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IBD Flashcards

1
Q

what is IBD?

A
  • Chronic disease
  • Causes inflammation of the digestive tract
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2
Q

what are the two main forms of IBD?

A

– Ulcerative Colitis
– Crohn’s Disease

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3
Q

what is the key difference between UC and CD?

A

Key differences between the two are the LOCATION and
EXTENT of the inflammation

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4
Q

what complications occurs in UC?

A

pancolitis- all
distal colitis-
proctitis-

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5
Q

how/where does CD affect the intestines?

A

terminal ileum
ilecolon- patchy inflam and stricture
colon

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6
Q

what is CD?

A

Typically involves the distal ileum or colon but can affect the ENTIRE digestive tract.
* Starts as an inflammatory lesion which develops into ulceration of the mucosa and then progresses to deeper
layers

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7
Q

what is CD characterised by?

A

– Areas of healthy tissue .v. diseased tissue giving characteristic
‘skip lesions’
– Cobblestone appearance

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8
Q

what is the most common type of IBD?

A

UC

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9
Q

what is UC characterised by?

A

– Characterised by diffuse inflammation and crypt abscesses

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10
Q

how often does IBD occur?

A

Both diseases following a relapsing/remitting
course
* Patients can be well going long periods without (or with very few) symptoms, however, this is often followed by periods of active disease when symptoms flare up

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11
Q

where does CD affect?

A

– Typically involves distal ileum,
proximal colon
* Can affect the entire digestive tract
– Inflammation can go through entire
thickness of the bowel wall

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12
Q

where does UC affect?

A

– Only affects the colon
– Diffuse inflammation
– Affects the colonic mucosa

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13
Q

how do signs and symptoms vary for IBD?

A

depending on the site and severity of inflammation

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14
Q

what are the overlapping symptoms in UC and CD?

A

– Abdominal pain/cramping
– Diarrhoea
– Fever
– Tiredness/Fatigue
– Weight loss/Reduced appetite
– Mouth sores

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15
Q

where does abdominal cramping affect?

A
  • In U.C this is usually in the lower abdomen and
    tends to be a colicky type pain. Pain is usually
    severe in severe colitis.
  • In C.D pain is often in the RLQ and more
    prevalent than in U.C
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16
Q

what causes abdominal pain in IBD?

A

Inflammation/ulceration can affect the normal
movement of the intestines/colon and its
contents resulting in pain/cramping

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17
Q

is diarrhoea common in IBD?

A

– Common problem
– Intestinal cramping can contribute to it
– Blood can be present
– U.C: tend to get bloody, mucoid diarrhoea due to the
inflammation of the mucosa
– Can occur during the night as well

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18
Q

why would someone get a fever with IBD?

A

– Usually low grade and due to underlying inflammation
(and or infection)

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19
Q

why would someone be tired with IBD?

A

– Can be in part due to the development of
anaemia

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20
Q

why would weightloss/ reduced appetite be a probelm in IBD?

A

– Due to reduced ability to digest/absorb food
– Often get malabsorption
– Many IBD patients have a reduced BMI

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21
Q

what are some extra-intestional manifestations of IBD?

A

Inflammation of the skin, eyes, joints and liver
failure to thrive in children

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22
Q

what are the potential complications of IBD?

A

– Increased risk of colon cancer
– Surveillance monitoring is in place as per NICE
recommendations with colonoscopies for this patient
group
– Malnutrition
– Due to excess diarrhoea and malabsorption
– Anaemia
– Iron deficiency; bleeding from the GI tract due to
inflammation
risks ass with medication
blood clots
primary sclerosing cholangitis

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23
Q

what are potential complications of CD?

A

Narrowing of the bowel wall
* Obstruction
– Due to strictures caused by spasms, scarring, oedema
and luminal narrowing, this can lead to fistulas
* Fistulas
– Abnormal connection between two areas of the intestine
– Ulcers
– Anal fissures and perianal lesions such as
skin tags and abscesses

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24
Q

what are the potential complications of UC?

