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Year 3 - primary care + medicine > MSK general / rheum > Flashcards

MSK general / rheum Flashcards

1
Q

What is osteoarthritis?

A

Breakdown of the joint cartilages due to wear and tear meaning the bones rub together. This presents with pain and stiffness in the joints

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2
Q

What joints are commonly affected by osteoarthritis?

A

Hips, knees, sacro-iliac joints, hands ( DIP and CMC), wrists, lumbar spine, cervical spine (cervical spondylosis)

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3
Q

What are the X-ray signs of osteoarthritis?

A

(L)oss of joint space
(O)steophytes (bony spurs)
(S)ubarticular sclerosis (increased bone density)
(S)ubcondral cysts (fluid filled holes in the bone)

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4
Q

What are risk factors for osteoarthritis?

A 
Obesity
old age
occupation (e.g. manual labour)
trauma
family history
female
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5
Q

What are the common symptoms of osteoarthritis?

A
  • Stiffness in joint (commonly unilateral)- generally worse with movement and at the end of the day
  • Pain in joint
  • Crepitus / grinding
  • Restricted range of movement
  • joint effusions
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6
Q

What signs in the hands indicate osteoarthritis?

A 
Heberden's nodes (DIP joint swelling)
Bouchards nodes (PIP joint swelling)
Squaring at the base of the thumb (carpometacarpal joint)
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7
Q

How is osteoarthritis managed?

A 
Weight loss
Physiotherapy
Occupational therapy
Analgesia (paracetamol, NSAIDS, opiates)
Steroid injections (only work temporarily)
Joint replacement
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8
Q

What is often co prescribed with an NSAID and why?

A

A proton pump inhibitor such as lansoprazole to decrease risk of gastritis and peptic ulcers.

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9
Q

What are some side effects of NSAIDS?

A

GI side effects - gastritis and peptic ulcers
Renal - AKI
Cardio - hypertension, heart failure, MI
Exacerbates asthma

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10
Q

What is rheumatoid arthritis?

A

Autoimmune condition causing chronic inflammation of the synovial lining of joints, tendons and bursa. It is normally symmetrical and affects multiple joints

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11
Q

What are risk factors for rheumatoid arthritis?

A
  • smoking
  • obesity
  • female
  • family history
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12
Q

What is the most common gene associated with rheumatoid arthritis?

A

HLA DR4

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13
Q

What antibodies can be tested for that indicate rheumatoid arthritis?

A

Anti - CCP (cyclic citrullinated peptide)

Rheumatoid factor

Rheumatoid factor

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14
Q

How does rheumatoid arthritis typically present?

A
  • Symmetrical joint pain, swelling and stiffness
  • Is normally worse in the mornings >30 mins and improves with activity
  • Systemic systems such as fatigue, weight loss, muscle aches
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15
Q

What joints are commonly affected by rheumatoid arthritis?

A

Small joints of the hands and feet (MCP , PIP, MTP)
Wrists and ankles
Cervical spine
Can also affect large joints such as the knees, hips and shoulders

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16
Q

What signs in the hands indicate rheumatoid arthritis?

A

Swan neck deformity
Boutonnieres deformity
Ulnar deviation of the knuckles
Z shaped deformity of the thumb

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17
Q

What is felty’s syndrome?

A

Rheumatoid arthritis, neutropenia and splenomegaly

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18
Q

What are the X-ray changes seen in rheumatoid arthritis?

A

Joint deformity
Bony marginal erosions
Soft tissue swelling
Periarticular osteopenia

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19
Q

What are some extra-articular manifestations of RA?

A
  • pulmonary fibrosis
  • felty’s syndrome ( RA, neutropenia and splenomegaly)
  • Sjogrens syndrome
  • Anaemia of chronic disease
  • CVD
  • eye conditions
  • rheumatoid nodules
  • lymphadenopathy
  • amyloidosis
  • bronchilolitis obliterans
  • caplan syndrome (pulmonary nodules if exposed to coal, silica or asbestos)
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20
Q

What investigations are done to diagnose rheumatoid arthritis?

A
  • antibodies - rheumatoid factor and anti-CCP
  • inflammatory markers - CRP and ESR
  • X-rays
  • ultrasound / MRI for synovitis
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21
Q

What scoring system is used to monitor RA?

A

DAS28 (disease activity score)

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22
Q

What is the management for rheumatoid arthritis?

A
  • DMARDs (disease modifying anti-rheumatic drugs) such as methotrexate or sulfasalazine.
  • Steroids can be used in flare ups.
  • If still not controlled can add other medications - biologics - such as a TNF inhibitor (infliximab) or rituximab.
  • surgery if severe disease
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23
Q

What are the risks of using biological therapies such as infliximab or rituximab?

A

Cause immunosuppression

Can cause reactivation of dormant infections (e.g. TB and Hep B)

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24
Q

What is osteoporosis?

A

Reduction in mineral density of bones, reducing strength and making them more prone to fractures.

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25
Q

What are the risk factors for osteoporosis?

A 
Old age
Female (particularly post menopause)
Reduced mobility and activity
Low BMI (<18.5)
Rheumatoid arthritis
Alcohol and smoking
Certain medications (long term corticosteroids, PPIs, anti-epileptics, SSRIs etc.)
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26
Q

Why are post menopausal women at a higher risk of osteoporosis?

A

Oestrogen is protective against osteoporosis. Levels of oestrogen fall post menopause.

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27
Q

How is bone mineral density measured?

A

Using a DEXA scan.

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28
Q

What is the difference between osteopenia and osteoporosis?

A

Osteopenia is a less severe reduction in bone density than osteoporosis

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29
Q

How is osteoporosis managed?

A 
Activity and exercise
Maintain a healthy weight
Adequate calcium and vitamin D intake
Avoid falls
Stop smoking and reduce alcohol consumption
Medications - bisphosphonates 
Hormone replacement therapy if suitable
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30
Q

How to bisphosphonates work for osteoporosis?

A

Reduce osteoclasts activity, present reabsorption (breakdown) or the bone.

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31
Q

What are some key side effects of bisphosphonates?

A

GORD (reflux)
Atypical fractures
Osteonecrosis (of jaw or external auditory canal)

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32
Q

What is an example of a bisphosphonate?

A

Alendroate
Risedronate
Zoledronic acid

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33
Q

What is gout?

A

A condition where excess uric acid causes urate crystals to be deposited in the joint causing it to become acutely hot, swollen and painful.

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34
Q

What are gouty tophi?

A

Subcutaneous uric acid crystals - typically seen on hands, elbows and ears.

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35
Q

What is an important differential to gout?

A

Septic arthritis

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36
Q

What joints are most commonly affected by gout?

A

Hands
Base of thumb (CMC) / big toe (MTP)
Wrists
But can also affect bigger joints such as the knee and ankle.

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37
Q

What are some risk factors for gout?

A 
Male
Obesity
High purine diet (meat and seafood)
Alcohol 
Diuretics (particularly thiazide)
CVD or kidney diseases
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38
Q

How is gout diagnosed?

A

Joint aspiration - will show urate crystals.
These are needle shaped and negatively birefringent of polarised light.

Joint X-RAY

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39
Q

What are the XRAY changed seen in gout?

A
  • joint space is often maintained
  • lytic lesions
  • punches out erosions with sclerotic borners and overhanging edges
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40
Q

How is an acute flare up of gout managed?

A

1st line - NSAIDs (co prescribe with PPI)
2nd line - colchicine (used if patient has CKD or heart disease)
3rd line - oral steroids (prednisolone)

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41
Q

What is the prophylaxis for gout?

A

Allopurinol - works to reduce uric acid levels. Ensure to start this after the initial flare has been managed.

Lifestyle changes - losing weight, keeping hydrated, reduce alcohol consumption and eating less purine backed foods (meat and seafood)

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42
Q

What is sciatica?

A

Irritation of the sciatic nerve.

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43
Q

What are the symptoms of sciatica?

A

Unilateral pain (shooting) from the buttock radiating to the back of the thigh to the knee or foot.
Pins and needles
Motor weakness
Lower back pain

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44
Q

What is bilateral sciatica a red flag of?

A

Cauda equina syndrome

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45
Q

What nerve roots make up the sciatic nerve?

A

L4 - S3

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46
Q

What are the main causes of sciatica?

A

Lumbrosacral nerve compression due to

  • herniated disc
  • spondylolisthesis
  • spinal stenosis
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47
Q

What is spondylolisthesis?

A

Anterior displacement of a vertebrae compared to the one below.

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48
Q

What cancers commonly metastasise to bones?

A 
Prostate
Renal
Thyroid
Breast 
Lung 
(Spells out PoRTaBLe)
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49
Q

What are causes of mechanical back pain?

A 
Muscle or ligament sprain
Facet or sacroiliac joint dislocation 
Herniated disc
Spondylolisthesis 
Scoliosis 
Degenerative changes (arthritis)
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50
Q

How is mechanical back pain managed?

A

Analgesia - normally NSAIDs
Stay active - mobilising the spine
Improve posture
Physiotherapist

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51
Q

How is sciatica managed?

A 
Neuropathic meds - amytriptyline or duloxetine
If severe and chronic:
- Epidural corticosteroid injections
- local anaesthetic injections
- spinal decompression
52
Q

What is bursitis?

A

Inflammation of the bursa which are fluid filled sacs that cushion the joints.

53
Q

What are the symptoms of bursitis?

A 
Dull, achy pain
tenderness
warm around the joint
redness
swelling
54
Q

How is bursitis managed?

A

Rest
Ice
Painkillers - iBuprofen or paracetamol
If caused by an infection give antibiotics
Steroid injection may be used to reduce swelling
If severe may need to be surgically drained

55
Q

How can bursitis be prevented?

A

Maintain a healthy body weight
keep any cuts clean to decrease risk of infections
Warm up before exercise
Use joint pads/cushioning
Take regular breaks from activities such as kneeling

56
Q

What can cause bursitis?

A

Friction from repetitive movements
Trauma
Inflammatory conditions
Infection (septic bursitis)

57
Q

What is psoriatic arthritis?

A

inflammatory arthritis associated with psoriasis.

58
Q

What are some signs that may indicate psoriatic arthritis?

A

Plaques of psoriasis on skin (dry, scaly areas)
Pitting of the nails
Onycholysis (separation of the nail from the nail bed)
Dactylitis (inflammation of the full finger)
Enthesitis (inflammation where the tendons insert into the bone)

59
Q

What tool can be used to screen for psoriatic arthritis?

A

PEST tool (psoriasis epidemiological screening tool)

60
Q

How can psoriatic arthritis be managed?

A

NSAIDs
DMARDs - e.g. methotrexate
Anti TNF - e.g. infliximab

61
Q

What is ankylosing spondylitis?

A

An inflammatory condition affecting the spine that causes progressive stiffness and pain. It can lead to fusion of the spine. It is related to a HLA B27 gene.

62
Q

What are the key joints affect ankylosing spondylitis?

A

Sacroiliac joints

Vertebral column

63
Q

How does ankylosing spondylitis present?

A

Commonly presents in young adults - particularly males.
Lower back pain and stiffness
Sacroiliac pain in the buttock
This pain is worse with rest (and at night) and improves on movement
‘Bamboo spine’ due to fusion of the spine

64
Q

What is Schober’s test used for?

A

It is used to assess mobility of the spine.

65
Q

How can ankylosis spondylitis be managed?

A 
Physiotherapy and exercise
Avoid smoking
NSAIDs
Steroids
Anti TNF - e.g. infliximab
Surgery is sometimes needed for certain deformities
66
Q

What is Osgood-Schlatters disease?

A

A condition that occurs during the growth spurt of puberty that causes pain and swelling below the knee joint anteriorly where the patellar tendon attaches to the tibia.

67
Q

What causes Osgood-Schlatters disease?

A

Repetitive movements such as jumping and running

Growth spurt

68
Q

What are the symptoms of Osgood-Schlatters disease?

A

Pain and swelling below the knee anteriorly - normally unilateral. This is worse on exercising.
Tender
Limp may be present

69
Q

What is Perthes disease?

A

A rare childhood (<10y.o) condition affecting the hip joint where blood supply is lost to the femoral head. This can cause pain in the groin/thigh/hip as well as stiffness. Often there is also a short stature.

70
Q

How is Osgood-Schlatters disease managed?

A

Reduce amount of physical activity
Ice
NSAIDS / pain relief
Stretching and physio may also be useful to strengthen the joint when the symptoms settle.

71
Q

What is pseudogout?

A

Crystal arthropathy caused by calcium pyrophosphate crystal deposition in the joints

72
Q

What are differentials for an acutely hot and swollen joint?

A

Septic arthritis
Reactive arthritis
Gout
Pseudogout

73
Q

What is another name for pseudogout?

A

Chondrocalcinosis

74
Q

What crystals are involved in pseudogout?

A

Calcium pyrophosphate

75
Q

How does pseudogout present?

A
  • often asymptomatic and picked up incidentally on xray
  • can be chronic pain and stiffness in multiple joints
  • can be an acutely, hot, swollen and stiff joint
76
Q

Which joints are most commonly affected by pseudogout?

A
  • knee
  • shoulders
  • hips
  • wrists
77
Q

How is pseudogout diagnosed?

A

** ensure to rule out septic arthritis**

  • joint fluid aspiration - shows calcium pyrophosphate crystals that are rhomboid shaped and are positively birefringent of polarised light
78
Q

What Xray changes are seen in pseudogout?

A
  • Chrondrocalcinosis - a thin white line of calcium deposit in the middle of the joint space
  • LOSS similarly to osteoarthritis.
79
Q

How is pseudogout managed?

A

Symptomatic management
- NSAIDs ( alongside PPI)
- colchicine
- intra-articular steroid injections
- Oral steroids

80
Q

What is osteomalacia?

A

Softening of the bones due to insufficient vitamin D causing defective bone mineralisation

81
Q

What causes osteomalacia?

A
  • Insufficient vitamin D (e.g. due to lack of sun exposure) means less calcium and phosphate is absorbed in the intestines and reabsorbed through the kidneys.
  • Calcium and phosphate are required for construction/ mineralisation of bone
  • low calcium = increased PTH = calcium resorption from the bones. Further worsening the bone mineralisation.
82
Q

What are risk factors for osteomalacia?

A
  • darker skin - need more prolonged sun exposure to generate vit D
  • low exposure to sunlight
  • living in colder environments
  • malabsorption disorders e.g. IBD
  • CKD
83
Q

How does osteomalacia present?

A
  • often asymptomatic
    Can have
  • fatigue
  • bone pain
  • muscle weakness
  • muscle aches
  • pathological or abnormal fractures
84
Q

What investigations are done for osteomalacia and what do they show?

A

Bloods
- serum vitamin D levels (low)
- serum calcium (low)
- phosphate (low)
- ALP (high)
- PTH (high)

XRAY- osteopenia
DEXA scan - low bone mineral density

85
Q

How is osteomalacia managed?

A
  • colecalciferol (Vitamin D3 replacement)
86
Q

What is the equivalent of osteomalacia in children?

A

Rickets

87
Q

What is the role of osteoclasts vs osteoblasts?

A
  • Osteoclasts - dissolve down old bone
  • Osteoblasts - build up new bone
88
Q

What is Paget’s disease of the bone?

A

Where there is excessive uncoordinated burn turnover leading to to patchy areas of sclerosis and lysis of the bones.
This causes misshapen bones, structural issues and increased risk of fractures.

89
Q

How does Paget’s disease of the bone present?

A
  • may be asymptomatic
  • bone pain
  • bone deformities
  • abnormal fractures
  • hearing loss (if affecting the bones in the ear)
90
Q

What are the XRAY findings in Paget’s disease of the bone?

A
  • bone enlargement and deformities
  • osteoporosis circumscripta ( well defined osteolyic lesions)
  • cotton wool appearance of the skull (poorly defined pathcy areas of increased and decreased density)
  • V shaped osteolytic defects in long bones
91
Q

How is Paget’s disease of the bone managed?

A
  • bisphosphoantes
  • analgesia for bone pain
92
Q

What are some of the complications of Paget’s disease of the bone?

A
  • hearing loss
  • heart failure (due to hypervascularity of abnormal bone)
  • increased risk of osteosarcoma
  • spinal stenosis + spinal cord compression
93
Q

What is Behcet’s disease?

A

Complex inflammatory condition affecting blood vessels and tissues that causes reccurent oral and genital ulcers alongside other symptoms.

94
Q

What gene is associated with Behcet’s disease?

A

HLA B51

95
Q

What are some differentials for mouth ulcers?

A
  • simple aphthlous ulcers
  • squamous cell carcinoma
  • herpes simplex virus
  • hand, foot and mouth disease
  • IBD
  • Coeliac disease
  • connective tissue disorders (e.g. RA, SLE)
  • vitamin deficiencies (iron, B12, folate, vit D)
  • HIV
  • Behcet’s disease
96
Q

What are the features of Behcet’s disease?

A
  • oral ulcers > 3 times a year.
  • gentical ulcers

Can affect many other organs
- skin - erythema nodosum
- eyes - e.g. uveitis, retinal artery or vein thrombosis
- MSK pain
- GI ulceration
- arterial aneurysms
- venous abnormalities - e.g. DVT

97
Q

How is behcet’s disease managed?

A
  • topical steroids
  • systemic steroids
  • topical anaesthetics (e.g. lidocaine)
  • immunosupressants
  • biologic therapies
98
Q

What is systemic lupus erythematosus (SLE)?

A
  • a multi-systemic chronic autoimmune disease that follows a relapsing-remitting course
  • causes a variety of symptoms as affects multiple organs and systems in the body
99
Q

Who is most commonly affected by SLE?

A
  • females
  • onset in 20s/30s
  • ethnicity - more common in afro-carribean and asian origin
100
Q

What can trigger SLE flares?

A
  • exposure to oestrogen (e.g. contraception, pregnancy)
  • overexposure to UV light / sun
  • infections
  • stress
  • certain medications
101
Q

How can SLE present?

A
  • fatigue
  • weight loss
  • skin changes - photosensitive malar rash
  • arthralgia / myalgia
  • fever
  • lymphadenopathy
  • splenomegaly
  • SOB
  • pleuritis
  • pericarditis
  • mouth ulcers
  • hair loss
  • raynauds
  • oedema due to nephritis
102
Q

What are some dermatological features that can be present in SLE?

A
  • photosensitivity
  • malar (butterfly shaped rash across the cheeks)
  • discoid rash (round, raised plaques)
  • recurrent mouth ulcers
  • nonscarring alopecia
103
Q

What investigations can be done for SLE and what can these show?

A
  • Autoantibody tests - looking for anti-nuclear antibodies and anti-double stranded DNA.
  • FBC - may show anaemia, thrombocytopenia and leucopenia
  • CRP and ESR may be raised with active inflammation
  • C3 and C4 may be decreased
  • Urinalysis - proteinuria in lupus nephritis
  • renal biopsy can also be done to investigate for renal nephritis
104
Q

What autoantibodies are associated with SLE?

A
  • Anti-nuclear antibodies (ANA) - most sensitive but not specific
  • Anti-double stranded DNA (anti-dsDNA) - highly specific
105
Q

What can be used for monitoring disease activity in SLE?

