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mpharm y3s1 > Inflammatory Clinical > Flashcards

Inflammatory Clinical Flashcards

1
Q

Does paracetamol have any anti-inflammatory effects?

A

Doesn’t have any significant anti inflammatory effects

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2
Q

What are special patient groups to look out for when paracetamol is being prescribed?

A

Children
Low body weight (less than 50kg)
Liver impairment (or those with risk factors for hepatotoxicity) -dose seen 500mg TDS

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3
Q

When would paracetamol be the preferred analgesic to prescribe over NSAIDs?

A

Elderly patients
Pts with hypertension, CVD, renal impairment, GI issues
Pts on medicines interacting with NDAIDs e.g warfarin

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4
Q

How does aspirin work as an anti platelet?

A

Inhibit thrombus formation in arteriole system, thrombi composed of little platelets with fibrin
Used for prevention of 1º and 2º CVD

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5
Q

What is the dose of aspirin as an antiplatelet?

A

75-300mg (LD dependent on indication)
No anti-inflammatory effect

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6
Q

What is the dose of aspirin for an analgesic effect?

A

300-900mg every 4-6 hrs when required
Max dose 4g

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7
Q

What are special patient groups to take into consideration when prescribing aspirin?

A

CI in children under 16
CI in pts with previous or active peptic ulcers, bleeding disorders, severe cardiac failure, previous hypersensitivity to NSAID
Elderly, increase SEs
Caution in pts with asthma- can cause bronchospasm

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8
Q

Why is aspirin contraindicated in children under 16?

A

It can cause a rare Reyes disease, leads to swelling in liver or brain
Only seen under very specialist use in Kawasaki syndrome

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9
Q

What are interactions with aspirin?

A

Drugs that increase risk of GI irritation and bleeding - steroids, NSAIDS, SSRIs, anticoagulants
Drugs that increase risk of renal SEs- biphosphonates
Drugs where aspirin can increase toxicity, therefore decrease clearance of other drugs- methotrexate

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10
Q

What are the available preparations of aspirin?

A

Tablet
Enteric coated
Dispersible
Suppository
Compound preparations

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11
Q

How long after does the analgesic and anti-inflammatory effects work of NSAIDS?

A

Analgesic effects starts soon after after first dose and full effect obtained within a week
Anti-inflammatory effect may not be achieved for up to 3 weeks

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12
Q

What is the difference in the different anti-inflammatory effect of the different NSAIDS?

A

Difference is small
Diclofenac and naproxen have slightly increased efficacy but they have increase side effects
Coxibs have similar effects as diclofenac and naproxen but have decreased SEs but increase CV risk

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13
Q

If an NSAID is indicated, how long should it be used for?

A

The LOWEST effective dose should be used for the SHORTEST duration

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14
Q

Name standard NSAIDs which are non selective:

A

Ibuprofen
Indomethacin
Mefenamic acid
Naproxen

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15
Q

Name standard NSAIDs which are non selective but preference for COX 2:

A

Diclofenac
Etodolac
Meloxicam

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16
Q

What are the GI side effects of NSAIDS and how are they caused?

A

Epithelial damage, ulceration and bleeding caused by:
1. Suppression of physiological homeostatic prostanoid (COX1) inhibition:
-reduced mucus production
-reduced bicarbonate production
-reduced mucosal blood flow

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17
Q

Group the NSAIDs from highest to lowest risk of SEs:

A

Highest risk: Piroxicam, Ketoprofen
Intermediate: Indomethacin, diclofenac, naproxen
Low risk: Ibuprofen (low dose)
Lowest risk: coxibs

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18
Q

What are the monitoring conditions for pts taking NSAIDS?

A

Pts have to report symptoms of dyspepsia/ GI irritation
Pts haemoglobin
Signs of GI bleeding/ haemoptosis/ dark stools

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19
Q

What effects do NSAIDs have on CV events?

A

Believed to be due to increase in selectivity for COX2 over COX 1 of vasculature, platelets and potential effects from the kidney
Ibuprofen 2.4g or more can increase CV risk

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20
Q

Group the NSAIDs from highest to lowest risk of CV events:

A

Highest risk: COX 2 inhibitors, diclofenac (150mg daily), Ibuprofen (2.4g daily)
Lower thrombotic risk: Naproxen (1g daily)
No evidence for Ibuprofen 1.2g or less

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21
Q

Which NSAIDs are contraindicated for which CV events?

A

COX 2 inhibitors, diclofenac and high dose ibuprofen in ischaemic heart disease, cerebrovascular disease and some stages of heart failure

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22
Q

When are NSAIDs cautioned in the use for which CV events?

A

Heart failure
Cerebrovascular disease
Ischaemic heart disease
Risk factors for CVD

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23
Q

What are CV interactions of NSAIDs?

A

Antihypertensives (opposite effect)
Antiplatelet dose aspirin (75mg)

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24
Q

When are renal side effects from NSAIDs seen?

A

In individuals where compensatory PGs are playing an important role to maintain renal function i.e advanced age, renal impairment, HF, volume depletion, liver cirrhosis
PGs have a limited effect in healthy individuals

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25
Q

Which effects on the kidney can NSAIDs cause?

A

Decrease in renal blood flow and increase the risk of acute kidney injury
Na and H2O rention, oedema and hypertension

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26
Q

What are renal interactions of NSAIDs?

A

Co-prescribed nephrotoxic meds (diuretics -ACEi)
Anti-hypertensive (opposite effect)
Lithium and methotrexate, decrease renal elimination causing toxicity (narrow therapeutic window)

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27
Q

What are the renal monitoring requirements when taking NSAIDs?

A

Renal function- eGFR, urine output, urea
BP
Electrolytes -Na/K
Oedema -weight/ visual signs

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28
Q

What is the risk of bronchospasm when taking NSAIDs?

