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Phase 2A > MSK + Rheumatology > Flashcards

MSK + Rheumatology Flashcards

1
Q

What is osteoarthritis?

A

Degenerative joint disorder involving the entire joint and characterised by joint pain, stiffness and functional limitation.

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2
Q

What is the aetiology of osteoarthritis?

A

result of mechanical and biological events which destabilise the normal process of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix, and subchondral bone

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3
Q

What are the risk fators osteoarthritis?

A

obesity
age
occupation
trauma
being female
family history

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4
Q

What is the pathophysiology of osteoarthritis?

A

Imbalanced cartilage breakdown > repair; ↑chondrocyte metalloproteinase secretion
Bone attempts to overcome this w/ T1 collagen; abnormal bony growths (osteophytes)

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5
Q

What are the key presentations of osteoarthritis?

A

Joint pain
Stiffness
Deformity, instability and reduced joint function
Heberden nodes (affects DIP joints)

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6
Q

What are the investigations for osteoarthritis?

A

NICE suggests that diagnosis can be made without any investigations if the patient is >45yrs, has typical activity related pain and no morning stiffness or stiffness lasting less than 30 minutes

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7
Q

What are the XR signs for osteoarthritis?

A

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

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8
Q

What are some differentials for osteoarthritis?

A

Bursitis
Gout
Pseudogout

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9
Q

What is the management for osteoarthritis?

A

Pt education and lifestyle advice
Physiotherapy and occupational therapy +/- orthotics
Analgesia for symptomatic relief:
Oral paracetamol and topical NSAIDs
Add oral NSAIDs and consider also prescribing a PPI
Consider opiates such as codeine and morphine
Intra articular steroid injections provide temporary inflammation and pain reduction
Joint replacement in severe cases

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10
Q

What are the most commonly affected joints in osteoarthritis?

A

hips, knees, sacro-iliac joints, distal-interphalangeal joints in the hands (DIPs), carpo-metacarpal joint at the base of the thumb, wrist, cervical spine

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11
Q

What is rheumatoid arthritis?

A

autoimmune condition causing chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa

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12
Q

What is the epidemiology of RA?

A

3 times more common in women than men
Affects around 1% of the population
Most common inflammatory arthritis seen by physicians

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13
Q

What are the risk factors for RA?

A

Age 30-50 yrs
Female
FHx
Smoking

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14
Q

What is the pathophysiology of RA?

A

arginine –> citrulline mutation in T2 collagen => anti-CCP formation
IFN-a causes further pro-inflammatory recruitment to synovium
- synovial lining expands and tumour -like mass (pannus) grows past joint margins
- pannus destroys subchondral bone + articular cartilage

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15
Q

What are the key presentations of RA?

A

symmetrical distal polyarthopathy
key symptoms: pain, swelling, stiffness of the joint (often worse in the morning and eases as day goes on)

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16
Q

What are some signs of RA?

A

Swan neck deformity
Boutonniere’s deformity (flexion at PIP joint)
Ulnar deviation
Rheumatoid nodules
Vasculitic lesion

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17
Q

What are some associated symptoms of RA?

A

fatigue, weight loss, flu-like illness, muscle aches and weakness

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18
Q

What are the investigations for RA?

A

Usually clinically diagnosed
Bloods = ↑ESR/CRP, normocytic normochromic anaemia (mc as can also cause microcytic and macrocytic)
Serology = +ve anti-CCP (80% specific), +ve RF (70% non-specific)
Radiographs
ultrasonography

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19
Q

What are the XR signs of RA?

A

LESS
Loss of joint space
Eroded bone
Soft tissue swelling
Soft bones (osteoporosis)

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20
Q

What are some differentials for RA?

A

Psoriatic arthritis
infectious arthritis
Gout
SLE
Osteoarthritis

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21
Q

What is the management of RA?

A

Short course of steroids at first presentation and during flare-ups to settle disease
DMARD (disease modifying antirheumatic drugs)- methotrexate
NSAID analgesia
Intra-articular steroid injection if very painful
Biologics 1st line- TNF-a inhibitor (infliximab
2nd line - B cell inhibitor - Rituximab

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22
Q

What are the commonly affected joints in RA?

A

the small joints of the hands and feet, the wrist, ankle, MCP and PIP

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23
Q

What are the extra-articular effects of RA?

A

lungs (PE, pulmonary fibrosis), heart (↑IHD risk), eyes (episcleritis, keratoconjunctivitis sicca), spinal cord compression, kidney (CKD), rheumatoid skin nodules

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24
Q

What is gout

A

Type of crystal arthropathy associated with chronically high blood uric acid levels

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25
Q

What is the aetiology of gout?

A

Urate crystals are deposited in the joint causing it to become hot, swollen and painful

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26
Q

What are the risk factors for gout?

A

Male
Obesity
High purine diet (meat and seafood)
Alcohol diuretics
Existing cardiovascular or kidney disease
Family history

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27
Q

What is the pathophysiology of gout?

A

↑uric acid/CKD –> impaired excretion of uric acid –> monosodium urate

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28
Q

What are the 4 clinical phases of gout when left untreated?

A

asymptomatic

hyperuricaemia - uric acid is building up in the blood and starting to form crystals around joints

acute/recurrent gout - symptoms start to occur, causing a painful gout attack

inter-critical gout - periods of remission between gout attacks

chronic tophaceous gout - frequent gout pain and tophi form in jointsf

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29
Q

What are the key presentations of gout?

A

Monoarticular and typically big toe
Sudden onset, severe swollen big toe - can’t put weight on it!

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30
Q

What are the investigations for gout?

