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Exam 1 Year 3 > Crohn's VS Ulcerative Colitis > Flashcards

Crohn's VS Ulcerative Colitis Flashcards

1
Q

I affect any part of the GI tract from mouth to rectum. Inflammation extends through all layers of the gut wall. This inflammation is patchy in distribution. What am I?

A

Crohn’s

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2
Q

I affect the colon and rectum only. I only affect the mucosa and submucosa. The inflammation is continuous. What am I?

A

Ulcerative colitis

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3
Q

I affect younger people with a mean onset of age 26, What am I?

A

Crohn’s

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4
Q

I affect older people with a mean age onset of 34, What am I?

A

Ulcerative Colitis

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5
Q

50% of people relapse each year, what am I?

A

Ulcerative colitis

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6
Q

I am more common in females with a ratio of: 1:1.2 What am I?

A

Crohn’s

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7
Q

I am more common in males with a ratio of: 1.2:1 What am I?

A

Ulcerative Colitis

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8
Q

Smoking makes me worse, oral CC increases the chance of getting me due to vascular changes. 40% of patients with me smoke. What am I?

A

Crohn’s

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9
Q

10% of patients are smokers, and smoking can help to prevent the onset of me, as the chemicals affect the colon smooth muscle. What am I?

A

Ulcerative Colitis

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10
Q

What are some common causes of symptoms for Crohn’s and Ulcerative Colitis?

A

*Environmental
*Genetic then triggered by infection

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11
Q

Having what high within your diet can make UC/C worse?

A

Fibre

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12
Q

Why can enteric microflora cause IBD?

A

As the loss of immunological tolerance to intestinal microflora an the body then rejects normal flora.
-Antibiotics can change enteric microflora

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13
Q

What drugs can exacerbate IBD?

A

NSAIDs

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14
Q

Why can stress trigger IBD?

A

As it activates the inflammatory mediators at the enteric nerve endings in the gut wall.

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15
Q

What procedure can have a protective effect, with no reason to why?

A

Appendectomy

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16
Q

I have issues with lymphocyte differentiation, lots of cells and this is hard for me to switch off.
Gene CARD15/NOD2 in chromosome 16
Gene OCTNI chromosome 5 and DLG5 on the chromosome 10. These can be altered in this condition, what am I?

A

Crohn’s

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17
Q

70% of people with me have p-ANCA (Anti-neutrophil cytoplasmic antibodies). What am I?

A

Ulcerative colitis

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18
Q

My T Cells are resistant to apoptosis after inactivation due to having too much inflammation, this usually affects the terminal ileum and ascending colon. What am I?

A

Crohn’s

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19
Q

My affected areas are thickened, oedematous and lumen of the gut is narrow. What am I?

A

Crohn’s

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20
Q

I can make deep ulcers appear, What am I?

A

Crohn’s

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21
Q

I make fissures in the mucous membrane and have a cobblestone appearance, what am I?

A

Crohn’s

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22
Q

I can progress to deep fissuring ulcers, fibrosis and strictures. What am I?

A

Crohn’s

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23
Q

I can cause bowel obstructions, abscesses and gut perforations, what am I?

A

Crohn’s

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24
Q

On first presentation
-40% in the rectum (proctitis)
-40% Sigmoid & descending colon (L side)
-20% whole colon

What am I?

A

Ulcerative colitis

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25
Q

I have purulent and granular with superficial ulceration, and in severe inflammation pseudo-polyps are formed. What am I?

A

Ulcerative colitis

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25
Q

I form crypt abscesses and mucosal ulceration, I can cause the mucosa to look red, inflamed and easily bleed. What am I?

A

Ulcerative colitis

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26
Q

What happens to lymphocytes and cytokines in Ulcerative colitis and Crohn’s?

A

-Increased activity of effector lymphocytes and proinflammatory cytokines that override normal control mechanisms
-Primary failure of regulatory lymphocytes and cytokines

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27
Q

The cells associated with me are Th1, What am I?

A

Crohn’s

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28
Q

The cells associated with me is Th2, IL-10, IL-4, IL-5, IL-6.
Inflammatory cells. What am I?

A

Ulcerative colitis

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29
Q

Dysplasia can be seen from biopsies which can then progress to carcinomas, what am I?

A

Ulcerative colitis

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30
Q

The chronic inflammation I cause, can cause cancer. What am I?

A

Crohn’s

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31
Q

You have a patient with the following symptoms:
*N&V
*Weight loss
*Acute/insidious onset
*Pain (LRQ)
*Anaemia
*Palpable masses
*Small bowel obstructions
*Abscesses
*Fistulas
*Gut perforations
What is this associated with?

A

Crohn’s

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32
Q

You have a patient with the following symptoms:
*Diarrhoea with/without blood/mucus, up to 10-20 loose stools OD
*Abdo cramps with fever
*Constipation
What is this associated with?

A

Ulcerative colitis

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33
Q

What IBD complications can happen to the skin and why?

A

Cytokine release in these areas which can cause:
-Erythema nodosum - tender hot nodules on the skin
-Pyoderma gangrenosum - ulcer formation

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34
Q

What IBD complications can happen to the eyes and why?

A

-Episcleritis - intense burning and itching of the blood vessels involved
-Uveitis - headache, burning red eye, blurred vision

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35
Q

What IBD complications can happen to the liver and why?

A

-Sclerosing cholangitis
-Chronic inflammation of the biliary tree
-This leads to progressive fibrosis and biliary strictures

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36
Q

Your patient is p-ANCA positive, what are they likely to have?

A

Ulcerative colitis

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37
Q

Your patient is p-ANCA negative, what are they likely to have?

A

Crohn’s

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38
Q

What procedure is used to diagnosis ulcerative colitis ?

A

Sigmoidoscopy

39
Q

What can an ultrasound find for a patient with Crohn’s?

A

Identifies thickened small bowel loops

40
Q

What blood tests will be requested for a patient initially?

A

Anaemia
Iron/folate deficiency
ESR and CRP and WCC (raised)
Hypoalbuminemia - shows protein loss in the gut, as mucosal wall is not working
LFT

41
Q

You have a patient who is inducing remission with mild-moderate proctitis (UC), what is the treatment plan?

A

1) Topical aminosalicylate (mesalazine/sulfasalazine)
-If cannot tolerate go straight to step 3

No remission within 4 weeks
2) ADD oral amino salicylate

3) ADD topical or oral cortico-steroid

42
Q

You have a patient who is inducing remission with mild-moderate proctosigmoiditis and left sided colitis (distal colitis), what is the treatment plan?

A

1) Topical aminosalicylate
-If cant tolerate -topical/oral steroid
2) High dose oral aminosalicylate or oral and topical steroid
3) Oral aminosalicyte and oral corticosteroid

43
Q

You have a patient with mild-moderate, extensive spread of UC, what is the treatment plan?

A

1) Topical aminosalicylate + high dose oral aminosalicyte
-If first presentation/exacerbation
-If the patient cannot tolerate aminosalicylates –> Oral Steroids
2) Stop topical treatment and offer oral steroids

44
Q

Inducing remission with ulcerative colitis which is moderate - severe what is the treatment plan?

A

1) Oral corticosteroids - pred 40-60mg
2) Biologics and JAK after failure of conventional therapy

45
Q

Inducing remission with ulcerative colitis which is acute - severe requiring hospitalisation affecting all areas, what is the treatment plan?

A

1) IV corticosteroids, 60mg Methyl pred or 100mg Hydrocortisone TDS-QDS
2) 72 hours later - if worse/no improvement
-> ADD IV Ciclosporin
BUT in practice they will add IV Infliximab

46
Q

We want to maintain remission in mild to moderate ulcerative colitis, whom has proctitis and proctosigmoiditis, what is the treatment plan?

A

1) Topical aminosalicylate
or Oral and topical aminosalicylate together

47
Q

We want to maintain remission in mild to moderate ulcerative colitis, affecting left sided and is extensive, what is the treatment plan?

A

Low maintenance dose of oral aminosalicylate

48
Q

We want to maintain remission in ulcerative colitis which affects all areas, the patient has had 2 + exacerbations in the past 12 months and has required steroids, remission is not maintained by aminosalicylate, what is the treatment plan?

A

Consider Mercaptopurine or Azathioprine

49
Q

We want to maintain remission in someone with ulcerative colitis, which affects all areas, and the patient has has a single acutely severe episode of there UC, what is the treatment plan?

A

Azathioprine, Mercaptopurine or Oral Aminosalicylate

50
Q

With a patient who is firstly presenting with Crohn’s disease or had a single exacerbation in a 12 month period, what is the treatment plan to induce remission?

A

1) Gluco-corticosteroid:
Pred 40mg / IV Methyl Pred / Hydrocortisone
Budesonide is beneficial for proximal disease
- If no steroids oral aminosalicylate - less effective but NICE recommend

ADD on therapy
*Azathioprine or Mercaptopurine

OR
Consider Methotrexate if can’t tolerate above or have low TPMT activity

51
Q

If the patient had moderate to severe active disease how do we induce remission when they have had no response to conventional therapy? Crohn’s

A

1) Infliximab or Adalimumab
2) Ustekinumab or Vedolizumab

52
Q

How do we maintain remission in Crohn’s?

A

1) Azathioprine or Mercaptopurine
*Consider methotrexate only in those who needed it at induction or cannot tolerate first option

53
Q

How do we maintain treatment if a patient decide to have no treatment? Crohn’s

A

Follow up’s, education on what to do when they relapse, how to access healthcare, smoking cessation

54
Q

How do we maintain remission after Crohn’s surgery?

A

Azathioprine with Metronidazole for 3/12 weeks post op.
Azathioprine ALONE if cannot tolerate Metronidazole.

55
Q

What class of drug is Sulfasalazine and Mesalazine?

A

Aminosalicylates

56
Q

Are Aminosalicylates brand specific?

A

YES

57
Q

Where are Aminosalicylates absorbed?

A

By the colon and metabolised by the liver and excreted in the urine.

58
Q

What monitoring does a patient need on aminosalicylates?

A

FBC, LFT, Creatine, eGFR
-Counselling on symptoms of myelosuppression

59
Q

What drug group may colour urine and stain contact lenses yellow?

A

Aminosalicylates

60
Q

Mercaptopurine and Azathioprine are what class of drug?

A

Thiopurines

61
Q

What monitoring needs doing when a patient is on Thiopurines?

A

Prior - FBC, U&E, LFT, HCV, HIV, HBV, VZV,
-Check TMPT,
-Check cervical screening is up to date

Ongoing monitoring
*FBC *U&E *LFT

62
Q

When does monitoring on thiopurines need doing?

A

At least week 2, 4, 8, 12, and then 3 monthly

-Counsel patient on myelosuppression

63
Q

What class of drug is Infliximab?

A

Anti-TNF

64
Q

What class of drug ends in ‘Nibs’

A

JAK inhibitors

65
Q

In moderate to severe active UC what drugs can be used?

A

Upadacitnib, Ozanimod, Filgotinib, Ustekinumab, Tofacitinib, Vedolizumab, Infliximab, Adalimumab, Golimumab

66
Q

In severe UC what IV ca be given?

A

Infliximab - given when ciclosporin is contraindicated or not appropriate

67
Q

In moderately to severely active Crohn’s disease what drugs can be offered?

A

Upadacitinib, Risankizumab, Ustekinumab, Vedolizumab, Infliximab and Adalimumab

68
Q

What enteric infections are IBD patients at a higher risk of getting?

A

Norovirus, Campylobacter, E.coli, C.Diff

69
Q

When is IV Ganciclovir followed by oral valganciclovir treatment given to IBD patients?

A

When they have Cytomegalovirus (CMV).

70
Q

What percentage of IBD patients are reliant on steroids?

A

14.9%

71
Q

What are the issues with prolonged steroid use?

A

*infection risk
*Osteoporosis
*Adrenal suppression
*Diabetes
*Weight gain
*CVD

72
Q

What is important to monitor in patients with long term steroid use?

A

FBC, Glucose/HbA1c, lipids, BP, eyes (cataracts and glaucoma), mood, sleep

73
Q

What dose of calcium should someone on Corticosteroids be on?

A

800-1000mg

74
Q

What dose of vitamin D should people on corticosteroids be on?

A

800 IU

75
Q

What deficiencies can someone with IBD be susceptible to?

A

*Magnesium
*Calcium
*Vitamin D
*Potassium (Sando K)
*Anaemia

76
Q

What must an IBD patient have annually

A

*FBC
*Ferritin
*CRP

77
Q

How many years after symptoms of IBD does the cancer risk begin?

A

8-10 years

78
Q

What is short gut syndrome?

A

Lack of functioning small bowel
-This may affect nutritional absorption
-May affect oral medication absorption

79
Q

What is the max dose of loperamide with a stoma?

A

64mg - can cause QT prolongation

80
Q

MOA of sulfasalazine

A

1) Mesalazine (5-ASA) bound to sulfapyridine via aza bond.
2) Colonic bacterial azo reductase breaks the bond
3) Sulfapyridine is absorbed by colon, metabolised by the liver and excreted in the urine

81
Q

Where is mesalazine metabolised?

A

Liver

82
Q

What monitoring needs to be done with someone on sulfasalazine?

A

Prior and every second week for the first 3 months, then monthly for three months then every three months.
FBC, LFT
Creatinine/eGFR - monthly for 3 months then as indicated.
Any sore throat, fever, myelosuppression

83
Q

What are the pH dependent formulations of Aminosalicylate?

A

Asacol, Mesren, Salafalk/granules, Mesasal

84
Q

What are the time dependent formulations of Aminosalicylates?

A

Pentasa/granules

85
Q

What are the multi-matrix systems for aminosalicylates?

A

Mezavant

86
Q

What is the purpose of having different delivery mechanisms to change the release of mesalazine in the GIT?

A

To attach to other carrier molecules!

87
Q

What does an enteric coating do ?

A

With a specific agent to release at a specific pH to prevent early disintegration in the stomach and upper GIT

88
Q

What pH does Eudragit S dissolve at?

A

7 - due to a methyl acrylate copolymer coating

89
Q

What pH does Eudragit L dissolve at?

A

6 - due to methyl acrylate copolymer coating

90
Q

What are the multi-matrix aminosalicylates have in them?

A

Mesalazine is incorporated into the lipophilic matrix and enterically coated, dissolves at pH 7.

91
Q

How do the multi-matrix systems work?

A

Matrix swells to form a gel - (slow diffusion) - gets the terminal ileum and entire colon release.

92
Q

What is Azathioprine converted to in the body?

A

Mercaptopurine

93
Q

When on Thiopurines what should the patient be counselled?

A

*Myelosuppression symptoms
*Exposure to the sun as increased risk of skin cancers
*Take with meals to avoid risk of nausea

94
Q

If a patient is on Allopurinol what should we do with the dose of Azathioprine?

A

Azathioprine dose should be 1/4 of prescribed dose. Example, pt is on 100mg initially - lower to 25mg

Exam 1 Year 3 (40 decks)

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