PBL 5: Monoarticular joint pain Flashcards
Discuss the presentation, initial investigation, key differential diagnosis & initial management of acute joint pain and and swelling
presentation is just an acute hot swollen joint.
Any affected joint - Tense effusion, be tender to palpation, active and passive movement.
Fully examine the other joints to know if it is mono-arthritis.
differential diagnosis:
Septic arthritis → Red Flag
Crystal Arthropathy
Gout
Pseudogout
Inflammatory arthritis (Explained next week)
Haemarthrosis → Bleeding to a Joint Space
Transient synovitis → Inflammation of the inner lining (the synovium) of the capsule of the hip joint
Investigations:
Blood tests, Xray, joint aspirations
Initial management:
Analgesia, specialist based on findings
MUST RULE OUT SEPTIC ARTHRITIS
TAKE FULL PATIENT HISTORY
Discuss the basic epidemiology, pathophysiology, presentation, investigation, management and prognosis of crystal arthropathies
GOUT AND PSEUDOGOUT
GOUT:
Epidemiology:
Most common inflammatory arthritis in men >40.
After menopause increase in women-loss of uricosuric effect of oestrogen.
Attacks of gout more severe and difficult to treat.
Ageing population
Comorbidities eg: renal failure contradicting many therapeutic options
Pathophysiology:
Overproduction of uric acid (exogenous or endogenous).
Underexcretion of uric acid (abnormal renal healing of urate).
Presentation:
4 different stages: asymptomatic hyperuricemia, A/C gouty attacks, intercritical gout, advanced tophaceous gout
70% of first attacks occur in the mtp joint of great toe.
Investigation:
Joint fluid analysis
WCC in joint fluid (5,000-50,000/mm3) neutrophils.
Culture to r/o infection
S. uric acid & WCC <15,000/mm3
Renal function
Urine dipstick – haematuria (gout and kidney stone)
Management
Acute attack:
Joint rest & local ICE
NSAIDs/COX II inhibitor
Oral seroids
Local steroid injection
Oral colchicine
Intercritical gout
Lifestyle changes: diet (lower purine intake), alcohol, losing weight.
Colchicine prophylaxis for the first 3-6 moths to reduce the frequency of attacks.
Urate lowering drugs (wait until acute attack subsides - around 2-3 weeks after acute attack):allopurinol, uricosuric drugs
Given when presence of kidney stones/tophi.
If 2 attacks in a year, uricosuric agents may be used: probenecid, sulfinpyrazone & benzbromarone
Small risk of uric acid stone formation
No h/o kidney stones
Supfinpyrazone & Probenecid – ineffective if CRF
Losartan & Fenofibrate & Atorvastatin.
Prognosis:
Septic arthritis
RA: degree of inflammation
Pseudogout
Podagra: gout of 1st MTP joint
Pseudogout
Epidemiology:
Hyperparathyroidism
Osteoartiritis
Metabolic bone disease
Pathophysiology:
Mostly unknown
Phosphate levels are raised with CPPD
Presentation:
Asymptomatic chondrocalcinosis: radiographic evidence without joint symptoms
Common in 8th decade
No attacks of pseudogout occur
CPPD deposition in joints: cartilage damage, acceleration of OA
Not treated
20% of elderly patients have chondrocalcinosis on x-ray with no history of pseudogout.
Investigation:
Radiographic appearance
Ca, s.uric acid, Mg, Ferritin, PTH
Synovial fluid analysis
Wcc 3000 -50,000. >70% Polymorphs.
Negative gram stain & negative cultures
CPPD crystals – rhomboid shaped and weakly positively birefringent.
Management:
Acute attack - joint aspiration, steroid injection, anti-inflammatories
Chronic - Anti-inflammatories, periodic intraarticular steroid injection, associated disease managed.
Prognosis:
Gout of 1st mtp; shoulder and hip involvement rare in gout.
Discuss the basic epidemiology, pathophysiology, presentation, investigation, management and prognosis of osteoarthritis
the cartilage within a joint breaks down and the bone underneath begins to change causing pain, stiffness and swelling of the joint
Cartilage matrix degrading enzymes are over expressed, causing progressive cartilage degration.
