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Phase 2a > MSK + rheumatology > Flashcards

MSK + rheumatology Flashcards

1
Q

What conditions fall into inflammatory arthritis?

A

Rheumatoid arthritis
Seronegative spondyloarthritis
Crystal arthritis (gout and pseudogout)

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2
Q

Difference between rheumatoid and seronegative arthritis

A

Rheumatoid: starts in small joints, bigger joints not affected until later in course of disease. Seronegative involves big joints from beginning
Rheumatoid: symmetrical, Seronegative: asymmetrical
Rheumatoid has no spinal involvement, seronegative involves spine
Rheumatoid more common in females, seroneg males

basically complete opposites

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3
Q

What is Raynaud’s?

A

vasospasm that causes digits to change colour to white (pallor) from lack of blood flow, usually brought on by cold temperatures

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4
Q

What is systemic lupus erythematosus?

A

SLE is an inflammatory autoimmune connective tissue disorder.
Chronic and affects multiple systems.

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5
Q

Who does SLE affect?

A

More common in Afro-Caribbean and Asian
9/10 patients are women
Peak age of onset ranges from 30 to 70 years in women and between 50 and 70 years in men

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6
Q

What can cause SLE?

incl. environmental possible triggers

A

Genetic + environmental
Environmental triggers
- UV radiation
- Drugs: procainamide, sulfasalazine, minocycline, isoniazid
- Viral: EBV, CMV, parovirus B19
- Hormonal: oestrogen

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7
Q

What is the pathophysiology in SLE?

A

Environmental trigger damages cells causing apoptosis.
leads to the release of nuclear antigens from the apoptosing cells.
B cells produce anti-nuclear antibodies in response and form antigen-antibody complexes.
These complexes travel and deposit in tissue causing an inflammatory response and tissue damage (type 3 hypersensitivity)

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8
Q

What are the risk factors for SLE?

A

Female sex
age >30 years
African descent in Europe and US
Certain meds
sun exposure
family history of SLE
tobacco smoking

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9
Q

What meds are associated with SLE?

A

procainamide
minocycline
terbinafine
sulfasalazine
isoniazid
phenytoin
carbamazepine

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10
Q

Why is the risk of thrombosis increased in SLE?

A

presence of antiphospholipid antibodies increases the risk

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11
Q

What are the symptoms of SLE?

A

Skin: malar rash, discoid rash, photosensitive rash
Haematological: anaemia (can be haemolytic), thrombocytopenia, neutropenia, lymphopenia
Fatigue
Weight loss
Fever
Oral ulcers
Arthralgia/ arthritis
Serositis: pleuritis, pericarditis
Thrombosis
Abdo pain, D&V
Raynaud’s
Hair loss
Nephrosis

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12
Q

What course does SLE follow?

A

relapsing-remitting course
with flares of worse symptoms and periods where symptoms settle

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13
Q

What autoantibodies are relevant in SLE?

A

ANA
anti-dsDNA
anti-Ro
anti-Sm
anti-La
antiphospholipid

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14
Q

What investigations should be done for SLE?

A

ANA: positive, but not specific for lupus
Double stranded DNA antibody (+ other autoantibodies)
FBC: anaemia, leukopenia, thrombocytopenia
Urea and creatinine: rise when renal disease advanced
Erythrocyte sedimentation rate and C-reactive protein: ESR raised, CRP normal/raised

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15
Q

In SLE, who has antiphospholipid syndrome?

A

Patients with thrombosis, recurrent miscarriages and persistent positive aPL blood tests

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16
Q

Differentials for SLE

A

Rheumatoid arthritis
Antiphospholipid syndrome
Systemic sclerosis
Mixed connective tissue disease
Lyme disease

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17
Q

What is the non-pharmacological treatment for SLE?

A

sun protection
diet and nutrition - avoiding CVD
exercise
psychological treatment
smoking cessation

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18
Q

Pharmacological treatment options for SLE

A

NSAIDs
Hydroxychloroquine
Corticosteroids (pred) + immunosuppressive drugs

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19
Q

What are some possible complications of SLE?

A

Haematological: anaemia, thrombocytopenia, leukopenia
Corticosteroid complications
Inflammation: myocarditis, endocarditis, pleuritis, pericarditis
Miscarriage in presence of aPL
Thrombosis

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20
Q

What can cause oedema in SLE?

A

Lupus nephritis causing inflammation in kidney, nephrotic syndrome (proteinuria) and hypoalbuminaemia

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21
Q

How is lupus nephritis diagnosed?

A

Renal biopsy showing crescent shaped swelling and a wire loop pattern

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22
Q

What is antiphospholipid syndrome?

A

persistently elevated antiphospholipid antibodies characterised by thromboses and pregnancy-related morbidity

1/3 of patients have SLE

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23
Q

What investigations would you run for antiphospholipid syndrome?

A
  • Anticardiolipin test:
  • Lupus anticoagulant test:
  • Anti-B2-glycoprotein I test:
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24
Q

What is Marfan’s syndrome?

A

Autosomal dominant connective tissue disorder characterised by loss of elastic tissue

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25
Q

What genetic mutation causes Marfan’s?

A

mutation of the FBN1 gene on chromosome 15q21
In 75% of patients this is autosomal dominant, the others occur spontaneously

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26
Q

What is the pathophysiology of Marfan’s?

A

FBN1 gene mutation makes abnormal fibrillin protein
Causes fewer functioning microfibrils in extracellular matrix Less tissue integrity and elasticity throughout connective tissue in body
Less functioning fibrillin means less removal of TGF-Beta, so excessive signalling and more tissue growth.

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27
Q

How does Marfan’s affect the aorta?

A

Marfan’s causes aorta to dilate over time, risk of aortic valve issues.
Aorta also undergoes cystic medial necrosis.
Both of these make aorta susceptible to aneurysms and dissection

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28
Q

According to ghent diagnostic criteria, what are the 2 cardinal features of Marfan’s?

A

aortic root aneurysm
ectopia lentis

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29
Q

What is needed to diagnose Marfan’s?

A

Aortic Root Dilatation Z score ≥ 2 AND Ectopia Lentis/ FBN1
or
Ectopia lentis AND a FBN1 mutation associated with Aortic Root Dilatation

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30
Q

What are the risk factors for Marfan’s?

A

family history of Marfan syndrome, or of aortic dissection or aneurysm
weak association with high paternal age

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31
Q

What signs can be seen in Marfan’s?

A

Positive thumb sign: if patient bens thumb across palm and covers with fingers, tip of thumb protrudes
Positive wrist sign: when wrapped around other wrist, 1st and 5th digits overlap

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32
Q

Clinical features of Marfan’s

A

ectopia lentis + aortic dilation
Tall stature
long limbs
arachnodactyly (long digits)
scoliosis
high level of pubic bone
high arched palate (can cause dental crowding)
pectus excavatum (sternum inwards) or pectus carinatum (sternum outwards)
flat feet
myopia and/or astigmatism
hypermobility

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33
Q

How can the aorta be viewed?

A

Echocardiography
CT/MRI, thorax if not clear on echo
CT/MRI, abdomen
Abdominal ultrasound

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34
Q

What investigations should be done for Marfan’s?

A

Echocardiography or other aortic imaging
Ophthalmic assessment
Consider blood screening for FBN1, however diagnosis usually made clinically

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35
Q

Differentials for Marfan’s

A

Aortic dissection not associated with Marfan syndrome
Bicuspid aortic valve
Ehlers-Danlos syndrome
Marfanoid hypermobility syndrome

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36
Q

Basic management of Marfan’s

A

No curative treatment exists, so management aims to prevent cardiac, ophthalmic, and musculoskeletal complications

e.g. lifestyle changes, beta blockers and ARBs, consider pregnancies as bigger risk of AAA

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37
Q

What can worsen the prognosis for Marfan’s?

A

Once aortic dissection occurs, survival is considerably reduced to between 50% and 70% at 5 years

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38
Q

Complications of Marfan’s

A

Aortic dissection
Spontaneous ptx
Aortic/mitral regurgitation
Hernia

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39
Q

What is Ehlers Danlos syndrome?

A

Ehlers-Danlos syndromes are inherited connective tissue disorders due to defective collagen,
characterised by joint hypermobility, skin hyperextensibility, and tissue fragility

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40
Q

Which is the most common and least severe form of EDS?

A

Hypermobile

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41
Q

What causes EDS?

A

genetic changes in genes for connective tissue proteins, such as collagen and matrix proteins
e.g. COL5a1

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42
Q

What are the effects on connective tissue due to the EDS gene defect?

A
  • ligament laxity and hypermobility
  • fragility of connectvie tissues
  • impaired healing
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43
Q

What systems are the primary manifestations in EDS?

A

Musculoskeletal
skin

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44
Q

What feature in EDS is present in all types?

A

joint hypermobility

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45
Q

What score is used to assess for hypermobility and what would the mark be for hypermobility?

A

Beighton score
5/9

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46
Q

List some manifestations/symptoms of EDS

A

MSK: joint pain and hypermobility, dislocation, spinal pain
Skin: easy bruising, stretchy and soft skin, stretch marks
Cardiovasc: POTS
GI: GORD, IBS
Poor wound healing
Chronic pain and fatigue
Gynae: abnormal bleeding, dysmenorrhoea
Uterine/rectal prolapse
abdominal wall, inguinal, or para-umbilical hernia

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47
Q

Risk factors for EDS

A

family history of joint hypermobility or EDS
genetic mutations for EDS

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48
Q

Examples of criteria of Beighton scoring for hypermobility

A

Place their palms flat on the floor with their straight legs
Hyperextend their elbows
Hyperextend their knees
Bend their thumb to touch their forearm
Hyperextend their little finger past 90 degrees

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49
Q

How is EDS diagnosed?

A

Clinically (assessment and beighton)
Genetic testing can reveal some mutations but no single confirmatory test

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50
Q

Differentials for EDS

A

Marfan’s syndrome
Fibromyalgia
Chronic fatigue syndrome

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51
Q

Management of EDS

A

Asymptomatic don’t require treatment
MDT: physiotherapy to strength joints, avoid contact sports and physically demanding jobs

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52
Q

Complications of EDS

A

Surgery complications: bleeding, impaired healing, difficulty suturing
Ruptured blood vessels
Reduced QoL

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53
Q

Which type of EDS is associated with shortened lifespan?

A

Vascular

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54
Q

Epidemiology of sjogrens syndrome

A

Women affected more than men
Peaks between 20-40 and 50s

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55
Q

Difference between primary and secondary sjogrens syndrome

A

Primary Sjögren’s is where the condition occurs in isolation. Secondary Sjögren’s is where it occurs due to other diseases such as SLE or RA

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56
Q

How is the Schirmer test carried out?

Sjogrens

A

inserting folded filter paper under the lower eyelid with the end hanging out.
Moisture from the eye will travel by diffusion along the filter paper.
After 5 minutes, the distance that the moisture travels along the filter paper is measured.

15mm is expected. Less than 10mm is significant

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57
Q

What investigations should be done for Sjogren syndrome?

A

Schirmer test
Screen for anti-60 kD (SS-A) Ro and anti-La (SS-B)

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58
Q

What is going wrong in Sjogrens?

A

focal lymphocytic infiltration of exocrine glands

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59
Q

What are the risk factors for sjogrens syndrome?

A

female
SLE
RA
systemic sclerosis (scleroderma)
HLA class II markers
age 40-70

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60
Q

What are the key diagnostic factors for sjogrens?

A

fatigue
dry eyes
dry mouth

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61
Q

What are the sicca symptoms in sjogrens?

A

dry eyes and mouth

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62
Q

Differentials for sjogrens

A

hypothyroidism
drug-induced or idiopathic sicca
SLE
RA
scleroderma
fibromyalgia

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63
Q

Management of sjogrens

A

Artificial tears/ eye drops
Artificial saliva
Vaginal lubricants
Pilocarpine to stimulate tear and saliva production

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64
Q

Why should anticholinergics, antihistamines, and diuretics be avoided in sjogrens?

A

Can exaccerbate dry eyes

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65
Q

Complications of sjogrens

A

Blepharitis (from dry eyes)
exacerbation of dry eyes and blurring vision
oral candidiasis
cholinergic side effects of medicine

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66
Q

What is healthy cartilage like?

A

matrix of collagen fibres, enclosing proteoglycans and water
Avascular
Chondrocytes secrete collagen and proteoglycans
balance between cartilage degradation from wear and production by chondrocytes

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67
Q

What type of collagen is normally in articular cartilage?

A

type 2

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68
Q

What is the pathophysiology of OA?

A

Injury to joint leads to inflammation
Cytokines released and break down lining of joint, more inflammatory cells produced.
Loss of cartilage and abnormal bone repair leads to sclerotic subchondral bone and overgrowths (osteophytes)

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69
Q

Risk factors of osteoarthritis

A

age >50 years
female sex
obesity
genetic factors (e.g. family history)
joint malalignment
physically demanding occupation/sport
post trauma/injury

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70
Q

What X-ray changes are seen in OA?

A

L – Loss of joint space
O – Osteophytes (bone spurs)
S – Subarticular sclerosis (increased density of the bone along the joint line)
S – Subchondral cysts (fluid-filled holes in the bone)

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71
Q

What is osteoarthritis?

A

OA is the result of mechanical and biological events that destabilise the normal process of degradation and synthesis of articular cartilage, extracellular matrix, and subchondral bone

Leads to loss of cartilage and sclerosis of subchondral bone

Clinically characterised by joint pain, stiffness, and functional limitation

affects the entire joint

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72
Q

What is the most common form of arthritis?

A

osteoathritis

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73
Q

What causes primary and secondary OA?

A

Primary: unkown
Secondary: pre-existing joint damage, e.g. RA, gout, spondyloarthritis

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74
Q

What joints are commonly affected in OA?

A

Hips
Knees
Distal interphalangeal (DIP) joints in the hands
Carpometacarpal (CMC) joint at the base of the thumb
Lumbar spine
Cervical spine (cervical spondylosis)

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75
Q

Signs of osteoathritis

A

Crepitus
Restricted movement
Bony enlargement
Joint effusion + inflammation
Bony instability + muscle wasting

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76
Q

What is morning stiffness like for OA?

A

shouldn’t last longer than 30 minutes
if longer, consider RA

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77
Q

Symptoms of OA

A

joint pain, stiffness, and sometimes swelling
functional difficulties and limited range of movement
bony deformities

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78
Q

How is OA diagnosed?

A

Clinically
Can consider (but diagnosis made clinically):
XR: if damage advanced
CRP and ESR: normal
RF and ANA: negative

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79
Q

What signs of OA can be seen in the hands?

A

Heberden’s nodes (in the DIP joints)
Bouchard’s nodes (in the PIP joints)
Squaring at the base of the thumb (CMC joint)

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80
Q

Differentials for osteoarthritis

A

Bursitis
Gout
Pseudogout
Rheumatoid arthritis (RA)
Psoriatic arthritis
Avascular necrosis (AVN)

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81
Q

Management options for OA

A

Non-pharmaceutical: exercise, weight loss if overweight
Pharmacological: topical NSAIDs, oral NSAIDs + PPI for gastroprotection
Surgical joint replacement

NSAIDs: best used intermittently, only for a short time during flares

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82
Q

Complications of OA

A

functional decline and inability to perform activities of daily living
spinal stenosis in cervical and lumbar OA
NSAID-related gastrointestinal bleeding
NSAID-related renal dysfunction

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83
Q

What can cause RA?

A

genetics and environment.
E.g. HLA-DR1 or HLA-DR4.
Environmental factors: infection

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84
Q

What is rheumatoid arthritis?

A

an autoimmune condition that causes chronic inflammation in the synovial lining of the joints, tendon sheaths and bursa.

a type of inflammatory arthritis

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85
Q

Who does RA tend to affect?

A

2-3x more common in women than men
most often develops in middle age but can present at any age

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86
Q

How long does morning stiffness last in RA?

A

1 hour (longer than OA)

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87
Q

What are the risk factors for rheumatoid arthritis?

A

genetic predisposition/ family hx
smoking

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88
Q

What joints does RA tend to affect and what is this called?

A

Metacarpophalangeal (MCP) joints
Proximal interphalangeal (PIP) joints
Wrist
Metatarsophalangeal (MTP) joints (in the foot)

can affect larger joints (more progressed) and c spine (not lumbar)

symmetrical distal polyarthrits

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89
Q

What joint symptoms are present in RA?

A

Pain
Stiffness
Swelling

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90
Q

What age do most patients with RA present?

A

between the ages of 40 and 60

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91
Q

Which arthritis may affect the DIP joints?

A

Enlarged and painful distal interphalangeal joints are more likely to represent Heberden’s nodes due to osteoarthritis, not RA.

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92
Q

How do patients with RA typically present?

A

hx of bilateral, symmetrical pain and swelling of the small joints of the hands and feet that has lasted for >6 weeks. Morning stiffness lasting over 1 hour

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93
Q

What hand deformities can be seen in advanced RA?

A

Z-shaped deformity to the thumb
Swan neck deformity (hyperextended PIP and flexed DIP)
Boutonniere deformity (hyperextended DIP and flexed PIP)
Ulnar deviation of the fingers at the MCP joints

not as common now as DMARDs usually given early

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94
Q

What are some extra-articular manifestations of RA?

A

Pulmonary fibrosis
Felty’s syndrome
Sjögren’s syndrome
Anaemia of chronic disease
CVD
Eye manifestations
Rheumatoid nodules
Lymphadenopathy
Carpel tunnel syndrome
Amyloidosis

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95
Q

What investigations should be done for RA?

A

Rheumatoid factor and anti-CCP: positive
Radiographs and ultrasonography

ESR and CRP

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96
Q

What are the differentials for RA?

A

Psoriatic arthritis
Infectious arthritis
Gout
SLE
Osteoarthritis

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97
Q

What scoring systems can be used in RA?

A

Health Assessment Questionnaire (HAQ) measures functional ability
Disease Activity Score 28 Joints (DAS28) score is used in monitoring disease activity and response to treatment, involves assessing 28 joints

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98
Q

What are the management options for RA?

medications

A

single DMARDs for low disease activity, e.g. methotrexate
short term corticosteroids during: flares, early disease, or when starting/changing DMARDs
NSAIDs
biological DMARDs with methotrexate (if methotrexate not working)

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99
Q

What is the prescription of methotrexate given for RA?

A

7.5mg given once a week, with 5mg folic acid taken the next day as it interferes with folate metabolism

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100
Q

Examples of common synthetic DMARDs given for RA

A

hydroxychloroquine
sulfasalazine
methotrexate
leflunomide

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101
Q

What are some of the biological DMARDs given for moderate to severe RA?

A

Tumour necrosis factor (TNF) inhibitors: adalimumab
Anti-CD20: rituximab
Anti-interleukin-6 inhibitors: sarilumab
JAK inhibitors: upadacitinib
T-cell co-stimulation inhibitors: abatacept

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102
Q

What medication is given to pregnant women (or considering pregnancy) with RA?

A

Corticosteroids
e.g. oral pred

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103
Q

Side effects of methotrexate

A

Mouth ulcers and mucositis
Liver toxicity
Bone marrow suppression and leukopenia
Teratogenic

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104
Q

What are some possible complications of RA?

A

work disability
increased joint replacement surgery
increased coronary artery disease
increased mortality
interstitial lung disease
carpal tunnel syndrome

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105
Q

What does spondyloarthritis mean?

A

an umbrella term for a group of conditions that affects the spine and peripheral joints with familial clustering and a link to type1 HLA antigens

(HLA-B27)

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106
Q

What types of arthritis fall into seronegative spondyloarthritis?

A

Axial & ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Enteropathic athritis

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107
Q

What tissue type are the spondyloarthropathies associated with?

A

HLA-B27

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108
Q

What is HLA-B27?

A

Human leukocyte antigen B27
Class 1 surface antigen (on all cells except for RBC)
Is an antigen presenting cell

associated with spondyloarthropathies

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109
Q

What is axial spondyloarthritis and what does it become?

A

An inflammatory disorder primarily affecting fibrous and synovial joints of the spine
When radiographic changes at the sacroiliac joints are present it is called ankylosing spondylitis

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110
Q

When is axial spondyloarthritis described as ankylosing spondylitis?

A

When radiographic changes at the sacroiliac joints are present

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111
Q

What is non-radiographical axial spondyloarthritis?

A

axial inflammation visible on magnetic resonance imaging (MRI) that has not caused substantial erosive damage to the sacroiliac joints

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112
Q

Epidemiology of AS

A

Men more affected than women
AS most commonly begins between 20 and 30 years of age, with 90-95% of people aged less than 45 years at disease onset

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113
Q

What percentage of patients with AS have HLA-B27 present?

A

90%

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114
Q

What are the symptoms of inflammatory back pain?

seen in AS

A

Early morning back stiffness
Improvement of stiffness with exercise
Resolution of symptoms using NSAIDs
Alternating buttock pain
Waking in the second half of the night with back pain

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115
Q

What are the risk factors for AS?

A

HLA-B27
ERAP1and IL23R genes
positive family history of AS
male sex

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116
Q

What are the criteria for classifying back pain as AS?

A

Age of onset less than 45
Insidious
Improvement of back pain with exercise
No improvement with rest
Pain at night that improves when getting up

4/5 suggest AS

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117
Q

Key presentations of AS

A

low back pain and stiffness: improves with movement, worst at night
sacroiliac pain in buttock region
stiffness lasting more than 30 minutes

enthesitis, iritis and uveitis may be present

typically young adult male

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118
Q

What may be visible on examination in AS?

A

loss of lumbar lordosis
peripheral joint involvement
kyphosis
tenderness at sacroiliac joints

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119
Q

What is seen in advanced AS on a spinal XR?

A

Bamboo spine

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120
Q

What test can be used to assess spinal mobility?

A

Schober’s test

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121
Q

What investigations should be done for AS?

A

Pelvic XR: sacroiliitis
Spine XR
MRI of the spine can show bone marrow oedema in early stages
Bloods: ESR and CRP raised

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122
Q

Differential diagnoses for AS

A

Other spondyloarthropathies
OA
Infection (e.g., discitis)
Vertebral fracture
Bony metastases

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123
Q

What are the management options for AS?

A

NSAIDs
Physiotherapy
If NSAIDs fail, TNF-alpha inhibitors drugs

DMARDs can be used for peripheral involvement but don’t help axial

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124
Q

What’s a complication of AS?

A

Higher risk of CVD

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125
Q

What does an increase in erythrocyte sedimentation rate (ESR) and C-reactive protein suggest?

A

Inflammation

Plasma viscosity may also be raised in inflammatory disease

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126
Q

Which ENA antibodies are commonly seen in Sjogrens?

A

Anti-Ro and anti-La

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127
Q

Which ENA antibodies are commonly seen in SLE?

A

Anti-SM
Anti-ro and anti-la

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128
Q

What antibodies are specific for systemic sclerosis?

A

anti-topoisomerase I (anti-Scl 70)

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129
Q

Which ENA antibodies occur in systemic sclerosis and are associated with pulmonary fibrosis?

A

anti-RNA polymerase I and III

130
Q

What are the 3 causes of lower back pain and which are the most common?

A

Mechanical - most common, 97%
Systemic
Referred

131
Q

What is the difference between a strain and a sprain?

A

Strain: disruption of the muscle fibres
Sprain: partial ligament damage

132
Q

What is mechanical lower back pain?

A

LBP that is triggered by movement and improves with rest
The most common causes of LBP (97%)

133
Q

What can cause mechanical lower back pain?

A

Lumbar spine strain/sprain
Degeneration of discs or facets
Disc herniation
Spinal stenosis
Spondylolysis
Compression fractures
Sacroiliitis
Scoliosis

134
Q

In mechanical LBP how does discogenic pain present?

A

increases with flexion, sitting, and coughing/sneezing due to an increase in intradiscal pressures

135
Q

In mechanical LBP how does facet joint pain present?

A

back pain that increases with extension as the facet joints are mechanically loaded

136
Q

What are risk factors for recurrent lower back pain?

A

female, increasing age, fibromyalgia, psychosocial

137
Q

When assessing lower back pain, what does pain on flexion and leg radiation suggest?

A

disc herniation / degeneration

138
Q

When assessing lower back pain, what does pain on extension suggest?

A

Facet involvement or spinal stenosis

139
Q

When assessing lower back pain, what does a young patient with reduced range of movement suggest?

A

ankylosying spondylosis

140
Q

What is the management for acute mechanical lower back pain?

A

adequate analgesia (NSAIDs), normal mobility and activities, heating devices, physio

141
Q

How does mechanical lower back pain typically present?

A

starts suddenly and usually short lived
may be recurrent
helped by rest
back is stiff
muscular spasm may be visible and palpable
local pain and tenderness

142
Q

What provocative tests can be done for lumbar disc herniation?

A

Straight leg raise: pain below 60degress of hip flexion
Femoral stretch: leg pain

143
Q

What provocative tests for sacroiliac joint (SIJ) pain are there?

A

Thigh thrust test
Distraction test

144
Q

What is sciatica?

A

symptoms associated with irritation of the sciatic nerve

indicated by sciatic stretch test

145
Q

What are some bad causes of lower back pain?

A

Cauda equina
Spinal fracture
Malignancy
Infection
AAA

146
Q

What are the red flags for back pain?

A

Saddle anaesthesia
Sphincter disturbance
Neurological deficit
History of malignancy with new onset back pain
Fever
Unexplained weight loss
IV drug use
UTI
Prolonged corticosteroid use/ immunosuppressed
Trauma
Age >50 years or <20

147
Q

Which cancers metastasize to bone?

A

Kidney
Prostate
Breast
Lung
Thyroid

148
Q

What is psoriatic arthritis (PsA)?

A

a chronic inflammatory seronegative arthritis associated with psoriasis

149
Q

What are the key features of psoriatic arthritis?

A

Mono or oligoarthritis (one joint or large joints)
Asymmetrical polyarthritis
Spondylitis
DIP arthritis + nail dystrophy + dactylitis
Arthritis mutilans: osteolysis causes shortening of digits

150
Q

Who does psoriatic arthritis tend to affect?

A

uncommon in the general population, it occurs frequently in patients with psoriasis

151
Q

What is thought to cause PsA?

A

Genetic + environmental triggers (trauma, infection smoking)

152
Q

What are the 5 patterns of psoriatic arthritis?

A

Distal interphalangeal joint (DIP) arthritis
Asymmetrical oligoarthritis
Symmetrical polyarthritis
Arthritis mutilans
Psoriatic spondylitis with sacroiliac and spinal involvement

153
Q

What are the risk factors for psoriatic arthritis?

A

psoriasis
family history of psoriasis or psoriatic arthritis
history of joint or tendon trauma
infection
smoking

154
Q

What is seen on XR for psoriatic arthritis?

A

erosion in the distal interphalangeal (DIP) joint
periarticular new-bone formation
osteolysis and pencil-in-cup deformity in advanced disease

155
Q

What investigations should be done for psoriatic arthritis?

A

Plain film XR of hands and feet
RF and anti-CCP
ESR and CRP

156
Q

What are the differentials for PsA?

A

Rheumatoid arthritis (RA)
Gout
Erosive osteoarthritis
Reactive arthritis
Mycobacterial tenosynovitis
Sarcoid dactylitis

157
Q

What is the management of PsA?

A

DMARDs for peripheral arthritis
NSAIDs
Intra-articular corticosteroid injections

Smoking cessation
Physiotherapy

158
Q

What bacteria can cause reactive arthritis?

A
  • Chlamydia
  • Salmonella
  • Campylobacter
  • Shigella
  • Yersinia

HLA-B27 increases risk

gram-negative, GI infection or STI most common triggers

159
Q

What are the risk factors for reactive arthritis?

A

male sex
HLA-B27 genotype
preceding chlamydial or gastrointestinal infection

160
Q

What are the symptoms of reactive arthritis?

A

Acute monoarthritis (most often the knee)
asymmetrical oligoarthritis
axial arthritis
Bilateral conjunctivitis (non-infective)
Anterior uveitis
Urethritis (non-gonococcal)
Circinate balanitis (dermatitis of the head of the penis)

typically 1-4 weeks after infection

161
Q

What investigations should be done for reactive arthritis?

A

ESR and CRP: elevated
ANA and RF: negative
Urogenital and stool cultures: may not show after onset of symptoms, earlier better

162
Q

What are the management options for reactive arthritis?

A

NSAIDS
Corticosteroids: better for peripheral than axial
DMARDs if NSAIDs don’t help

163
Q

Differentials of reactive arthritis

A

Ankylosing spondylitis (AS)
Psoriatic arthritis
Rheumatoid arthritis (RA)
Rheumatic fever
Arthritis associated with inflammatory bowel disease (IBD)
Gout
Septic arthritis
Post-viral arthritis

164
Q

Complications of reactive arthritis

A

secondary osteoarthritis
iritis/uveitis

165
Q

What does seronegative mean in relation to arthritis?

A

inflammatory arthritis but without a positive rheumatoid factor

166
Q

When does enteropathic arthritis occur?

A

10-15% of patients with ulcerative colitis or crohn’s

167
Q

How does enteropathic arthritis present?

A

asymmetrical
predominantly affects lower limb joints
sacroiliitis or spondylitis

168
Q

How is enteropathic arthritis managed?

A

IBD should be treated
NSAIDs
Mono-arthritis best treated by intra-articular corticosteroids
Sulfasalazine

169
Q

What is the definition of osteoporosis?

A

a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue, resulting in increased bone fragility and susceptibility to fracture

170
Q

What is the morbidity one year one post hip fracture?

A

20%

171
Q

What is the pathophysiology of post-menopausal osteoporosis?

A
  • Drop in oestrogen levels
  • Increase in bone turnover
  • Osteoclasts resorb bone faster than osteoblasts reform
  • Imbalance, resorption is greater than formation
  • Erosion through trabeculae
172
Q

What is the basic pathology of osteoporosis?

A

Osteoporosis results from increased bone breakdown by osteoclasts and decreased bone formation by osteoblasts, leading to loss of bone mass

173
Q

What is the prevalence of osteoporosis?

A

18.3% in the general population, increasing to 21.7% in older age groups

affects more women than men and increases with age

174
Q

What is the T score used in osteoporosis?

A

T score of the femoral neck measured on a dexa scan shows the number of standard deviations the patient is from an average healthy young adult

175
Q

What is a normal T score?

A

More than -1
(closer to 0, and less SD away)

176
Q

What is the T score for osteopenia?

A

-1 to -2.5

177
Q

What is the T score value for osteoporosis?

A

2.5 SD

178
Q

What is the T score value for severe osteoporosis?

A

-2.5 plus a fracture

179
Q

What are the risk factors for osteoporosis?

A

Older age
Post-menopausal women
Reduced mobility and activity
Low BMI (under 19 kg/m2)
Low calcium or vitamin D intake
Alcohol and smoking
Hx of fractures
Chronic diseases
Long-term corticosteroids (e.g., 7.5mg or more of prednisolone daily for longer than 3 months)
Certain medications (e.g., SSRIs, PPIs, anti-epileptics and anti-oestrogens)

180
Q

What can cause osteoporosis?

A

Inflammatory disease (increase bone resorption)
Hyperthyroidism and primary hyperparathyroidism (increases bone turnover)
Cushing’s (increases bone resorption and induces osteoblast apoptosis)
Oestrogen deficiency (e.g. menopause)
Male hypogonadism
Anorexia
Reduced skeletal loading (increases resorption)
Glucocorticoid medication

181
Q

How does osteoporosis present?

A

Asymptomatic until fracture occurs

182
Q

What is the gold standard for measuring bone mineral density in osteoporosis?

A

DEXA scan

183
Q

What can calculate the 10-year risk of a major osteoporotic fracture and a hip fracture?

A

QFracture tool
FRAX tool

based on results arrange a DEXA scan

184
Q

What are some differentials for osteoporosis?

A

Multiple myeloma
Osteomalacia
Chronic kidney disease-bone and mineral disorder
Primary hyperparathyroidism
Metastatic bone malignancy
Vertebral deformities

185
Q

What is the first-line treatment for postmenopausal women at high risk of fracture with prior hip or vertebral fractures and/or DXA T-score of ≤-2.5?

A

Bisphosphonates
E.g. alendronic acid

186
Q

Management for osteoporosis

A

Ensure adequate calcium and vitamin D intake
Regular weight baring exercise to maintain bone strength (if able)
Anti-resorptive drugs: bisphosphonates (alendronic acid)
Denosumab if bisphosphonates not suitable

187
Q

Whats the main complication of osteoporosis?

A

Fractures: e.g. hip, wrist, rib

188
Q

How can osteoporosis be prevented in at risk patients?

A

Adequate dietary intake of vitamin D and calcium
Exercise
Raloxifene in osteopenia

189
Q

What is given to patients with osteopenia to help prevent reaching osteoporosis?

A

Raloxifene

190
Q

What is gout?

A

An inflammatory crystal arthritis associated with hyperuricaemia and intra-articular sodium urate crystals

191
Q

Where does gout most commonly affect?

A

most commonly affects the first toe, foot, ankle, knee, fingers, wrist, and elbow

however, it can affect any joint

192
Q

What’s the epidemiology of gout?

A

more prevalent in men than women, and increases with age for both groups
prevalence of about 2.5% in UK

193
Q

What is podagra?

A

When gout affects the first metatarsal joint of the big toe

194
Q

What causes gout?

A

Hyperuricaemia: due to under excretion or over production/consumption of urate

195
Q

What is the pathology of gout?

A

Purines are converted into uric acid.
Uric acid has limited solubility: more uric acid than is soluble leads to hyperuricaemia
Uric acid forms monosodium urate crystals
these can form from: increased consumption or production of purines or decreased clearance of uric acid

196
Q

How is gout diagnosed?

A

arthrocentesis showing monosodium urate crystals
crystals are needle-shaped and negatively birefringent of polarised light

197
Q

Where does gout most commonly affect?

A

1st metatarsophalangeal (MTP) joint

198
Q

What does a hx of acute pain in a joint which becomes swollen, tender and erythematous and which reaches its crescendo over a 6- to 12-hour period suggest?

A

Crystal arthropathy of some sort

199
Q

What are the symptoms of gout?

A

Rapid onset of severe pain, redness or swelling of joints
Tophi
Acute episodes, typically at peak intensity after 12 hours

200
Q

What are gouty tophi?

A

subcutaneous uric acid deposits

201
Q

What investigations should be done for gout?

A

arthrocentesis with synovial fluid analysis: rule out septic arthritis, would show monosodium urate crystals
serum uric acid level

202
Q

What are the differentials for gout?

A

Pseudogout (calcium pyrophosphate deposition disease)
Septic arthritis
Trauma
Rheumatoid arthritis (RA)
Reactive arthritis
Psoriatic arthritis

203
Q

What is the acute management of gout?

A

NSAIDs (e.g., naproxen) first-line (co-prescribed with a proton pump inhibitor for gastroprotection)
Colchicine second-line
Oral steroids (e.g., prednisolone) third-line

204
Q

What’s the long term management of gout?

A

Long term management:
- Dietary modifications
- xanthine oxidase inhibitors such as allopurinol

205
Q

How should gout patients be monitored?

A

In patients taking uric acid-lowering agents, follow up uric acid levels every 1 to 3 months initially, then every 6 to 12 months (target level <360 micromol/L [<6 mg/dL]).
Annual monitoring of serum urate level is recommended for patients with gout who are continuing urate-lowering therapy after reaching their target serum urate level

206
Q

What are the complications of gout?

A

acute uric acid nephropathy
chronic kidney disease
nephrolithiasis

207
Q

What is pseudogout?

A

a crystal arthropathy caused by calcium pyrophosphate crystals collecting in the joints

calcium pyrophosphate deposition disease (CPPD

208
Q

What causes pseudogout?

A

deposition of calcium pyrophosphate (CPP) crystals in the mid-zone of articular hyaline and fibro-cartilage

209
Q

What joints are most commonly affected in pseudogout?

A

Knee
Wrist

210
Q

What are the risk factors for pseudogout?

A

advanced age
injury
hyperparathyroidism
haemochromatosis
family history of CPPD
hypomagnesaemia
hypophosphatasia

211
Q

What are the main presentations of pseudogout?

A

Red, swollen, painful, tender joints
Can have OA like symptoms of wrists and shoulders that aren’t commonly affected by OA
Sudden

212
Q

What investigations should be done for pseudogout?

A

arthrocentesis with synovial fluid analysis: positively birefringent rhomboid-shaped crystals, rule out septic arthritis
XR of affected joints

213
Q

What would a joint aspiration show in pseudogout?

A

positively birefringent rhombodial crystals

214
Q

What are the differentials of pseudogout?

A

Acute gouty arthritis
Acute septic arthritis
Milwaukee shoulder syndrome
Osteoarthritis
Rheumatoid arthritis
Polymyalgia rheumatica

215
Q

What is the management for pseudogout?

A

Symptomatic relief as no clear treatment:
* NSAIDs (e.g., naproxen) first-line (co-prescribed with a proton pump inhibitor for gastroprotection)
* Colchicine
* Intra-articular steroid injections (septic arthritis must be excluded first)
* Oral steroids

216
Q

Risk factors for fibromyalgia

A

family history of fibromyalgia (FM)
rheumatological conditions
age between 20 and 60 years
female sex
stressful events
sleep problems
infections

217
Q

What are the symptoms of fibromyalgia?

A

Chronic widespread pain
Allodynia
Cognitive impairment
Fatigue and sleep disturbance
Anxiety and depression
Nausea
Pins and needles
Muscle spasms
Dysmenorrhoea

218
Q

What is the epidemiology of fibromyalgia?

A

2:1 female: male
Most commonly diagnosed between 35-45
first-degree relatives of individuals with fibromyalgia are eight times more likely to have the condition

219
Q

What are the differentials for fibromyalgia?

A

Rheumatoid arthritis (RA)
Polymyalgia rheumatica (PMR)
Systemic lupus erythematosus (SLE)
Polyarticular osteoarthritis
Ankylosing spondylitis

220
Q

What is the management for fibromyalgia?

A

Individual therapy may include:
aerobic exercise: has the strongest evidence base
cognitive behavioural therapy
medication: pregabalin, duloxetine, amitriptyline
explaining it to the patient

221
Q

What is osteomyelitis?

A

an inflammatory condition of bone caused by an infecting organism, most commonly staph aureus

222
Q

What pathogen most commonly causes osteomyelitis?

A

staph aureus

223
Q

What are the risk factors for osteomyelitis?

A

Open fractures
Penetrating injury
Orthopaedic operations, particularly with prosthetic joints
Diabetes, particularly with diabetic foot ulcers
Peripheral arterial disease
IV drug use
Immunosuppression, e.g HIV
Previous osteomyelitis

224
Q

What is the basic pathology of acute osteomyelitis?

A

Bacteria reach bone and proliferative.
Nearby dendritic cells and macrophages fight infection.
Immune cells release chemicals and enzymes that cause local destruction of bone.

225
Q

What are the different routes of infection in osteomyelitis?

A

Haematogenous spread: bacteria reach bone via blood.
Direct innoculation: trauma or surgery cause bone to be exposed
Contiguous spread: infection can spread from elsewhere, e.g. cellulitis to bone
Can be a combo, e.g. a prosthetic joint infected during surgery then spreads (contiguous)

226
Q

Where does haematogenous osteomyelitis typically affect?

A

metaphysis of long bones in children or the vertebral bodies in adults

227
Q

Which pathogens typically cause osteomyelitis in patients with sickle cell?

A

s.aureus
salmonella

228
Q

What are the symptoms of osteomyelitis?

A

local inflammation, tenderness, erythema, or swelling
fever
fatigue and malaise
non-specific pain at infection site

229
Q

What investigations should be done for osteomyelitis?

A

WBC
ESR and CRP: raised
Blood culture
Plain XR

230
Q

What can be seen in later stage osteomyelitis on an XR?

A

Periosteal reaction (changes to the surface of the bone)
Localised osteopenia (thinning of the bone)
Destruction of areas of the bone

231
Q

What are the differentials for osteomyelitis?

A

Septic arthritis
Transient synovitis
Reactive arthritis
Cellulitis
Necrotising fasciitis
Metastatic bone cancer or primary bone tumour
Trauma

232
Q

How is osteomyelitis managed?

A

Check it’s not septic
6 weeks of flucloxacillin, clindamycin if penicillin allergy
Possible surgical debridement of the infected bone and tissues

233
Q

Difference between septic arthritis and osteomyelitis

A

Septic arthritis is infection of a joint
Osteomyelitis is infection of a bone

234
Q

What is the definition of septic arthritis?

A

the infection of 1 or more joints caused by pathogenic inoculation of microbes

235
Q

How does septic arthitis present?

A

a hot, swollen, acutely painful joint with restriction of movement

236
Q

What is the incidence of septic arthritis?

A

6 per 100,000 in developed countries
incidence increases 10 fold in patients with joint disease or prosthetic joints

237
Q

What pathogen is the most common cause of septic arthritis?

A

staph aureus

predominant causative organisms are staph or strep

238
Q

What causes septic arthritis?

A

Pathogenic inoculation of micro-organisms into the joint, either direct or haematogenous spread

239
Q

What can cause septic arthritis in sexually active patients?

A

Neisseria gonorrhoea (gonococcus)

240
Q

What should a hot, swollen, acutely painful joint with restriction of movement be seen as?

A

septic arthritis until proven otherwise

241
Q

What joints are most commonly affected by septic arthritis?

A

Large joints, e.g. hip/knee

242
Q

What are the risk factors for septic arthritis?

A

underlying joint disease
prosthetic joint
age over 80
immunosuppression
contiguous spread
exposure to ticks (lyme disease)
IV drug use
Recent joint surgery

243
Q

What investigations should be done for septic arthritis?

A

Aspirate joint for synovial fluid sample
- Synovial fluid microscopy
- Synovial fluid culture
Blood culture
White blood cell count
ESR and CRP

244
Q

Differential diagnoses of septic arthritis

A

Osteoarthritis
Psoriatic arthritis
Rheumatoid arthritis
Gout
Pseudogout
Haemarthrosis
Trauma
Bursitis
Cellulitis
Lyme disease

245
Q

What’s the treatment for septic arthritis?

A

IV then oral antibiotics for 4-6 weeks
antibiotics dependent on pathogen

246
Q

What are some possible complications of septic arthritis?

A

Joint destruction
Osteomyelitis (if infection not controlled in joint, spreads to bone)
Antibiotic allergic reaction

247
Q

What is vasculitis?

A

Inflammation of blood vessels

248
Q

What is the pathophysiology of vasculitis?

A

Immune activation
activated immune cells infiltrate into vessel wall and cause direct damage and remodelling
weakening and occlusion of vessel
ischaemia, infarction, aneurysm

immune-mediated blood vessel wall injury

249
Q

What are the main forms of large vessel vasculitis?

A

Takayasu’s arteritis
Giant cell arteritis.

250
Q

What are the main medium vessel vasculitides?

A

Polyarteritis nodosa
Kawasaki’s disease.

251
Q

What are the small vessel vasculitides?

A
  • ANCA associated vasculitis
  • Immune complex small-vessel vasculitis
252
Q

What are the systemic vasculitides?

A

autoimmune disorders characterised by inflammation of blood vessels

253
Q

Where does giant cell arteritis tend to affect?

A

extracranial branches of the carotid artery, e.g. temporal, carotid and facial

254
Q

What is giant cell arteritis?

A

Granulomatous vasculitis of large and medium-sized arteries
Primarily affects branches of the external carotid artery
Most common form of systemic vasculitis seen in over 50s

255
Q

What are the key features for granulomatosis with polyangiitis?

A

Nasal symptoms
Respiratory symptoms
Glomerulonephritis

small vessel, c-ANCA on lab findings

256
Q

What are the key findings for polyarteritis nodosa?

A

Renal impairment
Hypertension
Cardiovascular events
Tender skin nodules

medium vessel

257
Q

What subtype of vasculitis tends to affect kidneys?

A

Small vessel

258
Q

What investigations would you order for vasculitis?

A

Erythrocyte sedimentation rate or C-reactive protein: elevated
Anti-neutrophil cytoplasmic antibodies (ANCA)

259
Q

Who does vasculitis tend to affect?

A

young children or older adults

260
Q

What are the main differentials for vasculitis?

A

Infective endocarditis
Hypercoagulability syndromes
Systemic lupus erythematosus (SLE)
Levamisole-induced vasculitis

261
Q

How is granulomatosis with polyangiitis managed?

vasculitis

A

remission induction: corticosteroids
remission maintenance: rituximab

262
Q

What are the risk factors for GCA?

A

age >50 years
female sex
smoking
atherosclerosis
genetic + environmental factors

263
Q

What is the basic pathology of GCA?

giant cell arteritis

A

immune-mediated vasculitis characterised by granulomatous inflammation in the wall of medium-sized and large arteries

264
Q

What would a presentation of GCA look like?

A

new onset of headache
limb, jaw, or tongue claudication
acute visual symptoms
unexplained raised inflammatory markers

aged over 50

265
Q

What are the symptoms of giant cell arteritis?

A

Scalp tenderness
Headache
Vision loss
Jaw, tongue and limb claudication

266
Q

What are the possible differentials for GCA?

A

Polymyalgia rheumatica (PMR)
Takayasu’s arteritis
Chronic infection
Rheumatoid arthritis
Amyloidosis
SLE
Hypothyroidism

267
Q

What would a temporal artery biopsy show in GCA?

A

granulomatous inflammation
multinucleated giant cells

268
Q

What is the management for GCA?

A

High-dose glucocorticoids: oral prednisolone

269
Q

What are the complications of GCA?

A

Vision loss
Glucocorticoid adverse reaction
Aortic aneurysm
Arterial stenoses

270
Q

What is Paget’s disease of bone?

A

A chronic bone disorder that is characterised by focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone

271
Q

Epidemiology of Paget’s

A

second most common chronic bone-remodelling disorder after osteoporosis
UK prevalence of 2%
mean age of onset is 55 years
equal distribution among men and women

272
Q

What are the pathological phases in Paget’s?

A

Short-lived osteoclast activity increasing resorption
Clast and blast activity leads to increased levels of bone turnover and deposition of structurally abnormal bone
Sclerotic phase where bone formation overtakes resorption

273
Q

What are the 2 different degrees of boney involvement in Paget’s?

A

Monostotic: involves only one bone, most commonly femur, 25% of patients
Polyostotic: involves more than one bone, e.g. femur, tibia, vertebrae, skull, pelvis, and occurs in 75% of patients.

274
Q

What are the symptoms of paget’s?

A

Most patients are asymptomatic

Bone pain
Bone deformity
Fractures
Hearing loss

275
Q

What are the risk factors for Paget’s?

A

Family hx of paget’s
Age over 50

276
Q

What investigations should be done for Paget’s?

A

XR
Alkaline phosphatase: raised
Serum calcium: normal

277
Q

What may be seen on an XR in paget’s?

A

Bone enlargement and deformity
Osteolytic lesions
Cotton wool appearance of the skull
V-shaped osteolytic defects in the long bones

278
Q

What is the first line therapy for Paget’s?

A

Bisphosphonates, e.g. alendronic acid, to inhibit bone resorption

279
Q

What are the possible complications of Paget’s?

A

Arthritis
Hearing loss
Fractures
Osteosarcoma
Spinal stenosis

280
Q

What are the most common causes of secondary bone tumours?

A

Kidney
Prostate
Breast
Lung
Thyroid

281
Q

What are primary and secondary bone tumours?

A

primary arise from bone
secondary metastasize

282
Q

What are the most common benign bone tumours?

A

Osteochondroma (most common)- metaphysis of long bones (tibia, femur), has exotosis
Giant cell tumour- epiphysis of long bone
Osteoma- skull

283
Q

What are the malignant bone tumours and what do they affect?

A

Most common is osteosarcoma: metaphysis, affect age 10-20
Ewing’s sarcoma: femur and sacrum
Chondrosarcoma: axial skeleton, can affect femur and humerus

284
Q

What would be seen on an XR for osteochondroma?

A

Exostosis

285
Q

What is dermatomyositis?

A

idiopathic autoimmune inflammatory myopathy characterised by distinctive skin manifestations

286
Q

At what age are the peaks of incidence for dermatomyositis?

A

5 and 15 years of age
40 and 60 years

287
Q

What can cause dermatomyositis?

A

Genetic: HLA DR3/5
Environmental: Infection, e.g. coxsackie virus

unclear but thought to be gen/env combo

288
Q

What skin changes are visible in dermatomyositis?

A

Gottron papules affecting the backs of the hands and heliotrope rash affecting the eyelids.

289
Q

What are the risk factors for dermatomyositis?

A

genetic predisposition
female sex
black race
ultraviolet radiation

290
Q

What are the signs and symptoms of dermatomyositis?

A

Muscle weakness, atrophy and pain
Heliotrope rash on upper eyelids, shoulders, upper chest and back
Photosensitivity
Gottron’s lesions/papules

291
Q

What is the main investigation for dermatomyositis?

A

Serum creatine kinase: raised

292
Q

What investigations should be done for dermatomyositis?

A

Serum creatine kinase: high
ANA: positive
Serum aldolase: high
Muscle and skin biopsy

293
Q

What are the differentials for dermatomyositis?

A

SLE and subacute cutaneous LE
Psoriasis
Scleroderma

294
Q

What’s the first line treatment for dermatomyositis?

A

corticosteroids: pred

295
Q

What are the complications of dermatomyositis?

A

Respiratory tract infections
Interstitial lung disease
Cardiac disease
Dysphagia

296
Q

What is systemic sclerosis?

aka scleroderma

A

an autoimmune connective tissue disease involving inflammation and fibrosis (hardening or scarring) of the connective tissues, skin and internal organs

women affected much more than men

297
Q

What are the features of limited cutaneous systemic sclerosis?

CREST

A

C – Calcinosis
R – Raynaud’s phenomenon
E – oEsophageal dysmotility
S – Sclerodactyly
T – Telangiectasia

298
Q

What are the 2 types of systemic sclerosis?

A

Limited cutaneous
Diffuse cutaneous

299
Q

What are the features of diffuse cutaneous systemic sclerosis?

A

C – Calcinosis
R – Raynaud’s phenomenon
E – oEsophageal dysmotility
S – Sclerodactyly
T – Telangiectasia

+ organ (CV, lung, kidney) problems

300
Q

What are the risk factors for systemic sclerosis?

A

family history of scleroderma
immune dysregulation (e.g., positive ANA)

301
Q

What autoantibodies would be seen in systemic sclerosis?

A
  • ANA: positive
  • Anti-centromere antibodies: limited cutaneous systemic sclerosis.
  • Anti-Scl-70 antibodies: diffuse cutaneous systemic sclerosis
302
Q

What medication can be given for Raynaud’s?

A

CCB: nifedipine

303
Q

What are the complications of systemic sclerosis?

A

Skin ulcers and infection
Hypothyroidism

304
Q

What is polymyalgia rheumatica?

A

an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck

305
Q

Whats the association between polymyalgia rheumatica and GCA?

A

15% to 20% of patients with PMR have giant cell arteritis
40% to 60% of GCA patients have PMR

306
Q

What are the risk factors for polymyalgia rheumatica?

A

giant cell arteritis, age over 50 years, and female gender

306
Q

How may a patient with polymyalgia rheumatica describe their symptoms?

A

difficulty rising from seated or prone positions
significant shoulder and hip girdle stiffness
varying degrees of muscle tenderness,
shoulder/hip bursitis
oligoarthritis

acute onset

307
Q

What are the main features of polymyalgia rheumatica?

A

Pain and stiffness in shoulder, pelvic girdle and neck
Acute onset
Rapid response to corticosteroids

308
Q

What investigations are done for polymyalgia rheumatica?

A

FBC
ESR and CRP: elevated

309
Q

What are the differentials for polymyalgia rheumatica?

A

Giant cell arteritis (GCA)
Early rheumatoid arthritis (RA)
Hypothyroidism
Fibromyalgia
Paraneoplastic syndrome
Polymyositis

310
Q

What’s the management for polymyalgia rheumatica?

A

low-dose corticosteroids; response usually occurs within 24 to 72 hours

311
Q

What is osteomalacia?

A

Metabolic bone condition where defective bone mineralisation causes softening of the bones

312
Q

What is the link between osteomalacia and rickets?

A

Different manifestations of the same pathological process

(rickets in children)

313
Q

What is the primary cause of osteomalacia?

A

Vitamin D deficiency

314
Q

What are the risk factors for osteomalacia?

A

dietary calcium and vitamin D deficiency
chronic kidney disease
limited sunlight exposure
inherited disorders of vitamin D and bone metabolism
hypophosphatasia
anticonvulsant therapy

315
Q

What are the symptoms for osteomalacia?

patients tend to be asymptomatic

A

Lower bone pain
Fractures
Fatigue
Muscle weakness

316
Q

What would invesitgations show for osteomalacia?

A

low serum vitamin D
Low serum calcium
Low serum phosphate
High serum alkaline phosphatase
High parathyroid hormone

317
Q

How would osteomalacia show on imaging?

A

X-rays may show osteopenia (more radiolucent bones)
DEXA scan shows low bone mineral density

318
Q

What are the differentials for osteomalacia?

A

Osteoporosis
Paget’s disease

319
Q

How is osteomalacia treated?

A

Vitamin D

320
Q
A

Phase 2a (14 decks)

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