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Phase 2 Mine > Revision List Rheum > Flashcards

Revision List Rheum Flashcards

1
Q

What is a crystal?

A

Homogenous solid, stable high density, hard

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2
Q

When are crystals pathological?

A
  1. Deposition causes inflammatory response and tissue damage

2. Deposition at abnormal sites

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3
Q

Give 3 examples of pathological crystals?

A
  1. Joints: Crystal arthropathies, urate, calcium pyrophosphate, hydoxypatite
  2. Kidney: stones - calcium oxalate (nephrolithiases)
  3. Gallbladder: cholesterol
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4
Q

What is crystal arthropathy?

A

Arthritis caused by deposition of crystals in joint lining

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5
Q

What is gout?

A

Monosodium urate crystal deposition in the joints causing inflammation

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6
Q

Epidemiology of gout?

A

M

>40

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7
Q

Risk factors of gout?

A
  1. Purine rich foods e.g. red meat
  2. High saturated fat diet
  3. High alcohol intake
  4. High fructose intake
  5. Drugs - low dose aspirin
  6. IHD
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8
Q

Renal causes of gout?

A

URAT1 transporter defect
Diuretics
High insulin levels

All impair uric acid excretion

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9
Q

What can cause increased production of urate?

A
  1. Metabolic syndromes: hyperlipidaemia
  2. Proliferative: myelo/lymphoproliferative disorders, cytotoxic drugs
  3. Psoriasis
  4. Diet: alcohol, XS meat, shellfish, meat extract, yeast extract, fructose sweetened drinks
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10
Q

What is the pathophysiology of gout?

A

Xanthine oxidase controls hypoxanthine –> xanthine –> uric acid and excreted by kidney - not very efficient –> hyperuricaemia

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11
Q

Normal serum uric acid levels?

A

0.3micromol/l

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12
Q

Hyperuricaemia plasma levels?

A

> 0.36umol/l

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13
Q

Causes of underexcretion of urate?

A
  1. Alcohol
  2. Renal impairment
  3. Hypertension
  4. Hyperthyroid/PTH
  5. Obesity, diabetes
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14
Q

Clinical presentation of acute gout?

A

Hot swollen red joint
Painful
Crescendo over 6-12 joint
Usually 1st MTP

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15
Q

Clinical presentation of chronic polyarticular gout?

A

Rare only in elderly on diuretics+renal failure

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16
Q

Clinical presentation of chronic trophaceous gout?

A

Persistently high levels of uric acid crystals –> large crystal depositis –> irregular nodules on fingers, forearms, achilles tendon
Asymmetrical tophi - chalky appearance under skin

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17
Q

What are tophi?

A

0nion like aggregates of MSU with inflammatory cells

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18
Q

How do tophi cause damage?

A

Cause deformity, crepitus, and decreased movement

May secrete proteolytic enzymes causing punched out lesions

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19
Q

Precipitators of acute gout attack

A
  1. Sudden cessation/aggressive introduction to hypouricaemic therapy
  2. Alcohol, shellfish binges
  3. Sepsis/MI/Acute severe illness
  4. Trauma, surgery, dehydration
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20
Q

Diagnosing gout?

A
  1. Clinical exam
  2. Joint aspiration fluid - microscopy and polarised light, gram stain exclude septic arthritis as cannot co-exist
  3. Serum UA raised
  4. Imaging - x-rays chronic gout - areas of sclerosis, punched out lesions, areas of sclerosis
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21
Q

Non pharmacological management of gout?

A

Weight loss, decrease alcohol, avoid shellfish, avoid purine rich food

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22
Q

Treatment of Acute Gout?

A
  1. NSAIDs - naproxen, ibuprofen
  2. Colchicine Se: diarrhoea, abdominal pain
  3. IM/oral/intra-articular corticosteroid e.g. prednisolone
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23
Q

Prevention of Gout?

A
  1. Stop diuretics e.g. thiazides, switch to ARB
  2. Allopurinol act on Xanthine oxidase - start 3 weeks after acture episode SE: rash, fever, decreased WCC
  3. Febuxostat: non purine xanthine oxidase inhibitor
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24
Q

What crystals in pseudogout?

A

Calcium pyrophosphate

25
Q

Risk factors for pseudogout?

A
  1. Diabetes
  2. HyperPTH
  3. Haemochromatosis
  4. Hypothyroidism
  5. Old age
26
Q

Clinical presentation of pseudogout?

A
  1. Knee>Wrist
  2. Typical inflammed joint
  3. Fever
  4. Marked synovitis
27
Q

Triggers of acute pseudogout attack?

A
  1. Direct trauma to joint
  2. Most are spontaneous
  3. Blood transfusion/IV fluid
28
Q

Diagnose pseudogout?

A
  1. Joint fluid aspiration and microscopy - positively birefringent rhomboids on polarised light, joint fluid is pus like, culture to exclude septic arthritis
  2. X ray - chondrocalcinosis
29
Q

Management of acute pseudogout?

A
  1. NSAIDs
  2. Analgesia
  3. Aspiration, injection
  4. Physiotherapy
30
Q

Management of long term pseudogout?

A

Continued inflammatory changes e.g. methotrexate, hydroxychloroquine
Synovectomy
Surgery

31
Q

Systemic Lupus Erythematous

A

Inflammatory, multisystem autoimmune disorder with athralgia and rashes

32
Q

Epidemiology of SLE?

A

More common in women

Afrocarribeans

33
Q

Risk factors for SLE?

A
  1. Genetic predisposition
  2. Fhx
  3. Drugs - hydralazine, isoniazid,
  4. UV light
  5. EBV
34
Q

Pathophysiology of SLE?

A
  1. Failure of immune system to inactivate T and B cells that recognise self antigens and availability of self antigens.
  2. Development of autoantibodies that are either circulating complexes or deposited by directly binding tissue.
  3. Complement activation and neutrophil influx leads to inflammation of tissues and abnormal cytokine production –> increase IL10, and interferon alpha
35
Q

Clinical presentation of SLE?

A 
Arthritis - non erosive - peripheral joints 
Renal failure
ANA+ve
Serositis - pleuritis/pericarditis
Haematological - Leukopoenia, thombocytopoenia etc
Photosensitivity
Oral ulcers
Immunological - Anti- dsDNA,Anti-sm, Anti-Rho, 
Neurological - seizures and psychosis
ts
Malar rash
Discoid rash
36
Q

SLE differential diagnosis?

A 
Acute pericarditis
Antiphospholipid syndrome
Fibromyalgia
Lymphoma
Scleroderma
Sjorgren Syndrome
37
Q

SLE investigations?

A
  1. Raised ESR, normal CRP
  2. FBC - normochromic normocytic anaemia
  3. Urinalysis - proteinuria/haematuria
  4. Autoantibody test:
    - ANA+ve highly sensitive
    - anti-dsDNA - highly specific
  5. Histologically:
    - SLE of skin and kidneys: deposition of compliment and IgG antibodies and influx of neutrophils and leukocytes
    - Vasculitis - affects arterioles, capillaries, venules
    - Haemotoxylin bodies are seen in inflammatory infiltrates = result of ANA and inflammatory body
38
Q

How to manage SLE?

A
  1. Education and support
  2. Reduce UV exposure
  3. Assess lupus activity - clinical/immunological
  4. Screen for major organ development
  5. Identify patients with phospholipid Ab
  6. Assess and mange atherosclerosis and CVD risk - identify patients at risk of blood clots
  7. Planned pregnancy
39
Q

How to treat SLE?

A
  1. No treatment
  2. Topical:
    - sunscreen, steroids, toxic for rashes
  3. NSAIDs
  4. Antimalarial drugs - chloroquine
  5. Steroids - high dose prednisolone
  6. Cytotoxics: azathioprine, methotrexate, cyclophosphamide
  7. Anticoagulants
  8. Biological - target inflammatory cytokine, usually mAb, e.g. Rituximab
  9. Stem cell transplant
40
Q

What is giant cell arteritis?