A

– Toxic megacolon
– Dilation of the colon causing severe abdominal
pain, tenderness and distention
– At a significant risk of bowel perforation
– Associated with a 50% mortality rate
– Perforated colon

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25
Q

what are the risk factors of IBD?

A

– Age
– Family History
(10 – 20%)
– Infection (50%)
– Smoking
– Medication
* NSAIDS

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26
Q

what are the causes for IBD?

A

– Not well understood
– Genetics
– Environmental
triggers
– Autoimmune

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27
Q

what type of IBD has an autoimmune component?

A

CD

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28
Q

what are environemtal risk factors for IBD?

A
  • Smoking
    – Associated with increased risk of developing C.D whereas with U.C at a greater risk of developing if you don’t smoke
  • Diet
    – Certain foods might affect the already damaged mucosal lining and trigger a flare e.g. caffeine, spicy, fatty foods
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29
Q

how is diagnosis made?

A

Based on a combination of factors, not just
one element:
– Examination and history taking
* Abdomen may be tender and slightly distended;
PR may show presence of blood
– Colonoscopy/sigmoidoscopy
* Biopsies
* 2 biopsies from 5 different sites
– Stool cultures
* Relapses can be associated with pathogens,
therefore, always check in a flare

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30
Q

what blood test will be done for diagnosis and why?

A

Anaemia
* FBC: looking for presence of iron or B12 deficiency due to chronic
inflammation, blood loss and/or malabsorption
– Inflammation
* Increase in WCC, platelets, ESR an CRP (all useful markers of
active inflammation)
– LFT’s may be abnormal
* Reduced albumin due to malabsorption
* Raised ALP, AST, ALT and bilirubin due to primary sclerosing
cholangitis
– U&E’s
* Dehydration and electrolyte imbalances
– Faecal calprotectin
* Calprotectin: protein released into faeces when neutrophils gather
at the site of inflammation
* Help guide management and diagnosis
* Determine if urgent imaging is needed and has prevented
unnecessary referrals for colonoscopy

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31
Q

how will x-rays and endoscopy help in diagnosis?

A

Abdominal x-ray
– Rule out toxic megacolon
* Endoscopy
– If you suspect inflammation is higher up in the GI
Tract

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32
Q

what is it important to ruele out in the differential diagnosis?

A

– Colorectal cancer
– Other forms of IBD/colitis e.g. ischaemic
– Infection
– Diverticular disease
– Irritable bowel syndrome
– Appendicitis
– Ectopic pregnancy
– Pelvic inflammatory disease

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33
Q

what general support should you give to someone with IBD?

A

– Fertility and contraception
– Monitoring
– Advice
– Interactions
– Side-effects

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34
Q

what are general supportive issues that are important to inform patient of?

A
  • Possible delay of growth and puberty in children
    and young people
  • Diet and nutrition
    – Avoid fatty, sugary foods – encourage a healthy high fibre diet
  • Fertility
    – Can be reduced in active disease (women)
  • Prognosis
  • Side effects of their treatment
  • Cancer risk
  • Smoking cessation
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35
Q

when are aminosalicylates mostly used?

A

UC
dont use a lot in CD

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36
Q

when are antibiotics used in therapy?

A
  • Used if underlying infection
  • In fistulating C.D
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37
Q

what is the treatment aim in IBD?

A
  • Heal the inflammation and in turn reduce
    symptoms during a flare up i.e. induce
    remission
  • OR
  • Prevent flare ups from happening
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38
Q

what should you treat a patient when inducing remission in CD?

A

Corticosteroids
– Offer monotherapy with a conventional glucocorticosteroid (prednisolone, methylprednisolone or intravenous hydrocortisone) to induce remission in people with a first presentation or a single inflammatory exacerbation of Crohn’s disease in a 12-month period.

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39
Q

what should you offer In people with one or more of distal ileal, ileocaecal or right-sided colonic disease who decline, cannot tolerate or in whom a conventional glucocorticosteroid is
contraindicated?

A

budesonide
less effective but fewer side effetcs

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40
Q

what should you consider when prescribing corticosteroids as treatment?

