Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2A revision > rheumatology to work on COPY > Flashcards

rheumatology to work on COPY Flashcards

1
Q

What investigations might you do in someone you suspect to have psoriatic arthritis?

A

X-ray

- Erosion in DIPJ + periarticular new-bone formation  - Osteolysis  - Pencil-in-cup deformity

Bloods

  • ESR + CRP - normal or raised
  • Rheumatoid factor -ve
  • anti-CCP - negative

Joint aspiration - no bacteria or crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What investigations might you do in someone you suspect to have reactive arthritis?

A 
ESR + CRP - raised
ANA - negative
RF - negative
X-ray - sacroiliitis or enthesopathy
Joint aspirate - negative (exclude septic arthritis + gout)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give 4 properties of bone that contribute to bone strength

A
  1. Bone mineral density
  2. Bone size
  3. Bone turnover
  4. Bone micro-architecture
  5. Mineralisation
  6. Geometry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give 5 risk factors for osteoporosis

A
  • old age, women, FHx, previous fracture, smoking, alcohol, Asian/Caucasian

‘SHATTERED’

  • Steroid use
  • Hyperthyroidism, hyperparathyroidism, hypercalciuria
  • Alcohol + tobacco use
  • Thin (BMI < 18.5)
  • Testosterone (low)
  • Early menopause
  • Renal or liver failure
  • Erosive/inflammatory bone disease (e.g. myeloma or RA)
  • Dietary low calcium /malabsorption or Diabetes type 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are is the clinical presentation of giant cell arteritis?

A
  1. Headache, typically unilateral over temporal area
  2. Temporal artery/scalp tenderness
  3. Jaw claudication
  4. Visual symptoms - vision loss (painless)
  5. Systemic symptoms - fever, malaise, lethargy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the investigations for giant cell arteritis?

A
  • ↑ESR and/or CRP (=highly sensitive) ESR >50 mm/hr
  • Halo sign on US of temporal and axillary artery
  • Temporal artery biopsy = gold standard for Dx (show giant cells, granulomatous inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the treatment for giant cell arteritis

A
  1. High dose corticosteroids - prednisolone ASAP
  2. DMARDs - methotrexate (sometimes)
  3. Osteoporosis prophylaxis is important - lansoprazole, alendronate, Ca2+, vit D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the pathophysiology of Wegener’s granulomatosis?

A

Necrotising granulomatous vasculitis affecting arterioles and venules
ANCAs can activate primed circulating neutrophils which leads to fibrin deposition in vessel walls and deposition of destructive inflammatory mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What investigations might you do in someone you suspect to have Wegener’s Granulomatosis?

A

ANCA testing - c-ANCA
Tissue biopsy - (renal biopsy best) - shows granulomas
CT - assessment of organ involvement
FBC - high eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the treatment for Wegener’s Granulomatosis?

A
  • Glucocorticoids (prednisolone)
  • Immunosuppresive drugs (cyclophosphamide OR rituximab)
  • plasma exchange for specific complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give 5 risk factors for developing OA

A
  1. Genetic predisposition - females, FHx
  2. Trauma
  3. Abnormal biomechanics (e.g. hypermobility)
  4. Occupation (e..g manual labor)
  5. Obesity = pro-inflammatory state
  6. Old age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the pathophysiology of osteoarthritis

A

Mechanical stress –> progressive destruction and loss of articular cartilage
exposed subchondral bone becomes sclerotic
cytokine mediated TNF/IL/NO involved
deficiency in growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the pathogenesis of SLE

A

Type 3 hypersensitivity reaction = immune complex mediated

Autoantibodies to a variety of auto antigens result in formation and deposition of immune complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A
  1. Blood tests = anaemia, neutropenia, thrombocytopenia, RAISED ESR and NORMAL CRP
  2. Serum autoantibodies - ANA, anti-dsDNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the pharmacological treatment for SLE

A 
● Avoid excessive sunlight and reduce CVS risk factors 
● NSAIDs - ibuprofen
● Chloroquine and hydroxychloroquine 
● Corticosteroids - prednisolone
● cyclophosphamide
● methotrexate
● Topical steroids

first line = hydroxychloroquine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give 5 signs of limited scleroderma

A

CREST
1. Calcinosis - skin calcium deposits
2. Raynauds
3. Esophageal reflux/stricture
4. Sclerodactyly - thick tight skin on fingers/toes
5. Telangiectasia - dilated facial spider veins
Pulmonary arterial hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give 4 signs of diffuse scleroderma

A

Skin changes develop more rapidly and are more widespread than inlimited cutaneous scleroderma/CREST

  1. Proximal scleroderma
  2. Pulmonary fibrosis
  3. Bowel involvement
  4. Myositis
  5. Renal crisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is a diagnostic test for scleroderma?

