general Flashcards
list the different types of arthritis
- osteoarthritis:
- starts with roughening of cartilage ‘repair cartilage’
- osteophyte growth
- increased amount of thick fluid inside joint
- joint capsule can stretch, and the joint may lose its shape
- > Rx = paracetamol, NSAIDs, keeping active - gout:
- due to too much urate/uric acid. crystals form in joints
- inflammatory arthritis that can cause painful swelling in the joints
- red hot skin, looks shiny and can peel
- > Rx = allopurinol, felauxostat, NSAIDs, paracetamol - Rhumatoid arthritis:
- AI inflammatory condition
- inflammation and increased fluid can cause: painful joint; chemicals in the fluid can damage bone, joint and nerve endings (painful); increased fluid stretches capsule
- often starts in small joints - hands - bilateral
- symptoms include pain/tender joints, stiffness/swelling in the morning >30mins, fatigue, general feeling of being unwell
- 40-60y/o W>M
- > Rx = DMARDs (slow down over-active IS and therefore reduce pain and swelling in joints). if don’t work -> biological therapies - spondylosis/ spondyloarthritis:
- number of conditions that cause pain and swelling mainly around around joints of the spine. there is inflammation of the entheses
- e.g. 1) ankylosing spondylitis - in response to inflammation around the spine, the body responds by making more calcium –> new bone growth causing pain and stiffness. typically causes pain in the second 1/2 of the night and swelling >30mins in the morning
- 20-30y/o M>W
- > Tx = drugs to slow process down. posture to help prevent curvature
- e.g. 2)psoriatic arthritis - AI condition causing painful swelling and stiffness within and around joint, as well as red scaly itchy rash + fatigue
- > Tx =DMARD creams and meds
- e.g. 3) JIA - diagnoesed with inflammatory arthritis before 6y/o
what features in a pt history are consistent with osteoarthritis and what features suggest an inflammatory arthropathy
inflammatory:
- worse in morning
- physical exercise makes it better
- morning stiffness lasts >1hr
- associated fatigue and malaise
- small joints
- bilateral
OA:
- worse at night
- exercise doesn’t make it better
- no morning stiffness
- oler pt
- previous injury to joint
- larger joints
- unilateral
what are the main features seen on plain radiographs to the type of arthritis
osteoarthritis:
- sub-articular sclerosis
- osteophyte growth
- bone cysts
- joint space narrowing
inflammatory arthritis:
- joint subluxation
- soft tissue swelling
- osteolysis
- erosions
- periarticular osteoporosis
- joint space narrowing
(NB: first signs of RA are not osseous - MRI and CT better at detection, but plain radiographs remain the mainstay of diagnosis and follow up)
what are the non-operative treatment of osteoarthritis
pharmacological:
- heat creams
- paracetamol
- topical NSAIDs
- oral cox 2 inhibitors
- oral NSAIDs
- intra-articular glucocorticoids
- duloxetine
non-pharmocological:
- strength training
- weight management
- self management and education
- land/water based exercises
- biomechanics intervention e.g. knee brace
*surgical after these have been exhausted
for knee replacement surgical operations, which risks should be discussed with the pt?
- venous thromboembolism
- infection
- stiffness
- fracture
- revision
- pain
- neuromuscular injury
- amputation
after a total knee replacement there are concerns of a haematoma around the operation site and could be an infected wound. what appropriate test would be included in this case? what would be the appropriate management?
- FBC: to looks for increased WCC which would be consistent with infection
- inflammatory markers (ESR+CRP) that might indicate and underlying infection
- wound swab to look for culprit bacteria
- radiograph
- undergo a washout of the haematoma and primary closure of the wound
list 2 developmental abnormalities to bone
osteopetrosis:
- marble bone disease
- makes bone abnormally dense, hardened and deformed
- failure of osteoclasts
osteogenesis imperfecta:
- brittle bone disease
- group of genetic disorders that affect bone
- mutations in genes responsible for making type I collagen (usually found in.bine)
what is the order of fracture healing?
injury/necrosis/haemorrhage -> acute then chronic inflammation -> repair-callus -> mineralisation -> remodelling
what is Paget’s disease and how does it present?
- rare bone disease of bone that disrupts the normal cycle of bone renewal (osteoblasts + osteoclasts become overactive), causing bones to become enlarged and weakened
- usually present as bone pain with unclear cause
- common in the elderly
- XR shows increased reabsorption of bone and later on, the accumulation of large amounts of bone
- familial or sporadic
- single bone or more diffuse
- 4% of the elder
- possible viral trigger
- modelling gone wrong
- pain
how does osteomyelitis affect bone architecture?
- infection of the cavity of the bone, most commonly staph aureus or TB
- Hx of fracture, recent orthopaedic surgery, immunocmpressed pt to unwell child
- sets up inflammatory, osteoblast and osteoclast response
- not just typical inflammation and granulation. cartilage and bone is ‘coming in’
- goes away with ABS, but chronic osteomyelitis can lead to gross distortion of the bone
- bacterial infection. -> inflammation -> progressive bone destruction + loss of vasculature
what re the 3 risks associated with osteomyelitis?