A

When long term corticosteroid therapy is used in some chronic diseases, the adverse effects of treatment may become greater than the disabilities of the disease.
* To minimise side-effects the dose should be kept as low as possible and used for the shortest possible time

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41
Q

what are some early and delayed side effects of corticosteroids?

A
  • Early effects
    – Acne
    – Oedema
    – Sleep & mood disturbance
    – Dyspepsia
    – Impaired Glucose tolerance
  • Delayed Effects
    – Cataracts
    – Osteoporosis & osteonecrosis
    – Myopathy
    – Susceptibility to infection
    – Moon face
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42
Q

what are glucocorticoids side effects?

A

– Diabetes
– Osteoporosis
– Muscle wasting
(myopathy)
– Peptic ulceration
and perforation
– Psychiatric reactions

43
Q

what are mineralocorticoid side effects?

A

– Hypertension
– Sodium retention
– Water retention
– Potassium loss
(more of an issue
with longer term
use)
– Calcium loss

44
Q

when do you use oral corticosteroids?

A

Moderate to severe– Budesonide potent corticosteroid with reduced systemic toxicity -only effective in ileal disease due to site of release– Tapering – the more severe the exacerbation the slower the schedule should be. Average 5 mg / week– May need to adjust / slow down to cover introduction of aza/6mp (3 months to effect)

45
Q

when do you use topical steroids?

A

Depend on the site of inflammation – used more in U.C– Suppositories - proctitis

46
Q

when do you use IV steroids?

A

– Severe; patients are vomiting – Hydrocortisone

47
Q

why may adrenal suppression occur? what are the signs and symptoms?

A

Acute withdrawal after a prolonged period can
lead to acute adrenal insufficiency, hypotension or death.

48
Q

when should gradual withdrawl be used in steroid treatment?

A

– Received more than 40mg of prednisolone (or equivalent) for
more than 1 week
– Been given repeated doses in the evening
– Received more than 3 weeks treatment
– Recently received repeated courses
– Taken a short course within 1 year of stopping long term therapy.

49
Q

why is osteoporosis linked to IBD?

A

due to higher levels of corticosteroid use but also:
– Lower BMI
– Reduced physical activity
* Increased risk of poor posture, balance and muscle weakness
– Disease activity

50
Q

how do you manage osteoporosis in IBD?

A

– Management of underlying disease, good nutrition, avoidance of steroids as far as possible.
– Lowest effective dose or steroids for shortest time possible
– Aza/6MP use at early stage
– Biological therapy or surgery should be considered if patient is unable to maintain a steroid free remission

51
Q

when should bisphosphonates be given in patients with osteoporosis in IBD?

A

– When on steroids for all >65 years
– If <65 but need steroids for >3 months
– Stopped when steroids stopped unless indicated on other grounds

52
Q

how should you induce remission in a patient with crohn’s disease?

A

In people who decline, cannot tolerate or in whom a conventional glucocorticosteroid is contraindicated,consider 5-aminosalicylate treatment for a first presentation or
a single inflammatory exacerbation in a 12-month period.

53
Q

when would you consider as an add on treatment when inducing remission in CD?

A

Consider adding azathioprine or 6-mercaptopurine to a
conventional glucocorticosteroid or budesonide to induce
remission of Crohn’s disease if:
– there are two or more inflammatory exacerbations in a
12-month period, or
– the glucocorticosteroid dose cannot be tapered

54
Q

what should you assess before add on treatment?

A

Assess TPMT activity before offering azathioprine or
mercaptopurine. Do not offer azathioprine or 6-mercaptopurine if TPMT activity is deficient (very low or absent). Consider azathioprine or mercaptopurine at a lower dose if TPMT activity is below normal but not deficient

55
Q

when should you consider adding methotresate to steroid to induce remission in CD?

A

people who cannot tolerate azathioprine or
mercaptopurine, or in whom TPMT activity is deficient.

56
Q

what should people be warned about on azathioprine?

