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Rheumatology > Rheumatology/ Immunosuppressants > Flashcards

Rheumatology/ Immunosuppressants Flashcards

1
Q

What is rheumatoid arthritis?

which age does it occur?

pattern of join involvment of RA?

A

Rheumatoid arthritis (RA)

Autoimmune disease associated with antibodies to Fc portion of IgG (rheumatoid factor) and anti citrullinated cyclic peptide (anti-CCP)

Usually 30-50 years old, females, although the disease can occur at any age

  • Presenting with progressive, peripheral and symmetrical polyarthritis.
  • Usually affects MCPs/PIPs/MTPs and typically spares DIPs (cf OA) but may affect any joint inc hips/knees/shoulders/c-spine.
  • Must have hx ≥ 6 weeks for ∆.Morning stiffness > 30 mins duration.
  • Commonly c/o fatigue/malaise.
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2
Q

what is a prodrug?

A

A prodrug is a medication or compound that, after administration, is metabolized (i.e., converted within the body) into a pharmacologically active drug

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3
Q

what is this image showing?

A
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4
Q

RA pathogenesis

A

balance btw proinflammatory cytokines and antiinflammatory cytokines > is tipped towrds the pro,

Tcells & macrophages r all in OVERDRIVE!

  1. Pathogenesis involves citrullination of self antigens which are then recognized by T & B cells which can then produce antibodies (RF & anti-CCP).
  2. Stimulated macrophages and fibroblasts release TNFα.
  3. Inflammatory cascade leads to proliferation of synoviocytes (resulting in the ‘boggy’ joint swelling typical of RA)
  4. these grow over the cartilage and lead to restriction of nutrients and cartilage is damaged.
  5. Activated macrophages stimulate osteoclast differentiation contributing to bone damage.

There is persistent synovitis, causing chronic symmetrical polyarthritis with systemic inflammation.
There is over-activation of the inflammatory process. Chemoattractants produced in the joint recruit circulating inflammatory cells

Over-production of tumour necrosis factor (TNF)> activates IL-6 leads to synovitis and joint destruction.
Interaction of macrophages and T and B lymphocytes drives this over-production.

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5
Q

deformities of RA on hand?

A
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6
Q

what is butonniere deformity? what cuases it?

A

“or button-hole deformity”

extensor tendon splits, & head of proxiaml phalages pokes through, like a button through a button hole!

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7
Q

Is RA symmetrical or asymmetrical?

A

Symmetrical!

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8
Q

What is the main auto-antibody found in blood tests?

A

Autoantibodies to the Fc portion of immunoglobulin G (rheumatoid factor)

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9
Q

What other autoantibodies can occur in RA? Suggest 2

A
  • Anti-cyclic citrullinated peptide (anti-CCP)
  • Also referred to as Anti-citrullinated protein antibody (ACPA)
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10
Q

give 4 syndromes in the body that RA can cause

A

Felty’s syndrome

Caplan’s syndrome

carpal tunnel syndrome

Sjogren’s syndrome

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11
Q

Give 2 other non-articular manifestations of RA

A
  • *3Cs** – Carpal tunnel syndrome, elevated Cardiac risk (CVD), Cord compression (due to atlanto- axial subluxation)
  • *3As** – Anaemia (normochromic & normocytic), Amyloidosis (very rare now due to improved treatment, can cause nephrotic syndrome and CKD), Arteritis (rare now due to improved treatment, can cause nail fold infarcts, cutaneous vasculitis & mononeuritis multiplex) 3Ps – Pericarditis (uncommon), Pleural disease (common), Pulmonary disease (common) e.g. bronchiectasis, bronchiolitis obliterans, fibrosis

3Ss – Sjögren’s (common), Scleritis/episcleritis (uncommon), Splenic enlargement (together with neutropaenia = Felty’s syndrome, rare)

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12
Q

What can occur in the lungs of patients with RA?

A

Nodules

Other lung diseases including pleural effusion, interstitial lung disease and others.

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13
Q

what investigations should we do?

A
  • RF & anti-CCP
  • FBC – normocytic anaemia (chronic disease),

WCC if concerns re septic arthritis.

  • Inflammatory markers – elevated
  • X-ray changes apparent in established disease –

USS/MRI more sensitive in early disease
- Other investigation guided by history & exam e.g.

may need PFTs and HRCT chest if lung involvement (e.g. pulmonary fibrosis).

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14
Q

In history of RA, look for the three S’s

A

* Stiffness – early morning joint stiffness lasting over 30mins

* Swelling – persistent swelling of one joint or more, especially hand joints

* Squeezing – squeezing the joints is painful (particularly MCP)

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15
Q

How do we diagnose RA?

Symptoms

A
  • Morning stiffness  1 hour
  • Arthritis of more than 3 joints
  • Arthritis of hand joints
  • Symmetrical arthritis
  • Rheumatoid nodules>> shouldnt seen it early RA
  • Serum rheumatoid factor
  • X-ray changes >> happens later on!
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16
Q

Diagnosis chart

A
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17
Q

RA treatment goals?

A
  • Symptomatic relief
  • Prevention of joint destruction
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18
Q

RA treatment strategy?

what about corticosteroids?

A

Initially DMARD monotherapy – usually methotrexate.

Consider combination DMARDs (leflunomide, hydroxychloroquine, sulfasalazine).

  • Steroids (acutely) – PO/IM or intra-articular.
  • Symptom control with NSAIDs (with PPI cover) if

no contraindication.

  • If disease still severe after combination DMARDS

then consider biologics (e.g. anti-TNFs like

etanercept) .
- Non-drug – OT/PT, podiatry, psychological.

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19
Q

Systemic lupus erythematosus (SLE)

  • causes, symptoms, diagnosis & pathology
A
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20
Q

Vasculitis

  • causes, symptoms, diagnosis, treatment, pathology
A

LFT

Lots of consolidation in lung bases

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21
Q

Treatment goals in SLE & vasculitis

A
  • Symptomatic relief e.g arthralgia, Raynaud’s phenomenon (well controlled, make sure their fingers arent dropping off)
  • Reduction in mortality
  • Prevention of organ damage
  • Reduction in long term morbidity caused by disease & by drugs
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22
Q

name the typical Immunosuppressants

A

MY CCAT

  • Corticosteroids
  • Azathioprine
  • Ciclosporin
  • Tacrolimus
  • Mycophenolate mofetil
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23
Q

DMARDs>> disease-modifying anti-rheumatic drugs

A

Theres biologics and nonbiologics

wdna ib kakaw MARS

  • Methotrexate
  • Anti-TNF agents
  • Rituximab
  • Sulphasalazine> B

Cyclophosphamide (cytotoxic) >> (only in extreme cases of lupus & SLE)

24
Q

common side effects of all dmards

A

N + V

myelosuppression

abnormal LFT’s

25
Q

corticosteroids: mechanism of action

A

Its a bazuka! It just shot down everything, which is why lama

SE STERIODS>> symptoms nafs someone going through old age!

act quickly, releive symptoms, control inflammation

inhibit TRANSCRIPTION FACTORS by binding directly onto DNA>> rapidly inhibit inflammation.

  1. prevent interleukin (IL)–1 and IL-6 production by macrophages
  2. inhibit all stages of T-cell activation
26
Q

Gold standard treatment for RA

A

Methotrexate

27
Q

Methotrexate

  • mechanism of action
  • pharmacokinetics
  • ADRs
  • clinical monitoring
A
28
Q

Sulphalazine

  • mechanism of action
  • pharmacokinetics
  • ADRs
  • clinical monitoring
A
29
Q

Cyclophosphamide

  • mechanism of action
  • pharmacokinetics
  • ADRs
  • clinical monitoring
A
30
Q

Mycophenolate mofetil

  • mechanism of action
  • pharmacokinetics
  • ADRs
  • clinical monitoring
A
31
Q

Calcineurin inhibitors (ciclosporin and tacrolimus)

  • mechanism of action
  • pharmacokinetics
  • ADRs
  • clinical monitoring
A
32
Q

Azathioprine

  • mechanism of action
  • pharmacokinetics
  • ADRs
  • clinical monitoring
A
33
Q

the newer ‘biologicals’ and their range of indications

which one r commonly used?

