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Year 2 > MSK: Part 4 > Flashcards

MSK: Part 4 Flashcards

1
Q

What are all vasculitis associated with

A

Anaemia and raised ESR

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2
Q

What conditions are associated with vasculitis

A 
Infective:
1. Subacute infective endocarditis
Non-infective:
1. Vasculitis with RA
2. SLE
3. Scleroderma
4. Polymyositis/Dermatomyositis
5. Good pasture syndrome and UC/Crohn's
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3
Q

What patients are effected by Polymyalgia Rheumatica and Giant Cell Arteritis (large vessel vasculitis)

A

Patients older than 50

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4
Q

What is associated with PMR and GCA

A

Finding of GCA on temporal artery biopsy (THEY COEXIST)

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5
Q

What is giant cell arteritis

A

Arteries of the head and neck inflame

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6
Q

What gender is effected by Polymyalgia Rheumatica

A

FEMALES

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7
Q

Risk factors of Polymyalgia Rheumatica

A
  1. SLE

2. Polymyositis/dermamyositis

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8
Q

Clinical presentation of Polymyalgia Rheumatica

A
  1. Sudden onset of severe pain and stiffness of the shoulders and neck, and of the hips and lumbar spine; a limb girdle pattern
  2. Symptoms are worse in the morning, lasting from 30 mins to several hours
  3. Mild polyarthritis of peripheral joints
  4. 1/3rd experience: fatigue, fever, weight loss, depression
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9
Q

Differential Diagnosis of Polymyalgia Rheumatica

A
  1. RA, spondyloarthropathies, SLE, polymyositis
  2. Osteoarthritis, malignancy
  3. Chronic pain syndrome (fibromyalgia and depression)
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10
Q

Diagnosis of POlymyalgia Rheumatica

A
  1. ALWAYS over 50
  2. ESR and CRP RAISED
  3. ANCA negative
  4. Serum alkaline phosphatase raised
  5. Normochromic, normocytic anaemia present
  6. Giant cell arteritis upon temporal artery biopsy
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11
Q

What FBC content is used to distinguish polymyalgia Rheumatica from myositis

A

Creatinine Kinase is normal

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12
Q

How is Polymyalgia Rheumatica treated

A
  1. CORTICOSTEROIDS (reduce symptoms of PMR) - ORAL PREDNISOLONE
  2. If improvement does not occur then diagnosis should be questioned
  3. Decrease SLOWLY
  4. Used long-term to give GI and bone protection (e.g. LANSOPRAZOLE, ALENDRONATE and Ca/vit D)
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13
Q

What is Giant cell arteritis

A

Inflammatory granulomatous arteritis of large CEREBRAL ARTERIES as well as large vessels associated with PMR

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14
Q

Risk factors for giant cell arteritis

A
  1. Over 50
  2. Female
  3. RA, SLE, scleroderma
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15
Q

What happens to arteries in Gaint cell arteritis

A
  1. Arteries become inflamed, thickened and obstruct blood flow
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16
Q

What arteries are effected in giant cell arteritis

A
  1. Cerebral arteries (temporal artery) and ophthalmic artery = temporary vision loss)
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17
Q

Clinical presentation of giant cell arteritis

A
  1. Temporal pulsations (headaches)
  2. Tenderness of scalp or temple
  3. Claudication of the jar when eating (pain)
  4. Tenderness and welling of one or more temporal or occipital arteries
  5. Sudden painless vision loss (arteritis anterior ischaemic optic neuropathy - optic disc is very pale)
  6. Malaise, lethargy, fever
  7. Associated symptoms of PMR
  8. Dyspnoea, morning stiffness and unequal pulses

Morning Stiffness Does Seem Very Convenient This Hour

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18
Q

Differential diagnosis of giant cell arteritis

A
  1. Migraine
  2. tension headache
  3. Trigeminal neuralgia
  4. Polyarteritis nodosa

The Magnus Nasty Neil

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19
Q

Diagnostics of Giant cell arteritis

A
  1. Over 50
  2. New headache
  3. Temporal artery tenderness
  4. ESR raised
  5. Abnormal artery biopsy (inflammatory infiltrates present)

ONE OF 3

AND TEMPORAL ARTERY BIOPSY

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20
Q

FBC tests for Giant Cell arteritis

A
  1. ESR raised
  2. Normochromic, normocytic anaemia
  3. ANCA negative
  4. CRP VERY HIGH
  5. Serum alkaline phosphatase RAISED
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21
Q

When should temporal artery biopsy be done for giant cell arteritis

A
  1. BEFORE or within 7 days of starting high dose

2. Lesions are patchy so take a big chunk

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22
Q

Histological features of Giant cell arteritis

A
  1. Cellular infiltrates of CD4+ T cells, macrophages and giant cells in the vessel wall
  2. Granulomatous inflammation of the intima and media
  3. Breaking up of internal elastic lamina
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23
Q

Treatment of Giant cell arteritis

A
  1. PREDNISOLONE to stop vision loss
  2. Long-term to protect GI and bones (LANSOPRAZOLE, ALDENRONATE and Ca/Vit D)
  3. Monitor treatment progress by looking at fall in ESR/CRP
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24
Q

Name two medium-vessel vasculitis

A
  1. POLYARTERITIS NODOSA

2. CRYSTAL ARTHROPATHIES

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25
Q

How common is Polyarteritis Nodosa in the UK

A

Rare

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26
Q

What does PAN effect

A

Middle-aged men

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27
Q

What disease is PAN associated with

A

Hep B

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28
Q

Risk factors for PAN

A
  1. Male
  2. Hep B
  3. RA, SLE and scleroderma
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29
Q

What is the pathophysiology of Polyarteritis Nodosa

A
  1. Necrotising vasculitis that causes aneurysms and thrombosis in medium-sized arteries leading to infarctions in affected organs

HAS SEVERE SYSTEMIC SYMPTOMS

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30
Q

Clinical presentation of PAN

A
  1. Fever, malaise, weight loss and myalgia

Neurological: Mononeuritis multiplex due to arteritis of vast nervorum (arterial supply to peripheral nerves) -
Numbness, tingling, abnormal/lack of sensation and inability to move part of the body

Abdominal: Pain due to arterial involvement of the abdominal viscera, mimicking acute cholecystitis, pancreatitis or appendicitis

Renal: Haematuria and Proteinuria

Hypertension and CKD can occur

Cardiac: Coronary arteritis causes MI and HF

Skin: Subcutaneous haemorrhage and gangrene occur

Lung involvement is rare

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31
Q

Differential diagnosis of PAN

A
  1. Fever caused by infection
  2. Crohn’s
  3. Connective tissue disease
  4. Other vasculitis
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32
Q

Diagnosis of PAN

A
  1. FBC
  2. Biopsy of kidney for hypertension and damage
  3. Angiography (micro-aneurysms in hepatic, intestinal or renal vessels)
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33
Q

FBC result for PAN

A
  1. Anaemia
  2. WCC raised
  3. ECR raised
  4. ANCA negative (sometimes positive)
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34
Q

Treatment for PAN

A
  1. ACEI - Ramipril
  2. CORTICOSTEROIDS - Prednisolone with AZATHIOPRINE or CYCLOPHOSPHAMIDE
  3. Hep B should be treated with antiviral after treatment alongside steroids
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35
Q

What two crystals tend to cause Crystal arthropathies

A
  1. MONOSODIUM URATE CRYSTALS

2. CLACIUM PYROPHOSPHATE CRYSTALS

36
Q

Characteristics of monosodium rate crystals

A

1, needle-shaped rate crystals

2. Negatively bifringent under polarised light

37
Q

Characteristics of calcium pyrophosphate crystals

A
  1. Small rhomboid brick-shaped pyrophosphate crystals

2. Positively bifringent under polarised light

38
Q

How do crystals cause arthropathies

A
  1. Neutrophils ingest crystals and initiate a pro-inflammatory reaction
39
Q

What is GOUT

A
  1. Inflammatory arthritis associated with hyperuricaemia and intra-articular monosodium rate crystals
40
Q

Where is GOUT common

A

MALES in older people

41
Q

Risk factors for GOUT

A
  1. High alcohol intake (highest risk for beer then spirits then wine)
  2. Purine rich foods (red meat)
  3. High fructose intake reduces uric acid excretion
  4. High saturated fat diet
  5. Low-dose aspirin
  6. Ischaemic heart disease
  7. Family history of gout
42
Q

What are renal causes for GOUT

A

1, Defective gene for URAT1 transporter in kidney (this reabsorbs rate and secretes it)

  1. High insulin levels lower rate excretion
  2. Diuretics impair uric acid excretion (thiazides)
43
Q

What factors can influence increased production of uric acid

A
  1. Increased purine turnover
  2. Myeloproliferative (polycthaemia vera)
  3. Lymphoproliferative disorders (leukaemia)
  4. Carcinoma and psoriasis - due to increased cel turnover
  5. Cell damage - surgery
  6. Cell death - chemotherapy
44
Q

How is uric acid broken down

A
  1. HYPOXANTHINE to XANTHINE to URIC ACID by XANTHINE OXIDASE

final product is usually allantoin which is harmless in the body

45
Q

Why can’t we produce allantoin in the human body

A

No URICANSE present

46
Q

What happens to Uric acid in the human body

A

Excreted via the kidneys

47
Q

What happens to uric acid when there is hyperuricaemia

A

Converted to monosodium urate crystals which causes GOUT and PAIN

48
Q

In what gender are serum uric levels higher

A

Men

49
Q

What defines hyperuricaemia

A

Serum levels higher than 420 micro moles/L or 360 micro moles/L in females

50
Q

What joints are more prone to attacks of gout in hyperuricaemia

A

Osteoarthritic joints

51
Q

What four factors increase serum uric acid levels

A
  1. AGE
  2. OBESITY
  3. DIABETES MELLITUS
  4. ISCHAEMIC HEART DISEASE and HYPERTENSION
52
Q

Where do monosodium rate crystals tend to form

A

Joints in which previous traumas have occurred: Big toe

53
Q

At what temperatures do crystals form

A

Lower so they form at peripheral joints (coolest)

54
Q

Why do monosium rate crystals cause pain

A

Trigger intracellular inflammation

55
Q

Clinical presentation of ACUTE GOUT

A
  1. Middle-aged men
  2. Sudden onset of agonising pain, swelling and redness of first MTP joint
  3. Usually just one joint affected by can sometimes be polyarthritic
  4. Attack is precipitated by excess food (especially red meat) , alcohol, dehydration or diuretic therapy, cold, trauma or sepsis
  5. Urate renal stone formation
  6. Gout increases risk of hypertension, renal disease, CVS disease, type 2 diabetes and osteoargitic damage to joints
  7. Recurrent gout attacks can lead to renal impairment
56
Q

What people have chronic polyarticular gout

A

Patients in renal failure or been started on ALLOPURINOL too soon

57
Q

Differential diagnosis of acute gout

A

TOPHACEOUS GOUT

58
Q

Clinical presentation of tophaceaous gout

A

1, Persistently high levels of uric acid causes monosodium rate forming smooth white deposits (top) in skin and round joints on ear, fingers or Achilles tendon

59
Q

What are Topphi

A

Onion like aggregates of monosodium rate crystals with inflammatory cells

60
Q

How do Tophi cause damage

A

Release proteolytic enzymes and erosions to bone

61
Q

What is TOphaceous gout associated with

A

Renal impairment and long-term use of diuretics

62
Q

Differential diagnosis of gout

A

Septic arthritis in acute monoarthropathy

63
Q

How is Gout diagnosed

A
  1. Joint fluid aspiration and microscopy (DIAGNOSTIC)
  2. SERUM uric acid is raised
  3. Serum urea, creatinine and eGFR monitored for renal impairment
64
Q

What does joint fluid aspiration show in GOUT

A

long needle shaped crystals that are NEGATIVELY bifringent under polarised light

65
Q

How is Gout treated

A
  1. Lose weight
  2. Less alcohol
  3. Avoid purine rich food
  4. Diary can reduce gout
66
Q

Treatment of ACUTE GOUT

A
  1. NSAIDs (IBUPROFEN) or ASPIRIN
  2. NSAID not tolerated then COLCHICINE (targets uric acid crystallisation)
  3. IM PREDNISOONE
67
Q

Problems with Colchicine

A
  1. TOXIC in overdose

2. DIARRHOEA and abdo pain

68
Q

How is Gout prevented

A

1, Stop diuretics (LOSARTAN - promotes uric acid excretion)

  1. ALLOPURINOL
  2. FEBUXOSTAT
69
Q

Role of ALLOPURINOL

A
  1. Inhibits Xanthine Oxidase so less uric acid production and less monosodium rate production
  2. Reduces serum urate levées rapidly
70
Q

Side effect of ALLOPURINOL

A
  1. Rash
  2. Fever
  3. Low WCC
71
Q

When do we give ALLOPURINOL

A

3 weeks AFTER an attack as it can trigger attacks too

72
Q

What is FEBUXOSTAT

A

Non-purine Xanthine Oxidase inhibitor

73
Q

When is FEBUXOSTAT given

A

When ALLOPURINOL is inhibited

74
Q

What is PSEUDOGOUT

A

Deposition of calcium pyrophosphate crystals on joint surface

75
Q

What kind of people are effected by pseudo gout

A
  1. Old age
  2. Diabetes
  3. Osteoarthritis
  4. Joint Trauma/injury
  5. Hyperparathyroidism
  6. Haemochromatosis
76
Q

Pathophysiology of pseudo gout

A
  1. Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue producing radiological appearance of chonedrocalcinosis (linear calcification parallel to the articular surfaces)
77
Q

Clinical Presentation of pseudo gout

A
  1. Shedding of crystals into a joint produces acute synovitis that resembles ACUTE GOUT but effects knee or wrist
  2. Swollen and hot wrist or knee
  3. Presents with hot joint and fever (septic arthritis - if steroids given then DEVASTATING)
78
Q

Diagnosis of pseudo gout

A
  1. Joint fluid aspiration and microscopy
  2. X-ray
  3. FBC
79
Q

What does joint fluid aspiration and microscopy show in pseudo gout

A
  1. Small rhomboidal crystals under microscopy
  2. Positively bifringent crystals under polarised light
  3. Joint fluid looks purulent so should be send for culture to exclude septic arthritis
80
Q

What does X-ray show in pseudo gout

A
  1. CHONEDROCALCINOSIS - linear calcification parallel to articular surfaces
81
Q

What does FBC show in pseudo gout

A
  1. RAISED WCC count
82
Q

Treatment of pseudo gout

A
  1. IBUPROFEN or ASPIRIN
  2. Colchicine if not tolerated
  3. PREDNIOSOLNE

Aspiration of joint reduces pain

83
Q

Name a small-vessel vasculitis

A
  1. Necrotising, granulomatous vasculitis of small vessels
84
Q

Effect of GPA on the body

A
  1. Upper Resp tract: Sinusitis, nasal crusting and bleeding, saddle nose deformity
  2. Lungs: Pulmonary nodules/haemorrhage
  3. Kidney: Glomerulonephritis
  4. Skin: Purpura
  5. CNS: Mononeuritis Multiplex
  6. Eye: Bilateral periorbital oedema and chemises (swelling of conjunctiva)
  7. MSK: Synovitis
  8. CV: Pericarditis
85
Q

How is GPA treated

A
  1. Cyclophosphamide

Non-severe:
METHOTREXATE and AZATHIOPRINE

Year 2 (155 decks)

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