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notes to flashcards year 2 - LCRS1 > IBD > Flashcards

IBD Flashcards

1
Q

what are the 2 major forms of IBD?

A
  • ulcerative colitis

- Chron’s disease

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2
Q

whata re the risk factors of IBD?

A
  • genetic predisposition
  • environmental factors (smoking, diet, obesity, gut microbiome)
  • obesity (only for CD)
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3
Q

what is the pathogenesis of IBD?

A
  • defective interactions b/ mucosal immune system and gut flora
  • leads to disrupted innate immunity
  • physical damage
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4
Q

what immune cytokines are involved in UC?

A
  • Th2 mediated

- dependant on IL-5 and IL-13 cytokines

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5
Q

what does UC affect?

A
  • mucosa and submucosa
  • starts in rectum, spreads proximally
  • always continuous
  • surgery can be curative
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6
Q

what cytokines are involved in Chron’s?

A
  • Th1 mediated (worst inflammatory response)

- dependant on TNF-alpha

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7
Q

what does Chron’s affect?

A
  • penetrates all of gut wall
  • affects any point of GIT
  • causes patchy inflammation
  • abscesses, fissures and fistula
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8
Q

what are the clinical features of IBD?

A
  • R iliac fossa pain
  • skin rash
  • diarrhoea, blood, mucus
  • weight loss
  • arthritis, athralgia
  • abdo pain
  • anaemia
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9
Q

what are the supportive therapies for IBD?

A
  • fluid/ electrolyte replacement
  • blood transfusion
  • nutritional support
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10
Q

what are the classic symptomatic treatments?

A
  • glucocorticoids e.g. prednisolone
  • aminosalicylates e.g. mesalazine
  • immunosuppressives e.g. azathioprine
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11
Q

what are the potentially curative treatments?

A
  • manipulation of microbiome
  • anti-TNF alpha
  • anti-alpha-4-integrins
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12
Q

give 2 aminosalicylates and what are they?

A

mesalazine
olsalazine
anti-inflammatory drugs

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13
Q

are aminosalicylates used in UC and CD treatment?

A
  • UC: 1st line in inducing and maintaining remission

- CD: not effective in active disease

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14
Q

what is the MoA of aminosalicylates?

A
  • inhibition of IL-1, TNF-alpha, PAF
  • dec. antibody secretion
  • non-specific cytokine inhibition
  • reduce cell migration
  • localized inhibition of immune responses
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15
Q

describe the metabolism of mesalazine?

A
  • does not need to be metabolised

- absorbed by small bowel and colon

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16
Q

describe the metabolism of olsalazine

A
  • metabolised by gut flora

- absorbed by colon

17
Q

give examples of glucorticoids

A
  • prednisolone
  • flucticasone
  • budesonide
18
Q

are GC used in UC and CD?

A
  • UC: use in decline

- CD: drug of choice for inducing remission

19
Q

give general info about glucocorticoids

A
  • powerful anti-inflammatories and immunosuppressives

- activate intracellular GC receptors –> +/- TF

20
Q

what are the pharmacokinetics for glucocorticoids?

A
  • have long term side effects
  • administer topically
  • use low dose in combo with another drug
21
Q

give examples of immunosuppressives

A
  • azathioprine
  • methotrexate
  • cyclosporine
22
Q

what is azathioprine used for?

A
  • CD: used to maintain remission
  • UC: useful for maintaining remission in some
  • slow onset of action (3-4 months treatment before clinical benefits seen)
23
Q

what does methotrexate do?

A
  • efficacy in some IBD pt
  • folate antagonist
  • reduces synthesis of thymidine and other purines
  • significant side effects
24
Q

what is the MoA of azathioprine?

A
  • Aza is pro-drug activated by gut flora to 6MP

- 6MP is purine antagonist (interferes with DNA synthesis and cell replication)

25
Q

what does azathioprine impair?

A
  • humoral and innate immune responses
  • lymphocyte proliferation
  • mononuclear cell infiltration
  • synthesis of antibodies
26
Q

what does azathioprine promote?

A

T cell apoptosis

27
Q

what side effects are azathioprine associated with?

A
  • pancreatitis
  • bone marrow suppression
  • hepatotoxicity
  • x4 inc. risk of lymphoma and skin cancer
28
Q

what are the 3 main routes of metabolism of 6MP?

A
  • HRPT: beneficial but causes myelosuppression
  • TPMT: hepatotoxic metabolites
  • XO: inert metabolites (ideal and main pathway)
29
Q

are nutrition based therapies useful?

A

CD: no evidence
UC: evidence for probiotics in induction and maintenance of remission

30
Q

is antibiotic treatment (Rifaximin) useful?

A
  • CD: induces and sustains remission in moderate cases

- UC: may be beneficial, interferes with bacterial transcription by binding to RNA polymerase

31
Q

give an example of biological therapy

A

Anti-TNF-alpha e.g. infliximab

32
Q

is anti-TNF alpha successful?

A

CD - successful, potentially curative, 60% responsive within 6 weeks
UC: some, UC is not TNF alpha mediated, mainly IL mediated

33
Q

what is the MoA of this biological therapy?

A
  • reduces activation of TNF-alpha receptors in gut
  • down regulated other cytokines and infiltration of leukocytes
  • induces cytolysis of cells expressing TNF-alpha
34
Q

what are the pharmacokinetics of this?

A
  • very long half life (9.5 days)
  • benefits last for 30 weeks after infusion
  • pt relapse after 8-12 weeks
35
Q

what are the adverse effects of this biological therapy?

A
  • consequences of knocking out key cytokine inflammatory cascades
  • x5 incidence of TB
  • inc. risk of septicaemia (downregulated inflammation)
  • worsening of HF
  • can be immunogenic
36
Q

what are other targets in biological therapy?

A
  • alpha-4 integrin (cell adhesion molecule)
  • IL-13 (esp in UC)
  • Janus kinases 1,2,3 (block signally of IL-2,4,9,15,21 and INF-gamma)

notes to flashcards year 2 - LCRS1 (58 decks)

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