Inflammation Flashcards
(171 cards)
1
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
2
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
3
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
4
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
5
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
6
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
7
Q
What is low and high dose methotrexate used for?
A
Low: Autoimmune diseases
High: Cancer chemo
8
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
9
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
10
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
11
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
12
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
13
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
14
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
15
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
16
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
17
Q
What are key side effects of MTX that mostly require cessation?
A
Bone marrow suppression
GI toxicity
Liver toxicity
Pulmonary toxicity
Skin reactions
18
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
19
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
20
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
21
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
22
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
23
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
24
Q
Why else would a prescriber temporarily stop MTX?
A
Prior to surgery or acute renal impairment
25
What should a pt do if they miss their dose of MTX?
Doses can be taken within 2 days, after than then mark it as a missed dose
Continue the following week as normal
26
What are key interactions with MTX and why?
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
27
What are the recommend vaccines to have when taking MTX?
Pnemonoccoal (one off) and Influenza
28
Can pts drink alcohol while taking MTX?
Alcohol can increase liver toxicity and so does MTX
The occasional drink is fine but not excessively
29
What is the indication for Leflunomide?
Psoratic arthritis
RA
30
What is the dosing schedule of Leflunomide?
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
31
How long after do the effects of Leflunomide begin to work?
Can start after 4-6 weeks and may further improve up to 4-6 months
32
What are the monitoring requirements when taking Leflunomide?
LFTs, FBC, BP
Prior to administration (pregnancy needs to be excluded)
Every 2 weeks for the first 6 months
Then every 8 weeks thereafter
33
Why does there need to be blood tests every 2 weeks (frequently) for the first six months of taking leflunomide?
Most cases of severe side effects (hepatic impairment) occurs there
34
What are the cautions when prescribing leflunomide?
Co administration with haemotoxic or hepatotoxic drugs
History or TB, can cause reactivation
Bone marrow suppression
35
What are the contraindications when prescribing leflunamide?
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
36
What are the requirements when wanting to get pregnant after stopping leflunamide?
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)
37
Describe the washout procedure for leflunamide:
Stop leflunamide
Give colestyramine 8g TDS or activated charcoal 50g QDS for 11 days
Can be repeated if required
38
What are the additional counselling points for pts taking leflunomide?
Avoid live vaccines
Avoid alcohol (increase risk of hepatic impairment)
Can be taken with or without food
39
What are the indications for ciclosporin?
IBD
Psoriasis
Immunosuppressive therapy in transplant patients (solid organ and bone marrow transplant)
Severe atopic dermatitis
RA
40
Name some severe side effects of ciclosporin?
Immunosuppression- increase risk of infection and increase risk of developing lymphomas and malignancies in skin
Important to limit exposure to UV light
41
What are the contraindications of ciclosporin?
Abnormal baseline renal function
Malignancy
Uncontrolled hypertension
Uncontrolled infection
42
Why would abnormal baseline renal function be a contraindication in ciclsporin?
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
43
What are the cautions in ciclosporin?
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)
44
What are the monitoring (baseline and throughout) requirements whilst taking ciclosporin?
Renal function
Hepatic function
BP
Lipids
Electrolytes e.g K, Mg
Uric acid
45
What are the common interactions with ciclosporin?
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
46
What is the difference in the oral and IV preparations of ciclosporin?
The oral dose of ciclosporin is around 3x that of IV formation
The oral has poor bioavialibility
47
What should be the specific administration requirements when using oral solution ciclosporin?
Required dose should be diluted down (mixed with orange or apple juice (no grapefruit)) immediately before admin
48
What are the counselling points for ciclosporin?
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
49
What are the inflammatory blood tests in RA?
Erythrocyte sedimentation rate (ESR)
Measure of degree of inflammation within joints
Can see increase with 24-48 hrs after inflammation
C reactive protein (CRP)
50
Name the immunological parameters for testing for RA:
Rheumatoid factor (RF)
Antinuclear antibody (ANA)
Anti-cyclic citrullinated peptide (anti-CCP)
51
What are the other tests when testing for RA?
Hb test (anaemia)
Radiology- can show damage and inflammation within the joints, in early disease it isn't always visible on an x-ray
52
What does being seropositive mean?
In RA where the patient has a positive result for RF/ anti-CCP
General indicator of more severe disease
53
What are the symptoms of RA on examination?
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
54
What is DAS-28 monitoring?
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'
55
What are the DAS-28 scores and what do they mean?
more than 5.1= active disease
Less than 3.2= low disease activity
Less than 2.6= remission
56
What are possible non-pharmalogical treatments for RA?
Physiotherapies
Occupational therapists- helping with ADLs, excerises
Orthotics- ADLs
Surgery in severe patients
57
What are the classes of treatment for RA?
Analgesics- NSAIDs
Glucocorticoids- decrease inflammation/pain
Conventional DMARDs
Biological DMARDs- Anti TNF/ other biologics
Targeted DMARDS- JAK inhibitors
58
What is the target for patients when on therapy for RA?
Treat to target
Remission (DAS<2.6)
Low activity (DAS<3.2)
59
What is the initial first line NICE treatment for RA?
First line cDMARD as monotherapy ASAP (ideally within 3 months of onset of symptoms)
e.g methotrexate, Leflunomide, Sulfasalazine
60
Why should glucocorticoids be used in initial treatment of RA?
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
61
Give examples of corticosteroids used initially in RA and their dosing:
Prednisolone PO 7.5mg/10mg OD up to 30mg
Methylprednisilone IV/IA/IM 120mg OW
62
What should be the second line NICE treatment for RA?
Add an additional cDMARD
More intense monitoring required
63
For those with a moderate disease, what is the response they should have to the third line treatment?
Moderate response
DAS ≥0.6 and ≥1.2 at 6 months to continue
64
For those with a severe disease, what is the response they should have to the third line treatment?
Moderate response
DAS greater than 1.2 at 6 months to continue
65
When would step down therapy be considered?
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
66
What is a major risk of biologics and why?
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
67
What are the guidelines when initiating a biologic regarding increased infection risk?
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
68
What is the correlation between biologics and malignancy and why?
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
69
Can pts drink alcohol while on biologics?
All biologics can be consumed within normal limits however if on DMARDs then cautioned
70
What is the correlation between cardiac failure and biologics?
Increase in potential risks with cardiac failure (class III or IV)
In TNFi can increase severity of symptoms, no problem in non TNFi
71
What are the monitoring requirements before and during being on biologics?
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
72
What would need to occur if someone has latent TB if needing to take biologics?
Require chemoprophylaxis prior to biologics as can cause reactivation
73
When should ongoing biologic therapy be reviewed?
At least every 6 months and for higher risk patients every 3 months
74
What is the indication for infliximab?
RA
IBD
Alkylosing spondylitis
Psoriatic arthritis
Psoriasis
75
What is the clinical response time for infliximab?
Clinical response achieved within 12 weeks if not may need to increase dose
76
Describe the process for the IV infusion of infliximab:
Over 2 hours and required 1-2 hours of observations afterwards
Pre-treatment- anti-histamine, hydrocortisone and/or paracetamol
77
Why does there need to be observations after the IV infusion of infliximab?
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
78
What is the NICE recommend diagnosis for OA?
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
79
What are the pharmacological treatments for OA?
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
80
What are the 5 stages of clinical presentation in gout?
Asymptomatic hyperuricaemia
Acute gouty arthritis
Interval gout/ intercritical gout
Chronic tophaceous gout
Gouty nephropathy
81
Describe the diagnosis process for gout:
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
82
What is the basic advice when having an acute gout attack?
Rest
Prompt treatment with full dose NSAIDS
83
Why shouldn't you give aspirin to someone experiencing a gout attack?
Competes with uric acid for excretion and can worsen attack
84
What is the first line treatment for an acute gout attack and describe them:
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
85
What is the second line treatment for an acute gout attack and describe it:
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
86
What is the dose of colchicine used for an acute gout attack?
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
87
What is the efficacy like of colchicine?
Response after 6 hours, pain relief after 12 hours and resolution after 48-72 hrs
88
What can be the interactions with colchicine?
CYP450i:
Clarithromycin, erthroymycin, dilitazem, verapamil
As can increase the levels of colchicine
89
What are the side effects of colchicine?
