates osteoclasts to break down bone and release Ca
2) leads to increased Ca absorption - PTH acts on nephron, increases Ca reabsorption from DCT
3) increases synthesis of vit D - increases rate of vit D formation within kidney (higher vit D = increased Ca absorption from gut)

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10
Q

what does kidney disease lead to and why

A

renal osteodystrophy

kidneys produce less vit D

reduced Ca absorption from gut

leads to hypocalcaemia so PTH released

but PTH breaksdown bone -> weakening

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11
Q

why is there an increased risk of developing osteoporosis after menopause

A

menopause = low oestrogen

oestrogen inhibits osteoclasts - it stimulates OPG which inhibits RANK-l and thus prevents osteoclast activation

however, low oestrogen leads to less OPG and less inhibition of osteoclasts = greater bone breakdown = osteoporosis

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12
Q

which cells are activated more/less in osteoporosis

A

breakdown is faster than formation

so osteoclasts are activated more
osteoblasts are activated less

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13
Q

which bones are at greatest risk of fracture in osteoporosis

A

ribs
scapula
vertebrae

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14
Q

what is the FRAX tool

A

screening tool
assess person risk of fragility fracture over 10 years
performed in women 65+, men 75+
involves - age, BMI, comorbidities, smoking, alcohol, fhx, bone mineral density

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15
Q

what would blood tests shown in osteoporosis

A

all normal

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16
Q

what is the gold standard for osteoporosis investigation

A

DEXA scan
reading of the hip

generates 2 score - T and Z

T= value of bone density vs normal healthy population 
Z= value of bone density vs normal value for patient age
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17
Q

