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BRS YEAR2 > Musculoskeletal and Rheumatology > Flashcards

Musculoskeletal and Rheumatology Flashcards

1
Q

How is trauma fractures managed

A

ABCD: resuscitate to keep patient alive
then usually reduce (closed or open), retrict/hold, rehabilitate

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2
Q

How is a fracture assessed, investigated

A

Pain, Swelling, Crepitus, Deformity, Collateral nerve or vessel damage.

Investigations XRay, CT if want to see if goes into joint

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3
Q

How are fractures described

A

closed or open
pieces: simple fracture or comminuted/multi fragmented
pattern: transverse (straight across), spiral
displaces/undisplaced
rotated/translated/angulated : varus vs valgus, in hand volar/dorsal

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4
Q

What are the two types of fracture healing

A

Direct/Primary: bones end in contact so can get anatomical reduction, absolute stability/compression, low strain without callus. fixed with compression, involves endochondral and intramembranous bone healing

Indirect/Secondary: only sufficient fracture healing, micromovement, callus will form. Endochondral ossification only

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5
Q

What are the phases of indirect fracture healing

A

Inflammation: haematoma forms, cytokines released which recruit osteoclasts, granulation tissue and blood vessels form
Repair: soft callus forms (type II collagen), converted to hard callus (type I collagen)
Remodelling: callus responds to activity, external forces. functional demands and growth

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6
Q

What law describes how bone grows and remodels in response to forces put upon it

A

Wolff’s Law

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7
Q

How is reduction of a fraction achieved

A

Can be
Closed: by manipulation (pull and put in plaster) or traction (skin or skeletal, pins in bones to slowly move back into place)

Open: mini-incisions or full exposure

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8
Q

What types of fracture hold/restriction options are there

A

Closed: plaster or traction through skin or skeletal pins/splints

Fixation: can be internal such as: extramedullary plates, screws and pins or intramedullary pins and nails OR external such as monoplana or multiplanar

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9
Q

What types of rehabilitation options are there

A

use : pain relief and retrain
move
strengthen
weight bear

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10
Q

What are the complications of fractures

A

fat embolus: fat from bone marrow can cause pulmonary embolus
DVT
infection
prolonged immobility can cause UTI, chest infections

The fracture itself can injure structures:
neurovascular injury
muscle/tendon injury
non union/mal union
local infectio
Degenerative change: pressure can kill condrocytes

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11
Q

What factors affect fracture healing

A

Mechanical environment : movement and force applied

Biological environment : blood supply, immune function, infection, nutrition

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12
Q

What are the causes of a fractured neck of femur

A

Osteoporosis in older patients
trauma in younger patient

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13
Q

Describe the anatomy of the femoral neck

A

Triple blood supply to femoral head
iliopsoas muscle attaches to lesser trochanter
gluteus medius, minimus, piriformis, obturator externus and obturater internus attaches to greater trochanter

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14
Q

What are the four types of neck of femur fractures

A

Subcapital/ intracapsular: just under femoral head at the capsule
Transcervical/extracapsular: at femoral neck
Basicervical/extracapsular: below femoral neck, at the base
Subtrochanteric- below lesser trochanter
Part intertrochanteric : goes through/ around the trochanter

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15
Q

In which neck of femur fracture is avascular necrosis and non union likely to occur

A

Intracapsular as has a triple blood supply so more likely to be compromised

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16
Q

What sign on an x-ray indicates a neck of femur fracture

A

Shentons line ( a line from inside/medial of the femoral neck to bottom of superior pubic ramus, if displaced then means theres a problem.

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17
Q

How are neck of femur fractures managed

A

Extracapsular: internal fixation (plate and screws or nail)

Intracapsular
- if displaced : less than 55yrs then reduce and fix with screws, if over 65 replace (fit and mobile is total hip replacement, if not then hemiarthroplasty- aka femur head only)

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18
Q

How would a shoulder dislocation present, what hsould you examine and investigate

A

due to trauma often so pain, restricted movement, shoulder doesnt look normal
examine axillary nerve function
investigate: x-ray first to check if theres a fracture

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19
Q

How is a dislocated shoulder managed

A

traction-counter traction + gentle internal rotation
make sure patient relaxed
stimson manouvre

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20
Q

What are the complications of shoulder dislocation

A

Hill-Sachs defect : dent on humerus
Bankart lesion : injuries of the anteroinferior aspect of the glenoid labral complex , glenoid head usually makes

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21
Q

How are distal radius fractures managed

A

Cast/splint
Mua and k-wire: if unstable and extra-articular
ORIF: diplaced, unstable fracture not suitable for k wire get open reduction with internal fixation

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22
Q

What is a tibial plateau fracture and how is it managed

A

Tibial joint surface has medial and lateral plateaus with a central tibial spine insertion point
Any extreme loading or valgus/varus force can cause

management: only non operatuve if truly undisplaced, most have to have operation to restore articular surface with plates and screws, bone graft to prevent further depression

