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Phase 2a Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Give 3 causes of inflammatory joint pain.

A
  1. Autoimmune disease e.g. RA, vasculitis, connective tissue disease.
  2. Crystal arthritis.
  3. Infection.
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2
Q

Give 2 causes of non-inflammatory joint pain.

A
  1. Degenerative e.g. osteoarthritis.

2. Non-degenerative e.g. fibromyalgia.

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3
Q

What are the 5 cardinal signs of inflammation?

A
  1. Rubor (redness).
  2. Calor (heat).
  3. Dolor (pain).
  4. Tumor (swelling).
  5. Loss of function.
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4
Q

How does inflammatory pain differ from degenerative non-inflammatory pain?

A

Inflammatory pain tends to ease with use whereas degenerative pain increased with use.

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5
Q

Are you more likely to see swelling in inflammatory or degenerative pain?

A

In inflammatory pain you are likely to see synovial swelling. There is often no swelling in degenerative pain.

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6
Q

Name 2 inflammatory markers that can be detected in blood tests.

A
  1. ESR (erythrocyte sedimentation rate).

2. CRP.

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7
Q

Explain why ESR levels are raised in someone with inflammatory joint pain.

A

Inflammation leads to increased fibrinogen which means the RBC’s clump together. The RBC’s therefore fall faster and so you have an increased ESR.

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8
Q

Explain why CRP levels are raised in someone with inflammatory joint pain.

A

Inflammation leads to increased levels of IL-6. CRP is produced by the liver in response to IL-6 and therefore is raised.

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9
Q

Describe the ESR and CRP levels in someone with lupus.

A

ESR is raised and CRP is low.

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10
Q

With what tissue type are all spondyloarthritis conditions associated?

A

They are all associated with tissue type HLAB27.

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11
Q

Give 5 conditions that fall under the umbrella term spondyloarthritis.

A
  1. Ankylosing spondylitis.
  2. Reactive arthritis.
  3. Psoriatic arthritis.
  4. Enteropathic arthritis.
  5. Juvenile idiopathic arthritis.
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12
Q

What is the function of HLAB27?

A

It is an antigen presenting cell.

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13
Q

Describe the ‘molecular mimicry’ theory for explaining why HLAB27 is associated with spondyloarthritis.

A

Infectious agents have peptides very similar to HLAB27. An auto-immune response is triggered against HLAB27.

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14
Q

Name 3 theories that can explain why HLAB27 is associated with spondyloarthritis.

A
  1. Molecular mimicry.
  2. Mis-folding theory.
  3. HLAB27 heavy chain hypothesis.
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15
Q

Give 6 signs of spondyloarthritis.

A
  1. Psoriasis.
  2. Inflammatory spine and buttock pain.
  3. Good response to NSAIDS.
  4. Enthesitis.
  5. Arthritis.
  6. Crohn’s/colitis associated.
  7. Uveitis.
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16
Q

What is the general treatment for all spondyloarthritis?

A

Initially DMARDs and then biological agents if DMARDs fail e.g. TNF blockers.

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17
Q

Describe the pathophysiology of ankylosing spondylitis.

A

Inflammation of spine -> erosive damage -> repair/new bone formation -> irreversible fusion of spine.

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18
Q

Give 5 symptoms of ankylosing spondylitis.

A
  1. BACK PAIN!
  2. Morning stiffness.
  3. Waking in the second half of the night.
  4. Buttock pain.
  5. Insidious onset.
  6. Usually <40y/o at onset.
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19
Q

What investigations might you do in someone who you suspect to have ankylosing spondylitis?

A
  1. X-ray.
  2. MRI.
  3. HLAB27 test.
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20
Q

What is the diagnostic criteria for ankylosing spondylitis?

A
  1. > 3 months back pain.
  2. Aged <45 at onset.
  3. Plus one of the SPINEACHE symptoms.
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21
Q

Give 3 locations that psoriasis commonly occurs at.

A
  1. Elbows.
  2. Knees.
  3. Fingers.
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22
Q

What is reactive arthritis?

A

Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually GI or genital.

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23
Q

What gut infections are associated with reactive arthritis?

A

Salmonella, shigella.

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24
Q

What sexually transmitted infections are associated with reactive arthritis?

A

Chlamydia.

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25
Q

What is the triad of symptoms for reactive arthritis?

A
  1. Arthritis.
  2. Conjunctivitis.
  3. Urethritis.
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26
Q

What type of spondyloarthritis occurs in 20% of patients with IBD?

A

Enteropathic arthritis.

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27
Q

What is the criteria for making a clinical diagnosis of juvenile idiopathic arthritis?

A

Joint swelling/stiffness >6 weeks in children <16 and no other cause is identified.

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28
Q

What is the aetiology of JIA?

A

Unknown - idiopathic!

However, it is autoimmune so there are genetic factors associated.

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29
Q

Why is it important to check the eyes in JIA?

A

The lining of the eyes and the joints is very similar. Children with JIA are at a high risk of developing uveitis!

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30
Q

What type of JIA affects <4 joints and is usually ANA positive?

A

Oligoarthritis.

High risk of developing uveitis!

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31
Q

What JIA is similar to adult ankylosing spondylitis?

A

Enthesitis related JIA - inflammation of where the tendon joins a bone. HLAB27 positive.

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32
Q

Describe the non-medical treatment for JIA.

A
  1. Information.
  2. Education.
  3. Support.
  4. Liaison with school.
  5. Physiotherapy.
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33
Q

Describe the medical treatment for JIA.

A
  1. Steroid joint injections.
  2. NSAIDS.
  3. Methotrexate.
  4. Systemic steroids.
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34
Q

Give 5 potential consequences that can occur if you fail to treat JIA.

A
  1. Damage.
  2. Deformity.
  3. Disability.
  4. Pain.
  5. Bony overgrowth.
  6. Uveitis.
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35
Q

What is the diagnostic criteria for fibromyalgia?

