GIT DISEASE Flashcards

1
Q

gastric pits

A

site of hydrochloric acid synthesis

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

oesophagitis

A

innflammation of oesophageal mucosa, most frequently due to reflux of gastric contents

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

Gastro-oesophageal reflux disease (GORD)

A

recurrent backflow of gastric contents into the oesophagus

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

dyspepsia

A

indigestion

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

GORD prevalence

A
  • 20% of adult population in Western countries
  • Age-dependent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

GORD aetiology

A
  • Dysfunction of the oesopho-gastric junction due to:
  • transient lower oesohpageal sphincter relaxation
  • conditions that decrease closure strength or efficiency of LES
  • Hiatal hernia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

complications of GORD

A
  1. strictures leading to fibrotic scarring and swallowing difficulties
  2. barrets oesophagus- metaplastic change in mucosa, where normal squamous epithelium is replaced with columnar epithelium
    - incomplete intestinal metaplasia (goblet cells)
    - shares similar driver mutations to adenocarcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute gastritis

A

inflammation of the stomach lining

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

acute gastritis aetiology

A

injurious agents or impaired defences including:
- non-steroidal anti-inflammatory drugs
- ageing
- ingestion of harsh chemicals
- ischaemia

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

pareital cells

A

secrete HCl

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

cheif cells

A

secrete pepsinogin

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

Mucous cell

A

secrete mucus

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

prostoglandins

A
  • inflammation mediators
  • in our GI tract, are protective and help mucousal cells to produce mucus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Acute gastritis pathogenesis

A
  1. mucosal damage
  2. erosions that can casue haemorrhages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic gastrits aetiology

A

infection with bacillus Helicobacter pylori and chronic NSAID use

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

chronic gastritis pathogenesis

A
  • Virulence
  • Bacillis + inflammation increases gastrin secretion
  • in time, loss of parietal cells function, gastric atrophy and intestinal metaplasia
17
Q

peptic ulcer disease

A

acis induced ulcer formation in GIT
- commonly in gastric antrum or duodenum
- H. pylori erodes mucosal cells, resulting in less mucus and hydochloric acid penetrates gastric wall

18
Q

inflammatory bowel disease (IBD)

A

-chronic inflammatory condition of the intestinal mucosa (include both crohn’s disease and ulcerative colitis)

19
Q

idiopathic

A

aetiology of a disease is unknown

20
Q

NOD2 (IBD pathogenesis)

A

the first gene to be associated with Crohn’s disease, in about 30% of diagnosed people have a ‘gain of function’ mutation of NOD2.
this means it is more likely to recognise bacteria, and cause more inflammatory cytokines to be produced

21
Q

autophagy

A

the natural, conserved degradation of the cell that removes unnecessary or dysfunctional components through a lysosome-dependent regulated mechanism.

22
Q

intestinal microbiota (IBD pathogenesis)

A

enormous amounts of microbes in intestines, influences by diet, pre and probiotics, antibiotics, enzymes, fecal transplantation

23
Q

environmental factors (IBD pathogenesis)

A
  • industrialization
  • diet high in vegetables and fruit (decrease ibd)
  • smoking
  • psychological stress
  • appendectomy
24
Q

non-specific physiologic immunity (IBD)

A
  • intestinal epithelial barrier
  • antibacterial products
  • acidic pH of stomach
  • innate immune cells
25
Q

specific physiologic immunity (IBD)

A
  • pathogen-specific
  • generation of B and/or T cell response
26
Q

Dysregulation of non-specific immunity

A

an immunologic abnormality in IBD where the epithelial barrier is disrupted and increased numbers of dendritic cells

27
Q

dendritic cell

A

an antigen presenting cell, boosts immune responses by showing antigens on its surface to other cells of the immune system.

28
Q

Dysregulation of specific immunity

A

an immunologiv abnormality in IBD where the microbial antigen that is presented to the CD4+ cell induces differentiation into certain sub-types of T-helper cells.
- if T helper 1 type cells are produced, Crohn’s disease is more likely to develop
- if T helper 2 type cells are produced, ulcerative colitis is more likely to develop

29
Q

ulcerative colitis locations

A

begins in the rectum and is limited to the mucosal and submucosal layers

30
Q

crohns disease locations

A

can involve any part of the GI tract, often in ‘skipped lesions’ and involves transmural inflammation - the muscle layer of the tract

31
Q
A