Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 > Week 11 MSK > Flashcards

Week 11 MSK Flashcards

1
Q

Types of joint disorders

A

Infection (septic arthritis)

Inflammatory (reactive arthritis)

Crystal arthropathy (Gout, pseudo gout)

Degenerative (OA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Septic arthritis

A
  • Bacterial infection of joint
  • Synovium inflamed with fibrin exudation and neutrophil polymorphs
  • Medical emergency

Clinical features: Sudden onset, fever, swollen, hot joint, loss of function, mostly hips or knees, usually one joint

Causes: Staph. aureus, neisseria gonorrhoea, haemophilus influenzae (children)

  • If have loss of cartilage can cause secondary OA
  • Pott’s disease: TB from spine

Risk factors: steroids, biologics, RA, joint prosthesis, IV drug abuse, sexually active

Investigations:

Bloods - FBC, CRP

Blood culture

Joint aspirate - for microbiology culture

Treatment

IV antibiotics

Drainage

Types of SA

Lyme disease (due to borrelia burgdoferi)

Brucellosis

Sphyilitc arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Crystal arthropathy - Gout

A

Includes Gout and pseudogout

Gout:

  • Inflammatroy arthritis due to excess levels of uric acid
  • Urate cystals deposited in joint (tophi)

Acute gout: deposition stimualtes acute inflammatory reaction

Chronic gout: tophi formation

Clinical features: Acute onset (<24 hours), swelling, erythema, tenderness of involved joint, big toe

Investigations:

  • Synovium fluid aspirate: negatively birefringent

needle shaped crystals on polarised microscope

  • Urate levels

X-ray

Primary - hyperuricaemia due to genetic predisposition e.g. Lesch Nyhan syndrome

Secondary - high uric acid due to myeloproliferative disorder, thiazides, chronic renal disease

Risk factors: obesity, age, alcohol, diabetes, HTN, diuretics

Management

Short term:

NSAIDs

Cholchicine (inhibits IL-1, chemotactic factor. Statins should be stopped)

Corticosteroids

Long-term:

Lifestyle factors (though not enough)

Urate lowering therapy:

Allopurinol (xanthine oxidase inhibitor - reduces production of uric acid)

Risks: SJS/TEN, hepatitis, vasculitis

Rasburicase (recombiant uric oxidase - metabolises urc acid in blood)

  • effective but risk of anaphylaxis with repeated doses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Crystal arthropathy - pseudo gout

A

Deposition of calcium pyrophosphate

Synvoium (pseudo gout)

Cartilage (chondrocalcinosis)

Clinical features: Acute onset (<24 hours), swelling, erythema of joint

Acute (acute inflammatory arthritis) or Chronic (mimics OA or RA)

Primary or secondary (hyperparathyroidism and haemochromatosis)

Investigations

Aspiration: positively birefringent rhomboid shaped crystals

X-ray

Serum calcium and parathyroid hormone

Management

NSAIDs

Colchicine

Intra-articular joint corticosteroids

Joint aspiration (reduce pain and swelling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Reactive arthritis

A

Defintion: Sterile, inflammatory arthritis that occurs after infections, usually GI or genitourinary

  • Salmonella, Shigella, Chlamydia trachomatis

Clinical features: Onset days/weeks post infection, asymmetrical lower limb arthritis

Assoc. symptoms:

Classic triad (not needed for diagnosis): conjunctivitis, non-gonococcal urethritis, post infectious arthritis (can’t see, pee or climb a tree)

Risk factors:

Male, HLA-B27, previous GI or chlamydial infection

Signs:

  • Dactylitis (swollen digits)
  • Enthesitis (inflammation of entheses - where tendons insert into bone)
  • Keratoderma blenorrhagica (“blenno: mucousy, “rrhagia” discharge) - yellow, waxy lesion usually on palms, soles

Complications

  • Aortic regurgitation, aortitis

Management

- Usually self-limiiting (can last up to 6 mnths)

  • NSAIDs
  • Intra-articular steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Enteropathic (IBD) arthritis

A

Form of reactive synovitis that’s assoc with IBD

Asymmetrical lower limb arthritis. enthesitis

Treatment

  • Treat bowel disease
  • NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Definition, Presentation, Risk factors, Investigations, Treatment of OA vs RA

A

Definition: Degnerative joint disease characterised by loss of articular cartilage

Commonest form of arthritis

Risk factors: female, age (more common in elderly), obesity

Primary: Wear and tear

Secondary: Trauma, avascular necrosis, other arthropathies e.g. RA, Paget’s disease, haemachromotosis

Pathophysiology:

Loss of balance between cartilage production and breakdown causing loss of articular cartilage and:

  • irregular cartilage surface
  • articulation of bone on bone causing thickening of subarticular bone (eburnation)
  • ostephytes forms - due to bone trying to repair itself producing cartilagenous outgrowths which calcifiy
  • loss of joint space leading to deformity
  • immbolity of joint

Macroscopically: loss of articular cartilage with eburantion of surface, subarticular cysts, osoteophytes, sclerosis (thickening of subchondral bone)

Clinical presentation: characterised by joint pain, stiffness (morning <30 mins) and loss of function, usually hip or knee

Clinical examination: pain (worse on movement, better with rest) muscle wasting, limited ROM, joint deformity, antalgic gait

Investigations

X-Ray: Joint space narrowing, osteophytes, subchondral sclerosis, bony cysts

(Subarticular cysts due to raised intraarticular cysts)

Synvoium becomes hyperplastic, mild inflammation, bony detritus (broken down material)

Bloods:

FBC (normal), CRP/ESR (normal) , RF/Anti-CCP (negative), Ca2+, phosphate, Alk phos (normal)

Secondary OA due to gout - high levels uric acid, or due to Paget’s - high Alk Phos

Treatment:

Analgesics

Physiotherapy

Reducing load - weight loss, walking stick

Surgical:

  • arthrodesis (fusion of bones. Considered in young pts where joint replacement would be expected to fail as demands are higher)
  • joint replacement (weigh up benefits of pain relief and improved function, against risks of surgery)
  • excision arthroplasty (affected jointis removed and space is filled with fibrous tissue)

RA

Definition:

Multisystem autoimmune disease characterised by chronic, symmetrical polyarthritis

Risk factors:

HLA-DR4, smoking, infections (TB, EBV), hormones

Affects 1% population, usually middle aged, female 3:1

Pathophysiology:

  • IgM and IgA directed against Fc portion of IgG - forms large immune complexes. Synovitis occurs, immune cells (macrophages, T cells, plasma cells) invade normally acellular synovium. Immune cells secrete cytokines which activate enzymes in synovium.