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23
Q

What is a trimalleolar fracture

A

Medial malleous
Lateral malleous/ medial side of fibula
Posterior malleous all broken

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24
Q

How are lateral malleus ankle fractures managed

A

Weber ankle fracture classification:
Type A: below the level of the syndesmosis between tibula and fibula, tibiofibular syndesmosis is intact. usually transverse/avulsion fractures
Type B: At level of tibiofibular syndesmosis but tibiofibular syndesmosis usually intact. usually torsion/spiral
Type C: above the level of the syndesmosis and tibiofibular syndesmosis disruption

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25
Q

How are ankle fractures managed

A

non operative: if Weber A or B then cast for 6-8 weeks non weight bearing, walking boot then physiotherapy.

operative: if Weber C or unstable Weber B. will need elevation as otherwise will swell, open reduction and internal fixation with syndesmosis repair

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26
Q

What are the three main functions of the spine

A

Locomotor: rigid for stability and mobile to bend
Bony armour/Protection: protect spinal cord
Neurological: spinal cord transmission between brain and periphery

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27
Q

Where does the spinal cord end

A

L2

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28
Q

What is lordosis and typhosis

A

lordosis: lumbar vertebrae curves outwards normally, c shaped
kyphosis: mirrored c shape, thoracic and cervical usually curved inwards

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29
Q

Before the spinal cord becomes the cauda equina what is it called

A

Conus medularis

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30
Q

How is chronic back pain categorised

A

back pain that lasts more than 12 weeks

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31
Q

What are the common symptoms and causes of mechanical back pain

A

Worse with movement, better at rest
common causes: muscular tension. muscle sprain/spasm, degenerative disk disease, osteoarthritis of facet joints

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32
Q

What symptom usually accompanies back pain

A

Sciatica : due to disk herniation ( a tear in the annulus fibrosis causes nucleus pulposus to move out and impede on the nerve. This causes pain radiating down one leg

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33
Q

What are some serious causes of back pain?

A

tumour
infection
referred pain
Inflammatory spondyloarthropathy
fracture
large disk prolapse casuing neurological compromise

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34
Q

What are the red flag symptoms of back pain

A

pain at night, or pain when laying supine
constant or progressive pain
thracic pain
weight loss and previous malignancy
fever/night sweats
immunosuppressed
bladder or bowel disturbance
leg weakness
sensory loss
younger than 20 yrs or older than 55

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35
Q

What is cauda equina syndrome, what investigations and treatment is needed

A

caused by large disk herniation, bony metastases, TB, myeloma

Signs:
saddle anaesthesia
bladder/bowel incontinence
loss of anal tone on PR
radicular leg pain
ankle jerks absent

Treatment: surgery , according to cause

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36
Q

What is the treatment for lower back pain that has no red flags

A

time to see if improves
analgesia
keep moving, no bed rest
physiotherapy: soft tissue work and corrective exercises

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37
Q

Why four causes of back pain are blood tests useful for and what would be the results

A

myeloma- high ESR, low FBC, high Calcium
Inflammation- high ESR, high CRP, high WCC
TB- high ESR
Bony metastases: high calcium, high PSA (prostate cancer specifically)

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38
Q

What imaging modalities are preferred in back pain cases

A

MRI is the best visualisation of soft tissue and spinal imaging

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39
Q

What pathology is a wedge fracture indicative of

A

Osteoporosis (causes vertebral collapse so see a squished door wedge shaped fracture rather than square vertebral body from side will look triangular

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40
Q

How would TB affect the spinal cord and what would show up on an MRI

A

Looks like the vertebral body has been eaten away, cerebrospinal fluid moves out

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41
Q

What is the treatment for a herniated disk

A

normally improves spontaneously

1- if back pain without sciatica: NSAIDs and physiotherapy
2- nerve root injection of local anaestheric and glucocorticoid
3- surgeruif neurological impact

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42
Q

What is inflammatory spondyloarthritis

A

group of immune mediated inflam diseases. causes spondylitis which is inflammation of the spine, inflam of sacro-iliac joint (sacro-ilitis). Affects peripheral joints especially tensor insertions

get AAAA: anterior uveitis (ocular inflam), Apical lung fribrosis, Aortic regurg, Amyloidosis

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43
Q

What are the symptoms and pathophysiology of ankylosing spondylitis

A

is chronic spinal inflammation that can lead to spinal fusion, inflammation at enthesis (where tendon or ligament attaches), no autoantibodies
Loose spinal movements, head can get stuck in forward flexion, get morning stiffness, enthesitis (inflammation of entheses) , pain and swelling in the inflamed areas. NSAIDs like ibuprofen make better

Genetic component: HLA-B7 is the risk factor , is a diagnostic biomarker but HLA-B7 positive doesnt mean AS always.(HLA Class I molecules o infective sells bind to B7 on T cell).

