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Phase 2a med mine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What kind of arthritis is osteoarthritis?

A

Non-inflammatory degenerative mechanical shearing

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2
Q

Name some risk factors for developing osteoarthritis

A

Age:>50
Female
Obesity
Occupation: sports/manual labour
Genetic: COL2A1

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3
Q

Which gene is associated with osteoarthritis?

A

COL2A1

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4
Q

Describe the pathophysiology of osteoarthritis.

A

Imbalance between cartilage breakdown and repair
Increased chondrocyte metalloproteinase secretion degrades T2 collagen and causes cysts
Bone tries to overcome this with T1 collagen leading to abnormal bony growths(osteophytes) and remodelling

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5
Q

How is osteoarthritis diagnosed?

A

Ruel out other causes: normal CRP and ESR, anti-CCP, RF etc
X-ray:
LOSS
L-loss of joint space
O-osteophytes
S: subchondral sclerosis
S: subchondral cysts

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6
Q

What are osteophytes?

A

Spurs of bone on ends of joints

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7
Q

What is subchondral sclerosis?

A

Increased bone density along joint line

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8
Q

What are subchondral cysts?

A

Fluid filled holes in bone along joint line

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9
Q

How do patients with osteoarthritis typically present?

A

<30min mornign pain
Pain increases with use
Asymmetrical, hard, non inflamed joints
No extra-articular symptoms
Bouchard(PIPJ) and Heberden(DIPJ) nodes on fingers

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10
Q

Which joints are typically affected by osteoarthritis?

A

Knees
Hips
Hands: DIPS, PIPS
Spine ,especially cervical

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11
Q

What can be seen/felt on the hands of patients with osteoarthritis

A

Bouchard nodes: PIPJ
Heberden nodes: DIPJ

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12
Q

Describe the treatment for osteoarthritis

A

Lifestyle changes: weight bearing and physio
NSAID pain relief
Last resort: surgery-arthroplasty-knee and hip replacement

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13
Q

What kind of arthritis is rheumatoid arthritis?

A

Inflammatory autoimmune polyarthritis
Symmetrical

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14
Q

Name some risk factors for developing rheumatoid arthritis

A

Smoking
Women 30-50 pre-menopausal
Genetic link: HLADR4/HLADR1

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15
Q

Describe the male:female distribution of rheumatoid arthritis

A

Pre menopausal: 3 times more likely in women than men
Post menopause: M=F

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16
Q

What genes is rheumatoid arthritis linked to?

A

HLA-DR4
HLADR1

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17
Q

How do rheumatoid arthritis symptoms change throughout the day?

A

Worse in morning-30 minutes
Pain improves with use

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18
Q

Describe the presentation of patients with rheumatoid arthritis

A

Symmetrical, hot, inflamed joints, most commonly hands and feet
Hands: boutonniere, swan neck, ulnar deviation, Z thumb
Extra articular: lungs, heart, eyes, kidneys, skin

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19
Q

How can rheumatoid arthritis affect the lungs?

A

PE
Pulmonary fibrosis

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20
Q

How can rheumatoid arthritis affect the heart?

A

Increased IHD risk

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21
Q

How can rheumatoid arthritis affect the eyes?

A

Episcleritis
Keratoconjunctivitis sicca(dry eyes)

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22
Q

How can rheumatoid arthritis affect the skin?

A

Rheumatoid skin nodules-often on elbows

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23
Q

How can rheumatoid arthritis affect the kidneys?

A

CKD

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24
Q

Which hand joint is commonly spared in rheumatoid arthritis and in which kind of arthritis is commonly affected?

A

DIPJ
Psoriatic arthritis

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25
Q

Name some hand signs seen in rheumatoid arthritis

A

Boutonniere
Swan neck
Ulnar deviation
Z thumb

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26
Q

What is Boutenniere’s sign

A

Extensor tendon splits
PIP flexion, DIP hyperextension

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27
Q

What is swan neck sign?

A

PIP hyperextension, DIP flexion

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28
Q

What is ulnar finger deviation?

A

Fingers deviate towards ulnar(pinkie)

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29
Q

What is Z thumb?

A

Carpometacarpal flexion, MP hyperextension, IP flexion

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30
Q

Describe the pathophysiology of rheumatoid arthritis

A

Arginine->Citruline mutation in T2 collagen->anti-CCP mutation
IFN-alpha also causes more pro-inflammatory recruitment to synovium
Results in expansion of synovial lining and pannus to grow past joint margins
->Destruction of subchondral bone and articular cartilage

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31
Q

What is a pannus?

A

Tumour like mass

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32
Q

What is Felty syndrome?

A

Triad of:
Rheumatoid arthritis
Granulocytopenia
Splenomegaly

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33
Q

What is the main cause of death in patients with Felty syndrome?

A

Life-threatening risk of infection

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34
Q

What tests can be used to help diagnose rheumatoid arthritis?

A

Bloods: CRP and ESR elevated, anaemia
Serology: anti CCP and RF
X-rays:
LESS
Loss of joint space
Eroded bone
Soft tissue swelling
Soft bones(osteopenia)

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35
Q

How useful are anti-CCP and RF in diagnosing RA?

A

anti-CCP: 80% specific
RF: 70% non specific

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36
Q

What can be used to monitor RA disease progression?

A

Bloods: ESR and CRP

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37
Q

What x-ray features show rheumatoid arthritis?