A

can be diagnosed clinically or using joint fluid aspirate (no bacteria + needle shape crystals, negatively birefringent of polarised light, monosodium urate crystals)

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31
Q

What is the management for gout

A

Diet changes - ↓purines, ↑dairy
NSAIDs then consider colchicine, then steroid injection
prevention : allopurinol (xanthine oxidase inhibitor)

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32
Q

Which joints are most commonly affected by gout?

A

Most commonly seen in the metatarsophalangeal joints (base of big toe), wrists and carpometacarpal joints (base of thumb)

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33
Q

What is pseudogout?

A

calcium pyrophosphate crystals deposit along joint capsule
Also known as chondrocalcinosis

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34
Q

What are the risk factors for pseudogout?

A

Elderly females (70+)
Diabetes
Metabolic diseases
osteoarthritis

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35
Q

What are the key presentations for pseudogout?

A

Often polyarticular with knee commonly involved
Swollen hot red joint

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36
Q

What are the investigations for pseudogout?

A

Joint aspiration + polarised light → +vely birefringent, rhomboid shaped crystals

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37
Q

What are the XR signs for pseudogout?

A

chondrocalcinosis (thin white line in the middle of joint space caused by calcium deposition)
+ LOSS

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38
Q

What is the management for pseudogout?

A

Only acute management - NSAIDS, then colchicine, then steroid injection (no prevention drug here)

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39
Q

What is osteoporosis?

A

reduced bone density

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40
Q

What is osteopenia

A

reduction in bone density like osteoporosis but less severe

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41
Q

What are the risk factors for osteoporosis?

A

Steroids
Hypothyroid/hyperparathyroid
Alcohol + smoking
Thin (↓BMI)
Testosterone↓
Early menopause (↓oestrogen)
Renal /liver failure
Erosive + inflammatory disease
DMT1 or malabsorption

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42
Q

What are the key presentations of osteoporosis?

A

Fractures (proximal femur (falls), Colles’ forked wrist; fall on outstretched wrist), compression vertebral crush (may cause kyphosis))

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43
Q

What are the investigations for osteoporosis?

A

DEXA scan (produces T score 1<T≤2.5)
FRAX score

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44
Q

What is the management for osteoporosis?

A

Bisphosphonates (alendronate, risedronate, inhibit RANK-L signalling —> osteoclast inhibition)
mAB denosumab (inhibit RANK-L)
HRT - oestrogen, testosterone
Oestrogen receptor modulator -raloxifene
Recombinant PTH - teraparatide

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45
Q

What does direct inoculation mean in osteomyelitis?

A

When trauma or surgery results in direct access for polymicrobial or monomicrobial infection

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46
Q

What is contiguous spread in osteopmyelitis?

A

When infection spreads from adjacent soft tissues and joints
- can be poly or monomicrobial
- most common in older adults with DM, chronic ulcers, vascular disease, arthroplasties

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47
Q

What is haematogenous seeding in osteomyelitis?

A

Infection caused by bacterial seeding from the blood
- Most common in long bones in children and vertebrae in adults
- monomicrobial

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48
Q

What is gonococcal arthritis?

A

joint inflammation which occurs with disseminated gonococcal infection
Sx: fever, arthritis, tenosynovitis, maculopapular rash

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49
Q

What is osteomalacia?

A

defective bone mineralisation resulting from insufficient vitamin D and causing “soft” bones

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50
Q

What is the prevalence of osteomalacia?

A

2%

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51
Q

What are the causes of osteomalacia?

A

Hypoparathyroidsim (↑Ca2+ release from bone –> less available for mineral formation)
Vitamin D deficiency (malabsorption/reduced intake/poor sunlight)
CKD/renal failure (↓active vit D production (25-dihydroxyvitamin D → 1,25-dihydroxyvitamin D))
Liver failure (↓reaction in vit D pathway (cholecalciferol → 25-hydroxyvitamin D)
Anticonvulsant drugs (↑CYP450 metabolism of vit D)

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52
Q

What are the risk factors for osteomalacia?

A

Decreased sunlight to skin exposure.
Diet.
Dark skin.
Obesity.
Elderly.
Medications that may precipitate vitamin D deficiency.
Renal or hepatic disease.
Malabsorptive syndromes.

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53
Q

What is the pathophysiology of osteomalacia?

A

inadequate vitamin D leads to a lack of calcium and phosphate in the blood which are required for the constriction of bone
low levels result in defective bone mineralisation

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54
Q

What are the key presentations of osteomalacia?

A

Fatigue
Bone pain
Muscle weakness
Muscle aches
Pathological or abnormal fractures
Difficulty weight bearing
Can be asymptomatic

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55
Q

What are the investigations for osteomalacia?

A

Bloods (hypocalcemia, ↑PTH, ↓serum Ca2+, ↓25(OH) vitamin D
BM biopsy - incomplete mineralisation (GS)
XR = looser zones (defective mineralisation)

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56
Q

What is the management for osteomalacia?

A

Vitamin D replacement (colecalciferol) + ↑dietary intake (D3 tablets, eggs)

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57
Q

What percentage of women over 50 yrs old will have a fracture due to osteoporosis?

A

50%

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58
Q

What percentage of men over the age of 50 will have fractures due to osteoporosis?

A

1/5

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59
Q

What is Paget’s disease?

A

Excessive bone turnover due to uncoordinated excessive activity of both osteoblasts and osteoclasts leading to patchy areas of high and low density bone.

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60
Q

What are the key presentations of Paget’s?

A

Pain in bone
Arthralgia
Nerve compression/neural deafness
Increased bone density
Cardiac failure
Skull or vertebral sclerosis

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61
Q

What are the x-ray findings of Paget’s?

A

Bone enlargement and deformity
Osteoporosis circumscripta (well defined less-dense lesions of bone)
Cotton wool appearance of the skull (poorly denied patchy areas of sclerosis and lysis)
V-shaped defects in the long bones (osteolytic v-shaped lesions

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62
Q

What are the investigations for Paget’s disease?