Cytokines are involved: TNF-alpha, IL-17 and IL-23
aberrant aminopeptidases in E.R

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44
Q

How may MRI scans look in patients with ankylosing spondylitis

A

Joints irregular and not smooth, increased whiteness on bone either side of joint :sclerosis
see shiny corners of the vertebral body: which is spinal inflammation

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45
Q

Why does untreated ankylosing spondylitis result in spinal fusion/ being stuck in positions

A

Spinal inflammation at entheses (spinal enthesitis)
this causes bridging syndesmophytes and there is bone growth between adjacent vertebra which becomes calcified and get stuck in positions

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46
Q

How is ankylosing spondylitis managed

A

1) physiotherapy with life long exercise programme
2) NSAIDs (ibuprofen): at risk of peptic ulcer, renal probelms, asthma exacerbation and higher atherothrombosis risk.
Selective COX2 inhibitors reduce GI ulcer risk as COX1 isnt inhibited
3) Biological therapies: monoclonal antibodies such as anti-tnf alpha or anti IL-17 (all end in mab)

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47
Q

Why do NSAIDs help ankylosing spondylitis

A

NSAIDs inhibit COX-1 and COX-2 (cyclooxegenase). COX converts arachadonic acid to prostaglandins. Prostaglanding cause imflammation, pain, platelet inhibition. Instead of prostaglandin arachadonic acid is converted to leukotrienes and causes bronchoconstriction.

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48
Q

What is an example of a selective COX2 inhibitor

A

celecoxib

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49
Q

Describe the two types of bone development

A

Intramembranous : mesenchymal cells in embryonic skeleton differentiate into osteoblasts, osteoblasts cluster to make the ossification centre. Osteoblasts then secrete osteoid which calcifies and traps osteoblasts making them osteocytes. clusters of osteoid form around capillaries make the trabecular matrix , and clusters on the spongey bone surface form the periosteum (outside of bone). spongey bone crowds nearby blood vessels and condenses to red bone marrow and the superficial layer becomes cancellous/compact bone : MESENCHYMAL TO BONE: BONE FORMS FROM FIBROUS MEMBRANES

endochondral: mesenchymal cells become chondroblasts which make hyaline cartilage. Perichondrium is vascularised, nutrients from blood stimulate mesenchymal cells to become osteobblasts, osteoblasts for spongey bone at primary ossificcation, osteoblasts around diaphysis to form bone collar, whch causes calcification of the matrix , causes cell death = hollow bone. Chondrocytes at epiphysal plate still depositing cartilage and elongating the bone. Periosteal bud invades cavity and makes sponget bone. osteoblasts deposit bone at ephiphysis and diaphysisi to make epiphyseal plate , this is the secondary ossification centre where the bone grows

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50
Q

What types of bone do each bone development types create

A

Intamembranous- flat bones : skull clavicle and mandible
Endochondral- long bones

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51
Q

What is the difference between primary ossification centres and secondary ossification centres

A

Primary: pre-natal bone growth through endochondral ossification at the diaphysis

Secondary: post-natal at the physis

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52
Q

Describe the layers of the physis

A

growth plate zone (chondrocytes change)
Reserve zone: matrix production
Proliferative zone: mitosis
Maturation and hypertrophy (lipids, glycogen, alkaline phosphatase)
Calcified matrix (cell death)

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53
Q

Describe where longitudinal and positional growth occur

A

longitudinal at the physis
positional at the periosteum

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54
Q

what investigation needs to be done if you want to visualise cartilage

A

arthrogram

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55
Q

Differences between adult and childrens bones

A

PHYSIS : growth occurs at physis until closes girls 15-16, men 18-19. Therefore, physical injuries can cause growth arrest and deformity in younger children

ELASTICITY: children have immature bone: less dense, lamellae more porous, increased density of haversian canals so bone bends before breaks

SPEED AND REMODELLING: thick periosteum allowing for remodelling as gives nutrition and blood supply, so if bone breaks periosteum will correct

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56
Q

What two type of fractions are common in children

A

Buckle fracture: axial force squash radius then cortices can’t sustain force so cracks and buckles, doesn’t snap but buckles and doesn’t displace as the periosteum stays in tact.

Greenstick Fracture: bending force, cracks on one cortex but stay intact the other, in adults as their bones are brittle both sides will snap.

