MSK diseases Flashcards

1
Q

What are the 2 microscopic appearance of bone?

Explain them

A

Woven bone
- Made quickly (in fetal bone)
- Disorganised
- No clear structure

Lamellar bone
- Made slowly
- Organised
- Has a clear layered structure

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2
Q

What are the 5 different types of bones?

List examples

A

Long bones - Tubular shape with hollow shaft, - articulates with other bones (humerus, radius, ulna, metacarpals, phalanges)

Short bones - Cuboidal in shape (carpals in the wrist - scaphoid, lunate, triquetral)

Flat bones - plates of bone which are often curved and have a protective function (skull, pelvis, thoracic cage)

Irregular bones - appear in various shapes (vertebrae, bones in ears)

Sesamoid bones - round, oval nodules in a tendon (protects tendons from wear and tear) –> Patella, two sesamoid bones at the thumb, mcp joint

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3
Q

What are the 2 macroscopic appearances of bone?

Describe them

A

Cortical (Compact)
- Dense outer shell of bone
- Has lamellae which are organised into concentric circles that surround vertical haversian canals
- Vertical haversian canals are connected by horizontal volkmann’s canals
- Osteocytes are located in lacunae (cavities between lamellae) which are are connected by canaliculi

Trabecular (spongy)
- Makes up the interior of bone
- Contains many large spaces giving it a honeycombed appearance
- Spaces between trabeculae are filled with bone marrow

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4
Q

What are the categories of joints, give examples.

A

Synarthroses - Immovable joints –> skull sutures, teeth
- Mostly fibrous joints

Amphiarthroses - slightly moveable joints - intervertebral discs, pubic symphysis
- Mostly cartilaginous joints

Diarthroses - freely movable joints –> hip, knee, shoulder
- Mostly synovial joints

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5
Q

What are ligaments and tendons?

A

Ligaments - Bone - Bone

Tendons - Muscle - Bone

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6
Q

Osteoarthritis

RF

Pathology
Symptoms
Investigations
Treatment

A

NON INFLAMMATORY wear and tear of the joints
- Typically occurs in synovial joints

RF - Obesity, increased age, occupation (where there is high usage of particular joints), FEMALE, family history

PATHOLOGY
- A result of imbalance between cartilage worn down and the chondrocytes repairing the cartilage (leads to structural issues in the joint)
- There is increased (matrix) metalloproteinase which catalyse degradation of Type 2 collagen and proteoglycan. - produced by chondrocytes
- Bone attempts to compensate with Type 1 collagen –> resulting in abnormal bony growth which present as Osteophytes.
- Commonly affects hips and knee joints. Also DIP and CMC joint (hand)

SYMPTOMS
- Joint pain and stiffness which is worse on activity and transient/little in the morning (in contrast to inflammatory arthritis)
- Deformity of joints
- Instability
- Reduced function
- Limited range of motion (due to pain) - limited bilateral flexion of knees

Signs
- Heberden’s nodes - DIP joints
- Bouchard’s nodes - PIP joints
- Weak or reduced grip strength
- Squaring of base of the thumb (CMC joint)

(No extraarticular symptoms)

INVESTIGATIONS
X-ray - LOSS
L- Loss of joint space (bones are closer to each other)
O- Osteophytes (spurs of bone protruding from either end of the joint)
S - Subarticular sclerosis (increased density of the bone - causing bone to come into contact with each other)
S - Subchondral cysts (fluid filled holes in the bone along joint line)

MOSTLY A CLINICAL DIAGNOSIS (X-ray can help but not necessary if presentation is typical)
- >45 YEARS OF AGE
- ACTIVITY RELATED PAIN
- MORNING STIFFNESS <30 MINS

Treatment
1st (non pharmacological) Lifestyle changes- exercise, physiotherapy, occupational therapy
- patient education

1st (pharmacological) Analgesia - Topical NSAID (topical diclofenac) – if topical doesn’t work then Oral first

Definitive - surgery (Arthroplasty - knee/hip replacement)

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7
Q

Rheumatoid arthritis
-Biological therapies you could give

RF

Pathology
Symptoms
Investigations
Treatment

Complications

A

An autoimmune condition that causes chronic inflammation in the synovial lining of the joints (Type of inflammatory arthritis) - polyarthritis

RF - Females, genetics (HLA DR4), smoking, post menopausal

LESS
- Loss of joint space
- Erosion of bone
- Soft tissue swelling
- Soft bones

PATHOLOGY
- Affects multiple small joints symmetrically across both sides of the body –> Symmetrical polyarthrtitis (BILATERAL)

Citrullination - Conversion of arginine to citrulline by peptidylarginine deaminase (PAD). Anti CCP (cyclic citrullinated peptide) antibodies target citrullinated proteins - healthy tissue in joints. - autoimmune (anti-CCP antibodies are more sensitive and specific than rheumatoid factor)

Rheumatoid factor - mostly IgM targets the Fc portion of IgG

SYMPTOMS
- Pain that is worse in the morning and eases as the day goes on
- JOINT PAIN, STIFFNESS AND SWELLING - Symmetrical distal polyarthritis affects the small joints of hands and feet (MCP, PIP, wrist and MTP joint- foot) -

LESS COMMON SIGNS
- Swan neck deformity –> DIP hyperflexion and PIP hyperextension
- Boutonniere’s deformity –> PIP flexion with DIP hyperextension
(Z shaped deformity in the thumb)

Can lead to extra articular complications –> Lungs (PE, pulmonary fibrosis), heart (increased IHD risk), carpal tunnel syndrome

INVESTIGATIONS
FBC - Elevated ESR/CRP, normocytic normochromic anaemia (haemolytic anaemia)

GS - Serology - Anti CCP antibodies (80% specific), RF (70% specific)

TREATMENT
1st - Disease modifying anti-rheumatic drug (DMARD) (give folic acid alongside it)
- Methotrexate (sulfasalazine for PREGNANT patients)

Biological therapies
- TNF inhibitor - Infliximab (TNF- cytokine that stimulates inflammation)
- Anti CD20 on B cells - Rituximab

NSAID - analgesia

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8
Q

What score is used to monitor disease activity in rheumatoid arthritis and response to treatment?