A

Limited - ACAs

Diffuse - 
Anti-topoisomerase, 
Anti scl-70
ANAs
ESR (normal)

If renal involvement, there may be anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the management of scleroderma

A

avoid smoking, handwarmers

GI - PPIs, Antibiotics
Renal - ACEi
Pulmonary fibrosis - cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give 5 symptoms of sjögren’s syndrome

A
  1. Dry eyes and dry mouth
  2. dry skin and dry vagina
  3. Inflammatory arthritis
  4. Rash
  5. Neuropathies
  6. Vasculitis
  7. fatigue
  8. salivary and parotid gland enlargement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Serum auto-antibodies –> anti-RO, anti-La, RF, ANA

Raised immunoglobulins and ESR

Schirmer’s test
- ability for eyes to self-hydrate - <10mm in 5 minutes

Rose bengal staining and slit lamp exam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the treatment for sjögren’s syndrome?

A
  • Artificial tears, artificial saliva, vaginal lubricants
  • Hydroxychloroquine
  • NSAID
  • M3 agonist - pilocarpine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give 3 symptoms of dermatomyositis

A
  1. Rash
  2. Muscle weakness
  3. Lungs are often affected too (e.g. interstitial lung disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A
  1. Muscle enzymes raised
  2. Electromyography (EMG)
  3. Muscle/skin biopsy
  4. Screen for malignancy
  5. CXR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the treatment for dermatomyositis?

A

Steroids - prednisolone

Immunosuppressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

which organisms can cause septic arthritis?

A
  1. Staphylococcus aureus
  2. Streptococci
  3. Neisseria Gonorrhoea
  4. Gram negative = E. coli, pseudomonas aeruginosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the risk factors for septic arthritis?

A 
Pre-existing joint disease (OA or RA)
Joint prostheses
IVDU
Immunosuppression
Alcohol misuse
Diabetes
Intra-articular corticosteroid injection
Recent joint surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe the treatment for septic arthritis

A 
Aspirate joint 
Empirical Abx - flucloxacillin 
- if allergic to penicilin = clindamycin
- if MRSA = vancomycin
- if gram negative = cefotaxime
Analgesia - NSAIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What organisms can cause osteomyelitis?

A
  1. Staph. aureus
  2. Coagulase negative staph (s. epidermidis)
  3. Aerobic gram negate bacilli (salmonella)
  4. haemophilus influenza
  5. Mycobacterium TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Name 2 predisposing conditions for osteomyelitis

A
  1. Diabetes

2. PVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Give 4 host factors that affect the pathogenesis of osteomyelitis

A
  1. Behavioural (risk of trauma)
  2. Vascular supply (arterial disease, DM)
  3. Pre-existing bone/joint problems (RA)
  4. Immune deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

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

A
  1. Inflammatory cells
  2. Oedema
  3. Vascular congestion
  4. Small vessel thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

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

A
  1. Necrotic bone - ‘squestra’
  2. New bone formation ‘involucrum’
  3. Neutrophil exudates
  4. Lymphocytes and histiocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

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

A
  • Inflammation in BM increase intramedullary pressure exudate into bone cortex which rupture through periosteum
  • this causes interruption of periosteum blood supply which results in necrosis and sequestra
  • therefore new bone forms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is acute osteomyelitis associated with?

A

Associated with inflammatory bone changes caused by pathogenic bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is chronic osteomyelitis associated with?

A

Involves bone necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are the signs of acute osteomyelitis?

A
  1. Tender
  2. Warm
  3. Red swollen area around OM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are the signs of chronic osteomyelitis?

A
  1. Acute OM signs
  2. Draining sinus tract
  3. Non-healing ulcers/fracture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the differential diagnosis of osteomyelitis?

