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Pharmacology > Inflammatory Bowel Disease > Flashcards

Inflammatory Bowel Disease Flashcards

1
Q

What is IBD?

A

A chronic inflammatory disease if the GI tract of unknown aetiology

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2
Q

What conditions does IBD include?

A

Crohn’s disease
Ulcerative colitis

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3
Q

How is IBD characterised?

A

As a multi focal infarction
Pathogenic infection
Relapsing and remitting course that may lead to surgical intervention

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4
Q

What are the risk factors of IBD?

A

Thought to be a genetic predisposition
Infection
Local ischaemia
Altered immune state
Maybe Cigarette smoking

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5
Q

What aspects of the GI system does ulcerative colitis affect?

A

Confined to the mucosal and sub mucosal layers
Restricted to the large intestine
(Especially the rectum)

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6
Q

How is UC characterised?

A

Crypt abscesses and ulceration
Continuous inflammation rather than patchy

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7
Q

What are the symptoms of UC

A

Bloody diarrhoea
Abdominal tenderness
Abdominal distension

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8
Q

Are there any extra colonic symptoms of UC?

A

Reactive arthritis
(Possibly due to the proliferation and migration of activated T lymphocytes)
Anaemia
Fever
Weight loss

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9
Q

What is Crohn’s disease?

A

A transmural granulomatous condition characterised by macrophages lesions

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10
Q

Where does Crohn’s disease normally affect?

A

Can involve any section of the gut
Usually spares the rectum

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11
Q

How is inflammation caused by Crohn’s normally categorised?

A

Discontinuous and segmental inflammation
There will be inflamed portions next to healthy region of tissues
(Skipper areas)

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12
Q

What abnormalities can help diagnose Crohn’s?

A

Fistulas
(Abnormal connections between sections of the bowel)
Small bowel strictures
(Narrowing of the intestine making it hard for things to pass through)
Abscesses
Anal fissures

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13
Q

What are the symptoms of Crohn’s?

A

Diarrhoea
Abdominal pain
Fatigue

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14
Q

What is the molecular pathophysiology of IBD?

A

Poorly understood
Thought to be linked to a dysfunction in the intestinal epithelial barrier
(NOD2 gene mutation)
Or to dysregulation of innate immunity
Abnormal chemokine production
Impaired barrier repair and maintenance function
T lymphocyte migration

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15
Q

How does the innate immune system affect the chances of Crohn’s?

A

Defects in the innate immune system are associated with a predisposition to infections and autoimmune diseases

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16
Q

Describe how immune cell imbalances may influence IBD
T cells

A

Imbalances between pro inflammatory T helper 1 and T helper 2 cells and anti inflammatory T helper 3 and T regulatory cells
Disruption to this system may contribute to the pathophysiology of IBD

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17
Q

Molecular pathophysiology 2

A

Aggressive activation of adaptive immunity (cytokines)
Dysfunctional neuro immune regulation
Excessive production of nitric oxide and other radicals
Enhanced expression of matrix metalloproteinases

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18
Q

What is the point of therapeutic management

A

To induce and maintain remission
High failure rate usually results in surgery

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19
Q

What drugs are used in the treatment of IBD?

A

Corticosteroids
Aminosalicylates
Immunomodulators
TNF alpha antibodies

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20
Q

What are two immunomodulators used for IBD?

A

Thiopurines
Methotrexate

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21
Q

Give two examples of TNF alpha antibodies

A

Ciclosporin
Anti microbial agents

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22
Q

What do corticosteroids do?

A

Dampen the general inflammatory response
Reduce expression of cytokines, COX and adhesion molecules
Induce remission of active disease (particularly Crohn’s

23
Q

What are some of the formulation of corticosteroids?

A

Oral prednisolone
Foam/ enemas for left sided distal UC
Novel drug delivery (extended controlled release)
Budesonide topically active (extensive first pass metabolism - few side effects)
IV hydrocortisone (sever disease not responding to oral therapy)

24
Q

What are the side effects of using corticosteroids?

A

Cushing like syndrome
Metabolic disturbance
Diabetes
Fat redistribution
Bone / muscle breakdown
Growth suppression
Peptic ulcer
Hypertension
Acne
Behavioural changes

25
Q

What is associated with prolonged use of corticosteroids?

A

Dependence
Resistance
Increased susceptibility to infections

26
Q

Are there risk factors associated with stopping corticosteroid treatments?

A

Withdrawal symptoms
Acute adrenal insufficiency
Advised to taper off the treatment
1 year treatment = 2 months tapering roughly

27
Q

What are aminosalicylates?

A

Prodrugs metabolised by enteric bacteria to 5-aminosalicylate

28
Q

How can aminosalicylates be administered?

A

Sulfasalazine
Mesalazine
Rectal foams
Suppositories of 5-ASA
Slow oral release preparations of pro drugs

29
Q

What are the three types of aminosalicylates?

A

Azo-bonded prodrugs
oh-dependent drugs
Time-dependent drugs

30
Q

What sites do specific types of 5-ASAs treat?

A

Azo - colon
pH - ileum and colon
Time - duodenum, small bowel, colon

31
Q

What is the mechanism of action for aminosalicylates?

A

Mechanism is unclear
Suppression of inflammation
Induces remission of mild active disease (UC > Crohns)
Maintenance of UC remission

32
Q

What pathways can 5-ASAs target?

A

PPAR gamma agonist
Increase TGF-beta
Decreases NF-kB
MAPK
COX-2
Pro inflammatory cytokines
Scavenges ROS and RNS

33
Q

What are the side effects of taking aminosalicylates?

A

Diarrhoea
Nausea
Abdominal pain
Headache
Rash
Allergic reactions
Lupus like syndrome
Nephritis
Reversible oligospermia

34
Q

Give two examples of thiopurines

A

6-mercaptipurine
Azathioprine (pro drug)

35
Q

How do thiopurines work?

A

Metabolised to active 6-thioguanine phosphates
Randomly incorporated into nucleic acid as false purine analogs
Inhibit gene transcription
Inhibits activation and proliferation
Promotes apoptosis of T lymphocytes

36
Q

What are the side effects of thiopurines?

A

Nausea
Diarrhoea
Abdominal pain
long term use:
Hepatotoxicity
Allergic reactions
Pancreatitis
Bone marrow suppression
Lymphoma
Infection

37
Q

What is the treatment plan for thiopurines?

A

Slow onset (>3 months)
Given for over five years
Mainstay for remission (steroid dependent Crohns)

38
Q

What sort of things must be monitored when using thiopurines?

A

6-mercaptopurine metabolite levels
(Guides dosing regime and monitors compliance)
Serum amylase (predictor for pancreatitis)
Regular FBC and liver function tests

39
Q

What is methotrexate?

A

Folic acid analogue that interferes with nucleic acid synthesis

40
Q

How does methotrexate work?

A

Inhibits dihydrofolate reductase (purine and pyrimidine synthesis)
Reduces cytokine expression
Increases T cell apoptosis

41
Q

When and how often is methotrexate used?

A

Controls inflammation and allows withdrawal from steroids while maintaining remission
Given weekly by mouth or injection

42
Q

What are the minor side effects of methotrexate?

A

Mild headache
Nausea
Abdominal pain
Diarrhoea
Rarely opportunistic infections

43
Q

What are the more severe side effects of methotrexate?

A

Bone marrow suppression
Blood disorders
Hepatotoxicity
Sperm toxicity?
Teratogenic?
Spontaneous abortions?

44
Q

How is methotrexate use monitored?

A

Regular FBC, renal and live function tests (initially every 1-2 weeks)
Methylene tetrahydrofolate reductase mutations used as a predictor for toxic effects

45
Q

When should methotrexate be avoided?

A

Avoids in hepatic and renal impairment
Avoid in pregnancy for 3 months following cessation

46
Q

What is ciclosporin?

A

An immunosuppressant

47
Q

How does ciclosporin work?

A

Inhibits calcineurin to attenuate transcription of pro inflammatory cytokines and lymphocyte proliferation
Effective in severe steroid refractory or dependent UC

48
Q

What are the side effects of ciclosporin?

A

Renal toxicity
Tremor
Increased infection
Hypertension
Nausea
Headache
Gingival hyperplasia
Diarrhoea
Fatigue

49
Q

How is ciclosporin wise monitored?

A

Liver and renal function tests
Blood pressure
Lipid profile

50
Q

Give three examples of anti bacterials used for IBD

A

Metronidazole
Ciprofloxacin
Ornidazole

51
Q

Why are antibacterial used to treat IBD?

A

They promote remission and reduce post operative relapse
Combine with steroids in active Crohns to reduce the overgrowth of bacteria in the small bowel

52
Q

Are there any risks when using anti bacterials?

A

Potential risk of nerve damage

53
Q

Describe how changes to the adaptive immune system might affect IBD

A

The adaptive immune system is defined by the presence of T or B lymphocytes including CD 8+ cytotoxic T cells, CD 4+ helper T cells and B cells that present antigens and produce antibodies
Disruption to this system may contribute to the pathophysiology of IBD

Pharmacology (18 decks)

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