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Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Describe the term Seropositive Inflammatory Arthritis.

A

Umbrella term for joint inflammation caused by autoantibodies e.g. RA (anti-CCP and RF), SLE (ANA, dsDNA, Anti-Sm, Anti-Ro, Anti-SRP), Scleroderma (anti-Scl70 + anti-centromere), Sjogren’s (Anti-La + Anti-Ro) and Dermatomyositis (anti-Jo)

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2
Q

Positive Anti-CCP is seen in what condition?

A

RA

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3
Q

Positive dsDNA is seen in what condition?

A

SLE

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4
Q

Positive Anti-SM is seen in what condition?

A

SLE

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5
Q

Positive anti-Ro is seen in what condition?

A

SLE; Sjogren’s

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6
Q

Positive anti-La is seen in what condition?

A

Sjogrens

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7
Q

Anti-centromere Abs being positive is suggestive of what condition?

A

Systemic sclerosis (limited)

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8
Q

Anti-Scl70 Ab being positive is indicative of what condition?

A

Systemic sclerosis (diffuse)

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9
Q

What does anti-Jo1 Ab suggest?

A

Myositis

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10
Q

What does positive Anti-cardiolupin Ab suggest?

A

Anti-Phospholipid Syndrome

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11
Q

What does positive Lupus anticoagulant suggest?

A

Anti-phospholipid syndrome

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12
Q

What does positive Lupus anticoagulant suggest?

A

Anti-phospholipid syndrome

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13
Q

What is the difference between cANCA and pANCA?

A

Two types of ANCA, each target a different protein within the cytoplasm of neutrophils and monocytes.

pANCA targets MPO

cANCA targets PR3

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14
Q

What group of conditions are present if ANCA Abs are present?

A

Small vessel vasculitis (GPA; EGPA; MPA)

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15
Q

State 3 RFs for SLE.

A
  • Female sex
  • Young onset: 15-45 years
  • Drugs: Procainamide/Sulfasalazine/Isoniazid/ Phenytoin/ Carbamazepine
  • Infection: EBV
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16
Q

How may Lupus present?

A
  • Fever
  • Tiredness
  • Weight loss
Skin
•	Butterfly rash: cheeks + bridge of nose 
•	Vasculitic lesions
•	Urticaria 
•	Photosensitivity
•	Alopecia 
Nervous system
•	Epilepsy
•	Migraine
•	Cerebellar ataxia
•	CN lesions
•	Polyneuropathy

Lungs
• Pleurisy/ pleural effusion

CV
•	Pericarditis/ Pericardial effusion 
•	Myocarditis 
•	Thrombosis 
•	Atherosclerosis 
GI
•	Abdominal pain
•	Vomiting
•	Diarrhoea
•	Dysphagia
•	Mesenteric vasculitis

Kidneys
• Glomerulonephritis

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17
Q

What skin lesion is typically present in Lupus?

A

Butterfly rash on cheeks and nasal bridge. Rash is photosensitive.

Urticaria

Vasculitis lesions

Alopecia

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18
Q

What blood test(s) are clinically suggestive of SLE?

A

• Antibodies: Anti-dsDNA; ANA; Anti-Ro; Anti-La and Anti-RNP may be seen in SLE

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19
Q

How do you treat SLE with joint symptoms and systemic disease?

A 
•	Anti-malarial: Hydroxychloroquine 
\+
•	NSAIDs: Ibuprofen/Naproxen
\+
•	Corticosteroids: Prednisolone

± (Systemic disease)
• Immunosuppressants: Azathioprine/ Mycophenolate mofetil

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20
Q

How would you treat SLE which causes severe organ disease?

A

Severe Organ Disease
• IV Steroids
+
• Cyclophosphamide

and seek help from HDU

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21
Q

Describe Sjogrens syndrome.

A

Autoimmune disease featuring immunologically mediated destruction of epithelial exocrine glands via lymphocytic infiltration which also causes polyarthritis. Sjogrens syndrome may be primary or secondary to another autoimmune disorder – SLE, RA.

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22
Q

How may Sjogrens syndrome present?

A
  • Dryness of the mouth (xerostomia)
  • Dry eyes (keratoconjunctivitis sicca)
  • Parotid gland swelling (parotitis)
  • Arthralgia and fatigue
  • Raynaud’s Phenomenon
  • Angular stomatitis may occur
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23
Q

What are the diagnostic criteria for Sjogren’s Syndrome?

A

4 or more of:
• Ocular symptoms- dry eyes > 3 months (keratoconjunctivitis sicca), foreign body sensation, use of tear substitutes > 3 x daily
• Ocular signs- Schirmer’s test performed without anaesthesia (essentially see how wet some filter paper gets)
• Oral symptoms-dry mouth, recurrently swollen salivary glands, liquids aids used to swallow
• Oral signs- abnormal salivary scintigraphy
• Autoantibodies: Anti-Ro or Anti La antibodies

Mnemonic: Eyes, (Anti-)Ros and Mouth

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24
Q

What are the diagnostic criteria for Sjogren’s Syndrome?

A

4 or more of:
• Ocular symptoms- dry eyes > 3 months (keratoconjunctivitis sicca), foreign body sensation, use of tear substitutes > 3 x daily
• Ocular signs- Schirmer’s test performed without anaesthesia (essentially see how wet some filter paper gets)
• Oral symptoms-dry mouth, recurrently swollen salivary glands, liquids aids used to swallow
• Oral signs- abnormal salivary scintigraphy
• Autoantibodies: Anti-Ro or Anti La antibodies

Mnemonic: Eyes, (Anti-)Ros and Mouth

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25
Q

State the name of the test for eye dryness in Sjogrens syndrome.

A

Schirmer test

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26
Q

What does a Schirmer test consist of?

A

Schirmer’s test performed without anaesthesia (essentially see how wet some filter paper gets)

Filter paper placed in lower conjunctival sac with positive being < 5mm

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27
Q

How do you manage Sjogrens syndrome?

A
  • Artificial tears/lubricating eye drops
  • Pilocarpine- can stimulate salivary gland production (however also produces flushing)
  • Hydroxychloroquine can help with arthralgia and fatigue
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28
Q

What are the side effects of Pilocarpine?

A

Cholinergic parasympathomimetic agent thus SLUDGE

Sweating 
Lacrimation
Urinary disorders
Defaecation 
GI upset 
Emesis

Flushing of skin

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29
Q

Describe Scleroderma.

A

Autoimmune disorder which affects multiple systems involving the activation of immune system featuring upregulation of adhesion molecules (VCAM, E-selectin, ICAM-1) which stimulates production of ECM via fibroblasts yielding abnormal connective tissue growth.

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30
Q

What type of molecules are upregulated in systemic sclerosis?

A

Upregulation of adhesion molecules - VCAM, E-selectin, ICAM-1 thus ECM production via fibroblasts

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31
Q

What are the two types of Scleroderma?

A
  • Limited: Begins in hands, fingers, face and progresses to body (Anti-Centromere)
  • Diffuse: Less common but more aggressive; earlier organ involvement with arthralgia and myalgia occurring as well as pulmonary disease and cardiac disease (Anti-Scl70)
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32
Q

What are the pentad of features in Limited Systemic Sclerosis?

A

CREST

Calcinosis cutis

Raynaud’s

Oesophageal dysmotility

Sclerodactyly

Telangiectasia

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33
Q

What symptoms may be present in diffuse scleroderma (in addition to limited scleroderma)?

A

Diffuse Scleroderma
• Cough
• SOBE
• Rales at lung bases

  • Dysphagia
  • Heartburn/Reflux
  • Bloating
  • Malabsorption
  • Bowel dysmotility
  • Esophageal dysmotility
  • Arthralgia
  • Inflammatory arthritis
  • Myositis
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34
Q

What investigation may confirm oesophageal dysmotility in Systemic Sclerosis?

A

• Barium swallow: Reduced peristalsis; Gastroparesis; Reduced sphincter tones; Strictures

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35
Q

What investigation may confirm thoracic involvement in Systemic Sclerosis?

A

• CXR: Interstitial infiltrates; Cardiomegaly

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36
Q

What autoantibodies will be positive in Systemic Sclerosis?

A

• Serum auto-antibodies: ANA; Anti-Scl70 (anti-topoisomerase I) positive = diffuse; Anticentromere Ab positive = limited

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37
Q

How would you manage Systemic Sclerosis?

A

Tx dependent on Sx and Organ involvement

Renal Crisis
• ACEi: Captopril/ Enalapril/ Lisinopril
+
• Antihypertensives: CCBs (Lercanidipine)

2nd
• RRT: Dialysis or Transplant

Raynaud’s phenomenon
• Supportive: Exercise/Warmth
+
• CCB: Nifedipine

± (Ulcers)
• PDE5: Sildenafil

GI
• PPI: Omeprazole/ Esomeprazole

± (Gastroparesis)
• Prokinetic agent: Domperidone/ Octreotide

Myopathy/ Synovitis/ Arthritis
• Oral corticosteroid: Prednisolone

Interstitial lung disease
•	Immunomodulator: Cyclophosphamide/Mycophenolate mofetil/Azathioprine
\+ 
•	Oral corticosteroid: Prednisolone 
\+
•	Oxygen

Cardiac arrhythmia
• Antiarrhythmics

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38
Q

How may you medically treat Raynaud’s Phenomenon?

A

Nifedipine

Sildenafil

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39
Q

How may you manage ILD in Diffuse Systemic Sclerosis?

A 
•	Immunomodulator: Cyclophosphamide/Mycophenolate mofetil/Azathioprine
\+ 
•	Oral corticosteroid: Prednisolone 
\+
•	Oxygen
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40
Q

Describe Antiphospholipid Syndrome.

A

Autoimmune disease caused by antibodies targeting the phospholipid cell membrane which causes arterial and venous thrombosis. This can be primary or secondary to other immune disorders.

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41
Q

How may Antiphospholipid Syndrome present?

A
  • Stroke
  • TIA
  • MI
  • Valvular heart disease
  • DVT
  • Budd-Chiari Syndrome (occlusion of hepatic veins  ascites, abdo pain + hepatitis)

• Recurrent miscarriages = 3≤

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42
Q

What is the triad of clinical features observed in Budd-Chiari Syndrome?

A

Ascites

Abdominal Pain

Hepatomegaly

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43
Q

What would bloods show in a patient with Anti-Phospholipid Syndrome?

A

• APTT: Increased
• FBC: Thrombocytopenia
• Antibodies: Anti-cardiolipin; Lupus anticoagulant (LA)
-> LA is an autoimmune phospholipid antibody

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44
Q

Which clotting pathway is increased in Anti-phospholipid syndrome?

What blood test reflects this?

A

Intrinsic

APTT thus problem with clotting factors 8, 9, 11 and 12

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45
Q

How do you manage a patient with Antiphospholipid Syndrome?

A

Aspirin 75mg

Warfarin

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46
Q

How do you manage Anti-phospholipid syndrome in a pregnant woman?

A

LMWH 1mg/kg (‘check BNF’)

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47
Q

Describe Polymyositis and Dermatomyositis.

A

Autoimmune disorder featuring necrosis of skeletal muscle fibres (polymyositis) and/or skin (dermatomyositis) which is of unknown aetiology (idiopathic) characterised by proximal muscle weakness, myalgia, dysphagia, SOB and Shawl sign (V-shaped superior truncal rash), Heliotrope rash (reddish purple rash around eyelids), Gottron’s papules (violaceous bumps on outside of joints)

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48
Q

What classic dermatological clinical features of Dermatomyositis are there?

A

Gottron’s papules

Shawl Sign

Heliotrope rash

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49
Q

What is the term for the rash around the eyes in Polydermatomyositis?

A

Heliotrope rash

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50
Q

What is the term for the V-shaped truncal rash in Polydermatomyositis?

A

Shawl sign

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51
Q

What is the term for violaceous bumps on the outside of the joints?

A

Gottron’s papules

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52
Q

What investigations would you run in a suspected case of polymyositis/dermatomyositis?

A

• Muscle biopsy: T-cell infiltration and necrosis
• Serum muscle enzymes (CK; ALT; aldolase): Elevated
• Abs: Anti-JO positive; ANA positive; anti-SRP positive
-> Antisynthetase Ab = Anti-Jo (Ab in polymyositis and ILD); Anti-signal recognition particle = Anti-SRP (present in necrotising myopathy)
• ESR: Normal; Raised
• EMG: characteristic changes
• MRI: Muscle inflammation

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53
Q

How do you treat an acute bout of Polymyositis/Dermatomyositis?

A

Oral corticosteroids: Prednisolone 1/12

Immunosuppressants: Azathioprine/ Methotrexate/ Ciclosporin

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54
Q

Describe Undifferentiated Autoimmune Rheumatic Disease.

A

Seropositive inflammatory arthritis which combines features of more than one arthritic rheumatoid disease.

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55
Q

What clinical feature is almost always present in Undifferentiated Autoimmune Rheumatic Disease?

A

Raynaud’s (90%)

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56
Q

Describe Rheumatoid Arthritis.

A

Chronic inflammatory condition affecting small joints of hands and feet which is characterised by joint pain, swelling and persistent morning swelling resulting in reduced mobility and reduced quality of life.

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57
Q

What finger swellings are more prevalent in RA? Which joint do these impact?

A

Bouchard’s Nodes

PIP

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58
Q

Which deformities may be present in RA? Describe the joints and the deformity in each example.

A
  • Swan neck deformity: DIP hyperflexion + PIP hyperextension
  • Boutonniere’s deformity: DIP hyperextension + PIP hyperflexion
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59
Q

Outline the clinical features of Felty’s Syndrome.

A

Splenomegaly

RA

Neutropenia

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60
Q

The presence of pneumoconiosis and RA is termed…

A

Caplan Syndrome

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61
Q

What investigations would you order in an individual with suspected RA?

A
  • Rheumatoid factor (RF): Positive
  • Anti-cyclic citrullinated peptide (anti-CCP) Ab: Positive
  • XR/CT: Erosions
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62
Q

How may you manage RA?

A

• DMARDs: Methotrexate/ Sulfasalazine/ Leflunomide

±
• Corticosteroid: Prednisolone
+
• NSAID: Ibuprofen/Naproxen/ Diclofenac

Pregnancy
• Corticosteroid: Prednisolone

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63
Q

Describe what a Seronegative Arthritis is.

A

Umbrella term for conditions associated with predilection for axial (spinal and sacroiliac) inflammation with asymmetrical peripheral arthritis, in the absence of antibodies (seronegative) with enthesis inflammation.

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64
Q

Describe ankylosing spondylitis.

A

Type of seronegative Spondyloarthritis which is a chronic, progressive disease characterised by severe pain, spinal stiffness, fatigue, sleep disturbance, SI joint tenderness and kyphosis.

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65
Q

What is the term of the diagnostic criteria used in Ankylosing Spondylitis?

A

Calin Criteria

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66
Q

Outline the Calin Criteria.

A
  • Age < 40 years
  • Back pain > 3 months
  • Insidious onset
  • Improves with exercise
  • Early morning stiffness
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67
Q

What gene mutation is strongly associated with ankylosing spondylitis?

A

HLA-B27

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68
Q

Outline the presentation of Ankylosing Spondylitis.

A
  • Inflammatory back pain: Early morning back stiffness; improves with exercise; insidious onset; back pain > 3 months
  • Fatigue
  • SI joint tenderness
  • Kyphosis:
  • Enthesitis
  • Iritis/Uveitis
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69
Q

What investigations would have positive findings in Ankylosing Spondylitis?

A
  • CRP: Raised
  • XR-Pelvis: Sacroiliitis
  • XR-Cervical/Thoracic/Lumbar spine (lateral): erosions; sclerosis; syndesmophytes; bamboo spine (late disease)
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70
Q

How would you manage Ankylosing Spondylitis?

A

• Supportive: Stretches/ Group sessions/ Assess for CV risk
+
• NSAIDs: Naproxen/ Ibuprofen

± (Local IA inflammation/enthesitis)
• IA Corticosteroid injection: Hydrocortisone

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71
Q

How would you manage Ankylosing Spondylitis in the case of peripheral joint involvement?

A

DMARDs

Biologics

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72
Q

What are the guidelines for using Biologics in Ankylosing Spondylitis?

A

• Biologics: Adalimumab/ Infliximab/ Etanercept

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73
Q

Describe Psoriatic Arthritis.

A

Type of seronegative inflammatory arthritis which is associated with psoriasis characterised by joint pain, joint stiffness, history of psoriasis and family history of psoriasis.

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74
Q

What is Arthritis Mutilans?

A

Deformity of joints of hands and feet, usually in conjunction with Psoriatic Arthritis, resulting in shortening of digits due to deformity at MCP and IP joints resulting in retraction of skin transversely into the space left - known as ‘opera glass’ hands or feet.

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75
Q

How may Psoriatic Arthritis present?

A
  • Joint pain: prolonged morning stiffness ≥ 30 minutes; improves with use; worsened with prolonged rest
  • Joint stiffness
  • Dactylitis (uniform swelling of entire digit)
  • Entheseal inflammation (pain at site of tendon attachment)
  • Spinal stiffness + reduced ROM: Schober test
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76
Q

What investigations may suggest Psoriatic Arthritis?

A

Seronegative, unremarkable joint fluid aspirate and radiological finds on XR

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77
Q

How would you manage Psoriatic Arthritis?

A

Supportive: Physiotherapy; Exercise

Medical: NSAIDs; DMARDs; Steroids IA; Biologics

Surgery: joint fusion; arthroplasty

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78
Q

Describe Reactive Arthritis?

A

Inflammatory, seronegative arthritis occurring after exposure to GI and GU infections characterised by joint pain, joint stiffness and possibly a classical post-infectious triad (Reiter’s Syndrome): arthritis, urethritis and conjunctivitis

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79
Q

Outline the 3 clinical features of Reiter’s Syndrome.

A

Arthritis

Uveitis

Conjunctivitis

‘Can’t see, can’t wee, can’t climb a tree’

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80
Q

How may Reactive Arthritis present?

A
  • Joint pain
  • Joint stiffness
  • Skin rash: Keratoderma blenorrhagicum (vesicular lesion becoming plaque/pustular on volar surfaces)
  • Circinate balanitis (painless ulcers on glans of penis)
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81
Q

How may Reactive Arthritis be diagnosed?

A

Clinical diagnosis

Aided by exclusion of other differentials… seronegative; unremarkable arthrocentesis

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82
Q

How may you manage Reactive Arthritis?

A

NSAIDs

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83
Q

How may enterohepatic arthritis present?

A
  • Joint pain: Mono (one joint) or Oligoarthritis
  • Joint stiffness

• Known diagnosis of UC or CD

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84
Q

What investigations may aid your diagnosis of Enterohepatic arthritis?

A
  • Arthrocentesis: Negative; Sterile
  • Rheumatoid factor: Negative
  • CRP: Elevated
  • XR: Erosions
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85
Q

How would you manage enterohepatic arthritis?

A 
•	DMARD: Methotrexate/ Sulfasalazine/ Leflunomide 
±
•	Corticosteroids: Prednisolone 
±
•	Analgesia: Ibuprofen/ Naproxen
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86
Q

UVB converts 7-dehydrocholesterol into?

A

Cholecalciferol

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87
Q

Where is cholecalciferol stored?

A

WAT

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88
Q

Where is Cholecalciferol activated?

A

Liver, by 25-alpha hydroxylase

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89
Q

What converts cholecalciferol to 25-hydroxycholecalciferol?

A

25-alpha hydroxylase

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90
Q

What is the location for the formation of calcitriol?

A

Kidneys

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91
Q

What is the reactant used to convert 25-hydroxycholcalciferol into calcitriol?

A

1 alpha hydroxylase

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92
Q

Describe Osteoporosis.

A

Bone disease caused by reduction in bone mass and micro-architectural deterioration of bone tissue leading to fragility and increased fracture risk

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93
Q

Outline the difference between osteopenia and osteoporosis.

A

Osteopenia is a reduced bone mass between -1 to -2.5 SDs whilst Osteoporosis is a reduced bone mass greater than -2.5 SDs

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94
Q

State 5 RFs for Osteoporosis.

A
  • Female sex
  • Caucasian
  • Increasing age
  • Hypogonadism
  • FHx Hip Fx
  • Disease: DM; Multiple myeloma; Cushing’s syndrome; Hyperthyroidism; Hyperparathyroidism
  • Immobilisation
  • Low BMI
  • Smoking
  • Alcohol abuse
  • Vitamin D intake
  • Drugs: Heparin/Ciclosporin/ Anticonvulsants
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95
Q

How may Osteoporosis present?

A
  • Fractures: Vertebral/ Proximal femur/ Distal radius (Colles’ Fx)
  • Kyphosis
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96
Q

What is the gold standard investigation for Osteoporosis?

A
  • DEXA: T-score < 2.5 SDs

* XR: Osteopenia; Fx

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97
Q

What tool is used to assess Osteoporotic fracture risk?

A

FRAX Score

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98
Q

How may you manage a patient with Osteoporosis?

A

Bisphosphonates are first line with Vitamin D and Calcium as an Adjunct.

Second line is Denosumab, a RANKLi

If there is a high risk fracture and vertebral fractures, PTH-R antagonist Teriparatide could be used

In a postmenopausal woman, Oestrogen may be added

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99
Q

When might you use Teriparatide in an Osteoporotic patient?

A

High risk fractures with T-Score <3 and vertebral fractures

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100
Q

Describe Osteopetrosis.

A

Condition caused by reduced bone resorption by osteoclasts leading to craniofacial abnormalities, chest wall deformities and skeletal enlargement

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101
Q

List some clinical features of Osteopetrosis.

A
  • Facial nerve paralysis
  • Macrognathia
  • Teeth infections
  • Vision loss
  • Deafness
  • Cranial nerve palsies
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102
Q

What is the gold standard investigation for Osteopetrosis?

A

DEXA

XR

103
Q

Outline the management for a patient with osteoporosis.

A 
•	Analgesia: Ibuprofen
\+
•	Corticosteroids: Prednisolone
\+
•	Vitamin D: Ergocalciferol 
±
•	Surgery
104
Q

In adults, what is hypomineralisation of the bone secondary to vitamin D deficiency called?

A

Osteomalacia

105
Q

In children, hypomineralisation of the bone secondary to Vitamin D deficiency is termed?

A

Rickets Disease

106
Q

How may Osteomalacia/Rickets present?

A
  • Proximal muscle weakness

* Bone deformities: bowing + genu valgum

107
Q

What investigations would you order in a patient with suspected Osteomalacia?

A
  • Vitamin levels: OHD low
  • Serum biochemistry: ALP high
  • XR: Defective mineralization; Looser’s pseudofractures (low-density bands perpendicular to cortex) seen in pelvis and femur
108
Q

What is the term for low-density bands seen perpendicular to the cortex as a clinical feature of Osteomalacia?

A

Looser’s Pseudofractures

109
Q

How would you manage Osteomalacia?

A

• Vitamin replacement: 25-hydroxyvitamin D at 50 000U for 8/52

110
Q

What is the second treatment of choice for Osteomalacia?

Why may someone use this?

A

Ergocalciferol (Vitamin D2(

Cultural, dietary or religious - does not contain gelatine

111
Q

State some side effects of Vitamin D.

A

Abdominal pain
Headache
Nausea
Skin reactions

112
Q

What disease features aberrant remodelling due to osteoclast resorption and osteoblast deposition causing weaker bone with sclerotic and lytic areas observed on XR.

A

Paget’s disease of the bone

113
Q

Outline the clinical features of Paget’s disease.

A
  • Bone pain
  • Deformities: skull enlargement; tibial bowing
  • Nerve compression: Deafness; paraparesis
  • Fractures
  • Osteogenic sarcoma
  • High-output cardiac failure
114
Q

Outline the process by which high-output cardiac failure may occur in Paget’s disease.

A

Hyperactive osteoblasts deposit new bone matrix which is hyperperfused thus increased blood flow there, reducing blood in systemic circulation hence reduced EDV and F-S Principle compromised

115
Q

How do you manage Paget’s Disease?

A

• Bisphosphonates: Zoledronate

116
Q

What investigations would positively identify Paget’s disease?

A
  • Bone markers: ALP raised; Normal Calcium; Normal Phosphate
  • XR: Bone enlargement; distortion; sclerotic changes; osteolytic areas
  • Radionuclide bone scan: Increased uptake of bone-seeking radionuclides
117
Q

Describe osteonecrosis.

A

Bone disease causing death of bone and marrow cells due to hypoperfusion

118
Q

Outline 3 causes of osteonecrosis.

A
  • Drugs: Glucocorticoids/ Bisphosphonates
  • Sickle cell disease
  • Trauma
  • Radiation
  • HIV infection
119
Q

Describe Osteochondritis dissecans.

A

Idiopathic subchondral bone lesion causing sequestration of bone and instability – generally in young, athletic patients.

120
Q

What are the clinical features of Osteochondritis dissecans.

A
  • Pain:  on activity; ankle/ knee/ heel
  • Effusion
  • Crepitus
  •  ROM
  • Young patient
121
Q

How may you manage Osteochondritis Dissecans?

A

Stable
• Conservative: Ibuprofen ± Paracetamol; physiotherapy; technique correction

Unstable
• Surgery: Arthroscopy

122
Q

What is Hyperparathyroidism?

A

Endocrine cause of bone disease featuring excessive secretion of parathyroid hormone (PTH) from the parathyroid gland which can be categorized into primary, secondary or tertiary dependent on biochemical abnormalities and aetiology.

123
Q

Describe Hyperparathyroidism.

A

Endocrine cause of bone disease featuring excessive secretion of parathyroid hormone (PTH) from the parathyroid gland which can be categorized into primary, secondary or tertiary dependent on biochemical abnormalities and aetiology.

124
Q

How do the types of Hyperparathyroidism differ from eachother?

A
  • 1º: Hyperactive PT gland = RANKL secreted to RANK on Oc = activation thus osteoclast resorption yielding elevated Ca2+, elevated PTH, low Pi
  • 2º: Low calcium feedback to PT gland thus PTH elevated, Ca2+ low, Pi normal and ALP may be elevated
  • 3º: Untreated secondary hyperparathyroidism causes chronic elevated PTH, elevated Ca2+ and elevated Pi and ALP
  • Malignant HyperPT: Squamous cell carcinoma of lung or renal cell carcinoma produces PTH-p to elevated Ca2+
125
Q

A solitary adenoma secreting excess parathyroid hormone would be what type of Hyperparathyroidism?

A

Primary

126
Q

Chronically untreated parathyroid cancer would be classified as what type of Hyperparathyroidism?

A

Tertiary

127
Q

Dietary deficiency detected by low Ca2+ and elevated PTH would be what type of hyperparathyroidism?

A

Secondary

128
Q

Give an example of a cancer which may cause malignant hyperparathyroidism.

A

Breast
Lung - Squamous Cell Carcinoma
Renal
Multiple Myeloma

129
Q

What are the clinical features of hyperparathyroidism.

A
  • Fatigue
  • Malaise
  • Depressed
  • Thirsty
  • Dehydrated
  • Renal stones
  • Abdominal pain
  • Pancreatitis
  • Ulcers (duodenal > gastric)
130
Q

What electrolyte and hormone patterns are seen in primary hyperparathyroidism regarding?

A

Elevated PTH
Elevated Calcium
ALP high
Pi decreased (normal in CKD)

131
Q

What electrolyte and hormone patterns are seen in secondary hyperparathyroidism regarding?

A

PTH: Elevated
Ca: Low
ALP: N
Pi: N

132
Q

What electrolyte and hormone patterns are seen in tertiary hyperparathyroidism regarding?

A

PTH: High
Ca: Elevated
ALP: Elevated
Pi: Elevated

133
Q

How would you treat primary hyperparathyroidism?

A

• Conservative: Fluid intake (reduce calculi)
+
• Cinacalet

+
Tx cause

134
Q

How would you manage secondary hyperparathyroidism?

A 
•	Tx underlying condition 
\+
•	Hyperphosphatemia: Binders/ Diet (Calcium acetate; Ferric citrate)
\+
•	Vitamin D intake
135
Q

How would you treat tertiary hyperparathyroidism?

A 
•	Surgery
\+ 
•	Hyperphosphatemia: Binders/ Diet
\+
•	Vitamin D intake
136
Q

Describe gout.

A

Syndrome caused by hyperuricemia and deposition of urate crystals causing attacks of inflammatory arthritis

137
Q

State 3 RFs for Gout.

A
  • Older age
  • Male
  • Consumption of meat, seafood and alcohol
  • Use of diuretics
  • Drugs: Cyclosporine (urate reabsorption)/ Pyrazinamide (urate reabsorption)/ NSAIDs (reduce GFR)
138
Q

How does cyclosporine increase your risk of gout?

A

Increased urate reabsorption/reduced renal excretion

139
Q

How does pyrazinamide increase the risk of gout?

A

Reduced urate reabsorption

140
Q

How do NSAIDs increase the risk of gout?

A

Reduced eGFR

141
Q

Outline the pathophysiology of Gout.

A

• Uric acid super-saturation = crystal formation -> DAMPs bind to macrophages and PRRs -> inflammatory response featuring TNF-a; IL-1ß; IL-8 and neutrophil influx

142
Q

Outline the clinical features of gout.

A
  • Severe pain: Rapid onset;
  • Joint stiffness: Distributed in the feet (1st MCP/TMT and ankle); Monoarticular or oligoarticular (< 4 joints)
  • Joint swelling
  • Joint effusion
  • Tenderness
  • Tophi: Present on extensor surface joints – e.g. hands, elbows, knees, Achilles tendons
143
Q

What investigation would you order for suspected cases of gout?

A

• Arthrocentesis: Leukocytosis; Needle-shaped crystals

144
Q

How do you manage an acute episode of gout?

A

• NSAIDs: Naproxen/Ibuprofen/Diclofenac/ Celecoxib

145
Q

How do you treat recurrent gout?

A

• Xanthine oxidase inhibitors: Allopurinol
+
• Uric Acid Transporter Inhibitor: Lesinurad
+
• NSAIDs: Naproxen/Ibuprofen/Diclofenac/ Celecoxib

146
Q

Describe Pseudogout.

A

Type of seronegative, inflammatory arthritis which is a crystal arthritis caused by deposition of calcium pyrophosphate (CPP) crystals

147
Q

State 3 RFs of Pseudogout

A
  • Advanced age
  • FHx of CPPD
  • Hypomagnesemia
  • Hypophosphatemia
  • Hyperparathyroidism
  • Wilson’s Disease
148
Q

Outline the clinical presentation of pseudogout.

A
  • Joint pain
  • OA-like involvement: wrists/shoulders/knee
  • Exacerbation of OA
  • Joint effusion
  • Erythema
  • Swollen joint
149
Q

What would the investigations and results would you anticipate in a case of Pseudogout?

A
  • Arthrocentesis: Rhomboid-shaped crystals
  • XR: Linear deposits in fibro-cartilage or hyaline articular cartilage (chondrocalcinosis); rapid joint degeneration
  • Serum Calcium: Normal; Elevated
  • Serum PTH: Normal; Elevated
  • Serum Mg: Normal; Elevated
150
Q

How do you manage Pseudogout?

A

Acute
• NSAIDs: Naproxen/ Diclofenac
±
• Analgesia: Paracetamol

± (Monoarticular disease)
• IA Corticosteroids: Dexamethasone

Chronic
•	Surgery: Joint replacement 
±
•	NSAIDs: Naproxen/ Diclofenac
± 
•	Analgesia: Paracetamol
151
Q

How may Vasculitides be classified?

A
  • Vessel size
  • ANCA
  • IgE
152
Q

Define Takayasu’s Arteritis.

A

Chronic progressive, inflammatory disease of the aorta causing occlusion. Takayasu’s arteritis commonly affects young females (15-35).

153
Q

Outline the clinical features of Takayasu’s Arteritis.

A
  • Systemic Sx: Fever, malaise, fatigue
  • Claudication pain
  • Tenderness on palpation of artery
  • Bruit
  • Loss of pulses
154
Q

How do you manage Takayasu’s arteritis?

A

• Corticosteroids: Prednisolone 40-60mg

± (Stenosis)
• Surgery: Angioplasty

155
Q

Define Polymyalgia Rheumatica.

A

Chronic inflammatory condition of the large vessels of unknown cause characterised by bilateral proximal muscle stiffness (neck and shoulders) and ache affecting > 50 age group

156
Q

Outline the clinical features of Polymyalgia Rheumatica.

A
  • Morning stiffness >1 hour; improve in day
  • Myalgia: hip and shoulder girdle
  • Systemic Sx: Fever, malaise, weight loss
  • Often associated with GCA
157
Q

What investigation and result is suggestive of Polymyalgia Rheumatica in clinical context.

A
  • ESR: Elevated

* CRP: Elevated

158
Q

How do you manage Polymyalgia Rheumatica.

A
  • Corticosteroids: Prednisolone 15mg

* Bone protection: Vitamin D; Alendronic acid

159
Q
  1. Condition involving transmural inflammation of all 3 arterial layers with lymphocytes, macrophages and multinucleate giant cells.
  2. Clinical features (3)
  3. Gold standard investigation (1)
  4. Investigation to confirm (2)
  5. Treatment
A
  1. GCA
  2. Headache; Scalp tenderness; Visual changes; Jaw claudication
  3. ESR
  4. Biopsy of temporal artery
  5. Corticosteroids
160
Q

Cough, haemoptysis, malaise and oral ulceration featuring a blood film of schistocytes, haematuria, cANCA and Granulomas in the kidneys.

Diagnosis?

Clinical Features?

Ix to order?

Tx?

A

Granulomatosis with Polyangiitis (Wegener’s Syndrome)

  • Cough
  • Chest pain: Pleurisy
  • SOB
  • Haemoptysis
  • Malaise
  • Arthralgia
  • Haematuria
  • Purpura
  • Oral ulceration
  • Pleural effusion
  • Conjunctivitis

Urinalysis; Bloods; Abs; Autoantibodies; CXR; Kidney biopsy

Immunosuppressants - cyclophosphamide and prednisolone

161
Q

Patient presenting with a cough, SOBE, haemoptysis and purpura on the leg. IgE is raised on bloods and ANCA is positive.

Diagnosis?

Triad of features?

Management?

A

Churg-Strauss Syndrome

Asthma + Eosinophilia + Vasculitis

Prednisolone

162
Q

Young adult presenting with purpuric rash on buttocks, abdominal pain and vomiting. Usually well, last had a cold 2 weeks ago. IgA is positive and urinalysis shows blood and protein.

Diagnosis?

Treatment?

A

IgA Nephropathy/ HSP

Supportive - NSAIDs/ Anti-emetics/ Fluids

163
Q

Patient presents with distal fingers being blue, dry eyes and dry mouth, a rash along the legs. Bloods show proteins which precipitate in the cold. Urinalysis shows nephritic syndrome.

Diagnosis?

Name of proteins?

Name of group of symptoms featuring dryness.

Treatment?

A

Cryoglubulinaemic vasculitis

Cryoglobulins

Sicca symptoms - keratoconjunctiva sicca; xerostomia; hypohydrosis

• Antivirals: Grazapravir + Elbasavir
+
• Corticosteroids: Prednisolone

164
Q

Patient of Turkish descent presents with ulcers

A
165
Q

35 y/o F with asymmetrical pain and stiffness in the fingers and feet with plaques on the extensor surface of elbow and some nail changes.

What is your diagnosis?

What are the nail changes observed?

What us the term for inflammation of an entire digit?

What may the most severe form with osteolysis and telescoping of the digits cause?

A

Psoriatic arthritis

Nail pitting; Onycholysis

Dactylitis

Arthritis mutilans

166
Q

What are the causes of trochanteric bursitis?

A

Trauma

Inflammatory

Infection

Friction

167
Q

What special test is used to assess hip weakness?

A

Trendelenberg Test

168
Q

What movements elicit pain in trochanteric bursitis?

A

Abduction

Internal rotation

External rotation

169
Q

What are the key radiographic features for OA?

A

Mnemonic: LOSS

Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts

170
Q

In Arthritis, swelling of the joints furthest along the fingers are known as?

A

Heberden’s Nodes

171
Q

In Arthritis, swelling of the joints nearest along the fingers are known as?

A

Bouchards’s nodes

172
Q

How is OA managed?

A

Supportive: weight loss; patient education; physiotherapy; orthotics
+
Medical: Oral analgesia; Topical analgesia; IA injections
±
Surgery: TKR; HA; HTO

173
Q

Which is the most common gene association with RA?

A

HLA DR4

174
Q

In which proportion of patients is RF positive?

A

70%

175
Q

A 25 year old female presents with joint pain in her knuckles. The pain is present in the morning and improves as the day goes on. The pain lasts 1-2 days then resolves. These episodes have been happening for several months.

She is positive for anti-CCP and RF.

What is your diagnosis?

A

Palindromic Rheumatism - likely to develop full rheumatoid arthritis

176
Q

Outline the process by which Boutonnieres deformity occurs.

A

Tear in the central slip of extensor components of fingers.

When patients straighten fingers, lateral tendon around the PIP pull on the distal phalynx thus DIPs extend and and PIP flex

177
Q

What is the referral criteria for Rheumatoid Arthritis?

A

Persistent synovitis > 3 months = MSK referral

178
Q

How is rheumatoid arthritis managed?

A

Supportive: Referral; Review; Exercise; Physiotherapy
+
Medical: Methotrexate

2nd line = ± Hydroxychloroquine/Sulfasalazine

3rd line
Methotrexate + Adalimumab

4th line
Methotrexate + Ritixumab

179
Q

Which type of biologic is Adalimumab?

A

Anti-TNFa

180
Q

Which type of biologic is Infliximab?

A

Anti-TNFa

181
Q

Which type of biologic is Rituximab?

A

Anti-CD20

182
Q

Which type of biologic is Sarilumab?

A

Anti-IL6

183
Q

Which type of biologic is Tocilizumab?

A

Anti-IL6

184
Q

Which type of biologic is Tofacitinib?

A

JAKi

185
Q

Which drug is taken as an adjunct when on Methotrexate?

A

Folic acid 5mg - take on a different day to the methotrexate

186
Q

List 5 common side effects of Methotrexate.

A 
Anaemia 
Anorexia 
Diarrhoea/Vomiting 
Nausea 
Headache
GI discomfort
Leucopaenia - infections 
Pulmonary fibrosis 
Teratogenesis 
Hepatotoxicity
187
Q

What are the side effects of Leflunomide?

A 
Mouth ulcers
Rashes
Peripheral neuropathy
Liver toxicity 
Bone marrow suppression and leukopenia
Teratogenic
188
Q

What effect can Salfasalazine have on male sexual health?

A

Reduced sperm count

189
Q

What are the side effects of hydroxychloroquine?

A

Nightmares
Reduced visual acuity (macular toxicity)
Liver toxicity
Skin pigmentation

190
Q

What are the side effects of Rituximab?

A

Rituximab is a monoclonal antibody against CD20 protein on B cells

Vulnerability to severe infections
Night sweats
Thrombocytopaenia
Liver and lung toxicity 
Peripheral neuropathy
191
Q

Destruction of a whole joint due to severe psoriatic arthritis is known as?

A

Arthritis Mutilans

192
Q

What are the different patterns in Psoriatic Arthritis?

A

Symmetrical - similar to RA, hands, wrist, ankles and DIP joints affected; mainly F

Asymmetrical - affects few joints (Pauciarthritis)

Spondylitic pattern: AA joint; back stiffness; sacroillitis; mainly M

193
Q

What tool may be used to assess risk fo Psoriatic Arthritis in a patient with Psoriasis?

A

Psoriasis Epidemiological Screening Tool (PEST)

194
Q

What are the clinical features of Reiter Syndrome?

A

Urethritis

Conjunctivitis

Arthritis

195
Q

Which gene is associated with reactive arthritis?

A

HLA B27 gene

196
Q

What is the management for reactive arthritis?

A

Tx cause
+
NSAIDs ± IA injection

197
Q

Which gene mutation is associated with Ankylosing Spondylitis?

A

HLA B27

198
Q

Advanced changes from ankylosing spondylitis may result in which radiographic feature being observed?

A

Bamboo spine due to fusion of the VBs

199
Q

What proportion of patients positive for HLAB27 gene will get ankylosing spondylitis?

A

2%

200
Q

What proportion of patients with ankylosing spondylitis have HLAB27 gene?

A

90%

201
Q

What are the referral criteria for back pain?

A

Age <20 or >50

Thoracic pain

Weight loss; Night sweats; Itch

Widespread neurology

Structural deformity/Trauma

CES: Saddle anaesthesia; Urinary retention; Faecal incontinence; Bilateral radiculopathy

202
Q

What clinical test is used to assess the spine in suspected Ankylosing Spondylitis?

A

Schober’s Test

L5 vertebrae to 10cm above

> 20cm = normal

203
Q

What skin changes are noted in SLE?

A

Photosensitive malar rash
Mouth ulcers
Raynaud’s Phenomenon

204
Q

Which autoantibodies are specific to SLE?

A

Anti-dsDNA

205
Q

Which criteria can help you make a diagnosis of SLE?

A

ACR

Positive ANA + clinical features of SLE

206
Q

What are some of the complications presenting with SLE?

A

Anaemia

Neuropsychiatric SLE - optic neuritis, transverse myelitis, psychosis

CVD
Pericarditis

VTE
Interstitial lung disease
Pleuritis

Lupus nephritis

Anaemia of chronic disease - leucopenia, neutropenia, thrombocytopenia

Recurrent miscarriages

207
Q

What is the first line treatment for mild SLE?

A

Hydroxychloroquine

208
Q

What is the risk of developing SLE in a patient with DLE?

A

<5%

209
Q

A 30 year old female patient presenting with lesions on the face, ears and scalp that are circular shaped and sensitive to light. There is some scarring alopecia and the areas can become hypo and hyperpigmented.

They are positive for dsDNA.

What is your most likely Ddx?

A

Discoid lupus erythematosus

210
Q

How do you manage DLE?

A 
Supportive: avoid sun; sunscreen
\+
Topical steroid 
\+
Intralesional steroid (hyperkeratotic)
211
Q

What are the two main types of Systemic Sclerosis?

A

Limited (anti-centromere) and Diffuse (anti-Scl70)

212
Q

What are the features of limited cutaneous systemic sclerosis?

A

Mnemonic: CREST

Calcinosis cutis
Raynaud's phenomenon 
Esophageal dysmotility
Sclerodactyly
Telangiectasia
213
Q

A patient is positive for anti-Scl70 Abs, what is your ddx?

A

Diffuse systemic sclerosis

214
Q

How can you examine the nail bed in suspected systemic sclerosis?

A

Nailbed microscopy

215
Q

Which investigations are key to making a diagnosis of Polymyalgia Rheumatica?

A

Clinical features
AND
Inflammatory markers - ESR, CRP, plasma viscosity

216
Q

How do you manage a patient with suspected polymyalgia rheumatica?

Outline the process

A

Steroids - do a steroid taper

15mg 1 week, see if reduces

When symptoms controlled fully, begin taper

12.5mg for 3-4 weeks

10mg for 4-6 weeks

Reduce by 1mg every 4-8 weeks

If relapse at an interval, escalate or stay.

217
Q

What aspects of oral prednisolone management must you consider?

A

Mnemonic: DONT STOP

Dont suddenly stop - Steroid dependent after 3 weeks thus risk of adrenal crisis.

Sick day rules

Treatment card

OP - bone protection

PPIs - GI protection

218
Q

Which artery is affected in Giant Cell Arteritis?

A

Temporal artery

219
Q

What gives a diagnosis of GCA?

A

Clinical diagnosis

Raised ESR >50mm/hour

Temporal biopsy: multinucleate giant cells

220
Q

What is the management of Giant Cell Arteritis?

A

40-60mg Prednisolone started immediately

Review in 48 hours

221
Q

Which antibodies are present in Dermatomyositits/Polymyositis?

A

Anti-Jo; ANA

222
Q

what is the target INR for a patient with Antiphospholipid Syndrome?

A

2-3

223
Q

What is Livedo Reticularis? Which condition is it associated with?

A

purple lace like rash that gives a mottled appearance to the skin

Antiphospholipid Syndrome

224
Q

How is gout diagnosed?

A

Clinically

Joint aspiration - monosodium urate crystals, needle-shaped crystals, negatively birefringent of polarised light

225
Q

What is the first line management of an acute gout flare up?

A

NSAIDs > Colchicine > Steroids

Secondary prevention: Lifestyle + Allopurinol; Febuxostat

226
Q

How do you reach a definitive diagnosis of pseudogout?

A

Joint aspirate which shows no bacterial growth, positive birefringent of polarised light with calcium pyrophosphate crystals which are rhomboid shaped

227
Q

What XR changes may be seen in pseudogout?

A

Chondrocalcinosis - thin whit line in middle of joint space due to calcium deposition

228
Q

How should you take Oral Bisphosphonates?

A

Oral bisphosphonates are taken on an empty stomach sitting upright for 30 minutes before moving or eating to prevent this.

Prevents reflux/oesophageal erosions

229
Q

What are the side effects of Bisphosphonates?

A

Reflux/GI upset
ONJ
ON of external auditory canal
Atypical fractures

230
Q

Should bisphosphonates be continued continuously in a patient?

A

No, every 3-5 years a treatment holiday is required.

Check to see if BMD has improved and XR to check if fragility fractures.

Break for 18 months then re-assess.

231
Q

What radiographic finds may be present in Osteomalacia?

A

Looser zones (fragility fractures going partially through the bone)

Bowing of the long bones

232
Q

What are the thresholds for 25-hydroxyvitamin D?

A

> 75 nmol/L = optimal

25-50nmol/L = vitamin D insufficiency

<25nmol/L = vitamin D deficiency

233
Q

What is the treatment for Osteomalacia?

A

50 000IU once weekly for 6 weeks

234
Q

What is the cause of Paget’s Disease of the Bone?

A

Unknown

235
Q

What are the phases involved in Paget’s disease?

A

3 phases:
1) Osteoclast activity - excessive bone resorption

2) Mixed phase of osteoclastic and osteoblastic activity - increased levels of bone turnover
3) Final chronic sclerotic phase with bone formation > resorption

236
Q

What radiographic finds would you see in Paget’s disease?

A

Combinations of lytic bone regions and sclerosis

Osteoporosis circumscripta - well defined osteolytic lesions appearing less dense cf normal bone

Cotton wool appearance (lysis vs sclerosis)

V-shaped defects in long bones

237
Q

Which biochemical marker will be markedly raised in Paget’s disease of the bone?

A

ALP

238
Q

What are the potential complications of Paget’s disease of the bone?

A

Osteosarcoma

Spinal stenosis

Spinal cord compression

239
Q

How may Vasculitis be classified?

A

Classified based on vessel affected: Large, Medium and Small Vessel

ANCA associated or non-ANCA associated

240
Q

Which ANCA-associated vasculitis is detected by the presence of cANCA?

A

Mnemonic: Wegener was a classicist

cANCA

241
Q

pANCA is directed against which cellular component?

A

MPO

242
Q

cANCA is directed against?

A

PR3

243
Q

What are the clinical features of Henoch-Schonlein Purpura?

A 
Purpura
Joint pain
Abdominal pain
Renal involvement (nephritic syndrome)
244
Q

What proportion of patients with Henoch-Schonlein Purpura will go on to develop end-stage renal failure within 6 months?

A

1%

245
Q

What blood test finding may be suggestive of Churg-Strauss syndrome?

A

Raised mast cells

Raised eosinophils

IgE level elevated

246
Q

What are the clinical features of Wegener’s Granulomatosis?

A

Sinusitis
Recurrent epistaxis
Saddle shaped nose (from perforated nasal septum)

Cough, wheeze and haemoptysis

Glomerulonephritis

247
Q

Which condition is polyarteritis nodosa most associated with?

A

HBV

248
Q

Which skin rash is most associated with polyarteritis nodosa?

A

Livedo reticularis

249
Q

What are the clinical features of Kawasaki disease?

A 
Persistent high fever >5 days 
Strawberry tongue 
Erythematous rash 
Bilateral conjunctivitis 
Erythema and desquamation of skin at solar surfaces
250
Q

What is the most concerning complication risk in Kawasaki disease?

A

Coronary Artery Aneurysms

251
Q

How is Kawasaki’s disease managed?

A

Aspirin
+
IVIG

252
Q

What gene is associated with Behcet’s Disease?

A

HLA B51 gene

253
Q

What are the clinical features of Behcet’s disease?

A

Ulcers: mouth; genital
Skin: Erythema nodosum; Papules and pustules; Vasculitic type rash
Eyes: Anterior/posterior uveitis; Retinal vasculitis; Retinal haemorrhage
MSK: arthralgia; oligoarthritis
GI system: ileum; caecum; ascending colon
CNS: memory impairment; headaches; migraines; aseptic meningitis; meningoencephalitis;
Veins: Budd-Chiari syndrome; DVT; CVS
Lungs: Pulmonary artery aneurysms

254
Q

Which investigation may be used in Behcet’s Disease?

A

Skin pathergy test - sterile needle to create a SC abrasion; review after 24-48 hours to look for a weal 5mm

Medicine (18 decks)

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