Pannus (tissue made of fibrous vascular connective tissue) is formed which destroys cartilage and bone.

Clinical features:

Synovitis of any joint, symmetrical, PIP joints of fingers, wrists, elbows, knees, morning stiffness (>30mins) - better as day goes on

  • Pain, erythema, swelling, fatigue, weight loss

Late signs:

Boutonniere deformity joints nearest knucle (PIP) flexion (bent towards palm) and DIP hyperextension (bent away))

Swan neck deformity

Extra-articular features:

  • lungs: pleural effiusions (due to inflammation and rubbing)
  • cardiac: pericarditis, vasculitis
  • skin: rhematoid nodule
  • Felty’s syndrome (triad of RA, splenomegaly, neutropenia)
  • higher risk of malignancy (as chronic inflammation leads to higher cell turnover)

Invstigations:

Bloods - FBC (low HB)

Blood film:

  • normocytic normochromic anaemia of chronic disease
  • pts who take NSAIDs can have IDA from upper GI bleeding
  • pts with Felty’s syndrome (RA+spenomegaly) can have haemolytic anaemia

ESR/CRP (high)

LFT (elevated Alk phos. gamma GT during acute flare ups)

ANA (exclude SLE, may be postive in 20% RA pts)

RF (IgM against Fc portion of IgG) - 70% sensitive

Anti-CCP (anti-cyclic citrullinated peptide) - more sen and specific

Complement (normal. Exclude SLE, vasculitis)

Immunuglobulins: increased IgA and IgG but normal IgM

Xray (LESS): loss of joint space, erosions, soft tissue swelling, soft bone (osteopenia)

US

MRI: bone marrow oedema

DAS-28 (disease activity score) in 28 joints

Treatments:

NSAIDs: symptomatic

1nd line: DMARDS - sulfasalazine, methotrexate

Corticosteroids

Biologics: anti-TNF (infliximab), Anti CD20 (B cell) (rituximab)), Anti-IL6 (tociluzumab), anti CTLA4 ((T cell) (Abatacept)

Physio: maintains movement, prevents muscle atrophy

OT: adaption to pt’s lifestyle and housing improves long-term outlook

Podiatry: shoe wear alteration, good feet hygeiene as feet almost always involved

Surgical:

tendon repair

joint replacement - esp for knee

joint fusion - ankles and wrist (last resort)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Tendinopathy

A

General term that describes tendon degeneration characterised by pain, swelling, impaired performance

Tendinitis (inflammation of tendon)

Tendinosis (degenerative)

Tenosynovitis (inflammation of tendon sheath)

Tendinopathy can also be:

Insertional (damage where tendon attaches to bone)

Non-insertional (damage to damage itself)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is a tendon, what does it do?

A
  • Attaches muscle to bone
  • Transmits force from muscle to to achieve movement
  • Made up mostly of parallel collagen fibres with tenocytes. Surrounded by paratenon (e.g. achilles tendon) or tendon sheath (e.g. fingers)
  • Mostly avascular, receives nutrition from tendon sheath/paratenon. So slow to heal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pathologyof tedinopathy

A

Repetitive loading/over use leads to chronic tendon injury: - Degeneration and disorganisation of collagen fibres

  • Increased vasuclarity around tendon (as body tried to heal it)
  • Increased cellularity
  • Little inflammation
  • Inflammatory mediators released - NO, prostoglandins, IL-1 which causes pain, degeneration by release of matrix mellanoproteinases
  • Failed healing mechanisms in repsonse to micro damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Risk factors of tendinopathy

A

Age, chronic disease, diabetes, RA, repetitive exercise, quinolones (ciprofloxacin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Common tendinopathies

A

Achilles tedinopathy

Tennis elbow (lateral epicondylitis)

Golfers elbow (medial epicondylitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical features of tedinopathy

A

Pain

Swelling

Thickening of tendon

Tenderness

Provocative tests - pain elciited, when ask pt to contract muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Diagnosis of tedinopathy

A

Ultrasound (can see shape of tendon, neovascularisation)

MRI (tedinopathy best seen on T1 weighted MRI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Management of tedinopathy

A

Non-operative

NSAIDs

Physiotherapy - eccentric loading (contract of musculotedinous junction whilst it elongates)

GTN patches - vasodilator (increases local perfusion)

PRP (plalelet rich plasma) injections

Prolotherapy - inject irritant (dextrose) to stimulate a bit of damage, which stimulateshealing

Extracoporeal shockwave therapy - breaks down calcifcation, and causes little areas of trauma to stimualate healing

Steroid inejections

Operative treatment

Debridement - excise diseased tissue. Can debride 50% without loss of function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Compartment syndrome: definition

A

Increased interstitial pressure in a closed fascial compartment leading to decreased perfusion of tissue

  • Leg, forearm, thigh
  • Orthopeadic emergency (loss of function/life)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of compartment syndrome

A

Increased interstitial pressure:

  • trauam: bleeding
  • muscle oedema
  • administration drugs/fluids

Increased external compression:

  • Impaired conciousness (loss of protective reflexes e..g moving aorund)
  • Positioning in theatre - lithotomy
  • Bandaging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pathophysiology of compartment syndrome

A
  • Pressure in compartment beomes greater than the pressure in capillaries
  • Leads to decreased blood flow, muscles become ischaemic and develop oedema (through increased endothelial permeability) - leads pressure
  • Necrosis starts after 4 hours of muscles being ischaemic, and myoglobin released (toxic esp. to kindeys)
  • Ischaemic nerves become neuropraxic (blockage of nerve conduction )
  • Loss of function

Increased pressure leads to reduced blood flow due to Local Blood Flow (LBF)=(Pa-Pv)/R

(difference between between arterial and venous pressure, divided by peripheral resistance)

leading to reduced tissue perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical significance of timely management of compartment syndrome

A

1 hr - muscle viable, nerve conduction normal

4 hrs - muscle ischaemia (reversible) neuropraxis in nerves (reversible)

8hrs - muscle necrosis, nerve axonotmesis (damage to axon, irreversible)

End-stage

  • Stiff, fibrotic muscle compartments
  • Nerve damage
  • Clawing of limbs
  • Loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical features of compartment syndrome

A

Pain - out of proportion to injury

  • Pallor
  • Parathesia
  • Pulselessness
  • Paralysis
  • Pershingly cold
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Diagnosis compartment syndrome

A

Mostly clinical diagnosis

Site: Leg, forearm, thigh

  • Swelling, shiny skin, autonomic repsonses (tachycardia)

If patient has impaired consiousness:

  • compartment pressure measurement: Compare compartment pressure (CP) to diastolic BP: if <30mmHg than it is diagnostic, or if CP alone is >30mmHg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Management compartment syndrome

A

Open restricting bandages

Peri-operative:

  • fluids, monitor electrolytes, correct acidosis, renal function

Surgical release - decompression across all compartments, excise dead muscle, wound closure/skin graft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the normal function and structure of bone

A

Function: Movement, protection, support, stores Ca and phosphate

Structure:

Cortical bone (compact/tubular):

  • Outer layer
  • Slow turnover rate/metabolic activity
  • High Young’s modulus (resistane to tension and bending)

Cancellous bone (spongy/trabeculae):

  • Fills centre of bone
  • Higher turnover rate, undergoes remodelling
  • Lower Young’s Modulus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Anatomy of bone

A

Diaphysis - main shaft

Epiphysis - ends of the bone

Metaphysis - between diaphysis and epiphysis

Physis (growth plate): feature of children’s bones

  • repsonsible for skeletal growth, allows remodelling after fracture, blood supply to physis damaged then will lead to stopping growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Understand the process of indirect and direct bone healing

A

Indirect bone healing (secondary, via callus formation) - formation of bone via callus formation to restore skeletal continuity

  • IRR (inflammation, repair and remodelling)

1. Fracture haematoma and inflammation (6-8 hours after)

  • Blood (from broken blood vessel) forms clot
  • Swelling and inflammation occur.

2. Fibrocartilage (soft) callus (lasts 3 weeks)

  • New capillaries allow haematoma to become granulation tissue (procallus)
  • Fibrobalsts form collagen, which join ends together
  • Chrondroblasts form fibrocartilage

3. Bony (hard) callus (lasts 3 months)

- Osteoblasts form woven bone

4. Bone remodelling

- Osteoclasts remodel woven bone into coritcal and spongy bone

  • No fracture line on X-ray

Direct bone healing (primary)

  • Artifical surgical situation
  • Direct formation of bone, without callus formation to restore skeletal continuity
  • No callus formed
  • Lead by formation of cutting cones (osteoclasts at front (resorption) followed by osteoblasts to lay down new bone
  • Leads to formation of osteons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Bone blood supply

A
  • Bone must have blood supply to heal
  • Endosteal (nutrient artery) supplies inner 2/3rds
  • Periosteal supplies outer 1/3rd
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Understand factors which compromise blood supply to bone

A

Surgical factors (iatrogenic)

Anatomical factors

  • some fractures are prone to necrosis due to problems in blood supply
    e. g. proximal pole of scaphoid, talar neck, intracapsular hip, surgical neck of humerus fractures

Patient factors

- Age, diabetes, hypothyroidism, malnutrition

Medication

  • NSAIDs (esp. those that inhibit COX2)
  • Steroids
  • Bisphosphonates (inhibits osteoclast activity. Delays fracture healing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Composition of bone

A

ECM and cells (osteoprogenitor cells, osteocytes, osteoblasts, osteoclasts)

ECM is organic (40%) and non-organic salts (60%

Organic: collagen I

Non-organic salts: hydroxyapatite crystals (Ca and phosphate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Know the types of tumours which affect the bones and their demographics

A

Primary bone tumours: rare

  • Myeloma: commonest primary bone tumour

Secondary bone tumours: common

  • Metastatic carcinoma: lung, prostate, thyroid (follicular) kidney, breast (LP Thomas Knows Best)
  • Childhood: neuroblastoma, rhabdomyosarcoma

Long bones, vertebrae usually affected as have good blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

The clinical presentation of bone tumours and their management

A

Effects of metastases:

  • Often aysmptomatic
  • Bone pain
  • Bone destruction
  • Pathological fractures

Spinal metastases: vertebral collpase, spinal cord compression, nerve root compression

  • hypercalcaemia

Management:

PET-CT: Anatomical and metabolic data

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Differentials of acute hot joint

A
  • Septic arthritis
  • Crystal arthropathy
  • Trauma
  • Early presentation of polyarthropathy e.g. RA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Histology of bone

A

(A) Compact bone organised into osteons (Haverisan systems) - concentric lamellae (rings of calcified matrix where osteocytes are embedded in)

(B) Spongy bone: Arranged in trabeculae, with spaces between filled with bone marrow. White spaces is meduallary cavity (haemapoeitc marrow)

(D) Immature osteoprogenitor cells forms osteoblasts (mononuclear) which form osteoid

Osteoclasts (multi nucleated giant cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

2 different types of metastasis

A

Lytic (bone is destroyed) or sclerotic

Lytic:

More common e.g. in lung cancer

Tumour activates cyotkines which activate osteoclasts

Inhibited by bisphosphonates

Sclerotic:

New bone is formed due to tumour cells

e.g. prostate, breast

looks whiter (sclerotic) on Xray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Solitary bone metastases

A

Renal and thyroid carcinomas

Often long survival as can be surgically removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Myeloma

A

Commonest malignant primary bone tumour

Monoclonal proliferation of plasma cells

Plasmacytoma (single tumour) or multiple myeloma

Clnical effects:

CRAB

hyperCalcaemia

Renal infsufficiency

Anaemia (Pancytopenia ((as occurs in bone marrow) - Anaemia, leucopenia (decreased WBCs) and thrombocytopenia (decreased platelets)

Bone Lytic lesions

Diagnosis:

Immunoglobulin excess

  • Increased CRP
  • Urine/Serum electrophoresis - monoclonal band
  • Immunoglobulin light chain (normally have both kappa and lambda light chains produced. In myeloma, only one type of light chain is produced)

FBC: normocytic normochromic anaemia

Ca2+

Bone marrow aspirate and biopsy: plasma cell infiltrate >10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Histology myeloma

A

Sheets of malignant plasma cells (nucleus that looks like clockface, clear cytoplasm (Hoff), variation in nuclear size)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Primary bone tumours

A

Benign

  • Osteoid osteoma
  • Enchrondroma
  • Osteocartilagenous exostosis

Malignant

- Osteosarcoma

  • Chrondrosarcoma
  • Ewing’s tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Osteoid osteoma

A

Benign tumour of osteoblasts surrounded by rim of reactive bone

Common in adolescnece

Any bone esp. diaphysis of long bones

If tumours near joint (juxta-articular tumours) - sympathetic synovitis

Presentation: Pain worse at night, relieved by aspirin

Radiology: nidus (network of osteoblasts, woven bone) surrounded by sclerotic bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Osteosarcoma

A

Malignant proliferation of osteoblasts

Metaphysis of long bone

  • Teenagers, or less commonly elderly

Presentation: pain, swelling, inability to move limb

Natural history:

Aggressive

Commonly metastasise to lungs

Risk factors: Paget’s disease of bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Paget’s disease

A

Type of osteosarcoma

  • Excessive bone turnover
  • Increased osteoclasts, body tried to compensate by increasing osteoblast activity, so weak bone formed
  • vertebrae, pelvis, skull
  • usually lytic
  • common in elderly

Clinical features: bone pain, deformity, bowing of legs, pathological fractures, high cardiac output failure (as lots of blood goes to the bones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Enchondroma

A

Benign tumour of cartilage, usually arises in medulla

Mostly in hands and feet, long bones

Usually asymptomatic in long bones

Hands - swelling, pathological fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Osteocartilagenous exostosis (osteochondroma)

A

Most common benign tumour of bone

Benign outgrowth of cartilage on surface of bone

Common in adolescence

Arises from lateral projection of from growth plate

Complications:

  • In Multiple diaphyseal aclasis (AD form) - multiple tumours, can form into malignant chondrosarcoma in cartilage cap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Chondrosarcoma

A

De novo (primary) or from endochondroma or exostosis (secondary)

Malignant cartilage forming tumour, usually arises in medulla

Mostly middle aged/elderly

Shoulder girdle, ribs, pelvis

Better prognosis than osteosarcoma

Management:

Surgery, not chemo/radiotherapy

44
Q

Ewings sarcoma

A

Malignant proliferation of poorly differentiated cells derived from neuroectoderm (small, round, blue cell tumour)

Children

Long bones (Diaphysis), pelvis

Early metastases to lungs, bone marrow

Repsonds well to chemo/radio

Investigations:

Stain: CD99

Molecular genetics/karyotyping: chromosomal translocation 11:22

Management:

Chemotherapy/radiotherapy

45
Q

Describe the vasculitides by vessel size and immune-pathology

A

Primary vasculitidies - group of autoimmune disorders characterised by inflammation of blood vessels

  • Normally blood vessels of skin, nerves, kidneys, lungs

Classified by vessel size:

Large vessel vasculitis e.g. Temporal Giant cell arteritis, Takayasu arteritis

Medium vessel vasculitis e.g. Kawasaki disease, polyarteritis nodosa

ANCA-associated small vessel vasculitis e.g.

Granulomatosis with polyangiitis (GPA), Microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (Churg Strauss)

Immune complex small vessel vasculitis e.g. IgA vasculitis (Henoch-Schonlein pupura)

46
Q

Giant cell artertitis

A

Systemic vasculitis that affects aorta and major branches

>50 years old.

More common in females, caucasians

Clinical presentation: subacute temporal headache, visual symptoms (due to ischaemia of optic nerves), jaw claudication (pain upon chewing), polymyalgia rheumatica (pain and stiffness of msucles esp. shoudlers and hip)

Clinical examination findings:

Thickening and loss of pulse of temporal artery

Complications:

Blindness, vascular aneuryms, CVA

Investigations:

ESR (increased)

Temporal artery biopsy (TAB):

  • gold standard for diagnosis
  • Infiltration of mononuclear cells (macropahges, lymphocytes) into vessel wall. Granulotamous inflammation. Multinucleated giant cells seen but absence doesn’t exlcude a diagnosis

Affects arteries segmentally - skip lesions, so requires long sample of blood vessel

Temporal artery ultrasound

MRI

PET-CT

Management:

Start corticosteroids if clinical suspiscion, dont wait for investigations (due to risk of visual loss)

Prednisolone for 1 month

Methylprednisolone (if visual symptoms)

Aspirin

Corticosteroid sparing therapy in pts with relapse:

  • Methotrexate
  • Tocilizumab (IL-6 inhibitor)
47
Q

Cutaenous vasculitis

A

Small vessel vasculitis

Pathology: leukocytoclastic (damage due to infiltrating neutrophils) vasculitis

Differentials:

Drugs, infection (HCV, HBV), secondary RA, malignancy,

  • Henoch Schonlein pupura is a subtype of cutaneous vasculitis
48
Q

Henoch Schonlein pupura (IgA vasculitis)

A

Small vessel vasculitis due to IgA complex deposition

  • Most common vasculitis in children, most under 10
  • Triggered by streptococcal sore throat
  • Usually self-limiting

Presentation - characterised by 4 features: pupuric (non-blanching), abdominal pain, arthritis, glomerulonephritis

Complications: GI bleeding, IgA nephropathy

Investigations

  1. Exclude secondary causes - history, examination, immunology (RF, ANA, ANCA), virology (Hep B/C)
  2. Urinalysis (assess renal involvement)

Treatment:

Self limiting

  • Analgesics
  • Corticosteroids complications e.g. abdominal pain, testicular torsion
49
Q

Granulomatosis with polyangiitis (Wegener’s granulomatosis)

A

ANCA-associated small vessel vasculitis

Characterised by granulotamous necrotising inflammatory lesions involving upper (nasopharyngeal) and lower respiratory tract, kidneys

Presentation: Classical triad of upper (sinusitis otitis media )and lower respiratory tract (haemoptysis, lung nodules) and pauci-immune glomerulonephritis (haematuria)

  • Constitutional symptoms: fever, weight loss, fatigue

Other symptoms:

Conjuctivitus, ulcers in oral mucosa, pupura

Investigations

ANCA (anti-neutrophil cytoplasmic antibodies) : tested by 2 methods -

  • indirect immunofluorescence: p or cANCA staining pattern (cytoplasmic or peri-nuclear anit-neutrophil cytoplasmic anitbody)
  • ELISA: proteinase 3 (PR3) or myeloperoxidase antigens (MPO)

cANCA + PR3: Granulomatosis with polyangiitis

pANCA + MPO: MPA (microscopic polyangiitis) or Churg Strauss syndrome

Postive ANCA by indirect immunofluorescence but -ve PR3/MPO ELISA - no significance

Management

  • Prednisolone AND

Severe disease: rituximab (anti- B cell biologic)

Moderate disease: Methotrexate

Remission maitenance: methotrexate, azothioprine

50
Q

Clinical presentation of rheumatoid arthritis, its epidemiology and demographics

A

Chronic inflammatory condition, affects 1% population

  • Usually 50s, female 3:1

Risk factors:

HLA-DR4, smoking, infection (TB), hormonal

Pathophysiology:

  • Synovitis occurs, immune cells invade normally acellular synovium, forming pannus

Pannus (hyperplastic, invasive, granulation tissue) formation leads to breakdown of cartilage, erosions, reduced function

Clinical features:

Synovitis of any joint, symmetrical, usually hands and feet

  • Pain, erythema, swelling, fatigue, weight loss

Late signs:

Boutonniere deformity (joints nearest knucle (PIP) bent towards palm whilst DIP is bent back)

Swan neck deformity

Extra-articular features: lungs e.g. pleural effiusions (due to inflammation and rubbing), cardiac e.g. pericarditis, vasculitis, higher risk of malignancy (as chronic inflammation leads to higher cell turnover)

Invstigations:

FBC, U&Es, LFT, ESR/CRP

  • RF (autoantibody against Fc portion of IgG) - 60% sens, 80% spec
  • anti-CCP (anti-cyclic citrullinated peptide) - 60% sens, 90% spec

Xray: soft tissue swelling, joint space narrowing, erosions

US

MRI: bone marrow oedema

DAS-28 (disease activity score) in 28 joints

51
Q

Differential diagnosis of patients presenting with new inflammatory arthritis

A

OA

SLE

Psoriatic arthritis

Reactive arthritis

52
Q

jUnderstand the relevant pharmacological management (DMARDS, steroids, NSAIDS and biologic drugs) monitoring requirements, screening and some side effects

Appreciate the range of MOA of the biologic drugs, special precautions, vaccination issues, malignancy and infection risks

A

1st line: DMARDS (and NSAIDs, corticosteroid)

Methotrexate (dihydrofolate reducatase inhibitor)

Side effects: GI upset, liver toxicity, BM supression

Contra-indicated: pregnancy, infection, antibiotics

  • Sulfasalazine
  • Anti-inflammtory effects

Side effects: GI upset, rash, bone marrow supression. Can be used in pregnancy.

Biologics

Anti-TNF: infliximab, entaracept,certolizumab (can be used in pregnancy)

  • TB, infection risk, worsen MS symptoms

Anti CD20: rituximab

  • Hypogammaglobulinaemia

Anti-IL6: tocilizumab

  • Infections, high lipids

CTL4-Ig (comprises CTL4 linked with IgG): Abatacept (stops second signal needed for T cell activation)

JAK inhibitors: tofacitinib

Infections:

Increaseed risk e.g. TB, VZV

Vaccines:

  • pts should be vaccinted against influenza and pneumococcal annually

Vaccines should be given before IL-6, CTLA4-Ig administered

Live vaccines avoided

53
Q

X ray changes OA vs RA

A

OA:

(LOSS)

Loss of joint space

Osteophytes

Subchondral sclerosis

Subchondral cysts

RA:

(LESS)

Loss of joint space

Erosions

Soft tissue swelling

Soft bone (osteopenia)

54
Q

Describe the presentation, pathology and management of OA

A

Presentation: pain, stiffness (esp. in morning), swelling, crepitus, deformity, nearby joint problems (e.g. hip OA can present with knee pain)

Pathology:

  • Preotelytic breakdwon of cartilage due to increased production of enzymes e.g. matrix mellanoproteinases
  • Proteoglycan and collagen fragments released into synovial fluid as disease progresses.
  • Erosion to cartilage roughens surface of bone, and fibrillation narrows joint space
  • Increased production of synovial mellanoproteinases, cytokines which diffuse back into cartilage to destroy soft tissue

Clinical Examination:

  • General examination (include antalgic gait)

Systemic examination

Specific joint examintion (look/feel/move/special tests inc. leg length measurement)

Hip - pain on flexion and internal rotation, wasting of buttock muscles, limited ROM

55
Q

Appreciate the clinical indications for joint replacement

A

Kellgren Lawrenece Stages of OA on radiographs

Stage 1 (Minor): If pt not predisposed to OA, no special treatment. Mainly weight loss, if obese will slow progression

Stage 2 (mild) - physiotherapy

Stage 3 (moderate) - NSAIDs, intra-articular steroid injections

Stage 4 (severe) - surgery: replacement (most common), realignment, excision, fusion

56
Q

Understand the outcomes following joint replacement

A

Complications (total knee and hip replacement) - DVT/PE, infection, failure of procedure, revision

Specific to hip - dislocation, fracture, leg length discrepancy

Specific to knee - fracture, ligament or tendon damage

57
Q

Presentation, diagnosis, investigation and management of SLE

A

Presentation:

Chronic multi-system autoimmune disorder, charcterised by deposition of antinuclear antibodies (autoanitbodies agianst nucleus) in tissues (skin, kidneys) leading to systemic inflammation.

  • Mostly affects women in repdroductive years.

Most frequenlty affects skin, joints, kidneys.

Diagnosis:

ACR (American Collge of Rheumatology) critera: at least 4 criteria

Revised by SLICC requires: biopsy proven lupus nephritis with antinuclear antibodies or 4 classification with i clinical and 1 immunological.

Presentation:

Triad of fever, joint pain, and rash

Constiotional symtpms: fatigue, weight loss

Cutanous symptoms: butterfly shaped malar rash over cheeks and bridge of nose, discoid lupus (plaque-like rash that develops in sun exposed areas)

MSK symptoms: arthalgia (joint pain), arthritis (inflammatory), Jaccoud’s arthropathy (non-erosive, reversible conditions which occurs after bouts of arthritis)

Renal symptoms: Nephritic syndrome, Nephrotic syndrome

Resp: pleurisy, pleural effusions

Cardio: pericarditis, myocarditis, coronary heart disease

Avascular necrosis, fibromylagia, OP

Neuro: headache, anxiety

Gastro: dysphagia

Haemoatological: anaemia of chronic disease

Investigations:

Serum ANA (98% sesitive, but not specific)

ENA (extractable nuclear antibodies):

  • Anti-dsDNA (confirms diagnosis SLE)
  • Anti-Smith: (confirms diagnosis SLE)
  • Anti-Ro and anti-LA: SLE, Sjogrens

Serum Complement (low due to activation of complement system)

Management:

  • Hydroxychloroquine (1st line)
  • Steroids
  • Belimumab

Mild disease: topical therapies, sunblock for cuteanous symptoms

NSAIDs, IM steroids (MSK symptoms)

Moderate: treatment as mild+

  • oral prednisolone, methotrexate, azothioprine, belumimab

Severe: treatment as mod+

  • high dose steroid, cyclophosphamide (immuno suppressive), IV Ig (IV immunoglobulin), plasmapheresis

Adjunt therapy:

  • Ca2+ blockers for Raynoads
  • fatigue management groups
58
Q

ENA (extractable nuclear antigens)

A
  • Autoantibodies to these antibodies assoc with connective tissue disorders

Anti-dsDNA - SLE

Anti-smith - SLE

Anti-Ro/LA - SLE, Sjogrens

RNP - mixed CTD

Centromere - limited SScl (systemic sclerosis)

