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Year 2 PBL > U11W3: Rheumatoid Arthritis > Flashcards

U11W3: Rheumatoid Arthritis Flashcards

1
Q

Compare and contrast the pattern of joints affected in rheumatoid and osteoarthritis

A

RA: more common in symmetrical pattern in the MCP and PIP and the MT/foot joints
OA: more common in lumbar/cervical vertebrae, hips, knees and the MCP/DIP
Both can affect the elbow and shoulders.

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2
Q

What terms are used to describe when the PIP and DIP are affected by arthiritis?

A

Bouchards nodes - PIP
Herbedens nodes - DIP

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3
Q

How does the onset of different types of arthitis vary?

A

Trauma - immediate/hours
Inflammatory arthirits - over 24 hours or more insidioulsy (acute)
Crystal arthirtis - over 8-12 hours, often wake patient up overnight
Septic arthirtis - 1 to 2 days
Degenerative arthritis - years.

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4
Q

What are some important characteristics of pain to consider in MSK history?

A

Penetrating, deep or boring - worse at night (red flag) - indicate bone pain
Fracture pain - sharp and stabbing
Muscle pain - stiff and aching
Nerve pain - shooting, pins and needles, burning or stabbing

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5
Q

What are some common associated symptoms of joint pain?

A

Swelling
Stiffness (morning>30 indicates inflammatory)
Locking - physical block such as meniscus damage
Systemic symptoms - fever, night sweats, chills, rigour and rash - septic arthritis

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6
Q

What is a common cause of gout flare-ups?

A

Alcohol use

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7
Q

What exacerbating/relieving factors are important for differentials?

A

OA - worse with exercise
RA - worse with rest
Septic arthritis - present at rest and movement
Unable to walk or weight bear - red flag
Over-the-counter medications

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8
Q

What does pain disproportionate to injury indicate?

A

Compartment syndrome

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9
Q

What factors are important about the mechanism of injury in an MSK injury?

A

How,when and where did the injury occur?
Playing sport? At home?
Foot planted? Twisting? Landing after jumping?
What were the conditions like? Wet?
Sound or feeling on injury - pop, giving way, swelling. redness, knocking.

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10
Q

What questions should help characterise the pain of MSK injury?

A

TIMING: Time between pain and injury
Pain intermittent or constant
Severity of immediate pain - need to stop activity
Delayed pain

ACTIVITY: weight bearing, resting, flexion of joint., pain at night.

PREVENTION: sport, work or activities of daily living.

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11
Q

What are some important risk factors for joint injury?

A

Prior injury or surgery.

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12
Q

What are the different classifications of MSK joint problems?

A

ACUTE
- infective (septic arthiritis)
- traumatic

CHRONIC
- Degenerative (ostearthirtis)
- Inflammatory
1) seropositivie (+RF) RA
2) Seronegative (-RF)
-crystal (gout/pseudogout)
- non-crystal (IBD, reactive arthiritis, ankylosing spondylitis, psoriatic)

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13
Q

What is the specific information that should be asked about a joint in an MSK history?

A

Joint tenderness
Joint swelling
Joint redness
Joint stiffness
Joint locking
Limb weakness

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14
Q

What joints are normally affected in Rheumatoid Arthiritis?

A

Synovial Joints
Normally in a symmetrical pattern
Mostly small joints in the feet and hands (often spares the DIP).
Symstemic small joint inflammatory polyarthiritis.

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15
Q

What are some common risk factors for Rheumatoid arthritis?

A

Biological:
1)Age - normally diagnosed between 40-60 years - may be associated with immune ageing.
2)Sex - female - 3:1 - tend to have an early onset and early disease onset - oestrogen thought to increase the survival of autoreactive cells and enhance B cell response.
3)Genetic predisposition - HLA:DR:1Beta: 04 variation - better at presenting epitope - common in European populations

Lifestyle:
Smoking - increased risk of extraarticular lung complications, can activate PADI type 2 enzymes - results in Anti-CPP antibodies - can also interact with silica or asbestos as a risk factor.
Diet - higher red meat/protein and lower vegetables and vitamins, low omega-3 to omega-6 ratio is associated with inflammatory conditions such as RA.
Infections such as Epstein Barr Virus - help overcome immune tolerance e.g. molecular mimicry, cryptic antigen or antigen spreading. Infection of B cells tends to be higher in RA patients.*
Previous joint injury - trigger localised chronic inflammatory disorder.

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16
Q

What forms the wrist joint?

A

Is a synovial joint
The distal end of the radius (concave) and the articular disk over the ulnar, scaphoid, lunate and triquetrum (convex).

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17
Q

What are the features of the carpometacarpal joints?

A

Metacarpal 1 and triquetrum - saddle joint - wide range of mobility to thumb
Metacarpal 2 to 5 to carpal bones - are synovial plane joints.

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18
Q

What are the features of the metacarpophalangeal joints?

A

Are condylar synovial joints
Are reinforced by palmar ligamesn and medial/lateral collateral ligaments

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19
Q

What are the features of interphalangeal joints in the hand?

A

Are synovial hinge joints - allow flexion and extension of the digits.
Are reinforced by medial and lateral collateral ligaments and palmar ligaments

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20
Q

What are the signs and symptoms of rheumatoid arthritis in early disease?

A

Symmetrical joint involvement
Morning stiffness (lasting more than 30 minutes/normally 1 hour)
Throbbing and aching pain in may joints - polyarthralgia
Fatigue
Swollen Joints
Warm and red joints
Stiffness in joint
Rheumatoid nodules

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21
Q

What are the signs and symptoms of rheumatoid arthiritis in late disease?

A

Ulnar deviation
Swan necking and Boutonniere deformity
Z deformity of the thumb
Muscle atrophy.

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22
Q

What clinical assessments should you order for an Rheumatoid arthiritis patient?
Expected results

A

Examinations: GALS exam, wrist and hand exam and other focused on affected joints
Blood test: markers of inflammation, ESR,CRP, auto-antibodies such as RF and anti-CPP.
X-ray: to identify bony joint deformities (subluxation of the joints) and may identify joint swelling
Chest x-ray: to eliminate pulmonary complications such as lung effusion and fibrosis.
Joint aspiration - to examine synovial fluid - excess synovial fluid, presence of immune cells and antibodies.
Doppler ultrasound - indicate increased blood flow to the joint, identify increased soft tissue swelling and tenosynovitis.

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23
Q

What tests might a doctor order to rule out differential diagnosis for rheumatoid arthritis?

A

Blood test: Anti-nuclear antibodies - more common in SLE.
X-ray: help distinguish with osteoarthirits - more likely to see osteophytes and subchondral bone cysts, and narrowed bone space.

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24
Q

Why is a chest x-ray often done of a rheumatoid arthritis patient before starting their treatment?

A

TO identify any extra-articular respiratory manifestations such as pulmonary fibrosis and pleural effusions
Rule out pre-existing chest infections or significant pulmonary conditions before starting methotrexate with is reported to cause severe pneumonitis.
Identify rheumatoid nodules that may have formed in the lungs
Repeated to monitor extra-articular disease symptoms progression - looking for pulomnoary and cardiovascular complications

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25
Q

What is the function of a DAS28 score?

A

Used to assess the progression of a functional ability by giving a disease activity score.
Based on 28 joints
Count the number of tender joints
Count the number of swollen joints
Erythrocyte sedimentation rate
Patient Global Health Score (0-100) -this is the patients self-assessment of disease activity.
Combined in an online calculator to give a value between 0 and 10 - with 10 indicating a more active disease.

26
Q

Describe the mechanism of action of methotrexate in rheumatoid arthritis?

A

Clinical: non-biological DMARD, reduce symptomatic inflammation - first line drug
Chemistry: is an anti-metabolite, anti-folate. produrig converted to active metabolite in the body
Pharmacology: is a structural analogue of DHF that Inhibits DHFR preventing the conversion of DHF to THF
Also inhibits thymidate synthase - prevents the conversion of dUMP to dIMP this inhibts thymine synthesis.
These have combined effects to inhibit DNA synthesis, which prevents cell growth and proliferation - in particular, benefit prevents the proliferation of inflammatory cells.
Also inhibits AICART, preventing the conversion of AICAR to IMP, this increase in AICAR has anti-inflammatory effects by leading to adenosine accumulation in the extracellular space.
Physiology: fewer inflammatory cells, decreased production of inflammatory cytokines, leads to decreased inflammatory response.

27
Q

What is the mechanism of action of trimethoprim?

A

Chemistry: Antifolate antibiotic - antibacterial agent
Pharmacology: Reversible inhibitor of DHFR preventing the conversionof DHF to THF, binds with stronger affinity to bacterial DNF compared to mammalian DHFR, therefore selectivly interfering with the bacterial biosynthetic processes
Phyiology: Reduces THF available for purine and pyrimidine nucleotide synthesis, this reduces DNA synthesis and limits bacterial cell growth and proliferation - bacteriostatic.
Clinical: Used to treat gram-negative bacteria to treat UTIs, RTI and GITs. Often used in combination with sulfamethoxazole to cause bacteriocidal effects.

28
Q

Why are folic acid supplements are prescribed alongside methotrexate?

A

Timing of prescription is important: methotrexate on monday, folic acid the day after.
Methotrexate inhibits the conversion of folic acid to active metabolite - can lead to megoblastic anemia
Prescription of folic acid can reduce megaloblastic anemia.
As methotrexate selectivly effects rapidly divding cells can cause mouth ulcers/mucositis without folic acid prescription

29
Q

Why can trimethoprim and methotrexate not be prescribed together?

A

Both inhibits DHFR
Leads to significantly lower levels of THF, this can impede DNA synthesis and cell proliferation
This mostly effects rapidly dividing cells
Can lead to bone marrow suppression, present as bruising due to low platelets. May also have fever and mout ulcers.

30
Q

What is the pharmacology of sulfasalazine in rheumatoid arthritis?

A

Chemistry: is an aminosalicylate, breaks down in sulfapyridine and 5-aminosalicylic acid.
Pharmacology: precise mechanism is unknown, the suggested mechanisms include the inhibtion of COX, lipoxygenase and serine kinase.
This reduces PG and leukotrieene synthesis and the activation of NFkB.
Physiology: reduce inflammatory mediators the immune and inflammatory response, prevent pro-inflammatory cytokine production, (PG) - reduce pain and inflammation, reduce immune cell migration as fewer adhesion molecules, inhibit synovial vascularisation, inhibit chemotaxis.
Clinica: DMARD for RA.
* Need to check for aneamia as causse folate malabsoprtion and inhibit folate enzyme synthesis.

31
Q

What is the pharmacology of hydroxychloroquine in rheumatoid arthiritis?

A

Chemistry: Quinacrine derivative
Pharmacology: Antagonist at TLR-7 and TLR-9 receptors
Binds to nuclei acid fragments
Physiology: Leads to elevated pH in endosome this inhibits the proteolytic enzymes - inhibits the peptide processing fo epitope is not created to bind to MHC2.
Prevents recognition of non-self material contained within the endosome as unable to bind to TLRs.
This inhibits antigen processing
Inhibits MHC2 presentation as peptide unable to bind to MHC2, Reduces the release of cytokines such as IL-1 and TNF, leads to an reduced inflamamtory response such as inhibited phagoytosis, chemotaxis and free radical production.
Clinical: DMARD used to treat the symptoms of inflammation in rheuamtoid arthiritis.

32
Q

What are the guidelines for drug prescription in rheumatoid arthiritis?

A
  1. Methotrexate as first line DMAR - followed by change to sulfasalzine or hydroxychloroquine if needed
  2. NSAIDs may be used to treat flare up of symptoms, lowest dose possible and with a PPI
  3. Glucocorticoids may be used for bridging treatment between two DMARDs or severe flare-ups
33
Q

Evaluate the use of DMARDs in rheumatoid arthiritis

A

+Varied mechanisms of actions - can be more individualised to patientes specific pathogenesis of arthiritis - applies nicely to the treat to target approach
+symptomatic approach - improve patient quality of life
+ pill form, relativly easier to manufacture and adminster

  • Risks of side effects such as mouth ulcers and anaemia with methotrexate
  • suppress the overall immune system, immunocompromised - risk of serious infections or cancers.
  • can take a few months to notice if a DMARD is working
34
Q

Evaluate the use of biologics in Rheumatoid Arthiritis?

