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Phase 2a Sheffield Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What secretes the rank ligand?

A

Osteoblasts

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2
Q

What does the RANK ligand do?

A

Binds to osteoclasts and is essential for their formation, function and survival

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3
Q

What protein inhibits the rank ligand?

A

OPG

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4
Q

What is the function of OPG?

A

Inhibits osteoclast formation, function and survival by binding to RANK ligands, preventing them from binding to osteoclasts.

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5
Q

What happens if you have an unopposed RANK ligand?

A

increased bone loss, more osteoclasts are stimulated due to lack of OPG

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6
Q

What is responsible for bone resorption?

A

Cathepsin K

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7
Q

What is the best treatment for symptomatic relief of ankylosing spondylitis?

A

Exercise.

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8
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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9
Q

What are 3 causes of inflammatory joint pain?

A
  1. AI disease e.g. RA, vasculitis and connective tissue disease
  2. Crystal arthritis
  3. Infection
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10
Q

What are 2 causes of non-inflammatory joint pain?

A
  1. Degenerative e.g. osteoarthritis

2. Non-degenerative e.g. fibromyalgia

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11
Q

How does inflammatory joint pain differ from degenerative pain?

A

inflammatory pain eases with use whereas degenerative pain increases with use

Synovial swelling is much more likely to be witnessed in inflammatory pain, whereas in degenerative pain there is often no swelling.

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12
Q

What blood tests can be used to detect inflammatory markers?

A
  1. ESR (Erythrocyte sedimentation rate)

2. CRP

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13
Q

Why would you have a high ESR?

A

ESR levels are high in inflammatory joint pain as Inflammation causes increased fibrinogen which means RBC clump together

  • RBC fall faster and so you have increased ESR
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14
Q

Why would you have a high CRP?

A

CRP levels are high in inflammatory joint pain as Inflammation causes increased levels of IL-6

  • CRP is produced in the liver as a response to IL-6 and therefore is raised

In lupus ESR is raised but CRP is low.

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15
Q

What are 3 things that increase the volume of pain?

A
  1. Substance P
  2. Glutamate
  3. Serotonin
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16
Q

What are 3 things that decrease the volume of pain?

A
  1. Opioids
  2. GABA
  3. Cannabinoids
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17
Q

What 4 diseases are fibromyalgia associated with?

A
  1. Depression
  2. Chronig fatigue
  3. Chronic headache
  4. IBS
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18
Q

What are two examples of NSAIDs?

A

Ibuprofen

Naproxen

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19
Q

What are the side effects of NSAIDs?

A

Peptic ulcer disease, renal failure and increased risk of MI and CV disease

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20
Q

How can you prevent gastric ulcers and bleeding?

A
  • Co prescribe PPi’s

- Prescribe low doses and short courses

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21
Q

What are the 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
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22
Q

What is an example of a DMARD?

A

Methotrexate or hydroxychloroquine or sulfasalazine

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23
Q

How do DMARDs work?

A

Nonspecific inhibition of inflammatory cytokine cascade

This reduces joint pain, stiffness and swelling

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24
Q

How often should methotrexate be taken?

A

Once weekly.

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25
Q

What are the side effects of methotrexate?

A

Bone marrow suppression, abnormal liver enzymes, nausea, diarrhea, teratogenic

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26
Q

What should be given alongside methotrexate?

A

Folic acid should be prescribed alongside methotrexate to reduce the risk of side effects

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27
Q

What is dermatomyositis?

A

A rare disorder of unknown cause –> inflame and necrosis of skeletal muscle fibers and skin

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28
Q

What are the symptoms of dermatomyositis?

A
  1. Rash
  2. Muscle weakness
  3. Lungs are often affected
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29
Q

What investigations would you do in dermatomyositis?

A
  1. Muscle enzymes –> Raised
  2. EMG
  3. Muscle/skin biopsy
  4. Screen for malignancy
  5. CXR
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30
Q

What is the treatment for dermatomyositis?

A

Steroids and immunosuppressants

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31
Q

What is dactylitis?

A

Inflammation of of an entire digit.

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32
Q

What is a physis?

A

growth plate in the pediatric bone –> thick perisoteum means it can heal rapidly.

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33
Q

What are the initial steps for fracture management?

A
  1. Reduce fracture –> restore the length, alignment and rotation
  2. Immobilise
  3. Rehabilitate
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34
Q

What is the first line management for paediatric fractures?

A
  1. Non operative management e.g. traction, casts, splints

2. This is because pediatric bone heals quickly anyways

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35
Q

What happens if the physis is damaged?

A

growth arrest = deformity.

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36
Q

What is the salter harris fracture classification?

A

Name of classification used for fractures involving the physis

Type 1 fracture –>Transverse fracture through the growth plate.
Type 2 fracture –> fracture through growth plate and metaphysis.
Type 3 Fracture –> Fracture through the growth plate and epiphysis
Type 4 Fracture –> Fracture through metaphysis, physis and epiphysis –> need fixation.

Type 5 Fracture –> Crush injury of growth plate –> poor prognosis and growth arrest

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37
Q

What are red flags of non accidental injury in children?

A

Long bone fracture in child unable to walk, multiple bruises and fractures.

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38
Q

What is the management of non accidental injury in children?

A
  • Admit the child
  • Skeletal muscle
  • Referal to paediatric medics and safeguarding services
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39
Q

How does a child get a supracondylar fracture?

A

Falling on an outstretched hand.

There is often median nerve involvement.

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40
Q

What is the treatment for a supracondylar fracture?

A

K wires.

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41
Q

What are the 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 and blisters.
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42
Q

What is osteoarthritis?

A

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

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43
Q

Why does osteoarthritis increase with age?

A

OA increases with age due to cumulative effect of trauma and a decrease in neuromuscular function

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44
Q

What cells are responsible for Osteoarthritis?

A

Chondrocytes

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45
Q

What are the risk factors for osteoarthritis?

A
  1. Genetic predisposition
  2. Trauma
  3. Abnormal biomechanics
  4. Occupation e.g. manual labour
  5. Obesity – pro inflammatory state
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46
Q

What are the symptoms of osteoarthritis?

A
  1. Morning stiffness of over 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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47
Q

What are the radiological features of 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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48
Q

What are 3 joints in the hands which are commonly affected in OA?

A
  1. Distal interphalangeal joint
  2. Proximal Interphalangeal joint
  3. Carpal metacarpal joint
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49
Q

What area of the knee is commonly affected in OA?

A

Medial surface of knee

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50
Q

What investigation should be ordered in OA?

A

X-ray –> Asymmetric loss of joint space, sclerosis, cysts and osteophytes

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51
Q

What are the features of non-medical management of OA?

A
  1. Education
  2. Exercise
  3. Weight loss
  4. Physio
  5. OT
  6. Walking aids
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52
Q

What is the pharmacological management of OA?

A
  1. NSAIDs –> topical better
  2. Paracetamol
  3. Intra-articular steroid injections
  4. DMARDs
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53
Q

What is the surgical management of OA?

A
  1. Arthroscopy for loose bodies
  2. Osteotomy (changing bone length)
  3. Arthroplasty (Joint replacement)
  4. Fusion – usually ankle and foot.
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54
Q

What are some indications for surgery for OA?

A
  1. Significant limitation of function
  2. Uncontrolled pain
  3. Waking at night from pain
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55
Q

What is the treatment for loose bodies?

A

Arthroscopy

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56
Q

A patient complains of knee locking, what could be the cause?

A

A loose body

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57
Q

What is the pathway leading to monosodium urate formation?

A

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

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58
Q

What is the function of xanthine oxidase?

A

It converts hypoxanthine to xanthine.

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59
Q

What are 5 factors leading to an increased level of monosodium urate?

A
  1. Increased intake e.g. alcohol, red meat and seafood
  2. Cell turnover
  3. Cell damage due to surgery
  4. Cell death e.g. due to chemo
  5. Reduced excretion (Renal problems)
  6. Drugs e.g. Bendroflumethiazide  diuretics impair urate excretion
  7. High insulin
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60
Q

What is the epidemiology of gout?

A

most common in men over 75 y/o.

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61
Q

What are the symptoms of gout?

A

Hot and swollen joints, toes are commonly effected

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62
Q

What are tophi?

A

onion like aggregates of urate crystals with inflame cells

- Proteolytic enzymes are released –> erosion

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63
Q

What 4 diseases is someone with gout likley to develop?

A
  1. Hypertension
  2. CV disease
  3. Renal disease
  4. T2DM Treatment aim –> to get urate to <300umol/L
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64
Q

What is the treatment options for gout?

A
  1. Lifestyle modification e.g. diet, weight loss and reduced alcohol
  2. Allopurinol (blocks xanthine oxidase)
  3. Colchicine or NSAIDs
  4. Switch from Bendroflumethiazide to cosartan
  5. Rasburicase – rapid urate reduction
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65
Q

If a patient is taking Bendroflumethiazide, what would you replace their drug with to treat gout?

A

Cosartan as BFT is a diuretic so impairs urate excretion.

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66
Q

What 6 things can cause a sudden acute attack of gout?

A
  1. Sudden overload
  2. Cold
  3. Trauma
  4. Sepsis
  5. Dehydration
  6. Drugs
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67
Q

What is giant cell arteritis?

A

Temporal arteritis

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68
Q

What is the epidemiology of GCA?

A
  • Affects those >50y/o
  • Incidence increases with age
  • Twice as common in women
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69
Q

What are the symptoms of GCA?

A
  • Headache
  • Scalp tenderness
  • Jaw claudication
  • Acute blindness
  • Malaise
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70
Q

What investigations would you order in suspected GCA?

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

2. Temporal artery biopsy

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71
Q

What clinical investigation findings could you see in GCA?

A
  • Palpable and tender temporal arteries w reduced pulsation

- Sudden monocular visual loss, optic disc is swollen

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72
Q

What is the diagnostic criteria for GCA?

A
  • Age >50
  • New headache
  • Temporal artery tenderness
  • Abnormal artery biopsy
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73
Q

What is the treatment for GCA?

A
  • Prompt corticosteroids e.g. prednisolone
  • Methotrexate sometimes
  • Osteoporosis prophylaxis is important  lifestyle advice and vit D
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74
Q

What is a complication of arthroplasty surgery?

A

Prosthetic joint infection

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75
Q

How can prosthetic joint infections be prevented?

A
  • Asceptic environment and laminar air flow

- Systemic prophylactic AB

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76
Q

What investigations would you do in suspected prosthetic joint infection?

A
  1. Aspirate –> Microbiology
  2. Bloods for inflammatory markers and FBC
  3. X-rays

You must never give AB before aspirating a joint

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77
Q

What are the aims of treatment in prosthetic joint infections?

A
  1. Eradicate sepsis
  2. Relieve pain
  3. Restore function
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78
Q

What treatment would you choose for a patient that is unfit for surgery with a prosthetic joint infection?

A

AB suppression.

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79
Q

What is the gold standard treatment for prosthetic joint infections?

A

Exchange arthroplasty

  1. Radical debridement of all infected and dead tissue
  2. Systemic and local ab cover
  3. Sufficient joint and soft tissue reconstruction
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80
Q

What is scleroderma?

A

A multi-system disease characterized by skin hardening and raynauds phenomenon

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81
Q

What are the signs of limited scleroderma?

A
  1. Calcinosis
  2. Raynauds phenomenon
  3. Oesophageal reflux
  4. Sclerodactyly – Thickening and tightening of the skin
  5. Telangiectasia – visible small red blood vessels
  6. Pulmonary arterial hypertension
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82
Q

What are the signs of diffuse scleroderma?

A
  • Proximal scleroderma
  • Pulmonary fibrosis
  • Bowel involvement
  • Myostitis
  • Renal crisis
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83
Q

What is the pathophysiology of scleroderma?

A
  1. Various factors cause endothelial lesion and vasculopathy

2. Excessive collagen deposition (Skin hardening) –> inflammation and auto-AB production

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84
Q

What is the management of Scleroderma?

A
  1. Raynauds –> physical protection and vasodilators
  2. GORD – PPIS
  3. Annual echo and pulmonary function tests
  4. ACEi to prevent renal crisis
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85
Q

What is wegener’s granulomatosis and what is it associated with?

A

It is characterized by inflammation in various tissues, including blood vessels (vasculitis), but primarily parts of the respiratory tract and the kidneys.

Wegners Granulomatosis is associated with c-ANCA

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86
Q

What is the effect on URT in WG?

A

Sinusitis, otitis and nasal crusting

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87
Q

What is the effect on the lungs in WG?

A

Pulmonary haemorrhage/nodules + Inflam infiltrates are seen on xray

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88
Q

What is the effect on the kidney in WG?

A

Glomerulonephritis

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89
Q

What is the effect on the skin in WG?

A

Ulcers

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90
Q

What is the effect on the eyes in WG?

A

Uveitis, Scleritis and episcleritis

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91
Q

What is the treatment for wegeners granulomatosis?

A
  1. If severe – high dose steroids

2. If non-end organ threatening – moderate steroids

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92
Q

What is vasculitis?

A

Inflammation of the blood vessels.

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93
Q

What would you see histologically in vasculitis?

A
  • Neutrophils and giant cells
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94
Q

What is the chapel hill classification?

A
  • Used to classify vasculitis
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95
Q

What is an example of a large primary artery disorder?

A

Giant cell arteritis

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96
Q

What is an example of a large secondary artery disorder?

A

Aortitis in RA

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97
Q

What is an example of medium/small artery primary disorder?

A

Wegeners granulomatosis

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98
Q

What is an example of a medium/small artery secondary disorder?

A

Vasculitis secondary to AI disease, malignancy and drugs.

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99
Q

What is the common cause of septic arthritis?

A

Staph aureus

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100
Q

What are the causes of septic arthritis?

A
  1. Staph aureus
  2. Streptococci
  3. Neisseria

Consider clinical context of patient.

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101
Q

What are the risk factors of septic arthritis?

A
  1. Any cause of bacteremia e.g. cannula and UTI
  2. Local skin breaks/ulcers
  3. Damaged prosthetic joints
  4. RA
  5. Elderly
102
Q

What are the symptoms of septic arthritis?

A
  1. Painful
  2. Red
  3. Swollen
  4. Hot
  5. Fever
103
Q

What is the treatment for septic arthritis?

A
  1. AB guided by aspirate cultures
  2. Joint wash out/repeated aspiration
  3. Rest/splint/physio
  4. Analgesia
104
Q

What is a sarcoma?

A

A rare tumour of mesenchymal origin –> a malignant connective tissue neoplasm

105
Q

Describe the nature of sarcomas?

A

80% soft tissue and the remaining 20% are boney.

106
Q

What are 3 soft tissue sarcomas?

A
  1. Liposarcoma
  2. Leiomyosarcoma
  3. Rhabdomyosarcoma
107
Q

What is a liposarcoma?

A

A malignant neoplasm of adipose tissue

108
Q

What is a leiomyosarcoma?

A

A malignant neoplasm of smooth muscle

109
Q

What is a rhabdomyosarcoma?

A

A malignant neoplasm of skeletal muscle

110
Q

What are 3 bony sarcomas?

A
  1. Osteosarcoma
  2. Ewing’s sarcoma – responds well to chemo
  3. Chondrosarcoma – malignant neoplasm of cartilage
111
Q

What are 3 features of sarcomas?

A
  1. Fast growing
  2. Aggressive
  3. Typically affects 15-17 yo
112
Q

What are red flag symptoms for sarcoma?

A
  1. Non-mechanical pain

2. Pain at night

113
Q

What are 4 signs that could suggest malignancy to diagnose soft tissue sarcoma?

A
  1. Lump >5cm
  2. Lump increases in size
  3. Lump is deep in fascia
  4. Pain
114
Q

What are the investigations in suspected sarcoma?

A
  1. MRI
  2. Core needle biopsy
  3. CT scan
115
Q

What is the treatment of sarcomas?

A
  1. MDT meeting
  2. Surgery for localized soft tissue sarcomas
  3. Amputation
  4. If non resectable –> Adjuvant Chemo and radiotherapy
116
Q

What is sjorgen’s syndrome?

A
  • Immunologically mediated destruction of epithelial exocrine glands especially lacriminal and salivary glands.
117
Q

When does sjorgens syndrome often occur?

A

Often occurs secondary to other auto-immune disorders e.g. SLE, RA and scleroderma

118
Q

What are the symptoms of sjorgen’s syndrome?

A
  1. Dry eyes + mouth
  2. Inflam arthritis
  3. Rash
  4. Neutrophils
  5. Vasculitis
119
Q

What are the investigations in Sjorgen’s syndrome?

A
  1. Serum auto-antibodies e.g. Anti – RO, RF, ANA

2. Also raised ESR and raised immunoglobulins

120
Q

What is the treatment of sjorgen’s syndrome?

A

Tear and saliva replacement + immunosuppression for systemic complications

121
Q

What is the pathophysiology of pseudogout?

A
  • Calcium pyrophosphate crystals are deposited on joint surfaces
  • The crystals elicit an inflame response
122
Q

What is the cause of pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Diabetes
  3. Haemochromatosis
  4. Magnesium levels
123
Q

What are the symptoms of pseudogout?

A

Acute, hot and swollen joints  typically wrists and knees

124
Q

What is the investigations of pseudogout?

A
  1. Aspiration –> fluid for crystals or blood cultures

2. X-rays –> Can show chondrocalcinosis

125
Q

What is the differential diagnosis of pseudogout?

A

Infection

126
Q

What is the treatment for pseudogout?

A

Treat underlying cause and use methotrexate for inflammation

127
Q

You do some investigations on a 30 yo woman who has painful red and swollen MCP and PIP joints. 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

- Patient has rheumatoid arthritis

128
Q

An elderly man presents with worsening bone pain and is found to bhave an enlarged and bowed tibia, what is the most likely diagnosis?

A

Pagets disease of the bone

129
Q

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

A

Osteomalacia

130
Q

With which disease would you associate positively birefringent crystals ?

A

Pseudogout – pyrophosphate crystals are rhomboid shaped.

131
Q

With what disease would associate negatively birefringenet crystals?

A

Gout – Monosodium urate crystals are thin and needle shaped

132
Q

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

A

Gout and septic arthritis

133
Q

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

A

Joint aspirate

  • If septic arthritis –> high WCC and neutrophilia and baceteria on gram stain
  • If Gout –> urate crystals
134
Q

What is fibromyalgia?

A

A symptom characterized by widespread MSK pain accompanied by fatigue, sleep, memory and mood issues.

135
Q

What are 3 diseases included in the differential diagnosis of fibromyalgia?

A
  1. Hypothyroidism
  2. SLE
  3. Low Vit D
136
Q

What are the 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. Walking unrefreshed
  7. Low mood, irritable and weepy
  8. Headache and IBS common
137
Q

What are the triggers of fibromyalgia?

A
  1. Physical trauma
  2. Distress
  3. Hormonal alterations e.g. hypothyroid
  4. Infections
  5. Certain catastrophic events
138
Q

What is the diagnostic criteria for fibromyalgia?

A
  • Chronic widespread pain lasting for over 3 months with other causes excluding
  • Pain is at 11 of 18 tender point sites
139
Q

What is the management of fibromyalgia?

A
  1. Educate the patient and family
  2. Low dose amitriptyline can help with sleep
  3. Graded aerobic exercise
  4. Acupuncture
140
Q

What is essential to the management of fibromyalgia?

A
  • Explaining sleep disturbance is central to what they’re feeling
  • Emphasise the importance of exercise and fitness
141
Q

What is reactive arthritis?

A

Sterile inflammation of synovial membrane, tendons and fascia triggered by an infection at a distant site (usually Gut or genital)

142
Q

What are some associated gut infections with reactive arthritis?

A

Salmonella, shigella

143
Q

What are associated STIs with reactive arthritis?

A

Chlamydia

144
Q

What are the triad symptoms for reactive arthritis?

A
  • Arthritis
  • Conjunctivitis
  • Urethritis
145
Q

What is the aetiology of juvenile idiopathic arthritis?

A
  • Unknown as its idiopathic

- It is an AI disease so genetic factors must be associated.

146
Q

Why is it important to check the eyes in JIA?

A

Risk of uveitis

147
Q

What is the criteria for diagnosing JIA?

A
  • Joint swelling and stiffness for over 6 weeks in children <16 with no other cause identified
148
Q

What is the presentation of oligoarthritis?

A

Oligoarthritis affects over 4 joints and usually is ANA positive
- It has a high risk of developing uveitis

149
Q

What is enthesitis related JIA?

A

Enthesitis related JIA – inflammation of where tendon joins a bone – HLAB27 positive

  • Like ankylosing spondylitis
150
Q

What is the non-medication treatment for JIA?

A
  1. Information
  2. Education
  3. Support
  4. Liaison with school
  5. Physiotherapy
151
Q

What is the medical treatment for JIA?

A
  1. Steroid joint injections
  2. NSAIDs
  3. Methotrexate
  4. Systemic steroids
152
Q

What are consequences if you fail to treat JIA?

A
  1. Damage
  2. Deformity
  3. Disability
  4. Pain
  5. Bony overgrowth
  6. Uveitis
153
Q

What is spondylarthritis?

A

An umbrella term for the following conditions

  1. Ankylosing spondylitis
  2. Reactive arthritis
  3. Psoriatic arthritis
  4. Enteropathic arthritis
  5. Juvenile idiopathic arthritis
154
Q

What is spondylarthritis associated with?

A

Tissue type HLAB27 –> Antigen presenting cell.

155
Q

What is the molecular mimicry theory for why HLAB27 is associated with spondylarthritis?

A
  • Infectious agents have peptides similar to HLAB27

- An AI response is triggered against HLAB27

156
Q

What are other theories of Spondylarthritis and HLAB27 association?

A
  1. Molecular mimicry
  2. Misfolding theory
  3. HLAB27 heavy chain hypothesis
157
Q

What are the signs of spondylarthritis?

A
  1. Psoriasis
  2. Inflammatory spine and buttock pain
  3. Good response to NSAIDs
  4. Enthesitis
  5. Arthritis
  6. Crohn’s/UC association
  7. Uveitis
158
Q

What is the general treatment for spondylarthritis?

A
  • Initially DMARDs (disease modifying anti-rheumatic drugs)
  • Biological agents if DMARDs fail
  • Responds well to NSAIDs
159
Q

What is the pathophysiology of anklylosing spondylitis?

A

Inflammation of spine –> erosive damage –> repair/bone formation –> irreversible fusion of spine

160
Q

What are the symptoms of anklyosing spondylitis?

A
  1. Back Pain
  2. Morning stiffness
  3. Waking in second half of night
  4. Usually above 40 at onset
  5. Buttock pain
  6. Insidious onset
161
Q

What are the investigations neccesary in diagnosing anklyosing spondylitis?

A
  • X-ray
  • MRI
  • HLAB27 test
162
Q

What is the diagnostic criteria for ankylosing spondylitis?

A
  • > 3 months back pain
  • Aged <45 at onset
  • Plus one of the SPINEACHE symptoms

Enteropathic Arthritis is a type of spondylitis occurring in 20% of patients with IBD.

163
Q

Where does psoriasis usually occur at?

A
  1. Elbows
  2. Knees
  3. Fingers
164
Q

What is ANCA?

A

Anti-neutrophil cytoplasmic antibodies

165
Q

What is the protocol for treating trauma patients?

A

ATLS  Greatest threat to life first (ABCDE)

166
Q

What is a cytokine?

A

Short acting hormone

167
Q

What is a TNF blocker example?

A

Adalimumab

168
Q

How does rituximab work?

A

Binds to cd20 on the B cell leading to b cell depletion

169
Q

Why is osteomyelitis difficult to treat with ABx?

A

Abx dont penetrate bone well.

170
Q

What type of erosion is seen in psoriatic arthritis?

A

pencil in cup.

171
Q

How can you stop bone turnover?

A

Give bisphosphonates e.g. aldendronate

172
Q

How does aldendronate work?

A

bone turnover by inhibiting osteoclast mediated bone resorption

173
Q

What are two drugs that work on the HMGCoA pathway?

A
  1. Bisphosphonates e.g. alendronate

2. Statins e.g. simvastatin

174
Q

What AB present in people with RA?

A

RF and anti-CCP

175
Q

Nodal osteoarthritis affects the DIP and PIP Joints. What is the name for these nodes?

A
  • PIP –> Bouchard’s nodes

- DIP –> Herbeden nodes

176
Q

What joint is most commonly affected in gout?

A

MTP of big toe.

177
Q

What joints are affected in seronegative spondyloarthropathies ?

A

asymetrical large joints

178
Q

Which joints are affected in RA?

A
  1. MCP
  2. PIP
  3. Wrist
179
Q

How does antiphospholipid syndrome present?

A

thrombosis

recurrent miscarriage

180
Q

What is polymyalgia rheumatica?

A

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

181
Q

How can you differentiate between fibromyalgia and PR?

A

PMR shows raised inflam markers.

182
Q

What can cause raynaud’s syndrome?

A

Beta blockers

183
Q

What is the treatment of raynauds syndrome

A

Nifedipine – CCB –> relaxes blood vessels and stops vasospasm

184
Q

What joint is commonly affected in psoriatic arthritis?

A

DIP joint.

185
Q

What are the symptoms of osteomalacia?

A
  1. Bone pain and tenderness
  2. Fractures
  3. Wadding gait
186
Q

What would the x-ray in someone with ankylosing spondylitis be like?

A
  1. Sacroilitis

2. Syndesmophytes (Bamboo spine)

187
Q

What are the two features of psoriatic plaque?

A
  • Pink, scaling lesions

- Occur on extensor surfaces on the limbs

188
Q

What are the differences between RA and psoriatic arthritis?

A

Psoriatic –> psoriatic lesions, sausage like swelling on DIP joint, pencil cup erosion and HLAB27 associated

RA –> Hands and wrists typically affected –> periarticular erosion on x-ray and rheumatoid nodules

189
Q

What is the swelling like in psoriatic arthritis?

A

Dactylitis and sausage like swelling would be seen in psoriatic arthritis

190
Q

What is the systemic lupus erythematosus?

A

inflame multi-system disease characterized by presence of ANA

191
Q

What is the epidemiology of SLE?

A

90% young women, genetic component and more common in afro-Caribbean’s

192
Q

What is the pathogenesis of SLE?

A

Ineffecient phagocytosis causes cell fragments to be transferred to lymphoid tissue

Take up by APC. T Cells stimulate B cells to produce antibodies against self antigens

Immune complex deposition –> Neutrophil and cytokine influx = inflame and tissue damage

193
Q

Why may thrombosis occur in SLE?

A

Thrombosis can be caused by the presence of antiphospholipid antibodies

194
Q

What is anti-dsDNA specific to?

A

SLE

195
Q

What are the symptoms of SLE?

A
  1. Butterfly rash
  2. Mouth ulcers
  3. Raynaud’s phenomenon
  4. Fatigue
  5. Depression
  6. Weight loss
196
Q

What are the investigations for SLE?

A
  • Blood count –> may show normocytic anaemia –> neutropenia
  • Raised ESR and normal CRP
  • Serum autoantibodies –> ANA and Anti-dsDNA
197
Q

What is the non-medical treatment of SLE?

A
  1. Education and support
  2. UV protection
  3. Screening for organ involvement
  4. Reduce CV risk factors e.g. smoking cessation
198
Q

What is the medical treatment of SLE?

A
  • Corticosteroids
  • NSAIDs
  • Anti-malarials (DMARDs)
  • Anticoagulants – for those with antiphospholipid antibodies
  • Bio therapy –> targeting B cells e.g. rituximab
199
Q

What are the signs of SLE?

A
  1. Glomerulonephritis
  2. Thrombocytopenia
  3. Photosensitivity
  4. Vasculitis
  5. Anaemia
  6. Deforming arthritis
  7. Pericarditis
200
Q

What is a cause of inflammatory joint pain?

A

AI disease

201
Q

What is two examples of inherited connective tissue disease?

A
  1. Marfan’s syndrome

2. Ehler Danlos syndrome

202
Q

What is 3 examples of AI connective tissue disease?

A
  1. SLE
  2. Systemic Sclerosis
  3. Sjorgen’s syndrome
  4. Dermatomyositis
203
Q

What is osteomyelitis?

A

Bone inflammation secondary to infection

204
Q

What causes osteomyelitis?

A
  1. S.aureus
  2. Coag neg staphylococci e.g. s. epidermidis
  3. Aerobic gram negative bacilli
  4. Mycobacterium TB
205
Q

What histological changes would you see in someone with acute osteomyelitis?

A
  • Inflammmatory cells
  • Oedema
  • Vascular congestion
206
Q

What histological changes would you see in someone with chronic osteomyelitis?

A
  1. Necrotic bone – sequestera
  2. New bone formation
  3. Neutrophil exudates
207
Q

What are the signs of osteomyelitis?

A
  1. Fever, Rigors, Sweats, Malaise, Tenderness, Swelling and Erythema
    Sign specific to chronic osteomyelitis  Sinus formation
208
Q

What investigations would you order in suspected osteomyelitis?

A
  1. Bloods –> Raised inflame markers and WCC
  2. Plain radiographs and MRI
  3. Bone biopsy
  4. Blood cultures
209
Q

What are the differential diagnoses for osteomyelitis?

A

Cellulitis, Avascular necrosis and Gout

210
Q

What is the treatment of osteomyelitis?

A
  1. Large does IV AB tailored to culture findings often flucloxacillin
  2. Surgical treatment –> debridement
211
Q

What is the difference in osteomyelitis and TB caused ostemyelitis?

A
  1. Slower onset
  2. Epidemiology is different
  3. Biopsy is essential – case eating granuloma
  4. Longer treatment
212
Q

How can pathogens get into the bone?

A
  • Easy – Inoculation of infection into bone e.g. trauma or open wound
  • Quite easy – contagious spread of infection to bone from adjacent tissues
  • Difficult – hematogenous seeding e.g. due to cannula infection ( vertebrae in adults, long bones in kids)
213
Q

Why do the vertebrae get infected more often?

A

become more vascularised

214
Q

Why do long bones get infected more often?

A

as they have a high blood flow and BM are absent meaning bacteria can move from the blood to bone.

215
Q

Which Group of people at risk of hematogenous osteomyelitis?

A

IVDU and other groups at risk from bacteraemia

216
Q

Give 3 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
217
Q

How does chronic ostemyelitis lead to sequestra and bone formation?

A
  • Inflammatory exudate ruptures periosteum –> blood supply impaired –> necrosis –> sequestera –> new bone forms
218
Q

What is rheumatoid arthritis?

A

An AI inflammatory synovial joint disease.

219
Q

What is the epidemiology of RA?

A
  • 2-3 times more common in women

- 1% of pop effected

220
Q

What is the aetiology of RA?

A
  • Auto-antibodies e.g. RF and anti CCP lead to defected cell mediated immune responses
221
Q

What is the pathophysiology of RA?

A
  • Chronic inflammation –> BT Cells and neutrophils infiltrate
  • Proliferation –> Pannus formation
  • Pro inflammatory cytokines –> proteinases –> cartilage destruction
222
Q

What are the symptoms of RA?

A
  1. Early morning stiffness for over an hr
  2. Pain that eases with use
  3. Swelling
  4. General fatigue and malaise
  5. Extra-articular involvement
223
Q

What are the signs of RA?

A
  1. Symmetrical
  2. Deforming
  3. Polyarthropathy
  4. Erosion on X-ray
  5. 80% are RF positive
224
Q

What investigations would you associate with RA?

A
  1. Bloods for inflammatory markers – ESR and CRP will be raised
  2. Test for anaemia
  3. Test for RF and Anti-CCP
225
Q

What is the treatment for RA?

A
  1. NSAIDs
  2. Corticosteroids
  3. DMARDs
  4. Biological agents
226
Q

Describe the RA extra-articular involvement effects on Soft tissues

A
  • Nodules, Bursitis and Muscle wasting
227
Q

Describe the RA extra-articular involvement effects on the eyes

A
  • Dry eyes, Scleritis and Episcleritis
228
Q

Describe the RA extra-articular involvement effects on neurology

A
  • Sensory peripheral neuropathy
  • Entrapment neuropathies e.g. carpal tunnel syndrome
  • Instability of C spine
229
Q

Describe the RA extra-articular involvement effects –> haematology

A
  • Palpable lymph nodes, Splenomegaly and Anaemia
230
Q

Describe the RA extra-articular involvement effects on the pulmonary system.

A

pleural effusion

231
Q

Describe the RA extra-articular involvement effects on the heart

A

Pericardial rub and effusion

232
Q

Describe the affect of RA on the kidneys

A

Amyloidosis

233
Q

What is rheumatoid factor?

A

An antibody against the Fc portion of IgG

234
Q

What are 2 factors for predicting the likelihood of osteoporotic fracture?

A

Propensity to fall and bone strength

235
Q

Give 4 factors that contribute to bone strength

A
  1. Bone mineral density
  2. Bone size
  3. Bone turnover
  4. Bone micro-architecture
  5. Mineralisation
  6. Geometry
236
Q

What can control osteoclast action and bone turnover?

A

Oestrogen can control osteoclast action so control bone turnover.
Women over 50 are likely to be post-menopausal –> less estrogen so osteoclast isn’t inhibited

  • There is a high rate of bone turnover –> bone loss and deterioration –> fracture risk
237
Q

What happens when to our bones when we get older?

A
  • Trabecular thickness decreases especially in horizontal plane.
  • There are fewer connections between trabecular so there’s a decrease in strength
  • This causes an increased fracture risk
238
Q

How can RA cause osteoporosis?

A

RA is an inflammatory disease –> high levels of IL-6 and TNF so are responsible for bone resorption.

239
Q

How can high cortisol cause osteoporosis?

A

cortisol increases turnover, leads to increased bone resorption so induces osteoblast apoptosis

240
Q

How can cushings sydrome cause osteoporosis?

A

cortisol leads to increased bone resorption and osteoblast apoptosis

241
Q

How can hyperparathyroidism and hyperthyroidism cause osteoporosis?

A

TH + PTH –> increased bone bone turnover.

242
Q

What skeletal areas does a dexa scan focus on?

A

Lumbar spine

Hip

243
Q

What is a T score?

A

T score –> Standard deviation that is compared to a gender-matched young adult mean.

T score

244
Q

What is FRAX?

A

A tool that can be used to assess someone’s risk of osteoporotic fracture.

245
Q

What are 2 examples of anti-resorptive treatments used in osteoporosis management?

A
  1. Bisphosphonates
  2. HRT

they reduce osteoclast activity.

246
Q

What is an example of anabolic treatment in OP?

A

Teriparatide –> Anabolic treatments increase osteoblast activity

247
Q

Give 3 advantages of HRT treatment in OP?

A
  • Reduces fracture risk
  • Stops bone loss
  • Prevents menopausal symptoms
248
Q

Give 3 disadvantages of HRT treatment in OP?

A
  • Increased risk of breast cancer
  • Increased risk of stroke and CV disease
  • Increased risk of thrombo-embolism
249
Q

What is osteoporosis?

A

A systemic skeletal disease characterized by low bone mass and micro-architectural deterioriation –> patient is at increased risk of fracture.

250
Q

What is the epidemiology of osteoporosis?

A

50% of women over 50 and 20% of men –> incidence increases w/ age.

251
Q

What investigation would be done in osteoporosis?

A
  1. DEXA scan –> A T score will be generated.
252
Q

What are the risk factors for osteoporosis?

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

Phase 2a Sheffield Medicine (10 decks)

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