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
90
Describe oral corticosteroids which can be given in an acute gout attack:
Prednisolone 30-35mg daily for 5 days
Can be as effective as naproxen 500mg BD for 5 days
91
What is the treatment for resistant acute gout attacks?
Combo therapy:
NSAID with colchicine or coticosteroid
92
What is the name for the prophylaxis of gout and when is it started?
Urate Lowering Therapy
Important to prevent long term complications
Consider when pts suffer 2 or more acute gout attacks per year
93
Should you start URL during an acute gout attack, why/why not?
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
94
What should be taken for the phrophylaxis while uptitrating UTL?
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
95
What are the doses of allopurinol?
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)
96
What is the target serum urate levels?
Less than 300µmol/L
97
When should you start allopurinol after an acute attack, or what should happen if the patient is already on allopurinol?
Start 1-2 weeks after attack has subsided
If patient is already on allopurinol then continue and also treat the acute attack
98
What is the an alternative treatment for gout and why?
Febuxostat
If intolerant to allopurinol or GI side effects
99
What are the doses for febuxostat?
80mg OD, increase to 120mg if uric acid levels are more than 375µmol/L after 2-4 weeks
100
What is the second line treatment for gout and name 2 examples:
Uricosuric agents
Sulfinpyrazone
Probenecid (unlisenced)
101
How does the second line treatment for gout work?
Increase in uric acid secretion by direct action on renal tubule
Can be used with xanthine oxidase inhibitor
102
What are cautions and CIs of uricosic agents?
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
103
Name a major interaction with allopurinol and why?
With azathioprine
Azathioprine is metabolised to mercaptopurine
Mercaptopurine is metabolised by xanthine oxidase
Allopurinol causes accumulation
Potentially fatal by bone marrow suppression
104
Describe how smoking can influence IBD:
Worsens the clinical course of the disease
Increase risk of relapse and need for surgery
40% of CD patients are smokers (10% UC)- more likely to be an ex smoker (quit within first 2-5 years) or non smoker
Shows smoking may help prevent onset of UC
-chemicals affect colon sm, nicotene incline NO which alters gut motility and transit time
105
What are the different types of UC?
Starts in rectum- proctitis
SI+rectum- left sided colitis
LI+SI+rectum- universal= dancolitis
Not patchy, works its way up
106
What are the symptoms of IBD?
Depends on site, severity and extent:
-diarrhoea
-abdominal pain
-fever
-malaise
-lethargy
-N&V, more common in CD as related to upper GI
-weight loss, more common in CD as more severe and small bowel affected so decreased absorption
-malabsorption
-growth retardation in children
107
What are the clinical features of CD?
Tends to be more disabling than UC
Pain (particularly in lower right quadrant)
Palpable masses- can feel a lump
Anaemia
Small bowel obstructions
Abscesses
Fistulas
Gut perforation
108
What are the clinical features in UC?
Diarrhoea- possible with blood/ mucus
-up to 20 liquid stools a day
Abdominal cramp with fever
Constipation- due to narrowing
50% of UC pts have a relapse each year
-severe attacks can be life threatening
109
What parts of the body can experience complications of IBD?
Joints and bones
Skin
Eyes
Liver
110
Why do complications occur in patients with IBD?
50% of patients with IBD will get at least 1
Inflammation will spill over into other tissues, immune cells in gut can go to different areas
111
Describe the joint and bone complications in IBD:
Arthropathies (arthritis) and osteopenia (weakness bone matrix- cytokines activates OCs)
112
Describe the skin complications in IBD:
Erythema nodosum- tender hot red nodules, subside over a few days to leave brown skin discolouration
Pyoderma gangrenosum- pustule, develops into an ulcer
113
Describe the eye complications in IBD:
Episcleritis- intense burning and itching of BVs involved
Uveitis- headache, burning red eye, blurred vision
114
Describe the liver compilcations in IBD:
Sclerosing cholangitis
-chronic inflammation of the biliary tree
-leads to progressive fibrosis and biliary structures
115
What is the morbidity like in IBD?