A

Commonest large vessel vasculitis

- inflammatory granulomatosis arteritis of cerebral arteries and other large vessels.

41
Q

Epidemiology of GCA?

A
  1. F>M

2. >50

42
Q

Pathophysiology of GCA?

A
  1. Activation of dendritic cells in the adventitia
  2. Recruitment and activation of T cells
  3. Recruitment of CD8+cells and monocytes
  4. Vascular damage and remodelling
43
Q

Clinical presentation of GCA?

A
  1. Headache
  2. Scalp tenderness
  3. Jaw claudication
  4. Acute vision loss
44
Q

Medical emergencies associated with GCA?

A

Stroke

Blindness

45
Q

Signs of GCA?

A

Scalp tenderness leads to scalp ischaemia
Superficial temporal artery tenderness
Decreased or absent pulsation of artery

46
Q

GCA differential diagnosis?

A
  1. Migraine
  2. Tension headache
  3. Trigeminal neuralgia
  4. Polyarteritis nodosa
  5. Herpes zoster
47
Q

GCA diagnostic criteria?

A
  1. > 50 with:
    a. New onset localised headache
    b. temporal artery abnormality - tenderness, thickening
    c. Occasional overlying red skin and decreased pulsation
48
Q

Investigations for GCA?

A
  1. ESR/CRP raised
  2. Normochromic normocytic anaemia
  3. US/PET
  4. Temporal artery biopsy = diagnostic
49
Q

How to treat GCA?

A
  1. High dose glucocorticoids
  2. Uncomplicated: 40mg prednisolone
  3. Complicated: 60mg prednisolone/ IV methylprednisolone
  4. GI protective drugs - PPI
  5. If fail to wean off glucorticoids -
    - DMARDs: methotrexate
    - Tocilizumab
50
Q

Ankylosing Spondylitis what is it?

A

Chronic inflammatory disorder of spine, ribs, and sacroiliac joints

51
Q

Epidemiology of ankylosing spondylitis?

A

M>F

<30 years

52
Q

Risk factors of AS?

A
  1. HLA B27

2. Environment: shigella, salmonella, klebsiella

53
Q

Pathophysiology of AS?

A

Lymphocyte and plasma infiltration occurs with local erosion of bone at attachments of ligament
- heal with new bone formation.
= SYNDESMOPHYTE

54
Q

What is syndesmophyte?

A

New bone formation and vertical growth from anterior vertebral corners

55
Q

Diagnostic criteria of clinical presentation of ankylosing spondylitis?

A
  1. Morning stiffness > 30 minutes
  2. Improve with exercise /not with rest
  3. Waking in second half of night because of pain
  4. Insidious onset
  5. Duration of back pain >3months
  6. <45 years
56
Q

Two characteristic spinal abnormalities with AS?

A
  1. Loss of lumbar lordosis (inward curve of spine) and increased kyphosis - top of spine becomes more rounded
  2. Limitation of lumbar spine mobility in both the sagittal and frontal planes –> decrease spinal flexion
57
Q

How to diagnose AS?

A
  1. ESR/CRP raised
  2. Normochromic normocytic anaemia
  3. HLA B27 +ve
  4. X ray - can be normal but erosion, sacrolitis, fusion of sacroiliac joint
  5. MRI - with gadolinum - show sacrolitis before on X ray
58
Q

How to treat AS?

A

QUICK -to prevent irreversible syndesmophytes formation and progressive calcification

  • morning exercise to maintain posture and spinal mobility
  • NSAIDs at night
  • Methotrexate aids peripheral arthritis but not spinal disease
  • TNF alpha blocker - improve spinal and peripheral joint inflammation - infliximab
  • Local steroid injection - temporary relief
  • Surgery - hip replacement to improve pain and function

Phase 2 Mine (12 decks)

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