A

10% of patients suffer (2-20%, up to 40%)

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29
Q

What are the recommendations when taking NSAIDs and asthma?

A

Cross sensitivity, pt who has had a reaction to 1 is likely to have a reaction to another
Not recommended to asthmatics who have not taken NSAIDs previously
If they have successfully used them in the past then they can use them but need to be aware of the risks and need to carry receiver therapy at all times, stop if any deteriorating symptoms

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30
Q

What is the relation between topical NSAIDs and systemic absorption?

A

Systemic absorption is much lower but can occur if pt uses it over a large area or using heat therapy along side it

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31
Q

What is low and high dose methotrexate used for?

A

Low: Autoimmune diseases
High: Cancer chemo

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32
Q

What is the oral bioavailability of MTX?

A

64-90%
Decreases at higher doses due to saturation of carrier

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33
Q

What is the frequency of admin of low dose MTX and why, how should this be portrayed on a Rx?

A

Once weekly on the same day each week
Reduce the risk of fatal overdose by inadvertent daily dosing
Prescriber should document this on the prescription in full, never as directed

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34
Q

What are the medicinal forms of MTX?

A

Oral
IM
SC

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35
Q

What medicinal forms are used first line for MTX and why would the second route be used?

A

Oral is first route
Parenteral routes may be used for pts suffering with GI SEs with measures already tried

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36
Q

Why is a test dose needed prior to MTX therapy and what is this dose?

A

To rule out idiosyncratic adverse effects
Dose is 2.5mg

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37
Q

What strength does MTX come in and which of these should be prescribed for low dose MTX treatment and why?

A

2.5mg tablets and 10mg
2.5mg should be used as a single strength tablet, never 10mg even if needing 10mg (use 4x 2.5)
To avoid confusion and overdose

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38
Q

How long can MTX take to have an effect on RA?

A

It can take 6 weeks for it to begin to work and 12 weeks to feel the maximum effect

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39
Q

What are the rules for dose escalation in MTX for RA?

A

To reach to optimal dose
Starting dose around 7.5mg and increase by 2.5-5mg every 1-3 weeks
Aim for optimal dose within 4-6 weeks

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40
Q

What are the baseline assessments needed when MTX is started?

A

Full blood count (FBC)
Liver function test (LFT)
Urea and electrolytes (U&E)
Renal function (creatinine, Cr or estimated Glomerular Filtration Rate eGFR)
Chest X -ray

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41
Q

Why would you need to check renal function when starting MTX?

A

Greater than 8% of MTX is excreted unchanged in urine so need to see how the kidney can handle this

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42
Q

Why would you need a chest X-ray when starting MTX?

A

Monitor signs of pulmonary toxicity

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43
Q

What are the ongoing assessments/monitoring needed while taking MTX and how often?

A

LFT
Renal function
FBC
Every 1-2 weeks until therapy is stabalised
Once stabilised every 2-3 months

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44
Q

What are the symptoms patients need to monitor for in themselves when taking MTX and why?

A

Signs of an infection i.e sore throat, bruising, bleeding- indicating blood disorders
Nausea, vomiting, abdominal discomfort and dark urine- indicating liver toxicity
Shortness of breath- respiratory effects

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45
Q

What are key side effects of MTX that mostly require cessation?

A

Bone marrow suppression
GI toxicity
Liver toxicity
Pulmonary toxicity
Skin reactions

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46
Q

What are key side effects of MTX which can come with solutions before cessation of therapy?

A

Acute reactions:
-sore throat, mouth ulcers (check WBC)
Sickness, diarrhoea, nausea
Generally improves after stabilising

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47
Q

What are the measures taken to improve acute side effects of MTX if pts experience them?

A

Can increase dose of folic acid
Can give an antiemetic short term
Can change MTX to sc admin

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48
Q

Why is folic acid always co-prescribed with MTX and give the dosing?

A

To reduce the risk of hepatotoxicity and GI side effects
5mg OD (1 to 6 days a week) not on the day of MTX

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49
Q

Describe the side effect of bone marrow suppression for MTX:

A

Evident as neutropenia in WCC
Thrombocytopenia - low platelet
Anaemia- red cell count
Pancytopenia- low everything
These symptoms are signs of infections, bleeding and bruising

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50
Q

Describe the side effect of severe GI (GI toxicity) for MTX:

A

Mucositis- inflammation of mucous membrane
Stomatitis- inflammation of mouth e.g ulcers
Oral or GI ulcers and GI bleeding

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51
Q

Describe the side effect of hepatotoxicity for MTX:

A

Yellowing of whites of eyes
Consistent nausea and vomiting
Monitoring LFTs, increase in ALT
May need to decrease dose but in large increase of ALT may need cessation

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52
Q

Describe the side effect pulmonary toxicity for MTX:

A

Dry cough, breathlessness, thoracic pain

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53
Q

What are the key contraindications for prescribing MTX?

A

Active infection- wait until gone
Severe renal impairment- as MTX mainly renal excreted
Hepatic (liver) impairment
Bone marrow suppression
Immunodeficiency
Pregnancy and breast feeding

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54
Q

What is the counselling point for patients of child bearing age while taking MTX?

A

Effective contraception during and for 3-6 months after stopping
No to breastfeeding

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55
Q

What are the key cautions and why for prescribing MTX?

A

Surgery- effects on bone marrow, increase infection
Renal impairment- reduce dose, extra monitoring
Diarrhoea- can cause renal impairment
Ascites- fluid collects in spaces within abdomen, MTX naturally accumulates there so increase accumulation
Peptic ulcer- increase GI toxicity
Elderly- naturally reduced folate, reduced renal and hepatic impairment

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56
Q

What should pts on MTX do if they come into contact with someone with chicken pox/ shingles if you haven’t had it before?

