GIT DISEASE

Question 1

gastric pits

Answer 1

site of hydrochloric acid synthesis

Question 2

oesophagitis

Answer 2

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

Question 3

Gastro-oesophageal reflux disease (GORD)

Answer 3

recurrent backflow of gastric contents into the oesophagus

Question 4

dyspepsia

Answer 4

indigestion

Question 5

GORD prevalence

Answer 5

• 20% of adult population in Western countries
• Age-dependent

Question 6

GORD aetiology

Answer 6

• Dysfunction of the oesopho-gastric junction due to:
• transient lower oesohpageal sphincter relaxation
• conditions that decrease closure strength or efficiency of LES
• Hiatal hernia

Question 7

complications of GORD

Answer 7

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

Question 8

Acute gastritis

Answer 8

inflammation of the stomach lining

Question 9

acute gastritis aetiology

Answer 9

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

Question 10

pareital cells

Answer 10

secrete HCl

Question 11

cheif cells

Answer 11

secrete pepsinogin

Question 12

Mucous cell

Answer 12

secrete mucus

Question 13

prostoglandins

Answer 13

• inflammation mediators
• in our GI tract, are protective and help mucousal cells to produce mucus

Question 14

Acute gastritis pathogenesis

Answer 14

1. mucosal damage
2. erosions that can casue haemorrhages

Question 15

Chronic gastrits aetiology

Answer 15

infection with bacillus Helicobacter pylori and chronic NSAID use

Question 16

chronic gastritis pathogenesis

Answer 16

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

Question 17

peptic ulcer disease

Answer 17

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

Question 18

inflammatory bowel disease (IBD)

Answer 18

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

Question 19

idiopathic

Answer 19

aetiology of a disease is unknown

Question 20

NOD2 (IBD pathogenesis)

Answer 20

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

Question 21

autophagy

Answer 21

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

Question 22

intestinal microbiota (IBD pathogenesis)

Answer 22

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

Question 23

environmental factors (IBD pathogenesis)

Answer 23

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

Question 24

non-specific physiologic immunity (IBD)

Answer 24

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

Question 25

specific physiologic immunity (IBD)

Answer 25

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

Question 26

Dysregulation of non-specific immunity

Answer 26

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

Question 27

dendritic cell

Answer 27

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

Question 28

Dysregulation of specific immunity

Answer 28

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

Question 29

ulcerative colitis locations

Answer 29

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

Question 30

crohns disease locations

Answer 30

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