- septicaemia - source of inflammation that can discharge into the circulation
- amyloidosis - deposition of an abnormally processed protein in tissue, effectively starving them from O2 and nutrients reaching the tissue. in this case, the protein comes from the acute phase response proteins generated from the liver. abnormally modified and deposited
- fracture - because may lead to abscess forming, new bone forming might end up with weaker bones
how might metabolic disease manifest itself in bone?
-disorders of bone strength usually caused by abnormalities of minerals (such as calcium or phosphorus), vitamin D, bone mass or bone structure
- osteoporosis:
- is the most common
- characterized by decrease in bone mass and density combined with loss of bone matrix and demineralization (loss calcium + osteoid)
- presents when severe: bone pain, fracture, nerve trapping
- particularly in females and postmenopausal - osteomalacia:
- metabolic bone disease characterised by incomplete mineralisation of the bone matrix (osteoid). so, instead of having calcified bone, you end up with non calcified matrix/ soft bone
(- in children, defective mineralisation of the epiphyseal growth plate cartilage –> rickets, resulting in skeletal deformities and growth retardation)
- caused by severe vit D def (lack of sunlight, inadequate diet, malabsorption, renal failure)
- often non-specific muscle pain presentation - hyperparathyroidism:
- caused by parathyroidism adenoma or parathyroid hyperplasia. secondary cause is renal failure
- causes increased reabsorption from bone (activates osteoclasts)
- lead to osteoporotic type.
- more acute, so often presents with hypercalcemia (‘bones, moans, groans, stones’)
what is the pathophysiology and different subtypes of osteoporosis?
type 1:
- postmenopausal osteoporosis
- decrease in oestrogen, genetic, endocrine and environmental factors -> secretion of bone resorptive cytokines -> increase bone resorption -> osteoporosis
type 2:
- happens in ill and old aged men
- secondary osteoporosis, disuse or steroids -> decrease bone formation -> osteoporosis
briefly describe the pathophysiology of OA
involves a degradation of cartilage and remodelling of bone due to an active response of chondrocytes in the articular cartilage and the inflammatory cells in the surrounding tissues.
The release of enzymes from these cells break down collagen and proteoglycans, destroying the articular cartilage. The exposure of the underlying subchondral bone results in sclerosis, followed by reactive remodelling changes that lead to the formation of osteophytes and subchondral bone cysts (cracks with leakage of synovial fluid into the bone). The joint space is progressively lost over time.
briefly describe the pathophysiology of RA
- rheumatoid antibody
- RF and anti-ccp
- something triggers damage to the synovial cells (maybe virus) -> sets up recurrent AI response.
- plasma cells produce antibody, mast cells releasing histamine and other inflammatory cells
- set up inflammatory setting
- in joint get fibrin, oedema, new blood vessel formation -> chronic inflammatory reaction
- the presence of growth factors will cause synovial cells to proliferate (hyperplasia) thrown into folds, lymphoid follicles present, plasma cells pilling out antibody.
- all this happening beside the joint and bones so get secondary changes occurring
Rx = physio, NSAIDs (GI haemorrhage), steroids (risk of osteoperosis), DMARDs (pathogenic cytokines inhibitors) … prescribe with care
what are the risk factors for developing avascular necrosis?
elderly
F>M
post fall
made worse by osteoporosis
what is the pathophysiology of gout?
problem of uric acid metabolism (increased intake, decreased removal or increased cell turnover or death)
M>F
age 40-50
family Hx common
symptoms variable
inflammation and pain
renal stones
what are the main classes of malignant bone tumours?
diaphysis:
- Ewing sarcoma
- chondrosarcoma (from cartilage producing cells)
metaphysis:
- osteosarcoma (from bone producing cells)
- juxtacortical osteosarcoma
*commonest tumours in bone is metastatic
where are the main sites of bone metastases
breast kidney lung prostate colon thyroid
list organisms responsible for septic arthritis
s.aureus
s. pyogenes
s. epidermis
m. tuberculosis
salmonela
bucella
N. gonorrhoea in sexually active
list organism responsible for osteomyelitis
S. aureus (>80%)
S. pyogenes
M. tuberculosis
(fungal in severe immunocompromised pt’s)
what is the pathogenesis, Ix and Mx of septic arthritis (joint infection, and medical emergency, characterised by hot, swollen, red, restricted joints)
- infection can be introduced into the joint by haematogenous spread or direct inoculation e.g. trauma or iatrogenically
- 1-2 week Hx of red, painful and restricted joint
Ix:
- urgent joint aspiration
- culture + sensitivity joint fluid
- peripheral blood culture
- PCR is suspect N. gonorrhoeal cause
- joint XR
Mx:
- most common cause of acute SA is staph aureus -> IV flucloxacillin 2g qds 2 weeks and then oral therapy for further 4wks
- washout may be required
- microbiology and infective diseases advice
(DD - inflammatory arthritis, crystal arthritis, trauma, bursitis or cellulitis)
what is the pathogenesis of reactive arthritis, Ix and Mx (triad - conjunctivitis, urethritis and arthritis)?