A

Contact the doctor as need to be treated due to chance of severe infection

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57
Q

What should occur if a patient has a severe infection while on MTX?

A

May have their MTX stopped until the infection has improved to improve the bodies natural ability to fight the infection

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58
Q

Why else would a prescriber temporarily stop MTX?

A

Prior to surgery or acute renal impairment

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59
Q

What should a pt do if they miss their dose of MTX?

A

Doses can be taken within 2 days, after than then mark it as a missed dose
Continue the following week as normal

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60
Q

What are key interactions with MTX and why?

A

Anti-folates e.g co-trimoxazole, trimethoprim, increase toxicity
NSAIDs- decrease excretion of MTX, can be taken together but needs to be closely monitored under direction of prescriber
Live vaccines
Ciclosporin- increases toxicity

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61
Q

What are the recommend vaccines to have when taking MTX?

A

Pnemonoccoal (one off) and Influenza

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62
Q

What if a patient takes too much MTX?

A

Seek medical help immediately

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63
Q

Can pts drink alcohol while taking MTX?

A

Alcohol can increase liver toxicity and so does MTX
The occasional drink is fine but not excessively

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64
Q

What is the indication for Leflunomide?

A

Psoratic arthritis
RA

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65
Q

What is the dosing schedule of Leflunomide?

A

PO
100mg OD for 3 days (loading dose)
Then decrease to 10-20mg OD (maintenance dose)
The LD can increase risk of adverse events, so LD can not be included if needed

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66
Q

How long after do the effects of Leflunomide begin to work?

A

Can start after 4-6 weeks and may further improve up to 4-6 months

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67
Q

What are the monitoring requirements when taking Leflunomide?

A

LFTs, FBC, BP
Prior to administration (pregnancy needs to be excluded)
Every 2 weeks for the first 6 months
Then every 8 weeks thereafter

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68
Q

Explain why there are specific monitoring requirements when taking Leflunomide?

A

Hepatic impairment- increased when used with other hepatotoxic meds, slight changes in LFTs may require a dose change but higher increase in LFTs may require cessation and wash out
Bone marrow suppression- leucopenia, anaemia, thrombocytopenia, pancytopenia, increase when other drugs cause same problems, may need cessation and wash out
Can increase BP (common)

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69
Q

Why does there need to be blood tests every 2 weeks (frequently) for the first six months of taking leflunomide?

A

Most cases of severe side effects (hepatic impairment) occurs there

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70
Q

Name common side effects of leflunomide:

A

GI (pain, anorexia, diarrhoea, vomiting)
Alopecia
Skin reactions (rash)- severe may require cessation

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71
Q

Name rare side effects of leflunomide:

A

Respiratory reactions: dyspnoea, cough, severe lung diseases
Dizziness

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72
Q

What are the cautions when prescribing leflunomide?

A

Co administration with haemotoxic or hepatotoxic drugs
History or TB, can cause reactivation
Bone marrow suppression

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73
Q

What are the contraindications when prescribing leflunamide?

A

Hepatic impairment- due to risk of accumulation as metabolism in liver
Severe immunodeficiency
Severe infection
Severe hypoproteinemia- drug is highly protein bound, so low protein can cause high drug plasma levels
Moderate to severe renal impairment
Pregnancy and breast feeding

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74
Q

What are the requirements when wanting to get pregnant after stopping leflunamide?

A

Effective contraception during and for 2 years after for women and 3 months after in men
Waiting time can be reduced if effective washing out system (plasma conc levels are low on 2 separate occasions)

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75
Q

What is the half life of leflunamide and how long does this mean it stays in the body for?

A

The half life is 1-4 weeks and it isn’t cleared from the body until 5 half lives have passed

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76
Q

Describe the washout procedure for leflunamide:

A

Stop leflunamide
Give colestyramine 8g TDS or activated charcoal 50g QDS for 11 days
Can be repeated if required

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77
Q

How and why is the wash out process needed in leflunamide?

A

Due to it staying in the body for a long time even after discontinuation
Believed to involve interruption of enterohepatic cycling or GI dialysis process

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78
Q

What are the additional counselling points for pts taking leflunomide?

A

Avoid live vaccines
Avoid alcohol (increase risk of hepatic impairment)
Can be taken with or without food

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79
Q

How does ciclosporin work?

A

A calcineurin inhibitor

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80
Q

What are the indications for ciclosporin?

A

IBD
Psoriasis
Immunosuppressive therapy in transplant patients (solid organ and bone marrow transplant)
Severe atopic dermatitis
RA

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81
Q

What are the medicinal forms of ciclosporin?

A

Capsules/ liquid
IV

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82
Q

What are very common and common side effects of ciclosporin?

A

Very:
Headache, tremor, hypertension, hirsutism, renal impairment
Common:
GI, fatigue, muscle cramps/ pain, hyperkalaemia/glycaemia, hypomagnesia

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83
Q

Name some severe side effects of ciclosporin?

A

Immunosuppression- increase risk of infection and increase risk of developing lymphomas and malignancies in skin
Important to limit exposure to UV light

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84
Q

What are the contraindications of ciclosporin?

A

Abnormal baseline renal function
Malignancy
Uncontrolled hypertension
Uncontrolled infection

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85
Q

Why would abnormal baseline renal function be a contraindication in ciclsporin?

A

Due to the common side effect of renal impairment
If occurs further on, then dose reductions and if it doesn’t improve within a month then cessation is required

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86
Q

What are the cautions in ciclosporin?

A

Elderly (decrease in renal/hepatic function) more likely to increase bp
Gout (increase in uric acid is a side effect)
Hepatic impairment (dose should be lowered)

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87
Q

What are the monitoring (baseline and throughout) requirements whilst taking ciclosporin?

A

Renal function
Hepatic function
BP
Lipids
Electrolytes e.g K, Mg
Uric acid

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88
Q

How regular should therapeutic drug monitoring of ciclosporin be carried out?

