Rheum Flashcards
what is osteoporosis
loss of bone density without loss of bone mineralisation
results in increased susceptibility to bone fractures
what are the different types of osteoporosis
type 1 = post menopausal
type 2 = senile
secondary = disease process or medical tx
what are the risk factors for type 2 osteoporosis
fhx alcohol RA immobility untreated menopause
what are the risk factors for secondary osteoporosis
Steroid use Hyperthyroidism, hyperparathyroidism Alcohol Thin BMI <18 Testeosterone Early menopause Renal failure Erosive bone disease Diet - low vit D or Ca
how do steroids cause osteoporosis
cortisol inhibits osteoblasts and activares osteoclasts
bone breaks down, reduced bone density
how does hyperthyroidism cause osteoporosis
thyroxine inhibits osteoblasts
increased bone breakdown than formation
also hypercalcaemia
what is the clinical presentation for osteoporosis
usually asymptomatic
fragility or pathological fracture
- compression fracture - back pain, loss of height, loss of spine curve, hunched
- colles fracture - distal radius
- NOF fracture
3 cells within bone
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
describe the effects of PTH
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)
what does kidney disease lead to and why
renal osteodystrophy
kidneys produce less vit D
reduced Ca absorption from gut
leads to hypocalcaemia so PTH released
but PTH breaksdown bone -> weakening
why is there an increased risk of developing osteoporosis after menopause
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
which cells are activated more/less in osteoporosis
breakdown is faster than formation
so osteoclasts are activated more
osteoblasts are activated less
which bones are at greatest risk of fracture in osteoporosis
ribs
scapula
vertebrae
what is the FRAX tool
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
what would blood tests shown in osteoporosis
all normal
what is the gold standard for osteoporosis investigation
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
which score do we use to assess the severity of osteoporosis in DEXA
T-score
-1 = normal
management for osteoporosis
lifestyle advice - adequate ca and vit D intake
medical management
-bisphosphonates = aledronate or etidronate
how do bisphosphonates help osteoporosis
cause apoptosis of osteoclasts - stops bone degradation
side effects of bisphosphonaetes
oesophagtis
GORD
hypophosphataemia
osteonecrosis of jaw/external auditory canal
what is osteopenia
reduced bone density - not to the severity of osteoporosis
what is osteomalacia
disorder of impaired bone mineralisation and formation causing soft bones
loss of bone mineralisation but no loss of bone
what is rickets disease
childhood presentation of osteomalacia
impaired mineralisation of cartilagenous growth plates
only happens if patient has osteomalacia during bone regrowth
what is paget’s disease of the bone/osteitis deformans
increased bone turnover
associated with increased numbers of osteoclasts and osteoblasts
causes excessive bone breakdown and formation
leads to poor bone quality
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
what is the cause of osteomalacia and rickets
lack of vit D so poor ca reabsorption from gut -> hypocalcaemia
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)
what is the clinical presentation of rickets
growth retardation
hypotonia
apathy
valgus and varus bone deformities
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
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
how would osteomalacia appear on x-ray
transluscent
thin cortices
pseudo-fractures or looser zones = transevrse bands across bone
how would rickets appear on x-ray
transluscent
thin cortices
wide epiphysis
clear bone deformities
management for osteomalacia/rickets
ensure adequate vit D and calcium in body
vit D supplements - cholecalciferol to increase vit D and ca
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
what blood test result would we get in pagets and what is the management
raised ALP
bisphosphonates
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
risk factors for rheumatoid arthritis
Female (3:1)
50-75 Years of Age
HLA-DR4 and HLA-DR1 Haplotypes
Family History
Smoking
Obesity
risk factors for psoriatic arthritis
psoriasis
HLA-B27
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
hand deformities associated with RA
z-shaped deformitiy of thumb
swan neck
boutonnieres
ulnar deviation of MCP
clinical presentation of psoriatic arthritis
symptoms
- joint pain
- joint stiffness
- joint swelling
- joint warmth
signs
- skin changes
- onycholysis
- dactylitis
- enthesitis
- uveitis
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
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
what is the pathophysiology of psoriatic arthritis
T-cell mediated attack of joints
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
what are the investigations for psoriatic arthritis
psoriasis epidemiological screening tool - PEST
lack of RF and anti-CCP (bloods)
x-ray results in hands and feet for rheumatoid arthritis
joint destruction and deformity
soft tissue swelling
periarticular osteopenia - redcued bone density
bony erosions
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
special test for rheumatoid arthritis
DAS28 score - assess 28 joints
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)
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
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
management of psoriatic arthritis
similar to RA - NSAIDs, DMARDs, anti-TNF