QoL generally lower in CD than UC, especially because of recurrences after surgery
Increase risk of peritonitis (abdominal cavity) and malignancy
Malnutrition and chronic anaemia common in long standing CD
116
Describe blood tests for diagnosis of IBD:
Anaemia is common (iron and/or folate)
Raised ESR and CRP and a raised WCC
Hypoalbuminemia- some protein loss in gut
LFTs may be abnormal
117
Describe serological tests for diagnosis of IBD?
SC antibody usually present in CD
pANCA antibody, -ve in CD, +ve in UC
118
What is the Crohn's disease activity index (CDAI) score?
<150 or Harvey Bradshaw Index 4 or below = patient in remission
≥300 or HBI more than 8= severe active disease
119
Define what acute severe UC is:
Medical emergency
More than 6 bloody stools a day + 1 more:
-pulse >90bpm
-temp>37.5ºC
-Hb<10.5g/dL
-ESR>30mm/h
120
Describe the Montreal classification in UC:
E= extent
E1= proctitis E2= left sided E3= extensive
S=severe
S0=clinical remission S1=mild S2= moderate
S3= severe
121
Explain the severe section meanings in the Montreal classification:
S0= asymptomatic
S1= 4 or less stools, +/- blood, no systemic illness, normal inflammatory markers
S2= more than 4 stools, minimal toxicity
S3= more than 6 stools a day and rest
122
What is the first line treatment for inducing remission for mild to moderate UC- proctitis?
Topical aminosalicylate
Suppositories preferred over enemas due to delivering drug to rectum than further up
Suppositories increase mucosal conc and work better than oral
If patient decline topical consider oral aminosalicylate
123
What is the second line treatment for inducing remission for mild to moderate UC-proctitis?
If remission not achieved by 4 weeks, consider adding oral aminosalicylate (higher response with both together)
124
What is the third line treatment for inducing remission for mild to moderate UC- proctitis?
Consider adding topical or oral corticosteroid- time limited
Oral prednisolone- 40mg OD for 6-8 weeks
or prednisolone 5mg suppositories OD
125
What is the first line treatment for inducing remission for mild to moderate UC- proctosigmoiditis and left sided?
Topical aminosalicylate
Enemas preferred as go up further
1g day
126
What is the second line treatment for inducing remission for mild to moderate UC- proctosigmviditis and left sided?
If remission not achieved by 4 weeks,
add a high dose oral aminosalicylate or
switch to a high dose oral aminosalicylate and time limited topical corticosteroid
127
What is the third line treatment for inducing remission for mild to moderate UC- proctosigmviditis and left sided?
Stop topical treatment and offer oral aminosalicylate and time limited oral corticosteroid
128
What is the dosing for high dose oral aminosalicylates?
OD dosing is as effective as divided dosing
Greater than 2g a day were more effective at inducing remission, most pts respond to 2-3g day, higher doses are reserved for non-responders/severe
129
What is the first line treatment for inducing remission for mild to moderate UC-extensive?
Topical aminosalicylate AND high dose oral aminosalicylate
130
What is the second line treatment for inducing remission for mild to moderate UC-extensive?
If remission not achieved in 4 weeks,
stop topical treatment and offer a time limited course of oral corticosteroids
131
What is the treatment for inducing remission for moderate to severe UC?
Oral corticosteroid
Prednisolone 40mg-60mg OD (OD as causes less adrenal suppression)
Greater than 40mg doses lead to increased SEs
50% experience short term corticosteroid events
Improvements may be seen within 2 weeks of treatment
132
What are short term corticosteroid events?
Glucose intolerance
Oedema
Acne
Sleep disorders
133
What would be the weening off dosing for patients on long term, high dose corticosteroids?
2.5-10mg every week over 6-8 weeks
134
What is the first line therapy for inducing remission in acute severe UC (all areas)?
IV corticosteroids and assess likelihood of needing surgery
Methylprednisolone 60mg daily
Hydrocortisone 100mg QDS
Consider IV ciclosporin in these intolerant/decline/CI to corticosteroids
Symptoms should improve by day 3
135
What is the second line therapy for inducing remission in acute severe UC (all areas)?
If symptoms worsen or little improvement within 72 hours, consider adding IV ciclosporin to the corticosteroid
If ciclosporin CI, infliximab is an option
Also increase in VTE so need thromoboprophylaxis
136
What is the treatment for maintaining remission for mild to moderate proctitis and protosigmoiditis in UC?