A

LESS
Loss of function
Eroded bone
Soft tissue swelling
Soft bones (osteopenia)

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38
Q

What anaemia is most commonly associated with rheumatoid arthritis?

A

Normocytic normochromic->anaemia of chronic disease

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39
Q

Which anaemias can occur in patients with rheumatoid arthritis?

A

Normocytic normochromic->anaemia of chronic disease
Microcytic->NSAID use->PUD->Fe deficiency anemia
Macrocytic->Methotrexate use->folate deficiency

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40
Q

How can rheumatoid arthritis cause microcytic anaemia?

A

NSAID use->PUD->Fe deficiency anaemia

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41
Q

How can rheumatoid arthritis cause macrocytic anaemia?

A

Methotrexate use inhibits folate

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42
Q

Describe the treatment of rheumatoid arthritis

A

NSAID analgesia
Intra-articular steroid injections for pain
DMARD-methotrexate
Biologics: 1st line: infliximab: TNF alpha inhibitor
2nd line: rituximab: B cell inhibitor

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43
Q

Which biologics can be used to treat rheumatoid arthritis?

A

Infliximab: TNF alpha inhibitor
Rituximab: B cell inhibitor (CD20 target)

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44
Q

When is methotrexate contraindicated?

A

Pregnancy->folate inhibitor so can affect DNA synthesis

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45
Q

Name 2 crystal arthropathies

A

Gout
Pseudogout

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46
Q

What kind of arthritis is gout?

A

Crystal arthritis

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47
Q

How does hyperuricaemia affect gout?

A

Increases risk, doesn’t cause it!

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48
Q

Describe the pathophysiology of gout

A

Hyperuricaemia->sodium urate crystal deposition along joints and intra-articularly

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49
Q

What is the most common inflammatory arthritis in the UK?

A

Gout

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50
Q

Name some risk factors for developing gout

A

Middle-aged, overweight men
Purine rich foods (meat, beer, seafood)
CKD+diuretics

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51
Q

Name some purine-rich foods

A

Meat
Beer
Seafood

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52
Q

Which food group can be anti-gout?

A

Dairy products

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53
Q

What is the equation linking purine and monosodium urate?

A

Purines->uric acid->monosodium urate
Purines->uric acid catalysed by xanthine oxidase
Uric acid secreted by kidneys

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54
Q

How is CKD a risk factor for gout?

A

Kidneys are responsible for excreting uric acid so CKD leads to impaired uric acid secretion and therefore increased monosodium urate deposits

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55
Q

Name a differential diagnosis for gout

A

Septic arthritis

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56
Q

Describe the symptoms of gout

A

Sudden onset, severe swollen, red toe, can’t put weight on it
Monoarticular, typically metatarsophalangeal joint (big toe)

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57
Q

How is gout diagnosed?

A

Joint aspirate and polarised microscopy
Negative birefringent needle-shaped crystals

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58
Q

Describe the treatment for gout

A

Diet: low in purines, high in dairy
NSAIDS, then colchicine, then steroid injections for acute flare
Prevention: allopurinol

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59
Q

How does allopurinol help prevent gout?

A

Xanthine oxidase inhibitor
Will decrease uric acid production and therefore decrease monosodium urate

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60
Q

What is the difference in pathophysiology between gout and pseudogout?

A

Gout: monosodium urate crystals
Pseudogout: calcium pyrophosphate crystals

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61
Q

What is the difference in diagnosis between gout and pseudogout?

A

Gout: Negatively birefringent needle shaped crystals
Pseudogout: Positively birefringent rhomboid shaped crystals

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62
Q

What is pseudogout?

A

Calcium pyrophosphate crystals deposited along joint capsule

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63
Q

What is the difference in treatment between gout and pseudogout?

A

Gout: Allopurinol as prevention
Pseudogout: No preventative treatment

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64
Q

Name some risk factors for developing pseudogout

A

Most commonly seen in females, >70yrs
Diabetes
Metabolic diseases
Osteoarthritis

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65
Q

Name a differential diagnosis for pseudogout

A

Septic arthritis

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66
Q

Describe the symptoms of pseudogout

A

Often polyarticular with knee involvement
Swollen, red, hot joint

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67
Q

How is pseudogout diagnosed?

A

Joint aspirate and polarised light microscopy
Positively birefringent rhomboid-shaped crystals

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68
Q

Describe the treatment of pseudogout

A

NSAIDS, then colchicine, then steroid injections
No preventative treatment

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69
Q

Define osteoporosis

A

Decreased bone density by >2.5 standard deviations below young adult mean value (T<2.5)

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70
Q

What is the difference between osteomalacia and osteoporosis?

A

Osteoporosis: low bone density
Osteomalacia: low bone mineralisation

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71
Q

What characteristic group tends to be affected most by osteoporosis?

A

> 50 post-menopausal caucasian women

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72
Q

Name the risk factors for osteoporosis

A

SHATTERED
Steroids
Hyperthyroidism/hyperparathyroidism
Alcohol and smoking
Thin (low BMI)
Testosterone-low
Early menopause(low oestrogen)
Renal/liver failure
Erosive and inflammatory disease
DMT1/malabsorption

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73
Q

Describe the symptoms of osteoporosis

A

Fractures!
Proximal femur-falls
Colles’-forked wrist
Compression of vertebrae-may cause kyphosis/widow stoop

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74
Q

How is osteoporosis diagnosed?