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57
Q

In the leg and arm which two physis’ remodel faster

A

physis at he knee and at extreme of upper limb (shoulder)

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58
Q

What is avulsion

A

Bone pulled off from ligament or tendon

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59
Q

What is the difference between intra articular and extra articular fractures and their preferred bone healing process

A

Intra articular: affects the joint , want primary/direct bone healing so no callous is formed
Extra articular: doesnt impact the joint so secondary/indirect is okay

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60
Q

How are physical injuries classified

A

Salter-Harris

TYPE 1: physeal separation
Type 2: fracture is through physis and exits through metaphysis
Type 3: Fracture through physis and exits epiphysis
Type 4: Through epiphysis, physis and metaphysis
Type 5: crush injury to physis= growth arrest

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61
Q

What causes growth arrest

A

injuries to the physis

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62
Q

Describe the difference between damage to the whole physis and partial damage to the physis

A

Whole: limb length discrepancy
Partial: angultion as other side keeps growing

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63
Q

What are the treatment options for growth arrest

A

1) limb length correction: shorten the long side, or lengthen the short side

2)angular deformities:stop growth of the unaffected side or osteomy (reforming the bone)

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64
Q

What is an example of closed reduction

A

Gallows traction: hold the skin, reduce the long bones of the lower limb

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65
Q

What restriction methods in fracture healing is preferred when the patient is a child

A

Splints and plaster as remodelling is achieved from the healing potential of children
If not then elastic or nails try to do the least damage as physis is still growing, if put metal in will remove in the future

66
Q

Describe a congenital condition that affects the hip joint

A

Developmental dysplasia of the hip : femur is unstable or incongruous with the acetabulum. Normal development relies on concentric reduction and balanced forces being put on it. Get a spectrum can get subluxation where the joint surfaces are still in contact or complete dislocation

67
Q

What are the risk factors for Developmental dysplasia of the hip

A

Being female
first born
breech (head isnt the first to be birthed)
family history
Native Americans swaddle the hip
Oligohydramnios (little amniotic fluid)

68
Q

What is the examination, investigation and treatment of Developmental dysplasia of the hip

A

Baby checks : reduction of hip movement (abduction especially), check leg length (galeazzi)
If older than 3m then Barlow and Ortalani test where pop femoral head out is non-sensitive
shorter leg or uneven skin folds

Investigate- ultrasound used if less than 4 months, if older than X-ray. This is used to measure acetabular dysplasia and the hip position

Treatment: less than 6 month and have a reducible hip then Pavlik harness to align the legs and stimulate the acetabulum to deepen. If too old or pavlik harness doesnt work due to secondary soft tissue and capsule changes then MUA+ closed reduction

69
Q

If developmental dysplasia of the hip is left untreated what problems will occur

A

abnormal gait
pain during activity
limited range of motion

70
Q

Name a congenital deformity of the foot in children

A

Congenital Talipes Equinovarus

71
Q

What groups of people are most affected by congenital talipes equinovarus

A

hawaiians
males more
genetic
PITX1 gene

72
Q

What symptoms do those with congenital talipes equinovarus have

A

CAVE deformity
Cavus: high arch tight glexor digitorum longus (FDL) and flexor hallucis longus
Adductus of foot: tight tibialis posterior and anterior
Varus: tight tendoachillies, tibialis post and ant
Equinou: tight tendo achilles

looks like riding horse with foot bent/ adduction

73
Q

What is the treatment of congenital talipes equinovarus

A

Ponseti method: casts to correct,might have operation for soft tissue releases

74
Q

What congenital condition is also called brittle bone disease

A

Osteogenesis imperfecta : is hereditary and causes decreased Type 1 collaged (low secretion and produced abnormal collagen instead
also insufficient osteoid production

75
Q

What are the effects of osteogenesis imperfecta

A

bones: fragile, short stature, scoliosis
also: heart problems, BLUE SCLERA (because type 1 collagen is needed for sclera), dentinogenesis imperfecta (brown soft teeth), hypermetabolism, wormian skill (small round ish extra part of skull inbetween skull sutures)

76
Q

What is a common skeletal dysplasia

A

Achondroplasia
autosomal dominant
G380 mutation of FGFR3 (FGFR23 is the phosphate regulator). Inhibits condrocyte proliferation in the physis’ prolferative zone resulting in defect in endochondral bone formation

Rhizomelic dwarfism: humerus is shorter than foreaem and femus shorter than tibia, normal trunk and short high, spinal issues but no cognitive issues

77
Q

If a child is limping what are the four most probable causes, differentiate them

A

Septic Arthritis : is emergency, Kochers classficiation: non weight bearing, ESR over 40, WBC over 12000, temp over 38. wont happen after trauma, worried if had recent illness as infection and if they have joint pain. fever, joint pain, swelling, redness, and warmth.

Transient Synovitis: inflamed joint due to systemic illness. CRP less than 20 so only need AB’s, pain improves over the day

Perthes Disease : necrosis of proximal femoral epiphysis, in 4-8 year olds usually male, use support as treatment. Get pain in knee thigh or groin

Slipped Upper Femoral Epiphysis: proximal epiphysis slips in relation to metaphysis (lower than perthes like top of bone neck). Obsese young male- over 10, athletic injury, may have hypo thyroidism or pituitarism. Operative screw fixation to prevent further slip

78
Q

Describe the different bone cell types and their functions

A

Osteogenic cell: bone stem cell are in deep layers of periosteum and the bone marrow
Osteoblast: bone formin, makes osteoid, catalyses the mineralisation of osteoid. in periosteum and endosteum
Osteoclast: bone breaking, dissolves and reabsorbs bone via phagocytosis, from bone marrow, are at bone sites of old or injured bone
Osteocyte: mature bone cell, when osteoblast is imbedded/trapped in secretions become osteocytes- directs osteoblast and osteocyte function, is in matrix