Topical aminosalicylate alone (daily, at night or intermittent, every third night)
Oral aminosalicylate+ topical aminosalicylate (daily or intermittent)
Oral aminosalicylate alone- explain this isn't as effective as combined
137
What is the treatment for maintaining remission for left sided and extensive UC?
Offer low maintenance dose oral amino salicylate
138
What is the treatment for maintaining remission in UC in all areas after aminosalicylates fail/other reasons?
Consider mercaptopurine or azathioprine
-after 2 or more inflammatory exacerbations in 12 months that require systemic corticosteroids or if remission is not maintained by aminosalicylates
139
What is the treatment for inducing remission in CD?
Monotherapy with traditional glucocorticoid steroid (at first presentation or single inflammatory exacerbation in 12 months)
Prednisolone- PO 40mg OD
Methylprednisolone
Hydrocortisone IV
140
What is the second line treatment for inducing remission in CD and why?
Budesonide may also be considered
CI/ refusal to conventional corticosteroids
Not for severe presentations as not effective
Less effective than conventional but has fewer SEs
141
What is the third line treatment for inducing remission in CD?
Aminosalicylates if patient CI/decline corticosteroids- less effective than above but has fewer SEs
142
What would be the add on therapy for CD if 2 or more exacerbations in 12 months or if glucocorticoid dose cant be tapered?
Consider adding azathioprine (2.5mg/kg/day) or mercaptopurine (1-1.5mg/kg/day) to glucocorticoid or budesonide to induce remission
Slow onset of action 8-12 weeks
Consider MTX to GC or budesonide in those who can't tolerate aza/mer or low TPMT levels
143
Name and describe the biological agents used to treat CD:
Infliximab and adalimumab
For adults with moderately/ severe (fistulating) active disease, who hasn't responded to conventional therapy
Should be given as a planned course until treatment failure or 12 months after initiation
Continue if there is clear evidence or ongoing active disease
May also see therapy given with immunosuppressant
144
What are the symptoms of severe CD?
Very poor general health and/ more of the following:
-weight loss
-fever
-severe abdominal pain
-usually frequent 3-4 stools a day
145
What is the treatment for CD for maintaining remission?
Offer azathioprine or mercaptorupine when previously used in induction or if not previously received with adverse onset
MTX (15mg OD) only in those who needed it in induction, tried and did not tolerate/ CI azathioprine/ mercaptopurine
DON'T offer conventional glucocorticoid/ ASA/ budesonide
146
What is the treatment for maintaining remission in CD after surgery?
After completing macroscopic resection
Within the last 3 months, consider azathioprine in combo with metronidazole (for up to 3 months post op)
Azathioprine alone in those who cant tolerate metronidazole, don't offer biologics/ budesonide
147
What infections are associated with IBD and what should occur?
Novovirus
Camplybacter
Ecoli
C difficile - increase colectomy and mortality
If present, treatment needed
148
What should occur if a patient with IBD has cytomegalovirus (CMV)?
Potentially associated with refractory disease, immunomodulatory therapy and corticosteroids:
IV ganciclovir followed by oral valganciclovir treatment
149
What should be the infection monitoring requirements for a patient with IBD before starting immunosuppressive therapy?
Assess at diagnosis:
-infection history -HSV (oral/genital), VSV
-immunisation status
If history unclear- serology should be tested for immunity
Treat active HBV, latent/active TB, HCV or HIV prior to initiating therapy
150
What are the monitoring requirements before and during corticosteroid treatment for IBD?
FBC
Glucose/HbA1c
Lipids
BP
Eyes (cataracts)
Sleep/mood
151
What should all patients on corticosteroids take to help prevent osteoporosis?
800-1000mg Ca
800IU vit D
152
What should be the non pharmacological recommendations for an IBD patient to help prevent iron deficiency?
Annual FBC, ferritin and CRP monitoring
Dietary improvements- iron fortified foods, non haem iron and haem iron promotors of Fe absorption (via C rich) avoiding inhibitors (caffeine)
153
What are the pharmacological treatments for an IBD patient with an iron deficiency?
