Gastro Physiology Flashcards
Enteric nervous system
Myenteric plexus / Auerbach’s
- Motor
- Runs bewtween circular and longitudinal muscle layers
Submucosal / Meissner’s
- Sensory
- Runs in submucosal layer
Parasympathetic: synapses with myenteric plexus
Sympathetic: synapses with myenteric and submucosal plexus
Saliva types
Parotid gland
- Watery
- No mucous
- IgA
- Amylase
- 25%
Submandibular
- Mixed mucous/serous
- 70%
Sublingual
- Contains mucoproteins
- Only 5% of saliva secretion
Ductal modifications of saliva
Glands secrete isotonic fluid
During duct movement
- K+ and HCO3- are added
-NA+ and Cl- are removed
Control of saliva production
Salivary nucleus in medulla
Parasympathetic supply from facial and glossopharnygeal nerve
Oesophageal sphincter
Physiological not anatomical
Pressure ~ 15-25mmHg
Characteristics reducing reflux:
- Right crus of diaphragm presses on oesophagus as it passes through diaphragm
- Acute angle of oesophagus as it enters somach through diaphragm
- Mucosal folds in the lower oesophagus act as a valve
Closure of the sphincter is under vagal control
Hormone gastrin causes the sphincter to contract
Secretin, CCK and glucagon cause it to relax
Cells of the gastric mucosa
Two broad types:
Columnar epithelium: secrete protective mucus layer
Gastric galnds: secretory role
- Mucus cells: secrete mucus located at opening of gastric gland
- Peptic/chief cells: secrete pepsinogen and ar elocated at base of gastric gland
- Parietal cells: secrete HCl and IF
- Neuroendocrine cells: secrete a number of peptides that regulate GI motility and secretion, i.e. gastrin.
Gastric secretory cells
- Mucus cells: secrete mucus located at opening of gastric gland
- Peptic/chief cells: secrete pepsinogen and ar elocated at base of gastric gland
- Parietal cells: secrete HCl and IF
- Neuroendocrine cells: secrete a number of peptides that regulate GI motility and secretion, i.e. gastrin.
Cells found most at fundus and body of stomach
Parietal cells
Peptic cells
Cells found most at pylorus and antrum of stomach
Mucus cells
Neuroendocrine (secreting gastrin) cells
Cells of the cardia of the stomach
Mucus cells make up all of gastric gland
Factors that stimulate parietal cells acid production
Vagal innervation ACh
Gastrin secreted from G-cell
Histamine secreted from entero-chromaffin cells and mast cells
Factors that inhibit paroetal cell acid production
Secretin produced by duodenal mucosa
CCK produced by duodenal mucosa
GIP produced by duodenal mucosa
Somatostatin producerd by D-cells
Pepsinogen
Secreted by chief/peptic cells
Activated by HCl (and pepsin) to produce pepsin
Pepsin proteolytic enzyme that hydolyses peptide bonds in proteins
Factors protecting the epithelium of the gastric mucosa
Mucus is secreted from cells in the bottom of the gastric gland to coat the epithelium
Contains bicarbonate to off-set pH
Tight-epithelial junctions prevents gastric juices reaching deeper structures
Prostagland E increases thickness of mucus layer
- Stimulating HCO3 production
- Increasing blood flow in the mucosa (bringing nutrients to any damaged areas).
Phases of gastric secretion
Cephalic
- Appeptite centre in thalamus
- 30%
- Stimulation of parietal cells via G cells and from G-cells producing gastrin
Gastric
- 60%
- Distension of the stomach and the chemical composition of food lead to acetylcholine release from the vagus
Intestinal
- 5%
- Stimulation is the presence of food in the duodenum; this results in the release of gastrin from G-cells in the duodenal mucosa
Enterogastric reflex
Food entering duodenum causes release of secretin, CCK and GIP
All inhibit gastrin and parietal cell activity
Factors altering transit into duodenum through pylorus
Increased gastric volume leads to quicker emptying
Fats: CCK and GIP are released which cause contraction of pyloric sphincter
Proteins: stimulate gastrin secretion –> causes contraction of pylorus constriction
Low pH / Acid: causes vagus-mediated delay in passage + secretin release
Secretin
–> Inhibits contractions in gastric antrum
–> Contraction of pylorus
–>Increased production of bicarbonate release from pancreas to off-set acidic pH
Hypertonic chyme –> delays gastric emptying
Vomiting reflex
Coordinated by vomiting centre in the medulla
Impulses along
- CN V
- CV VII
- CV IX
- CN XII
- Intercostals
- Diaphragm
- Andominal muscles
Action of proton pump inhibitors
Inactive at neutral pH but is activated by the acidic conditions in the stomach
Irreversibly binds to sulphydryl groups on the proton pump
Gastric protection drugs
Sucralfate
-Polymerises at pH <4 and adheres to base of ulcer
Bismuth chelate
-Acts similar to sucralfate and ?eradicates H.Pylori
Misoprostol
- Prostaglandin E2 analogue
- Increases bicarb and blood flow
Complications post gastrectomy
Iron deficiency
B12 deficiency
Dumping syndrome
Diarrhoea
Billous vomiting
–> refluxed bile can also lead to gastritis –> recurrent ulcers
Gastric cancer from bile salt reflux gastritis
Early dumping syndrome
30–45 min after eating
Rapid gastric emptying of a hyperosmolar meal into the small bowel
Results in fluid moving into the small bowel by osmosis (third space loss) and rresults in dizziness, weakness and palpitations
Complications of a vagotomy
Reduced gastric acid secretion (therapeutic intent)
Delayed gastric emptying
–> failure of pylorus to relax
Reduced pancreatic secretions
Diarrhoea secondary to loss of vagal control of small bowel
Increased risk of large bowel cancer due to excess of bile salts reaching large bowel
Components of small bowel crypts
Undifferentiated stem cell precursor
D-cell: somatostatin
S-sell: secretin
N-cell: neurotensin
Enterochromaffic cells: 5-hydroxytrptamine
Activates pancreatic trypsinogen
Enterokinase
Brunner’s gland
Present in duodenum only (not jejunum or ileum)
Secrete mucus-rich bicarbonate
Glucose and galactose absorbtion
Secondary activae transport using NA-K ATPase
Fructose absorbtion
Distinct Na-independent absorbtion
‘Facilitate’ diffusion
Absorbtion of triglycerides
Absorbed into enterocytes
–>Smooth endoplasmic reticulum reforms triglycerides from the absorbed monoglycerides and FFAs
Reformed triglycerides are formed into chylomicrons, which are released from basal layer of the enterocyte to diffuse into the lacteals within the villi
From here they enter the lymphatic circulation and then into the venous circulation
Fat-soluble vitamins
A, D, E and K
Water-soluble vitamins
B and C
Vitamin C is absorbed by a Na+-dependent mechanism in the jejunum
Vitamin B12 is absorbed in the ileum after intrinsic factor (secreted in the stomach) binds to its specific receptor.