A

Levels of ciclosporin for non transplant pts can be done when unexpected response or it pt is showing sighs of toxicity
Levels of ciclosporin for transplant patients should be done very regularly

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89
Q

What are the common interactions with ciclosporin?

A

Cyp450 inhibitors: macrolides, diltiazem, verapamil, lercandidpine, ‘ozoles’, grapefruit juice (all increase levels of ciclosporin)
Cyp450 inducers: rifampicin, carbemzapine st johns wort (all decrease blood ciclosporin)
Statins: avoid or dose reductions (increase exposure to statins which causes renal failure)
Nephrotoxic drugs: NSAIDs/DMARDS
Any drugs causing same effects as ciclosporin e.g K+ sparing diuretics like spironolactone

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90
Q

What is the difference in the oral and IV preparations of ciclosporin?

A

The oral dose of ciclosporin is around 3x that of IV formation
The oral has poor bioavialibility

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91
Q

What should be the specific administration requirements when using oral solution ciclosporin?

A

Required dose should be diluted down (mixed with orange or apple juice (no grapefruit)) immediately before admin

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92
Q

What are the counselling points for ciclosporin?

A

Twice daily preparation
Should be maintained on the same brand
Consistency of admin- same time of day and proximity to food as exposure can increase with high fat meals
Avoid live vaccines

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93
Q

What is the pathophysiology of RA?

A

Autoimmunity, including Ab such as anti-citrullinated peptide antibodies (ACPAs) and RFs
Immune disregulators, Ab responses to modified peptides and increase production of cytokines and chemokines

94
Q

Name the signs and symptoms of RA?

A

Insidious onset (gradual changes or not at all)
Symmetrical inflammation
Progressive articular deterioration over time
Weight loss, fatigue, changes in mental health
Extra articular manifestations
Swan neck deformity- boutonniere deformity
RA nodules

95
Q

Describe insidious onset as a symptom of RA:

A

Fever, malaise, weakness, arthralgia (pain in joints)

96
Q

Describe symmetrical inflammation as a symptom of RA:

A

Pain, tenderness, swelling, stiffness (less than 30 mins from getting up), redness and joint warmth
Usually on the small synovial lined joints of the hands and wrist or feet, can affect any joint (Polyarthritis)

97
Q

Describe progressive articular deterioration over time in RA:

A

=Loss of function
Increase inflammation, destruction of bone and cartilage
Deformity, limited motion, pain on motion

98
Q

Describe extra articular manifestations as a symptom of RA:

A

Systemic
Lungs- pulmonary fibrosis
Heart- stroke/ cardiac failure, 2x increase of MI, increase in CVD
Eyes- sjogrens syndrome
Bone- osteoporosis

99
Q

What are RA nodules?

A

20% of patients get them
Firm lump that appears in sc round joints e.g fingers, toes, elbows
Poor prognostic factor, meaning increase of severity of disease

100
Q

What is the clinal course of RA?

A

It can vary between patients
Generally exacerbations/ flares and remissions with general chronic progressions- each flare not improving as much as last
Less likely self limiting

101
Q

What are the increased co-morbidities with RA?

A

CV risk, heart disease leads to 1/3 of RA deaths
Risk of infection
Risk of respiratory disease
Risk of osteoporosis
Risk of malignancy (decrease in bowel and breast, increase in lung and lymphoma)
Risk of depression

102
Q

What are the inflammatory blood tests in RA?

A

Erythrocyte sedimentation rate (ESR)
Measure of degree of inflammation within joints
Can see increase with 24-48 hrs after inflammation
C reactive protein (CRP)

103
Q

What is the ESR blood test?

A

Blood is left to settle in a solution in a column for 1 hr
Measure distance blood has moved
A more rapid fall down column indicated more inflammation due to inflammatory molecules attached to RBCs causing more clumping and to descent quicker
Not specific to RA

104
Q

What is the CRP blood test?

A

Protein that is produced from the innate immune response in liver
Begins to increase around 4-6 hrs after inflammation, peaks up to 38-50hrs
CRP can increase for a number of reasons including surgery/injury

105
Q

Name the immunological parameters for testing for RA:

A

Rheumatoid factor (RF)
Antinuclear antibody (ANA)
Anti-cyclic citrullinated peptide (anti-CCP)

106
Q

Describe the test for RF:

A

Type of autoantibody, but 30% of patients with RA don’t have it present
There are other inflammatory conditions which can give a +ve result for RF
It isn’t essential in diagnosis but presence can indicate a more severe disease

107
Q

Describe the test for ANA:

A

Type of autoantibody directed against components of nucleus
Present in 40% of patients with RA
Indicator of poor prognosis factor

108
Q

Describe the test for anti CPP:

A

More specific for RA than RF but not all patients have it
It is an antibody against citrilline (unusual a.a. formed when arginine altered)
Sign of more severe disease

109
Q

What are the other tests when testing for RA?

A

Hb test (anaemia)
Radiology- can show damage and inflammation within the joints, in early disease it isn’t always visible on an x-ray

110
Q

What does being seropositive mean?

A

In RA where the patient has a positive result for RF/ anti-CCP
General indicator of more severe disease

111
Q

What are the symptoms of RA on examination?

A

Limitation of motion e.g difficult to form a tight fist
Metacarpophalangeal (MCP) on hands or metatarsophalangeal (MTP) on feet - squeeze knuckle joints on hand or foot, if they have RA, will feel some gelling feeling and cause extreme pain

112
Q

What are the complete history notes needing to be taken to help with a diagnosis for RA?

A

Morning stiffness for greater than 30 mins
Stiffness after quiescence
FH, lifestyle
Other conditions that could predispose them

113
Q

What should the referral process be like in RA in primary care?