A

DEXA scan
Dual x-ray absorptiometry
Yields T score
FRAX score

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75
Q

What is T score-osteoporosis?

A

Compares patient’s bone mineral density to reference
0-1: normal
1-2.5: Low BMD-osteopenia
>2.5: Osteoporosis

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76
Q

What is the FRAX score?

A

Fracture risk assessment score
Assessess 10 year fracture risk in osteoporotic patients

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77
Q

Describe the treatment for osteoporosis

A

Bisphosphonates:(alendronate, risedronate)
mAB denosumab
HRT
Oestrogen receptor modulator: raloxifene
Recombinant PTH-teriparatide

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78
Q

How can HRT help treat osteoporosis?

A

Increases testosterone and oestrogen levels

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79
Q

How do bisphosphonates help treat osteoporosis?

A

Inhibit RANK-L signalling and osteoclastic inhibitors

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80
Q

How does mAB denosumab work to treat osteoporosis?

A

Inhibits RANK-L

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81
Q

What is the precursor to osteoporosis?

A

Osteopenia

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82
Q

What T score indicates osteopenia?

A

1<T<2.5-Low BMD so osteopenia

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83
Q

What is fibromyalgia?

A

Chronic widespread MSK pain >3 months and all other causes ruled out
Non-nociceptive pathway affected

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84
Q

What characteristic group is usually affected by fibromyalgia?

A

Typically: females with depression/stress/poor
>60

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85
Q

Describe the symptoms of fibromyalgia

A

Stressed, depressed females, >60
Fatigue
Sleep disturbance
Morning stiffness (especially neck and back)
Pain

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86
Q

What is the difference between nociceptive and non-nociceptive pain?

A

Nociceptive: painful stimuli like trauma
Non-nociceptive: neuropathic pain and CNS processing of pain, neuropathies, sciatica etc

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87
Q

Which pain pathway is affected by fibromyalgia?

A

Non-nociceptive

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88
Q

Name a differential diagnosis for fibromyalgia

A

Polymyalgia rheumatica

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89
Q

How is fibromyalgia diagnosed?

A

Bloods: normal ESR and CRP
Serology: negative ANA, aPL, anti-CCP, RF
Clinical: Pain in >11/18 specific regions

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90
Q

What are the 18 specific regions to test for pain in a patient with fibromyalgia?

A

Front:
Base of skull
Shoulders
Top of butt
Top of femur
Back:
Base of neck
2nd rib
Lateral elbows
Knee

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91
Q

Describe the treatment for fibromyalgia

A

Educate patient
Physiotherapy
Antidepressants if severe neuropathic pain
(TCA’s, amytriptyline)
CBT

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92
Q

What is polymyalgia rheumatica?

A

Large cell vasculitis that presents as a chronic pain syndrome
Muscles and joints

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93
Q

What characteristic groups are affected by polymyalgia rheumatica?

A

Females, >50

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94
Q

Which condition is closely linked to polymyalgia rheumatica?

A

Giant cell arteritis

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95
Q

Describe the symptoms of polymyalgia rheumatica

A

Chronic pain syndrome
Often bilateral shoulder pain and/or pelvic girdle aching discomfort for >2 weeks
Morning stiffness
Systemic: fever, weight loss, fatigue, depression etc

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96
Q

How is polymyalgia rheumatica diagnosed?

A

High ESR and CRP
Temporal artery biopsy may show GCA
Might have anaemia of chronic disease: normocytic normochromic

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97
Q

How is polymyalgia rheumatica treated?

A

Oral prednisolone

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98
Q

What is Sjogren’s syndrome?

A

Autoimmune exocrine dysfunction
Can be primary or secondary

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99
Q

Name some conditions that can cause secondary Sjogren’s syndrome

A

Other AI diseases:
SLE, RA

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100
Q

Name some risk factors for developing Sjogren’s

A

Females
40-50yrs
fHx
Other AI diseases
HLAB8/DR3

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101
Q

Which genes are associated with Sjogren’s

A

HLAB8/DR3

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102
Q

Describe the symptoms of Sjogren’s

A

Dry eyes: keratoconjunctivitis sicca
Dry mouth: xerostomia
Dry vagina

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103
Q

How is Sjogren’s diagnosed?

A

Serology: anti-Ro and anti-La antibodies positive
ANA also often positive
Schirmer test: induce tears and place filter paper under eyes-tears travel <10mm

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104
Q

What is the Shirmer test?

A

Induce tears and place filter paper under eyes
Tears travel<10mm-dry eyes
(Should be >20mm)

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105
Q

Describe the treatment for Sjogren’s

A

Artificial tears
Artificial saliva
Lube for sexual activity
Sometimes hydroxychloroquine

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106
Q

Name a complication that can arise from Sjogren’s

A

Increased risk of lymphomas

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107
Q

What is antiphospholipid syndrome characterised by?

A

Thrombosis, recurrent miscarriage and aPL antibodies

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108
Q

Is APS commonly seen in males or females?

A

Females

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109
Q

Name a condition associated with APS

A

SLE

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110
Q

Describe the symptoms of APS

A

CLOTS
Coagulopathy
Livedo reticularis
Obstetric issues-miscarriages
Thrombocytopenia

Also increased risk of arterial (stroke, MI) and venous thrombosis (DVT)

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111
Q

How is APS diagnosed?

A

Symptoms and positive antibodies
Lupus anticoagulant
Anticardiolipin antibodies (IgG/M)
Anti B2 glycoprotein-1-antibodies

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112
Q

Describe the treatment for APS

A

Warfarin long term if have had a thrombosis
Prophylactic(not had thrombosis)-aspirin
Aspirin and heparin if pregnant instead of warfarin

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113
Q

Describe the treatment of APS in a pregnant patient

A

Aspirin and heparin

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114
Q

What is SLE?

A

Hypersensitivity T3 reaction->antigen-antibody complex deposition->autoimmune systemic inflammation

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115
Q

Which groups of people are more commonly affected by SLE?

A

Females
Afro/Caribbeans
20-40(pre-menopausal)

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116
Q

Name some risk factors for developing SLE

A

Females (12 times more than men)
HLAB8/DR2/DR3
Drugs (isoniazid, procainamide)

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117
Q

Name 2 drugs that can cause SLE

A

Isoniazid
Procainamide

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118
Q

Describe the pathophysiology of SLE

A

Impaired apoptotic debris presented to TH2->B cell activation->antigen-antobody complexes

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119
Q

Describe the symptoms of SLE

A

Butterfly rash and hypersensitivity
Glomerulonephritis(nephritic syndrome)
Seizures and psychosis
Mouth ulcers
Serositis(pleural/peritoneal/pericardial inflammation of lungs)
Anaemia
Joint pain
Raynaud’s
Pyrexia

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120
Q

How is SLE diagnosed?

A

Bloods: anaemia
High ESR and normal CRP
Urine dipstick: haematuria, proteinuria
Serology: ANA, anti dsDNA
Anti Ro, anti Sm, anti La
Low C3 and C4

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121
Q

Describe the treatment for SLE

A

Lifestyle changes(decrease sunlight exposure)
Corticosteroids
Hydroxychloroquine
NSAID’s
Azathioprine if severe

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122
Q

What is scleroderma?

A

Autoimmune systemic condition

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123
Q

What is the most common type of scleroderma?

A

Limited cutaneous scleroderma
CREST

124
Q

Describe the signs and symptoms of limited cutaneous scleroderma (CREST)Q

A

Calcinosis-Ca deposits in SC tissue-renal failure
Raynaud’s-digit ischaemia due to sudden vasospasm
Eosophageal dysmotility/strictures-GI sx
Sclerodactyly-local skin thickening or tightening on fingers/toes-movement restriction
Telangiectasia-spider veins->risk of pulmonary hypertension

125
Q

What is calcinosis?

A

Ca deposits in SC tissue->renal failure

126
Q

What is raynaud’s?

A

Digit ischaemia due to sudden vasospasm
Often precipitated by cold, relieved with heat

127
Q

What is sclerodactyly?

A

Local skin thickening/tightening on fingers/toes->movement restriciton

128
Q

What is telangiectasia?

A

Spider veins->risk of pulmonary hypertension

129
Q

How is scleroderma diagnosed?

A

Anti centromere antibodies (ACA’s)-70% cases
ANA often positive

130
Q

How is scleroderma treated?

A

No cure
Treat symptoms
Raynauds-hand warmers
GI symptoms: PPI

131
Q

What is polymyositis/dermatomyositis?

A

Inflammation and necrosis of skeletal muscle

132
Q

What is the difference between polymyositis and dermatomyositis?

A

If it also involves skin->dermatomyositis

133
Q

Name some risk factors for developing polymyositis/dermatomyositis

A

Females
HLAB8/DR3 genetic link

134
Q

Describe the symptoms of polymyositis/dermatomyositis

A

Symmetrical wasting of muscles of shoulders and pelvic girdle->hard to stand from sitting, hard to squat, hard to put hands on head
Dermatomyositis-skin changes too

135
Q

Name some skin changes associated with dermatomyositis

A

Gottron’s papules->scales on knuckles
Heliotrope rash->purple/red eyelids
Shawl sign

136
Q

How is polymyositis/dermatomyositis diagnosed?

A

Muscle fibre biopsy->necrosis
LDH and CK raised
Anti-Jo1 antibodies: both
Anti-Mi2 antibodies: dermatomyositis

137
Q

Which antibody is specific to dermatomyositis and what dermatological sign is it associated with?

A

Anti-Mi2 antibodies
Shawl sign

138
Q

How is polymyositis/dermatomyositis treated?

A

Bed rest
Prednisolone for 1 month then tapering regime

139
Q

Describe the mutation and inheritance of Marfan’s

A

Autosomal dominant FB1 mutation->decreases connective tissue tensile strength

140
Q

Describe the signs and symptoms of Marfan’s

A

‘Marfan’s body habits’-tall and thin, arachnodactyly, pectus excavatum(sunken breastbone) pectus carinatum(protruding breastbone)
And aortic complications
aortic regurgitation, AAA, aortic disseciton

141
Q

Name some aortic complications associated wtih Marfan’s

A

Aortic regurgitation, AAA, aortic dissection

142
Q

How is Marfan’s diagnosed?

A

Clinical presentation and FBN-1 mutation

143
Q

What is EDS caused by?

A

Autosomal dominant mutations affecting collagen proteins
13 subtypes

144
Q

Describe the symptoms of EDS

A

Joint hypermobility, stretchy skin, easy bruising, CV complications (mitral regurgitation, AAA, aortic dissection)

145
Q

Name some CV complications associated with EDS

A

Mitral regurgitation
AAA
Aortic dissection

146
Q

How is EDS diagnosed?

A

Clinical presentation-Beighton score
Collagen mutations

147
Q

Name a common cause of back pain in people aged 20-55

A

May be normal and self limiting
Trauma/work related

148
Q

Name some signs for serious pathology when a patient presents with mechanical lower back pain

A

Elderly-e.g. myeloma
Neuropathic pain-spinal cord compression

149
Q

What is lumbar spondylosis?

A

Degeneration of IV disc->loses its compliance and thins over time

150
Q

What age group is most commonly affect by lumbar spondylosis?

A

Older patients

151
Q

Describe the symptoms of lumbar spondylosis

A

Initially asymptomatic, progressively worsens
L4/5 or L5/S1

152
Q

Name an investigation for mechanical lower back pain if serious pathology is suspected

A

X-ray or MRI

153
Q

Describe the treatment for simple mechanical lower back pain

A

Analgesia and physio

154
Q

What connects bone to bone?

A

Ligaments

155
Q

What connects muscle to bone?

A

Tendons

156
Q

Name the primary bone tumours

A

Osteosarcoma
Ewing sarcoma
Fibrosarcoma
Chondrosarcoma

157
Q

Are primary or secondary bone tumours more common?

A

Secondary

158
Q

Which age group is predominantly affected by primary bone tumours

A

Children

159
Q

Where do secondary bone tumours arise from?

A

BLT KP
Breast
Lung
Thyroid
Kidneys
Prostate

160
Q

Name a cancer that can cause bone pain

A

Myeloma (OLD CRAB)

161
Q

Which secondary bone tumours are osteolytic?

A

Breast
Lung

162
Q

Which secondary bone tumours are osteosclerotic?

A

Prostate

163
Q

What is the most common primary bone malignancy?

A

Osteosarcoma

164
Q

What disease is osteosarcoma associated with?

A

Paget’s

165
Q

What age group is most affected by osteosarcoma?

A

15-19 years

166
Q

Where does osteosarcoma often metastasise to?

A

Lungs

167
Q

How is osteosarcoma diagnosed?

A

X-ray: ‘sunburst’ appearing bone

168
Q

What is chondrosarcoma?

A

Cartilage cancer

169
Q

What cells does Ewing sarcoma arise from?

A

Mesenchymal stem cells

170
Q

What is the most common age Ewing sarcoma presents?

A

15yrs

171
Q

Describe the symptoms of bone cancer

A

Local severe pain, worst at night
Decreased range of motion of longbone/verterbrae
Pathological fractures
Systemic: weight loss, fever, malaise, fatigue

172
Q

How is bone cancer diagnosed?

A

Skeletal isotope scan (shows changes before x ray)
X-ray->osteolysis (osteosclerosis->prostatic mets)
High ALP, high ESR/CRP, hypercalcemia of malignancy

173
Q

Describe the treatment for bone cancer

A

Chemo/radiotherapy
Bisphosphonates

174
Q

What should be considered when prescribing long term steroids?

A

Bone protection-bisphosphonates
Stomach protection-PPI

175
Q

What is the general treatment for vasculitis?

A

Corticosteroids

176
Q

Name some conditions that cause large vessel vasculitis

A

Giant cell arteritis
Takayatsu arteritis

177
Q

What groups are mainly affected by Takayatsu arteritis?

A

Asian women

178
Q

What does Takayatsue arteritis mainly affect?

A

Aortic arch

179
Q

Name some conditions that cause vasculitis of medium-sized vessels

A

Polyarteritis nodosa
Buerger’s disease
Kawasaki disease

180
Q

What groups are most affected by Buerger’s disease?

A

Male smokers aged 20-40

181
Q

What is Buerger’s disease also called?

A

Thromboangiitis obliterans

182
Q

What does Buerger’s disease cause?

A

Peripheral skin necrosis

183
Q

What group does Kawasaki disease affect?

A

Children

184
Q

What does Kawasaki disease cause?

A

Coronary artery aneurysms

185
Q

Name some conditions that cause vasculitis of the small vessels

A

Granulomatosis with polyangiitis(Wegener’s)
Eosinophilic granulomatosis with polyangitis (EGPA/Churg Strauss disease)
Henoch Schonlein purpura

186
Q

What is eosinophilic granulomatosis with polyangitis also called?

A

Churg Strauss disease

187
Q

What test can be used to diagnose Churg Straus disease?

A

pANCA

188
Q

What is granulomatosis with polyangitis also called?

A

Wegener’s disease

189
Q

What test can be used to diagnose Wegener’s granulomatosis?

A

cANCA

190
Q

Name some signs and symptoms of Wegener’s granulomatosis

A

Saddle shaped nose
Pulmonary renal syndrome: glomerulonephritis and diffuse alveolar haemorrhage
(Glomerulonephritis and pulmonary symptoms)

191
Q

What is Henloch Schontein purpura?

A

IgA vasculitis
DDx for IgA nephropathy

192
Q

How is Henloch Schontein purpura different to IgA nephropathy

A

HSP has a purpuric rash on shins and affects other organs-joints, abdomen, renal
IgA nephropathy-renal only

193
Q

What groups tend to be affected by GCA

A

50+ caucasian female

194
Q

How do patients with GCA typically present?

A

50+ caucasian females
Unilateral temple headache
Jaw claudication with/without vision changes
Temporal scalp tenderness

195
Q

Which vessel is affected by GCA?

A

External carotid branches

196
Q

What causes scalp tenderness in GCA patients?

A

Vasculitis of temporal branch of external carotid

197
Q

What causes vision changes in GCA patients?

A

Vasculitis of ophthalmic branch of external carotid

198
Q

What causes jaw claudication in GCA patients?

A

Vasculitis of facial branch of external carotid

199
Q

How is GCA diagnosed?

A

High ESR: normal/high CRP
Temporal artery biopsy is diagnostic: granulomatous inflammation of intima and media->patchy skip lesions so you need a big chunk

200
Q

What would you expect to find on a temporal artery biopsy in a GCA patient?

A

Granulomatous inflammation of intima and media
Patchy skin lesions

201
Q

What is the treatment for GCA?

A

Corticosteroids-prednisolone

202
Q

Name a complication of GCA

A

Sudden painless vision loss in one eye-optic neuropathy-can become permanent if not treated quickly

203
Q

What is temporary vision loss in one eye called and when does it typically occur?

A

Amaurosis fugax-typically seen in TIA

204
Q

How is amaurosis fugax from GCA treated?

A

High does IV methylprednisolone

205
Q

Does polyarteritis nodosa typically affect males or females?

A

Males

206
Q

What disease is polyarteritis nodosa associated with?

A

Hepatitis B

207
Q

Describe the symptoms of polyarteritis nodosa

A

Severe systemic symptoms:
Multineuritis multiplex(ischaemia of vasa nervosum)
GI bleeds-mesenteric artery
CKD/pre-renal AKI (renal artery)
Skin SC nodules and haemorrhage

208
Q

How is polyarteritis nodosa diagnosed?

A

CT angiogram-‘Beads on string’ microaneurysm
Biopsy, e.g. kidney->necrotising vasculitis, e.g. due to hypertension

209
Q

Describe the treatment for polyarteritis nodosa

A

Corticosteroids
Control hypertension->ACEi
Hep B treatment after corticosteroids

210
Q

What is enteric arthritis?

A

Arthritis associated with IBD

211
Q

What are spondyloarthropathies?

A

Asymmetrical, seronegative inflammatory arthritis, associated with HLAB27-an MHC1 serotype

212
Q

Which gene is associated with spondyloarthropathies?

A

HLAB27

213
Q

Name some spondyloarthropathies

A

Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Enteric arthritis

214
Q

What are the general features of spondyloarthropathies?

A

SPINEACHE
Sausage fingers-dactylitis
Psoriasis
Inflammatory back pain
NSAID’s-good response
Enthesitis
Arthritis
Crohn’s/colitis
HLA B27
Eyes-uveitis

215
Q

What is reactive arthritis?

A

Sterile inflammation of synovial membranes and tendons , reacting to distant infections, usually GI or STI

216
Q

Which organisms can cause reactive arthritis?

A

GI: gastroenteritis
C.jejuni
Salmonella
Shigella
STI:
C.trachomatis
N.gonorrhoea

217
Q

Name a differential diagnosis for reactive arthritis

A

Septic arthritis
Painful, hot, red, swollen joint
Signs/history of infection

218
Q

What triad is associated with reactive arthritis?

A

Reiter’s triad
Uveitis, Urethritis, arthritis/enthesitis
Can’t see, can’t pee, can’t climb a tree

219
Q

Describe the symptoms of reactive arthritis

A

Reiter’s triad: urethritis/balanitis, uveitis, arthritis/enthesitis
May also have keratoderma blenorrhagicum(skin lesions)

220
Q

How is reactive arthritis diagnosed?

A

Joint aspirate:
mc+s:no organisms
Polarised light microscopy: no crystal arthropathy
High ESR and CRP
HLAB27 positive
Sexual health review and stool culture for cause

221
Q

How is reactive arthritis treated?

A

Symptoms: NSAIDs, steroid injecitons
Methotrexate, anti-TNFa if this doesn’t work

222
Q

Is reactive arthritis acute or chronic?

A

Mostly an single acute attack
>6months recurrence-chronic

223
Q

Is reactive arthritis acute or chronic?

A

Mostly a single acute attack
>6months recurrence-chronic

224
Q

What is ankylosing spondylitis?

A

Abnormal stiffening of joints (sacroiliac and verterbral) due to new bony formation

225
Q

Are males or females more affected by ankylosing spondylitis?

A

young Males

226
Q

What gene is associated with ankylosing spondylitis

A

HLAB27

227
Q

Describe the pathophysiology of ankylosing spondylitis

A

Syndesmophytes replace spinal bone damaged by inflammation which decreases spine mobility

228
Q

What are syndesmophytes?

A

Vertical abnormal bony growths-cause fusion of verterbral bodies

229
Q

What body parts are commonly inflamed with ankylosing spondylitis?

A

Vertebrae and sacroiliac joints
Tendons
Eyes
Fingers

230
Q

Describe the typical presentation of a patient with ankylosing spondylitis

A

Young male, progressively worsening back stiffness
Worst in morning and night, better with movement

231
Q

Name the signs of ankylosing spondylitis

A

Anterior uveitis
Enthesitis
Dactylitis
Lumbar pathology: decreased natural lumbar lordosis->more kyphosis
Schober test: decreased lumbar flexion (<20cm)

232
Q

What is the Schober test used for?