A
  1. Cellulitis
  2. Charcot’s joints (sensation loss –> degeneration)
  3. Gout
  4. Fracture
  5. Malignancy
  6. Avascular bone necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A
  1. Bloods - raised inflammatory markers (CRP, ESR) and WCC
  2. X-rays (cortical erosion, sequestra, sclerosis) and MRI (delineates inflammatory layers, marrow oedema)
  3. Bone biopsy - gold standard
  4. Blood cultures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Describe the usual treatment for osteomyelitis

A

Large dose IV antibiotics tailored to culture findings (S. aureus = flucloxacillin)
immobilisation
Surgical treatment = debridement +/- arthroplasty of joint involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Name 3 risk factors of RA

A
  1. Smoking
  2. Women
  3. family history
  4. Other AI conditions
  5. genetic factors - HLA-DR4 and HLA-DRB1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the pathophysiology of RA

A
  1. Chronic inflammation - B/T cells and neutrophils infiltrate
  2. Proliferation –> pannus formation (synovium grows out and over cartilage)
  3. Pro-inflammatory cytokines –> proteinases –> cartilage destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are the symptoms of RA?

A
  1. Early morning stiffness (>60 mins)
  2. Pain eases with use
  3. Swelling
  4. General fatigue, malaise
  5. Extra-articular involvment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are the signs of RA?

A
  1. Symmetrical polyarthorpathy
  2. Deforming –> ulnar deviation, swan neck deformity, boutonniere deformity
  3. Erosion on X-ray
  4. 80% = RF positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

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

A

Nodules
Bursitis
Muscle wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

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

A

Dry eyes
Scleritis
Episcleritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

RA extra-articular involvement: describe the pulmonary effects

A

Pleural effusion

Fibrosing alveolitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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

A

Pericardial rub

Pericardial effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

RA extra-articular involvement: describe the effects on the skin

A

Vasculitis - infarcts in nail bed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is seen on an X-ray of someone with RA?

A

LESS:

  • Loss of joint space (due to cartilage loss)
  • Erosion
  • Soft tissue swelling
  • Soft bones = osteopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the pathophysiology of gout

A

Purine –> (by xanthine oxidase) xanthine –> uric acid –> monosodium rate crystals OR excreted by kidneys

Urate blood/tissue imbalance –> rate crystal formation –> inflammatory response through phagocytic activation

Overproduction/under excretions of uric acid causes build up and precipitated out in joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Give 3 causes of gout

A

= Hyperuricaemia

  1. Impaired excretion - CKD, diuretics, hypertension
  2. Increased production - hyperlipidaemia
  3. Increased intake - high purine diet = red meat, seafood, fructose, alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Name 3 common precipitants of a gout attack

A
  1. Aggressive introduction of hypouricaemic therapy
  2. Alcohol or shellfish binges
  3. Sepsis, MI, acute severe illness
  4. Trauma
55
Q

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

A
  1. Hypertension
  2. CV disease - e.g. stroke
  3. Renal disease
  4. Type 2 diabetes
56
Q

What investigations might you do in a patient you think has gout?

A

first line = bloods

  • U&E and eGFR - renal failure
  • Uric acid levels - 4-6 weeks after to confirm hyperuricaemia
  • gold standard = joint aspiration
57
Q

what is the management for chronic gout?

A

1st line = allopurinol - inhibits xanthine oxidase

2nd line = febuxostat

consider co-prescribing colchicine with allopurinol for 6 months

58
Q

Name 6 factors that can cause an acute attack of gout

A
  1. Sudden overload
  2. Cold
  3. Trauma
  4. Sepsis
  5. Dehydration
  6. Drugs
59
Q

What can cause pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Haemochromatosis
  3. Diabetes
  4. Magnesium levels
60
Q

What investigations might you do in someone you suspect might have pseudogout?

A

Aspiration –> fluid for crystals and blood cultures = positive birefringent rhomboid crystals

X-rays –> can show chondrocalcinosis

61
Q

What is the most likely differential diagnosis for pseudogout?

A

Infection

62
Q

How can you distinguish OA from pseudogout?

