Microanatomy of the GI tract 2 Flashcards
epithelium type of oesophagus
Stratified squamous because its protective epithelium
What’s the muscular layer like of the oesophagus (how does it change)
1st third: skeletal (voluntary)
Middle third: mixed
Last third: smooth (involuntary)
Outer layer of oesophagus in thorax vs abdomen
Adventitia in thorax
Becomes serosa in last part beyond diaphragm (which allows it to secrete water to reduce friction)
What is Barrats oesophagus and why does it occur
Metaplasia. Change from stratified to columnar in oesophagus due to repeated damage from gastric reflux
–> Happens because columnar epithelium is more likely to protect against acid in oesophagus
What are rugae
Folds which increase the surface area and enable max contact between stomach contents and gastric mucosa
What is the luminal surface of the stomach composed entirely of
Columnar epithelial mucous cells for protection
What do gastric pits contain
Epithelial cell types which break down food
What is the oblique muscle layer of the stomach used for
Facilitates the churning of the food in all directions
What cells are there in gastric pits
Mucous cells
Parietal cells
chief cells
Enteroendocrine cells
Where are and What do mucous cells produce
At the surface
-Produce mucus and bicarbonate (protect surface from acid and digestion)
What are parietal cells
Produce HCl and intrinsic factor
What are chief cells
Produce enzymes e.g. pepsinogen
What are enteroendocrine cells
Produce hormones e.g. gastrin, serotonin, somatostatin, and VIP
HOW do parietal cells produce HCl
By active transport of H+ and passive transport of Cl into the lumen. Stimulated by gastrin, Ach and histamine
Why don’t antihistamines prevent the secretion of stomach acid production
Antihistamines target H2 receptors bu histamines in stomach are H2
What bacteria cause gastric ulcers
H. Pylori
How does H. Pylori cause gastric ulcers
Breaks down protective mucus layer. so not producing mucus so there is no protection from stomach acid. Acid eats down layers of stomach. Initiates acute inflammatory response and becomes chronic (damage and repair happening at the same time) and so a gastric ulcer forms
How can you fix a gastric ulcer caused by H. Pylori
1) Get rid of the infection
2) give PPI to enable the mucus cells to grow back over the surface
Why can H. pylori survive acidic conditions
Has an alkaline surface
What are the distinguishing features of the duodenum
- Have Brunners glands in the submucosa
- Receives secretions from the liver and pancreas via pancreatic and bile ducts
What are Brunners glands and why does the duodenum have them
Because pyloric sphincter allows control of release of chyme so with that comes a lot of HCl. You don’t want acidic attack in duodenum. Brunners glands release alkaline secretions which neutralise chyme when sphincter opens
Distinguishing features of jejunum and why
Has lots of plicae and vili because lots of absorption takes place
Distinguishing features of lieum and why
Peyers patches (prominent lymphoid tissue clusters that help do lymphoid surveillance) and shorter, sparser plicae and vili
Folds in the small intestine in descending size and where they are found
Plicae (mucosa and submucosa)
Villi (mucosa)
Microvilli (on the surface of columnar epithelium) (enterocytes)
What are villi lined with
Simple columnar epithelium
what is the impact of the small intestine epithelium having a high cell turnover
If you damage small intestine, it will easily repopulate itself
Function of enterocytes in the small intestine epithelium
Columnar cells with microvilli
ABSORPTION
Brush border enzymes aid digestion
Function of goblet cells in small intestine epithelium
Secrete mucus (more numerous distally)
Function of panted cells
Large cytoplasmic granules
DEFENSINS
Protect against infection
Function of enteroendocrine cells in the small intestine
Triangular cells with small haloed granules. Secrete locally acting hormones regulating secretion and motility
Where are brush border enzymes produced
Vili
What is luminal digestion done by
chyme and pancreatic secretions mix to break down food into component parts
What is membrane digestion done by
Brush border enzymes
How are proteins digested
By stomach and in duodenum by pancreatic enzymes. Enterocytes have membrane peptide hydrolyses to finally break down proteins to amino acids
How are carbohydrates digested
Salivary and pancreatic amylase converts starch to glucose and maltose. Membrane sacharridases form monosaccharides
How are lipids digested
Broken down by bile to a fine emulsion of triglycerides then pancreatic lipases to monoglyceride and free fatty acids. In the enterocytes they are reconstituted to triglycerides and coated with phospholipid and protein for transport (as chylomicrons)
How do amino acids and monosaccharides enter the blood
Enter the intestinal capillaries and are taken to the liver in the portal system
Causes of malabsorption in the small intestine
- Insufficient pancreatic enzyme (e.g. CF)
- Insufficient bile
- Loss of small intestinal surface area
- Lack of mucosal brush border enzymes
What is celiac disease
Intolerance to gluten. Response to that is build up of lymphocytes in epithelial layer in villi. It is a chronic inflammatory response so the villi are damaged. You lose the villi gradually. Very important to exclude gluten from diet
Manifestations of malabsorption
- Dairrhoea (water) and steatorrheoea (fat)
- Haemopoietic (anaemia due to deficiency in iron, folate and B12. Bleeding due to vitamin K deficiency (fat soluble)
- Skeletal (osteopenia (more porous bones) due to Ca, Mg, vit D and protein deficiency)
- Endocrine (impotence, infertility, amenorrhea. Hyperparathyroidism due to low Ca and Via D)
- Skin : oedema and dermatitis (vit A)
- Nervous system: peripheral neuropathy (vit A and B12)
Symptoms of coeliac disease in adults and children
Diarrhoea, abdominal distension, malnutrition
-failure to thrive in children
What cells do the large intestine contain and what do they do
goblet cells for lubrication
Enterocytes: absorption
Enteroendocrine cells and stem cells
Why are there more goblet cells in the large intestine
More difficult to shift the solid waste so goblet cells lubricate it
What is the colon specialised for
Water absorption
What cells are numerous in the colon
Goblet cells
What influences transit rate in the GI tract
Slower: Constipation due to dehydration/lack of fibre. Consquence can be diverticulosis
Faster rate: IBS and diarrhoea
Blocked: Obstruction
What causes diverticulosis
Low fibre. Harder to move contents of bowel so puts pressure on bowel
How does diverticulosis present
Inflammation/perforation of diverticula. Lower left quadrant pain and tenderness. Mild fever and raised WBC
How to treat diverticulosis
Antibiotics and withhold solid food
What is the obstruction of small bowel due to
mechanical obstruction or impairment of peristalsis (due to nerve or muscle damage e.g. after abdominal surgery)
What does the obstruction of the small bowels result in
Distension and loss of fluids and electrolytes
-Interruption of blood flow (strangulation due to increased pressure), necrosis and rapid bacterial growth, gangrene and perforation
Symptoms of obstruction of small bowel
Pain, absolute constipation, abdominal distension and vomiting, no passing of stool, vomiting if they’re trying to eat
Two main inflammatory diseases of colorectal area
Crohn’s disease and ulcerative colitis
What are the two sphincters in the anal canal and are they involuntary or voluntary
Internal anal sphincter: smooth muscle thickening at the end of the rectum (involuntary)
External anal sphincter: skeletal muscle- under voluntary control
What epithelium is the rectum
Columnar epithelium
venous supply of the anal canal
Haemorrhoidal plexi which can become distended due to congestion: piles