Scl-70 - diffuse SScl

Histone - drug induced lupus

59
Q

Presentation, diagnosis, investigation and management of the systemic sclerosis (SScl) (scleroderma)

A

Multisystem autoimmune disease where fibroblasts are activated leads to deposition of collagen in tissues inc. blood vessels

  • Usually middle aged females

Presentation: Raynaud’s phenomenon (most common), oedema of hands, thickened skin, ulcers on fingers

GI symptoms: dysphagia, malabsorption

Resp symptoms: pulmonary hypertension, respiratory failure

Investigations:

Serum ANA (90%)

Anti-DNA topoisomerase antibody

Centromere: limited SScl (systemic sclerosis)

Scl-70: diffuse SScl

FBC (microcytic anaemia, GI bleed), ESR/CRP, ECG (cardiac disease), CXR (lung disease)

Management:

Raynaud’s: Sidenafil (enothelin 1 receptor inhibitor) adjunct Ca+ channel blocker

Skin: Topical emoillient, corticosteroids, methotrexate

60
Q

Presentation, diagnosis, investigation and management of myositis

A

Dermatomyositis: Chronic inflamation of skin and skeletal muscle with rash

In elderly, assoc. with malignancy e.g. gastric carcinoma

Clinical presentation

  • painful, proximal muscle weakness,
  • inflammation in muscle (biospy or MRI)
  • elevation muscle enzymes
  • characteristic EMG pattern
  • Skin changes: rash of upper eyelids (heliotrope rash), malar rash, red papules on elbows

Investigations

Serum creatine kinase, myglobin (increased)

Serum ANA (90%)

Anti Jo-1 antibodies

ESR/CRP

EMG (muscle dysfunction)

Muscle biopsy (muscle necrosis)

Management

IV corticosteroids, adjunct creatinine

Polymyositis: chornic inflammation of skeletal muscles, doens’t involve skin

61
Q

Presentation, diagnosis, investigation and management of Sjogren’s

A

Systemic autoimmune destruction of lacrimal and salivary glands. Lymphocyte mediated Type IV HS.

Presentation: dry eyes, mouth, throat, myalgias, arthalgias, renal disorders

Assoc. with RA

Investigations:

Schirmer’s test (quantitatively measures tears)

Anti-Ro and Anti-LA (Anti-Ro also in SLE)

Management:

Artificial tears

Ciclosporin eye drops (immunosuppressant)

Pilocarpine (Cholinergic drug - stimulates secretion of glands)

62
Q

Drugs used in the treatment of vasculitis and the implications of these

A

Moderate:

  • Mycophenolate (immunosuppressant)

Methotrexate

Risks: teratogen, hepatotoxicity

Severe:

  • Cyclophosphamide (immunosuppressant)

Risks: infections, malignancy, infertility

  • Rituximab (anti-B cell)

Risks: less risk of malignancy, no risk of infertility

Remission maintenance:

  • Prevent relapse, lower drug toxicity, more prolonged therapy
  • Methotrexate
  • Azothioprine

Risks: BM supression, agranulocytosis

63
Q

Describe common indications for immunosuppressant drugs and biologic therapies

A

Steroids are good immunosuppressants (rapid onset, easy to administer) however causes: weight gain, OP, hepatoxicity. Though does not cause BM suppression.

MOA: Binds to glucocorticoid receptors, activates anti-inflammatory transcription factors and inhibits pro-inflammatory transcription factors

Steroid sparing agents

Inhibitors DNA synthesis

  • Methotrexate
  • Azothoprine

Lymphocyte signalling inhibitors:

  • Cyclosporin
  • Tacrolimus

Biologics:

Therapeutic agents synthesised bioligcally rather than chemically

  • Targets specific components of immune system, with minimal off-target effects
  • Usually delivered parenteral
  • Favourable side effect profile
64
Q

Methotrexate

A

MOA:

Inhibits dihydrofolate reducatase (enzyme involved in tetrahydrofolate synthesis) and thymidylate synthetase - needed for DNA, RNA synthesis

  • Leads to S-phase arrest in cell cycle

Indications:

1st line for RA. psoriatic arthritis

Giant cell ateritis

High dose: chemotherapeutic agent

Adverse effects: teratogen, hepatoxicity, BM suppression (increaed infections), pulmonary fibrosis

Clinical use:

Given once a week, with folic acid 4 days later

Normally orally

Pts need regular blood monitoring

65
Q

Azathioprine

A

MOA: metabolised to 6-mercaptopurine which incoporates in DNA and RNA chains leading to termination of nucleic acid strands. Stops cell growth and metabolism

Preferential action on lymphocytes (as other cells have pruine salvage pathways)

Also inhibits T ell co-stimulation by interfering with CD28

Adverse effects: BM suppression (leukopenia, thrombocytopenia, increased infections), N&V, hepatitis

Clincal use:

  • TPMT enzyme which reduces active metabolite (6-mercaptopurine). Without TPMT - accumulation of active metabolites causing severe toxicity
  • Need to check TPMT acvitiy in pts (0.6% pts lack TPMT)
  • Given orally
  • Monitor bloods
66
Q

Cyclosporin

A

Small molecule inhibitor of calicneurin, which leads to inhibition of signalling transduction from activated TCR. Leads to inhibition of T-cell activation

Indications:

Organ transplantation (liver, kidney)

Topically for skin, eye

Adverse effects:

Nephrotoxicity, Hypertension, Hepatotoxicity, does not cause BM suppression

Tacrolimus similar MOA, more potent

Clincal use:

  • Given orally
  • Drug interactions through CYP450
  • Monitor bloods
67
Q

Risks and common types of infection associated with these drugs

A

Immunosuppressants:

Effectiveness:

Not enough to control inflammatory disease if it progresses

Usually have slow rate onset, limiting use in acute severe conditions

Toxicity:

Even with low dose, has significant toxicities e.g. BM suppression, frequent infections

Biologics:

Adverse events:

Hypersensitivty, infusion reactions, mild GI toxicity

Infections not significantly higher than placebo

Infliximab (Anti-TNF): Increased risk of TB, salmonella, listeria (screen for latent TB)

Abatacept (AntiCD86 (T cell)): Increased risk of pneumonia, respiratory tract infections. Increased risk of TB but less than antiTNF

Rituximab (Anti-CD20 (B cell)): Increased generalised serious infections. Increased risk of Hep B (need to screen and prophylax)

Anti-IL1: increased of respiratory infections, pneumonia

68
Q

Identify common fractures on X-Ray

A

Transverse: straight through bone

Oblique: oblque line through bone

Comminuted: more than 2 parts to fracture

Compound fracture: broken bone peirces skin

Angular fracture: Axis of bone displaced so distal pprtion of bone points at a diff direction

Overriding: proximal and distal fragments overlap

69
Q

Intra-articular fractures vs Extra-articular fractures

A

Intra-articular fractures: fractures that involves a joint space, resulting in damage to cartilage. Higher risk of developing long term complications.

