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Gen Med > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What are the cardinal features of Scleroderma

A

excessive collagen production
vascular damage
immune system activation by autoantibody production

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2
Q

What is localised scleroderma?

A

Causes one of more hard patches of skin - thickened, discoloured, hair loss over patch

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3
Q

What is the pathophysiology behind localised scleroderma

A

Fibroblasts make too much collagen
Plaque morphea - oval patches
Linear - in some severe cases just beneath the skin, it can cause scarring

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4
Q

Which creams are used in localised scleroderma

A

Cream containing calcipotriol
Tacromilus ointment
Steroid treatments/ointments

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5
Q

Which autoantibodys are associated with limited systemic scleroderma

A

Anti-centromere

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6
Q

Where does limited scleroderma affect predominantly

A

Affects the face and distal limbs predominantly

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7
Q

What is CREST

A

Calcinosis - calcium deposits usually on fingers
Raynauds Phenomenon - treated by Nifedipine (calcium channel blocker)
oEsophageal dysmotility - collagen deposition and loss of smooth muscle function
Sclerodactyly - thickening of the skin
Telangiectasisa - red spots

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8
Q

Which type of scleroderma has the poorer prognosis

A

Diffuse

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9
Q

Which antibodies are assciated with diffuse scleroderma

A

Scl-70 antibodies

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10
Q

Which other body systems are involved in diffuse scleroderma

A

Heart –> myocardial fibrotic change - secondary to Pulmonary artery hypertension
Blood vessels - Hypertension
Lungs - lung fibrosis –> pulmonary artery hypertension causing
Exertional Dyspneoa
syncope
RV strain
Renal –> due to vascular complications e.g. hypertension, can go into renal crisis with apparently normal BP
MSK - flexion contractures, arthralgia, myalgia and stiffness

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11
Q

Which parts of the skin are involved in diffuse scleroderma

A

Skin of the trunk
upper arms
thighs
Skin changes within 1 year of Reynauds

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12
Q

What is a renal crisis in scleroderma patients

A 
Characterised by acclerated BP with symptoms 
- oliguria 
- headache 
- fatigue 
- oedema 
Investigations show 
- riase in creatinine 
- proteinuria 
- microscopic haematuria
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13
Q

Why is regular BP monitoring important in diffuse scleroderma

A

Important to monitor it so its known what normal is for the patient as a scleroderma renal crisis can occur in a apparently normal BP but is higher than baseline

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14
Q

How is a scleroderma renal crisis treated

A

ACE inhibitors

Dialysis if needed

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15
Q

Which investigations would be done in suspected Scleroderma

A 
Bedside: BP, Urine dip - if presenting with renal crisis 
Bloods 
FBC 
U+Es
LFTs
ESR and CRP 
Autoantibodies - anti-centromere (limited)
Scl-70 (diffuse) 
Barium swallow 
Endoscopy - if presenting with dysphagia 
CXR
Lung function tests
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16
Q

Which investigations are done to monitor scleroderma

A 
Regular BP monitoring 
Renal function 
BNP
Lung function 
CT chest 
ECG
Endocscopy - dilatation of strictures
Cardiac MRI 
Oesophageal manometry +24hr pH studies
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17
Q

What is psoriatic arthropathy

A

A condition that affects both the skin and joints
Referred as one of the seronegative spondyloarthropathy - inflammatory arthritis that is negative for RF
Often precedes the development of skin lesions

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18
Q

What are the clinical features of psoriatic arthritis

A

Oligoarthritis - 2-5 joints affected, usually asymmetrical and weight bearing
Sometimes spinal involvement - typically at the sacrum
Osteolysis - as bone in fingers are lost - telescoping on X ray –> pencil in cup
Plaques on exstensor surfaces - check scalp, natal cleft and umbilicus
Nail changes
- discoloured
- ridging
- onycholysis
- psoriatic nail dystrophy –> pitting, leukonychia

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19
Q

How is psoriatic arthropathy treated

A

DMARDs - methotrexate and leflunomide
- same as RA
NOT hydroxychloroquine as this exacerbates skin conditions
Anti-TNF alpha

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20
Q

What is rheumatoid arthritis

A

Systemic inflammatory disorder - affects multiple joints usually 5 or more symmetrically
Autoimmune
causes progressive symmetrical joint destruction esp in hands

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21
Q

Where else in the body can be affected in rheumatoid arthritis

A

Brain - interleukin 1 and 6 –> fever
Skeletal muscle - protein breakdown
Liver - hepicidin produced due to inflammatory cytokines causing a decrease in iron absorption
Blood vessels - atheroma - strokes, MI and ischaemia
Skin - rheumatoid nodules, necrosis centre surrounded by macrophages (found at pressure points)
Lungs - interstitium –> fibroblasts proliferate causing fibrosis and decrease in gas exchange
PLeural cavity - becomes inflamed and causes pleural effusion (exudative) - SOB

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22
Q

How does RA typically present

A

Swollen, tender painful joints in hands and feet
Stiffness worse in morning which lasts longer than 30 mins
Systemic symptoms: tiredness, depression
typical patient in a young woman

23
Q

What is the pathophysiology of RA

A

Immune cells - activated T cells and plasma cells with antigens reach the joint space
T cells secrete cytokines and recruit macrophages which produce more cytokines and causs granular cells to proliferate
causes thick swollen synovial membrane - which damage cartilage and erodes bone
Joints are red due to increased blood flow
Swollen due to increased blood flow and inflammatory process
painful due to the nerve endings in the joint being irritated by the cytokines

24
Q

Which specific deformities are associated with RA

A

Ulnar deviation
Boutonnieres deformity - extensor tendon splits (PIP flexion and DIP hyperextension)
Swan neck deformity - PIP hyperextended and DIP flexion
Bakers cysts - synovial sac bulges into popliteal fossa

25
Q

Which Score is used in to determine the severity of RA

A

DAS-28

26
Q

What is Felty syndrome

A

Rheumatoid arthritis
Splenomegaly
Agranulocytosis
increased risk of infections - life threatening

27
Q

How is rheumatoid arthritis investigated

A 
Bedside: BP
Bloods 
- FBC 
- U+Es
- LFTs
- CRP
- Rheumatoid factor 
- Anti CCP
- May test for other Rheumatological conditions such as SLE e.g anti dsDNA

Imaging
Xray - different to OA

28
Q

What are the features of RA on XRay

A 
Narrowing of joint space 
Bony erosions - periarticular erosions
Soft tissue swelling 
Decreased bone density 
subluxation
29
Q

How is newly diagnosed RA treated

A

2 DMARDs - MTX and other

Short course of prednisolone

30
Q

Which drugs are used to treat RA

A

DMARDS

  • Methotrexate –> pulmonary toxicity, weekly dose
  • Hydroxychloroquine - can result in severe and permanent retinopathy, also exacerbates skin conditions
  • Sulfasalazine - can be used during pregnancy, give folate

Biologics
e.g. Infliximab TNF inhibitor

31
Q

Which drugs are used in acute flares of RA

A

NSAIDs

Glucocorticoids - short term use

32
Q

When are Biologics used

A

if there is an inadequate response to at least 2 DMARDs including Methotrexate

33
Q

How else is RA managed other than DMARDs

A

Physiotherapy
Analgesia
Surgery

34
Q

What are some of the ocular manifestations of RA

A

Keratoconjunctivitis sicca - dryness of the conjunctiva and cornea
Episcleritis
Scleritis - erythema and pain
Corneal ulceration
Keratitis
Iatrogenic: Steroid induced Cataracts and chloroquine retinopathy

35
Q

What are the risk factors for RA

A

Smoking

Family history

36
Q

What are the differentials for RA

A

Psoriatic Arthropathy
Reactive arthritis - would only affect one or two joints, post infection, uvetitis and urethritis
SLE - other systemic symptoms
Polymyalgia rheumatica - stiffness in proximal muscles rather than joints, rapid onset
Gout - usually seen in first metatarsal
Osteoarthritis - usually weight bearing joints and stiffness wears off <30mins and worse at end of day