A

– Patients should be warned about the possibility of bone marrow suppression i.e. infection or unexplained bleeding or bruising
– Should report to prescriber immediately

57
Q

what monitoring should be done for azathioprine?

A

– TPMT before prescribing
– FBC every 2 weeks for 3 months, then 3 monthly
– ALT* Increases in response to drug toxicity
– CRP * If levels reduce – good marker that the treatment being used is being successful
– U&Es* Check renal function for excretion of the drugs

58
Q

what are the main interactions to be aware of for azathioprine?

A

Allopurinol
– high risk of increased toxicity.
– Life-threatening reaction
* Warfarin
– Possible reduction in INR
– Monitor closely and remember may take 3 months for effect
* Trimethoprim / co-trimoxazole
– Increased risk of thrombocytopenia & neutropenia – avoid
* Clozapine
– Increased risk of agranulocytosis - avoid

59
Q

what is 6MP?

A

Metabolite of azathioprine
* Better tolerated and may be more effective
than AZA
* Interactions, side effects and monitoring –
as for azathioprine

60
Q

what is TPMT?

A

Thiopurine Methyl Transferase
* Enzyme responsible for metabolism of azathioprine / 6MP

61
Q

what happens to people with no TPMT enzyme?

A

can become severely ill if treated with normal doses of thiopurine drugs

62
Q

what should you use if methotrexate is not tolerated?

A

Use if Azathioprine / 6MP not effective or not tolerated
* Avoid in women of child bearing potential as it is teratogenic

63
Q

what monitoring needs to be done with methotrexate?

A

– FBC & LFTS before and every month

64
Q

what are the side effects of methotrexate?

A

bone marrow sup
liver tox
pulmonary tox
GI tox

65
Q

what are the interactions with methotrexate?

A

Drugs which reduce the renal excretion of
methotrexate including NSAIDs
– Drugs with antifolate activity such as
trimethoprim

66
Q

what is TNF-a ? what does it do?

A

umour necrosis factor alpha (TNF-α) is a pro-
inflammatory mediator:
– Over expressed in IBD
– Partly responsible for the chronic inflammatory processes in the
intestinal tissue
– Therefore indicated in certain patient groups who have failed
previous therapies/other therapies not appropriate

67
Q

when is TNF-a used?

A

Now recommendations for use to induce remission as a
monotherapy or in combination with an
immunosuppressant

68
Q

what are biologics?

A

Large, complex molecule
* Sometimes referred to as biotherapeutics or
biopharmaceuticals
* Chemically synthesized
– Made from protein and other substances which occur in nature
– Manufactured in a living system e.g. modified plant and animal cells

69
Q

what are the main biologics used in IBD?

A

Infliximab - Remicade®
* Adalimumab - Humira

70
Q

how do you prescribe biologics?

A

Prescribed by BRAND

71
Q

who are infliximab and adalimumab recommended for?

A
  • as treatment options for adults with severe
    active Crohn’s disease
  • whose disease has not responded to
    conventional therapy or
  • who are intolerant of or have contraindications
    to conventional therapy.
72
Q

how should these main biologics be given?

A

as a planned course of treatment until
treatment failure (including the need for
surgery), initiated by a specialist or
– until 12 months after the start of treatment,
whichever is shorter.

73
Q

who are biologics C/I in?

A

Crohn’s related abscess (infection)
– Moderate to severe heart failure
– Multiple sclerosis (exacerbates symptoms)
– TB
– Need to check for dormant TB as they significantly aggravate the dormant cells, therefore screening prior to treatment is essential
– Lymphoma
– Recurrent infections
– Hepatitis B infection (adalimumab only)
– Active infection

74
Q

what are the signs and symptoms of an infusion reaction of infliximab?

A

itching, fever, chills, chest pain, changes in blood pressure and problems with breathing (monitor for signs of throughout).
– May be attenuated by reducing the rate of infusion or by stopping it for a while
– Rarely, reactions are severe and the infusion must be stopped.

75
Q

how is adalimuab given?

A

s/c injection
– Patients can inject at home (no need to come
to hospital as with infliximab)
– Watch for injection site reactions and
infections

76
Q

what are the side effects of these biologics?