A

Refer to specialist with suspected persistent synovitis
Urgently if its affecting small joints of hands/feet, more than one joint, and/or a delay of more than 3 months before seeking advice

114
Q

What should the diagnosis process be like in RA once a referral has been made?

A

If found to have synovitis on clinical examination:
Blood test for RF, (for Anti-CCP abs if RF negative), x-ray on hands and feet

115
Q

What should be the additional investigations be like in RA once diagnosis has been made?

A

Any blood tests not done in diagnosis e.g Anti-CCP if RF was present in addition to a Health Assessment Questionnaire (HAQ)

116
Q

What is DAS-28 monitoring?

A

A measure of disease activity- 4 different measures
-Number of swollen joints (out of 28)
-Number of tender joints (out of 28)
-Measure of ESR or CRP
-‘Global assessment of health’

117
Q

What are the DAS-28 scores and what do they mean?

A

more than 5.1= active disease
Less than 3.2= low disease activity
Less than 2.6= remission

118
Q

What are the disadvantages of the DAS-28 scoring system?

A

The feet aren’t included, only arms and knees
Some patients don’t have an increase in ESR so lower score than disease is showing

119
Q

What are the 2 sets of guidelines that are looked at for the management for RA?

A

NICE guidance
EULAR- European League Against Rheumatism

120
Q

What are possible non-pharmalogical treatments for RA?

A

Physiotherapies
Occupational therapists- helping with ADLs, excerises
Orthotics- ADLs
Surgery in severe patients

121
Q

What are the aims of treatment for RA?

A

Minimise joint pain and swelling
Preventing deformity and radiological damage
Delay progression of disease
Maintain pts QoL
Control extra-articular manifestations

122
Q

What are the classes of treatment for RA?

A

Analgesics- NSAIDs
Glucocorticoids- decrease inflammation/pain
Conventional DMARDs
Biological DMARDs- Anti TNF/ other biologics
Targeted DMARDS- JAK inhibitors

123
Q

What is the target for patients when on therapy for RA?

A

Treat to target
Remission (DAS<2.6)
Low activity (DAS<3.2)

124
Q

What is the initial first line NICE treatment for RA?

A

First line cDMARD as monotherapy ASAP (ideally within 3 months of onset of symptoms)
e.g methotrexate, Leflunomide, Sulfasalazine

125
Q

Why should glucocorticoids be used in initial treatment of RA?

A

Short term (by 3 months) bridging when starting a new DMARD as it helps patient to adhere to therapy as DMARDs can take a while to work

126
Q

Give examples of corticosteroids used initially in RA and their dosing:

A

Prednisolone PO 7.5mg/10mg OD up to 30mg
Methylprednisilone IV/IA/IM 120mg OW

127
Q

What should be the second line NICE treatment for RA?

A

Add an additional cDMARD
More intense monitoring required

128
Q

What are the different types of DMARDs used in moderate RA, third line?

A

Anti-TNF
Targeted DMARDs
Ab blocking T cell activation

129
Q

What are the different types of DMARDs used in severe RA, third line?

A

Anti-TNF
Targeted DMARDs
Ab blocking T cell activation
Anti IL6
Anti B cell

130
Q

What is the score for third line moderate and severe disease?

A

Moderate (DAS between 3.2-5.1)
Severe (DAS greater than 5.1)

131
Q

Name 3 examples of Anti-TNF agents used in moderate RA:

A

Adalimumab +/- MTX
Etancercept +/- MTX = latex free
Infliximab +MTX

132
Q

Name 2 examples of Anti-TNF agents used in severe RA:

A

Certolizumab +MTX
Golimumab +MTX

133
Q

Name 2 examples of targeted DMARDs used in moderate RA:

A

Good as can be taken orally
Filgotinib +/- MTX
Upadacitinib +/- MTX

134
Q

Name 2 examples of targeted DMARDs used in severe RA:

A

Baricitinib +/- MTX
Tofacitinib +/- MTX

135
Q

Name 2 examples of Anti IL6 used in severe RA:

A

Sarilumab +MTX
Tocilizumab +MTX

136
Q

Name an example of an Ab blocking T cell activation used in both moderate and severe RA:

A

Abatacept + MTX

137
Q

Name an example of an anti B cell used in severe RA:

A

Rituximab +/- MTX

138
Q

For those with a moderate disease, what is the response they should have to the third line treatment?

A

Moderate response
DAS ≥0.6 and ≥1.2 at 6 months to continue

139
Q

For those with a severe disease, what is the response they should have to the third line treatment?

A

Moderate response
DAS greater than 1.2 at 6 months to continue

140
Q

When would step down therapy be considered?

A

If maintained for at least 1 year (without corticosteroids for a flare) consider step down stratergy
Cautiously reduce dosing/ stopping, return to previous DMARD therapy

141
Q

What is a major risk of biologics and why?

A

Increase risk of infection
e.g TNF inhibitors inhibit inflammation and modulates cellular IR, needed to be clear of intracellular infections as hosts defence compromised and infections may last longer and more severe

142
Q

What are the guidelines when initiating a biologic regarding increased infection risk?

A

Shouldn’t start it when having a severe infection
Have a flu and pnemoniccical vaccine
Inform doctor immediately if come into contact with chicken pox/shingles and haven’t had it before - should have the VSZ vaccine before starting
Pts over 50 should be given the herpes zoster vaccination if not CI before initiating treatment as a LAV

143
Q

What is the correlation between biologics and malignancy and why?

A

Increase risk of malignancy
Caution on other diseases e.g RA as can increase malignancy
Shouldn’t be used in those with clinical signs of malignancy who are under investigation, lower incidence in non-TNF

144
Q

Can pts drink alcohol while on biologics?

A

All biologics can be consumed within normal limits however if on DMARDs then cautioned

145
Q

What is the correlation between cardiac failure and biologics?