A

Pattern of involvement –> Pseudo = wrists, shoulders, ankle, elbows
Marked inflammatory component –> Elevated CRP and ESR Superimposition of acute attacks

63
Q

Name 4 diseases that fibromyalgia is commonly associated with

A
  1. Depression
  2. Choric fatigue
  3. IBS
  4. Chronic headache
64
Q

Give 4 symptoms of fibromyalgia

A
  1. Neck and back pain
  2. Pain is aggravated by stress, cold and activity
  3. Generalised morning stiffness
  4. Paraesthesia of hands and feet
  5. Profound fatigue
  6. Unrefreshing sleep
  7. poor concentration, brain fog
65
Q

Give 3 disease that might be included in the differential diagnosis for fibromyalgia

A
  1. Hypothyroidism
  2. SLE
  3. Low vitamin D
66
Q

Define sarcoma

A

A rare tumour of mesenchymal origin

A malignant connective tissue neoplasm

67
Q

where do secondary bone tumours come from?

A

Metastases from:

  1. Lungs
  2. Breast
  3. Prostate
  4. Thyroid
  5. Kidney
68
Q

How are malignant bone cancers staged using Enneking grading?

A 
G1 = Histologically benign
G2 = Low grade
G3 = High grade
A = intracompartmental
B = extracompartmental
69
Q

How are benign bone cancers staged using Enneking grading?

A 
G1 = Latent
G2 = Active 
G3 = Aggressive
70
Q

Where do osteosarcomas usually present?

A

Knee - distal femur, proximal humerus

71
Q

Where does Ewings sarcoma arise from?

A

mesenchymal stem cells

72
Q

Give 3 side effects of NSAIDs

A
  1. Peptic ulcer disease
  2. Renal failure
  3. Increased risk of MI and CV disease
73
Q

Give 5 potential side effects of steroids

A
  1. Diabetes
  2. Muscle wasting
  3. Osteoporosis
  4. Fat redistribution
  5. Skin atrophy
  6. Hypertension
  7. Acne
  8. Infection risk
74
Q

How do DMARDs work?

A

Non-specific inhibition of inflammatory cytokines cascade = reduces joint pain, stiffness and swelling

75
Q

Give 3 potential side effects of methotrexate

A
  1. Bone marrow suppression
  2. Abnormal liver enzymes
  3. Nausea
  4. Diarrhoea
  5. Teratogenic
76
Q

Describe the mechanism of action of infliximab

A

Inhibits T cell activation

77
Q

How does alendronate work?

A

Reduces bone turnover by inhibiting osteoclast mediated bone resorption

78
Q

what are the complications of rheumatoid arthritis?

A

Cervical spinal cord compression- weakness and loss of sensation
Lung involvement- interstitial lung disease, fibrosis.

79
Q

what is the difference between the presentation of early and late septic arthritis

A

● Early infection presents with inflammation, discharge, joint effusion, loss of function and pain
● Late disease presents with pain or mechanical dysfunction

80
Q

what are the risk factors for gout?

A

Middle age overweight males.
high purine diet,
increased cell turnover

81
Q

what are the complications of gout?

A

Infection in the tophi

Destruction of the joint

82
Q

what are the risk factors for osteomyelitis?

A 
Previous osteomyelitis
Penetrating injury
IVDU
Diabetes
HIV
Recent surgery
Distant or local infection
Sickle cell disease
RACKD
Children → upper resp tract  or varicella infection
83
Q

what are the different types of psoriatic arthritis?

A

● Distal interphalangeal arthritis – most typical pattern of joint involvement – dactylitis is characteristic
● Mono- or oligoarthiritis
● Symmetrical seronegative polyarthritis – resembling RA
● Arthritis mutilans – a severe form with destruction of the small bones in the hands and feet
● Sacroiliitis – uni- or bilateral

84
Q

what treatment should be used if reactive arthritis relapses?

A

methotrexate or sulfasalazine

85
Q

what is the pathophysiology of reactive arthritis?

A

● Bacterial antigens or DNA have been found in the inflamed synovium of affected joints – suggests persistent antigenic material is driving the inflammatory response

86
Q

what are the complications of Sjogren’s syndrome?

A
  • eye infections- oral problems (dental cavities, candida infections)
  • vaginal problems (candidiasis, sexual dysfunction)

RARE

  • pneumonia and bronchiectasis
  • non-hodgkin’s
  • vasculitis
  • renal impairment
  • peripheral neuropathy
87
Q

what is antiphospholipid syndrome?