which score do we use to assess the severity of osteoporosis in DEXA

A

T-score

-1 = normal

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18
Q

management for osteoporosis

A

lifestyle advice - adequate ca and vit D intake

medical management
-bisphosphonates = aledronate or etidronate

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19
Q

how do bisphosphonates help osteoporosis

A

cause apoptosis of osteoclasts - stops bone degradation

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20
Q

side effects of bisphosphonaetes

A

oesophagtis
GORD
hypophosphataemia
osteonecrosis of jaw/external auditory canal

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21
Q

what is osteopenia

A

reduced bone density - not to the severity of osteoporosis

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22
Q

what is osteomalacia

A

disorder of impaired bone mineralisation and formation causing soft bones

loss of bone mineralisation but no loss of bone

23
Q

what is rickets disease

A

childhood presentation of osteomalacia

impaired mineralisation of cartilagenous growth plates

only happens if patient has osteomalacia during bone regrowth

24
Q

what is paget’s disease of the bone/osteitis deformans

A

increased bone turnover

associated with increased numbers of osteoclasts and osteoblasts

causes excessive bone breakdown and formation

leads to poor bone quality

25
what are the risk factors for osteomalacia and rickets
those at risk of vit D deficiency reduced sunlight low intake of oral vit D reduced intestinal absorption due to CF coeliac disease, gastrectomy liver disease and CKD
26
what is the cause of osteomalacia and rickets
lack of vit D so poor ca reabsorption from gut -> hypocalcaemia
27
clinical presentation of osteomalacia
fatigue bine pain muscle cramps due to hypocal pins and needles due to hypocal ``` proximal myopathy fractures waddling gait bone deformities trousseau sign (spasm in hand BP) chvostek sign (spasm of facial nerve) ```
28
what is the clinical presentation of rickets
growth retardation hypotonia apathy valgus and varus bone deformities
29
how does vit D deficiency lead to osteomalacia and rickets
lack of vit D -> hypocalcaemia bones will lack mineralisation as calcium is not able to form the bone mineral leads to soft bones (osteomalacia) and inability to mineralise growth plates (rickets) hypocalcaemia also leads to increased release of PTH - removes ca from bone making bones weaker
30
what blood tests would you order for suspected osteomalacia/rickets
- FBC to rule out infection or anaemia - U&Es for hypocalcaemia (due to lack of vit D), hypophosphataemia (excess PTH) - LFTs rasied ALP (from bone) - vit D (serum 25-hydroxy) low - PTH levels raised due to low Ca levels = secondary hyperparathyrodism
31
how would osteomalacia appear on x-ray
transluscent thin cortices pseudo-fractures or looser zones = transevrse bands across bone
32
how would rickets appear on x-ray
transluscent thin cortices wide epiphysis clear bone deformities
33
management for osteomalacia/rickets
ensure adequate vit D and calcium in body vit D supplements - cholecalciferol to increase vit D and ca
34
what is paget's disease a disease of and how can it present
disease of osteoclasts - increased and disordered breakdown and turnover rare <40 asymptomatic but can get pain in bones - pathological fracture = nerve compression - hearing loss due to narrow auditory foramen
35
what blood test result would we get in pagets and what is the management
raised ALP bisphosphonates
36
what is the difference between seronegative and seropositive arthritis
seronegative = patient is not +ve for RF or anti-CCP - affects tendons and large joints - psoriatic arthritis ankylosing spondyloarthritis seropositive = patients +ve for FR or anti-CCP -have worse prognosis
37
risk factors for rheumatoid arthritis
Female (3:1) 50-75 Years of Age HLA-DR4 and HLA-DR1 Haplotypes Family History Smoking Obesity
38
risk factors for psoriatic arthritis
psoriasis | HLA-B27
39
how would someone with rheumatoid arthritis present
symptoms - joint pain - joint swelling - fever - myalgia - fatigue signs - rheumatoid nodules on elbows - anaemia - pallor - warm joints - joint deformities - uveitis
40
hand deformities associated with RA
z-shaped deformitiy of thumb swan neck boutonnieres ulnar deviation of MCP
41
clinical presentation of psoriatic arthritis
symptoms - joint pain - joint stiffness - joint swelling - joint warmth signs - skin changes - onycholysis - dactylitis - enthesitis - uveitis
42
differentiating between RA and psoriatic arthritis
RA - affects MCPs, PIPs (NOT DIPs) - can affect shoulders, knees, ankles, elbows - morning stiffness - pain worse after REST, improves with ACTIVITY PA - affects DIPs (NOT MCPs) - can affect spine, wrists, ankles, hands - pain worse after rest, improves with activity
43
pathophysiology of rheumatoid arthritis
autoimmune attack of joints due to citrullination of proteins (arginine replaced with citrulline) which -> immune system unable to recognise cells citrullination can occur due to smoking or genetic factors autoimmune cells attack joint -> cytokine release (pro-inflamm = TNF-a, IL-1/6) -> systemic sx attack of joint leads to proliferation of synovial joints -> panus (filled with granulation tissue) overtime, the panus leads to damage of cartilage, soft tissue and bone release of RANK-l -> increased osteoclast activation -> increased breakdown of joint
44
what is the pathophysiology of psoriatic arthritis
T-cell mediated attack of joints
45
blood test results for rheumatoid arthritis
FBC - anaemia of chronic disease LFTs - raised CRP and ESR RF - positive (indicated worse prognosis) anti-CCP - positive, more specific for RA
46
what are the investigations for psoriatic arthritis
psoriasis epidemiological screening tool - PEST lack of RF and anti-CCP (bloods)
47
x-ray results in hands and feet for rheumatoid arthritis
joint destruction and deformity soft tissue swelling periarticular osteopenia - redcued bone density bony erosions
48
x-ray results for psoriatic arthritis
``` periostitis ankylosis - joining of bones osteolysis - bone destruction dactylitis - soft tissue swelling pencil in cup appearance - central erosions of bone ```
49
special test for rheumatoid arthritis
DAS28 score - assess 28 joints
50
management of RA
disease modifying anti-rheumatic drugs - methotrexate, leflunomide, hydroxychloroquine if patient has DASS28 score of >5.1 qualify for biologic therapy - adalimumab, inflixamab (anti-TNF), rituximab (anti-CD20)
51
how does methotrexate help in RA
inhibits action of dihydrofolate reductase (converts folic acid to tetrahydrofolate) - required for DNA synthesis therefore limits anti-inflammatory effects by inhibiting IL-6/8, TNF-a dampens down inflammation
52
important measures while on methotrexate
prescribe folic acid take FBCs and LFTs to ensure BM suppression and hepatotoxicity does not occur take folic acid on different day to methotrexate
53
management of psoriatic arthritis
similar to RA - NSAIDs, DMARDs, anti-TNF

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