Extra-articular fractures: fracture outside of the joint

70
Q

Supracondylar fractures

A

If fracture heals in deformed position (malunion) results in gunstock deformity (part of it is deviated towards midline)

Mostly in children

Complications:

Nerve injury - neuroprxis which resolves

Vascular injury - pulseless but pink hand

71
Q

Femoral neck fracture

A

Are intracapsular fractures:

Subcapital - femoral head

Transcervical - midportion of femoral neck

Basicervical - base of femoral neck

Can cause disruption of blood supply to femoral head (avascular necrosis)

72
Q

Paget’s disease

A

Blade of grass sign (candle flame appearence)

Characteristic of lytic phase of Paget’s

73
Q

How arthritis Xray changes can be classified

A

Degenerative - Bone production

Inflammatory - Periarticular erosions

Depositional - Periarticular soft tissue masses

74
Q

OA radiography

A

Primary degenerative arthritis

Intrinsic degeneration of articular cartilage

Excessive wear and tear

Commonly in hips and knees

X ray features: (LOSS)

Loss of joint space

Osteophytes

Subschondral sclerosois

Subchondral cysts

Hands:

DIP, PIP, 1st MCP joint (whereas RA in PIP or MCP)

More common in females

Secondary degenerative arthritis

Another process destorys articular catilage

Atypical location, appearence age

Causes: Trauma, infection, any arthritis esp. RA, avascular necrosis

75
Q

RA with secondary OA

A

Loss of joint space

Mild subarticular sclerosis

No osteophytes

76
Q

Calcium Pyrophosphate dihydrate deposition disease (CPPD)/Pseudo gout

A

Idiopathic or associated with hyperparathyroidism or haemochromatosis

Symmetrical

Similar to OA but unusual distribution:

Calcification of articular cartilage (chondrocalcinosis) in knee, hip, shoulder, symphysis pubis

77
Q

Classification of inflammatory arthritis

A

Infective/septic arthritis

Sero-positive (RA)

Sero-negative:

  • psoriatic arthritis
  • reactive arthritis

Ankylosing spondylitis

IBD

Other connective tissue diseases

  • SLE
  • Systemic sclerosis
78
Q

RA radiography

A
  • Symmetrical

X ray findings: (LESS)

  • loss of joint space
  • erosion
  • soft tissue swelling
  • soft bone (osteopenia)

Others:

  • MCP ulnar deviation (swelling of MCP joint causes deviation to ulnar (little finger) side
  • MCP joint erosions
79
Q

Sero-negative inflammatory arthropathies

A

Heterogenous group of conditions that are RF negative with overlapping clinical manifestations and assoc HLA B27

Differs from RA:

  • normal bone density
  • periositis (inflammtion of membrane covering bone)
  • asymmetrical
  • ankylosis (fusion)

Psoriatic, reactive, ankylosing spondylitis, IBD

80
Q

Psoriatic arthritis

A

Both male and female, young adults

Skin and nail changes

DIP joints of hands>feet

  • Pencil in cup defomity (erosions and bone resorption giving appearence of pencil in a cup)
81
Q

X ray features of Ankylosing spondylitis

A

Chronic, progressive inflammatory arthropathy which presents as low back pain and spinal stiffness which leads to spinal fusion

More common in young males

Complications: uvetitis, aortic regurgitation

Pathology:

Spinal joints affected

Inflammation starts in lumbar vertebral and sacroiliac joints and extends up (symmetrical)

Pathology starts at entheses (where ligments, tendons insert) causing enthesiopathy

Xray:

Romanus lesions (erosions in anterior and posteior vertebral bodies)

Bamboo spine (vertebral body fusion)

Spinal fractures (as vertebrae is rigid and fused together, brittle, more likely to fracture)

82
Q

Anatomy of synovial joint (6 points)

A
  1. Bones which make contact with each other covered by articular cartilage ( type II collagen)
  2. Joint surrounded by connective tissue capsule which encloses the 3. joint cavity (contains synovial fluid)
  3. Inner surface of capsule and non-articular surfaces of bone is lined with synovial membrane which secretes synovial fluid
  4. Capsule supporte by ligamens which stabilise joint
  5. Joint allows wide range of movement
83
Q

Histology of OA vs RA

A

OA

Microscopically:

Fissuring, flaking then full thickeness loss of articular cartilage

Subarticular cysts

Osteophytes at joint margins

Subchondral sclerosis

Histology:

Increased water content

Alteration in proteoglycans, collagen, binding of proteins to hyaluronic acid

Rate of DNA, collgen, proteoglycan synthesis increased

Detritus synovitis - bone and cartilage broken off from damaged joint and embedd into synovium causing villous hyperplasia and inflammation

RA

Histology:

Villous hypertrophy

Hyperplasia of synoival lining

Fibrin exudate

Chronic inflmmation - aggregrates of lymphoid cells and plasma cells

84
Q

When ultrasound, MRI, CT and DXA scanning are indicated for arthritis)

A

US:

  • shows joint and surrouding soft tissue, mostly those located near surface of skin e.g. hands, use them to guide difficult joint injections

MRI:

  • shows detailed picture of bone and surrounding tissue (cartilage, ligaments) detects joint damage esp. spine, synovitis, bony erosions

CT: more detailed for bone and soft tissue, bony erosions

MRI/CT indicated to see SC and patients with subluxation (atlanto-axial subluxation in RA)

DXA:

  • detects bone mineral density.