1st line IV iron (iron sucrose, ferric carboxymaltose,) active IBD
PO up to 100mg (elemental iron), mild anaemia with clinically active disease
Monitor every 3 months for a year, then every 6-12 months thereafter
154
What is the correlation with smoking and IBD?
Always check status
UC is more common in non smokers and more likely to arise in those who quit, linked to decreased surgery rates, less extensive disease, decrease need for therapy but should be encouraged to stop
155
What is the correlation with NDAIDs and IBD?
Conflicting data
May lead to increase in disease activity
May predicate relapse
Short term, low dose in patients with controlled disease (remission), potentially safe but try to avoid in practice
156
Which vaccinations should a patient with IBD receive?
Shouldn't receive live vaccinations if on immunosuppressants
Should receive covid-19
Aminosalicylate or no treatment, the vaccine should work as well as in the general population
Those on IS are though to have a decreased antibody response
Influenza vaccination- especially if on IS
Pneumococcal- 2 weeks before immunosuppressant initiation
157
What are the drug considerations for patients who have a stoma?
Pain control- non opioid, liquid or non coated tablets (not EC/MR)
High dose loperamide used, up to 64mg, QT prolongation (CV effects)
Antisecretory drugs (PPI) somatostatin decreases stoma output
Restrict oral hypotonic fluid (1L), use ORT
Hypocalcaemia risk- increase risk of digoxin toxicity
158
What are the cautions of sulfasalazine?
Hx of asthma- can cause dyspnoea and cough
Risk of haematological toxicity- causes blood disorders
Renal/ hepatic impairment- metabolism/ excretion routes
G6PD deficiency
Slow acetylator status
159
What are the common side effects of sulfasalazine?
Headache- 1/3 patients (less likely to occur if dose is uptitrated)
Nausea
Fever
Raised temp
Reversible infertility in men
Reduced WBC
Can colour urine and stain contact lenses yellow
160
What are the monitoring requirements for sulfasalazine and describe when:
FBC, LFT before and every 2nd week for first 3 months, then monthly for 3 months, then every 3 months
Creatinine, eGFR monthly for 3 months then as indicated
161
What are the symptoms a patient should report if on sulfasalazine and why?
Sore throat, fever, malaise, jaundice, unexpected non specific illness, may indicate myelosupression, haemolysis or hepatoxicity
162
What are the monitoring requirements prior to having mesalasine?
Renal function, U&Es, LFTs, FBC, and periodically until stabilised
Renal function- 6 monthly
Urea electrolytes, FBC, LFTS 6 monthly to annually
163
What are rectal enemas of aminosalicylates used for?
Foam enemas used to treat the proximal sigmoid colon
Liquid enemas can go up to the splenic flexure
Equally effective in proximal UC
Foam enemas preferred as easier to administer and retain
164
What are suppositories of aminosalicylates used for?
Indicated for use in disease up to rectosigmoid junction
Deliver drug more effectively to rectum than enema
165
What is the dosing regime for thiopurines and how long do they take to work?
Start at full dose
3-6 months to see effects
166
What are the monitoring requirements prior to initiation of thiopruines for IBD?
FBC, U&E, LFT
Screen for HCV, HIV, HBV/ VZV
Vaccinate
Ensure cervical screening up to date (increase cervical dysplasia with IBD)
Check TPMT and alter dose dependant on result- avoid in very low TMPT
167
What are the ongoing monitoring requirements for thiopurines for IBD?
FBC,U&E,LFT at least 2,4,8 and 12 weeks and then 3 monthly
168
What are the CI of thiopurine therapy for IBD?
Hypersensitivity, serious infections, pancreatitis, impaired bone marrow
169
What are the cautions of thiopurine therapy for IBD?
Decreased TPMT, renal and hepatic impairment
170
What are the counselling points for thiopurine therapy?
Inform about signs of myelosuppresion
Reduce exposure to sun due to increase risk of skin cancer
Take with meals to decrease risk of nausea- usually decreases within a few weeks
171
What is a major interaction with azathioprine and what should be the actions of this?
With allopurinol- reduce azathioprine to 1/4 of usual dose
Can switch to mercaptopurine