A

ankylosing spondylitis
Detects reduced flexion

233
Q

Describe the Schober test

A

While standing, mark 5th lumbar spinal process(usually dimple of Venus) and 10cm above
On forward flexure, space between 2 marks should increase to >20cm

234
Q

How is ankylosing spondylitis diagnosed?

A

ESR ad CRP raised
HLA B27 positive-but not needed for diagnosis
Xray
MRI

235
Q

Is MRI or xray better for diagnosis ankylosing spondylitis?

A

MRI can detect sacroilitis before x ray so is a better screening tool

236
Q

What x ray findings would you expect in a patient with ankylosing spondylitis?

A

Bamboo spine
Sacroiliitis
Squared verterbral bodies
Syndesmophytes

237
Q

Describe the treatment for ankylosing spondylitis

A

Exercise, NSAIDs
DMARD
TNFa blockers-infliximab, etanercerpt

238
Q

Name 2 TNFa blockers used to treat ankylosing spondylitis

A

Infliximab
Etanercept

239
Q

Describe the symptoms of moderate psoriatic arthritis

A

Inflamed DIPJ’s
Nail dystrophy
Dactylitis
Enthesitis
Psoriatic rash on skin

240
Q

What are the hidden sites for a psoriatic rash?

A

Behind ears, scalp, under nails, penile

241
Q

Descirbe the symptoms of severe psoriatic arthritis

A

Arthritis mutilans
Penicl in cup deformity (fingers telescope in on themselves-osteolysis of bone->progressive shortening)

242
Q

Describe the treatment for psoriatic arthritis

A

NSAIDS/steroid injection sot improve symptoms
Methotrexate
If fails: antiTNFa: inflixumab, etanercept
If fails: IL12+23 inhibitor: ustekenumab

243
Q

Name an IL12+23 inhibitor and what i might be used to treat

A

Ustekenumab: treat psoriatic arhtritis when methotrexate and snti TNF alpha fails

244
Q

Name 2 infective arthritis

A

Septic arthritis
Osteomyelitis

245
Q

What is septic arthritis?

A

Direct bacterial infection of joints (either direct access or haematogenous spread)

246
Q

What is meant by haematogenous spread?

A

Spreads from elsewhere in the body

247
Q

Why is septic arthritis a medical emergency and what can this look like?

A

Acutely inflamed joint with fever, very painful
Can destory knee in <24 hours
(Typically knee)

248
Q

What organism most commonly causes septic arthritis?

A

S.aureus

249
Q

Which organism is often the cause of septic arthritis in prosthetic joints?

A

Coagulase negative staphs
S epidermis

250
Q

Which organisms commony cause septic zrthritis?

A

H influenza(children, less common due to vaccination now)
N. gonorrhoea
E.Coli/pseudomonas (IVDU)

251
Q

Name some risk factors for developing septic arthritis

A

IVDU
Immunosuppression
Recent surgery
Trauma
Prosthetic joints and inflammatory joint disease, especially RA

252
Q

How is septic arthritis diagnosed?

A

Urgent joint aspirate
mc+s and polarised light microscou
Spetic arthritis will show causative organism

253
Q

Name some differential diagnoses for septic arthritis and how you can distinguish between them

A

Reactive arthritis: Sterile, crystal free joint
Gout: sterile, negative befringent needle crystals
Pseudogout: sterile, positive befringent rhomboid crystals

254
Q

Describe the treatment of septic arthritis

A

Joint aspirate(drainage) them epirical antibiotics
Stop methotrexate/anti TNF
If on steroids, double dose
NSAIDS for analgesia

255
Q

Which antibiotics would you use to treat septic arthritis caused by gram negative bacteria like E.coli and p. aeruginosa

A

Flucoxacillin

256
Q

Which antibiotics would you use to treat septic arthritis caused by MRSA or s aureus

A

Vancomycin

257
Q

Which antibiotics would you use to treat septic arthritis caused by N. gonorrhoea?

A

ceftriaxone and azithromycin

258
Q

What would you do if a patient on prednisolone develops septic arthritis?

A

Double the dose-stress response

259
Q

What is osteomyelitis?

A

Acutely inflamed infected bone marrow, haematogenous or local spread

260
Q

Which organism most commonly causes osteomyelitis?

A

S.aureus

261
Q

Which organism most commonly causes osteomyelitis in sickle cell patients?

A

Salmonella

262
Q

Name some risk factors for developing osteomyelitis

A

IVDU
Immunosuppression
PVD, DM
Sickle cell anaemia
Inflammatory arthritis
Trauma

263
Q

Describe the pathophysiology of osteomyelitis

A

Direct inoculation/local spread/haematogenous spread
All result in acute bone changes->inflammation and bone oedema
Chronic bone changes->sequestra and involucrum

264
Q

What is sequestra and involucrum

A

Sequestra: necrotic bone embedded in pus
Involucrum: thick sclerotic boneplaces around sequestra to compensate for support

265
Q

Describe the acute symptoms of osteomyelitis

A

Dull bony pain
How and swollen
Worse with movement

266
Q

Describe the chronic symptoms of osteomyelitis

A

Dull bony pain, hot and swollen, worse with movement
Also deep ulcers (sequestrate)

267
Q

Name a differential diagnosis to osteomyelitis

A

Charcot joint: damage to sensory nerves due to diabetic neuropathy->causes progressive degeneration of weight bearing joint and bony destruction
Often affects foot-diabetic feet’

268
Q

How is osteomyelitis diagnosed?