‘Wear and tear’ arthritis
Degenerative
Hands, Knees, Hips
Risk Factors:
women (over 50)
joint injury
Repeated stress on joint
age
Overwieght/obesity
Genetics
Race
pain/aching in joints
Stiffness in joints
Decrease range of motion in joints
Swollen joints
History, physical exam, xray
Weight loss, steroid injections, NSAIDS, joint replacement, joint fusion
Discuss the basic epidemiology, pathophysiology, presentation, investigation, management and prognosis of septic arthritis
Septic arthritis is an infection within a synovial joint.
Most common with groups with reduced immune systems
Leukocytes release enzymes to fight bacterium within the joint, these damage the joint
· Acutely hot swollen joint
· Fever
· Systemically unwell
Intense pain
· WCC (white cell count), CRP and ESR will be elevated (due to inflammation)
· X-ray images will be normal initially and show joint damage late.
· Any joint suspected of infection must be aspirated (withdrawal of fluid, tissue or other substance) for GRAM stain, culture and examination for crystals.
· Relieve pain by splinting the limb
· Aspiration needs to be done as soon as possible so that the appropriate antibiotics can be given.
· A surgical solution may be needed resulting in an arthroscopy (keyhole surgery for diagnosing and treating joint problems) or arthrotomy (Surgical exploration of a joint, involving the inspection of cartilage). This is done alongside antibiotics.
· Serial aspiration
Good prognosis if treated quickly. There can be permanent joint damage
Treat with broad spectrum antibiotics until organism is confirmed
Describe the indications for joint replacement
Joint replacement is just one form of operation that can be used. There is also fusion and excision arthroplasty.
total and hemi arthroplasty.
Total is more commonplace now, to prevent doing more work further down the line.
However, depends on individual circumstances such as age, mobility, occupation etc.
Severity of symptoms needed to be thought of, conservative treatment always to be tried first
joint replacement maintains mobility, but is less durable.
If the patient is young, and has good mobility, a full joint replacement will allow for greater quality of life, but the joint may wear out
If a patient is going to be doing hard manual labor with that joint (e.g in the hands) a fusion may be more appropriate to prevent further surgery
If there is arthritis, that is unable to be managed by analgesics or physiotherapy or steroid injections, a joint replacement will alleviate pain and allow for greater movement
Describe the main mechanisms behind haematogenous spread of pathogens and their complications
Haematogenous spread → pathogen is spread via the bloodstream
Causes? → previous infections (pneumonia/UTI), artificial joints/heart valves, cuts, dental procedures, injecting recreational drugs, vigorous toothbrushing
How? → Bacteria enters through cuts, can spread into the lymphatic system and gain access to the bloodstream.
Complications → Sepsis, meningitis (brain), osteomyelitis (bone), endocarditis + pericarditis (heart)
Diagnoses→ culture of a blood sample
Describe the development of the 3 germ layers and what they develop into
ectoderm/ mesoderm/ endoderm
Ectoderm:
the nervous system (formation of neural cord : neurulation)
Neural crest cells —> tissues and organs. Craniofacial skeleton. Meninges. Dorsal root ganglia of autonomic nervous system.
Mesoderm:
The Notochord - helps cell orientation
the paraxial mesoderm and develop into somites. Somites form axial skeleton (trunk). Somites split into:
dermatone (dermis)
Myotome (muscle)
Sclerotic (bones and cartilage)
The lateral plate mesoderm —> splits into visceral and parietal layers
Lateral plate: lines body cavity and lines organs.
Parietal: bone/skeletal muscle/ connective tissues of limbs, pelvis, sternum.
Visceral: smooth muscle,cardiac, gut tube
Intermediate mesoderm
adrenal cortex
Kidneys
Testes and ovaries
Endoderm:
linings of digestive tract and respiratory tract
Also: tonsils/ thyroid/ parathyroid glands/ thymus/ liver/ gallbladder/ pancreas
How the trilaminar disk arises:
1) from the bilaminar disc - two cell layers (week 2 post fertilisation).
2) formation of the primitive streak (linear band of epiblast cells)
3) Cell migration and proliferation from primitive streak = forms mesenchyme cells
4) invagination process of epiblast mesenchyme cells (neural tube formation)
5) Endoderm replaces hypoblast cells. Mesoderm in between. Epiblast cells on surface = ectoderm.