37
Q

What are the side effects of Methotrexate

A 
Anti-folate 
Myelosuppression 
Liver cirrhosis 
Pneumonitis 
Lung fibrosis
38
Q

What are the side effects of Sulfalazine

A

Rashes
Oligospermia
Heinz body anaemia
Interstitial lung disease

39
Q

What are the side effects of leflunomide

A

Liver impairment
Interstitial lung disease
Hypertension

40
Q

What are the side effects of Hydroxychloroquine

A

Retinopathy
Corneal deposits
Skin condition exacerbation

41
Q

What is SLE

A

An inflammatory autoimmune disease in which any tissue can be targeted by autoantibodies
It has a relapsing and remitting course

42
Q

What are the clinical features of SLE

A

MD SOAP N HAIR
Malar rash
Discoid rash
Serositis - pleuritis and pericarditis
Oral ulcer
Arthritis
Photosensitivity
Neurological abnormality –> psychosis and seizures
Haematological abnormalities –> Anaemia, thrombocytopenia and leukopenia
ANA positive, Anti ds DNA positive, anti smith - last two are more specific
Immunological abnormality
Renal involvement - abnormal urine protein,, diffuse proliferation, glomerulonephritis

43
Q

Describe the malar rash seen in patients with SLE

A

It is across the cheeks but spares the naso-labial folds and appears after sun exposure

44
Q

What is the pathophysiology behind SLE

A

Damage done to cells so parts of the nucleus (histones, DNA, proteins) go into circulation
B cells then create antibodies against nuclear antigens
Antinuclear antibodies formed
genetic factors then cause patients body to recognise the ANA as foreign and when they deposit there is an inflammatory reaction
Complement system activated
Type 3 hypersensitivity reaction occurs

45
Q

Which drugs can cause drug induced SLE

A

Hydralazine
Isoniazid
Procainimide

Anti-histone antibodies seen

46
Q

How is SLE managed

A 
Lifestyle:
avoid UV exposure 
Patient education
minimise cardiovascular risk factors 
Pharmacological
- Hydroxychloroquine - reduces flares and improves fatigue 
- Paracetamol/NSAIDs for analgesia 
- Steroids - in the short term to treat flares
- Methotrexate for chronic arthritis 
- Aziothioprine - moderate disease
CNS or renal involvement requires aggressive treatment 
- high dose steroids 
- azathioprine or mycophenalate 
- cyclophosphomide 
- ciclosporin 
(may require multiple agents)

Biologics
- used for refractory disease

47
Q

What are the complications of SLE

A

Cardiovascular disease
Infection
Antiphospholipid Syndrome
Osteoporosis

48
Q

How does polymyalgia rheumatica present

A

Proximal muscle aching and stiffness in the morning
bilateral shoulder pain with bilateral arm weakness - may be difficult to raise arms to brush hair
May have pain in neck or pelvis girdle also
Rapid onset
Typically > 60 years old
mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
flu like symptoms

49
Q

What is the pathophysiology of polymyalgia rheumatica

A

Histology shows vasculitis with giant cells, characteristically skips certain sections of affected artery whilst damaging others
Muscle bed arteries mostly affected

50
Q

Which investigations are done in polymyalgia rheumatica

A

Bloods

  • FBC - reduced CD8+ T cells
  • U+Es
  • LFTs
  • ESR >40mm/hr
  • CK - normal

Imaging
rule out OA

51
Q

What are the differentials for Polymyalgia rheumatica

A 
Inflammatory disorders:
Rheumatoid arthritis 
Ankylosing Spondylitis 
Psoriatic arthritis 
SLE 
Scleroderma 
Vaculitis 
Dermatomyositis 
polymyositis 
Non-inflammatory disorders:
OA
Drug induced myalgia e.g. statins
Rotator cuff disease 
Infections 
Malignancy
52
Q

What is the treatment in CREST syndrome

A

supportive
endothelin receptor antagonists
phosphodiesterase 5 inhibitors
ACE inhibitors in renal crisis

53
Q

Which antibodies is CREST syndrome associated with

A

Anticentromere antibodies

54
Q

What is the colour change in Reynauds syndrome

A

White to blue to red

Gen Med (10 decks)

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