Indicated:

  • Detect risk of OP (RA has increased risk of OP)
  • Condition that leads to low bone density e.g. RA
85
Q

Occasions when interventional radiology may be required for MSK diseases

A

Arthrocentesis - joint aspiration guided by US

86
Q

Features of mechanical back pain

A

Acute back pain: most resolves

Chronic back pain: >3 months. Most due to wear and tear but can be due to: cancers, medical emergencies, treatable conditions

Back pain = symptom

  • (97%) Non specific lower back pain
  • (3%) Radiculopathy, spinal stenosis, spondylolisthesis, cauda equina, compression fracture

Non-specific back pain:

Onset, any age

Worsens with movement or prolonged standing

Better with rest

Early morning stiffness <30 mins

Causes:

Lumbar strain

  • Most common
  • Muscle spasms settle within 24-48hrs

Degenerative discs (spondylosis):

  • increase with flexion, sneezing

Disc prolapse:

  • more localised
  • increased with extension

Treatment:

Education, promote self management

Physiotherapy

Analgesics

Acupuncture

87
Q

Causes of back pain

A

Mechanical:

  • (97%) Non specific lower back pain
  • (3%) Radiculopathy, spinal stenosis, spondylolisthesis, cauda equina, compression fracture

Systemic:

  • infection (e.g. discitis - infection of vertebral disc, usually staph. aureus)
  • malignancy (LP Thomas Knows Best - Lungs, Prostate, Thyroid, Kidneys Breast)
  • inflammatory (mostly in teens, symptom not a diagnosis)

Referred (no pathology in back):

  • Aortic aneurysm
  • Acute pancreatitis
88
Q

Mechnical back pain - radiculopathy

A

Disc prolapse: Herniated nucleus pulposus

May be acute

Usually leg

Straight leg raise +ve

Treatment:

Resolves within 12 wks

NSAIDs

Epidural cortiosteroid injections

<10% need surgery (helps leg, not back pain)

89
Q

Mechanical back pain - spinal stenosis

A

Anatomical narrowing of spinal canal

Presents with claudication of legs (too little blood flow - cramp)

  • Worse with walking, rest in flexed position
  • Xray, MRI
90
Q

Cauda equina syndrome

A

Back pain emergency

Compresison of SC nerve roots (below SC (L1/L2))

Neuropathic symptoms:

  • Bilateral sciatica
  • Saddle anaesthesia

Bladder/bowel dysfunction

  • Reduced anal tone
91
Q

Mechincal back pain - spondylolisthesis

A

Slipping of vertebrae, usually at base

Asymptomatic in most

Pain may radiate to post. thigh

Increase with extension

92
Q

Mechanical back pain - compression fracture

A

Sudden onset, severe

“belt” around chest, abdomen

Assoc OP

Investigations: Xray, DEXA

Treatment: Analgesia, calcitonin, vetebroplasty (cement), kyphoplasty (balloon)

93
Q

‘Red flags’ for sinister causes of back pain to diagnose serious back pathology

A

New onset aged <16 or >50

Previous malignancy

Recent serious infection

Fever, weight loss

After signfiicant trauma

IV drug abuse, immunosupressed

Urinary retention

Non-mechanical pain (Worse at rest/night)

Signs:

Saddle anaethesia

Reduced anal tone

Generalised neurological deficit

Yellow signs:

Attitudes, Beliefs, Compensation, Diagnosis

94
Q

Features of mechanical vs inflammatory back disease

A

Mechanical:

>40 years

Acute onset

Morning stiffness <30 mins

Exercise worsens pain

Rest imrpoves pain

May improve at night (due to rest)

Inflammatory:

<40 years

Onset: Insiduous

Morning stiffness >30 mins

Exercise improves pain

No improvement

May wake during night

95
Q

Define spondylolisthesis, spondylosis and spinal stenosis

A

Spondylosis: OA of spine, degernation of disc or facet joints

Spondylolisthesis: slipping of vertebrae

Spinal stenosis: Anatomical narrowing of spinal canal

96
Q

Describe the relevant diagnostic tests and treatments for axial spondyloarthritis

A

Diagnosis

Symptoms: inflammatory back pain, fatigue, enthesitis, extra-articular inflammation e.g. psoriasis, uveitis

Imaging

HLA-B27

CRP/ESR (usually normal)

Treatment:

Education, exercise phsyio

NSAIDs, biologics (TNF inhibitors, IL-17A inhibitors)

97
Q

Juvenile arthritis

A

Disease of childhood onset, characterised by arthritis persisting for more than 6 weeks, no known cause. It is a clinical diagnosis.

Subtypes:

Oligoarticular

Up to 4 joints, usually one

Polyarticular

RF positive polyarthritis (RA in adults)

RF -ve

Systemic onset:

Systemic features+arthritis

  • hepatosplenomegaly, pericarditis

Enthesitis related arthritis (Alkylosing spondylitis in adults)

Juvenile psoriatic arthritis - dactylitis (swelling of one joint)

98
Q

Kawasaki disease

A

Medium vessel vasculitis

<4 years, asian children

Fever, conjunctivitis

Erythematous rash on palms and soles, strawberry tongue, mucositis (lips peel)

Coronary artery involved so risk of aneursym formation and MI

99
Q

Juvenile dermatomyositis

A

Cutaneous signs:

Heliotrope rash: telangectasia on eyelids, rash across bridge of nose

Gottron’s papules: pale, red lesions over PIP and MCP joints

Nail fold changes e.g. megacapillaries

Calcinosis

Complications: vasculitis ulcers

100
Q

Juvenile SLE

A

Neuro symptoms: Headache, depression, cognitive impairment

Renal disease

Diagnosis: ANA

101
Q

Localised scleroderma

A

Linear or morphea (several patches occur)

Morphea: Leisons on trunk, abdomen, proximal limb. have purple halo

Linear: localised. Occur distally, band of discoloured skin. Growth of joint may be restricted.

Locaised scleroderma en coup de sabre: linear scleroderma which involves face. Ptosis, cataracts, scarring alopecia.

Localised scleroderma Parry Romberg sydnrome:

Changes in skull, reduced tongue development

102
Q

Osteonecrosis (avascular necrosis) - Clinical presentation, pathophys, risk factors

A

Infarction of bone near a joint

Leads to death of subchrondral bone and lead to joint collapse and arthritis

Most common in hip, then shoulder

Clinical presentation:

Limp, tenderness, limited ROM

Pts with osteonecrosis of femoral head present with groin pain that worsens with movement. Limitation in internal rotation, abduction.

Pathophysiology:

  • Necrosis involves medullary bone
  • Leads to empty lacunae which are surrounded by necrotic adipocytes which rupture and release fatty acids
  • FAs can bind to calcium and form insoluble Ca2+ soaps
  • necrotic cancellous bone collapses

Risk factors:

History trauma

Corticosteroid use

Alcohol

Sickle cell

103
Q

Osteonecrosis imaging

A

Crescent sign (subchoondral radiolucenecy)

Subchondral collapse

Joint space narrowing

Bone remodelling

104
Q

How does osteonecrosis cause arthritis?

A

If bone dies, does not remodel

So micro-damage doesn’t get repaired

Subchrondral bone weakens and collapses

Joitn surface becomes irregular, causing damage

105
Q

Prostatic breast - sclerotic

Lung - lytic lesions

Kidey, thyroid - solitary bone mets

A

Year 3 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions