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GI 11 Flashcards

1
Q

What is IBD?

A

Chronic inflammation of the GI

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2
Q

What is IBS?

A

is Multifactorial and different therapeutic approaches.

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3
Q

What is Inflammatory Bowel disease (IBD)?

A

Chronic Inflammation in the GI tract.

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4
Q

Where Chron’s Disease can affect?

A

Can affect any part of the gastrointestinal system. Mostly in the small intestine and colon. But it also a systemic disease can be from the mouth to your anas.

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5
Q

What are the Symptoms of Chrons disease ?

A

Mild: Frequent diarrhoea, Abdominal pain.

Moderate: Frequent diarrhoea abdominal pain or tenderness
Fever
Significant weight loss
Significant anaemia

Severe: High fever
Persistent vomiting 
Intestinal blockage
Intestinal infection 
More severe weight loss.
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6
Q

What is Ulcerative Colitis is?

A

also an inflammatory bowel disease but it just only in the colon.

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7
Q

What are the Symptoms of Ulcerative Colitis:

A

Mild to Moderate: Diarrhoea, Mild pain
Severe to very severe: Diarrhoea, Fever
Bloody stool. fatal complication.

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8
Q

What is the difference of inflammation between UC and CD?

A

Ulcerative colitis has uniform pain all the time whereas Chron’s disease has pain than skip and pain and skip in one part to another.

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9
Q

IBD also have some complications ?

A 
Like arthritis 
Heart kidney and eyes
Skin
Cancer 
Ocular manifestation
Gul stone
Fatty liver.
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10
Q

How the IBD occurs?

A

Gi Epithelium of your GI get damaged or leaky, as a result bacteria can get in through the leakage and the bacteria access to the APC (ANTIGEN Presenting Cells) .

For UC: APC cells get induce lots of Interleukin 4 into lots of TH2 helper cells.
For CD: APC cells get induce Interleukin IL-12 & 18 as a result lots of TH1 cells.

APC (antigen presenting cells) also produce TH17 cells which increase the inflammation as bacteria gets in through the epithelial cells of GI. whereas T reg cells try to keep the inflammation under control. Finally it becomes imbalance between TH17 and T reg cells as the proportion of inflammatory TH17 cells are higher than T reg cells, result, more and more inflammation and problems.

For CD disease TH1 cells produce TNF gamma and TNF alpha which activate macrophages and regulate Th1 cells so more inflammation, TH1 reproduce as like a cyclic process.TH1 is responsible for more and more inflammation.

For UC disease TH2 cells attract lymphocytes and monocytes as a result inflammation.

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11
Q

What is the Goals of therapy for IBD ?

A 
Induce and maintain remission 
Ameliorate symptoms 
Improves quality of life 
Adequate nutrition
Prevent complication of both the disease and medications.
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12
Q

Different classes of drugs used to treat IBD ?

A

1st stop: Anti inflammatory drugs
5 amino salicylate (Mesalazine) Sulfasalazine. Need regular colonoscopy’s to see the all the where is the inflammation is to give the right formulation. Because oral formulation is good for upper portion of the colon Liquid enemas is for middle colon and suppositories for lower part (rectum).

Note: Sulfasalazine is prodrug. Sulphapyridine and Mesalamine both separates into the body whereas the activate is 5 amino salicylate and sulphapyridine (metabolite) is inactive. 5 amino salicylate reduce inflammation whereas sulphapyridine gives some side effects of this drug.

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13
Q

What if we do not add metabolite with 5ASA ?

A

We need send this drug into the colon if we do not add sulphapyridine metabolite then it might end up in stomach and will not get effect to the colon.

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14
Q

For Oral and rectal formulation for treating IBD ?

A

MOA: Not known but they inhibit some of the mediator those are occurring.

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15
Q

What is the reason of using suppository?

A

If we use suppository than the effect would be just on the lower part of the colon. Local target.

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16
Q

But if we use enemas foams?

A

Then it will go a bit up then suppository to treat IBD which is more localised target and the oral therapy will reach rest of the part.

17
Q

Where Sulfasalazine works?

A

Sulfasalazine work in the colon as it has designed to cleave by the colons bacteria so it become 2 parts 5 Aminosalicylate (active) and sulphapyridine (metabolite). So the active part 5 Aminosalicylate helps with the inflammation but the sulphapyridine (metabolite part) cause side effects. So the reason of adding that part is to give more strength to reach to last part of the colon.

18
Q

Excessive numbers of T helper type 2 lymphocytes is indicative of crohn’s disease

A

False

19
Q

The active constituent of sulfasalazine is 5-ASA

A

True

20
Q

What is the reason of using Glucocorticoids?

A

Used as anti-inflammatory drugs.
Prednisone is the major steroid for the treatment of UC and CD for inflammation.
Oral Prednisone (for inflammation) induce remission 40 % (symptoms will go away) of acute condition of IBD within 1-2 weeks. after taper down 40 % symptoms might come back. However This medicine need to taper down.

21
Q

Why we tapper down prednisone ?

A

If we do not tapper down prednisone then patient will experience HPA axis crisis

22
Q

What Is HPA axis crisis ?

A

The hypothalamic pituitary adrenal (HPA)axisis our central stress response system.

H= Hypothalamus
P=Pituitary
C= Cortex
These 3 things are the normal HPA process of human body when we produce enough cortisol it gives a negative feedback and shut the inflammatory mediators down. When we expose to UC or CD HPA process does not shuts down and result lots of inflammation. However then we apply corticosteroids like prednisone to increase the level of cortisol as a result it suppress the inflammatory mediators through the negative feedback as a result inflammatory mediators starts turning off into our H and P and immune system and less or no inflammation.

23
Q

What is the MOA of Glucocorticoid (Immunosuppressant) ?

A

GR complex upregulates our anti-inflammatory proteins. And it decreases pro inflammatory proteins. This is the mechanism of immunosuppressant.

24
Q

What is the MOA of Glucocorticoid (anti-inflammatory)?

A

Glucocorticoid stop the enzyme phospholipase A2 and stop the pathway to prostaglandin, thromboxane and prostacyclin.

25
Q

What are the Long term risks of Glucocorticoids?

A
  • Adrenal axis suppression: Risk of death with sudden stopping of this medicine.
    - Require dose tapering
  • Effects on carbohydrate, protein and fat metabolism: Promote gluconeogenesis.
    - Can precipitate hyperglycaemia so diabetes monitoring required.
    - Hypertension
    - Skin thinning
    - Moon face look
26
Q

Treatment of IBD by using Immunosuppressant?

A

We only use immunosuppressant, when everything fails and this it the last step of out treatment. Immunosuppressants will work on our immunity by suppressing it activity when immunity gone out of control.

2 cytotoxic drugs commonly use, 6 mercaptopurine and azathioprine which impair PURIN biosynthesis and also suppress lymphocyte cells proliferation, cell immunity and antibody responses that can not respond inflammatory mediators of UC or CD.

27
Q

Immunosuppressant: Methotrexate use for ?

A

As immunosuppressant and a cytotoxic drug

Used for the treatment of arthritis and cancer.

28
Q

What is the MOA of Methotrexate

A

Folic acid antagonist. Methotrexate inhibit DHFR which is important for synthesis of thymidine (Nucleotide) as a result Inhibition of Tcells activation result reduction of inflammation.

29
Q

What is the main Side Effect of Methotrexate?

A

Is Blood dyscrasias and liver cirrhosis (so this are the red flags need to remember).

30
Q

Cyclosporin & Tacrolimus is used for immunosupprants?

A

used for transplant usually.

Inactivate the IL2 gene, as a result they decrease T Cells proliferation as a result inflammation got down.

31
Q

Cyclosporin Side effect?

A

Nephrotoxicity & hepatotoxicity & Neurotoxicity.

32
Q

What is the use of Tacrolimus?

A

For inflammation while transplant.
Inactivate the IL2 gene, as a result they decrease T Cells proliferation as a result inflammation got down.
Are way more than potent and popular than cyclosporin however

33
Q

Side effect of Tacrolimus?

A

Nephrotoxicity

34
Q

What is Infliximab?

A

Last step treatment.
Monoclonal antibody which Stops TNF alpha activity as a result reduces overexpression of chronic inflammation and immune response activation.
To get prolonged action need to give IV infusion at intervals of weeks or months.
Effective for maintaining remission and also sometimes used for Ulcerative Colitis

35
Q

Infliximab Half life is?

A

8- 10 days and usually given by IV at different intervals across long period of time.
So this are very good of reducing inflammation specially in severe case of inflammation. Decrease acute flares of CD and help to closing of fistulas in the skin.

36
Q

Infliximab binds to TNF alpha to reduce inflammation

A

True

37
Q

Oral corticosteroids are used as a first line treatment in IBD

A

False however if IBD happen in Anas then oral form is not first line treatment. Then suppository or foam enemas are the primary treatment options.

GI (16 decks)

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