A

Increase in potential risks with cardiac failure (class III or IV)
In TNFi can increase severity of symptoms, no problem in non TNFi

146
Q

What is the correlation between TNFi and demyelinating diseases?

A

Use with caution as known to worsen symptoms

147
Q

What are the monitoring requirements before and during being on biologics?

A

Co-morbitites e.g COPD/renal failure as higher risk of infection
FBC
Renal function
LFTs including AST,ALT and albumin
Test for TB
Heb B and C screening
Chest X-ray

148
Q

What would need to occur if someone has latent TB if needing to take biologics?

A

Require chemoprophylaxis prior to biologics as can cause reactivation

149
Q

When should ongoing biologic therapy be reviewed?

A

At least every 6 months and for higher risk patients every 3 months

150
Q

What is the correlation between brand and biologic?

A

Pts should remain on their specific brand of treatment unless it is converted under the direction of the prescriber

151
Q

What does it mean that a patient on biologics should be traceable?

A

All patients need to be traceable in the disease registry:
-batch number
-brand
-pts on agents
essential for pharmacovigilance

152
Q

What is the indication for infliximab?

A

RA
IBD
Alkylosing spondylitis
Psoriatic arthritis
Psoriasis

153
Q

What are the formulations of infliximab?

A

Powder for infusion (IV)
Pre filled pen (SC)- good so patients can do it at home

154
Q

What is the dosing with infliximab?

A

With MTX once a week
3mg/kg at week 0,2,6 and then every 8 weeks thereafter

155
Q

What is the clinical response time for infliximab?

A

Clinical response achieved within 12 weeks if not may need to increase dose

156
Q

Describe the process for the IV infusion of infliximab:

A

Over 2 hours and required 1-2 hours of observations afterwards
Pre-treatment- anti-histamine, hydrocortisone and/or paracetamol

157
Q

Why does there need to be observations after the IV infusion of infliximab?

A

Due to risk of acute infusion reactions
Fever, chest pain, hyper/hypotension, angiodema, anaphylaxis
Risk of reaction is greater during the first 2 infusions
The infusion rate may be lowered (to 1 hr min) if no previous reactions

158
Q

What are very common side effects of infliximab?

A

Infection (URT)
Headache
Infusion related reaction
Pain

159
Q

What are serious reactions of infliximab?

A

Serious infections and reactivations
New or worsening HF
Delayed hypersensitivity (due to increase duration of drug interval)
Haemotological reaction

160
Q

Why should infliximab be used with MTX?

A

As inflixiamb is a foreign protein
MTX decreases the risk of Abs being formed

161
Q

What are CI of infliximab?

A

Hypersensitivity to other murine proteins
Severe infection, TB, absecess, opportunistic infections
Moderate to severe HF

162
Q

What are the cautions of infliximab?

A

Chronic/ history recurrent infection/ immunosuppressive drugs
Pts with demyelinating diseases
Malignancy
Mild HF
Elderly

163
Q

How is infliximab excreted?

A

Reused in the body as peptides- a.a for de novo synthesis and excreted via the kidneys

164
Q

What is a synovial joint?

A

Articular capsule filled with synovial fluid, helps lubricate joint and holds bone together

165
Q

What joints does osteoarthritis normally affect?

A

Can affect any joint, but most common in:
-*knee, hip, small joints in hands, spine

166
Q

What is the epidemiology of OA?

A

8.75 million people in UK over 45+
Prevalence increases with age
More common in women than men

167
Q

What is the impact of OA?

A

Co-morbidities
15% increase in hospitalisation
20% of patients with OA experience anxiety/ depression
QoL: - pain, work 1/3 ppl give up work

168
Q

Describe the pathophysiology in OA:

A

Whole joint is involved
Rate of damage exceeds rate of repair- leads to degradation
When cartilage is injured leads to an inflammatory response
Joint fails to dissipate load effectively
Leads to cycle of degeneration
Exposes bone to more load- body attempts to repair damage causes cartilage growths, becoming calcified->osteophytes, the inflammatory mediators can lead to complete cartilage destruction
Narrowing of joint space=synovitis (painful and tenderness of lining of synovial) and effusion (swelling of joint)

169
Q

What is the aetiology of OA?

A

Primary: idiopathic- cause unknown
Secondary: specific cause- previous injury to joint, congenital abnormality, inflammatory arthritis e.g gout

170
Q

What are the risk factors for OA?

A

Age (45+)
Female, may be due to drop of oestrogen levels in menopause
Obesity (BMI>25) 2.5-4.6x more likely to develop

171
Q

What are the genetic factors of OA?

A

Estimated heritability of 40-65% depending on joint site
Polygenetic

172
Q

How does NICE recommend to diagnose OA and why?

A

Diagnose clinically without investigations due to damage on X-ray not correlating to pain

173
Q

What is the NICE recommend diagnosis for OA?

A

Activity related joint pain AND
morning stiffness lasting no longer than 30 mins (or no morning stiffness) AND
over 45 years
Blood tests and X-rays may help aid diagnosis

174
Q

What are lifestyle changes that could be implemented if someone has OA?

A

Weight loss- releases burden on joints
Exercise- stretching, muscle strengthening, aerobic exercises
Physical aids- dexterity products, good quality foot wear, braces/ splints

175
Q

What are the pharmacological treatments for OA?

A

Mainly pain relief
Topical NSAIDs or topical Capsaicin
Paracetamol
Oral NSAIDs (+PPI)
Opioids, instead of NSAID if taking low dose or can’t tolerate them
Intra-articular corticosteroids-adjunct to core treatment for moderate/ severe pain

176
Q

Describe topical capsaicin as a treatment for OA:

A

0.025% cream
Little interactions
Applied at regular intervals QDS, to adjust to burning sensation
Relief begins in first week

177
Q

What are non pharmacological treatments for OA?