A

Chronic widespread pain lasting for >3months with other causes excluded. Pain is at 11 of 18 tender point sites.

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36
Q

Give 3 factors that increase the volume of pain.

A
  1. Substance P.
  2. Glutamate.
  3. Serotonin.
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37
Q

Give 3 factors that decrease the volume of pain.

A
  1. Opioids.
  2. GABA.
  3. Cannabanoids.
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38
Q

Name 4 diseases that fibromyalgia is commonly associated with.

A
  1. Depression.
  2. Chronic fatigue.
  3. Chronic headache.
  4. IBS.
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39
Q

Give 5 symptoms of fibromyalgia.

A
  1. Neck and back pain.
  2. Pain is aggravated by stress, cold and activity.
  3. Generalised morning stiffness.
  4. Subjective swelling of extremities.
  5. Frequent waking during the night.
  6. Waking unrefreshed.
  7. Low mood, irritable, weepy.
  8. Headache and IBS common.
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40
Q

Give 5 triggers of fibromyalgia.

A
  1. Physical trauma.
  2. Distress.
  3. Hormonal alterations e.g. hypothyroid.
  4. Infections.
  5. Certain catastrophic events e.g. wars.
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41
Q

Give 3 diseases might be included in the differential diagnosis for fibromyalgia?

A
  1. Hypothyroidism.
  2. SLE.
  3. Low vitamin D.
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42
Q

Describe the management for fibromyalgia.

A
  1. Educate the patient and family.
  2. ‘Resent the pain thermostat’.
  3. Low does amitriptyline can help with sleep.
  4. Graded aerobic exercise.
  5. Acupuncture.
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43
Q

What 2 things are essential in the management of fibromyalgia?

A
  1. Explaining that sleep disturbance is central to what they’re feeling.
  2. Emphasising the importance of exercise and fitness.
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44
Q

What is vasculitis?

A

Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow.

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45
Q

What cells might you see on a histological slide taken from someone with vasculitis?

A

Neutrophils and giant cells.

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46
Q

Chapel Hill classification: give an example of a large artery primary disorder.

A

Giant cell arteritis.

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47
Q

Chapel Hill classification: give an example of a large artery secondary disorder.

A

Aortitis in RA.

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48
Q

Chapel Hill classification: give an example of a medium/small artery primary disorder.

A

Wegener’s granulomatosis (GPA).

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49
Q

Chapel Hill classification: give an example of a medium/small artery secondary disorder.

A

Vasculitis secondary to autoimmune disease, malignancy, drugs.

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50
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies.

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51
Q

Describe the epidemiology of giant cell arteritis.

A
  • Affects those >50y/o.
  • Incidence increases with age.
  • Twice as common in women.
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52
Q

Give 5 symptoms of giant cell arteritis.

A
  1. Headache.
  2. Scalp tenderness.
  3. Jaw claudication.
  4. Acute blindness.
  5. Malaise.
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53
Q

What might you find on clinical investigation in someone with giant cell arteritis?

A
  1. Palpable and tender temporal arteries with reduced pulsation.
  2. Sudden monocular visual loss, the optic disc is pale and swollen.
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54
Q

What is the diagnostic criteria for giant cell arteritis?

A
  1. Age >50.
  2. New headache.
  3. Temporal artery tenderness.
  4. Abnormal artery biopsies.
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55
Q

What investigations might you do in someone who you suspect has giant cell arteritis?

A
  1. Bloods for inflammatory markers e.g. CRP, ESR.

2. Temporal artery biopsy.

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56
Q

Describe the treatment for giant cell arteritis.

A
  • Prompt corticosteroids - prednisolone.
  • Methotrexate is sometimes adeed.
  • Osteoporosis prophylaxis is important e.g. lifestyle advice and vitamin D.
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57
Q

Is Wegener’s granulomatosis associated with c-ANCA or p-ANCA?

A

c-ANCA.

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58
Q

What organ systems can be affected by Wegener’s granulomatosis?

A
  1. URT.
  2. Lungs.
  3. Kidneys.
  4. Skin.
  5. Eyes.
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59
Q

What is the affect of Wegener’s granulomatosis on the URT?

A
  • Sinusitis.
  • Otitis.
  • Nasal crusting.
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60
Q

What is the affect of Wegener’s granulomatosis on the lungs?

A
  • Pulmonary haemorrhage/nodules.

- Inflammatory infiltrates are seen on X-ray.

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61
Q

What is the affect of Wegener’s granulomatosis on the kidney?

A

Glomerulonephritis.

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62
Q

What is the affect of Wegener’s granulomatosis on the skin?

A

Ulcers.

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63
Q

What is the affect of Wegener’s granulomatosis on the eyes?

A
  • Uveitis.
  • Scleritis.
  • Episcleritis.
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64
Q

What is the treatment for Wegener’s granulomatosis?

A
  • If severe: high dose steroids.

- If non-end organ threatening: moderate steroids.

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65
Q

What is rheumatoid arthritis?

A

An auto-immune inflammatory synovial joint disease.

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66
Q

Describe the epidemiology of RA.

A
  • 2 to 3 times more common in women.

- Approximately 1% of the population affected.

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67
Q

Describe the aetiology of RA.

A

Auto-antibodies e.g. RF and anti-CCP lead to a defective cell mediated immune response.

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68
Q

Describe the pathophysiology of RA.

A
  1. Chronic inflammation. B/T cells and neutrophils infiltrate.
  2. Proliferation -> pannus formation.
  3. Pro-inflammatory cytokines -> proteinases -> cartilage destruction.
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69
Q

Give 5 symptoms of RA.

A
  1. Early morning stiffness (>60 mins).
  2. Pain eases with use.
  3. Swelling.
  4. General fatigue, malaise.
  5. Extra-articular involvement.
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70
Q

Give 5 signs of RA.

A
  1. Symmetrical.
  2. Deforming.
  3. Polyarthropathy.
  4. Erosion on X-ray.
  5. 80% are RF positive.
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71
Q

RA extra-articular involvement: describe the effect on soft tissues.

A
  • Nodules.
  • Bursitis.
  • Muscle wasting.
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72
Q

RA extra-articular involvement: describe the effect on the eyes.

A
  • Dry eyes.
  • Scleritis.
  • Episcleritis.
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73
Q

RA extra-articular involvement: describe the neurological effects.

A
  • Sensory peripheral neuropathy.
  • Entrapment neuropathies e.g. carpal tunnel syndrome.
  • Instability of cervical spine.
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74
Q

RA extra-articular involvement: describe the haematological effects.

A
  • Palpable lymph nodes.
  • Splenomegaly.
  • Anaemia.
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75
Q

RA extra-articular involvement: describe the pulmonary effects.

A
  • Pleural effusion.
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76
Q

RA extra-articular involvement: describe the effects on the heart.

A
  • Pericardial rub.

- Pericardial effusion.

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77
Q

RA extra-articular involvement: describe the effect on the kidneys.

A

Amyloidosis.

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78
Q

What is rheumatoid factor?

A

An antibody against the Fc portion of IgG.

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79
Q

What investigations might you do in someone who you suspect has rheumatoid arthritis?

A
  • Bloods for inflammatory markers; ESR and CRP will be raised.
  • Test for anaemia.
  • Test for RF and anti-CCP.
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80
Q

Describe the treatment for rheumatoid arthritis.

A
  • NSAIDS.
  • Corticosteroids.
  • DMARDs.
  • Biological agents.
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81
Q

Define osteoarthritis.

A

A non-inflammatory degenerative disorder of moveable joints characterised by the deterioration of articular cartilage and the formation of new bone.

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82
Q

Why does the prevalence of OA increase with age?

A

Due to the cumulative effect of trauma and a decrease in neuromuscular function.

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83
Q

Give 5 risk factors for developing OA.

A
  1. Genetic predisposition.
  2. Trauma.
  3. Abnormal biomechanics e.g. hypermobility.
  4. Occupation e.g. manual labour.
  5. Obesity; pro-inflammatory state.
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84
Q

What are the most important cells responsible for OA?

A

Chrondrocytes.

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85
Q

Give 5 symptoms of OA.

A
  1. Morning stiffness (<30 minutes).
  2. Pain - aggravated by activity.
  3. Tenderness.
  4. Walking and ADLs affected.
  5. Joint swelling and bony enlargement.
  6. Deformities.
  7. Crepitus.
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86
Q

Give 5 radiological features associated with OA.

A
  1. Joint space narrowing.
  2. Osteophyte formation.
  3. Sub-chondral sclerosis.
  4. Sub-chondral cysts.
  5. Abnormalities of bone contour.
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87
Q

Name 3 joints of the hand that are commonly affected in osteoarthritis.

A
  1. Distal interphalangeal joint.
  2. Proximal interphalangeal joint.
  3. Carpal metacarpal joint.
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88
Q

Which surface of the knee is most commonly affected by OA?

A

The medial surface.

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89
Q

What is the primary investigation used to make a diagnosis of OA?

A

X-ray.

Look for asymmetric loss of joint space; sclerosis; cysts and osteophytes.

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90
Q

Describe features of the non-medical management for OA.

A
  • Education.
  • Exercise.
  • Weight loss.
  • Physiotherapy.
  • Occupational therapy.
  • Walking aids.
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91
Q

Describe the pharmacological management for OA.

A
  • NSAIDS (topical better than PO).
  • Paracetamol.
  • Intra-articular steroid injections.
  • DMARDs if there is an inflammatory component.
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92
Q

Describe the surgical management for OA.

A
  • Arthroscopy for loose bodies.
  • Osteotomy (changing bone length).
  • Arthroplasty (joint replacement).
  • Fusion (usually ankle and foot).
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93
Q

Give 3 indications for surgery.

A
  1. Significant limitation of function.
  2. Uncontrolled pain.
  3. Waking at night from pain.
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94
Q

A patient complains of ‘locking’, what is the most likely cause of this?

A

This is probably due to a loose body e.g. a bone or cartilage fragment.

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95
Q

What is the treatment for loose bodies?

A

Arthroscopy.

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96
Q

Give an example of an inherited connective tissue disease.

A
  1. Marfan’s syndrome.

2. Ehler Danlos syndrome.

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97
Q

Give an example of an autoimmune connective tissue disease.

A
  1. SLE.
  2. Systemic sclerosis.
  3. Sjögren’s syndrome.
  4. Dermatomyositis.
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98
Q

What is SLE?

A

Systemic Lupus Erythematosus is an inflammatory multi-system disease characterised by the presence of serum anti-nuclear antibodies (ANA).

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99
Q

Describe the epidemiology of SLE.

A
  • 90% of cases are in young women.
  • More common in afro-Caribbeans.
  • Genetic association.
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100
Q

Describe the pathogenesis of SLE.

A
  • Inefficient phagocytosis means cell fragments are transferred to lymphoid tissue where they are taken up by APC. T cells stimulate B cells to produce antibodies against self-antigens.
  • Immune complex deposition -> neutrophil and cytokine influx -> inflammation and tissue damage.
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101
Q

What can cause thrombosis in patients with SLE?

A

The presence of antiphospholipid antibodies.

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102
Q

What autoantibody is specific to SLE?

A

Anti-dsDNA.

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103
Q

Give 5 symptoms of SLE.

A
  1. Butterfly rash.
  2. Mouth ulcers.
  3. Raynaud’s phenomenon/’cold pale fingers’.
  4. Fatigue.
  5. Depression.
  6. Weight loss.
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104
Q

What investigations might you do in someone who you suspect has SLE?

A
  1. Blood count may show normocytic anaemia; neutropenia; thrombocytopaenia. Raised ESR, normal CRP.
  2. Serum autoantibodies: ANA, anti-dsDNA.
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105
Q

Describe the non-medical treatment for SLE.

A
  • Education and support.
  • UV protection.
  • Screening for organ involvement.
  • Reduce CV risk factors e.g. smoking cessation.
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106
Q

Describe the pharmacological treatment for SLE.

A
  • Corticosteroids.
  • NSAIDS.
  • Anti-malarials (DMARDs).
  • Anticoagulants (for those with antiphospholipid antibodies).
  • Biological therapy targeting B cells e.g. rituximab.
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107
Q

What is scleroderma?

A

A multi-system disease characterised by skin hardening and Raynaud’s phenomenon.

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108
Q

Give 5 signs of limited scleroderma.

A
  1. Calcinosis.
  2. Raynaud’s phenomenon.
  3. Oesophageal reflux.
  4. Sclerodactyly (thickening and tightening of the skin).
  5. Telangectasia (visible small red blood vessels).
  6. Pulmonary arterial hypertension.
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109
Q

Give 4 signs of diffuse scleroderma.

A
  1. Proximal scleroderma.
  2. Pulmonary fibrosis.
  3. Bowel involvement.
  4. Myositis.
  5. Renal crisis.
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110
Q

Describe the pathophysiology of scleroderma.

A
  • Various factors cause an endothelial lesion and vasculopathy.
  • There is excessive collagen deposition (skin hardening), inflammation and auto-antibody production.
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111
Q

Describe the management of scleroderma.

A
  1. Raynaud’s: physical protection and vasodilators.
  2. GORD: PPI’s.
  3. Annual Echo and pulmonary function tests to monitor arterial pulmonary pressure.
  4. ACEi to prevent renal crisis.
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112
Q

What is the pathophysiology of sjögren’s syndrome?

A

Immunologically mediated destruction of epithelial exocrine glands, especially lacrimal and salivary glands.

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113
Q

What does sjögren’s syndrome often occur secondary to?

A

Other auto-immune disorders e.g. SLE, RA, scleroderma, primary biliary cirrhosis.

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114
Q

Give 5 symptoms of sjögren’s syndrome.

A
  1. Dry eyes and dry mouth.
  2. Inflammatory arthritis.
  3. Rash.
  4. Neuropathies.
  5. Vasculitis.
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115
Q

Why does someone with sjögren’s syndrome have dry eyes and a dry mouth?

A

There is immunologically mediated destruction of epithelial exocrine glands meaning the lacrimal and salivary glands produce fewer secretions.

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116
Q

What investigations might you do in someone who you suspect to have sjögren’s syndrome?

A

Look for serum auto-antibodies e.g. anti-RO, RF, ANA.

Also, raised immunoglobulins and ESR.

117
Q

What is the treatment for sjögren’s syndrome?

A
  • Tear and saliva replacement.

- Immunosuppression for systemic complications.

118
Q

What is dermatomyositis?

A

A rare disorder of unknown aetiology. There is inflammation and necrosis of skeletal muscle fibres and skin.

119
Q

Give 3 symptoms of dermatomyositis.

A
  1. Rash.
  2. Muscle weakness.
  3. Lungs are often affected too e.g. ILD.
120
Q

What investigations might you do in someone who you suspect has dermatomyositis?

A
  1. Muscle enzymes - raised.
  2. EMG.
  3. Muscle/skin biopsy.
  4. Screen for malignancy.
  5. CXR.
121
Q

What is the treatment for dermatomyositis?

A

Steroids and immunosuppressants.

122
Q

What is the name given to inflammation of an entire digit?

A

Dactylitis.

123
Q

What is the approach used for managing trauma patients?

A

ATLS - treat the greatest threat to life first (ABCDE).

124
Q

Describe the physiological pathway that leads to monosodium urate formation.

A

Purines -> hypoxanthine -> xanthine -> uric acid -> monosodium urate.

125
Q

What enzyme converts hypoxanthine to xanthine?

A

Xanthine oxidase.

126
Q

Give 5 factors that can lead to increased levels of monosodium urate.

A
  1. Increased intake e.g. alcohol, red meat, seafood.
  2. Cell turnover (increased production).
  3. Cell damage e.g. due to surgery.
  4. Cell death e.g. due to chemotherapy.
  5. Reduced excretion (renal problems).
  6. Drugs e.g. bendroflumethiazide - diuretics impair urate excretion.
  7. High insulin.
127
Q

Name a drug that can lead to increased monosodium urate.

A

Bendroflumethiazide.

Diuretics impair urate excretion.

128
Q

Describe the epidemiology of gout.

A

Gout is most common in men over 75 y/o.

129
Q

Give a symptom of gout.

A

Hot and swollen joints.

The toes are commonly effected.

130
Q

What are tophi?

A

Onion like aggregates of urate crystals with inflammatory cells. Proteolytic enzymes are released -> erosion.

131
Q

Name 4 diseases that someone with gout might have an increased risk of developing.

A
  1. Hypertension.
  2. CV disease e.g. stroke.
  3. Renal disease.
  4. Type 2 diabetes.
132
Q

What is the aim of treatment for gout?

A

To get urate levels < 300μmol/L.

133
Q

Name 5 treatment options for gout.

A
  1. Lifestyle modification e.g. diet, weight loss, reduced alcohol.
  2. Allopurinol (blocks xanthine oxidase).
  3. Colchicine or NSAIDS.
  4. Switch from bendroflumethiazide to cosartan.
  5. Rasburicase - rapid urate reduction.
134
Q

Name a drug used in the treatment of gout that blocks xanthine oxidase.

A

Allopurinol.

135
Q

You see a patient with gout who is taking bendroflumethiazide. What drug might you replace this with to help treat their gout?

A

You would switch bendroflumethiazide to cosartan as bendroflumethiazide is a diuretic and so impairs urate excretion.

136
Q

Name 6 factors that can cause an acute attack of gout.

A
  1. Sudden overload.
  2. Cold.
  3. Trauma.
  4. Sepsis.
  5. Dehydration.
  6. Drugs.
137
Q

Describe the pathophysiology of pyrophosphate arthropathy (pseudogout).

A

Calcium pyrophosphate crystals are deposited on joint surfaces. The crystals elicit an inflammatory response.

138
Q

What can cause pyrophosphate arthropathy (pseudogout)?

A
  1. Hypo/hyperthyroidism.
  2. Diabetes.
  3. Haemochromatosis.
  4. Magnesium levels.
139
Q

Give a symptom of pyrophosphate arthropathy (pseudogout).

A

Acute, hot and swollen joints. Typically the wrists and knees.

140
Q

What investigations might you do in someone who you suspect might have pyrophosphate arthropathy (pseudogout)?

A
  1. Aspiration: fluid for crystals and blood cultures.

2. X-rays: can show chondrocalcinosis.

141
Q

What is the most likely differential diagnosis for pyrophosphate arthropathy (pseudogout)?

A

Infection.

142
Q

Describe the treatment for pyrophosphate arthropathy (pseudogout).

A

Treat the underlying cause and use methotrexate for inflammation.

143
Q

Define osteoporosis.

A

A systemic skeletal disease characterised by low bone mass and micro-architectural deterioration. The patient is at increased risk of fracture.

144
Q

Describe the epidemiology of osteoporosis.

A

50% of women and 20% of men over 50 are affected. The incidence increases with age.

145
Q

What 2 factors are important for determining the likelihood of osteoporotic fracture?

A
  1. Propensity to fall -> trauma.

2. Bone strength.

146
Q

Give 4 properties of bone that contribute to bone strength.

A
  1. Bone mineral density.
  2. Bone size.
  3. Bone turnover.
  4. Bone micro-architecture.
  5. Mineralisation.
  6. Geometry.
147
Q

Name a hormone that can control osteoclast action and so bone turnover.

A

Oestrogen.

148
Q

Why are so many women over 50 affected by osteoporosis?

A

Women over 50 are likely to be post-menopausal; they therefore have less oestrogen and so osteoclast action isn’t inhibited. There is a high rate of bone turnover -> bone loss and deterioration -> fracture risk.

149
Q

What happens to bone micro-architecture as we get older that leads to a reduction in bone strength?

A

Trabecular thickness decreases; especially in the horizontal plane. There are fewer connections between trabecular and so an overall decrease in trabecular strength -> increased risk of fracture.

150
Q

Why can RA cause osteoporosis?

A

RA is an Inflammatory disease. There are high levels of IL-6 and TNF; these are responsible for increased bone resorption.

151
Q

Name 3 endocrine diseases that can be responsible for causing osteoporosis.

A
  1. Hyperthyroidism and primary hyperparathyroidism: TH and PTH -> increased bone turnover.
  2. Cushing’s syndrome: cortisol leads to increased bone resorption and osteoblast apoptosis.
  3. Early menopause, male hypogonadism: less oestrogen/testosterone to control bone turnover.
152
Q

What is the affect of high cortisol levels on bone turnover?

A

Cortisol increases bone turnover. It leads to increased bone resorption and it also induces osteoblast apoptosis.

153
Q

Give 5 risk factors for osteoporosis.

A
  1. Previous fracture.
  2. FHx.
  3. Excessive alcohol.
  4. Smoking.
  5. Medications e.g. steroids, depo provera.
  6. Immobility.
154
Q

What investigation might you do in someone who you suspect to have osteoporosis?

A

DEXA scan.

A T score will be generated.

155
Q

Name 2 areas of the skeleton commonly affected by osteoporosis that the DEXA scan focuses on.

A
  1. Lumbar spine.

2. Hip.

156
Q

What is a T score?

A

A T score is a standard deviation that is compared to a gender-matched young adult mean.

157
Q

What T score signifies that a patient has osteoporosis?

A

T < -2.5

158
Q

What T score signifies that a patient has osteopenia?

A

-2.5 < T < -1

159
Q

What is a normal T score?

A

-1

160
Q

What tool can be used to assess someones risk of osteoporotic fracture?

A

FRAX.

161
Q

Give 2 examples of anti-resorptive treatments used in the management of osteoporosis.

A
  1. Bisphosphonates.
  2. HRT.

Anti-resorptive treatments decrease osteoclast activity.

162
Q

Give an example of an anabolic treatment used in the management of osteoporosis.

A

Teriparatide.

Anabolic treatments increase osteoblast activity.

163
Q

What cells do anti-resorptive treatments target in people with osteoporosis?

A

They decrease osteoclast activity.

164
Q

What cells do anabolic treatments target in people with osteoporosis?

A

They increase osteoblast activity.

165
Q

Give 3 advantages of HRT.

A
  1. Reduces fracture risk.
  2. Stops bone loss.
  3. Prevents menopausal symptoms.
166
Q

Give 3 disadvantages of HRT.

A
  1. Increased risk of breast cancer.
  2. Increased risk of stroke and CV disease.
  3. Increased risk of thrombo-embolism.
167
Q

Give an example of a bisphosphonate.

A

Alendronate.

168
Q

What pathway do bisphosphonates target?

A

HMGCoA pathway.

169
Q

What is the physis?

A

The physis is the growth plate in paediatric bone.

170
Q

What feature of paediatric bone means it can heal rapidly?

A

The thick periosteum.

171
Q

Describe the 3 initial steps in the management of fractures.

A
  1. Reduce the fracture e.g. restore the length, alignment, rotation.
  2. Immobilise.
  3. Rehabilitate.
172
Q

What is often the first line management option for paediatric fractures?

A

Non-operative management e.g. traction, casts, splints. This is because paediatric bone heals quickly due to the thick periosteum.

173
Q

What can happen if the physis is damaged?

A

Physis damage -> growth arrest -> deformity.

174
Q

What is the name of the classification used for fractures involving the physis?

A

Salter-Harris Fracture classification.

175
Q

Salter-Harris Fracture classification: describe a type 1 fracture.

A

Transverse fracture through the growth plate.

176
Q

Salter-Harris Fracture classification: describe a type 2 fracture.

A

A fracture through the growth plate and metaphysis.

177
Q

Salter-Harris Fracture classification: describe a type 3 fracture.

A

A fracture through the growth plate and epiphysis.

178
Q

Salter-Harris Fracture classification: describe a type 4 fracture.

A

A fracture through the metaphysis, physis and epiphysis. These fractures often need fixation.

179
Q

Salter-Harris Fracture classification: describe a type 5 fracture.

A

Crush injury of growth plate! These fractures have a very poor prognosis and growth arrest is likely.

180
Q

Give 2 ‘red flag’ signs of non-accidental injury in children.

A
  1. Long bone fracture in a child unable to walk.

2. Multiple bruises and fractures.

181
Q

Describe the management for non-accidental injury in children.

A
  1. Admit the child!
  2. Skeletal survey.
  3. Referral to paediatric medics and safeguarding services.
182
Q

What can cause a supracondylar fracture in children?

A

Falling on an outstretched hand.

183
Q

What nerve might be affected in a supracondylar fracture?

A

The median nerve.

184
Q

What is the treatment for a supracondylar fracture?

A

K-wires.

185
Q

Give 5 potential complications of fractures.

A
  1. Open fractures.
  2. Neurovascular compromise.
  3. Mal union - bone heals with deformity.
  4. Non union - bone fails to heal.
  5. Compartment syndrome.
  6. Cast problems e.g. tightness, compartment syndrome, plaster burns/blisters.
186
Q

Define osteomyelitis.

A

Bone inflammation secondary to infection.

187
Q

Describe the epidemiology of osteomyelitis.

A
  • Increasing incidence of chronic OM.

- Bimodal age distribution.

188
Q

What can cause osteomyelitis.

A
  1. S.aureus!
  2. Coagulase negative staphylococci e.g. s.epidermidis.
  3. Aerobic gram negative bacilli.
  4. Mycobacterium TB.
189
Q

Name 2 predisposing conditions for osteomyelitis.

A
  1. Diabetes.

2. PVD.

190
Q

Pathophysiology of osteomyelitis: describe the 3 ways in which the pathogen can get into bone.

A
  1. Easy: inoculation of infection into the bone e.g. trauma/open wound.
  2. Quite easy: contiguous spread of infection to bone from adjacent tissues.
  3. Difficult: hematogenous seeding e.g. due to cannula infection.
191
Q

What bones are likely to be affected by hematogenous seeding in adults?

A

Vertebrae.

192
Q

What bones are likely to be affected by hematogenous seeding in children?

A

Long bones.

193
Q

Why do vertebrae tend to be affected by hematogenous seeding in adults?

A

With age, the vertebrae become more vascular meaning bacterial seeding is more likely.

194
Q

Why do long bones tend to be affected by hematogenous seeding in children?

A

In children the metaphysis of long bones has a high blood flow and BM are absent meaning bacteria can move from the blood to bone.

195
Q

Name a group of people who are at risk of hematogenous osteomyelitis.

A

IVDU and other groups at risk from bacteraemia.

196
Q

Give 4 host factors that affect the pathogenesis of osteomyelitis.

A
  1. Behavioural e.g. risk of trauma.
  2. Vascular supply e.g. arterial disease.
  3. Pre-existing bone/joint problems e.g. RA.
  4. Immune deficiency.
197
Q

Acute osteomyelitis: what changes to bone might you see histologically?

A
  1. Inflammatory cells.
  2. Oedema.
  3. Vascular congestion.
198
Q

Chronic osteomyelitis: what changes to bone might you see histologically?

A
  1. Necrotic bone - ‘sequestra’.
  2. New bone formation.
  3. Neutrophil exudates.
199
Q

Why does chronic osteomyelitis lead to sequestra and new bone formation?

A

Inflammatory exudate ruptures periosteum -> blood supply impaired -> necrosis -> sequestra -> new bone forms.

200
Q

Give 5 signs of osteomyelitis.

A
  1. Fever.
  2. Rigors.
  3. Sweats.
  4. Malaise.
  5. Tenderness.
  6. Warmth.
  7. Swelling.
  8. Erythema.
201
Q

Give a sign specific to chronic osteomyelitis.

A

Sinus formation.

202
Q

What investigations might you do on someone who you suspect may have osteomyelitis?

A
  1. Bloods: raised inflammatory markers and WCC.
  2. Plain radiographs and MRI.
  3. Bone biopsy.
  4. Blood cultures.
203
Q

What is the differential diagnosis for osteomyelitis?

A
  1. Cellulitis.
  2. Avascular necrosis.
  3. Gout.
204
Q

Describe the usual treatment for osteomyelitis.

A
  • Large dose IV antibiotics tailored to culture findings (often flucloxacillin).
  • Surgical treatment: debridement.
205
Q

Give 4 ways in which TB osteomyelitis is different to other osteomyelitis.

A
  1. Slower onset.
  2. Epidemiology is different.
  3. Biopsy is essential - caseating granuloma.
  4. Longer treatment.
206
Q

What is the most common cause of septic arthritis?

A

Staphylococcus aureus.

207
Q

Give 3 causes of septic arthritis.

A
  1. Staphylococcus aureus.
  2. Streptococci.
  3. Neisseria.

Consider the clinical context of the patient!

208
Q

Give 5 risk factors for septic arthritis.

A
  1. Any cause of bacteraemia e.g. cannula, UTI.
  2. Local skin breaks/ulcers.
  3. Damaged/prosthetic joints.
  4. RA.
  5. Elderly.
209
Q

Give 4 symptoms of septic arthritis.

A
  1. Painful.
  2. Red.
  3. Swollen.
  4. Hot.
  5. Fever.
210
Q

Describe the treatment for septic arthritis.

A
  • Antibiotics guided by aspirate cultures.
  • Joint wash out/repeated aspiration.
  • Rest/splint/physio.
  • Analgesia.
211
Q

What is bacteraemia?

A

Bacteria in the blood.

212
Q

What is debridement?

A

The removal of damaged tissue.

213
Q

What is the most serious complication of arthroplasty surgery?

A

Prosthetic joint infection.

214
Q

Give 2 ways in which prosthetic joint infections can be prevented.

A
  1. Aseptic environment and laminar air flow.

2. Systemic prophylactic antibiotics.

215
Q

What investigations might you do on someone who you suspect might have a prosthetic joint infection.

A
  1. Aspirate -> microbiology.
  2. Bloods for inflammatory markers and FBC.
  3. X-rays.
216
Q

What must you never do before aspirating a joint?

A

Never give antibiotics before aspiration!

217
Q

What are the three aims of treatment for prosthetic joint infections?

A
  1. Eradicate sepsis.
  2. Relieve pain.
  3. Restore function.
218
Q

Prosthetic joint infections: what treatment might you choose for a patient that is unfit for surgery?

A

Antibiotic suppression.

219
Q

What is the gold standard treatment for prosthetic joint infections?

A

Exchange arthroplasty.

  • Radical debridement of all infected and dead tissue.
  • Systemic and local antibiotic cover.
  • Sufficient joint and soft tissue reconstruction.
220
Q

Define sarcoma.

A

A rare tumour of mesenchymal origin: a malignant connective tissue neoplasm.

221
Q

Soft tissue sarcomas make up what percentage of overall sarcomas?

A

80%. The remaining 20% are boney.

222
Q

Name 3 soft tissue sarcomas.

A
  1. Liposarcoma.
  2. Leiomyosarcoma.
  3. Rhabdomyosarcoma.
223
Q

What is liposarcoma?

A

A malignant neoplasm of adipose tissue.

224
Q

What is leiomyosarcoma?

A

A malignant neoplasm of smooth muscle.

225
Q

What is rhabdomyoscarcoma?

A

A malignant neoplasm of skeletal muscle.

226
Q

Name 3 boney sarcomas.

A
  1. Osteosarcoma.
  2. Ewing’s sarcoma.
  3. Chondrosarcoma.
227
Q

What is chondrosarcoma?

A

A malignant neoplasm of cartilage.

228
Q

Give 3 features of osteosarcoma.

A
  1. Fast growing.
  2. Aggressive.
  3. Typically affects 15 - 17 y/o.
229
Q

Name a boney sarcoma that responds well to chemotherapy.

A

Ewing’s sarcoma.

230
Q

Give 2 red flag symptoms for sarcoma.

A
  1. Non mechanical pain.

2. Pain at night.

231
Q

Give 4 signs that suggest malignancy and can be used to make a diagnosis of soft tissue sarcoma.

A
  1. Lump > 5cm.
  2. Lump is increasing in size.
  3. Lump is deep to fascia.
  4. Pain.
232
Q

What investigations might you do in someone who you suspect to have a sarcoma?

A
  1. MRI.
  2. Core needle biopsy.
  3. CT scan.
233
Q

What is the treatment for sarcomas?

A
  1. MDT meeting.
  2. Surgery for localised soft tissue sarcomas; ensure a wide margin.
  3. Amputation.
  4. If non resectable, chemotherapy and radiotherapy.
234
Q

If it is not possible to get a wide margin when resecting a sarcoma what might you do?

A

Give adjuvant radiotherapy.

235
Q

Name 2 NSAIDs.

A
  1. Ibuprofen.

2. Naproxen.

236
Q

Give 3 side effects of NSAIDs.

A
  1. Peptic ulcer disease.
  2. Renal failure.
  3. Increased risk of MI and CV disease.
237
Q

What can you do to reduce the risk of gastric ulcers and bleeding in someone taking NSAIDs?

A
  1. Co-prescribe PPI.

2. Prescribe low doses and short courses.

238
Q

Give 5 potential side effects of steroids.

A
  1. Diabetes.
  2. Muscle wasting.
  3. Osteoporosis.
  4. Fat redistribution.
  5. Skin atrophy.
  6. Hypertension.
  7. Acne.
  8. Infection risk.
239
Q

How do DMARDs work?

A

Non-specific inhibition of inflammatory cytokine cascade = reduced joint pain, stiffness and swelling.

240
Q

Give an example of a DMARD.

A

Methotrexate = gold standard.
Hydroxychloroquine.
Sulfasalazine.

241
Q

How often should methotrexate be taken?

A

Once weekly.

242
Q

Give 3 potential side effects of methotrexate.

A
  1. Bone marrow suppression.
  2. Abnormal liver enzymes.
  3. Nausea.
  4. Diarrhoea.
  5. Teratogenic.
243
Q

What can be co-prescribed with methotrexate to reduce the risk of side effects?

A

Folic acid.

244
Q

What are cytokines?

A

Short acting hormones.

245
Q

Name a TNF blocker.

A

Adalimumab.

246
Q

Name a monoclonal antibody that binds to CD20 on B cells.

A

Rituximab: binds to CD20 -> B cell depletion.

247
Q

Describe the mechanism of action of abatacept?

A

Inhibits T cell activation.

248
Q

Give one reason why osteomyelitis is difficult to treat.

A

The antibiotics struggle to penetrate bone and bone has a poor blood supply.

249
Q

With what disease would you associate the ‘pencil-in-cup erosion’ seen on a plain XR with?

A

Psoriatic arthritis.

250
Q

With what disease would you associate the Schirmer’s test?

A

Sjögren’s syndrome.

251
Q

You do some investigations on a 30 y/o woman who has presented with painful, red and swollen MCP and PIP joints. The XR shows swelling of soft tissues, deformity and loss of joint space. What auto-antibodies would you expect to see in the serum?

A

Anti-CCP and RF positive.

This patient has rheumatoid arthritis.

252
Q

How does alendronate work?

A

Alendronate reduces bone turnover by inhibiting osteoclast mediated bone resorption.

253
Q

What class of drug is alendronate?

A

Bisphosphonate.

254
Q

Name 2 drugs that act on the HMGCoA pathway.

A
  1. Bisphosphonates e.g. alendronate.

2. Statins e.g. simvastatin.

255
Q

Describe the treatment for an acute attack of gout.

A
  1. NSAIDs e.g. diclofenac.
  2. Colchicine if NSAIDs are ineffective.
  3. Corticosteroids - IM or IA.
256
Q

What auto-antibodies are often present in people with RA?

A

RF and anti-CCP.

257
Q

Nodal osteoarthritis can affect the DIP and PIP joints. What are the two terms used for nodes on these joints?

A
  1. PIP - Bouchard’s nodes.

2. DIP - Herbeden’s nodes.

258
Q

What joint is commonly affected in gout?

A

The MTP joint of the big toe.

259
Q

A patient presents with an acute mono-arthropathy of their big toe. What are the two main differential diagnoses?

A
  1. Gout.

2. Septic arthritis.

260
Q

A patient presents with an acute mono-arthropathy of their big toe. What investigations might you do?

A

Joint aspirate.

If septic arthritis - high WCC and neutrophilia and bacteria on gram stain.

If gout - urate crystals.

261
Q

What joints tend to be affected in seronegative spondyloarthropathies?

A

Asymmetrical large joints.

262
Q

What joints tend to be affected in RA?

A
  1. MCP.
  2. PIP.
  3. Wrist.
263
Q

Antiphospholipid syndrome is often characterised by 2 key clinical features. What are they?

A

Recurrent miscarriage (due to blood clots) and thrombosis.

264
Q

What is polymyalgia rheumatica (PMR)?

A

A condition that causes pain, stiffness and inflammation in the muscles around the shoulders, neck and hips

265
Q

How can you differentiate between polymyalgia rheumatica (PMR) and fibromyalgia?

A

PMR will show raised inflammatory markers.

266
Q

What disease is giant cell arteritis associated with?

A

Polymyalgia rheumatica.

267
Q

What class of drugs can cause Raynaud’s?

A

Beta blockers.

268
Q

What class of drugs does Nifedipine fall into and why can it be used to treat Raynaud’s?

A

Nifedipine - CCB.

It relaxes blood vessels and stops vasospasm.

269
Q

Psoriatic arthritis commonly involves swelling of what joint?

A

DIP joint.

270
Q

How would describe the swelling of fingers seen in psoriatic arthritis?

A

Dactylitis, sausage like swelling.

271
Q

Describe a psoriatic plaque.

A

Pink, scaling lesions. Occur on extensor surfaces of the limbs.

272
Q

Give 3 differences between RA and psoriatic arthritis.

A
  • Psoriatic: psoriatic lesions; sausage like swelling around DIP joint; pencil in cup erosion on XR; HLAB27 associated.
  • RA: hands and wrists typically affected; peri-articular erosion on XR; rheumatoid nodules.
273
Q

What 2 features would be seen on an X-ray taken from someone with ankylosing spondylitis.

A
  1. Sacroiliitis.

2. Syndesmophytes (bamboo spine).

274
Q

What condition must be always ruled out in a acutely inflamed joint?

A

Septic arthritis.

Aspirate the joint!

275
Q

Give 3 symptoms of osteomlacia.

A
  1. Bone pain and tenderness.
  2. Fractures.
  3. Wadding gait.
276
Q

An elderly man presents with worsening bone pain and is found to have an enlarged and bowed tibia. What is the most likely diagnosis?

A

Paget’s disease of bone.

277
Q

An elderly lady with bone pain is found to have hypocalcaemia, hypophosphataemia and a raised ALP. What is the most likely diagnosis?

A

Osteomalacia.

278
Q

What cells secrete RANK ligand?

A

Osteoblasts.

279
Q

What is the function of RANK ligand?

A

It binds to osteoclasts and is essential for their formation, function and survival.

280
Q

What protein inhibits RANK ligand?

A

OPG.

281
Q

What is the function of OPG?

A

OPG inhibits osteoclast formation, function and survival by binding RANK ligand; it prevents RANK ligand from binding to osteoclasts.

282
Q

What is the affect of unopposed RANK ligand?

A

Unopposed RANK ligand leads to increased bone loss. More osteoclasts are stimulated due to a lack of OPG.

283
Q

What enzyme, expressed by osteoclasts, is responsible for bone resorption?

A

Cathepsin K.

284
Q

What provides the best relief for the symptoms associated with ankylosing spondylitis?

A

Exercise.

285
Q

With which disease would you associate positively birefringent crystals?

A

Pseudogout - pyrophosphate crystals that are rhomboid shaped.

286
Q

With which disease would you associate negatively birefringent crystals?

A

Gout - monosodium urate crystals that are thin and needle shaped.

287
Q

What kind of crystals do you see in gout?

A

Monosodium urate crystals - negatively birefringent.

288
Q

What kind of crystals do you see in pseudogout?

A

Calcium pyrophosphate crystals - positively birefringent.

289
Q

Give 5 signs of SLE.

A
  1. Glomerulonephritis.
  2. Thrombocytopenia.
  3. Photosensitivity.
  4. Vasculitis.
  5. Anaemia.
  6. Deforming arthritis.
  7. Pericarditis.

Phase 2a Medicine (11 decks)

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