A

derived from proteins already in existence, through the use of recombinent DNA technology, we can transplant the DNA into bacteria & they can produce the drug for us!

& by creating Monoclonal antibodies, we can target ANY SYSTEM in the body!!!

Mechanism

  • have very similar structure to proteins or bound to other proteins
  • act to block certain pathways

indications

  • control inflammation
  • IBD
  • Asthma
  • CONTROL cancer (melanoma)
34
Q

action of drugs that block TNFα

-what considerations should u take into account?

A

TB REACTIVATION RISK!

make sure u screen patient for latent TB before anti-TNF treatment! using quantiferon gold test!

bc -TNF is used by the macrophages to help reinforce (strengthen) the Granuloma and keep the bacilius in check and make sure its walled off!

35
Q

which drug is NOT teratogenic ? IS?

A

teratogenic>> Methotreaxte

NOT teratogenic> sulfasalazine

36
Q

what drug is mostly used in transplantation?

A

Mycophenolate mofeti

37
Q

what is this? complication of what drug? how can this be prevented and time taken?

A

Cyclophosphamide-

Acrolein, metabolite of cyclophosphamide> is toxic to the bladder epithelium and can lead to hemorrhagic cystitis

  • aggressive hydration
  • Mesna >> orally 2 hrs b4 or IV w/ cyclophosphamide
38
Q

What is a good maintainence therapy for lupus nephritis?

A

Mycophenolate mofetil

39
Q

what is this? what caused it?

A

Mycophenolate mofetil >> mouth ulcers

40
Q

which drug causes renal toxicity & is not used much in rheumatology?

A

Calcineurin inhibitors

41
Q

what is this? which drug is used to cure this?

A

Azathioprine >> Bullous skin disease

42
Q

which drug is cytotoxic & only used in extreme cases of lupus & SLE?

A

Cyclophosphamide-

43
Q

what is used for atopic dermatitis & psoriasis ?

A

Calcineurin inhibitors

Ciclosporin & tacrolimus

44
Q

which drug can accelerate hypertension hence renal failure?

A

Ciclosporin

45
Q

what do immunosuppressents eventually lead to? (2)

A

All immunosuppressant’s result in increased susceptibility to infection& myelosuppression

46
Q

catagories of immunosuppressents

A
47
Q

which drug is can cause gum atrophy?

A

ciclosporin

48
Q

which drugs inhibit cyp450?

A

calcineurin inhbitiors

(C&T)

49
Q

all DMARDS take —–wks to have an effect

which one only takes 10 days?

A

6 wks

Cyclophosphamide

50
Q

give example of an induction and maintanence therapy?

A

give cyclophosphamide for induction for lupus,

but its cytotoxic if used for long!

so we then give MMF or Azathiporine for maintanece

51
Q

which drug is also used for cancer?

what r the diffrence in dosage btw the cancer therpy and rheumatology uses?

A

cyclophosmamide

cancer>> 4 or 5 g

Rheumatology> 1.5g

52
Q

which is a weekly drug!?

A

Methotrexate!

53
Q

Risk factors for RA?

why is bad dentition a risk factor?

A

Theres a protein in RA called “citrullin”, which the antibody against it is anti CCP

In bad dentition theres alot of citrullin, and so ppl with bad dentition can go on to develop RA!

and smoking also potentiates Bad dentition!

54
Q

If Rheumatoid factor is increased, does that mean she has RA?

A
55
Q

What is NOT a rheumatological cause of Joint pain?

A

Wegners granulamotis

rare multisystem autoimmune disease of unknown etiology. Its hallmark features include necrotizing granulomatous inflammation and pauci-immune vasculitis in small- and medium-sized blood vessels

Rheumatology (5 decks)

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