A

TENS machine
Heat cream isn’t recommended by NICE
Chondrotin/ glucosamine- can relieve pain
Surgery

178
Q

Give the evidence for taking Chondrotin/glucosamine for OA:

A

No stat sig benefit
NICE doesn’t advise it for routine advise
Chondrotin comes from shark cartilage
Glucosamine aids with synthesis of carb compounds in ligaments

179
Q

What is gout?

A

A group of diseases characterised by an increase in uric acid (hyperuricaemia)
Gout is a clinical manifestation where as the increased uric acid doesn’t mean you have gout

180
Q

What is gout caused by?

A

Increase production of uric acid or decrease excretion of uric acid or both
Deposition of monosodium rate monohydrate crystals in joints and soft tissues, leads to acute inflammation and tissue damage

181
Q

What is the epidemiology of gout?

A

2.49% prevalence in UK
More common in men (30-60yrs) and in older people (rare in under 20)
Ratio M:F 4.3:1
More likely with a family history

182
Q

How is uric acid excreted?

A

Uric acid is end product of purine metabolism
Uric acid excretion mainly in kidney, completely filtered by glomerulus
90-100% is reabsorbed in proximal tubule by URAT-1 specific anion transporter
50% actively secreted in DT
40-45% post secretary reabsorption
5-10% of original glomerular load is excreted in urine
2/3 of rate excreted in urine
1/3 of rate excreted through bile in GI tract

183
Q

What is the aetiology of gout?

A

Caused by:
-an increase in synthesis of purine precursors or uric acid (10%)
-a decrease in elimination of uric acid by kidney (90%)

184
Q

Name and describe the different types of gout?

A

Primary- due to the rare inborn errors of metabolism or renal excretion
Secondary- occur due to drugs or consequence of other disorder

185
Q

How can over consumption cause gout?

A

Over consumption of foods rich in purines
e.g offal (liver, kidney, heart, sweetbreads), game, oily fish, seafood, yeast or meat extracts

186
Q

How can over production cause gout?

A

Only 10% of cases
Excessive cell turnover (e.g neoplastic disease, psoriasis, haemolytic anaemias)
Cell lysis caused by chemo and radiology
Excessive synthesis of uric acid due to rare enzyme mutation defects

187
Q

How can under excretion cause gout?

A

90% of cases
Hyperuricaemia, large urate, loads filtered through glomerulus, leads to increase in rate reabsorption in patient to avoid dumping of insoluble rate in UT
Also decrease in tubular secretion
Overal reduction in excretion

188
Q

What can cause under excretion in gout?

A

Renal failure
Alcohol (beer), high levels of purine but also in itself
Drugs:
-*diuretics, especially thiazides (furosemide, bendro)- cause volume depletion, decrease in tubular excretion of uric acid
-aspirin, ciclosporin, omeprazole, etc
Physical stress, tight shoes, hill walking
Hypertension, obesity, hypertriglyceridemia

189
Q

What is the pathophysiology of gout?

A

Uric acid is a weak acid, pKa 5.8
At physiological pH it is ionised to MSU
If supersaturation occurs, it leads to crystal formation
Solubility is influenced by temp of environment, pH, cation conc

190
Q

What is the solubility limit of uric acid?

A

Greater than 380 micromol/ml

191
Q

Describe the crystals of uric acid and what can they cause?

A

Long thin crystals
Crystal deposition may continue for many months/ years without causing symptoms
Only cause symptoms when they shed into bursa (small sacs of synovial fluid surrounding joint) causing and inflammatory reaction

192
Q

What can the shedding of uric acid crystals be caused by?

A

Trauma
Dehydration
Rapid weight loss
Illness and surgery

193
Q

How can urate crystals control an inflammatory response?

A

Through humeral and cellular inflammatory mediators
Complement system

194
Q

What inflammatory response does urate crystals cause?

A

A pro inflammatory cascade of cytokines, chemotactic factors, TNF
Inflammatory cell accumulation (monocytes and mast cells in early phase and neutrophils later)
IL1B has been shown to to be related

195
Q

What are the 5 stages of clinical presentation in gout?

A

Asymptomatic hyperuricaemia
Acute gouty arthritis
Interval gout/ intercritical gout
Chronic tophaceous gout
Gouty nephropathy

196
Q

Describe where acute gouty arthritis occurs:

A

90% acute attacks are monoarticular (occur in 1 joint)
80% of first attacks in first metatarsophalangeal joint of big toe (podagra)
Other attacks: small joints of feet/ankles, hands, elbows, knees

197
Q

What are the symptoms of acute gouty arthritis?

A

Severe pain with hot, red, swollen and extremly painful joints
Begins abruptly- max intensity 8-12hrs
Weight bearing impossible
Erythema- redness
Synovitis- inflammation of synovial membrane
Leucocytosis- Increase in WCC
Confusion in elderly

198
Q

What if acute gouty arthritis is left untreated?

A

The attack lasts around 7 days but causes desquamation of overlying skin (shedding)

199
Q

What is intercritical gout?

A

Time between acute attacks of gout
Variable intervals of months/ years where there are no symptoms

200
Q

Describe chronic tophaceous gout:

A

Presence in tophi
White deposits of MSU (monosodium urate)
Nodule formation affecting joints
SC and periarticular areas- in skin and around joints (ears, fingers, Achilles tendon)

201
Q

Describe gouty nephropathy/ hyperuricamia induced renal disease:

A

Normally people who have presence of tophi- had it a long time
Crystals of urate deposited around renal tubules leading to inflammatory response (interstitial nephritis)
Proteinuria and renal impairment
Renal stone formation

202
Q

Describe the diagnosis process for gout:

A

Has to be based on clinical history and examinations
Uric acid levels can be useful but aren’t always raised when someone has an attack (repeat 2-3 weeks after if no raise)
Joint fluid microscopy- presence of crystals and absence of infection (to rule out septic arthritis), not always done as risk of infection
Joint x-ray
Standard bloods: RF, lipids, glucose

203
Q

What is the basic advice when having an acute gout attack?

