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Phase 2A Tom > MSK > Flashcards

MSK Flashcards

1
Q

What is osteoarthritis?

A
  • Progressive synovial joint damage resulting in structural changes, pain and reduced function
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2
Q

Who has the biggest muscles?

A

Jake wishes he did when the answer is actually louis

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3
Q

What is the epidemiology of osteoarthritis?

A
  • More common in women
  • Most common form of arthritis
  • 8.75 million people over 45 with it in the UK
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4
Q

What are the risk factors for developing osteoarthritis?

A
  • Age
  • high BMI
  • Joint injury or trauma
  • Excessive stress for exercise or certain occupations
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5
Q

What gene is related to an increased risk of osteoarthritis?

A

COL2A1- collagen type 2 gene

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6
Q

Describe the pathophysiology of osteoarthritis?

A
  • It is classified as non-inflammatory however inflammatory mediators play a role as inflammatory cytokines interrupt the normal repair of cartilage damage.
  • Cartilage is lost and joint space narrows this causes bone on bone interaction.
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7
Q

What are the mechanisms which cause osteoarthritis?

A
  • Metalloproteinases secreted by chondrocytes degrade the collagen and proteoglycan
  • IL-1 and TNF-alpha stimulate metalloproteinase production and inhibit collagen production
  • Deficiency in growth factors such as insulin-like growth factor impairs matrix repair
  • Gene susceptibility has a 35-60% influence
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8
Q

What areas are most affected by osteoarthritis?

A
  • Knees
  • Hips
  • Sacro-ileac joints
  • Cervical spine
  • Wrist
  • base of thumb (carpometacarpal)
  • finger joints (interphalangeal)
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9
Q

What are the signs of osteoarthritis?

A
  • Heberden’s nodes- swelling in the distal interphalangeal joints
  • Bouchard’s nodes- swelling in the proximal interphalangeal joint (tom has this on his deformed finger)
  • Weak grip
  • Reduced range of motion
  • alteration in gait
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10
Q

What are the symptoms of osteoarthritis?

A
  • Joint pain
  • Mechanical locking
  • giving way
  • Crepitus-crunching sensation when moving joint
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11
Q

How can a diagnosis of osteoarthritis be made?

A
  • If someone is over 45 and has typical activity related pain with no morning stiffness or stiffness lasting less than 30 minuets
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12
Q

What are the 4 key x-ray changes found in osteoarthritis?

A

L- Loss of joint space
O- Osteophytes
S- Subchondral sclerosis increased density of bone along the joint line
S- Subchondral cysts (fluid filled holes in the bone)

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13
Q

What is the management for osteoarthritis?

A
  • Patient education lifestyle changes such as weight loss and physiotherapy
  • Oral paracetamol and topical NSAIDs or topical capsaicin (chilli pepper extract)
  • Intra-articular steroid injection (don’t use these I’ve had loads and they destroy your joint even more)
  • Joint replacement
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14
Q

What is rheumatoid arthritis?

A

A chronic systemic inflammatory disease. It leads to a deforming and symmetrical inflammatory arthritis of the small joints which progress to involve larger joint and other organs such as the skin and lungs

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15
Q

What genes are implicated in rheumatoid arthritis?

A
  • HLA-DR1
  • HLA-DR4

They are both crucial in activating T-cells

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16
Q

What are some environmental causes of rheumatoid arthritis?

A
  • Smoking
  • Other pathogens e.g., bacteria
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17
Q

What are some risk factors for developing rheumatoid arthritis?

A
  • Female
  • Smoking
  • Family history
  • Infections
  • Post-menopause due to lack of oestrogen
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18
Q

Describe the pathophysiology of rheumatoid arthritis

A
  • Environmental triggers cause modification of self-antigens e.g., arginine is converted to citrulline in type 2 collagen.
  • Due to susceptibility due to genes the immune cells cannot differentiate between self and non-self antigen.

-This causes an inflammatory response and cytokines Interferon gamma, IL-17, TNF, Il-1 and IL6 are secreted

  • This creates a pannus (thick synovial membrane). This damages the cartilage, soft tissue and bones. The cytokines can also escape and affect multiple organ systems
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19
Q

What is arthritic sweat gland disease?

A

A complication of rheumatoid arthritis caused by a topoisomerase willebrand activation tree (TWAT)

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20
Q

What are two autoantibodies that are found in rheumatoid arthritis?

A
  • Rheumatoid factor- it is found in around 70% of patients with rheumatoid arthritis. It targets the Fc portion of the IgG antibody. This causes activation of the immune system against own IgG antibodies. RF is mainly IgM antibodies
  • Cyclic citrullinated peptide antibodies (anti-CCP antibodies) target citrullinated proteins. This forms immune complexes which can accumulate and activate the complement system. Often found before development of rheumatoid arthritis
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21
Q

What is the typical presentation of rheumatoid arthritis?

A

-Symmetrical polyarthritis: (on both sides of body)

  • Pain, swelling and stiffness in the small joints of the hands and feet. The onset can be rapid or over months to years
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22
Q

What are the systemic symptoms of rheumatoid arthritis?

A
  • Fatigue
  • Weight loss
  • Flu-like illness
  • Muscle aches and weakness
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23
Q

What joints are commonly affected in RA?

A
  • Proximal Interphalangeal Joints (PIP) joints
  • Metacarpophalangeal (MCP) joints
  • Wrist and ankle
  • Metatarsophalangeal joints
  • Cervical spine
  • Large joints can also be affected such as the knee, hips and shoulders

DIP is almost never affected

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24
Q

What are the x-ray changes seen in RA?

A
  • Joint destruction
  • Bone erosions
  • Joint swelling
  • Periarticular osteopenia

less - loss of joint space, erosions to bone, soft tissue swelling, soft bones (osteopenia)

as opposed to loss for osteoarthiritis

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25
Q

What are some signs of rheumatoid arthritis?

A
  • Z shaped deformity to the thumb
  • Swan neck deformity (flex at DIP)
  • Boutonnieres deformity- due to a tear in the central slip of the extensor components of the finger. This means when they try to straighten their finger it cause it to bend and flex at PIP
  • Ulnar deviation of the fingers at the knuckles
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26
Q

What are some extra-articular manifestations of rheumatoid arthritis?

A
  • Pulmonary fibrosis
  • Anaemia
  • Cardiovascular disease
  • Amyloidosis
  • Bronchiolitis obliterans (inflammation causing small airway destruction**
  • Felty’s syndrome (RA, neutropenia and splenomegaly)
  • Sjogren’s syndrome
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27
Q

What are some symptoms of rheumatoid arthritis?

A
  • Morning stiffness that lasts longer than 30 mins and improves throughout the day
  • Fever
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28
Q

What are some investigations for rheumatoid arthritis?

A
  • ESR and CRP will be elevated
  • Rheumatoid factor levels- can be a predictor can have high levels 15 years before the disease
  • Anti-CCP levels
  • Joint x-rays
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29
Q

What is the diagnostic criteria for rheumatoid arthritis?

A
  • Comes form the American college of rheumatology
    1. The joints involved (more and smaller joints score higher)
    2. Serology
    3. Inflammatory markers
    4. Duration of symptoms longer or less than 6 weeks

Score is added up and a score of greater than 6 indicates rheumatoid arthritis

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30
Q

Who is considered to have the worst prognosis with rheumatoid arthritis?

A
  • younger onset
  • Male
  • Presence of RF and anti-CCG
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31
Q

What is the first-lie monotherapy for rheumatoid arthritis?

A
  • Any one of methotrexate, leflunomide or sulfasalazine. Hydroxychloroquine can be considered in mild disease and is considered the “mildest” anti rheumatic drug.
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32
Q

What second line therapy for rheumatoid arthritis?

A

Two of methotrexate, leflunomide or sulfasalazine

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33
Q

What is third line treatment for rheumatoid arthritis?

A

Methotrexate plus a TNF inhibitor e.g., infliximab

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34
Q

What is fourth line treatment for rheumatoid arthritis?

A

Methotrexate plus rituximab

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35
Q

What is used to monitor rheumatoid arthritis?

A

CRP levels and DAS28

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36
Q

What is the leading cause of death in rheumatoid arthritis?

A

Accelerated atherosclerosis leading to cardiovascular disease

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37
Q

What is gout?

A

A type of crystal arthritis which is associated with chronically high levels of uric acid. Urate crystals are deposited in the joint causing it to become hot swollen and painful

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38
Q

What are the overproduction causes of gout?

A
  • Increased cell turnover
  • Cytotoxic drugs e.g., chemotherapy
  • Purine rich diet, seafood and alcohol
  • Obesity
  • Severe psoriasis
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39
Q

What are the decreased secretion of uric acid causes of gout?

A
  • CKD
  • Diuretics e.g., thiazide and loop
  • Pyrazinamide
  • Lead toxicity
  • High fructose intake

They are the more common cause they account for 90%

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40
Q

What are risk factors for developing gout?

A
  • Elderly
  • Men
  • Post-menopausal women
  • Alcohol
  • Diabetes
  • IHD
  • High diet intake of purines
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41
Q

Describe the pathophysiology of gout?

A
  • Uric acid is formed as a breakdown product if purines
  • Uric acid has a limited solubility in the blood and when there is too much uric acid it can become a urate ion and bind to sodium
  • This forms urate crystals which deposit in areas with slow blood flow the joints and kidney tubules
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42
Q

What the signs of Gout and where is affected?

A
  • Gout tophi are deposits of uric acid
  • Ears
  • Base of big toe
  • Wrists
  • Base of thumb
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43
Q

What are the symptoms of gout?

A
  • Red, tender, hot and swollen joints
  • Joint stiffness
  • Rapid onset of severe pain
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44
Q

How would you diagnose gout?

A

Can be made on just clinical presentation but excluding septic arthritis is key

  • Joint aspiration will show no bacterial growth, needle shaped crystals, Negatively birefringent of polarised light, Monosodium urate crystals
  • Measure serum urate levels 4-6 weeks after attack as they can be low at time of attack
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45
Q

What are the x-ray signs of gout?

A
  • Joint space maintained
  • Lytic lesions
  • Punched out erosions
  • Sclerotic borders with overhanging edges
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46
Q

What is the treatment of gout during an acute flare?

A
  • NSAIDs first line
  • Colchicine second line- severe diarrhoea is a side effect
  • Steroids as third line
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47
Q

What is used to prevent gout?

A

Lifestyle management and a Xanthine oxidase inhibitor

  • First-line Allopurinol
  • Second-line Febuxostat
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48
Q

What is pseudogout?

A

Is a form of inflammatory arthritis caused by the deposition of calcium pyrophosphate crystals in the synovium

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49
Q

What are risk factors of pseudogout?

A
  • Hyperparathyroidism
  • Hemochromatosis
  • Hypomagnesaemia
  • Hypophosphatemia
  • Wilson’s disease
  • Acromegaly
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50
Q

Describe the pathophysiology of pseudogout?

A

Deposition of calcium pyrophosphate triggers synovitis with the knee, shoulder and wrist most commonly being affected

  • Can be acute or chronic
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51
Q

What will joint aspiration for pseudogout show?

A
  • No bacterial growth
  • Calcium pyrophosphate crystals
  • Rhomboid shaped needles
  • Positive birefringent of polarised light
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52
Q

What would an x-ray of pseudogout show?

A

Chondrocalcinosis is the classic x-ray change in pseudogout. It appears as a thin white line in the middle of the joint space caused by the calcium deposition. This is pathognomonic (diagnostic) of pseudogout.

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53
Q

What is septic arthritis?

A

An infection of 1 or more joints caused by pathogenic inoculation of microbes.

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54
Q

What are the common bacteria that cause septic arthritis?

A
  • S.aureus the most common in all age groups
  • S.epidermis in prosthetic joints
  • Streptococcus pyogenes in children under 5
  • Gonorrhoeae in young sexually active people if a young person presents think this. (Watch out louis)
  • E.coli in immunosuppressant, elderly and IV drug use
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55
Q

What are some risk factors for developing septic arthritis?

A
  • Underlying joint disease
  • IV drug use
  • Immunocompromised
  • Prosthetic joint/recent joint surgery
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56
Q

What are the signs of septic arthritis?

A
  • Normally only one joint is affected. Most commonly the knee.
  • Hot tender and swollen joint
  • Limited range of movement
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57
Q

What are the symptoms of septic arthritis?

A
  • Difficulty weight bearing
  • Fever
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58
Q

What are the first line investigations for septic arthritis?

A
  • FBC
  • Elevated CRP and ESR
  • Blood cultures
  • Plain x-ray
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59
Q

What is the gold standard investigation for septic arthritis?

A

Joint aspiration will be yellow and cloudy and show presence of bacteria

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60
Q

What is the scoring criteria used for septic arthritis?

A

Kocher criteria a score of 2 suggests 40% likelihood and score of 3 suggest 93%

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61
Q

What is the treatment for septic arthritis?

A
  • Empirical therapy: flucloxacillin plus rifampicin is first-line
  • Penicillin allergy: clindamycin
  • Suspected or confirmed MRSA: vancomycin
  • Gonococcal arthritis or gram-negative infection: cefotaxime or ceftriaxone

Continue for 3-6 weeks

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62
Q

What is the prognosis for septic arthritis?

A

Mortality from septic arthritis ranges from 10 to 20% with treatment,

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63
Q

What is osteomyelitis?

A

An inflammatory condition of the bone caused by an infecting organism most commonly S.aureus.

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64
Q

What is the epidemiology of osteomyelitis?

A
  • Most common in children due to haematogenous spread
  • Adolescents and adults tend to get it due to an infection secondary to trauma
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65
Q

What can cause bacteria can cause osteomyelitis?

A
  • Staphylococcus aureus:A gram-positive cocci. Includes MRSA (Methicillin Resistant Staphylococcus Aureus) a penicillin resistant organism. MOST COMMON!
  • Mycobacterium tuberculosis:Acid fast bacilli. May cause osteomyelitis - characteristically in Pott’s disease (TB affecting the spine).
  • Salmonellaspp.:Gram-negative rods. Most commonly seen in patients with sickle cell anaemia.
  • Polymicrobial:More commonly seen in those with ulcers secondary to vascular disease, neuropathy and diabetes.
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66
Q

What are the risk factors for developing osteomyelitis?

A
  • Diabetes
  • Old age
  • Peripheral vascular disease
  • Immunocompromise
  • Malnutrition
  • Trauma/ injury
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67
Q

Describe the pathophysiology of osteomyelitis?

A
  • Can occur when there is breakdown of the protective barriers of the skin e.g., Open fracture, skin ulcer, surgery
  • Haematogenous spread - Most commonly affects the axial skeleton, primarily the vertebral bones. The next most frequently affected sites are other axial bones like the sternum and pelvis. In children, long-bone osteomyelitis is seen
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68
Q

What is the acute phase of osteomyelitis?

A
  • Bacteria reach the bone and start to proliferate. This alerts immune cells and they try and fight off the infection.
  • The immune cells release chemicals that cause local bone destruction and usually this is effective
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69
Q

What is chronic osteomyelitis?

A
  • If the lesion is not that extensive, and there’s viable bone the osteoblasts and the osteoclasts begin to repair the damage over a period of weeks. However, in some cases, the process turns into a chronic osteomyelitis - lasting months to years.
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70
Q

What are the signs osteomyelitis?

A
  • Redness
  • Swelling
  • Evidence of trauma or surgery
  • Tenderness
  • Ulcers/skin breaks
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71
Q

What are the symptoms of osteomyelitis?

A
  • Fever
  • Joint pain
  • Erythema
  • Muscle aches
  • Nausea
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72
Q

What are the investigations for osteomyelitis?

A

Blood tests will show raised inflammatory markers (e.g., WBC, CRP and ESR).

Blood cultures may be positive for the causative organism.

Bone cultures can be performed to establish the causative organism and the antibiotic sensitivities.

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73
Q

What is the gold standard test for osteomyelitis?

A

MRI- will show bone marrow oedema and abscesses

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74
Q

What is the treatment for osteomyelitis?

A
  • 6 weeks of flucloxacillin, possibly with rifampicin or fusidic acid added for the first 2 weeks
  • Clindamycin if penicillin allergy
  • Vancomycin in MRSA

Chronic requires 3 months of antibiotics

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75
Q

What are the complications of osteomyelitis?

A
  • Septic arthritis - if infection spreads to joints
  • Growth disturbance in children and adolescents
  • Amputations
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76
Q

What is the prognosis for osteomyelitis

A

Most patients with acute osteomyelitis recover with no long-term complications if osteomyelitis is diagnosed promptly and treated adequately.

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77
Q

What are spondyloarthropathies?

A

A group of related chronic inflammatory conditions. They tend to affect the axial Skelton adn share similar clinical features.

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78
Q

What are the shared clinical features of spondyloarthropathies?

A
  • Rheumatoid factor negative
  • HLA-B27 positive - louis strongly disagrees (not anymore) - thanks for correcting
  • Pathology in the spine
  • Asymmetrical inflammation of an entire jointsSausage fingers
  • Extra-articular manifestations
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79
Q

When should you suspect spondyloarthropathies?

A

S- Sausage digit
P- Psoriasis
I- inflammatory back pain
N- NSAIDs illicit a good response
E- Enthesitis inflammation where tendon meets joint (plantar fasciitis)
A- Arthritis
C- Crohn’s/colitis/CRP
H- HLA-B27
E- eye uveitis

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80
Q

What is ankylosing spondylitis?

A

A chronic progressive inflammatory arthropathy. It mainly affects the spine and cause progressive stiffness and pain.

Ankylosis= abnormal stiffening and immobility of a joint due to the fusion of a bone

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81
Q

What is epidemiology of ankylosing spondylitis?

A
  • More common in males
  • Most commonly presents in teens/20s
  • Women present later and are underdiagnosed
  • 90% are HLA-B27 positive
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82
Q

What is the pathology of ankylosing spondylitis?

A
  • There is lymphocyte and plasma infiltration with local erosion of bone at the attachments of the intervertebral and other ligaments.
  • Inflammation of these tendons/ligaments when they heal they heal with new bone formation
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83
Q

What are the key presentations of ankylosing spondylitis?

A
  • Symptoms tend to occur gradually over 3 months

-Lower back pain stiffness and sacroiliac pain in the buttock region.

  • The pain and stiffness is worse with rest and improves with movement it is worse at night and morning and improves throughout the day
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84
Q

What are some other signs and symptoms of ankylosing spondylitis?

A
  • Weight loss and fatigue
  • Chest pain
  • Anaemia
  • Heart block
  • Pulmonary fibrosis
  • Aortitis inflammation of the aorta

Note that any of the SPINEACHE symptoms may be present

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85
Q

What would the first line investigations for ankylosing spondylitis be?

A
  • FBC normocytic anaemia
  • CRP and ESR elevated
  • Genetic testing for HLA-B27
  • X-ray (MRI if x-ray of the spine is normal may show bone marrow oedema)
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86
Q

What would an x-ray for ankylosing spondylitis show?

A
  • Bamboo spine- calcification of ligaments
  • Syndesmophytes - areas of boney growth where the ligament normally inserts into the bone.
  • Ossification - structures such as ligaments turn into bone like tissue
  • Fusion - seen in facet joints, sacroiliac joints and costovertebral joints
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87
Q

What is the test used to asses mobility in the spine and help to diagnose ankylosing spondylitis?

A

Schober’s test

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88
Q

What is Schober’s test?

A

Have the patient stand straight. Find the L5 vertebrae. Mark a point 10cm above and 5cm below this point (15cm apart from each other). Then ask the patient to bend forward as far as they can and measure the distance between the points.

If the distance with them bending forwards is less than 20cm, this indicates a restriction in lumbar movement and will help support a diagnosis of ankylosing spondylitis.

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89
Q

What are the treatments of ankylosing spondylitis?

A
  • NSAIDs
  • Steroids
  • TNF-alpha infliximab
  • Monoclonal antibodies targeting IL-7 (secukinumab)
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90
Q

What are the complications of ankylosing spondylitis?

A
  • Vertebral fractures
  • Osteoporosis
  • Aortitis
  • Restrictive lung disease
  • Heart block
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91
Q

What is psoriatic Arthritis?

A

An inflammatory arthritis associated with psoriasis. Can vary in severity from mild stiffening and soreness in the joint or the joint can be completely destroyed arthritis mutilans

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92
Q

What % of people with psoriasis will develop psoriatic Arthritis?

A

10-20% and it usually occurs within 10 years of developing the skin change

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93
Q

What is the pathophysiology of psoriatic Arthritis?

A
  • It has a strong genetic component and although not fully understood the activation of CD8+ T cells is thought to play a crucial role
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94
Q

What are the signs of psoriatic Arthritis?

A
  • Joint tenderness and warmth
  • Dactylitis: swelling of the whole digit (sausage fingers)
  • Enthesitis: Inflammation of the tendons
  • Plaques of psoriasis on the skin
  • Pitting of the nails
  • Onycholysis (separation of the nail from the nail bed)
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95
Q

What are some other associations of psoriatic Arthritis?

A
  • Eye disease
  • Aortitis
  • Amyloidosis
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96
Q

What are the different patterns in which psoriatic Arthritis can present?

A

The condition does not have a single pattern of affected joints in the same way as osteoarthritis or rheumatoid. There are several recognised patterns:

Symmetrical polyarthritis presents similarly to rheumatoid arthritis and is more common in women. The hands, wrists, ankles and DIP joints are affected.

Asymmetrical pauciarthritis affecting mainly the digits (fingers and toes) and feet. Pauciarthritis describes when the arthritis only affects a few joints.

Spondylitic pattern is more common in men.

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97
Q

What is used to screen patients who have psoriasis for arthritis?

A

PEST screening tool
Patients are asked about: joint pain, swelling, nail pitting

Can also use the CASPAR criteria

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98
Q

What are some x-ray changes seen in psoriatic Arthritis?

A
  • Periostitis- thickened and irregular outline of the bone
  • Ankylosis- where bones are joined together
  • Pencil-in-cup appearance- the classic x-ray change to the digits is the “pencil-in-cup appearance”. This is where there are central erosions of the bone beside the joints and this causes the appearance of one bone in the joint being hollow and looking like a cup whilst the other is narrow and sits in the cup.
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99
Q

What is reactive arthritis (Reiter syndrome) ?

A

It refers to synovitis occurring due to a recent infective trigger. This is an autoimmune response to infection elsewhere in the body

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100
Q

What is the epidemiology of reactive arthritis?

A
  • 30-50 fold increase if someone is HLA-B27 positive
  • Women less commonly affected
  • Mainly occurs in adults
101
Q

What can cause reactive arthritis?

A
  • Gastroenteritis- Salmonella, shigella
  • Sexually transmitted disease- chlamydia, Gonorrhoea
102
Q

How does an infection cause reactive arthritis?

A
  • Immune system is responding to the recent infection. This results in antibodies and inflammation that also affect the joints
  • It presents a lot like septic arthritis without infection at site of the bone it is somewhere else in the body
103
Q

What is the key presentation of reactive arthritis?

A
  • Acute, asymmetrical monoarthritis typically in lower leg (knee).

Can also present with triad of: Urethritis, arthritis and conjunctivitis
Can’t see, pee or climb a tree

104
Q

What are some other signs and symptoms of reactive arthritis?

A
  • Iritis - swelling and irritation of eye
  • Keratoderma blennorrhagia - painless, red, raised plaques and pustules
  • Circinate balanitis - dermatitis of the head of the penis
  • Mouth ulcers
105
Q

What are the investigations for reactive arthritis?

A
  • Aspirate joints to rule out septic arthritis/Gout
  • Infectious serology
  • Sexual health review/ask about diarrhoea if present do a stool sample
106
Q

How should you treat reactive arthritis?

A
  • If patient presents with acute, warm, swollen and painful joint
    • Hot joint policy - presume patient has septic arthritis until its excluded
      • Antibiotics
      • Aspirate joint - MCS & crystal examination

NSAIDs
Steroid injections into the affected joints
Systemic steroids may be required, particularly where multiple joints are affected

107
Q

What is the prognosis of reactive arthritis?

A

Most cases resolve within 6 months

108
Q

What is systemic lupus erythematosus?

A
  • Is a chronic systemic autoimmune condition (type III hypersensitivity) due to a complex interplay between genetic and environmental factors.
  • It often takes a relapsing-remitting course. This results in chronic inflammation
109
Q

Why is SLE got the word erythematosus in it. Sounds a stupid question but actually useful information!!!!!

A

It refers to the typical red malar rash that occurs across the face. It is more common in women and Asians

110
Q

What are the leading causes of death in SLE?

A
  • Cardiovascular disease
  • Infections
111
Q

What are some environmental triggers of SLE?

A
  • UV light
  • Smoking
  • EBV (epstein barr virus)
  • Sex hormones
112
Q

What are some risk factors for SLE?

A
  • Middle aged
  • Female gender
  • HLA associations (HLA-B8/DR2/DR3)
113
Q

Describe the pathophysiology of SLE?

A
  • Environmental triggers e.g., UV light causes cell death. Due to genetic factors there is reduced clearance of these cellular debris
  • Also genetics play a further role as the immune system of these patients do not recognise the cellular debris as self so they attack them forming antibody-antigen complexes which get deposited in different tissues activating the complement pathway (type III hypersensitivity)
114
Q

What are the antibodies found in SLE called?

A

Anti-nuclear antibodies

115
Q

What are the symptoms of SLE?

A
  • Fatigue
  • Weight loss
  • Joint and muscle pain
  • Fever
  • Photosensitive malar rash. Get’s worse with sunlight and is butterfly shaped across the cheeks
  • Hair loss
  • Mouth ulcers
  • Shortness of breath
116
Q

What are some investigations for SLE?

A
  • Antibodies
  • FBC will show anaemia of chronic disease
  • C3 and C4 levels will be low
  • Increased CRP and ESR
  • Renal biopsy to asses for lupus nephritis
117
Q

What are the two main antibodies to screen for in SLE?

A

-Anti-nuclear antibodies (ANA): Around 85% of patients with SLE will be positive for ANA. The initial step in testing for SLE. Antinuclear antibodies can be positive in healthy patients and with other conditions (e.g. hepatitis). A positive result needs to be interpreted in the context of their symptoms.

  • Anti-double stranded DNA (anti-dsDNA): is specific to SLE, meaning patients without the condition are very unlikely to have these antibodies. Around 70% of patients with SLE will have anti-dsDNA antibodies
118
Q

What are some other antibodies used to test for SLE?

A

-Anti-Smith (highly specific to SLE but not very sensitive)

-Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis)

-Anti-Ro and Anti-La (most associated with Sjogren’s syndrome)

-Anti-Scl-70 (most associated with diffuse cutaneous systemic sclerosis)

-Anti-Jo-1 (most associated with dermatomyositis)

119
Q

How would you make a diagnosis of SLE?

A

Use the SLICC criteria or the ACR criteria: involves the presence of ANA antibodies and certain number of clinical features

120
Q

What are some complications of SLE?

A
  • CVD
  • Infections
  • Pericarditis
  • Lupus nephritis
  • Recurrent miscarriage
121
Q

What is the treatment for SLE?

A
  • NSAIDs
  • Steroids (prednisolone)
  • Hydroxychloroquine first line for mild
  • Sun cream for malar rash
122
Q

What are some other immunosuppressants used for more severe SLE?

A
  • Methotrexate
  • Mycophenolate mofetil
  • Azathioprine
  • Tacrolimus
  • Leflunomide
  • Ciclosporin
123
Q

What are some biological therapies for SLE?

A
  • Rituximab targets B cells
  • Belimumab targets B-cell activating factor
124
Q

What is antiphospholipid syndrome?

A

A disorder associated with antiphospholipid antibodies where the blood becomes prone to clotting as the patient is in a hypercoagulable state.

It presents with a variety of clinical features characterised by thromboses and pregnancy related morbidity

125
Q

What condition is associated with APS?

A

Systemic lupus erythematous in 20-30% of cases

126
Q

Describe the pathophysiology of APS

A
  • Antiphospholipid antibodies can cause thrombosis by binding to the phospholipid on the surface of cells such as endothelial cells, platelets and monocytes.
  • Once they bind to these cells it can result in thrombosis formation and/or miscarriage. They tend to affect cerebral and renal vessels
127
Q

What things do Antiphospholipid antibodies cause?

A

C- Coagulation defects
L- livedo reticularis - lace-like purplish discolouration of skin
O- Obstetric issues e.g., miscarriage
T- Thrombocytopenia (low platelets)

CLOT

128
Q

What are some of the venous complications of APL?

129
Q

What are the arterial complications of APL?

A
  • Stroke
  • MI
  • Renal thrombosis
130
Q

What are the pregnancy related complications of APL?

A
  • Recurrent miscarriage
  • Still birth
  • Preeclampsia
131
Q

What is another complication of APL?

A

Libmann-Sacks endocarditis: is a type of non-bacterial endocarditis where there are growths (vegetations) on the valves of the heart. The mitral valve is most commonly affected. It is associated with SLE and antiphospholipid syndrome.

132
Q

How would you make a diagnosis for APL?

A

Diagnosis would be made when there is a history of thrombosis or pregnancy related complications plus the presence of:

Lupus anticoagulant antibodies
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

The presence of them needs to be persistent positive test more than 12 weeks apart

133
Q

How would you treat APL?

A
  • Long term warfarin with an INR range of 2-3
  • Pregnant women are put on low molecular weight heparin plus aspirin
134
Q

What are polymyositis and dermatomyositis?

A

Autoimmune disorders where there is inflammation in the muscles.

Polymyositis refers to chronic inflammation of the muscles. Dermatomyositis is a connective tissue disorder where there is chronic inflammation of the skin and muscles

135
Q

What is the key enzyme for diagnosing polymyositis and dermatomyositis?

A
  • The creatine kinase blood test. It is an enzyme that is found inside muscle. Inflammation of the muscles can lead to the release of it.
136
Q

Other than polymyositis and dermatomyositis what can cause creatine kinase levels to rise?

A
  • Rhabdomyolysis
  • Acute kidney injury
  • Myocardial infarction
  • Statins
  • Strenuous exercise
137
Q

What can cause polymyositis and dermatomyositis?

A

They can be caused by an underlying malignancy. This makes them paraneoplastic syndromes

138
Q

What cancers are most associated with polymyositis and dermatomyositis?

A
  • Lung
  • Breast
  • Ovarian
  • Gastric
139
Q

What are the symptoms of polymyositis and dermatomyositis?

A
  • Muscle pain, fatigue and weakness
  • Occurs bilaterally and typically affects the proximal muscles
  • Mostly affects the Shoulder and pelvic girdle
  • Develops over weeks
140
Q

What are the skin features of polymyositis and dermatomyositis?

A

Polymyositis occurs without skin features

  • Gottron lesions
  • Photosensitive rash on back shoulders and neck
  • Purple rash on face and eyelids
  • Periorbital oedema
  • Subcutaneous calcinosis
141
Q

What is the antibody found in polymyositis?

142
Q

What are the two antibodies found in dermatomyositis

A

Anti-Mi-2 antibodies
Anti-nuclear antibodies

143
Q

How would you diagnose polymyositis and dermatomyositis?

A
  • Clinical presentation
  • Elevated creatine kinase levels
  • Autoantibodies
144
Q

What is the gold standard test for polymyositis and dermatomyositis?

A

Muscle biopsy

145
Q

What is the management for polymyositis and dermatomyositis?

A
  • Patients should be assessed for underlying cancer
  • Corticosteroids are first line
  • Then immunosuppressants
  • Then infliximab
146
Q

What is systemic sclerosis?

A

An autoimmune inflammatory and fibrotic connective tissue disease. It affects the skin in all areas and also the internal organs

147
Q

What are the two main patterns of disease in systemic sclerosis?

A

Limited cutaneous systemic sclerosis
Diffuse cutaneous systemic sclerosis

148
Q

What is Limited cutaneous systemic sclerosis?

A

Used to be called CREST syndrome.

C- calcinosis
R- Raynaud’s phenomenon
E- oEsophageal dysmotility (i hate this one)
S- Sclerodactyly
T- Telangiectasia

149
Q

What is diffuse cutaneous systemic sclerosis?

A

Includes the CREST symptoms but also has systemic features

  • Cardiovascular e.g., CAD and hypertension-
  • Lung problems e.g., pulmonary hypertension and fibrosis
  • Kidney problems causes glomerulonephritis and a condition called scleroderma renal crisis

C- calcinosis
R- Raynaud’s phenomenon
E- oEsophageal dysmotility (i hate this one)
S- Sclerodactyly
T- Telangiectasia

150
Q

What is scleroderma and Sclerodactyly?

A
  • Scleroderma refers to the hardening of the skin. It gives the appearance of shiny tight skin without normal folds

-Sclerodactyly describes skin changes in the hand where the skin tightens around the joints and restricts movement

151
Q

What is Telangiectasia?

A

Telangiectasia are dilated small blood vessels in the skin. They are tiny veins that have dilated. They have a fine, thready appearance.

152
Q

What is Oesophageal dysmotility?

A

Oesophageal dysmotility is caused by connective tissue dysfunction in the oesophagus. This is commonly associated with swallowing difficulties, acid reflux and oesophagitis

153
Q

What is Scleroderma renal crisis?

A

An acute condition where there is a combination of severe hypertension and renal failure.

154
Q

What are the antibodies associated with systemic sclerosis?

A
  • Antinuclear antibodies (ANA) are positive in most patients with systemic sclerosis.
  • Anti-centromere antibodies are most associated with limited cutaneous systemic sclerosis.
  • Anti-Scl-70 antibodies are most associated with diffuse cutaneous systemic sclerosis. They are associated with more severe disease.
155
Q

What test would you perform on someone with Raynaud’s to check for systemic scleropathy?

A
  • Nailfold capillaroscopy- examines the health of the peripheral capillaries.

micro-haemorrhages indicate systemic sclerosis

156
Q

What is used to treat Raynaud’s phenomenon?

A

Nifedipine

157
Q

What is osteoporosis/osteopenia?

A

Osteoporosis is a condition where there is a reduction in the density of the bones.

Osteopenia refers to a less severe reduction in bone density than osteoporosis. Reduced bone density makes bone less strong and more prone to fractures.

158
Q

What can cause osteporosis?

A
  • Primary disease
  • Malignancy
  • Endocrine dysfunction
  • COPD
  • IBD
  • CLD
  • CKD
159
Q

What are the risk factors for developing osteoporosis?

A

S- Steroid use
H- Hyperthyroidism, hyperparathyroidism
A- Alcohol and tobacco use
T- Thin
T- Testosterone decrease
E- early menopause- oestrogen is protective
R- renal or liver failure
E- Erosive/inflammatory bone disease
D- dietary e.g., reduced Ca2+, malabsorption, diabetes

160
Q

Why does bone mass decrease as we get older?

A
  • Osteoclasts are responsible for the breakdown of bone and osteoblasts are responsible for the formation. As we age osteoclast activity is increased however this is not matched by osteoblast activity
  • The peak mass we reach as young adults is key a higher peak bone mass can be protective
161
Q

How can a fall in levels of oestrogen cause bone mass to decrease?

A
  • Oestrogen deficiency leads to an increased rate of bone loss. It is key yo the activity of bone cell receptors found on osteoblasts, osteocytes, and osteoclasts.
  • It is thought that osteoclasts survive longer in the absence of oestrogen and there is an arrest of osteoblastic synthetic architecture
162
Q

How can glucocorticoids cause a reduction in bone mass?

A

They cause an increased turnover of bone. Prolonged use can result in reduced turnover state however the synthesis is affected resulting in bine mass reduction

163
Q

What is the symptom of osteoporosis and where is this most likely to occur?

A

There is an increased frequency of fractures.

The most common ones include, vertebral crush fracture, and those of the distal wrist (Colles’ fracture) and proximal femur

164
Q

What is the FRAX tool?

A

It gives a prediction of the risk of a fragility fracture over the next 10 years

It involves the inputting of information such as age, BMI, co-morbidities, smoking, family history and if done you can enter a bone mineral score from a DEXA scan

165
Q

What do the results of the FRAX tool give?

A

It gives the result as a percentage probability of a:

  • Major osteoporotic fracture
  • Hip fracture
166
Q

What is used to asses bone mineral density?

167
Q

What is a DEXA scan and what does it measure?

A

It stands for dual-energy x-ray absorptiometry. It assess how much radiation is absorbed by the bones indicating how dense the bone is. The measurement is usually taken from the Hip

168
Q

What are the T and Z scores of a DEXA scan and which one is more clinically relevant?

A

T-score: represents the number of standard deviations below the mean for a healthy young adult
Z-score: represents the number of standard deviations the bone density falls below a person for their age

T-score is more relevant

169
Q

What do the different T-scores represent?

A

More than -1: Normal

-1 to -2.5: Osteopenia

Less than -2.5: Osteoporosis

Less than -2.5 plus a fracture: Severe Osteoporosis

170
Q

What is the management for someone who has had a FRAX score without a DEXA scan?

A

Low risk- reassure
Medium risk- offer DEXA scan and recalculate the risk with the results
High risk: offer treatment

171
Q

What are some lifestyle management/light treatment for mild osteoporosis/osteopenia?

A
  • Activty and exercise
  • Weight control
  • Reduce alcohol/stop smoking

NICE recommend calcium supplementation with vitamin D in patients at risk of fragility fractures with an inadequate intake of calcium. An example of this would be Calcichew-D3, which contains 1000mg of calcium and 800 units of vitamin D (colecalciferol).

Patients with an adequate calcium intake but lacking sun exposure should have vitamin D supplementation.

172
Q

What is the treatment for someone at high risk of a fracture?

A

Bisphosphonates- they interfere with osteoclast activity reducing their activity. eg:

Alendronate 70mg once weekly
Riseronate 35mg once weekly
Zoledronic acid 5 mg once yearly (intravenous)

173
Q

What are the side effects of bisphosphonates?

A
  • Reflux and oesophageal erosions.
  • Osteonecrosis of the jaw and external auditory canal

They are taken on an empty stomach and person should sit upright for 30 minutes before taking

174
Q

What are some other treatment options for osteoporosis? (non bisphosphonates)

A

Denosumab is a monoclonal antibody that works by blocking the activity of osteoclasts.

Teriparatide anabolic treatment - increases bone density and improves trabecullae structure

Hormone replacement therapy should be considered in women that go through menopause early.

Strontium ranelate is a similar element to calcium that stimulates osteoblasts and blocks osteoclasts but increases the risk of DVT, PE and myocardial infarction.

Raloxifene is used as secondary prevention only. It is a selective oestrogen receptor modulator that stimulates oestrogen receptors on bone but blocks them in the breasts and uterus.

175
Q

What are some lifestyle management/light treatment for mild osteoporosis/osteopenia?

A
  • Activty and exercise
  • Weight control
  • Reduce alcohol/stop smoking

NICE recommend calcium supplementation with vitamin D in patients at risk of fragility fractures with an inadequate intake of calcium. An example of this would be Calcichew-D3, which contains 1000mg of calcium and 800 units of vitamin D (colecalciferol).

Patients with an adequate calcium intake but lacking sun exposure should have vitamin D supplementation.

176
Q

What are the side effects of bisphosphonates?

A
  • Reflux and oesophageal erosions. They are taken 30 minuets before food to prevent this
  • Osteonecrosis of the jaw and external auditory canal
177
Q

How should people be monitored who have osteoporosis or who are at risk of getting it?

A
  • Low risk patients should have a follow up within 5 years
  • Patients being treated should have a repeat FRAX and DEXA after 3-5 years and a treatment holiday if BMD has improved (this is 18months to 3 years of treatment before a repeat assessment)
178
Q

What is fibromyalgia?

A

Widespread chronic pain

179
Q

What are the risk factors for developing fibromyalgia?

A
  • female
  • Middle age
  • Genetics
  • Environmental e.g., child abuse, low household income divorced
180
Q

What causes fibromyalgia?

A
  • It is a problem with how the brain receives pain signals. Most patients have low levels of serotonin which is involved in inhibiting pain signals and elevated levels of substance P which increase pain signals
  • This together is though to paly a role in the hypersensitivity towards pain. Therefore the patient may perceive pain more readily compared to other people. The pain can be affected by lots of things e.g., sleep and emotions
181
Q

What are the key presentations of fibromylagia?

A

Allodynia- pain in response to non-painful stimuli
Hyperaesthesia- exaggerated perception of pain to mild stimuli

182
Q

What are the general symptoms of fibromyalgia?

A
  • Widespread pain that is aggravated by stress, cold and activity
  • Extreme tiredness
  • Sleep disturbance
  • Low mood
  • Poor concentration and headaches
183
Q

How would you diagnose fibromyalgia/

A
  • Chronic pain that has been present for at least 3 months
  • Widespread pain - involved left and right sides, above and below waist, and the axial skeleton.
  • Palpate tender point sites - severe pain in 3 to 6 different areas of your body, or you have milder pain in 7 or more different areas
  • No other reason for symptoms has been found

ALL INVESTIGATIONS WILL BE NORMAL

184
Q

What are the differentials for fibromyalga?

A
  • Rheumatoid arthritis
  • Chronic fatigue
  • Hypothyroidism
  • SLE
  • Polymyalgia rheumatica (PMR)
  • High calcium
  • Low vitamin D
  • Inflammatory arthritis
185
Q

What are the pharmacological: treatments for fibromyalgia?

A
  • Amitriptyline - tricyclic antidepressant
  • Serotonin-norepinephrinereuptake inhibitors (SNRIs) e.g. duloxetine

Help by elevating serotonin and norepinephrine levels.

  • Anticonvulsants like pregabalin and gabapentinwhich slow nerve impulses can help with sleep problems.
186
Q

What is Sjogren’s syndrome?

A

An autoimmune condition that affects the exocrine glands. It leads to symptoms such as dry mouth, eyes and vagina

187
Q

What are the tow types of Sjogren’s syndrome?

A

Primary SS: where the condition occurs in isolation

Secondary SS; where the condition occurs with SLE or rheumatoid arthritis

188
Q

What other autoimmune conditions can cause Sjogren’s syndrome?

A
  • Hepatitis
  • PBC
  • Graves’ disease
  • Antiphospholipid syndrome

normally is SLE or RA

189
Q

What are the tow main antibodies implicated in Sjogren’s syndrome?

A

Anti-Ro
Anti-La

190
Q

What is the Schirmer test for Sjogren’s syndrome?

A
  • Involves inserting a folded piece of filter paper under the lower eyelid with a strip hanging out over the eyelid
  • This is left for 5 minuets and the distance travelled along the strip is measured. Anything less than 10mm is significant
191
Q

What are the complications of Sjogren’s syndrome?

A
  • Eye infections
  • Oral problems such as cavities and candida infections
  • Vaginal problems such as candidiasis and sexual dysfunction
192
Q

What other things can be related to Sjogren’s syndrome?

A
  • Pneumonia and bronchiectasis
  • Non-Hodgkin’s lymphoma
  • Peripheral neuropathy
  • Vasculitis
  • Renal impairment
193
Q

What is the management for Sjogren’s syndrome?

A
  • Artificial tears
  • Artificial saliva
  • Vaginal lubricants
  • Hydroxychloroquine is used to halt the progression of the disease.
194
Q

What is vasculitis?

A

Inflammation of a blood vessel. It is characterised by the presence of an inflammatory infiltrate and destruction of vessel walls

195
Q

What are the types of vasculitis that affect the large vessels?

A
  • Giant cell arteritis
  • Takayasu’s arteritis
196
Q

What are the types of vasculitis that affect the medium sized vessels?

A
  • Polyarteritis nodosa
  • Kawasaki disease
197
Q

What are ANCA+ types of vasculitis that affect the small vessels?

A
  • Microscopic polyangiitis
  • Granulomatosis with polyangiitis (Wegener’s granulomatosis) ((nazi))
  • Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)
198
Q

What are the ANCA- types of vasculitis that affects the small vessels?

A

Henoch-schonlein purpura

199
Q

What are the blood tests done for vasculitis?

A

Anti neutrophil cytoplasmic antibodies (ANCA)

There are two types of blood test p-ANCA (anti-MPO) and c-ANCA (anti-PR3).

p-ANCA are positive in: Microscopic polyangiitis and Churg-Strauss syndrome
c-ANCA are positive in Granulomatosis with polyangiitis

200
Q

What is Giant Cell Arteritis (GCA)?

A

It is vasculitis of the medium and large arteries. It is the most common form of systemic vasculitis that affects and adults.

It usually affects branches of the carotid artery

201
Q

What are the risk factors for developing GCA?

A
  • Age usually over 50
  • Female
  • Caucasians
  • Polymyalgia rheumatica associated in 50% of cases
202
Q

What causes GCA and what arteries are affected?

A

It is a granulomatous vasculitis. Arteries become inflamed and thickened and there is a narrowed vascular lumen and can obstruct blood flow.

Cerebral arteries are particularly affected.:
Superficial temporal: headache and scalp tenderness
Mandibular: Jaw claudication
Ophthalmic artery: visual loss due to retinal ischaemia

203
Q

What are the signs of GCA?

A
  • Superficial temporal artery tenderness
  • Absent temporal pulse
  • Reduced visual activity
204
Q

What are the symptoms of GCA?

A
  • Main symptom is headache that us unilateral and around forehead and temple.
  • Irreversible painless complete sight loss
  • Jaw claudication
  • Scalp tenderness may be noticed when brushing hair
205
Q

What are the systemic symptoms of GCA?

A
  • Fever
  • Muscle aches
  • Fatigue
  • Weight loss
  • Loss of appetite
  • Peripheral oedema
206
Q

What are the investigations for GCA?

A
  • ESR a value of greater than 50mm/h makes up 1 of the 5 criteria
  • Definitive diagnosis- is made doing a temporal artery biopsy: will show the presence of Multinucleated giant cells. (negative results don’t rule out GCA due to presence of skip lesions)
207
Q

What should be used to make a diagnosis of GCA?

A

≥ 3 criteria should be met for a positive diagnosis of GCA

208
Q

What is the treatment of GCA?

A
  • Corticosteroids 40-60mg IV methylprednisolone
  • Oral aspirin to prevent ischaemic cranial complications
209
Q

What are the complications of GCA?

A
  • Aortic aneurysms
  • Glucocorticoid toxicity
  • Vision loss
  • Cerebrovascular accident
210
Q

What is the ongoing management for GCA?

A

Once the diagnosis is confirmed they will need to continue high dose steroids (40-60mg) until the symptoms have resolved. They then need to slowly wean off the steroids. This can take several years. This is a similar process to managing polymyalgia rheumatica.

211
Q

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

A

A multi-system disorder of unknown cause characterised by necrotising granulomatous inflammation

212
Q

What causes Granulomatosiswith polyangiitis (Wegener’s granulomatosis)?

A
  • B-cells mistakenly target their antibodies to granules made by a person’s own neutrophils.
  • These are ‘cytoplasmic anti-neutrophilic cytoplasmic antibodies’ or c-ANCAs. Once they are bound to the neutrophil it causes free radical release which damages nearby cells
213
Q

What are the symptoms of Granulomatosis with polyangiitis (Wegener’s granulomatosis)?

A

It affects the respiratory tract and the kidneys.

  • Nose bleeds
  • Sinusitis
  • Crusty nail secretions
  • Saddle shaped nose
  • Cough
  • Wheeze
  • Haemoptysis
  • glomerulonephritis
214
Q

What is the treatment for Granulomatosiswith polyangiitis (Wegener’s granulomatosis)?

A
  • Steroids combined with cyclophosphamide
  • Methotrexate and azathioprine usually used for maintenance
215
Q

What is polyarteritis nodosa?

A

Polyarteritis nodosa (PAN) is a medium vessel vasculitis. It is most associated with hepatitis B but can also occur without a clear cause or with hepatitis C and HIV.

It affects the medium sized vessels in locations such as the skin, gastrointestinal tract, kidneys and heart. This can cause renal impairment, strokes and myocardial infarction.

It is associated with a rash called livedo reticularis. This is a mottled, purplish, lace like rash.

216
Q

What is Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss syndrome)?

A

Eosinophilic granulomatosis with polyangiitis used to be called Churg-Strauss syndrome and is still often referred to by this name. It is a small and medium vessel vasculitis.

It is most associated with lung and skin problems, but can affect other organs such as kidneys.

It often presents with severe asthma in late teenage years or adulthood. A characteristic finding is elevated eosinophil levels on the full blood count.

217
Q

What is seen in Paget’s Disease of bone

A

Loads and loads of bone remodelling -
Excessive bone resorption and growth

Will lead to deformities and potential fractures

218
Q

Normal physiology - want stimulates osteoclasts to carry out bone resorption?

How is osteoclast activity stopped

A

Osteoblasts release RANKL, that binds to receptors on osteoclasts, activating them

Osteoblasts also release a substance call Osteoprotegerin, which blocks RANKL receptors on osteoclasts, so RANKL can’t bind to them and therefore prevents too much bone resorption

219
Q

What can trigger Paget’s disease of bone

A
  • Can be triggered by infections e.g. measles virus
  • Linked to genetic mutations e.g. SQSTM1
220
Q

What is some epidemology of Pagets Disease of bone

A
  • Typically affects older people (rare in under-40s)
  • Commoner in temperate climates and anglo-saxons
  • UK has highest prevalence in the world
221
Q

Outline the 3 phases of Paget’s disease of bone.

A

Phase 1 - lytic phase
- Osteoclasts which have up to 100 nuclei aggressively demineralise the bone (x20 more than normal).

Phase 2 - mixed phase (lytic and blastic)- rapid, disorganised proliferation of new bone tissue by a large number of osteoblasts. Collagen deposited in a haphazard way.

Phase 3 - sclerotic phase - New bone formation exceeds bone resorption. The bone is structurally disorganised and weak.

  • Osteoblastic activity slows down leading to dormant phase - ‘burned out state’
222
Q

What things can Paget’s disease of bone lead to?

A

Misshapen bone, that can impinge on nerves = pain

Overgrowth of bone, can lead to Hearing and vision loss

Can lead to osteosarcoma - Paget Sarcoma

Can lead to bony deformities, like
Kyphosis
Bow legs
pelvic asymmetry
Arthritis, joint inflammation, Easy fractures

223
Q

What are the investigations you would do for Paget’s disease of bone?

A

high levels of ALP

Lytic lesions and thickened bone cortices on xray

Bone biopsy to exclude malignancies

224
Q

What is the management for Pagets disease of bone?

A
  • pain relief
    • NSAIDs
  • Anti-resorptive medication - Biphosphonates e.g. alendronic acid
    • Along with calcium and vit D supplementation
  • Surgery -
    • Correct bone deformities
    • Decompress impinged nerve
    • Decrease fracture risk
225
Q

What is Marfan Syndrome? What gene is affected and what does it lead to,

A

Autosomal dominant condition affecting the FB1 gene which results in abnormal fibrillin production and therefore a reduced connective tissue strength

226
Q

Cancers of what bone cells are maligant?

A
  • Osteosarcoma - Arise from osteoblasts
  • Chondrosarcoma
    • Arises from the chondrocytes which are cartilage-producing cells.
  • Ewing sarcoma
    • Thought to arise from neuroectodermal cells
227
Q

Name and define some bengin bone cancers.

A
  • Osteochondroma - mutations in EXT1 + EXT2

arises from the growth plate, and it typically results in a lateral bony projection (exostosis) that has a cap, made mostly of hyaline cartilage.

  • Giant cell tumour
    • Risk factor: bony trauma e.g. fracture or radiation exposure
    • The tumor cells arises from osteoclasts cells, that develop into cells that have numerous nuclei - typically over 50 nuclei.
  • Osteoblastomas - large Nidus - Arise from osteoblasts
  • Osteoid osteomas- Small nidus - Arise from osteoblasts
228
Q

What are the key malignancies that can spread to bone to cause a secondary bone tumour?

A

BLT KP:
Breast
Lung
Thyroid
Kidney
Prostate

229
Q

Which secondary causes of bone cancer are osteolytic? What does osteolytic mean?

A

Breast and lung

Osteolytic = Causing the breakdown of bone

230
Q

Which Secondary causes of bone cancer are osteoslcerotic?

A

Prostate
Thyroid
RCC

Abnormal hardening of bone and an elevation in bone density

231
Q

What are the diagnostic investigations of bone tumours?

A

Local persistent severe pain often worse at night

Systemic:
Weight loss, fatigue, fever, malaise

Primary bone cancers only seen in the young

232
Q

What is the treatment of bone cancer?

A

Surgical resection - often limb amputation
Adjuvant Chemo/radiotherapy

Bisphosphonates

233
Q

Define Osteomalacia?

A

Defective bone mineralisation that has occurred after fusion of the epiphyseal growth plates therefore only occurs in adults.

234
Q

What is Rickets?

A

Disorder of defective bone mineralisation that has occurred prior to fusion of the epiphyseal growth plates and therefore occurs in children

235
Q

What is the pathophysiology of osteomalacia?

A

Commonly Vitamin D deficiency leading to reduced calcium and phosphate absorption from the GI tract.

Therefore there is inadequate production of Calcium Hydroxyapatite to mineralise bone

236
Q

What are the causes of Osteomalacia?

A

Vitamin D deficiency:
Malabsorption, Low intake, poor sunlight

CKD - low vitamin D activation cannot produce 1,25-hydroxyvit D)

Liver failure - Low reaction of Vit D pathway

Hyperparathyroidism - secondary to Vit D deficiency

237
Q

How can anti-convulsant drugs cause osteomalacia?

A

Increase CYP450 metabolism of vitamin D leading to deficiency and hence subsequent osteomalacia

238
Q

What are the symptoms of osteomalacia?

A

Generalised Bone Pain
Fractures of bone - most commonly femoral neck
Proximal weakness
Difficulty bearing weight

239
Q

What are the symptoms of Rickets?

A

Skeletal deformities

Knocked knees and Bowed Legs
Wide Epiphyses

240
Q

What is the Treatment for osteomalacia?

A

Correct initial Vit D and then maintenance:

Vitamin D replacement - Calcitriol

Increase dietary intake of Vit D (D3 tablets/eggs)

Treat underlying cause

241
Q

What are some causes of lower mechanical back pain?

A

Many causes, including

  • Strain
  • Heavy manual handling
  • Stooping and twisting whilst lifting
  • Pregnancy
  • Trauma
  • Lumbar disc prolapse
  • Spondylolisthesis (one vertebrae slips out of place causing back pain)
  • Osteoarthritis
  • Fractures
  • Exposure to whole body vibration
242
Q

What are some High-risk activities for MSK Problems

A

Heavy manual handling (>20kg)
Lifting above shoulder height
Lifting from below knee height
Incorrect manual handling technique
Forceful movements
Fast repetitive work, poor postures, poor grip

243
Q

What is a common cause of mechanical lower back pain?

A

Prolapse of the vertebral disc causing acute pain.
Vertebral disc degeneration

244
Q

What is the clinical presentation of a vertebral disc degeneration?

A

Sudden onset of severe back pain

often following a strenuous activity
Pain is often clearly related to position and is aggravated by movement
Muscle spasm leads to a sideways tilt when standing

Lower 3 discs

L4 - lateral thigh to medial calf

L5 - Buttock to lateral leg and top foot

S1 - Buttock down back of thigh to ankle/foot

245
Q

What are some red flags that would prompt you to take an xray of someone with lower back pain?

A

Red flags – TUNAFISH
T – trauma, TB
U – unexplained weight loss and night sweats
N – neurological deficits, bowel and bladder incontinence
A – age less than 20, or over 55
F - fever
I – IV drug user
S - steroid use or immunosuppressed
H – history of cancer, early morning stiffness

246
Q

What antibody is specific to SLE but not very sensitive?

A

Anti-Smith (highly specific to SLE but not very sensitive)
Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis)
Anti-Ro and Anti-La (most associated with Sjogren’s syndrome)
Anti-Scl-70 (most associated with systemic sclerosis)
Anti-Jo-1 (most associated with dermatomyositis)

247
Q

What antibody is specific to systemic sclerosis?

A
  • Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis).
  • Anti-Scl-70 (most associated with systemic sclerosis)
248
Q

What antibodies are specific to Sjogren’s syndrome?

A

Anti-Ro and Anti-La (most associated with Sjogren’s syndrome)

249
Q

What antibody is associated with dermatomyositis?

A

Anti-Jo-1 (most associated with dermatomyositis)

Phase 2A Tom (15 decks)

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