A

– headaches
– sore throat
– swallowing problems
– aches and pains in the muscles and joints
– swelling in the legs or face
– nausea, diarrhoea and abdominal pain
May take up to six months to be completely removed from the body, therefore, still monitor for side-effects after stopping therapyi
immunosuppressive

77
Q

what are the long term effects of these biologics?

A

– Possible increased risk of developing lymphoma
– Patients with COPD & heavy smokers may have an increased
risk of cancer with infliximab or adalimumab
– May exacerbate multiple sclerosis

78
Q

what is an example of an anti-tnf agent and when is it used?

A

Golimumab - Simponi®
Is licensed in moderate to severe ulcerative
colitis where other treatment has failed or is
not tolerated
s/c thigh to stomach

79
Q

what is Vedolizumab - Entyvio?

A

Gut selective integrin blocker – over production in WBC causes inflammation. Vedolizumab stops the WBC from entering the gut lining and selectively targets the gut = fewer
side-effects.
* Possible to use for adults with moderate to severe CD if anti-TNF therapy is not suitable, contra-indicated or has not worked well enough

80
Q

what is Ustekinumab - Stelara®? how does it work?

A

Moderate to severe active Crohn’s disease
– Where anti-TNF therapy not tolerated/CI
– IV infusion initially followed by s/c injection
* Targets IL-12 and IL- 23
– Which are increased in IBD and contribute to ongoing gut inflammation
– They therefore bind to IL-12 and 23 reducing
inflammation

81
Q

what are biosimilars?

A

Copy of an original biological agent (not
identical) already licensed for use
– Similar in terms of quality, safety and efficacy
– Not considered generic equivalents because the size and complexity of the medicine and the way they are produced results in natural variability in molecules
prescribed by brand

82
Q

when can person switch from origional product to biosimilar?

A

– Only in patients who are in remission or are having a stable
clinical response to originator product
– Same dose and dosing interval
– Based on evidence from use in RA and ankylosing spondylitis as
well as IBD
– Trials showed no difference in safety or effectiveness
– Currently trials ongoing in IBD
– Patient choice

83
Q

what is the maintenance therapy in CD?

A

patient specific
– Azathioprine or mercaptopurine
– Methotrexate
– Infliximab or adalimumab

84
Q

how do you induce remission for mild to moderate proctitis?

A

– Topical aminosalicylate alone
– Consider adding oral aminosalicylate to topical agent (more
effective than either agent alone)
– Consider oral aminosalicylate alone (least effective)
* Comes down to patient choice
* Once daily oral dosing has also been shown to be as effective as
conventional dosing and is as safe

85
Q

what if the patient cant tolerate/ decline remission therapy in proctitis?

A

– A time-limited course of topical CCS OR
– Consider oral prednisolone (if don’t respond to other treatments)

86
Q

how do you induce remission for mild to moderate proctosigmoiditis and left-sided ?

A

– Topical aminosalicylate first line
– High-dose of oral aminosalicylate OR
– Switch to high-dose oral aminosalicylate and a time-
limited course of topical CCS
– If unable to tolerate aminosalicylates, consider time-
limited topical or oral steroid

87
Q

how do you induce remission in mild to moderate extensive disease?

A

– Topical aminosalicylate + high dose oral
aminosalicylate
– Stop topical and give high dose oral
aminosalicylate with a time-limited course of
oral CCS

88
Q

when is tacrolimus C/I?

A

CI if history of hypersensitivity to macrolides (as
tacrolimus is a macrolide antibiotic)

89
Q

what monitoring needs to be done for tacrolimus?

A

Drug levels
– Blood pressure – can cause hypertension
– ECG
– U&E’s, renal, liver function; coagulation and
neurological parameters

90
Q

what is the general advice for tacrolimus?