A

Disease activity score 28 (DAS28–>joints)

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9
Q

Gout
Causes of hyperuricaemia
Treatment if patient was renally impaired

RF

Pathology
Symptoms
Investigations
Treatment

A
  • Crystal arthropathy which is characterised by HYPERURICAEMIA and deposition of ,monosodium urate crystals in the joint causing acute inflammatory arthritis. (- hot, swollen and painful)

RF - Male, obese, diet high in meat and seafood (purine), alcohol, family history. cardiovascular/kidney disease, diuretics

PATHOLOGY
Causes of hyperuricaemia (urate is a metabolite of purine)
- Renal under-excretion of urate
- Medications - diuretics
- High consumption of seafood, meat, alcohol (high in purines)

Deposition of monosodium urate crystals in joints causes:
- Acute inflammatory arthritis
- Tophi around the joints (subcutaneous deposits of uric acid under the skin, not in the joints) - DIP most common, joints of ears and elbow

Common joints
- Base of the big toe (MTP joint)
- Wrist
- Base of the thumb (CPC joint)
(Knees, ankles)

SYMPTOMS
- MONOARTICULAR (single), acute, hot, swollen, painful joint
- Tophi
(Can’t put weight on it - usually big toe (MTP joint)

INVESTIGATIONS
- Joint aspirate (arthrocentesis) + polarised light microscopy –> Negatively birefringent needle shaped crystals (under polarised light) - monosodium urate crystals (yellow when parallel, blue when perpendicular to axis of the polarised light)

(if there is bacteria means –> Septic arthritis)

TREATMENT
Acute -
1st line - NSAIDS - ibuprofen
Colchicine in patients with renal impairment or heart disease (NSAIDS CI)

Prophylaxis
- Allopurinol (xanthine oxidase inhibitor - reduces conversion of purines to uric acid - reduce production of uric acid)
- Diet - reduce intakes of high purine containing food - seafood, meat, alcohol

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10
Q

Pseudogout
- Where does it usually occur?
- Treatment

RF

Pathology
Symptoms
Investigations
Treatment

A

A crystal arthropathy caused by the deposition of calcium phosphate crystals in the joints

RF - 70+ females, hyperparathyroidism, diabetes, haemachromatosis (deposition of iron in joints)

SYMPTOMS
- Hot, swollen, painful joint (DDX of septic arthritis)
–> typically in knee, wrist, shoulder (often polyarticular)

Investigations
GS - Joint aspiration + polarised light microscopy –> positively birefringent, rhomboid shaped crystals - calcium pyrophosphate crystals —> Should not have bacterial growth (excludes septic arthritis)

X-ray - calcium deposits in the joint cartilage.

TREATMENT
Acute - First line
- NSAIDS
- then if needed - Colchicine
- then if needed - intra-articular steroid injections (dexamethasone)

(no prophylaxis)

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11
Q

Osteoporosis (and osteopenia)
-Which tool to assess 10 year fracture risk?

RF

Pathology
Symptoms
Investigations
Treatment

A

Osteoporosis - A significant reduction in bone density (osteomalacia - decrease in bone mineralisation)
Osteopenia - A less severe decrease in bone density

Most likely a 50+ postmenopausal caucasion woman

RF- SHATTERED
Steroids
Hyperthyroidism/hyperparathyroidism
Alcohol + smoking
Thin (low BMI)
Testosterone
Early menopause
Renal/liver failure
Erosive/inflammatory disease
Diabetes Mellitus (Type 1)

PATHOLOGY
- An oversupply of osteoclasts or undersupply of osteoblasts

SYMPTOMS
- Possible fractures which may present as
+ Patient has recently had a fall (proximal femur fracture)
+ Colles fracture (radius fracture) - fall on outstretched wrist - forked wrist
+ Kyphosis - evidence of vertebral fracture

INVESTIGATIONS
GS - DEXA scan (dual energy x ray absorptiometry) - see how much radiation absorbed by bones to indicate how dense the bone is.
–> It is used to yield the T score

Also can use Fracture risk assessment tool (FRAX)/QFracture assessment - assesses 10 year fracture risk

TREATMENT
1st line - Oral bisphosphonates + calcium and vitamin D3 supplements- Alendronic acid - osteoclast inhibitors
If bisphosphonate CI in kidney disease- DENOSUMAB (monoclonal antibody targeting osteoclasts)
or
TERIPARATIDE - recombinant PTH
or
Consider hormone replacement therapy - estrogen/testosterone (usually younger postmenopausal women with higher risk of fractures)
or
RALOXIFENE - selective oestrogen receptor modulator

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12
Q

What is the T score for young adult bone density

A

Normal - > -1
Osteopenia - -1 - -2.5
Osteoporosis < - 2.5

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13
Q

Fibromyalgia
-Treatment

RF

Pathology
Symptoms
Investigations
Treatment

A

A syndrome characterised by widespread pain in the body for at least 3 months. (with all other causes excluded)

RF- Female, 20-60 years, family history, rehaumatological conditions, depression, stress

PATHOLOGY
(MSK equivalent of IBS)

SYMPTOMS
Usually a stressed and depressed 60 year old woman
- Widespread pain and stiffness for at least 3 months (back and neck)
- Sleep disturbance (wake up frequently in the early morning + difficult getting back to sleep)
- Possible allodynia (pain due to a stimulus that does not normally provoke pain)

INVESTIGATIONS
Serology test to exclude differentials
- No serological markers
- No elevated ESR/CRP
++++++ PLUS pain in 11 or more out of 18 palpated regions –> CLINICAL DIAGNOSIS

TREATMENT
1st line - Patient education (can help improve physical function and reduce pain) + referral to physiotherapy

Pharmacological - Antidepressants - Amitriptyline
Can consider specialist referral - cognitive behavioural therapy, occupational therapy

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14
Q

Polymyalgia rheumatica
-Key symptom

RF

Pathology
Symptoms
Investigations
Treatment

A

Differential of fibromyalgia

An inflammatory condition causing pain and morning stiffness in the shoulders, pelvic girdle (hips) and neck

RF - >50 years, white, females, giant cell arteritis (GCA)

PATHOLOGY
Strong association with giant cell arteritis.