A

Bloods (↑ALP, normal Ca2+ and phosphate)
X-ray

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63
Q

What is the management for Paget’s disease?

A

Bisphosphonates
NSAIDs for bone pain
VItamin D + Calcium supplements

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64
Q

What are the key complications of Paget’s disease?

A

Osteogenic sarcoma (severe bone cancer)
Spinal stenosis and spinal cord compression (spinal canal narrowing which can compress spinal nerves)

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65
Q

What is fibromyalgia?

A

Chronic widespread musculoskeletal pain for 3+ months with all other causes ruled out

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66
Q

What is the prevalence of fibromyalgia?

A

Prevalence = 0.5-5%

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67
Q

What are the risk factors for fibromyalgia?

A

Females
Depression
Stress
20-60 yrs
FHx

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68
Q

What is the pathophysiology of fibromyalgia?

A

The primary pathology in fibromyalgia is in the CNS and involves pain and/or sensory amplification
A hallmark of these conditions is diffuse hyperalgesia (increased pain in response to normally painful stimuli) and/or allodynia (pain in response to normally non-painful stimuli)

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69
Q

What are the key presentations of fibromyalgia?

A

Chronic pain
Diffuse tenderness on exam
Fatigue unrelieved by rest
Sleep disturbance
Mood disturbance
Cognitive dysfunction
Headaches
Numbness /tingling sensations
Stiffness
Sensitivity to sensory stimuli such as bright lights, odours, noises

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70
Q

What are the investigations for fibromyalgia?

A

Clinical diagnosis - all other possible causes ruled out

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71
Q

What are the differentials for fibromyalgia?

A

Polymyalgia Rheumatica = large cell vasculitis presenting as chronic pain syndrome (↑ESR+CRP is diagnostic and treatment is prednisolone)
Myofascial pain syndrome
Chronic fatigue syndrome
Rheumatoid arthritis
Vitamin D deficiency

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72
Q

What is the management for fibromyalgia

A

Education + physiotherapy
Antidepressant for severe neuropathic pain (e.g. TCAs; amitriptyline) + CBT

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73
Q

What is Sjogren’s syndrome?

A

Chronic inflammatory and autoimmune exocrine disorder characterised by diminished lacrimal and salivary gland secretion

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74
Q

What are the risk factors for Sjogren’s?

A

Females
40-50 yrs
FHx
HLA B8/DR3
SLE
Rheumatoid arthritis
Systemic sclerosis

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75
Q

What are the key presentations for Sjogren’s?

A

Dry eyes (keratoconjunctivitis sicca)
Mouth (xerostoma)
Vagina
Fatigue

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76
Q

What are the investigations for Sjogren’s?

A

serology (anti-RO, anti LA, ANA +ve)
schirmer test +ve (induce tears and place filter under eyes, tears travel <10mm)

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77
Q

What is the management for Sjogren’s?

A

artificial tears, saliva + lubricant for sexual activity
*sometimes hydroxychloroquine given

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78
Q

What is SLE?

A

Systemic Lupus Erythematosus is autoimmune systemic inflammation due to hypersensitivity type 3 reaction

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79
Q

What is the epidemiology of SLE?

A

25 in 100,000
most commonly seen in females age 20-40 yrs

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80
Q

what are the risk factors for SLE?

A

Female
HLA B8/DR2/DR3
C4 A null allele
Drugs (e.g. isoniazid, procainamide)
Afro-caribbean descent
Sun exposure
Smoking
FHx

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81
Q

What is the pathophysiology of SLE?

A

Impaired apoptotic debris presented to TH2 → B cell activation → antigen-antibody complexes
Antinuclear antibodies cause the immune system to target proteins within the person’s cell nuclei resulting in an inflammatory response and tissue damage

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82
Q

What are the key presentations of SLE?

A

Butterfly rash + photosensitivity
Glomerulonephritis
Seizures + psychosis
Mouth ulcers
Fatigue
Weight loss

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83
Q

What are some other symptoms of SLE?

A

Serositis
Anaemia
Hair loss
Lymphadenopathy and splenomegaly
Joint pain, myalgia, Raynaud’s, pyrexia

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84
Q

What are the investigations for SLE?

A

FBC
C3 + C4 levels (decreased)
Raised CRP/ESR
Immunoglobulins
Urinalysis - hematuria +++, proteinuria ++
Renal biopsy
(GS) Autoantibodies - anti-dsDNA (specific to SLE, 70% of pts have), ANA (less specific but 85% pts have) + anti-RO, anti-SM, anti-LA

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85
Q

What is the management for SLE?

A

Lifestyle (↓sunlight + stop triggering drugs)
Corticosteroids (main) - prednisolone
Hydroxychloroquine
NSAIDs
Azathioprine if severe

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86
Q

What are the complications for SLE?

A

CVD, infection, anaemia of chronic disease, pericarditis, pleuritis, interstitial lung disease

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87
Q

What is antiphospholipid syndrome?

A

Persistent antiphospholipid antibodies resulting in a variety of clinical features characterised by thromboses and pregnancy-related morbidity.

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88
Q

What are the risk factors for antiphospholipid syndrome?

A

Systemic lupus erythematosus
Autoimmune rheumatological disorders (Sjogren syndrome, rheumatoid arthritis, systemic sclerosis)
Other autoimmune disease (e.g. hypo-/hyperthyroidism, pernicious anaemia, coeliac disease)

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89
Q

What are the key presentations of antiphospholipid syndrome?

A

CLOTS
Coagulopathy
Livedo reticularis
Obstetric issues - miscarriages, stillbirth, preeclampsia
Thrombocytopenia
↑risk of arteria (stroke, MI)l + venous thrombosis (DVT, PE)

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90
Q

What is the diagnostic history for antiphospholipid syndrome

A

Hx of thrombosis or pregnancy complication plus persistent antibodies as above

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91
Q

What is the management for antiphospholipid syndrome?

A

Long term warfarin
Low molecular weight heparin plus aspirin for pregnant women

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3
4
5
Perfectly
92
Q

What is systemic sclerosis?

A

autoimmune connective tissue disorder which causes damage to the small arteries, arterioles and capillaries due to excess collagen production which leads to thickening and tightening of the skin

93
Q

What is the pathophysiology of scleroderma?

A

hardening of the skin leading to shiny tight skin without normal skin folds

94
Q

WHat are the key presentations of scleroderma?

A

CREST
Calcinosis (Ca deposits in SC tissue) → renal failure
Raynaud’s →digit ischemia due to sudden vasospasm, often precipitated by cold, relieved with heat
Esophageal dysmotility/strictures → GI symptoms
Sclerodactyly (local skin thickening or tightening on fingers/toes) → movement restriction
Telangiectasia (spider veins) → risk of pulmonary hypertension

95
Q

WHat are the investigations for scleroderma?

A

Antibodies - ANA (+ve in most patients but not specific), Anti-centromere
Nailfold capillaroscopy

DIagnosis is based on classification criteria from ACR and EULAR (2013)

96
Q

What is the management for scleroderma?

A

No cure
Steroids and immunosuppressants
Treat symptoms (e.g. Raynaud - handwarmers, GI Sx - PPI)

97
Q

What is polymyositis/dermatomyositis?

A

Inflammation + necrosis of skeletal muscle, where skin involved = dermatomyositis

98
Q

Wha is the aetiology of Polymyositis/Dermatomyositis

A

can be caused by an underlying malignancy which makes them paraneoplastic syndromes
Common associated cancers are lung, breast, ovarian and gastric

99
Q

WHat are the risk factors for polymyositis/dermatomyositis?

A

female
HLA B8/DR3

100
Q

What are the key presentations of polymyositis/dermatomyostis?

A

Symmetrical wasting of shoulders + pelvic girdle (hard to stand from sitting, squat or put hands on head)
Muscle pain
Dermatomyositis - Gottron Papules (scales on knuckles), Heliotrope (purple eyelid), photosensitive erythematous rash, periorital oedema, subcutaneous calcinosis

101
Q

What are the investigations for polymyositis/dermatomyositis?

A

Creatinine kinase bloods (CK is raised)
Anti-Jo-1 + Anti-Mi-2 antibodies
Muscle fibre biopsy necrosis

102
Q

WHat is the management for polymyositis/dermatomyositis?

A

Bed rest + prednisolone
Immunosuppressive drugs

103
Q

What is polymyalgia rheumatica?

A

Inflammatory condition which causes pain and stiffness in the shoulders, pelvic girdle and neck

104
Q

What are the risk factors for polymyalgia rheumatica?

A

Older age (50+)
Female
Caucasian heritage
Strong association with GCA

105
Q

What are the key presentations of polymyalgia rheumatica?

A

Bilateral shoulder pain which can radiate to the elbow
Bilateral pelvic girdle pain
Worse on movement
Interferes with sleep
Stiffness for at least 45 mins in the morning

106
Q

What are the investigations for polymyalgia rheumatica?

A

Inflammatory markers (ESR, plasma viscosity and CRP) usually raised
FBC, U+Es, LFTS, calcium, etc. to exclude differentials
Based on clinical presentation and response to steroids

107
Q

What are some of the differential diagnoses for polymyalgia rheumatica?

A

Osteoarthritis, RA, SLE, myositis, cervical spondylosis

108
Q

What is the management for polymyalgia rheumatica?

A

Steroids: initially prednisolone 15mg per day, stopped if no response, can reduce if good response after 4 weeks

109
Q

What is osteomyelitis?

A

infection in the bone and bone marrow typically affects the metaphysis of the long bones

110
Q

What is the epidemiology of osteomyelitis?

A

10-100/100,000 p/y
Bimodal age distribution (children and older patients)

111
Q

What is the aetiology of osteomyelitis?

A

Most commonly caused by staphylococcus aureus.
Caused by salmonella in Sickle Cell patients
Can be introduced directly into the bone e.g. via an open fracture
Can also travel to the bone through the blood after entering the body via skin or gums etc.

112
Q

What are the risk factors for osteomyelitis?

A

ore common in boys and children under 10 yrs
Open bone fracture
Orthopaedic surgery
Immunocompromised
Sickle cell anaemia
HIV
Tuberculosis
IVDU
Diabetes
Peripheral vascular disease

113
Q

WHat is the difference between chronic and acute osteomyelitis?

A

Chronic = deep-seated, slow growing infection with slow development of symptoms
Acute = more rapid onset, particularly acutely unwell child

114
Q

WHat are the key presentations of osteomyelitis?

A

Refusing to use limb or weight bear
Dull bony pain
Swelling
Tenderness
Low grade fever
In acute can present with high fever

115
Q

What are the investigations for osteomyelitis?

A

XR
Bloods (raised CRP + ESR, WBCs)
Blood culture
Bone marrow aspiration or bone biopsy with histology and culture may be necessary
MRI (GS)

116
Q

What are the differential diagnoses for osteomyelitis?

A

Soft tissue infection
Charcto joint
Avascular necrosis of bone
Gout
Fracture
Bursitis
Malignancy

117
Q

What is the management for osteomyelitis?

A

Extensive antibiotic therapy (6 wks IV considered minimum)
may require surgery for drainage and debridement of the infected bone

118
Q

WHat is septic arthritis?

A

Infection within a joint which can affect native or prosthetic joints.
Emergency as infection can quickly destroy the joint and cause systemic illness
Mortality of around 10%

119
Q

What are the most common causative organisms of septic arthritis in native joints?