A

BM biopsy and culture(and blood mc+s) to ID causative organism
High ESR and CRP
XR: osteopenia
MRI after Xray can show bone marrow oedema

269
Q

Describe the treatment for osteomyelitis

A

Immobilise
Antibiotics

270
Q

Which antibiotics could be used to treat osteomyelitis caused by MRSA/S.aureus?

A

Vancomycin or teicoplanin

271
Q

What are the advantages and disadvantages of using teicoplanin over vancomycin

A

Longer lasting but more side effects (GI upsets and pruritus)

272
Q

Which antibiotics could be used to treat osteomyelitis caused by S aureus

A

Fusidic acid

273
Q

Which antibiotics could be used to treat osteomyelitis caused by salmonella

A

Flucoxacillin

274
Q

What must be ruled out when diagnosisng and treating osteomyelitis?

A

TB osteomyelitis

275
Q

How can TB osteomyelitis be ruled out?

A

Bone marrow biopsy-positive for caseating granuloma)

276
Q

What is osteomalacia?

A

Defective bone mineralisation after epiphyseal fusion

277
Q

What is rickets?

A

Defective bone mineralisation before epiphyseal fusion

278
Q

What is the main cause of osteomalacia/rickets?

A

Vitamin D deficiency, so causes decreased Ca2+ and PO43-

279
Q

Describe the vitamin D pathway

A

7-dehyrocholesterol->cholecalciferol(inactive D3) by UV light
Cholecalciferol->25-hydroxyvitamin D(liver)
25-hydroxyvitamin D->1,25-dihydroxyvitamin D(active D3/calcitrol) by kidneys

280
Q

Name the action of 1,25-dihydroxy-vitamin D

A

Overall increases serum calcium and phosphate
Increases Ca2+ bone and kidney resorption
Increases Ca2+ GI absorption

281
Q

Name the causes of osteomalacia/rickets

A

Hyperparathyroidism
Vitamin D deficiency
CKD/renal failure
Liver failure
Anticonvulsant drugs

282
Q

How does hyperparathyroidism cause osteomalacia/rickets?

A

Increased PTH->increased Ca2+ resorption from the bone so less available for mineral formation

283
Q

Name some primary causes of a vitamin D deficiency

A

Malabsorption
Low dietary intake
Poor sunlight exposure

284
Q

How does vitamin D deficiency result in osteomalacia/rickets?

A

Vitamin D responsible for increasing intestinal absorption of Ca2+
Low vitamin D->lose Ca2+ you would be getting from GI tract

285
Q

How does renal failure/CKD cause osteomalacia/rickets?

A

Kidneys responsble for converting 25-hydroxyvitamin D->1,25-dihydroxyvitamin D, so causes a decrease in active D3

286
Q

How does liver failure cause osteomalacia/rickets?

A

Liver responsible for cholecalciferol->25-hydroxyvitaminD, so decrease in hydroxyvitamin Dand therefore active D3

287
Q

How can anticonvulsant drugs result in osteomalacia/rickets?

A

Increase CY-450 metabolism of vitamin D

288
Q

Describe the symptoms of osteomalacia

A

Fractures
Proximal weakness and difficulties with weight bearing

289
Q

Describe the symptoms of rickets

A

Skeletal deformities
Knocked knees and bowed legs
Wide epiphyses

290
Q

How is osteomalacia diagnosed?

A

BM biopsy->incomplete mineralisation
Bloods: hypocalcaemia, high PTH, low 25(OH)D
Xray-Looser’s zones (defective mineralisation)

291
Q

Describe the treatment for osteomalacia

A

Vitamin D replacement(calcitrol) and increase dietary intake (D3 tablets, eggs

292
Q

What would you expect on a BM biopsy in a patient with osteomalacia?

A

Incomplete mineralisation

293
Q

What would you expect in the bloods of a patient with osteomalacia?

A

Hypocalcaemia
High PTH
Low 25(OH)D

294
Q

Why would you expect high PTH in a patient with osteomalacia?

A

Secondary to low Ca2+

295
Q

What would you expect on an xray of a patient with osteomalacia?

A

Looser’s zones: defective mineralisation

296
Q

What is Paget’s disease also called?

A

Osteitis deformans

297
Q

What is Paget’s disease?

A

Focal disorder of bone remodelling
Areas of patchy bone due to improper osteoblast/osteoclast action->areas of sclerosis and lysis

298
Q

What group is most commonly affected by paget’s disease/

A

Females, >40

299
Q

What is the most common cause of Paget’s disease?

A

Idiopathic

300
Q

Describe the signs and symtpoms of Paget’s

A

Bone pain
Bone changes-> bowed tibia and skull
Neurological symptoms-> nerve compression of CN8-deafness
Hydrocephalus due to sylvian aquaduct blockage

301
Q

How is Paget’s disease diagnosed?

A

Xray: osteoporosis circumscripta
Cotton wool skull(areas of lysis and sclerosis)
High ALP
Urinary hydroxyproline high

302
Q

Describe the treatment for Paget’s disease

A

Bisphpsphonates
NSAIDs for pain relief

303
Q

What is urinary hydroxyproline?

A

Protein consituent of bone collagen

304
Q

What can be useful for monitoring Paget’s disease progression?

A

Urine hydroxyproline

305
Q

Name 2 neurological complications of Paget’s disease

A

Deafness->compression of CN8
Hydrocephalus->compression of sylvian aqueduct

Phase 2a med mine (11 decks)

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