SYMPTOMS
-Sudden Shoulder/hip stiffness and pain (morning stiffness)
- Bilateral proximal muscle weakness
- Sleep disturbance
- Weight loss, depression, malaise, anorexia, low grade fever

INVESTIGATIONS
1st - ESR+CRP elevated

Rapid response to corticosteroids - prednisolone (patients with PMR will have a dramatic improvement in symptoms within 1 week.

Treatment - Oral prednisolone

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15
Q

Sjorgen syndrome

RF

Pathology
Symptoms
Investigations
Treatment

A

A systemic autoimmune disorder characterised by the presence of dry eyes and dry mouth as a consequence of lymphocytic infiltration into the lacrimal and salivary glands.

RF- Female, SLE, Rheumatoid arthritis, scleroderma

PATHOLOGY
2 types:
Primary - occurs alone
Secondary - occurs in associated with another autoimmune disease - SLE, RA, scleroderma (systemic sclerosis)

SYMPTOMS
- Dry eyes (keratoconjunctivitis sicca)
- Dry mouth (xerostomia)
- Dry vagina

INVESTIGATIONS
First line - Serology for Anti SS A antibodies (anti-Ro) and Anti SS B antibodies (anti-LA).

GS - Schirmer test - filter paper placed in the lower eyelid –> after 5 minutes if <10mm of the paper is wet, the test is POSITIVE.

(Rarely done but salivary gland biopsy - lymphocytic infiltration)

TREATMENT
Based on clinical features
- Artificial tears
- Artificial saliva
- Vaginal lubricants
- Pilocarpine - Cholinergic agonist)

Hydroxychloroquine - given if patient has joint pain, fatigue, rashes.

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16
Q

Main complication of giant cell arteritis?

A

(Amaurosis fugax) Vision loss - often irreversible if not treated with IV methylprednisolone ASAP.

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17
Q

Giant cell arteritis

RF

Pathology
Symptoms
Investigations
Treatment

A

A granulomatous vasculitis affecting large sized arteries (sometimes medium)
- Most common form of systemic vasculitis in adults.

RF - >50 years, female, genetics, smoking

PATHOLOGY
- It mainly affects branches of the external carotid artery
e.g. Temporal branch (scalp tenderness), ophthalmic branch (vision), facial branch (jaw)
The temporal artery may be tender and thickened to palpation.

SYMPTOMS
- Unilateral headache - around the temple
- Scalp tenderness (e.g. when brushing the hair)
- Jaw claudication
- Blurred or double vision
(Amaurosis fugax - transient loss of vision in one eye - possible loss of vision if untreated)

INVESTIGATIONS
1st - ESR and CRP elevated

GS- Temporal artery biopsy - shows granulomatous inflammation (possible presence of multinucleated giant cells) - inflammation can be in segmental skip lesions

TREATMENT
1st line - Prednisolone (corticosteroids)

For patients with recent vision loss (amaurosis fugax)- ASAP aggressive treatment with IV METHYLPREDNISOLONE –> otherwise vision loss can become permanent

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18
Q

Polyarteritis nodosa
-Symptoms
-Associated with?

RF

Pathology
Symptoms
Investigations
Treatment

A

Systemic vasculitis that affects medium sized vessels

RF - Hep B infection, 40-60 years, males

PATHOLOGY
- Associated with HBV

SYMPTOMS
- MONONEURITIS MULTIPLEX- peripheral neuropathy in at least 2 different areas (causes tingling, numbness, pain and paralysis)
- Paraesthesia
- Abdominal pain
- Renal impairment

INVESTIGATIONS
First line - ESR/CRP elevated
CT angiogram - Shows beads on a string –> microaneurysms

GS - Biopsy of affected tissue –> transmural necrotising inflammation

TREATMENT
1st line - Prednisolone (corticosteroids)

(if need to treat hypertension - Ace inhibitors)
Hep B treatment after giving corticosteroids

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19
Q

Give 2 examples of large vessel vasculitis

A
  • Giant cell arteritis - mainly affects branches of the external carotid artery
  • Takayasu’s arteritis - mainly affects the aortic arch
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20
Q

Give 3 examples of medium vessel vasculitis

A

Polyarteritis nodosa - Associated with HBV (40-60 year males)

Buerger’s disease - affects arms and legs (male smokers 20-40, peripheral skin necrosis) - thromboangiitis obliterans

Kawasaki disease - seen in children, can cause coronary artery aneurysms

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21
Q

Give 3 examples of small vessel vasculitis

A
  • Eosinophilic granulomatosis with polyangitis (Churg-Strauss syndrome) –> Tissue eosinophilia, granulomatous inflammation and vasculitis – pANCA positive
  • Granulomatosis with polyangitis (Wegener’s granulomatosis) - has upper/lower respiratory tract involvement and glomerulonephritis. – cANCA positive

Henoch schonlein purpura - IgA vasculitis - IgA deposition in GBM on kidney biopsy (has purpuric rash on shins)

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22
Q

What is the general treatment for vasculitis and what should be considered when giving steroids (in general) for long term.

A

Corticosteroids (prednisolone)

In general, steroids can cause GI effects (peptic ulcer) and bone loss (osteoporosis). So necessary precautions must be taken.

Give PPI for GI symptoms and bisphosphonates to help protect bones.

