GI tract diseases Flashcards

(46 cards)

1
Q

IBD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

principle types of IBD

A
  • crohns disease

- ulcerative colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

UC effects

A

the large intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Crohns effects

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

symptoms of IBD

A

pain, cramps or swelling in the tummy

  • bloody diarrhoea
  • weight loss
  • extreme tiredness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

causes of IBD

A

genetics and problems with the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

treating IBD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

medicines given for IBD

A
  • aminosalicylate
  • immunosuppressants
  • biologics (antibody based treatment given by injection)
    4) antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pro-infllamtory cytokines

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cytokines induce the expression of

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

down regulating over activated innate and adaptive immune repsonses

A

can successful ameliorate IBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Genes involved with IBD

A

NOD2
IBD5
IL-23R
AIEC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

NOD2

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IBD6

A

play a role in maintaining the integrity of epithelia barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IL-23R

A

play a role in a citation inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

AIEC

A

adhesive and invasive E.coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which bacterium is less common in patients with IBD

A

Faecalibacterium prausnitzii- ant-inflammatory role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
glycosuria
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
how is Type 1 treated
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
how is Type 2 treated
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
risk factor of type 1
Genetic predisposition linked to human leukocyte antigen (HLA)
29
risk factor of type 2
``` Age Obesity Ethnicity Family history Western diet Physical inactivity City dwelling ```
30
Bowel cancer
cancer of the large intestine e.g. colon or rectal cancer. Relating to the tumour suppressor gene DCC being switched off --> polyp formation
31
DCC
acts as a tumour suppressor and photo-oncogene
32
what are DCCs
receptors found the CSM of colorectal epithelium
33
what are part of the intracellular part of DCC
kinases- these activate the MAPkinase cascade
34
ligand of DCC is
Netrin-1- binds to the receptor and stimulates MAPK cascade
35
if DCC is over expressed
more MAPK cascade- more cell proliferation
36
intracellular cascade after entrain binds to DCC
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
DCC and Netrin
DCC's are dependence receptors
38
What are dependence receptors (2)
1. can act with netrin-1 bound: cause cell proliferation | 2. without entrain-1: activates caspases- apoptosis
39
without Netrin
DCC's are tumour suppressors- stoping overgrowth of tissue
40
Netrin is only expressed
at the bottom of villi
41
DCCs are expressed
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
cell proliferation
at the bottom
43
cell death
at the top- causes apoptosis when entry doesn't bind to DCC
44
if DCC is deleted via mutation
this process won't happen- no apoptosis at the top of the villi- polyp formation due to over proliferation.
45
when DCC is deleted
proto-oncogene
46
when DCC is there
tumour suppressor