79
Q

Describe the organisation of cortical bone

A

Functional units called osteons with have lamellae circled around the haversian canal which is (a nerve, lymphatic vessel and blood vessels). Lamellae also have lacunaeinbetween the layers which as small spaces that contain osteocytes, they have tiny canaliculi that radiate outwards filled with ECF. Blood vessels connect the centre of lamellaes horizontally are called vaklmanns canal

80
Q

What are the different types of mature bone

A

Cortical: compact and dense for weight bearing
Cancellous: spongey honeycomb cant have weight bearing

81
Q

Describe the stucture of long bones

A

Epiphysis -> Physis -> Metapysis -> Diaphysis

Yellow bone marrow in a medullary cavity -> endosteum lining the haversian canals, outer cortex of compact bone, spongey/cancellous bone at epiphysis and metaphysis, periosteum which is connective tissue covering the bone and a nutrient artery running through the periosteum

82
Q

What are the three mechanisms that can cause fractures

A

Trauma: low or high energy
Stress- abnormal stress on normal bone
Pathological: normal stress on abnormal bone

83
Q

Name at least 5 causes of a pathological/insufficiency fracture

A

Osteoporosis : soft bone
Malignancy
Vitamin D deficiency: osteomalacia and rickets
Osteomyelitis: bone infection
Osteogeneis imperfecta
Pagets

84
Q

How are fractures investigated

A

X ray first, CT if comminuted
MRI in soft tissue injury
Bone scan if have a prosthetic fracture

85
Q

Children have increased what in bone that contributes to the bones elasticity

A

Haversian canal density

86
Q

What is compartment syndrome

A

so much swelling trapped in a compartment so pushes on blood vessels or nerves and causes more pain

87
Q

How does the management of neck of femur fracture differ in older patients, younger patients and their mobility

A

Extracapsular: internal fixation (plate, screws and nails)

Intracapsular Undisplaced: screws

Intracapsular Displaced:
Younger patient: try to fix
Older patient: replace: if walk a lot, have few comorbidities then total hip replacement/ if lower mobility, comorbidities then hemiaarthroplasty

88
Q

How are joints classified

A

Fibrous : sutures syndesmosis and interosseous membrane
Cartilaginous: synchondroses like sine, symphyses (pubic symphyses)
Synovial: plane( between metatarsals) , hinge (elbow) , condyloid (radius and carpal bones), pivot (C1 and C2 vertebrae), saddle (trapezium carpal bone and metacarpal), ball&socket (hip)

89
Q

What stabilised synovial joints

A

Muscles and tendons
Ligaments
Bone surface congruity

90
Q

What are the components of a synovial joint

A

Synovium : cell lining containing macrophage like cells (type a synoviocyte), and firboblast-like cells that make hyalauronic acid (type b synoviocyte), also contains type 1 collagen.
Synovial fluid : hyalauronic acid rich
Articular cartilage : Type II collagen and proteoglycan

91
Q

What is cartilage composed of

A

Chondrocytes
ECM: water, collagen, proteoglycan

no blood supply

92
Q

What proteoglycan is in cartilage

A

Aggrecan: contains chondroitin sulfate and keratin sulfate chain. can interact with hyalauronic acid to form large proteoglycans

93
Q

What are the two main categories or arthritis

A

Osteoarthritis : degenerative arthritis
Inflammatory arthritis: rheumatoid arthritis

94
Q

What are the differences between rheumatoid arthritis and osteoarthritis

A

Rheumatoid arthritis: osteopenia and bony erosions

Osteoarthritis: osteophytes and subchondral sclerosis

both have joint space narrowing because arthritis

95
Q

What two places can osteophytes form nodes and what two types are there in rheumatoid arthritis

A

Distal interphalangeal joints: HEBERDENS NODES
proximal inter phalangeal joints: BOUCHARDS NODES

96
Q

What is the pathophysiology of osteoarthritis, risk factors and early vs late stage

A

Deterioration of cartilage causing bone rubbing together making stiffness, pain and impaired movement

Risk factors: age, gender (female), genetics, high BMI/obesity, low oestrogen, spondylarthritis or rheumatoid arthritis can cause, trauma or overload from exercise

Early stag : oedema of articular/chondral cartilage
Late stage: cartilage damaged, synovial inflammation: inflam mediators include MMRPs, aggrecanases, Il-1beta, TNF-alpha which cause upregulation of proteases and catabolic factors to degrade articular membrane, osteophytes forming nodes, sunchondral bone remodelling