IF–vitamin B12 complex is then taken up into the cell
The remaining B vitamins diffuse freely across the enterocyte cell membrane.
Absorption of Vitamin C
Vitamin C is absorbed by a Na+-dependent mechanism in the jejunum
Absorption of Iron
Absorbed in duodenum and jejunum
Ferrous Fe2+ form is absorbed (NOT ferric Fe3+)
Gastric acid converts iron to the ferrous form
Absorption transport protein transferrin
–> binds iron and links to a membrane-bound receptor, –> taken into the cell via endocytosis
Absorption of Calcium
Absorption is dependent on a calcium-binding
protein in intestinal cells
These receptors can be increased by vitamin D
Complications of duodenal resection
Ulceration
-Duodenum has Brunner’s glands to secrete mucus rich in HCO3-
Malabsorption
- Iron
- Calcium
- Phosphate
- Impaired fat emulsification
Dumping to uncontrolled passage of chyme
Complications of ileal resection
Impaired bile salt reabsorption
- -> Increased large bowel malignancy due to bile salts reaching colon
- -> Gallstones: decrease in bile salt pool; this predisposes to cholesterol gallstones
B12 deficiency
- -> Macrocytic anaemia
- -> Subacute degeneration of cord
Impaired water reabsorption
–> Diarrhoea
Pancreatic proteolytic enzymes
Secreted in inactive form = zymogen granules from pancreatic acinar cells
Activation of trypsinogen to trypsin –> activation of proteolytics
Activation of trypsinogen is by an enzyme secreted by the duodenum enterokinase and the alkaline environment
Procarboxypeptidase
Cleaves peptides at C-terminus
Secreted by pancreas
Chymotrypsin, trypsin and elastase
Cleave peptide bonds
Secreted by pancreas
Splits α-1,4-glycosidic bonds
Amylase
Amylase
Splits α-1,4-glycosidic bonds
Strach digestion resulting in oligosaccharides
Phases of exocrine secretion from pancreas
Cephalic: vagal
Gastric: vagal
Intestinal: CCK and secretin.
Complications of pancreatic resection
Malnutrition from malabsoption
- Inability to breakdown proteins
- Inability to breakdown fats
- Fat-soluble vitamin deficiency (ADEK)
Malabsorption: loss of alkaline pancreatic secretions
leads to failure to neutralise gastric chyme and leads
to Fe2+, Ca2+ and PO4
− malabsorption; this eventually leads to anaemia and osteoporosis
Diabetes mellitus: loss of the pancreas leads to an
absolute deficiency of insulin.
Cholic acid and chendeoxycholic acid
Bile ACIDS
Bile salts
Formed by linking glycine and taurine to bile acids
Cholic acid and chendeoxycholic acid = bile acids
Transport of bilirubin circulation
Poorly soluble
Bound to albumin
After glucoronidation –> becomes water soluble
25-hydroxycholecalciferol
Formed in liver by 25 - hydroxylation of Vit D3
Clinically detectable Jaundice
> 40
Complications of cholecystectomy
Inability to concentrate bile –> Increased flow of bile –> reflux and biliary gastritis
Formation of micelles during fat absorption is impaired
- -> fat intolerance and malabsorption
- -> abdominal pain and diarrhoea
Enteroglucagon
Inhibits gastric and small bowel motility
Released by distal ileum and colon
Presence of glucose of fats in colon or distal ileum
–> enteroglucagon –> inhibits gastric and small bowel motility
Essential amino acids
Cannot be synthesised
Isoleucine
Leucine
Lysine
Methionine Phenylalanine Threonine Typtophan Valine
Essential fats
Linolenic
Linoleic
Arachidonic acid
Selenium
Part of glutathioner peroxidase
AND
Responsible for convertign T4 –> T3 in liver microsomes
Chromium
Facilitates action of insulin
Copper
Required for synthesis of haemoglobin and is a component of coenzymes in the electron transport chain
Hunger or feeding centre
Lateral hypothalamus
Satiety centre
Ventromedial hypothalamus