Glaucoma, weight gain, insomnia, hypertension, diabetes mellitus, and Cushing’s syndrome

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23
Q

Granulomatosis with polyangitis (Wegener’s granulomatosis)
-Investigations

RF

Pathology
Symptoms
Investigations
Treatment

A

Systemic vasculitis typically involving small vessels (autoimmune)

RF- Genetic predisposition, infection, whites

PATHOLOGY
Classic triad of organs targeted
- Lower respiratory tract
- Upper respiratory tract
- Glomerulonephritis

SYMPTOMS
Upper resp tract
- Saddle shaped nose - due to nasal bridge collapse
- Epistaxis
- pain and muddled sensation in the ears
- Oral/nasal ulcers

Lower resp tract
- shortness of breath
- haemoptysis

Renal impairment (possible haematuria)

INVESTIGATIONS
1st ESR and CRP - elevated

GS - cANCA positive

Urinalysis and microscopy - haematuria, proteinuria
Tissue biopsy - shows granulomatous inflammation, necrosis and vasculitis.

TREATMENT
- Prednisolone

If needed rituximab (immunosuppressive agent)

24
Q

Paget’s disease of bone
-Symptoms

RF

Pathology
Symptoms
Investigations
Treatment

A

A chronic bone disorder characterised by focal areas of increased bone remodelling resulting in overgrowth of poorly organised bone.

RF - Family history, Male>50 years

Pathology
- Excessive bone turnover due to increased osteoclast and osteoblast activity.
- Excessive turnover is uncoordinated leading to patchy areas of high density (sclerosis) and low density (lysis) –> results in enlarged and misshapen bones.
(Particularly affects bones of the head and spine)

SYMPTOMS
- Bone pain
- Bone deformity (frontal bossing, prognathism - enlargement of mandible)
- Fractures
- Hearing loss

INVESTIGATIONS
1st line- Blood test - increased ALP (bone pathology)

GS- X-ray –> shows cotton wool skull (areas of lysis + sclerosis)

TREATMENT
1st line - Bisphosphonates (alendronic acid)

NSAIDS - analgesia

25
Q

What is a spondyloarthropathy? Name examples

A

An inflammatory arthritis affecting the spine

Examples
- Ankylosing spondylitis
- Psoriatic arthritis
- Reactive arthritis
- Enteric arthritis

26
Q

Ankylosing spondylitis
What tool would you use to assess spinal mobility?
INVESTIGATIONS

RF

Pathology
Symptoms
Investigations
Treatment

A

A chronic progressive inflammatory condition mainly affecting the spine.

RF - Young male with HLA B27

PATHOLOGY
- Seronegative spondyloarthropathy (rheumatoid factor not found in the blood)
- Associated with HLA B27
- Patients present with severe pain and stiffness of joints - at the sacroiliac and vertebral joints
–> overtime, inflammation destroys intervertebral joints and sacroiliac joints –> fibroblasts replace destroyed joint with fibrin –> forming a fibrous band around joints (limiting the range of motion) –> Osteoblasts are activated which leads to fibrous tissue becoming bone (ossification) - syndesmophytes (small bony outgrowth) form –> can make spine immobile

SYMPTOMS
- Typically a young male with progressively worsening back stiffness (that is worst in the morning) and better with exercise. (and back pain)
- Anterior uveitis (inflammation of uvea)
- Enthesitis - inflammation of connective tissue (tendons/ligaments) that attach to bones causing stiffness and pain
- Dactylitis - inflammation of the entire finger
- Loss of natural lumbar lordosis, presenting with kyphosis
- Buttock pain if sacroiliac joints are affected

INVESTIGATIONS
First line and GS - Pelvic X-ray –> Bamboo spine (ossification of annulus fibrosis) and sacroilitis + syndesmophytes (areas of bone growth) + squared vertebral bodies

MRI of the spine can show sacroilitis before any X ray changes. (better screening tool)

Genetic testing - HLA B27
ESR and CRP - elevated

  • Do Schober’s test to assess spinal mobility - (length less than 20cm indicates restriction in lumbar movement, supporting diagnosis)

TREATMENT
First line - NSAIDS - Ibuprofen

(For severe cases - intraarticular corticosteroid injection)

Second line- (DMARD) TNF alpha inhibitors (infliximab)

27
Q

Psoriatic arthritis

RF

Pathology
Symptoms
Investigations
Treatment

A

A chronic inflammatory musculoskeletal disease associated with psoriasis (flaky patches of skin)

RF - psoriasis, family history

PATHOLOGY
- 10-40% of patients with psoriasis develop it within 10 years
- Seronegative spondyloarthropathy/inflammatory arthritis
- It can vary in severity – mild stiffness in joint/joint can be completely destroyed (arthritis mutilans)

Could present with
1) Symmetrical polyarthritis (similar to RA)
- More common in women
- Affects DIP joints, hands, wrists, ankles

2) Asymmetrical pauciarthritis (only affecting a few joints)
- Affects digits and joints of feet

3) Sponylitic pattern
- More common in men
- Presents with back stiffness, sacroilitis, atlanto-axial joint involvement at top of the neck

SYMPTOMS
Moderate
- Inflamed DIP joints
- Onycholysis (Nail dystrophy - where nail separates from nail bed)
- Dactylitis - swelling of an entire digit
- Enthesitis (heel/elbow/lateral hip pain) - achilles tendon, plantar fascia and epicondyle (inflammation)

Severe
- Athritis mutilans - destruction of bones around the phalanx - pencil in cup deformity - fingers telescope on themselves

INVESTIGATIONS
X-ray - Erosion in DIP joint + periostitis + soft tissue swelling (dactylitis) — pencil in a cup appearance - only in advanced disease

Screening tool - Psoriasis epidemiological screening tool. (PEST) - high score triggers referral to rheumatologist

TREATMENT
1st line - NSAIDS - Ibuprofen
(Steroid injections for a lot of pain in a single joint)
If unresponsive to NSAIDS –> DMARDS - Methotrexate (Folate reductase inhibitor)
CI in pregnancy –> Sulfasalazine

If unresponsive –>
TNF alpha inhibitor - infliximab
If unresponsive to Anti-TNF –>
Ustekinumab is a monoclonal antibody that targets interleukin 12 and 23

28
Q

Differences between psoriatic arthritis and rheumatoid arthritis

A

Psoriatic - Associated with psoriasis
RA - Does not present with psoriasis

Psoriatic - often involves DIP joints
RA - often involves PIP and MCP joints

Psoriatic - Seronegative - typically negative for rheumatoid factor and anti-CCP antibodies.

