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ESA 5 > CPT S6 Rheumatology > Flashcards

CPT S6 Rheumatology Flashcards

1
Q

What is rheumatoid arthritis?

A

An autoimmune multi-system disease
Initially localized to the synovium
Cytokine involvement in inflammatory changes
Hyperplasia and proliferation of synovium

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2
Q

Give some diagnostic features of RA

A 
Morning stiffness of more than one hour
Arthritis of three or more joints
Involvement of hand joints
Symmetry
Rheumatoid nodules
Serum rheumatoid factor
X-ray changes
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3
Q

What are some important factors to remember when considering a diagnosis of RA?

A

Need to eliminate cancer first
It’s a clinical diagnosis rather than one dictated by test results
Not all symptoms must be present to diagnose as many are late-stage

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4
Q

What is the basic pathogenesis of RA?

A

overexpression of pro-inflammatory genes in comparison to anti-inflammatory genes

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5
Q

What are the treatment goals for RA?

A

Symptomatic relief

PREVENTION OF JOINT DESTRUCTION

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6
Q

What are the treatment strategies for RA?

A 
Early use of disease-modifying drugs
Use of combinations of drugs
Use of adequate doses
Aim to achieve good disease control quickly
Avoid use of long-term corticosteroids
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7
Q

What are the treatment goals in SLE and vasculitis?

A

Symptomatic relief
Mortality reduction by induction of disease remission the maintenance
Prevention of organ damage
Reduction in long term morbidity caused by disease and drugs

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8
Q

Give some examples of immunosuppressants

A 
Corticosteroids
Azathioprine
Ciclosporin
Tacrolimus
Mycophenolate mofetil
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9
Q

Give some examples of other disease-modifying anti-rheumatic drugs (DMARDs)

A 
Methotrexate (best)
Sulphasalazine
Anti-TNF agents (expensive)
Rituximab
Cyclophosphamide (cytotoxic though)
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10
Q

When is Azathioprine used in practice?

A 
Maintenence therapy in SLE & vasculitis
Rarely in RA
IBD
Bullous skin disease
Atopic dermatitis
As a 'steroid sparing' drug
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11
Q

What are the problems with Azathioprine?

A

Metabolized by TPMT, an extremely polymorphic gene, so need to test levels before prescribe because patients can develop myelosuppression

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12
Q

Give some azathioprine ADRs

A

Bone marrow suppression (so monitor FBC)
Increased risk of malignancy (as with all immunosuppressants)
Increased risk of infection
Hepatitis (so monitor LFTs)

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13
Q

How do ciclosporin & tacrolimus have their effect?

A

Both calcineurin inhibitors

So prevent IL-2 production by T-helper cells

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14
Q

What is the mechanism of action of mycophenolate mofetil?

A

Inhibits monophosphate dehydrogenase, an enzyme required for guanosine synthesis
This impairs B and T-cell proliferation but spares other rapidly dividing cells due to guanosine salvage pathways presence in other cell types.

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15
Q

Give some ADRs for mycophenolate

A

Nausea
Vomiting
Diarrhoea
Myelosuppression (not as bad as azathioprine
Metallic taste
May require monitoring
Toxicity more likely in renal and hepatic disease

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16
Q

When is mycophenylate used in practice?

A

Primarily for transplantation

Lupus Nephritis

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17
Q

What is the mechanism of action of cyclophosphamide?

A

Alkylating agent - crosslinks DNA to prevent replications

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18
Q

What are some indications for cyclophosphamide?

A 
Lymphoma
Leukaemia
Lupus nephritis*
Wegener's granulomatosis
Polyarteritis nodosum
*May not be as good as mycophenolate
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19
Q

What are the actions of cyclophosphamide?

A

Extremely strong anti-inflammatory

suppresses B and T cell activity

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20
Q

What are some ADRs for cyclophosphamide

A

May cause haemorrhagic cystitis
Renal excretion so adjust dose in renal impairment
Increased cancer risk
Infertility
Requires FBC monitoring
May not be the best drug for lupus nephritis and vasculitis.

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21
Q

What is the mechanism of action of methotrexate?

A

For malignancy, it works as an anti-folate, but the mechanism of action is unknown in non-malignant disease

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22
Q

What is methotrexate used for?

A

Gold standard for RA
Psoriasis
Crohn’s
Unlicensed for: inflammatory myopathies, vasculitis maintenance, steroid-sparing agent in asthma

23
Q

Give some ADRs for methotrexate

A 
Mucositis
Myelosuppression
Hepatitis
Cirrhosis
Pneumonitis
Increased infection risk
Highly teratogenic
Abortifacient
WEEKLY NOT DAILY DOSING
24
Q

What toxicity monitoring is required for methotrexate?

A

Baseline CXR
Baseline FBC, LFT, U+Es, creatinine
Followed by regular (eg monthly) FBC, LFT, U+E

25
Q

Give some actions of sulphasalazine

A 
T cell inhibition of proliferation
T cell apoptosis
Inhibition of IL-2 production
Reduced neutrophil chemotaxis
Reduced neutrophil degranulation
26
Q

Give some ADRs for sulfasalazine

A 
Myelosuppression
Hepatitis
Rash
Nausea
Abdominal pain
Vomiting
27
Q

Give some positives for sulfasalazine

A 
Safe in pregnancy
Effective
Favourable toxicity
Long-term blood monitoring may be unnecessary
Very few drug interactions
Not a carcinogen
28
Q

What are the effects of blocking TNF-alpha?

A

Inhibition of the cytokine cascade
Inhibition of leukocyte recruitent
Inhibition of elaboration of adhesion molecules
Reduced production of chemokines
Reduced angiogenesis due to reduced VEG-F and IL-8 levels
Reduced joint destruction due to reduced destructive enzyme release

29
Q

What is the stepwise management of asthma in adults?

A 
Step 1: mild intermittent asthma
Step 2: regular preventer therapy
Step 3: add-on therapy
Step 4: persistent poor control
Step 5: continuous or frequent use of oral corticosteroids
30
Q

What is prescribed for each step in the stepwise management of asthmatic adults?

A

1: Inhaled SABA as required
2: Inhaled corticosteroid
3: Inhaled LABA
4: Increased inhaled corticosteroid dose or addition of a fourth drug (leukotriene antagonist, SR theophylline)
5: Oral corticosteroids

31
Q

Describe good asthma control

A 
Minimal symptoms
Minimal need for reliever medication
No exacerbations
No limitation of physical activity
Normal lung function (FEV1 &/or PEFR>%predicted
32
Q

What should be done before initiating a stepping up of asthma control?

A

Check compliance with current therapies
Check inhaler technique
Eliminate trigger factors

33
Q

Briefly describe the pathophysiology of asthma

A

Th2-driven inflammation leads to:

  • Mucosal oedema
  • Bronchoconstriction
  • Mucus plugging
  • Bronchial hyperresponsiveness
  • (Potentially) Airway remodelling
34
Q

Give examples of SABAs

A

Salbutamol

Terbutaline

35
Q

What are the actions and mechanisms of SABAs?

A

Reversal of bronchoconstriction
Prevention of bronchoconstriction
Acts on bronchial smooth muscle to cause relaxation

36
Q

Why should SABAs not be used regularly?

A

Results in poor asthma control

Due to reduced inhibition of mast cell degranulation in response to allergens

37
Q

Give some side effects of beta 2 agonists

A

Tachycardia
Palpitations
Tremor

38
Q

What are the actions of inhaled corticosteroids?

A 
Improved symptoms
Improved lung function
Reduced frequency of exacerbations
Prevention of death
Due to reduced inflammation
39
Q

Give examples of corticosteroids used in asthma

A

Beclomethasone
Fluticasone
Budesonide

40
Q

Give examples of LABAs used in asthma

A

Formoterol

Salmeterol

41
Q

Can LABAs be prescribed alone?

A

No. They are not anti-inflammatory alone, and MUST be prescribbed with steroids. Failure causes increased incidence of exacerbations and deaths.

42
Q

How do Leukotriene receptor antagonists work?

A

Reduced LTC4 release by mast cells and eosinophils.

LTC4 can induce bronchoconstriction, mucus secretion and mucosal oedema, and promote inflammatory cell recruitment.

43
Q

Give some ADRs of LRAs

A 
Angioedema
Dry mouth
Anaphylaxis
Arthralgia
Fever
Gastric disturbance
44
Q

Give the mechanism of action of methylxanthines

A

We don’t really know

Could be phosphodiesterase of adenosine receptors

45
Q

Give some examples of methylxanthines

A

Theophylline (PO)

Aminophylline (IV)

46
Q

Give some methylxanthine ADRs

A 
Narrow therapeutic window
Nausea
Headache
Reflux
Toxic compilcations; arrhythmias, seizures
Many interactions
47
Q

Give some ADRs for LAMAs

A

Dry mouth
Urinary retention
Glaucoma

48
Q

Give some examples of LAMAs

A

Tiotropium

Ipratropium

49
Q

What are the clinical uses of LAMAs?

A

Mainly COPD
Can be used in step 4 or 5 of asthma control too
Reduces exacerbations in both

50
Q

Give some signs of severe acute asthma in adults

A

Any one of:

  • Unable to complete sentences
  • Pulse >110b/m
  • Respiration rate >25/m
  • Peak flow 33-50% predicted
51
Q

Give some features of life-threatening asthma

A 
PEF 4.5kPa
Silent chest
Cyanosis
Feeble respiratory effort
Hypotension
Bradycardia
Arrhythmia
Exhaustion
Confusion
Coma
52
Q

Give some features of near-fatal asthma

A

PaCO2 >6kPa

Mechanical ventilation

53
Q

What is the treatment of severe acute asthma?

A 
High flow O2 - aim for >94% sats
Nebulized salbutamol
Oral prednisolone 40mg for 10-14 days
Can add nebulized ipratropium if poor improvement
Consider aminophylline if no improvement

ESA 5 (17 decks)

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