A
  • Syndrome characterised by thrombosis (arterial or venous) and/or recurrentmiscarriages with positive blood tests for antiphospholipid antibodies (aPL) - hypercoagulable state
88
Q

what are the risk factors for antiphospholipid syndrome?

A
  • diabetes
  • hypertension
  • obesity
  • female
  • underlying autoimmune condition
  • smoking
  • oestrogen therapy
89
Q

what is the clinical presentation of antiphospholipid syndrome?

A
  • thrombosis
  • miscarriage
  • livedo reticularis - purple lace rash
  • ischaemic stroke, TIA, MI
  • DVT, budd-chiari syndrome
  • thrombocytopenia
  • valvular heart disease, migraines, epilepsy
90
Q

what is the pathophysiology of antiphospholipid syndrome?

A
  • Antiphospholipid antibodies (aPL) play a role in thrombosis by binding tophospholipid on the surface of cells such as endothelial cells, platelets andmonocytes
  • Once bound, this change alters the functioning of those cells leading tothrombosis and/or miscarriage
  • Antiphospholipid antibodies (aPL) cause CLOTs:
    • Coagulation defect
    • Livedo reticularis - lace-like purplish discolouration of skin
    • Obstetric issues i.e. miscarriage
    • Thrombocytopenia (low platelets)
91
Q

what are the investigations for antiphospholipid syndrome?

A

Hx of thrombosis/ pregnancy complications + Antibody screen with raised:

  - anticardiolipin antibodies
 - lupus anticoagulant
 - anti-beta-2 glycoprotein I antibodies
92
Q

what is the treatment for antiphospholipid syndrome?

A
  • long term warfarin
  • Pregnant women on low molecular weight heparin (e.g. enoxaparin) + aspirin
  • lifestyle - smoking cessation, exercise, healthy diet
93
Q

what is the clinical presentation of wegener’s granulomatosis?

A

Classic sign on exams: saddle shaped nose

Epistaxis - nosebleed

Crusty nasal/ ear secretions 🡪 hearing loss

Sinusitis

Cough, wheeze, haemoptysis

94
Q

what condition is osteosarcoma associated with?

A

Paget’s disease

95
Q

what is the clinical presentation of ewing’s sarcoma?

A

● Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk

● Painful swelling, redness in surrounding area, malaise, anorexia, weight loss, fever, paralysis and/or incontinence if affecting the spine, numbness in affected limb

96
Q

where is Ewing’s sarcoma commonly found?

A

Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk

97
Q

where does chrondosarcoma commonly present?

A

Common sites are pelvis, femur, humerus, scapula and ribs

98
Q

what is the clinical presentation of chrondrosarcoma?

A

Associated with dull, deep pain and affected area is swollen and tender

99
Q

what are the risk factors for scleroderma?

A
  • exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
  • bleomycin
  • genetic
100
Q

what is the clinical presentation of dermatomyositis?

A
  • heliotrope (purple) discolouration of eyelids
  • scaly erythematous plaques over knuckles (Gotton’s papules)
  • arthralgia, dysphagia and raynauds
101
Q

what are the investigations for polymyositis/dermatomyositis?

A

Muscle Biopsy

Bloods
- serum creatine kinase, aminotransferases, lactate dehydrogenase (LDH) and aldolase all raised

Immunology
ANA, Anti jo1, anti mi2

102
Q

what is the treatment for polymyositis/dermatomyositis?

A
  • bed rest + exercise plan
  • oral prednisolone
  • steroid sparing immunosuppressive - azathioprine, methotrexate, ciclosporin
  • hydroxychloroquine for skin disease
103
Q

what factors are used in the FRAX score calculation?

A
  • age
  • sex
  • height and weight
  • previous fractures
  • smoking
  • parent fractured hip (FHx)
  • steroid (glucocorticoid use)
  • RA
  • secondary osteoporosis
  • alcohol consumption (>3 units)
  • femoral neck bone mineral density
104
Q

what is the diagnostic criteria for RA?

A

RF RISES - >6 weeks and >4 of following:

  • RF positive
  • Finger/hand/wrist involvement
  • Rheumatoid nodules present
  • Involvement of >3 joints
  • Stiffness in morning >1 hr
  • Erosions on x-ray
  • Symmetrical involvement
105
Q

what is limited scleroderma?