A

Staph aureus (RA/diabetes)
Streptococci
Neisseria gonorrhoea (young/sexually active, MSM)
Gram -ve bacilli (extremes of age, systemically unwell, IVDU) - E. coli, pseudomonas
Anaerobes
Mycobacterium + fungi (immunocompromised)

120
Q

What are the risk factors for septic arthritis?

A

Prosthetic joints
Immunocompromised
RA
DM
Extremes of age
IVDU
Underlying joint disease
Exposure to ticks

121
Q

What are the clinical manifestations of septic arthritis?

A

Painful, red, swollen, hot joint
Stop using joint (children)
Fever
90% monoarthritis
Most common in knees, hips and shoulders

122
Q

WHat are the investigations for septic arthritis?

A

Bloods (FBC, ESR, CRP), Blood culture
Fluid aspirate → culture
Plain x-ray, USS

123
Q

What are the differential diagnoses for septic arthritis?

A

Osteoarthritis
Psoriatic arthritis
Rheumatoid arthritis
Gout

124
Q

What is the management for septic arthritis?

A

Aspiration
Antibiotics (6wk min)
- Flucloxacillin + rifampicin often first line
- Vancomycin + rifampicin for penicillin allergy, MRSA or prosthetic joint
Joint washout
rest/splint/physio
Analgesia
Stop immunosuppression if poss

125
Q

What are the spondyloarthropathies?

A

chronic inflammatory disease which most commonly affect SI joints and the axial skeleton and are associated with the HLA B27 gene

126
Q

What are the features of spondyloarthropathies?

A

Sausage digit (dactylitis)
Psoriasis
Inflammatory back pain
NSAID – > good response
Enthesitis (heel)
Arthritis
Crohn’s/colitis/↑CRP
HLA B27
Eye (uveitis)

127
Q

What is ankylosing spondylitis?

A

Inflammatory arthritis mainly affecting the spine which is part of the seronegative spondyloarthropathy group of conditions linked to the HLA B27 gene.
Symptoms develop gradually

128
Q

What are the risk factors for ankylosing spondylitis?

A

FHx
Male
HLA B27
ERAP1 and IL23R genes

129
Q

What are the key joints affected in ankylosing spondylitis?

A

sacroiliac joints and the joints of the vertebral column

130
Q

What are the key presentations of ankylosing spondylitis?

A

Lower back pain and stiffness
Sacroiliac pain in buttock region
Pain + stiffness worse with rest (e.g. at night and in morning >30mins ) and improves with movement
Vertebral fractures (key complication)
Can fluctuate with flares of worsening symptoms

131
Q

What are the x-ray signs of ankylosing spondylitis?

A

Bamboo spine
Squaring of vertebral bodies
Subchondral sclerosis and erosions
Syndesmophytes
Ossification
Fusion of the facet, sacroiliac and costovertebral joints

132
Q

WHat the systemic symptoms of ankylosing spondylitis?

A

Weight loss + fatigue
Chest pain
Enthesitis (inflammation of where tendons/ligaments insert into bone)
Dactylitis (inflammation in finger or toe)
Anaemia
Anterior uveitis
Aortitis
Heart block
Restrictive lung disease
Pulmonary fibrosis
Inflammatory bowel disease

133
Q

What are the investigations for ankylosing spondylitis?

A

Schober’s test (find L5 vertebrae and mark points 10cm above and 5cm below point, ask patient to bend over as far as they can and measure distance between points) - <20cm distance supports diagnosis of AS
Inflammatory markers
HLA B27 genetic test
X-ray of spine and sacrum
MRI of spine

134
Q

What are some differential diagnoses for ankylosing spondylitis?

A

Osteoarthritis
Diffuse idiopathic skeletal hyperostosis
Psoriatic arthritis
Reactive arthritis

135
Q

What is the management for ankylosing spondylitis?

A

NSAIDs for pain
Steroids in flare ups
Anti-TNF meds like etanercept or monoclonal antibodies like infliximab, adalimumab or certolizumab pegol

136
Q

What is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis which is variable in severity

137
Q

What are the risk factors for psoriatic arthritis?

A

Psoriasis
FHx
HX of joint or tendon trauma
HIV infection

138
Q

What is the mpst severe form of psoriatic arthritis?

A

Most severe form - arthritis mutilans which occurs in the phalanxes
Osteolysis leads to progressive shortening of the digit
Skin then folds as the digit shortens giving “telescopic finger” appearance

139
Q

What are the key presentations of psoriatic arthritis?

A

Has several patterns of affected joints:
Symmetrical polyarthritis (affects wrists, ankles and DIP joints but MCP less commonly affected)
Asymmetrical pauciarthritis (affecting mainly digits and feet, pauci- = few)
Spondylitic pattern (back stiffness, sacroiliitis, atlanto-axial joint involvement) - more common in men
The spine, achilles tendon and atlanto-axial joint can also be involved

140
Q

What are the signs of psoriatic arthritis

A

Plaques of psoriasis on the skin
Nail pitting
Onycholysis (separation of the nail from the nail bed)
Dactylitis (inflammation of the full finger)
Enthesitis (inflammation of the entheses)

141
Q

What are the x-ray changes in psoriatic arthritis?

A

Periostitis (results in thickened and irregular outline of bone)
Ankylosis (bones join together)
Osteolysis
Dactylitis (inflammation of whole digit)
Pencil-in-cup appearance (bone seems pointed and wears away at surface making it cup-like)

142
Q

What are the investigations for psoriatic arthritis?

A

PEST screening (questionnaire re joint pain, swelling, arthritis hx), ESR + CRP, RF, ACCP, lipid profile, uric acid
Xray

143
Q

What is the management for psoriatic arthritis?