A

Rest
Prompt treatment with full dose NSAIDS

204
Q

Why shouldn’t you give aspirin to someone experiencing a gout attack?

A

Competes with uric acid for excretion and can worsen attack

205
Q

What is the first line treatment for an acute gout attack and describe them:

A

NSAIDs
Releive pain and inflammation
Can abort attack if taken early enough (pt need to carry supplies)
Most important factor is how soon it is taken rather than the choice of the NSAID
Full therapeutic high dose for 24-48 hrs then lower doses for 7-10 days until completely resolved
Consider gastro protection

206
Q

What is the second line treatment for an acute gout attack and describe it:

A

Colchicine when NSAIDs are CI or ineffective e.,g CVD, renal disease, GI toxicity
Slower onset and higher level of toxicity
Inhibits neutrophil migration to joint
Administer ASAP as less effective over time

207
Q

What is the dose of colchicine used for an acute gout attack?

A

0.5mg 2-4 times a day until relief of joint pain or development of GI SEs or total of 6mg taken
Do not repeat course within 3 says
Lower dose of 0.5mg every 8 hrs in elderly and renal impairment

208
Q

What is the efficacy like of colchicine?

A

Response after 6 hours, pain relief after 12 hours and resolution after 48-72 hrs

209
Q

What can be the interactions with colchicine?

A

CYP450i:
Clarithromycin, erthroymycin, dilitazem, verapamil
As can increase the levels of colchicine

210
Q

What are the side effects of colchicine?

A

N&V
Abdominal pain
Diarrhoea- stop therapy immediately as has potential to cause direct mucosal damage and to lining of gut and this is a symptom
Rare:
Rashes, peripheral neuropathy

211
Q

Describe oral corticosteroids which can be given in an acute gout attack:

A

Prednisolone 30-35mg daily for 5 days
Can be as effective as naproxen 500mg BD for 5 days

212
Q

Describe intra-articular corticosteroids which can be given in an acute gout attack:

A

Triamcinolone, good safety profile
Consider in monoarthritis or easily accessible joint

213
Q

What is the treatment for resistant acute gout attacks?

A

Combo therapy:
NSAID with colchicine or coticosteroid

214
Q

What is the name for the prophylaxis of gout and when is it started?

A

Urate Lowering Therapy
Important to prevent long term complications
Consider when pts suffer 2 or more acute gout attacks per year

215
Q

Should you start URL during an acute gout attack, why/why not?

A

Traditionally no
Hyperuricaemic for several years, so no need to treat immediately
Decrease in serum uric levels leads to mobilisation of uric acid stores and may prelong/ precipitate another

216
Q

What should UTL achieve?

A

Reduces freq of flares
Once crystals dissolved avoids reccurance
Reduces size and number of tophi
Facilitates tophi disappearance- improve QoL

217
Q

What should be taken for the phrophylaxis while uptitrating UTL?

A

Recommend during the first 6 months of UTL or during a dose titration
Colchicine first line:
0.5-1mg daily, reduce in renal impairment
Where CI or not tolerated, a low dose NSAID should be used with gastro protection

218
Q

What is the first line prophylaxis for gout and why?

A

Allopurinol
Controls symptoms
Some improvement in tophi (usually after 6 months of treatment)
Xanthine oxidase inhibitor
Pro drug, undergoes hepatic metabolism to active metabolite, oxypurinol

219
Q

What are the doses of allopurinol?

A

Start with 100mg daily
Increase every 3-4 weeks according to response to achieve a decreased urate serum level
Maintenance 300mg daily (100-600mg)
Accumulate in renal impairment (50-100mg)

220
Q

What is the target serum urate levels?

A

Less than 300µmol/L

221
Q

What are common side effects of allopurinol?

A

Rashes
Hypersensitivity reactions
GI disturbances

222
Q

When should you start allopurinol after an acute attack, or what should happen if the patient is already on allopurinol?

A

Start 1-2 weeks after attack has subsided
If patient is already on allopurinol then continue and also treat the acute attack

223
Q

What is the an alternative treatment for gout and why?

A

Febuxostat
If intolerant to allopurinol or GI side effects

224
Q

What are the doses for febuxostat?

A

80mg OD, increase to 120mg if uric acid levels are more than 375µmol/L after 2-4 weeks

225
Q

What are side effects of febuxostat?

A

GI
Headache
Increased LFTs
Oedema
Rash

226
Q

What is the second line treatment for gout and name 2 examples:

A

Uricosuric agents
Sulfinpyrazone
Probenecid (unlisenced)

227
Q

How does the second line treatment for gout work?

A

Increase in uric acid secretion by direct action on renal tubule
Can be used with xanthine oxidase inhibitor

228
Q

What are cautions and CIs of uricosic agents?

A

Avoid in urate nephropathy
Ineffective in poor renal function (CrCl < 20-30ml/min)
Need to maintain high fluid intake to decrease risk of stone formation

229
Q

Name a sc treatment for the prophylaxis of gout:

A

Canakinumab

230
Q

What is the MoA Canakinmab?

A

Recombinant MAB
Severe, refractory tophaceous gout
Target IL1B, associated with inflammatory response induced by urate crystals

231
Q

What are the CI of Canakinmab?

A

In current infections as can increase the risk of sepsis

232
Q

Name a major interaction with allopurinol and why?

A

With azathioprine
Azathioprine is metabolised to mercaptopurine
Mercaptopurine is metabolised by xanthine oxidase
Allopurinol causes accumulation
Potentially fatal by bone marrow suppression

mpharm y3s1 (13 decks)

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