29
Q

Reactive arthritis (Reiter’s dynrome)
-Symptoms

RF

Pathology
Symptoms
Investigations
Treatment

A

An inflammatory arthritis - Synovitis (inflammation of synovium) that occurs after exposure to infections (GI/GU)

RF - Males, HLA B27, preceding chlamydial/GI infection

PATHOLOGY
- Seronegative spondyloarthropathy
Inflammation of synovial membranes and tendons due to infection
Infections can be caused by GI/STI infections
Gastroenteritis –> Campylobacter.jejuni, salmonella, shigella
STI –> CHLAMYDIA TRACHOMATIS (causes reactive arthritis) and Neisseria Gonorrhoea (causes gonococcal septic arthritis)

Immune system’s response to infection –> causes inflammation which affects the joints

SYMPTOMS
Triad of: Can’t see, Can’t pee, Can’t climb a tree
- Conjunctivitis
- Urethritis - pain on urinating (dysuria), blood in urine
- Arthritis (painful, swollen, warm, red and stuff joints, especially in the morning) - symptoms relieved by exercise

INVESTIGATIONS
ESR, CRP - elevated

Genetic testing for HLA B27

(Stool culture will be negative unless patients are tested very early after onset)

GS - Joint aspirate
- Microscopy and sensitivity tests - No organism (rules out septic arthritis)
- Plane polarised light microscopy - negative for crystalarthropathy

TREATMENT
1st line - NSAIDS (steroid injections if required)

Mostly a single attack which resolves within 6 months. But if there are recurrent cases (chronic), prescribe METHOTREXATE. if this doesn’t work then anti TNF - infliximab.

30
Q

Septic arthritis
- Investigation?

RF

Pathology
Symptoms
Investigations
Treatment

A

Infection of 1 or more joints caused by pathogenic inoculation of microbes. Can either occur via direct inoculation/access or via haematogenous spread. (MEDICAL EMERGENCY)

RF- prosthetic joint, immunosuppression, IVDU, recent surgery

PATHOLOGY
- Mortality of 10%

MOST COMMON ORGANISM –> S.aureus
Other bacteria:
- N.gonorrhoea - in sexually active individuals
- S.pyogenes
- Escherichia coli
- Haemophilus influenzae (children)

SYMPTOMS
Acute onset of
- Hot, red, swollen and painful joint (typically a single and large joint e.g the Knee)
- Stiffness and reduced range of motion
- Systemic symptoms –> fever, lethargy and sepsis

INVESTIGATIONS
URGENT JOINT ASPIRATE with microscopy and sensitivity and polarised light microscopy
To eliminate possible differentials:
1) Septic –> you can ID the causative organism
2) Reactive –> sterile, crystal free joint
3) Gout –> negatively birefringent needle crystals
4) Pseudogout –> positively birefringent rod-shaped crystals

ESR + CRP - elevated
Blood culture (bacteria may have spread via haematogenous methods)

TREATMENT
Can only give antibiotics AFTER joint aspirate and drainage of infected synovial fluid
1st line Flucloxacillin - E.coli and others
Clindamycin - penicillin allergy
Vancomycin - if MRSA - S.aureus
IM ceftriaxone (and azithromycin) - if Gonorrhoea

Can give NSAIDS for analgesia
(If they are on steroids, double the prednisolone dose - stress response)
(If on Methotrexate/anti-TNF –> stop )

31
Q

How would you differentiate between Gout, pseudogout, reactive arthritis, haemarthrosis?

A

Gout - Joint fluid shows urate crystals that are negatively birefringent of polarised light

Pseudogout - Joint fluid shows rod-shaped calcium pyrophosphate crystals that are positively birefringent

Reactive arthritis –> Triggered by urethritis or gastroenteritis and associated with conjunctivitis

Haemarthrosis –> bleeding into the joint that occurs usually after trauma

32
Q

Enteropathic arthritis (enteric arthritis)

RF

Pathology
Symptoms
Investigations
Treatment

A

Arthritis that occurs with IBD

RF - IBD, coeliac disease, HLA B27

Symptoms - ABD pain, blood in stools + arthritis symptoms

INVESTIGATIONS
ESR CRP - elevated
Genetic test for HLA B27

Stool culture microscopy and sensitivity test.

TREATMENT
NSAIDS - lessen pain and swelling
DMARDS - methotrexate
TNF alpha inhibitors - infliximab

Definitive - surgery (if affecting the spine)

33
Q

Osteomyelitis

RF

Pathology
Symptoms
Investigations
Treatment

A

Inflammatory condition of bone and bone marrow caused by an infecting organism, most commonly S.aureus.

RF - Open fractures, orthopaedic operations, diabetes, IVDU, immunosuppression

PATHOLOGY
Most common mode of infection in children –> haematogenous osteomyelitis (via haversian and volkmann canal system)
(Sometimes via direct contamination of bone e.g. at a fracture site/orthopaedic operation - more common in adults)

Mostly caused by S.aureus.
Salmonella (in sickle cell patients)

Complications –>
Acutely osteomyelitis leads to –> inflammation and bone oedema
Chronically it can cause –> Sequestra (necrotic bone separated from healthy bone) and involucrum (thick sclerotic bone formed around the sequestra - compensatory mechanism for support)

SYMPTOMS
Acute
- Fever, pain, swelling and erythema
- Dull bony pain

Chronic
- Persistent pain
- Soft tissue damage
- Sequestrum formation

INVESTIGATIONS
First line -
ESR and CRP elevated
X-ray - shows osteopenia

GS - Bone marrow biopsy and culture, microscopy and sensitivity to ID causative organism (rules out tuberculosis osteomyelitis - which would show caseating granulomas)

Treatment
Surgical debridement (removal) of the infected bone and tissues
+++ Plus
Prolonged courses of antibiotics (6 weeks)
- 1st line - Flucloxacillin
- Penicillin allergy - clindamycin
- MRSA - Vancomycin

34
Q

Systemic lupus erythematosus
-Lifestyle changes

RF

Pathology
Symptoms
Investigations
Treatment

A

An inflammatory autoimmune connective tissue disorder that affects multiple organs and systems. lack of complementary proteins –> buildup of immune complexes

RF - Women, asian, african, caribbean, young-middle aged adults

PATHOLOGY
- A type 3 hypersensitivity reaction (Antigen antibody complex deposition
- Characterised by Anti nuclear antibodies (IgG) –> autoantibodies against proteins within the cell nucleus –> thus generating a chronic inflammatory response.

