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Pharmacy Stage 2 > Inlammatory Bowel Disorders > Flashcards

Inlammatory Bowel Disorders Flashcards

1
Q

What is inflammatory bowel disease?

A

A structural problem with physical abnormalities in the GI tract. It is a chronic condition resulting from inappropriate mucosal immune activation.

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2
Q

What is it irritable bowel syndrome?

A

A functional GI problem with no structural abnormalities. It is characterised by abdominal pain and altered bowel habits

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3
Q

What gender is IBP more prevalent in and what age group?

A
  • more prevalent in women

- high prevalence in youth and middle aged people

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4
Q

What are the pathogenesis (causes) of IBS?

A

1) stress
2) diet
3) abnormal GI motility
4) Visceral hypersensitivity
5) infection
6) overgrowth of intestinal flora

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5
Q

How is IBS diagnosed?

A

1) if the individual has experienced discomfort for 3 days per month for over 3 months
2) if there’s a change in stool frequency/form
3) if the individual has any food allergies/intolerances resulting in bacterial growth

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6
Q

How is IBS treated?

A 
1-psychotherapy (antidepressants)
2-dietary fibre supplements
3-loperamide or laxatives
4-antibiotics
5-analgesics
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7
Q

What are the 2 most common IBD’s?

A

Ulcerative Collitis (UC) and Crohn’s disease

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8
Q

Where do Crohn’s disease and UC exist?

A

CD - any area in the GI tract

UC - Limited to the colon and rectum

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9
Q

What type of inflammation does CD cause?

A

Transmural inflammation

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10
Q

What type of inflammation does UC cause?

A

mucosal and submucosal inflammation

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11
Q

What type of lesions are caused by crohns and ulcerative?

A

CD- skip lesions

UC- continuous lesions

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12
Q

What are the symptoms of Crohn?

A
  • pain
  • diarrhoea
  • weight loss
  • anaemia
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13
Q

What are the symptoms of UC?

A
  • bloody diarrhoea
  • colicky
  • abdominal pain
  • urgency
  • fever
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14
Q

Which of the 2, UC or CD, can lead to relapse in 50% of patients?

A

Ulcerative Colitis

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15
Q

What is a colectomy?

A

Removal of the colon

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16
Q

What are the pathogenesis of IBD?

A

1) genetic factors
2) mucosal immune responses
3) epithelial defects
4) microbiota

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17
Q

What is the role of TH1 cells?

A
  • activate macrophages

- cause inflammation of the mucosa through release of TNF (tumour necrosis factors)

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18
Q

What is the role of TH17 cells?

A

-stimulated by IL-23 and activate neutrophils causing inflammation.

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19
Q

What is the role of TH2 cells?

A

-Secrete IL-13 found in the mucosa of ulcerative collitis patients.

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20
Q

What is used to support the theory that TH1 and TH17 cells play a role in UC?

A

The effectiveness of anti-TNF therapy on UC patients and the protective role that IL-23R polymorphisms have on UC patients.

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21
Q

What can happen if there are defects in the intestinal epithelial tight junction barrier?

A

Can activate innate and adaptive mucosal immunity and sensitize subjects to the disease

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22
Q

What polymorphism is associated with the intestinal epithelial tight junction barrier defect?

A

NOD2 polymorphism

23
Q

What does a mutation of the organic cation transporter SLC22A4 in Crohn disease suggest?

A

That defects in transepithelial transport may be related to this mutation

24
Q

What is the effect of the ATG16L1 polymorphism on Crohn disease patients?

A

it means they carry abnormal production of defensins (antibacterial peptides), which leads to defective ant-microbial function

25
Q

What happens to the microbiota of IBD patients?

A

-the diversity of the microbiota is reduced (less range of bacteria).
-Bacterial strands
associated with a role
in mucosal protection
are lost.

26
Q

What are microbiota alterations associated with?

A

genetic polymorphisms

27
Q

What is chronic inflammation?

A

inflammation of prolonged duration (weeks/months) in which inflammation, tissue injury and attempts at repairs coexist in varying combinations

28
Q

Causes of chronic inflammation?

A

1-persistent infections
2-immune-mediated inflammatory disease
3-immune reaction against individual’s tissues (autoimmune disease)
4-Unregulated immune-reactions against microbes
5-mmune-response against harmless environmental substances
6-prolonged exposure to toxic agents.

29
Q

What type of immune response is IBD?

A

An unregulated immune-reaction against microbes

30
Q

How is IBD diagnosed?

A

1-stool tests
2-blood tests (mainly for inflammatory markers)
3-GI investigations: radiology, imaging and endoscopy

31
Q

2 groups of drugs used to treat IBD?

A

1- DMARDs (Disease Modifying Anti-rheumatic Drugs)

2-Immunosuppressant drugs

32
Q

Examples of DMARDs

A

5 Aminosalicylic acid (5ASA)

Methotexate

33
Q

Examples of immunosuppressant drugs?

A
  • glucocorticoids
  • azathioprine
  • ciclosporin
  • biologicals
34
Q

What is the mechanism of action of 5ASA?

A
  • free radicals inhibit prostaglandin and leukotrienes production.
  • they decrease neutrophil chemotaxis
35
Q

what are the side effects to using 5ASA?

A
  • diarrhoea
  • salicylate sensitivity
  • interstitial nephritis
36
Q

Effect of 5ASA on UC?

A
  • less flare ups (less inflammatory responses)

- reduced risk of colorectal cancer

37
Q

Effect of 5ASA on chron’s disease?

A

-used after surgery to reduce chances of relapse

38
Q

Mechanism of action of methotrexate (MTX)?

A

folic acid antagonist (cytotoxic) and immunosuppressant activity.

39
Q

Effect of MTX on CD and UC?

A
  • induces remission and maintains it in CD.

- Has no role in UC.

40
Q

Side effects to using MTX?

A
  • bone marrow depression
  • develop intolerance to the drug
  • diarrhoea
  • stomatitis
  • GI epithelium damaged
41
Q

Mechanism of action of glucocorticoids?

A
  • reduce transcription of genes encoding COX-2, phospholipase A, pro-inflammatory cytokines and iNOS.
  • has immunosuppressive effect
42
Q

side effects to Glucocorticoids?

A
  • prolongesd use can result in -glaucoma, cataracts, osteoporosis, infections, diabetes mellitus.
43
Q

Mechanism of action of azathioprine?

A

interferes with purine synthesis (cytotoxic).
When metabolised to mercatopurine (a purine analogue), it inhibits DNA synthesis.
Also inhibits both cell-mediated and antibody-mediated immune reactions.

44
Q

Effect of azathioprine in CD?

A

induces remission and maintains remission for up to 4 years. Used after surgery as well.

45
Q

Effect of azathioprine in UC?

A

used to maintain remission for up to 4 years.

46
Q

Side effects of Azathioprine?

A
  • Depression of the bone marrow
  • nausea
  • vomitting
  • skin eruptions
  • mild hepatotoxicity
47
Q

Mechanism of action of cyclosporin in treatment of IBD?

A

inhibits IL-2 gene transcription hence decreasing the activation of clonal proliferation T-cells. This reduces the induction of cytotoxic T-cells, reduces the function of the effector T-cells, and reduces the T-cell-dependent B-cell responses.
(so overall reduces autoimmune response)

48
Q

When is Cyclosporin used in UC treatment?

A

if the condition is severe it is ‘typically used only as a rescue therapy’

49
Q

side effects of using Cyclosporin?

A
  • infections
  • hepatotoxicity
  • hypertension
  • renal impairment
50
Q

Mechanism of action of biologics?

A
  • directs monoclonal antibodies against TNF
  • has immunosuppressant activity
  • induces remission is steroids and immunomodulators are ineffective.
51
Q

problem with using biologics?

A

very costly-both drug and clinical administration

52
Q

side effects of using biologics?

A
  • risk of infections (TB)
  • psoriasis (rarely)
  • hypersensitivity
  • GI symptoms
  • increased risk of developing lymphoma (rarely)
53
Q

Examples of biologics?

A
  • infliximab

- adalimumab

Pharmacy Stage 2 (85 decks)

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