(urogenital or GIT. typically triggered by gram -ve bacteria)
- chlamydia trachomatis
- neisseria gonorrhoea
- escherichia coli
- shigella flexneri
- salmonella enteritis
- autoimmune condition that develops in response to an infection
- dermatological manifestations such as nail+ oral changes
Ix:
- ESR
- CRP
- rheumatic factor
Mx:
- symptomatic
- full dose NSAOD and gastric protection and treatment of precipitating factors e.g. chlamydia
what is the pathogenesis of osteomyelitis (inflammation of the bone and bone marrow usually caused by pyogenic baceteria and rarely by mycobacteria or fungi)?
- haematogenous spread; local spread (e.g. from septic joint); compound fracture; foreign body
- predisposition: sickle cell disease (salmonella); travel/foreign born (brucella); prosthesis (S.epidermis); children <5y/o (H.influenzae); UTI (E.coli)
- common bones = humerus, femur, tibia, fibula, calcaneum
- pain, swollen, fever, reduced movement, won’t weight bear
Ix:
- temp
- WBC
- eSR
- CRP
- blood cultures (Note - take 3)
- XR
- MRI/CT/Bone scan (increase uptake)
- pus
Mx:
- acute (prob staph. aureus) -> IV flucloxacillin (or clindamycin) 2g qds for 2 weeks -> or ABs further 2wks
- chronic (s.aureus, occasionally coliforms) -> oral glucloxacillin 1g qds
- MRSA osteomyelitis -> vancomycin IV
- drainage. removal or involucrum
define vasculitis
- inflammation in the blood vessel, characterised by inflammatory infiltrate and destruction of the vessel wall (thickening, weakening, scarring, narrowing)
- commonly refers to the systemic vasculitides -> AI disorders characterised by inflammation of blood vessels with widespread involvement (i.e systemic symptoms) and clinical severity
*2 features helpful in classification.nomenclature = size of vessel (small, medium and large) and ANCA )presence or absence of anti-neutrophil cytoplasmic antibody)
describe the different types of systemic inflammatory vasculitis
large vessel:
- Giant cell arteritis
- polymayalgia rhumatica
- takayasu’s arteritis (aorta)
medium vessel:
- polyarteritis nodosa (necrotising vasculitis in renalland visceral aa. adult pt’s.)
- Kawasaki disease (vasculitis in children <5y/o)
small:
- ANA associated = microscopic polyangitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis
- Henoch Schonlein Purpur (common in children; associated with rash, glomerulonephritis, arteritis, and sob pain)
what are the clinical features of vasculitis?
systemic: weight loss, fatigue, night sweats, arthralgia, fever
skin: rash, purpura, ulcers
kidneys: haematuria (hallmark of renal involvement in small vessel), proteinuria, AKI/CKD
neurological: nerve involvement - motor/sensory
respiratory: haemoptysis
ENT: epistaxis
deafness
sinusitis
what is polymyalgia rheumatica?
- large vessel vasculitis
- most common in adults >50y/o, peak 70-80y/o
- W>M
- causes pain and stiffness in the shoulders, neck and hips, which is often worse in the morning
- low-grade fever
- extreme tiredness
- loss of appetite and weight loss
- depression
- can be associated with GCA
- unknown cause - maybe infective trigger
DD -> RA (onset in older adults), local msk disease (bursitis or tendonitis), OA, hypothyroidism
describe the clinical assessment of a pt presenting with suspected PMR
Hx:
- aching stiffness in muscles/joints
- acute onset
- proximal/symmetrical, in limb girdles
- stiffness worse in morning or after inactivity >30mins
- systemic features - fatigue, weight loss, depression
- affect daily activities e.g. getting out of chair/dressed
examination:
- limited shoulder abduction
- reduced ROM
- distal synovitis
- normal muscle strength
IX:
- bloods (ESR/CRP - hallmark of disease, usually elevated; FBC - normocytic/normochromic, thrombocytosis; LFTs - raised ALP; CK - normal, Anti-CCP/ANA/RF - -ve)
- imaging (not required for Dx) -USS, MRI, PET
- mainly diagnosed based on clinical feature, lab findings and response to steroids
what is giant cell arteritis (GCA)
- most common large vessel vasculitis in the UK. AKA temporal arteritis
- key complication is vision loss. often reversible
- > 50y/o
- involvement of the cranial aa. that come off the aortic arch
describe the clinical assessment of a pt presenting with suspected GCA
Hx:
- unilateral headaches - temporal
- tenderness of the scalp or temples - unable to brush hair
- double vision/ vision loss - transient painless monocular visual loss
- dizziness or problems with coordination and balance
- jaw claudication
exam:
- erythema, thickening along course of the aa.
- tenderness on palpation
- reduced pulsation
- signs of superficial temporal artery inflammation
Ix:
- bloods (ESR/CRP - hallmark of disease, usually elevated; FBC - normovytic/normochromic, thrombocytosis; LFTs - raised ALP/ reflects systemic process)
- imaging (USS - increased diameter of superficial temporal a., and hypo echoic wall thickening)
- temporal a. biopsy