SYMPTOMS
RASH OR PAIN
Rash
Arthritis
Serositis - pericarditis and pleuritis
Haematological disorders - Pancytopenia
Oral ulcers
Raynaud’s phenomenon
Photosensitive rash
Anti nuclear antibodies
Immunologic disorders - Anti DS DNA antibodies
Neurologic disorder - tonic clonic seizure

CKD MOST COMMON CAUSE OF DEATH

INVESTIGATIONS
FBC - Anaemia
ESR - elevated with CRP normal (but CRP increases in severe inflammation)
C3 and C4 levels decreased

Urine dipstick - test for haematuria and proteinuria (nephritic syndrome)

GS - Serology for antinuclear antibodies (highly sensitive) and anti double stranded DNA antibodies (highly specific to SLE) –> both elevated diagnostic

TREATMENT
First line - Hydroxycholoroquine (reduce frequency of flareups - can lead to vision defects) + lifestyle changes e.g. wearing sun screen and avoiding the sun
+
NSAIDS - control joint stiffness and pain
+ Prednisolone

For more severe/resistant SLE infections –> DMARDS (Methotrexate)
(Rituximab - monoclonal antibody targeting CD20)

35
Q

Complications of SLE

A

1) Cardiovascular disease –> chronic inflammation in blood vessels lead to hypertension and coronary artery disease

2) Infection

3) Anaemia - anaemia of chronic disease, autoimmune haemolytic anaemia

4) Pericarditis - inflammation of the pericardial sac

5) Pleuritis - inflammation of the lining of the lungs - sharp chest pain on inspiration

36
Q

Antiphospholipid syndrome
-Treatment

RF

Pathology
Symptoms
Investigations
Treatment

A

An autoimmune disorder caused by antiphospholipid antibodies. (Characterised by thrombosis, recurrent miscarriage and anti phospholipid antibodies)

RF - History of SLE, history of other autoimmune diseases

PATHOLOGY
Can be primary - idiopathic
Can be secondary to other diseases –> especially SLE
Antiphospholipid antibodies bind to phospholipids on the surface of cells, causing inflammation and increasing the risk of thrombosis.

Specific antiphospholipid antibodies include:
- Lupus anticoagulant
- Anti cardiolipin antibodies
- Anti beta 2 glycoprotein 1 antibodies.

SYMPTOMS
CLOTS
C- Clot formation - venous thromboembolism (increased risk of arterial- stroke/MI + venous thrombosis (DVT)
L - Livedo reticularis - Mottled (spots/smears), purplish discolouration of the skin
O - Obstetric issues - Recurrent miscarriages, pre-eclampsia (condition causing high BP during and after labour)
T - Thrombocytopenia

INVESTIGATIONS
FBC - Thrombocytopenia

GS - One or more on 2 separate occasions (12 weeks apart)
Positive for
- Lupus anticoagulant
- Anti cardiolipin antibodies
- Anti beta 2 glycoprotein 1 antibodies.

TREATMENT
Long term warfarin with a target INR of 2-3 (if they have had a thrombosis)
IF NO THROMBOSIS- prophylactic aspirin

WARFARIN IS CONTRAINDICATED IN PREGNANCY
- Take Low molecular weight heparin + aspirin

COMPLICATION - catastrophic antiphospholipid syndrome (CAPS) - widespread clotting throughout the body

37
Q

Scleroderma (Systemic sclerosis)

RF

Pathology
Symptoms
Investigations
Treatment

A

An autoimmune disease characterised by fibrosis across multiple organ systems.

RF- Family history, positive ANA, 30-50 years women

PATHOLOGY
Diffuse cutaneous scleroderma - subcategory of the disease affecting multiple systems
CREST symptoms plus internal organ complications (hypertension, pulmonary hypertension, pulmonary fibrosis)

Limited cutaneous scleroderma (CREST SYNDROME)- subcategory of the disease affecting fewer organs. –> More common subtype

SYMPTOMS
CREST
C- Calcinosis –> hard calcified nodules under the skin
R - Raynaud’s phenomenon - colour change in fingers and toes due to poor blood flow - cold and blue
E - Esophageal dysmotility - food gets stuck on swallowing causing discomfort
S - Sclerodactyly - tightening and thickening of skin over the fingers distal to MCP joints
T - Telangiectasia - dilation of capillaries - spidery appearance on the skin.

(Patients may say they first noticed finger symptoms: skin of fingers becoming tight, fingers being stiff and inflexible, fingers turning cold and blue)

INVESTIGATIONS
Serum autoantibodies
- ANA positive in most patients
- Anti centromere antibodies - most associated with Limited scleroderma
- Anti SCl 70 antibodies - most associated with Diffuse scleroderma

(Nailfold capillaroscopy- examines health of peripheral capillaries) (may show abnormal capillaries, avascular areas and microhaemorrhages)

DIAGNOSTIC CRITERIA - American college of rheumatology

TREATMENT
Treat symptoms (no actual treatment for the condition)
Raynaud’s phenomenon –> Nifedipine (Calcium channel blocker)
GI symptoms –> omeprazole or metoclopramide (pro motility)
DMARDS
Steroids

Non pharmacological treatments
- Physiotherapy - promotes joint mobility and muscle strength
- Avoid smoking
- Avoid cold and use hand warmers –> Raynaud’s phenomenon)
- Occupational therapists