A

+ block specific parts of the immune system - reduce immune side effects
+ provide relief to patient, improve quality of life
+ some medications can start to take effect within 2 weeks

  • more complex and harder to produce, often need to be adminstered by an injection (risk of infection)
  • very expensive so limited funding for resources, ethical depate on who qualifies for what treatment.
  • may not necessary work for all patients, may work originally then stop working.
  • immunosuppression increase risk for serious infections and cancers.
35
Q

List the MDT involved in a RA case

A

Radiologist
Rheumatologist - initial diagnose and manages chronic inflammatory conditions, and helps coordinate treatment plans
Physiotherapist
Occupational therapist - give practical aids to help with tasks such as button hooks and can openers, and assess adaptations that may be needed at home. May give splints.
Pharmacist - check for drug interactions
Rheumatology Nurse Specialist -
Podiatrist - offer orthotics or foot wear advice to patients with arthiritis in the feet.

36
Q

What is the role of a rheumatology nurse specialist?

A

Dedicated rheumatology helpline, opportunities for education and self-management.
Teach the patient about the condition and treatments including medications.
Offer vital emotional support (reduce anxiety and depression).
Administer steroid injections and ultrasound diagnosis.

37
Q

What is the role of the physiotherapist in rheumatoid arthiritis?

A

offer strengthening and stretching exercises for affected joint - aim to preserve or increase motility and muscle mass and reduce pain
May offer steroid injections
Hydrotherapy
Therabands for strengthening

38
Q

What causes the walking on marbles sensation in rheumatoid arthiritis?

A

Arthiritis of the tarsal bones
Loss of fat pad over tarsal heads
Protruding metatarsal heads due to subluxation of joints.

39
Q

What is the mechanism of action of esomeprazole?

A

Chemistry; PPI
Pharmacology: basic in nature, sulfoxide group, attracted to acidic environment around gastric parietal cells converted to active sulfenic acid, inc to high conc in parietal cell canaliculi, binds to proton pump by forming a disulfide bond with cysteine residue, inhibits action of pump due to conformational change, reduces H+ and Cl- in the gastric lumen
Physiology: Reduces the concentration of HCL in the the gastric lumen, stomach pH increases, reduces damage associated with stomach acid
Clinical: Protective from side effects of NSAIDs, prevent stomach ulcers, GERS

40
Q

How does turmeric relieve pain?

A

Main active component is curcumin - has anti-inflammatory and anti-oxidant properties.
May modulate NFkB downregulating pro-inflammatory cytokines, COX-2 and phospholipase A2.
Also inhibits the production of TNFalpha.
Suppresses activation and cytokine productionof auto-reactive T cells and inhibits auto-antibody production by B cells.
Neutralises free radicals.
This can be useful for reducing pain and improving movement of patients with RA/OA arthiritis.

41
Q

Why is cod liver oil beneficial in rheumatoid arthiritis?

A

Active compound is omega-3 - has anti-inflammatory effects
Competes with omega-6 fatty acids for receptors, leads to reduced production of prostaglandins
Increased production of pro-resolving mediators such as protectins to promote the resolution of inflammation.
Regulate the balance of pro and anti-inflammatory cytokines
Modulate gene expression anti and pro genes.
Benefits: reduce pain, morning stiffness and tender/swollen joints.

42
Q

What is Versus Arthiritis?

A

Offer a helpine
Online community and virtual chat box assistant AI
Educational information about the different types of arthiritis
Resources for healthcare professionals
In person coffee mornings and social groups

43
Q

What is a nurse-led drug counselling clinic?

A

Experience and skilled nurses (often rheumatology specialist nurses) who work alongside rheumatologist consultants.
Review the patients current medications, assess which medications they would find the most beneficial, work with the patient to develop a treatment plan based on pharmacological treatment that will be effective, understood and followed.

44
Q

What is reflexology?
How might it benefit a rheumatoid arthiritis clinic?

A

Complimentary therapy that involves putting pressure to specific points on the feet, hands or ears.
This refelx areas correspond to different organs and systemis in the body, the pressure can promote relaxation and stimulate the bodies natural healing processes.
Helps enhance and balance energy flow to these areas.

45
Q

What is meant by a treat to target approach for DMARDs?

A

Creating a target for patients and finding an appropriate treatment for this, reviewing the treatment and progresses and adapting the treatment and goal as needed.

46
Q

How do anti-TNF injections benefit/work in rheumatoid patients?

A

Often adalimumab, certolizumab etc
Adalimumab - prevents TNF interactoin with p55 and p75, this reduces leukocyte migration, decreases epidermal thickness, causes apoptosis of mononuclear cells with TNFalpha receptors (lymphocytes) and inhibits the relies of IL-6 and acute phase proteins.
Reduces TNFalpha action - reducing synovitis and joint destruction
Reduces markers of inflammation and slows or halts structural damage
usually given in combination with methotrexate to reduce loss of efficacy due to anti-drug antibody formation.

47
Q

What is the eligibility criteria for anti-TNF injections for rheumatoid arthiritis?

A

Discredited for: ever had allergic reaction to a medicine, exposure to TB, heart failure, hepatitis B, ever had cancer, are pregnant or trying to get pregnant.
ONly offered if failing to manage condition with physio and other medications

48
Q

What are some potential side effects/complication of turmeric as a complimentary therapy for rheumatoid arthiritis?

A

Side effects are uncommon and generally limited to stomach distress
Topical can cause allergic contact dermatitis
Can stimulate the gallbladder leading to worse symptoms in patients with gallstones or bile duct obstruction.

49
Q

What are some potential side effects of TNFalpha injections?

A

Small risk of cancer development due to compromised immunity.
Risk of infection of the joint - septic arthiritis
Increased risk of infection
Drug-induced lupus
Dizzy or blurred vision after taking - not able to drive or use machinery.
As relatively new treatment concern that long-term side effects are not yet fully understood.

50
Q

What is the influence of ethnicity on the treatment and management of RA?

A

Cultural background and society - influence perceptions around healthcare and treatment - trust and reliance on Western medicine - may prefer CAM.
Affect attitudes towards disability and the importance of maintaining physical ability e.g common jobs
Attitude towards physical deformity of hands
Minority groups - face discrimination, slower to recieve treatment and recieve lower standard of care - health literacy and acsesibility.

51
Q

What are the benefits of exercise classes in RA treatment?

A

Promote mobility of the joint and reduce stiffness.
Helps maintains muscle mass
Reduce pain and fatigue
Promote psychosocial wellbeing - reduce depression and anxiety.
Social gym classess - encourage friendships and maintain patient identity outside of medical condition.

52
Q

What are the four main MSK disorders?

A

Rheumatoid Arthritis
Osteoarthiritis
Acute gout
Fibromyalgia

53
Q

What are the key parts of the history that indicate RA compared t other MSK conditions?

A

Acute onset
Warm tender swelling
Morning stiffness for more than an hour
Symmeterical synovial joints - normally hands, wrsts and feet
Gradually progresses to toher joints whilst persisting in initial joints.
More common in females

54
Q

What is the process of osteoarthiritis?

A

Degeneration adn progressive loss of joint cartilage from mechanical stress, which damage to the unerlying bone and formation of new bone at the cartilage marnings

55
Q

What are the presenting patterns of osteoarthiritis?

A

Commonly affects: DIP, wrist, knees, hips, previosuly injured joints, zygopophysial joints
Normally asymmetrical and may only involve one joint (but can spread)
Has a progressive and chronic onset
Crepitus on movement
Morning stiffnes in joint normally less than 30 minutes
More common in females

56
Q

What is the process of gout?

A

Inflammatory reaction to microcrystals of monosodium urate.

57
Q

What are the presenting features of acute gout?

A

Normally affects the first MTP joint or the dorsum of the feet to ankles. May spread to knees and elbows
Initial attacks are normally only one joint
Has a sudden onset normally at night
Occasional/isolated attacks
Is excruciating, hot and tender joints
No joint stiffness, motion is limited due to pain
Less common in females (1:3)

58
Q

What is the process of fibromyalgia syndrome?

A

Widespread musculoskeletal pain and tender points
Central pain sensitivity syndomre that may involved aberrant pain signalling and amplification

59
Q

How does fibromyalgia tend to present?

A

Can be symmetrical but varies in presentation
Worse after immobility, cold and excessive exercise
More common in females 7:1
Can have morning stiffness

60
Q

What is the link between body fat and rheumatoid arthritis?

A

Obesity is a risk factor for rheumatoid arthirtis - adipose tisse may promote systemic low grade chronic inflammation through the secretion of adipokines such as leptin.
Obesity has also been associated with decreased responses to some DMARDs - lead to less effective treatment of the condition, leading to worse progression and more likely to have deformity and extra-articular manifestation

Year 2 PBL (27 decks)

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