97
Q

How does osteoarthritis present

A

pain at exertion, rest, night all the time
disability and deformity

98
Q

How are orthopaedic conditions assessed

A

look - valgus/varus or scars
Feel- test for effusion
Move- angle of flexion

99
Q

What test is used to test the ACL

A

Lachmann test

100
Q

What signs are seen radiographically if the patient has osteoarthritis

A

Osteophyte- bony spurs
loss of joint space
Subchondral cyst
Sclerosis (whitening of bone edge)

101
Q

How is osteoarthritis managed

A

Analgesics, physio, walking aid, avoid strenuous activity, injections
replace joint, realign, excise and fuse

102
Q

What are the two types of bone/joint infection

A

Osteomyelitis: can be acute/chronic primary/secondary, causes pain, swelling, discharge/pus, fevers, sweating, weight loss, pain of bone/limp
Septic arthritis: pain, joint swelling/stiffness, fevers, sweats, weight loss

103
Q

What causes septic arthritis, risk factors, diagnosis and treatment

A

bacterial infection of a joint
RISK factors: immunosuppressed, already had a joint drainage, IV drugs
Diagnose by aspirating joint
Treatment: lavage (surgical wash out) and IV AB’s

104
Q

What type of septic arthritis can cause polyarthritis and is less likely to cause joint destruction

A

Gonococcal septic arthritis

105
Q

What are the markers of septic arthritis

A

CRP (seen in acute)
ESR (over 40, slower more chronic arthritis)
WCC over 12000
TB or PCR

106
Q

What scans can be used to investigate septic arthritis

A

MRI scan: see bony collections
CT if MRI isnt available
Bone scans if multifocal
Labelled WCC scans

107
Q

How is osteomyelitis treated

A

IV AB’s
surgical drainage
antibiotic suppression if chronic
amputate

108
Q

What is the treatment of septic arthritis

A

surgery: Joint lavage
IV AB’s
immobilise joint
after acute phase over then physio

109
Q

What is rheumatoid arthritis

A

chronic joint inflammation at the synovium= SYNOVITIS
autoantibodies cause
get bony erosions, joint space narrowing from cartilage degredation, synovitis, pannus formation

110
Q

What two autoantibodies are associated with rheumatoid arthritis

A

rheumatoid factor
CCP - anti-cyclic citrullinated peptide

111
Q

What 5 diseases are classified as connective tissue diseases

A

Systemic Lupus Erythematosus
Sjogrens syndrome
autoimmune inflammatory muscle disease
systemic sclerosis
overlap syndromes

112
Q

What is systemic lupus erythematosus

A

tissue inflammation due to antibodies directed against self antigen forming immune complexes.
inflammation and multiple sites: joints, skin and kidney especially

113
Q

What autoantibodies are associated with systemic lupus erythematosus

A

Antinuclear antibodies (not specific seen in many)
anti-double stranded DNA antibodies (serum level of this correlates with disease)
Anti-phospholipid antibodies: assoiated with arterial and VT risk

114
Q

What phenomenon is common in connective tissue disorders

A

Raynauds phenomenon: vsospasm of digits when exposed to cold, digits from white to blue to red

115
Q

What are the clinical manifestations of systemic lupus erythematosus

A

females from 15-45 yrs

malar rash
photosensitive rash
mouth ulcers
hair loss
Raynaids phenomenon
arthragia, sometimes arthritis
renal disease

116
Q

What is the pathogenesis of systemic lupus erythematosus

A

Apoptosis leads to translocation of nuclear antigens to membrane surface , apoptotic cells not cleared so nuclear antigen is presented to immune cells, Bcells autoimmunity leads to autoantibody production, tissue damage

117
Q

What investigations are needed is SLE is suspected

A

High ESR, normal CRP, platelets decrease, low albumin, low haemoglobin, low lymphocyte, high reticulocyte count, high WCC

renal: urine protein increase, the urine:protein to creatinine ration will increase

Immunological: antinuclear antibodies, anti-double-stranded DNA antibodies, complement consumption
complement consumption - low C3 and C4 (immune complexes activate the complement pathway)

clotting: anti-phospholipid antibodies cause clots

118
Q

How is SLE managed

A

Hydroxychloroquine : decrease immune systems activity
Glucocorticoids: rapid symptom relief but should be MINIMISED or WITHDRAWN
Immunomodulatory agents: methotrexate, azathioprine, mycophenolate)
If severe then cyclophosphamide and B cell targeted (rituximab and belimumab)

Check: antiphospholipid antibody status, their CVD risk, infection risk and plan for pregnancy

119
Q

What is sjogrens syndrome

A

autoimmune exocrinopathy: lymphocytes infiltrate exocrine glands which results in:

Xerophthalmia: dry eyes
Xerostomia: dry mouth
Parotid gland enlargement (infront of ear)
non-erosive arthritis and raynauds phenomenon

120
Q

What investigations are used for sjogrens syndrome

A

Salivary gland biopsy : chows t cell infiltration
Schirmers test: filter paper under eyelid and see tear production, more than 5mm abnormal

121
Q

What is inflammatory muscle disease

A

proximal muscle weakness due to autoimmuneinflammation with dermatomyositis (heliotrope/lilac coloured rask on eyelid/malar region/aso-labial folds , gottrons papules (red/purple flat or raised lesions on knuckles, subcutaneous calcinosis, mechanics hands (cracking of skin over finger pads). DONT HAVE A RASH THO

122
Q

A patient presents with dry eyes and mouth, has some joint pain and an enlargements at the side of his jaw, what is the diagnosis and what investigations should you try

A

Sjogrens syndrome

salivary gland biopsy and schirmers test

123
Q

What would tests show if the patient had inflammatory muscle disease

A

High creatinine phosphokinase (CPK) but creatinine is normal.
abnormal electromyography
muscle biopsy: polymyositis - high CD8 T cells, dermatomyositis- CD4 T cells and B cells

may also have malignancy an pulmonary fibrosis

124
Q

Describe systemic sclerosis

A

thickened skin with raynauds phenomenon : due to dermal firbosis, cutaneous calcinosis and telangiectasias

diffuse SS: fibrotic skin proximal to elbows or knees, anti-Scl-070 antibodies), pulmonary fibrosis and renal issues, raynauds phenomenon

Limited SS: fibrotic skin, hands, forearm and feet, anti-centromere antibodies, pulmonary hypertension, raynauds phenomemon for a long time

125
Q

What is overlap syndrome

A

features of more than 1 connective tissue disorder.

126
Q

What autoantibody is a serological marker of Mixed Connective Tissue Disease

A

Anti-U1-RNP antibody (U1-RNp= uridine rich small nuclear ribonucleoproteins)

127
Q

What is undifferentiated connective tissue disease

A

Have one connective tissue disorder and incomplete features of another disorder

128
Q

How can diffuse systemic sclerosis and limited systemic sclerosis be differentiated between on base of serology

A

Diffuse: Anti-Scl-70 antibody
Limited systemic sclerosis: anti-centromere antibodies

129
Q

What antibodies may be seen in inflammatory muscle disease

A

Dermatomyosilitis and Polymyosilitis causes anti-tRNA transferase antibodies

130
Q

Types of seronegative spondyloarthropathies

A

Ankylosing spondylitis
Reactive Arthritis
Psoriatic arthritis (have psoriasis with it)
Enteropathic synovitis (arthritis with GI inflam)

131
Q

what are the three causes of joint inflammation

A

1- infection: septic arthritis or TB : secondary and non-sterile
2) Crystal arthritis: gout (uric acid) or pseudogout (cppd crystals) : secondary and sterile
3) autoimmune : primary and sterile

132
Q

What are the two types of crystal arthritis, their risk factors and causes

A

Gout : deposition of monosodium urate/ uric acid crystals in and around the joint leading to inflammation
Risk factor: high uric acid levels
causes: genetics, intake of purine rich food, chemo causing inc cell turn over, kidney failure to clear the uric acid

Pseudo gout : deposition of calcium pyrophosphate dihydrate (CPPD) crystals
Risk factors: osteoarthritis, elderly, intercurrent infection

133
Q

What are the clinical features of gout

A

Gouty arthritis
Tophi ( deposits of MSU crystals around hands feet, elbows, ears ) - white lumps

abrupt onset, monoarthritis, big toe 1st metatarsophalangeal joint =podagra aka a bunion betty.

134
Q

How are the two types of gout tested

A

joint aspiration and synovial fluid analysis (get microbiology and polorasing light microscopy)

Gout : urate crystals, needle/long shape and no birefringence

Pseudogout: calcium pyrophosphate dihydrate, rhomboid/brick shape, positive birefringence

134
Q

How are the two types of gout tested

A

joint aspiration and synovial fluid analysis (get microbiology and polorasing light microscopy)

Gout : urate crystals, needle/long shape and no birefringence

Pseudogout: calcium pyrophosphate dihydrate, rhomboid/brick shape, positive birefringence

135
Q

How is genetic vs environmental contributions estimated

A

look at concordance rate
if concordance of monozygotic twins is more than dizygotic then likely genetic

136
Q

What environmental and genetic factors can contribute to rhematoid arthritis

A

HLA-DR gene especially if interacts with smoking
microbioe: porphyromas gingivalis, poor oral health

137
Q

What joints are most likely to be affected in rheumatoid arthritis

A

MCP, PIP, MTP

138
Q

How is a patient with rheumatoid arthritis likely to present

A

fever, weight loss, subcutaneous nodules (fibroid necrosis surrounded by histiocytes and connective tissue)

uncommon: lung disease, episcleritis (inflam of eye), vasculitis (digital ischameia) , neuropathies, fettys sundrome (splenomegaly, leukopenia, rheumatoid arthritis), amyloidosis

139
Q

What is the term used when the synovium becomes a proliferated mass of tissue, and how does it occur

