GI tract diseases Flashcards

1
Q

IBD

A

a group of inflammatory conditions of the colon and s.intestine.. long term conditions involving inflammation of the gut

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2
Q

principle types of IBD

A
  • crohns disease

- ulcerative colitis

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3
Q

UC effects

A

the large intestine

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4
Q

Crohns effects

A

any part of the digestive system from the mouth to the ans

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5
Q

symptoms of IBD

A

pain, cramps or swelling in the tummy

  • bloody diarrhoea
  • weight loss
  • extreme tiredness
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6
Q

causes of IBD

A

genetics and problems with the immune system

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7
Q

treating IBD

A

-aims to relieve symptoms and prevent them from returning: including diet, lifestyle, medicine and surgery

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8
Q

medicines given for IBD

A
  • aminosalicylate
  • immunosuppressants
  • biologics (antibody based treatment given by injection)
    4) antibiotics
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9
Q

the immune system and IBD

A

after exposure to abundant intestinal bacterial antigens, innate immune cells such as dendritic cell and macrophages are activated
- leading to the overproducing of chemises and proinflammmaotry cytokeind

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10
Q

pro-infllamtory cytokines

A

TNF, IL-12, IL-23, IL-1, IL-6

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11
Q

cytokines induce the expression of

A

adhesion meolce receptors in endothelia cels which together with chemokine initiate leukocytes to the site

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12
Q

down regulating over activated innate and adaptive immune repsonses

A

can successful ameliorate IBD

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13
Q

Genes involved with IBD

A

NOD2
IBD5
IL-23R
AIEC

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14
Q

NOD2

A

intracellular sensor for bacterial peptidoglycan. Polymorphisms can result in reduced activation of NF-kB in response to bacterial peptidoglycan

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15
Q

IBD6

A

play a role in maintaining the integrity of epithelia barrier

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16
Q

IL-23R

A

play a role in a citation inflammatory response

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17
Q

AIEC

A

adhesive and invasive E.coli

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18
Q

which bacterium is less common in patients with IBD

A

Faecalibacterium prausnitzii- ant-inflammatory role

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19
Q

Biomarkes for IBD

A
  • C-reactive proteins
  • Feal calprotectin
  • Stool lactoferrin
20
Q

Diabetes

A

a group of metabolic disorders which cause high blood sugar over a prolonged period of time due to either B cells of the pancreas not producing enough insulin or not responding to stimuli which would trigger insulin release

21
Q

Type 1

A

B cells don’t produce enough insulin

22
Q

Type 2

A

Insulin resistance- where ell do not respond to insulin properly- a lack of insulin may also occur

23
Q

symptoms of diabetes

A

frequent urination, increased thirst, increased hunger, tiredess

24
Q

chronic hyperglycemia

A

signif risk to cardiovascular disease, neuropathy and microvascular damage

25
Q

glycosuria

A

when glucose is found in the urine- usually filtered and reabsorbed
- if blood glucose reached the renal -threshold, then reabsorption mechanism of kidney becomes saturated and glucose will be found in urine

26
Q

how is Type 1 treated

A

Since b cells are destroyed, insulin is not naturally produced, therefore control of blood glucose is achieved by injecting insulin
Usually starts in childhood

27
Q

how is Type 2 treated

A

normal physiological response to insulin is impaired, meaning that blood glucose remains elevated for longer than normal after an oral doe of glucose or a meal
Insulin is also less effective at suppressing glucose output by the liver
Defect isnt to do with the receptor, but in the complex insulin signalling pathway
Treated through diet and exercise

28
Q

risk factor of type 1

A

Genetic predisposition linked to human leukocyte antigen (HLA)

29
Q

risk factor of type 2

A
Age
Obesity
Ethnicity
Family history
Western diet
Physical inactivity 
City dwelling
30
Q

Bowel cancer

A

cancer of the large intestine e.g. colon or rectal cancer. Relating to the tumour suppressor gene DCC being switched off –> polyp formation

31
Q

DCC

A

acts as a tumour suppressor and photo-oncogene

32
Q

what are DCCs

A

receptors found the CSM of colorectal epithelium

33
Q

what are part of the intracellular part of DCC

A

kinases- these activate the MAPkinase cascade

34
Q

ligand of DCC is

A

Netrin-1- binds to the receptor and stimulates MAPK cascade

35
Q

if DCC is over expressed

A

more MAPK cascade- more cell proliferation

36
Q

intracellular cascade after entrain binds to DCC

A

1)SRC kinases are attracted to intracellular portion of DCC receptor- phosphorylates it
2) promoting Grb2 to bind to the receptor
) then MAPK cascade commences
- cell migration and proliferation

37
Q

DCC and Netrin

A

DCC’s are dependence receptors

38
Q

What are dependence receptors (2)

A
  1. can act with netrin-1 bound: cause cell proliferation

2. without entrain-1: activates caspases- apoptosis

39
Q

without Netrin

A

DCC’s are tumour suppressors- stoping overgrowth of tissue

40
Q

Netrin is only expressed

A

at the bottom of villi

41
Q

DCCs are expressed

A

all along- no ligand at the top of villus- stop overgrowth and polo formation- therefore proliferation at the bottom, cell death at the top

42
Q

cell proliferation

A

at the bottom

43
Q

cell death

A

at the top- causes apoptosis when entry doesn’t bind to DCC

44
Q

if DCC is deleted via mutation

A

this process won’t happen- no apoptosis at the top of the villi- polyp formation due to over proliferation.

45
Q

when DCC is deleted

A

proto-oncogene

46
Q

when DCC is there

A

tumour suppressor