A
  • skin involvement limited to hands, face, feet and forearms
  • characteristic ‘beak’-like nose and small mouth
  • Microstomia - small mouth
106
Q

what is paget’s disease?

A

localized disorder of bone remodelling
↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)

107
Q

what is the pathophysiology of paget’s disease?

A

↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)

108
Q

what are the clinical features of paget’s disease?

A

60-80% are asymptomatic

  • bone pain
  • joint pain
  • deformities -> bowed tibia and skull enlargement
  • neurological complications
  • CN8 compression -> deafness
  • blockage of aqueduct of sylvius causing hydrocephalus
109
Q

what are the investigations for paget’s disease?

A

Bloods - Increased ALP, normal calcium and phosphate

Urinary hydroxyproline increase

X-rays - Findings of osteoarthritis, sclerotic changes, bone loss and reduced density

isotope bone scan

110
Q

what is the management for paget’s disease?

A

Bisphosphonates,

NSAIDS

111
Q

what is osteomalacia?

A

Defective mineralization of newly formed bone matrix or osteoid in adults, due to inadequate phosphate or calcium, or due to ↑ bone resorption (hyperPTH)

112
Q

what are the causes of osteomalacia?

A

malnutrition (most common)
drug induced
defective 1-alpha hydroxylation
Liver disease

113
Q

what is the clincial presentation of osteomalacia?

A 
Osteomalacia
widespread bone pain and tenderness
gradual onset and persistent fatigue
muscle weakness, parasthesia, waddling gait
fractures
114
Q

what is the clincial presentation of rickets?

A

leg-bowing and knock knees
- tender swollen joints
- growth retardation
- bone and joint pain
dental deformities – delayed formation of teeth, enamel hypoplasia
- enlargement of end of ribs (‘rachitic rosary’)

115
Q

what are the investigations for Osteomalacia / rickets?

A

Bloods - U&Es, Serum ALP, Vit D

X-rays - defective mineralisation, rachitic rosary

116
Q

what is the management for osteomalacia/rickets?

A

Lifestyle - nutrition, sunlight
Medications - Vit D replacement
Malabsorption/Renal disease - IM calcitriol

117
Q

what is the sepsis 6?

A
  1. administer O2
  2. take blood cultures
  3. give IV antibiotics
  4. give IV fluids
  5. check serial lactates
  6. measure urine output
118
Q

what are the common sites for bone changes in paget’s disease?

A

pelvis
vertebrae - thoracic + lumbar
femur
skull tibia

119
Q

what are the complications of Paget’s?

A

nerve compression - deafness and paraparesis
hydrocephalus
oestosarcoma
high output cardiac failure and myocardial hypertrophy

120
Q

what enzyme expressed by osteoclasts is responsible for bone resorption?

A

cathepsin K

121
Q

what is the effect of unopposed RANK ligand?

A

leads to increased bone loss

more osteoclasts stimulated due to less OPG

122
Q

what is the function of OPG?

A

inhibits osteoclast formation, function and survival by binding to RANK ligand
prevents RANK ligand from binding to osteoclast

123
Q

what protein inhibits RANK ligand?

A

OPG

124
Q

what is the function of RANK ligand?

A

binds to osteoclasts and is essental for formation, functio nand survivl

125
Q

what cells secrete RANK ligand?

A

osteoblasts

126
Q

what is the classification system for fractures involving the physis

A

salter-harris fracture classification

127
Q

what is the physiological pathway to monosodium urate formation

A

purine -> hypoxanthine -> xanthine -> uric acid -> monosodium urate

128
Q

name a drug that can increase monosodium urate?

A

bendroflumethiazide

impair urate excretion

129
Q

give 3 factors that increase pain

A

substance P
glutamate
serotonin

130
Q

give 3 factors that decrease pain volume

A

opioids
GABA
cannabanoids

131
Q

what is a complication of RA?

A

felty’s syndrome - anaemia and splenomegaly and neutropenia

132
Q

what are the extra-articular manifestations of RA?

A 
skin = nodules, vasculitis
sjogrens
glomerulonephritis
peripheral neruopathy
MI, pericarditis
pulmonary = pleuritis, effusions
133
Q

what type of crystals are seen in gout?

A

needle-shaped, negatively birefringent monosodium urate crystals

Phase 2A revision (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions