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Year 4: MSK > Rheumatology Revision 1 > Flashcards

Rheumatology Revision 1 Flashcards

1
Q

In which of the following conditions can tendinitis/tenosynovitis present without being swollen and tender?

Systemic sclerosis
Gout
Rheumatoid arthritis
Disseminated gonococcal infection
Reactive arthritis

A

In which of the following conditions can tendinitis/tenosynovitis present without being swollen and tender?

Systemic sclerosis
Gout
Rheumatoid arthritis
Disseminated gonococcal infection
Reactive arthritis

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2
Q

Describe how you manage fibromyalgia

A

Education; graded excerise programme

Psychological support
- CBT

Aerobic exercise - strong evidence

Analgesia
- amitriptyline; duloxetine; pregabalin

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3
Q

Describe the clinical features of PMR [+]

A

Patients may have a relatively rapid onset of symptoms over days to weeks:

Stiffness and pain in the
* Shoulders, potentially radiating to the upper arm and elbow
* Pelvic girdle (around the hips), potentially radiating to the thighs
* Neck

Systemic symptoms (40-50%).
* Includes low grade fever
* fatigue
* anorexia
* weight loss
* depression.

Peripheral oligoarticular arthritis (50%).

The characteristic features of the pain and stiffness are:
* Worse in the morning
* Worse after rest or inactivity
* Interfere with sleep
* Take at least 45 minutes to ease in the morning
* Somewhat improve with activity

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4
Q

Tx for PMR? [1]

Tx for TA? [1]

A

PMR:
- Prednisolone 15-20mg/day

TA:
- Prednisolone 60 mg/day

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5
Q

Describe conversation might have with a patient about how to manage their fibromyalgia [2]

A
  • FM is a chronic illness, akin to that of diabetes mellitus and congestive heart failure, selfmanagement of day-to-day symptoms is key and has been associated with decreased pain,
    depression, catastrophic thinking, and improved quality of life
  • Identify specific goals regarding health status and quality of life, that is encouraging exercise
    and sleep hygiene.
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6
Q

RA presents similiarly in the early stages of the disease to PMR.
What specifically should you look for give a ddx? [2]

A

Rheumatoid arthritis can have an initial phase that presents similarly to PMR and so the presence of synovitis or clinical features suggestive of rheumatoid arthritis should prompt consideration of this as a potential diagnosis and referral to secondary care for confirmation.

RA patients also do not respond well to corticosteroids, unlike PMR

RA antibodies (anti-CCP; RF)

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7
Q

Which type of bursitis is associated with PMR? [1]

A

subacromial bursitis is associated with PMR.

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8
Q

What are the key clinical features of GCA? [4]

A

unilateral headache
jaw claudication
visual disturbance
tender or thickened temporal artery on palpation

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9
Q

Describe the treatment regime for PMR

A

Oral corticosteroids 15mg prednisolone daily, initially and gradually weaned off them with dose adjustments typically being every 4-8 weeks and reviews (telephone or face to face) scheduled for one week after each dose adjustment.

Treatment with steroids typically lasts 1-2 years. NICE suggest the following reducing regime of prednisolone:
* 15mg until the symptoms are fully controlled, then
* 12.5mg for 3 weeks, then
* 10mg for 4-6 weeks, then
* Reducing by 1mg every 4-8 weeks

In secondary care, patients may be considered for DMARD treatment as 2nd line therapy (e.g. methotrexate) or tocilizumab as 3rd line.

NB: Patients with PMR have a dramatic improvement in symptoms (at least 70%) within one week. Inflammatory markers return to normal within one month. A poor response to steroids suggests an alternative diagnosis.

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10
Q

Temporal arteritis, also known as giant cell arteritis, is a vasculitis predominantly affecting medium and large arteries, particularly the branches of the [] artery

A

Temporal arteritis, also known as giant cell arteritis, is a vasculitis predominantly affecting medium and large arteries, particularly the branches of the carotid artery.

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11
Q

Describe the presentation of temporal arteritis [5]

A

Unilateral headache is the primary presenting feature, typically severe and around the temple and forehead. It may be associated with:
* Scalp tenderness (e.g., noticed when brushing the hair)
* Jaw claudication
* Blurred or double vision
* Loss of vision if untreated

Anterior ischemic optic neuropathy accounts for the majority of ocular complications

Lethargy, depression, low-grade fever, anorexia, night sweats

NB patients are typically > 60; rapid onset (< 1month)

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12
Q

Describe why vision testing is key in CGA [1]

A

Anterior ischemic optic neuropathy:
- occlusion of the posterior ciliary artery (a branch of the ophthalmic artery)
- causing ischaemia of the optic nerve head
- may result in temporary visual loss - amaurosis fugax
- permanent visual loss is the most feared complication of temporal arteritis and may develop suddenly

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13
Q

Describe investigations would conduct for CGA [3]

A

raised inflammatory markers

temporal artery biopsy
- skip lesions may be present
- multinucleated giant cells present

Duplex ultrasound
- showing the hypoechoic “halo” sign and stenosis of the temporal artery

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14
Q

Management of CGA? [

A

Steroids are the mainstay of treatment. They are started immediately, before confirming the diagnosis, to reduce the risk of vision loss. There is usually a rapid and significant response to steroid treatment. Initial treatment is:

  • 40-60mg prednisolone daily with no visual symptoms or jaw claudication
  • 500mg-1000mg methylprednisolone daily with visual symptoms or jaw claudication

Once the diagnosis is confirmed and the condition is controlled, the steroid dose is slowly weaned over 1-2 years.

low-dose aspirin should be considered to reduce the risk of ischemic complications
Proton pump inhibitor (e.g., omeprazole) for gastroprotection while on steroids
Bisphosphonates and calcium and vitamin D for bone protection while on steroids

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15
Q

How do you differentiate CGA to central retinal artery occlusion? [2]

A

Similarities: sudden onset, loss of vision

Differences: fundoscopy may reveal presence of cherry red spot with retinal whitening, no muscle stiffness

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16
Q

How do you different AS from mechincal back pain?

A

AS:
- Young men
- Lower back pain that can be so intense that wakes people up
- > 3 months
- Exercise improves pain
- More insidious onset

MBP:
- > 40 yrs
- typically acute pain
- excerise worsens the pain
- Pain uncommon at night
- No morning stiffiness

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17
Q

Describe the test used to quantify AS [1]

A

Schober’s test:
- Patient stands straight; L5 vertabrae is located
- Point is marked at 10cm above and 5cm below L5
- Patient bends forward
- A length of less than 20cm indicates a restriction in lumbar movement a supports a dx.

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18
Q

Describe the medical management of AS [3]

A
  • Regular exercise like swimming
  • First line treatment: NSAIDS
  • Physiotherapy
  • Second line: Anti-TNF: for patients with persistently high disease activity; e.g. adalimumab
  • Third line: IL-17 antibodies: Secukinumab or ixekizumab

  • DMARDs only useful in peripheral joint involvement
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19
Q

Which neurological complications are associated with AS? [1]

Which GI complications are associated with AS? [1]

A

Neurological complications:
- Atlantoaxial subluxation and cauda equina syndrome are rare but serious neurological complications associated with AS.

GI:
- Increased risk of IBD

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20
Q

Describe diagnositic criteria for AS

A

Limited lumber movement
Reduced chest expansion
Radiological changes:
- Progressive loss of joint space –> sclerosis –> fibrosis of joints
- CXR: apical fibrosis
- Syndesmophytes: formation of bony bridges that fuse - causes bamboo spine

Complete fusion of sacro-iliac joint on right photo

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21
Q

What are syndesmophytes? [1]

A

Syndesmophytes formation of bony bridges that fuse
- Syndesmophytes are calcifications or heterotopic ossifications inside a spinal ligament or of the annulus fibrosus.

OA osteophytes DONT fuse

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22
Q

Describe the basic pathophysiology of AS [2]

A

initial inflammatory stage:
- activation of the immune system leading to inflammation within the entheses.

reparative stage:
- ongoing inflammation leads to new bone formation in an attempt to repair the damage caused in the earlier phase
- However, this process is dysregulated in AS resulting in pathological bone formation.

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23
Q

What are the 7As of AS EAM? [7]

A

Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
and cauda equina syndrome

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24
Q

Which CV complications are AS patients at risk of? [4]

A

aortitis, aortic regurgitation, conduction abnormalities and ischemic heart disease.

25
Q

The [] is a commonly used scoring system in AS that helps to evaluate disease activity and ultimately can be used to assess response to treatment. The BASDAI is a six-part questionnaire where each question is scored 1-10. It is a subjective assessment of severity.

A

The Bath Ankylosing Spondylitis Activity Index (BASDAI) is a commonly used scoring system in AS that helps to evaluate disease activity and ultimately can be used to assess response to treatment. The BASDAI is a six-part questionnaire where each question is scored 1-10. It is a subjective assessment of severity.

26
Q

Infection from which organisms typically causes reactive arthritis? [1]

A

The most common triggers of reactive arthritis are gastroenteritis or sexually transmitted infections. - Chlamydia may cause reactive arthritis.

NB: Gonorrhoea typically causes septic arthritis rather than reactive arthritis.

27
Q

Investigations for ReA? [+]

A

Blood tests
- ongoing inflammation (raised ESR and CRP)
- ANA and RF: to rule out other forms of arthritis
- HLA B27 - present in 40% patients

Urine test:
- NAAT to detect Chlamydia trachomatis

Stool test:
- Test for Salmonella, Shigella, Campylobacter, and Yersinia

Radiological changes:
- Early stages - no specific changes
- chronic ReA - radiographic changes in 70%

Synovial fluid analysis:
- to exclude alternative diagnoses like septic arthritis; gout and pseudogout
- Synovial cultures are always negative.

NB - Stool cultures are usually negative by the time arthritis occurs, but should be considered if diarrhoea present or recently resolved.

28
Q

Describe the treatment used for ReA [+]

A

Treatment of arthritis
- first-line therapy for acute phase: NSAIDs
- Corticosteroids: during an acute flare, or unresponsive to NSAIDs.
- DMARDs: Sulfasalazine is effective in peripheral disease and has little or no effect on spinal disease; Methotrexate is effective in treating both acute and chronic ReA especially, in patients with spinal involvement.
- Anti-TNF-α therapy: Etanercept is an emerging therapy,

Antibiotics for acute Chlaymdia infection
- doxycycline or azithromycin

NB - Antibiotics may be given until septic arthritis is excluded.

29
Q

How would you treat cicinate balanitis or keratoderma blennorrhagica in ReA? [1]

A

topical steroids.

30
Q

Describe the pathophysiology of SLE [+]

A

Body produces B cells. Normally when they react to self they get destroyed.

In SLE they escape from peripheral circulation - they differentiate into plasma cells and produce antibodies to nuclear parts of cells (thus ANA)

Complexes of antibody-antigen deposit in the body and cause damage e.g. skin, joints and renal are most common

When deposited the immune system causes complexes. But in SLE, have complement dysfunction. This adds to the inflam cascade and actives inflam cytokines

Over the course of lifetime, get waxes and wanes of SLE

31
Q

Describe the clinical presentation of SLE

A

Joint pain & swelling (without joint destruction)

Malar rash - spares nasolabial folds. Feels inflammed

Mouth ulcers

Reynauds

Livedo reticularis - broken lattice work in inflam. disease

Photosensitivity

Lupus nephritis

Alopecia

Discoid erythematosus

Lymphadenopathy

32
Q

Which antibodies need to know that are associated with SLE? [6]

A

ANA -
DS-DNA - highly specific to SLE, meaning a positive result suggests SLE rather than other causes. But only half have ds-ANA
Anti-SM - highly specific but not very sensitive
Anti-RNP
Anti-Ro
Anti-La

33
Q

Describe the general principles for treating SLE

go over MORE

A

Skin:
- hydroxychloroquine or azathriopine.

Joints
- hydroxychloroquine or methotrexate

Vital organs:
- Azathriopine
- MMF
- Cyclophosphamide - esp. if renal involvement

PassMed:
All patients - hydroxychloroquine

Mild Disease:
- hydroxychloroquine & low dose pred.
- Methotrexate and NSAIDs can also be used

Moderate disease:
- hydroxychloroquine with short term pred.
- Additional agents may include methotrexate, azathioprine, mycophenolate and ciclosporin.

Severe disease:
- induction therapy of intense immunosuppressants and then maintenence
- DMARDs (methotrexate; MMF; cyclophoshamide) & Biologics (Rituximab; Belimumab) may also be used

34
Q

Describe the clinical presentation of Sjogrens

A

Sicca (dryness)
- eyes (keratoconjunctivitis sicca)
- mouth
- vagina

Arthralgia
Raynaud’s, myalgia
Sensory polyneuropathy
Gland swelling (parotitis)

35
Q

Describe how you diagnose Sjogrens

A

Assess clinical features:
- dry eyes > 3 months; use of tear substitutes more than three times daily or presence of keratoconjunctivitis sicca with ocular staining score ≥3.
- dry mouth consistently

Serology:
- anti-Ro; anti-La
- Elevated IgG levels

Further tests:
- Schirmer’s test - < 5 mm/5mins wetting and / or Rose Bengal scores of > 4
- Sialometry < 1.5ml/15mins

Histopathology
- Lip biopsy exhibiting focal lymphocytic sialadenitis with a focus score ≥1 per 4 mm² glandular tissue area.

36
Q

What are the antibodies seen in APS? [3]

A
  • anticardiolipin antibodies
  • anti-beta2 glycoprotein I (anti-beta2GPI) antibodies
  • lupus anticoagulant
37
Q

SLE symptoms

Other symptoms can be organ-specific caused by active inflammation these tend to develop within 5 years of diagnosis, such as:

A

Renal - lupus nephritis

Pleuritis; pneumonitis; PE

Pericarditis; Reynauds; Atherosclerosis

Headache or migraine; seizure; pyschosis

38
Q

Which other autoimmune conditons is SLE associated with? [3]

A

anti-phospholipid syndrome (20-30%), Sjogren’s disease (17.5%) and autoimmune thyroid disease (7.5%).

39
Q

Describe the diagnostic criteria for SLE

A

The European League Against Rheumatism (EULAR) / American College of Rheumatology (ACR) criteria (2019) can be used for diagnosis. This takes into account the clinical features and autoantibodies suggestive of SLE. uses 11 criteria of which 4 or more are required for diagnosis

40
Q

Describe the complications of SLE

A

Nephritis:
- Lupus nephritis: can lead to proteinuira; haematuria; end stage kidney disease

CV disease:
- CAD; myocarditis; pericarditis; heart failure

Pulmonary:
- ILD; pulmonary HTN; acute lupus pneumonitis

Neuropsyc:
- Head and mood to stroke or seizures

Hematologic abnormalities:
- leukopenia, lymphopenia, thrombocytopenia and autoimmune hemolytic anaemia.

41
Q
A

anti-Smith: highly specific (> 99%), sensitivity (30%)

42
Q

What is the most common cardiac manifestation of SLE? [1]

A

Pericarditis

43
Q
A

Type 3

44
Q

Describe the presentation of discoid LE [3]

A

Photosensitive lesions of the face
Scarring alopecia
Hyper & hypopigmentation

45
Q

What is the management for DLE? [3]

A
  • topical steroid cream
  • oral antimalarials may be used second-line e.g. hydroxychloroquine
  • avoid sun exposure
46
Q

Define Sjogrens syndrome [1]

A

Sjögren’s syndrome is an autoimmune condition where you get lymphocytic infiltration of exocrine glands notably the lacrimal and salivary glands, causing symptoms of dry mouth, eyes and vagina. Dry eyes and dry mouth can be called sicca symptoms.

47
Q

Describe the pathophysiology of Sjogren’s syndrome

A

Aberrant immune response - autoreactive T cells become activated and infiltrate exocrine glands.

Within the affected glands, there is a marked increase in pro-inflammatory cytokines including interleukin-1 (IL-1), tumour necrosis factor-alpha (TNF-α), and interferon-gamma (IFN-γ).

The local inflammatory milieu results in glandular dysfunction through both direct cytotoxic effects on acinar epithelial cells and disruption of normal glandular architecture.

B cell hyperactivity is another hallmark of Sjögren’s syndrome. There is increased production of autoantibodies such as anti-Ro/SSA and anti-La/SSB, which are directed complexes within the nucleus of glandular epithelial cells.

These autoantibodies may contribute to tissue damage either directly or via immune complex formation and deposition within glandular tissues.

Chronic inflammation leads to fibrosis and atrophy of the exocrine glands over time. The resultant loss of functional acinar cells impairs saliva and tear production, manifesting clinically as dry mouth and dry eyes.

48
Q

What is Schirmer’s test? [1]
Describe how you perform it [4]

A

Schirmer’s test is used to look at tear production.

Test procedure:
* Step 1: Folded sterile filter paper is placed over the margin of the lower eyelid
* Step 2: The patient is asked to gently close their eyes
* Step 3: The filter paper is left for 5 minutes
* Step 4: The extent of paper wetting is assessed after 5 minutes
Wetting of filter paper ≤5mm within 5 minutes is suggestive of aqueous tear deficiency

49
Q

Describe what is meant by Whole sialometry

How do you perform this test? [1]

A

Sialometry refers to the measure of saliva production.

Test procedure
* Step 1: Patient asked to expectorate at the start of the test
* Step 2: The patient then asked to collect all saliva in a pre-weighed container
* Step 3: Saliva should be collected over 5-15 minutes
* Step 4: The collection container is reweighed at the end of the time period

NB: Collection ≤ 0.1 mL/minute is indicative of abnormal salivary function.

50
Q

Describe the primary [5] and secondary [4] treatment options for Sjogrens

A

Primary treatment options:
* Artificial tears (e.g., polyvinyl alcohol eye drops during the day and carbomer gel at night)
* Artificial saliva
* Vaginal lubricants
* Pilocarpine (oral) can be used to stimulate tear and saliva production
* Hydroxychloroquine may be considered, mainly in patients with associated joint pain

Secondary treatment options are usually prescribed by an ophthalmologist and include:
* Topical NSAIDs or Corticosteroids: usually short-term use. Associated with corneal complications long-term.
* Topical cyclosporin: reserved for patients needing recurrent courses of topical steroid.
* Serum tear drops: application of autologous or allogenic serum. Variable efficacy.

NB: Pilocarpine stimulates muscarinic receptors, stimulating the parasympathetic nerves and promoting salivary and lacrimal gland secretion.

51
Q

The major complication of SS is [].

A

The major complication of SS is lymphoma.

52
Q
A

RF

53
Q
A

ANA

54
Q

Define antiphospholopid syndrome [1]

A

Antiphospholipid syndrome is an acquired disorder characterised by a predisposition to both venous and arterial thromboses, recurrent fetal loss and thrombocytopenia

55
Q

APS is most associated with which other condition?

A

SLE

56
Q

Which skin condition is associated with APS? [1]

A

livedo racemosa permanent Livedo reticularis

57
Q

Which cardiac complication is associated with APS? [1]

A

Libmann-Sacks endocarditis is a non-bacterial endocarditis with growths (vegetations) on the heart valves (most often the mitral and aortic valves). It is associated with SLE and antiphospholipid syndrome.

58
Q

Describe the primary [1] and secondary thromboprophylaxis (initial VTE; recurrent VTE; arterial thrombosis [3]

A

primary thromboprophylaxis
- low-dose aspirin

secondary thromboprophylaxis
* initial venous thromboembolic events: lifelong warfarin with a target INR of 2-3
* recurrent venous thromboembolic events: lifelong warfarin; if occurred whilst taking warfarin then consider adding low-dose aspirin, increase target INR to 3-4
* arterial thrombosis should be treated with lifelong warfarin with target INR 2-3

59
Q

How do you treat APS in pregnancy? [2]

A

low-dose aspirin should be commenced once the pregnancy is confirmed on urine testing
low molecular weight heparin once a fetal heart is seen on ultrasound. This is usually discontinued at 34 weeks gestation

Year 4: MSK (37 decks)

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