GIT DISEASE Flashcards
gastric pits
site of hydrochloric acid synthesis
oesophagitis
innflammation of oesophageal mucosa, most frequently due to reflux of gastric contents
Gastro-oesophageal reflux disease (GORD)
recurrent backflow of gastric contents into the oesophagus
dyspepsia
indigestion
GORD prevalence
- 20% of adult population in Western countries
- Age-dependent
GORD aetiology
- Dysfunction of the oesopho-gastric junction due to:
- transient lower oesohpageal sphincter relaxation
- conditions that decrease closure strength or efficiency of LES
- Hiatal hernia
complications of GORD
- strictures leading to fibrotic scarring and swallowing difficulties
- 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
Acute gastritis
inflammation of the stomach lining
acute gastritis aetiology
injurious agents or impaired defences including:
- non-steroidal anti-inflammatory drugs
- ageing
- ingestion of harsh chemicals
- ischaemia
pareital cells
secrete HCl
cheif cells
secrete pepsinogin
Mucous cell
secrete mucus
prostoglandins
- inflammation mediators
- in our GI tract, are protective and help mucousal cells to produce mucus
Acute gastritis pathogenesis
- mucosal damage
- erosions that can casue haemorrhages
Chronic gastrits aetiology
infection with bacillus Helicobacter pylori and chronic NSAID use
chronic gastritis pathogenesis
- Virulence
- Bacillis + inflammation increases gastrin secretion
- in time, loss of parietal cells function, gastric atrophy and intestinal metaplasia
peptic ulcer disease
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
inflammatory bowel disease (IBD)
-chronic inflammatory condition of the intestinal mucosa (include both crohn’s disease and ulcerative colitis)
idiopathic
aetiology of a disease is unknown
NOD2 (IBD pathogenesis)
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
autophagy
the natural, conserved degradation of the cell that removes unnecessary or dysfunctional components through a lysosome-dependent regulated mechanism.
intestinal microbiota (IBD pathogenesis)
enormous amounts of microbes in intestines, influences by diet, pre and probiotics, antibiotics, enzymes, fecal transplantation
environmental factors (IBD pathogenesis)
- industrialization
- diet high in vegetables and fruit (decrease ibd)
- smoking
- psychological stress
- appendectomy
non-specific physiologic immunity (IBD)
- intestinal epithelial barrier
- antibacterial products
- acidic pH of stomach
- innate immune cells
specific physiologic immunity (IBD)
- pathogen-specific
- generation of B and/or T cell response
Dysregulation of non-specific immunity
an immunologic abnormality in IBD where the epithelial barrier is disrupted and increased numbers of dendritic cells
dendritic cell
an antigen presenting cell, boosts immune responses by showing antigens on its surface to other cells of the immune system.
Dysregulation of specific immunity
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
ulcerative colitis locations
begins in the rectum and is limited to the mucosal and submucosal layers
crohns disease locations
can involve any part of the GI tract, often in ‘skipped lesions’ and involves transmural inflammation - the muscle layer of the tract
