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Pharmacology and Therapeutics 2 Y2 > Inflammatory Bowel Disease > Flashcards

Inflammatory Bowel Disease Flashcards

1
Q

2 MAJOR FORMS OF IBD:

A 
Ulcerative colitis (UC)
Crohn’s disease (CD)
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2
Q

risk factors for IBD? (11)

A
  • SMOKING
  • DIET
  • MICROBIOME
  • Medication
  • Sleep
  • Stress
  • Physical activity
  • Air pollution
  • UV exposure/vitamin D
  • Appendectomy
  • Heavy metal
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3
Q

How does IBD begin?

A

with an infection

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4
Q

Summarise IBD into 4 stages:

A

1) complex interplay between host and microbes
2) disrupted innate immunity and impaired tolerance
3) pro inflammatory compensatory mechanisms
4) physical damage and chronic inflammation

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5
Q

Gut layer affected by CD

A

all

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6
Q

Gut layer affected by UC

A

mucosa/submucosa

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7
Q

Regions affected by UC

A

Rectum, spreads proximally

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8
Q

Regions affected by CD

A

any part of GI

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9
Q

Cure success of surgery CD?

A

Not always curative

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10
Q

Cure success of surgery UC?

A

Curative

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11
Q

Pattern of inflammation, UC?

A

Continuous

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12
Q

Pattern of inflammation, CD?

A

Patchy

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13
Q

CD rarity of abscesses/fissures/fistulae?

A

Common

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14
Q

UC rarity of abscesses/fissures/fistulae?

A

Not common

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15
Q

Which IBD has IFN’s involved?

A

CD, gamma and alpha

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16
Q

Which IBD is TH1 mediated

A

CD

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17
Q

Which IBD is TH2 mediated

A

UC

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18
Q

IL in CD?

A

17 and 23

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19
Q

IL in UC?

A

5 and 13

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20
Q

T cell expansion and apoptosis in CD?

A

Florid expansion, defective apoptosis

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21
Q

T cell expansion and apoptosis in UC?

A

Limited clonal expansion, normal T cell apoptosis

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22
Q

Systemic clinical features of IBD?

A 
Anaemia, fevers, sweats, jaundice
Abdominal pain
Arthritis
Weight loss
Skin rash
Diarrhoea
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23
Q

Supportive therapies for IBD?

A

Fluids, blood, nutritional support

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24
Q

Symptom therapies for IBD: active disease?

A

Glucocorticoids, aminosalicylates and immunosuppressives

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25
Q

Symptom therapies for IBD: preventing remission?

A

Glucocorticoids, aminosalicylates and immunosuppressives

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26
Q

Curative therapies IBD? (2)

A

Microbiome manipulation, biologic therapies (anti TNFalpha antibodies)

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27
Q

Aminosalicylate examples?

A

Mesalazine or olsalazine

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28
Q

MoA of aminosalicylates? (3)

A
  1. Regulation of NF-B/MAPK- downregulates pro-inflammatory cytokines
  2. Regulation of COX-2- downregulates prostaglandin production
  3. (smaller way) they can scavenge oxidants
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29
Q

Relationship between Mesalazine and olsalazine

A

Olsalazine has to be activated by gut flora in the colon and split into the two mesalazine molecules

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30
Q

How can aminosalcylates be targeted at the colon

A

Olsalazine has to be activated by gut flora in the colon

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31
Q

What are aminosalicylates such as mesalazine AKA?

A

5-aminosalicylic acid

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32
Q

First line treatment for UC?

A

Aminosalicylates

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33
Q

Effectiveness of Aminosalicylates in UC?

A
  • First line in inducing and maintaining remission

- Good evidence base

34
Q

Effectiveness of Aminosalicylates in CD?

A
  • Ineffective in inducing remission
35
Q

First line treatment for CD?

A

Glucocorticoids

36
Q

Examples of glucocorticoids?

A

Prednisolone, Fluticasone, budesonide

37
Q

Effect of glucocorticoids?

A
  • Powerful anti-inflammatory and immunosuppressive drugs
38
Q

what are glucocorticoids Derived from

A

cortisol

39
Q

Main culprit in IBD? (the cell)

A

dendritic cells

40
Q

Difference in treatment for CD and UC?

A

First line is aminosalicylates in UC and glucocorticoids in CD

41
Q

Prednisolone vs budesonide?

A

Prednisolone for CD causes more side effects than budesonide but prednisolone is better at inducing remission in active CD

42
Q

First treatment for mild CD?

A
  • Budesonide
43
Q

What is budesonide used for?

A

Mild CD

44
Q

STRATEGIES FOR MINIMISING UNWANTED EFFECTS OF GCs: (3)

A
  • Administer topically - fluid or foam enemas or suppositories
  • Use a low dose in combination with another drug
  • Use an oral or topically administered drug with high hepatic first pass metabolism e.g. Budesonide so little escapes into the systemic circulation
45
Q

What does azathioprine do?

A

An immunosuppressive
Purine antagonist
Interferes with DNA synthesis and cell replication

46
Q

What type of nuceleotide does azathioprine interfere with

A

Purines

47
Q

What is the active form of azathioprine

A

6-mercaptopurine

48
Q

What is the prodrug of 6-mercaptopurine

A

Azathioprine

49
Q

2 ways 6-mercaptopurine interferes with DNA synthesis?

A

One active form of the drug inhibits de novo purine synthesis and the other gets incorporated into DNA

50
Q

Where/how is 6-mercaptopurine cleaved from Azathioprine

A

By gut flora in the gut

51
Q

Where does 6-mercaptopurine impair immune responses? (4)

A
  • cell- and antibody-mediated immune responses
  • lymphocyte proliferation
  • mononuclear cell infiltration
  • synthesis of antibodies
52
Q

What does 6-mercaptopurine enhance re. immune responses? (4)

A
  • T-cell apoptosis
53
Q

Azathioprine success in UC and CD?

A
  • Some success in inducing remission in Ulcerative Colitis
  • No benefit in CD active disease
  • Mainly used to maintain remission in CD
54
Q

Time for azathioprine to become useful in Crohns disease?

A

3 to 4 months treatment for clinical benefit

55
Q

What is azathioprine useful for re. CD?

A

It is effective in maintaining remission of CD

56
Q

Unwanted side effects of azathioprine? (5)

A
  • Nearly 10% patients have to stop treatment because of the serious side effects
  • Pancreatitis
  • Bone marrow suppression
  • Hepatotoxicity
  • Increased risk (~ 4 fold) of lymphoma and skin cancer
57
Q

How to deliver drugs more efficiently for IBD? (4)

A

1) Enteric coating ensures degradation in the colon as it resists degradation in acidic pH of stomach
2) Time dependent, self destructive polymer packaging
3) Pressure/osmotic controlled packaging that relies on the more aqueous environment of the colon, which allows water in and pushes drug out
4) Even more complex polymers combine time and pH factors as time can mean premature drug release if the digestion is slow, and pH factors can mean the drug is released prematurely in the small intestine rather than the colon

58
Q

Anti-TNFalpha drug?

A

Infliximab

59
Q

How can you manipulate the microbiome? (3)

A
  1. Nutrition-based therapies
  2. Faecal microbiota replacement (FMT) therapies
  3. Antibiotic Treatment - Rifaximin
60
Q

Success of probiotics in CD?

A

No evidence

61
Q

Success of probiotics in UC?

A

Is evidence for it

62
Q

Probiotics vs 5-ASA in UC

A

both equally effective

63
Q

Success rate of faecal microbiota therapies?

A

Not enough evidence

64
Q

how does rifaximin work?

A

Interferes with bacterial transcription by binding to RNA polymerase

65
Q

Successfulness of rifaximin in CD?

A

Induces and sustains remission

66
Q

Topical steroids vs 5-ASA in inducing UC remission?

A

topical 5-asa is more successful

67
Q

Successfulness of rifaximin in UC?

A

May be beneficial in UC

68
Q

What are biologic therapies in IBD?

A

Anti-TNFalpha antibodies

69
Q

Example of anti-TNFalpha antibody/biologic therapy?

A

Infliximab

70
Q

MoA of anti-TNFalpha Ab? (5)

A
  • Anti-TNF reduces activation of TNF receptors in the gut
  • Reduces downstream inflammatory events
  • Also binds to membrane associated TNF
  • Induces cytolysis of cells expressing TNF
  • Promotes apoptosis of activated T cells
71
Q

Route of admin of infliximab?

A

IV

72
Q

Half life of infliximab?

A

9.5 days

73
Q

Repeat infusion frequency?

A

Every 8 weeks

74
Q

Which IBD is ANTI-TNF therapy useful for

A

CD

75
Q

Success of ANTI-TNFalpha in CD?

A

Success

76
Q

Success of ANTI-TNFalpha in UC?

A

unsuccessful

77
Q

Why isANTI-TNFalpha much more useful in CD than UC?

A

Crohns is TH1 driven, UC is TH2, TH2 has TNF α much less involved

78
Q

Adverse effects of anti-TNFalpha therapy (7)

A
  • 4x - 5x increase in incidence of tuberculosis
  • Also risk of reactivating dormant TB
  • Increased risk of septicaemia
  • Worsening of heart failure
  • Increased risk of demyelinating disease
  • Increased risk of malignancy
  • Can be immunogenic – azothiaprine reduces risk, but raises TB/maligancy risk
79
Q

Combining infliximab with what improves its effectiveness?

A

Azathioprine

80
Q

New targets for IBD? (4)

A
  • Integrin (needed for cells to migrate)
  • Interleukins (IL12; IL17; IL23)
  • Interleukin receptors
  • Janus kinase (JAK) cytoplasmic cell signalling

Pharmacology and Therapeutics 2 Y2 (24 decks)

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