A

Pannus: due to neovascularisation, lymphangiogenesis, inflam cells: B and T, plasma, mast and macrophages, more pro inflammatory mediators

140
Q

what pro inflammatory mediators are most common in rheumatoid arthritis

A

TNF-alpha and IL-1
TNF-alpha especially
chondrocyte destruction (Metallaproteinase made and cartilage degradation)
osteoblast activation (bone reabsorption and bony erosion)
synoviocytes to cause joint inflammation - joint pain and swelling

141
Q

compare and contrast Hb, WCC, Platelet count , ESR and CRP in rheumatoid arthritis, osteoarthritis and septic arthritis

A

Rheumatoid: low Hb, normal WCC, high platelet, high ESR, high CRP

Osteoarthritis: everything normal

Septic arthritis: high WCC, high platelets, high ESR, high CRP

142
Q

Describe how the two autoantibodies in rheumatoid arthritis work

A

rheumatoid factor: recognise Fc portion of IgG by making IgM antibodies (IgM anti-IgG antibody)
IgM is pentameric and looks like a snowflake , recognises Y shaped IgG

anti-citrullinated protein antibodies (anti-CCP antibody): peptidyl argenine deiminases turn argenine into citrulline

143
Q

How is ACPA and smoking related

A

Smoking causes citrullination of proteins in the lung epithelium
ACPA attacks citrlinated proteins

144
Q

How will rheumatoid arthritis appear on different scans

A

X ray : soft tissue swelling, peri-articular osteopenia, bone erosions
US: synovial hypertrophy, increased blood flow-doppler signal, bony wrosions
MRI: may/may not be used

145
Q

How is rheumatoid arthritis treated and managed

A

Managed: prevent joint damage, early recognition, aggressive treatment to suppress inflammatory

1st line is : glucocorticoids (steroid) or short oral steroid then start combination DMARDs (disease-modifying anti-rheumatic drugs) are immunosuppresive : methotrexate with hydroxychloroquine or sulfasalazine

2nd line: biologicals: JAK inhibitors : tofacitinib and baricitinib

146
Q

What is one negative effect of glucocorticoids

A

Cushings syndrome

147
Q

How do glucocorticoids work

A

bind to glucocorticoid receptor in cytoplasm, when it binds it translocates into the nucleus and affects transcription

148
Q

How does methotrexate work

A

Inhibits dihydrofolate reductase (folate antagonist) is immuosuppressive and antiinflammatory

149
Q

What are the side effects of methotrexate

A

nausea, hair loss, low WCC, abnormal liver function, infection risk

150
Q

What are the for biological therapy types

A

1- Inhibit TNF-alpha :antibodies like infliximab or fusion proteins
2- B cell depletion- rituximab against B cell antigen CD20
3- Modulation of T-cell co-stimulation: abatacept is a fusion protein works on CTLA-4-Ig Fc portion
4- Inhibit IL-6: Tocilizumab and Sarilumab are antibodies against IL-6 receptor

151
Q

A patient presents with asymmetrical interphalangeal erosions and a scaly red plaque what is it

A

Psoriatic arthritis

152
Q

What is psoriatic arthritis

A

immune mediated, scaly red plaques on extensor surfaces like elbows and knees
pathogenic pathway is IL17, Il23
get asymmetrical arthritis affecting IPJ

153
Q

What is reactive arthritis

A

sterile inflammation in joints after being infected elsewhere in the body.
usually urogenital: chlamydia OR gastrointestinal cause like salmonella, shigella, campylobacter

get: enthesitis (tendon inflammation), skin inflammation, eye inflammation
may indicate HIV or Hep C infections

usually have HLA-B27 involvement and an infection to trigger

154
Q

What is the difference between reactive arthritis and septic arthritis

A

Septic arthritis: positive synovial fluid culture, needs AB’s and joint lavage
Reactive arthritis: joint is sterile so no AB’s or lavage

155
Q

What are the signs of ankylosing spondylitis

A

manifestation of psoriatic arthritis and IBd together
anterior uveitis, dactylitis (sausage finger)

156
Q

Differentiate the different types of arthritis by whether they are symmetrical or monoarthritis, what joints are likely affected, acute/chronic

A

Osteoarthritis: chronic and asymmetrical - weight bearing joints : DIP and PIP (heberdens and bouchards nodes)
Septic arthritis: acute, monoarthritis - usually knee
Crystals (gout and pseudogout): acute, monoarthritis - knee and big toe
Rheumatoid arthritis: chronic, polyarthritis, symmetrical, MCP and PIP
Seronegative arthritis: chronic, asymmetrical
Autoimmune ones like lupus: chronic

157
Q

Prolonged morning stiffness indicates what type of arthritis

A

Inflammatory

158
Q

What is the name of the phenomenon seen when fingers change to white, blue then red

A

Raynauds phenomenon

159
Q

What findings on x ray are associated with pseudogout

A

Chondrocalcinosis : white opacities within the joint space (crystals)

BRS YEAR2 (11 decks)

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