38
Q

Polymyositis/Dermatomyostitis

RF

Pathology
Symptoms
Investigations
Treatment

A

Autoimmune conditions that cause muscle inflammation (myositis)

PATHOLOGY
- They can be paraneoplastic syndromes caused by underlying cancer.
- They can be caused by viral triggers e.g. coxsackie virus, HIV

Presents with:
- Gradual onset, symmetrical, Proximal muscle weakness (top of arms and legs - due to muscle wasting) –> difficulties standing from a chair, climbing stairs or lifting items overhead
- Skin changes - GOTTRON PAPULES (scaly erythematous patches over knuckles, elbows and knees), HELIOTROPE RASH (on face and eyelids),PHOTOSENSITIVE ERYTHEMATOUS RASH over the back head and neck –> only in dermatomyositis (polymyositis have no skin changes)

INVESTIGATIONS
Creatine kinase blood test –> elevated
Inflammation of muscles causes release of creatine kinase. (but there are other causes of raised creatine kinase levels e.g. rhabdomyolysis, AKI, strenuous exercise, MI)

GS - Muscle biopsy –> perifascicular atrophy seen due to phagocytosis and necrosis of muscle fibres

Myositis specific antibodies
- Anti- Jo-1 antibodies –> associated with both
- Anti Mi 2 antibodies –> Associated with dermatomyositis

TREATMENT
1st line
- Prednisolone

If response to steroids are inadequate –> give methotrexate. if that doesn’t work –> infliximab

Physiotherapy
Occupational therapy
Assess for cancer

39
Q

Osteomalacia

RF

Pathology
Symptoms
Investigations
Treatment

A

A condition where defective bone mineralisation causes soft bones due to insufficient vitamin D (after epiphyseal fusion)
(defection bone mineralisation before epiphyseal fusion - Rickets (children))

RF - low dietary calcium, vitamin D deficiency, CKD, limited sunlight exposure

PATHOLOGY
Inadequate vitamin D leads to low serum calcium and phosphate. which are required for construction of bone. (low levels result in defective bone mineralisation and osteomalacia)

Causes:
- Vitamin D deficiency –> malabsorption, reduced intake, poor sunlight
- Hyperparathyroidism -secondary to Vit D deficiency increases calcium release from bone
- CKD/Renal failure –> decreases active vitamin D production
- Liver failure –> decrease in vitamin D pathway efficiency (vitamin D3 –>25 hydroxyvitamin D)

SYMPTOMS
- Fractures
- Bone pain and tenderness
- Proximal muscle weakness (may be associated with wasting) - waddling gait, difficulty climbing stairs

INVESTIGATIONS
1st line
Serum 25 hydroxyvitamin D - low (best marker as compensatory mechanisms can affect 1,25 dihydroxyvitamin D levels making it more inaccurate)

Serum calcium - decreased
Serum PTH - increased (secondary hyperparathyroidism)
X-rays –> Looser’s zones - pseudofractures/milkman fractures –> indicative of osteomalacia (defective mineralisation)

GS - Bone (Iliac crest) biopsy –>shows increased osteoid. but rarely performed due to invasive nature

TREATMENT
1st line - Colecalciferol (vitamin D replacement)

(may need to give calcium carbonate depending on serum calcium level)

40
Q

Osteosarcoma

RF

Pathology
Symptoms
Investigations
Treatment

A

Osteosarcoma
- Most common primary malignant tumour of bone where there is a abnormal proliferation of osteoblasts. - mainly seen in childhood (15-19)
- Associated with paget’s disease
Sx
- persistent bone pain that is worse at night time (may wake patient up) - affects the knee
- Fractures will occur due to minimal force or impact (structurally abnormal bone matrix)

Investigations
- X-ray shows sunburst appearing bone –> periosteal reaction - irritation of lining of the bone

  • Blood test - may show increased ALP

Treatment
- Surgically resect tumour + adjuvant chemotherapy (required as long as not low grade)

  • Can metastasise to the lungs
41
Q

What is the vitamin D pathway?

A

1) 7 dehydrocholesterol is converted into vitamin D3 under the influence of UV light (skin)

2) In the liver, vitamin D3 is converted into 25 hydroxyvitamin D (calcidiol) via 25 hydroxylase)

3) in the kidney, 25 hydroxyvitamin D is converted into 1,25 dihydroxyvitamin D (calcitriol) via 1 alpha hydroxylase

42
Q

Symptoms of rickets

A

Bone pain, failure to thrive, bony deformities - bowed legs and knocked knees, muscle weakness

43
Q

Ewing Sarcoma and chondrosarcoma

RF

Pathology
Symptoms
Investigations
Treatment

A

Malignant primary tumour of childhood and adolescence (between 10-20 years) that arise in soft tissue (mesenchymal stem cells)

  • Pain worse at night and can be accompanied by swelling or lump.
  • Highly malignant and commonly spreads to the lungs (can metastasise to the kidney, bone marrow, heart, etc)
  • X-ray shows destructive ‘moth eaten’ lesions.

Treat with chemotherapy + surgery

Only difference with chondrosarcoma is that it is cartilage cancer –> X-ray would show osteolysis

otherwise symptoms and treatment is the same

44
Q

Which tumours commonly metastasize to bone?

A

Breast, lung, prostate, thyroid, renal cell carcinoma

45
Q

Marfan’s syndrome
- Everything

RF

Pathology
Symptoms
Investigations
Treatment

A

An autosomal dominant condition disorder of connective tissue that is characterised by loss of elastic tissue. (Affects multiple systems e.f. MSK, cardio, neuro and resp)

RF- Family history of marfan’s, family history of aortic dissection/aneurysm

PATHOLOGY
Caused by a mutation in the fibrillin 1 gene.
This results in the production of abnormal fibrillin protein which leads to abnormalities in the mechanical stability and elastic properties of connective tissue. (decreased tensile strength - abnormal connective tissue)

SYMPTOMS
- Tall stature
- Long limbs, long neck
- Pectus carinatum (ribs and chest wall push outwards)
- Pectus excavatum (sternum may be pressed in)
- Long fingers (arachnodactyly)
Two tests
- Positive wrist sign –> if distal phalanges of the 1st and 5th digits overlap when hand is wrapped around the other wrist
- Positive thumb sign –> When patient bends the thumb toward the hand and covers it with the fingers, the tip of the thumb protrudes beyond the palm of the clenched hand.
++++++
Aortic complications
- Aortic regurgitation murmur
- AAA
- Aortic dissection

INVESTIGATIONS
Clinical diagnosis + genetic testing for fibrillin 1 gene.
(Use Ghent criteria)
Can do echocardiography to check for aortic regurgitation, Aortic root dilation, or aortic dissection

TREATMENT
Really to reduce the risk of complications (cardiac complications are at greater risk of developing)
- Lifestyle management - avoiding intense exercise and caffeine

  • Preventive medications include: Beta blockers and angiotensin 2 receptor blockers
    (yearly follow up and monitoring for complications –> echocardiograms and review by ophthalmologist)
46
Q

Ehler Danlos syndrome
- Symptoms
- Treatment

RF

Pathology
Symptoms
Investigations
Treatment

A

A group of inherited connective tissue disorder involving defects in collagen, causing hypermobility in the joints and abnormalities in connective tissue (of the skin, bones, blood vessels and organs)

RF - family history of joint hypermobility or EDS, genetic mutations

PATHOLOGY
Many subtypes
Most common - hypermobile Ehlers-Danlos syndrome
- Key features being joint hypermobility and soft stretchy skin.
Problem with type 3 collage.

SYMPTOMS
- Joint hypermobility –> established using the Beighton score.
- Recurrent joint dislocation (because ligaments are lax, making joints unstable)
- Joint pain
Other symptoms: Stretchy skin, stretch marks, easy bruising, abdominal pain, etc

INVESTIGATIONS
Clinical diagnosis + genetic testing

Beighton score used to assess hypermobility and support diagnosis. (Hyperextension of limbs, fingers and thumb)

TREATMENT
No cure –> focus on maintaining healthy joints
- Physiotherapy to strengthen and stabilise joints
- Occupational therapy to maximise function
- Moderating activities to minimise flares

47
Q

What is lumbar spondylosis?

Investigation and treatment

A

Progressively worsening, age related degeneration of the vertebrae and intervertebral discs (loss of disc height) of the lower back.

Leads to a loss of compliance and thinning over time.

(Essentially leads to persistent back pain) + (radicular leg pain as a result of nerve compression - due to loss of disc height)

(mainly L4/L5 or L5/S1)

Investigation –> X-ray

Treatment –> Analgesia and physiotherapy

48
Q

What drugs can cause psychosis?

A

Steroids, antiepileptics

49
Q

Triad associated with Rheumatoid arthritis

A

Felty’s syndrome

Extra articular manifestation of Rheumatoid Arthritis
(Characterised by persistent idiopathic neutropenia and frequently splenomegaly)

RF - RA >10 years, >50 years, white

PATHOLOGY
Triad of long standing RA, idiopathic neutropenia and splenomegaly.
- Strongly associated with Rheumatoid factor (95-100%) and HLA DR4
(sometimes ANA also (47% to 100%)

SYMPTOMS
Long standing erosive RA
- Z thumb, swan neck, boutonniere’s deformity)
- Splenomegaly
- Rheumatoid nodules (Hands and feet)

INVESTIGATIONS
FBC and Peripheral blood smear - Neutropenia (low neutrophil count)

Serum RA - elevated
Anti CCP and anti ANA - elevated

ESR, CRP - Elevated

TREATMENT
1st line - DMARD - methotrexate

if doesn’t work - rituximab

50
Q

How should you take bisphosphonates?

A

Always take bisphosphonates on an empty stomach with a full glass of water. Stand or sit upright for 30 minutes after taking them. You’ll also need to wait between 30 minutes and 2 hours before eating food or drinking any other fluids.

51
Q

Side effect of bisphosphonates

A

Osteonecrosis of the jaw

Oesophageal ulcers
Oesophagitis
Hypocalcemia
Renal toxicity

(associated with dyspepsia, GI ulcers and acid reflux)

52
Q

Rheumatoid arthritis extra articular complications

A

Pulmonary –> Pleuritis
Cardiac –> Pericarditis, atherosclerosis
Renal –> Glomerulonephritis
Oral –> Sjogren’s

53
Q

Complications of scleroderma
How to treat

A

Scleroderma can lead to renal crisis that presents with
- Abrupt onset of severe hypertension
- Renal failure/AKI

It can lead to acute kidney injury, hypertensive retinopathy, hypertensive encephalopathy, seizures and pulmonary oedema if left untreated.

Treat with ace inhibitors

(CAN ALSO CAUSE PULMONARY FIBROSIS)

54
Q

What are the general features of spondyloarthropathies?

A

SPINEACHE Includes: Akylosing spondylitis, psoriatic arthritis, reactive arthritis and enteric arthritis

S - Sausage fingers (Dactylitis)
P - Psoriasis
I - Inflammatory back pain
N - Nsaids - good response
E - Enthesitis (plantar fascitis, inflamed heel tendon - achilles tendon)
A- Arthritis
C - Crohn’s or colitis
H - HLA B27
E - Eyes (Uveitis)

55
Q

RF of osteoporosis

A

SHATTERED
Steroids
Hyperparathyroidism
Alcohol + smoking
Thin (low BMI)
Testosterone
Early menopause
Renal/liver failure
Erosive/inflammatory disease
Diabetes mellitus

56
Q

Methotrexate side effects

A

Nausea, vomiting, loss of appetite

Can cause bone marrow suppression
- Anaemia,
- Leucopenia
- Thrombocytopenia
(Agranulocytosis)

Can cause nephrotoxicity when prescribed with trimethoprim

57
Q
A