A

– Avoid excessive exposure to UV light including
sunlight
– May affect performance of skilled tasks e.g. driving
– Take 1 hour before or 2 – 3 hours after a meal
– Avoid grapefruit and grapefruit juice (increase levels)
– Report signs of bone marrow suppression
– Avoid in pregnancy; contraception is required during
treatment and for at least 3 months after stopping
treatment
– Passes through breast milk
– Potassium sparing medications may exacerbate
tacrolimus induced hyperkalaemia

91
Q

how do you induce remission in severe UC?

A

Step 1
– IV CCS
– Consider ciclosporin
* Can not tolerate CCS/CI/decline
* Step 2
– Add IV ciclosporin to IV CCS
* No improvement with 72 hours
* Symptoms worsen
– Consider biologic or surgery

92
Q

what is ciclosporin?

A

Used to induce or maintain remission
* Often notice improvement within a few days with IV
administration or within a few weeks with oral agent
* Prescribe by brand

93
Q

what interactions does ciclosporin have?

A

– Amiodarone
– Atorvastatin
– Carbamazepine
– Clarithromycin
– Dabigatran
– Diclofenac

94
Q

what monitoring does ciclpsporin require?

A

– Toxicity
– Drug associated mortality is 3%
– Check serum cholesterol must be checked prior to
starting (low levels can predispose to seizures)
– Monitor
* Blood pressure – causes hypertension
* Weekly for 4 weeks, then 2 weekly for 3 months
– Renal function
– Liver function
– Serum potassium, magnesium
– Drug levels

95
Q

what is budesonide?

A

Second-generation CCS are starting to
emerge as a treatment option
* Multi-matrix system – Cortiment® MMX®
– Licensed for mild to moderate active U.C in
adults where 5-ASA treatment is not sufficient

96
Q

how do you maintain remission in UC?

A
  • Proctitis and proctosigmoiditis
    – Topical and/or oral aminosalicylates (daily or
    intermittent)
  • Left-sided and extensive
    – Low dose oral aminosalicylate (superior to
    placebo)
97
Q

when do you consider oral aza or mercaptopurine to maintain remission in UC?

A

– After 2 or more exacerbations in 12 months requiring treatment with systemic CCS
* OR
– If remission is not maintained by aminosalicylates

98
Q

what should you give after a single epsoide of acute severe UC?

A

– Azathioprine or mercaptopurine
– Oral aminosalicylates as second line

99
Q

what medicne issues are there with UC?

A

Potassium levels & supplementation
– Supplements may be required if levels are low
– Key patient safety area
– Too much can cause life-threatening arrhythmias
– Avoid M/R formulations as they are associated
with GI ulceration
– Dose against clinical parameters
– Oral agents include Sando K and Kay Cee L
* Osteoporosis prevention & treatment

100
Q

what interactions should you be aware of for UC? especially for excretion

A

Consider MTX is renally excreted, therefore any
medication that can reduce renal function can
increase MTX levels
* Main 3 drugs = NSAIDs, Diuretics and ACEi

101
Q

what should you consider in UC with pregnancy or conception?

A

Consider teratogenic effects and also due to
malabsorption most effective types of contraception
– Many medications used in the management of IBD are teratogenic
* Azathioprine has emerging evidence for use in pregnancy
* If male, need to consider paternal risk
– Good pregnancy planning, speak with specialist
– During pregnancy also have additional dietary and nutritional needs

102
Q

what vaccinations should patients with IBD get?

A
  • Influenza (inactivated) vaccine annually
  • Pneumococcal vaccine
  • Hepatitis B vaccine (in all HBV seronegative
    patients)
  • Human papillomavirus
  • Varicella zoster vaccine (if no history of shingles
    or chicken pox in VZV seronegative patients)
103
Q

what considerations was made to patients medications during covid 19

A

Corticosteroids
* Avoid if possible but will still be needed for some –
they should observe shielding guidelines when on
prednisolone when dose is > 20mg daily
* Consider using budesonide 9mg/day for flares
– MMX
– Entocort
– Budenofalk
– Immunomodulators
* Azathioprine
* 6-Mercaptopurine
* Methotrexate
– Anti-TNF therapy
* Adalimumab
* Infliximab

MO1 (50 decks)

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