A
  • Anti-double stranded DNA antibodies - if present - levels vary with disease activity
  • CRP and ESR can also be used
106
Q

What are some complications of SLE?

A
  • cardiovascular disease - chronic inflammation in blood vessels = hypertension and coronary artery disease
  • infections
  • anaemia
  • pericarditis
  • pleuritis
  • interstitial lung disease that can progress into pulmonary fibrosis
  • neurological - seizures, psychosis
  • lupus nephritis
  • recurrent miscarriage
  • antiphospholipid syndrome secondary to SLE
107
Q

How is SLE managed?

A
  • avoid triggers where possible - e.g. sunscreen, immunisations

First options:
- hydroxychloroquine
- NSAIDs
- steroids

  • DMARDs
  • biologics - e.g. rituximab
108
Q

What is antiphospholipid syndrome?

A

An autoimmune disorder where elevated antiphopholipid antibodies cause inflammation and increased risk of thrombosis

109
Q

What are the specific antiphospholipid antibodies?

A
  • lupus anticoagulant
  • anticardiolipin antibodies
  • anti-beta-2 glycoprotein 1 antibodies
110
Q

What are the main features of antiphospholipid syndrome?

A

CLOT mneumonic

Clots - VTE (CVT/PE) or arterial (MI/stroke)
Livedo reticularis (mottled, lace like appearance of the skin)
Obstetric loss - recurrent miscarriages
Thrombocytopenia

111
Q

How is antiphospholipid syndrome managed?

A

Long term warfarin with a target INR or 2-3.

In pregnancy - LMWH and aspirin

112
Q

What other condition is antiphospholipid syndrome commonly associated with?

A

Systemic lupus erythematosis

113
Q

What is Sjogren’s syndrome?

A

An autoimmune condition affecting the exocrine glands - mostly lacrimal and salivary glands - causing dry mouth, eyes and vagina.

114
Q

What are the symptoms of Sjogren’s syndrome?

A
  • dry mouth
  • dry eyes
  • dry vagina / dyspareunia
  • dry skin
  • joint pain and stiffness
115
Q

What antibodies are associated with Sjogrens?

A

Anti-Ro
Anti-La

116
Q

What test can be done to test for Sjogrens and what does this involve?

A

Schirmer test - involves inserting folded filter paper under the lower eyelide. Look at the distance of moisture along the paper after 5 mins. Less than 10mm is significant (healthy is around 15mm)

117
Q

How is sjogrens syndrome managed?

A
  • artificial tears
  • artificial saliva
  • vaginal lubricants
  • oral pilocarpine can be used to stimulate tear and saliva production
118
Q

What are some complications of Sjogrens?

A
  • eye problems - keratoconjunctivitis + corneal ulcers
  • oral problems - cavities and candida infections
  • vaginal problems - candida infections and sexual dysfunction
119
Q

What is another name for giant cell arteritis?

A

Temporal arteritis

120
Q

What is giant cell arteritis?

A

Systemic vasculitis affecting medium and large arteries.

121
Q

What condition is strongly associated with giant cell arteritis?

A

Polymyalgia rheumatica

122
Q

How does giant cell arteritis present?

A
  • unilateral headache - severe around the temple and forehead
  • scalp tenderness
  • jaw claudication
  • blurred or double vision
  • loss of vision if untreated
  • may also have features of PMR - shoulder and pelvic pain
123
Q

How is giant cell arteritis diagnosed?

A
  • clinical presentation
  • raised inflammatory markets
  • temporal artery biopsy
124
Q

How is giant cell arteritis managed?

A

Immediately start high dose steroids
- 40-60mg oral pred is no visual symptoms
- 500-1000mg IV methylpred if visual symptoms

  • aspirin 75mg
  • bisphosphonates and PPIs should be co prescribed
125
Q

What are some complications of giant cell arteritis?

A
  • visual loss
  • stroke
  • steroid related complications

Year 3 - primary care + medicine (20 decks)

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