A

NSAIDs
DMARDS (methotrexate, leflunomide, sulfasalazine)
Anti-TNF meds (etanercept, infliximab or adalimumab)
Ustekinumab is last line

144
Q

What is reactive arthritis?

A

Synovitis in the joints as a reaction to a recent infective trigger
Previously known as Reiter Syndrome

145
Q

What are the risk factors for reactive arthritis?

A

Gastroenteritis (C. jejuni, salmonella, shigella)
STIs (chlamydia)
HLA B27 gene
Male
BCG immunotherapy

146
Q

What are the key presentations of reactive arthritis?

A

Acute, warm, swollen, painful joint
Reiter’s triad - uveitis, urethritis/balanitis, arthritis + enthesitis
Fever
Peripheral and axial arthritis
Dactylitis
Conjunctivitis and iritis
Skin lesions including circinate balanitis and keratoderma blennorrhagicum
Bilateral conjunctivitis
Anterior uveitis
Circinate balanitis (dermatitis of head of penis)

147
Q

What is the management for reactive arthritis?

A

NSAIDs
Steroid injections into affected joint/s
Systemic steroids in multi-joint presentations

148
Q

What is enteropathic arthritis?

A

form of chronic, inflammatory arthritis associated with the occurrence of an inflammatory bowel disease

149
Q

Which joints are most commonly affected in enteropathic arthritis?

A

peripheral joints and in some cases the spine is also involved

150
Q

WHat are the GI symptoms of enteropathic arthritis?

A

abdo pain, blood in stool, diarrhoea, weight loss

151
Q

What are the arthritic symptoms of enteropathic arthritis?

A

deformity, pain, redness, stiffness, swelling, tenderness, warmth

152
Q

What is the management for enteropathic arthritis?

A

DMARDs, NSAIDs, TNF-a inhibitors

153
Q

WHat is vasculitis?

A

inflammation of the blood vessels

154
Q

What is the pathophysiology of vasculitis?

A

→ Activated immune cells infiltrate into the vessel wall leading to direct damage and stimulates vascular smooth muscle cell remodelling
→ Vessel wall infiltration, proliferation and damage causes weakening and occlusion of blood vessel
→ Leads to ischaemia, infarction, aneurysm formation

155
Q

Which disease are large vessel vasculitis?

A

GCA
Takayasu’s arteritis (asian/japanese women, mainly affects aortic arch otherwise same as GCA)

156
Q

Which diseases are medium vessel vasculitis?

A

Polyarteritis nodosa - most associated with hep B and a rash called livedo reticularis (mottled, purplish, lace-like)
Buerger’s disease (male smokers 20-40, peripheral skin necrosis - “thromboangitis obliterans”
Kawasaki disease (Children, causes cornoary artery aneurysms)

157
Q

Which diseases are small vessel vasculitis?

A

Eosinophilic granulomatosis w/ polyangitis (EGPA) = “Churg strauss disease”, pANCA - mostly associated with lung and skin problems
Granulomatosis w/ polyangiitis (GPA) = “Wegener’s disease”, cANCA +ve, a cause of glomerulonephritis (+pulmonary symptoms, saddle shaped nose)
Henloch-Schonlein purpura - IgA vasculitis, a DDx for IgA nephropathy → both present as IgA deposition in GBM on kidney biopsy but HSP has purpuric rash on shins + affects other organs (joints, abdo, renal)

158
Q

What is giant cell arteritis?

A

Systemic vasculitis of the medium and large arteries, temporarily presents with symptoms affecting the temporal arteries.
Also known as temporal arteritis

159
Q

What are the 2 clinical patterns of disease in giant cell arteritis?

A

Cranial GCA
Large vessel GCA

160
Q

What are the primary and secondary causes of GCA?

A

Primary: Idiopathic autoimmune process
Secondary: Drugs, infection, other autoimmune disease

161
Q

WHat are the risk factors for GCA?

A

Age 50+ yrs
Female
Genetic factors
Smoking
Atherosclerosis
Environmental factors

162
Q

WHat is the pathophysiology of GCA?

A

Inflammation of the vessel lining leading to intimal expansion and hyperplasia which narrows and can occlude the vessel lumen, ultimately causing tissue ischaemia.

163
Q

WHat are the key presentations of GCA?

A

New localised headache (abrupt, temporal)
Visual symptoms (blurring, amaurosis fugax (veil over vision), diplopia (double vision), photopsia (flashing lights), visual loss)
Irreversible painless complete sight loss can occur rapidly
Scalp tenderness
Jaw and tongue claudication

164
Q

What are the systemic symptoms of GCA?Fever

A

Fatigue
Weight loss
Loss of appetite
Peripheral oedema
Polymyalgia
Limb claudication

165
Q

What are the investigations for GCA?

A

Clinical presentation, bloods (anaemia of chronic disease, thrombocytosis, raised CRP/ESR)
Temporal artery USS/biopsy
PET-CT and axillary USS (for extracranial disease)

166
Q

What are the steroid treatment protective measures?

A

Don’t - don’t stop taking steroids abruptly (risk of adrenal crisis)
S - sick day rules
T - treatment card
O - osteoporosis prevention with bisphosphonates and supplemental calcium and vitamin D
P - proton pump inhibitor for gastric protection

167
Q

What is the management for GCA?

A

Corticosteroid treatment immediately (prednisolone)
Methotrexate and or tocilizumab (use when high risk of corticosteroid toxicity)

168
Q

What are the potential complications of GCA?

A

Complications: stokes, blindness (stroke affecting retinal vessels, optic nerve)

169
Q

What is granulomatosis with polyangiitis (Wegener’s granulomatosis)?

A

Rare condition where the small to medium-size blood vessels become inflamed mainly affecting the ears, sinuses, kidneys and lungs)

170
Q

What are the risk factors for wegener’s granulomatosis?

A

genetic predisposition
Infective\
Environmental
White ethnicity

171
Q

What are the key presentations of wegener’s granulomatosis?

A

upper and lower respiratory tract involvement (cough, wheeze, haemoptysis)
Renal involvement (rapidly progressing glomerulonephritis)
Constitutional symptoms
Ocular manifestations
Nose bleeds

172
Q

What are the investigations for wegener’s granulomatosis?

A

Urinalysis + microscopy
CT chest
ANCA
FBC, serum creatinine, ESR, LFTs, serum calcium

173
Q

What are the differential diagnoses for wegener’s granulomatosis?

A

Eosinophilic granulomatosis with polyangiitis
Microscopic polyangiitis
Classic polyarteritis nodosa

174
Q

What is the management for wegener’s granulomatosis?

A

High dose corticosteroid
Immunosuppressant
Supportive care

175
Q

What is polyarteritis nodosa?

A

Rare medium vessel vasculitis which affects the skin, GI tract, kidneys and heart.

176
Q

What are the risk factors for polyarteritis nodosa?

A

40-60 yrs
Hep B infection
Hairy cell leukaemia
Hep C infection
male

177
Q

What is the pathophysiology of hep B-related PAN?

A

In Hep B-related PAN it is thought that the replicating virus causes direct injury to the vessel by replicating virus or by the deposition of immune complexes. Deposition of immune complexes leads to activation of the complement cascade, which results in an inflammatory response and subsequent damage to the vessel wall.

178
Q

What are the key presentations of PAN?

A

Mononeuritis multiplex (ischaemia of vasa nervosum)
GI bleeds (mesenteric artery)
CKD/AKI (renal artery)
Skin SC nodules + haemorrhage

179
Q

What rash is a key sign of polyarteritis nodosa?

A

Livedo reticularis (mottled, purplish, lace-like rash)

180
Q

What are the investigations for PAN?

A

CRP, ESR, FBC, complement, serum creatinine, MS urine analysis
CT angiogram ⇒ “beads on string” (microaneurysms)
Biopsy (e.g. kidney) → necrotising vasculitis

181
Q

What are the differential diagnoses for PAN?

A

Granulomatosis with polyangiitis
Microscopic polyangiitis
Churg-Strauss syndrome
GCA

182
Q

What is the management for PAN?

A

Corticosteroids
Control hypertension → ACEis
Hep B treatment after corticosteroids

183
Q

What is Marfan Syndrome?

A

Autosomal dominant condition affecting the gene responsible for creating fibrillin

184
Q

What is the epidemiology of Marfan syndrome?

A

3 in 10,000

185
Q

WHat is the pathophysiology of Marfan syndrome?

A

Mutations in the fibrillin-1 gene result in the production of an abnormal fibrillin protein, leading to abnormalities in the mechanical stability and elastic properties of connective tissue

186
Q

What are the key presentations for Marfan syndrome?

A

Tall stature
Long neck
Long limbs
Long fingers (arachynodactyly)
High arch palate
Hypermobility
Pectus carinatum or pectus excavatum
Downward sloping palpable fissures

187
Q

What are the aortic complications of Marfan syndrome?

A

aortic regurgitation murmur, AAA, aortic dissection, mitral/aortic valve prolapse (with regurgitation)

188
Q

What are the investigations for Marfan?

A

Clinical presentation
Genetic testing (FBN-1 mutation)

189
Q

What are the differential diagnoses for Marfan’s?

A

Unrelated aortic dissection
Bicuspid aortic valve
Ehlers-Danlos syndrome
Erdheim’s deformity

190
Q

What is the management for Marfan’s

A

Aim is to reduce ris kof cardiac complications
B-blockers, A-II receptor antagonists
Physiotherapy

191
Q

What is Ehlers Danlos?

A

Umbrella term encompassing a group of genetic conditions with cause collagen defects, resulting in hypermobility of the patient’s joints and abnormalities in connective tissue such as the skin, bones, blood vessels and organs.

192
Q

What are the different types of Ehlers Danlos?

A

Hypermobile (most common, least severe)
Classical
Vascular (most dangerous)
Kyphoscoliotic

193
Q

What is hypermobile EDS?

A

most common type seen in practice and the least sever type with key features if joint hypermobility and soft, stretchy skin

194
Q

What is the aetiology of EDS?

A

Caused by 1 or more genetic aberrations affecting genes and encoding for, or modifying, connective tissue proteins, such as collagen and matrix proteins.

195
Q

WHat is the pathophysiology of EDS?

A

Genetic aberration in genes encoding connective tissue proteins gives rise to a biochemical abnormality which in turn results in a biomechanical disorder with 3 effects:
Ligament laxity and resulting hypermobility + flexibility
Inherent fragility of connective tissues → increased injury risk
Impaired healing, often delayed and may be incomplete

196
Q

What are the presentations of EDS?

A

Joint hypermobility
Joint pain

Joint dislocations, for example the shoulders or hips
Cardiovascular complications (mitral regurgitation, AAA, Aortic dissection)
Soft stretchy skin
Easy bruising
Poor wound healing
Bleeding
Headaches
GORD
Abdo pain
Menorrhagia + dysmenorrhoea
Urinary incontinence

197
Q

What are the investigations for EDS?

A

Collagen mutations
Clinical diagnosis, Beighton score

198
Q

What is the management for EDS?

A

No cure, management focused on maintaining healthy joints, monitoring for complications and minimising symptoms
Physiotherapy/Occupational therapy
Painkillers
Psychology

199
Q

What is the Beighton score?

A

Beighton score - used to assess hypermobility, 1 point is scored for each side of the body, with a maximum score of 9:
Palms flat on floor with straight legs
Elbows hyperextend
Knees hyperextend
Thumb can bend to touch the forearm
Little finger hyperextends past 90 degrees

200
Q

What are the signs for serious pathology in mechanical lower back pain ?

A

elderly (e.g. myeloma), neuropathic pain (spinal cord compression)

201
Q

What is lumbar spondylosis?

A

degeneration of intervertebral discs which is initially asymptomatic and progressively worsens

202
Q

What vertebrae are most commonly affected in lumbar spondylosis?

A

L4/L5 or L5/S1

203
Q

What are the primary bone tumours?

A

Osteosarcoma
Ewing’s sarcoma
Fibrosarcoma
Chondrosarcoma

204
Q

WHat are the secondary bone tumours?

A

BLT KP
Breast (osteolytic)
Lung (osteolytic)
Prostate (osteosclerotic)
Thyroid
RCC
+ Myeloma can cause bone pain

205
Q

What is osteosarcoma?

A

Spindle cell neoplasms that produce osteoid.

206
Q

What are the different types of osteosarcoma?

A

Intramedullary (high grade)
Parosteal (low grade0
Periosteal (high grade)
Telangiectatic

207
Q

What is the epidemiology of osteosarcoma?

A

Usually presents in adolescents and younger adults aged 10-20 yrs
Most common non-haematological primary malignant neoplasm of bone

208
Q

What are the risk factors of osteosarcoma?

A

10-20yrs
Paget’s disease
Radiotherapy
Rothmund-Thomson syndrome (rare genetic disease)
Familial retinoblastoma syndrome
Li-Fraumeni syndrome (familial cancer syndrome resulting from germline mutations in the p53 tumour suppressor gene)
Fibrous dysplasia
Chemotherapy
male

209
Q

What bones are most commonly affected in osteosarcoma?

A

femur, tibia and humerus

210
Q

What are the key presentations for osteosarcoma?

A

Persistent bone pain which is worse at night
Bone swelling
Palpable mass
Restricted joint movements

211
Q

What are the XR signs of osteosarcoma?

A

Poorly defined lesion in bone with destruction of normal bone and a “fluffy” appearance
“Sun-burst “ appearance due to periosteal reaction

212
Q

What are the investigations for osteosarcoma?

A

Blood tests show raised ALP
Direct access x-ray (urgent <48hrs)
CT, MRI, bone, PET scans + bone biopsy for staging and better lesion definition

213
Q

What are the differential diagnoses for osteosarcoma?

A

Ewing’s sarcoma
Chondrosarcoma
Malignant fibrous histiocytoma

214
Q

What is the management for osteosarcoma?

A

Fatal if untreated, poor prognosis
Initial treatment with multi-agent chemotherapy pre-op 8-12 weeks - aims to kill tumour cells, reduce further spread, treat micro-metastases
Limb salvage surgery + adjuvant chemotherapy

215
Q

What is Ewing’s sarcoma?

A

very rare type of bone and soft tissue cancer most often affecting children and young adults.

216
Q

What is the aetiology of Ewing’s sarcoma?

A

Exact cause not fully understood
Not inherited
Most often fusion of genetic material between chromosomes 11 and 22 seen

217
Q

What are the risk factors for Ewing’s sarcoma?

A

10-20 yrs
Male
Most common in caucasians

218
Q

What cells does ewing’s sarcoma arise from?

A

neural crest cells

219
Q

What are the key presentations of Ewing’s sarcoma?

A

Classically a diaphyseal lesion (femur (mc), pelvis, distal tibia, proximal humerus)
Destructive lytic lesion (periosteum may be lifted off in multiple layers giving an onion skin appearance)
Pain around tumour site
Swelling and/or redness around tumour site
Fever
Weight loss
Anorexia
Fatigue
Paralysis and/or incontinence (if tumour is in spinal region)
Symptoms related to nerve compression from the tumour e.g. numbness, tingling, paralysis

220
Q

What are the investigations for Ewing’s sarcoma?

A

Bloods, XR
Bone biopsy (monotonous blue cell tumour, indistinct cell borders, no matrix production by the tumour cells)
Bone, MRI, CT, PET scans , tumour biopsy, bone marrow aspirate/biopsy

221
Q

What is the management for Ewing’s sarcoma?

A

Surgical removal
chemotherapy / radiotherapy
Amputation

222
Q

What is chondrosarcoma?

A

Cancer originating in the chondrocytes.

223
Q

What are the risk factors for chondrosarcoma?

A

Risk increases with age up to 70yrs
Enchondromas
Multiple hereditary exostoses (overgrowths of cartilage and bone which can develop into chondrosarcoma)
Ollier disease (clusters of enchondromas affecting hands and feet)
Maffucci syndrome (cause many enchondromas affecting hands and feet + benign tumours made up of blood vessels)
Li-Fraumeni syndrome

224
Q

What are the key presentations for chondrosarcoma?

A

Persistent bone pain
Lump on bone
Weakness and limited movement in limb or joint
Local swelling
Joint stiffness

225
Q

What are the investigations for chondrosarcoma?

A

Bloods, X-rays

CT, bone, PET, MRI scans, bone biopsy

226
Q

What is the management for chondrosarcoma?

A

Surgery to remove tumour
Radiotherapy / chemotherapy
Amputation

227
Q

What are the red flags for back pain

A

Trauma (osteoporosis)
Unexplained weight loss (cancer)
Neurological symptoms (cauda equina syndrome)
Age >50 or <20 (secondary bone cancer, ankylosing spondylitis, herniated disc)

Fever (infection)
IV drugs use (infection)
Steroid use (infection)
History of cancer (metastasis to spine)

228
Q

What are the non-medical managements for systemic sclerosis?

A

avoid smoking
gentle skin stretching
regular emollients
avoiding cold –> Raynaud’s
physiotherapy
occupational therapy

Phase 2A (18 decks)

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