Gastro Physiology Flashcards by Nathan Ashburner

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

How well did you know this?

Not at all

Perfectly

Saliva types

Parotid gland
-Watery
-No mucous
-IgA
-Amylase
-25%

Submandibular
-Mixed mucous/serous
-70%

Sublingual
-Contains mucoproteins
-Only 5% of saliva secretion

How well did you know this?

Not at all

Perfectly

Ductal modifications of saliva

Glands secrete isotonic fluid

During duct movement
- K+ and HCO3- are added

-NA+ and Cl- are removed

How well did you know this?

Not at all

Perfectly

Control of saliva production

Salivary nucleus in medulla

Parasympathetic supply from facial and glossopharnygeal nerve

How well did you know this?

Not at all

Perfectly

Lower 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

How well did you know this?

Not at all

Perfectly

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.

How well did you know this?

Not at all

Perfectly

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.

How well did you know this?

Not at all

Perfectly

Cells found most at fundus and body of stomach

Parietal cells

Peptic cells

How well did you know this?

Not at all

Perfectly

Cells found most at pylorus and antrum of stomach

Mucus cells

Neuroendocrine (secreting gastrin) cells

How well did you know this?

Not at all

Perfectly

Cells of the cardia of the stomach

Mucus cells make up all of gastric gland

How well did you know this?

Not at all

Perfectly

Factors that stimulate parietal cells acid production

Vagal innervation ACh

Gastrin secreted from G-cell

Histamine secreted from entero-chromaffin cells and mast cells

How well did you know this?

Not at all

Perfectly

Factors that inhibit parietal cell acid production

Secretin produced by duodenal mucosa

CCK produced by duodenal mucosa

GIP produced by duodenal mucosa

Somatostatin producerd by D-cells

Nausea

How well did you know this?

Not at all

Perfectly

Pepsinogen

Secreted by chief/peptic cells

Activated by HCl (and pepsin) to produce pepsin

Pepsin proteolytic enzyme that hydolyses peptide bonds in proteins

How well did you know this?

Not at all

Perfectly

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).

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Enterogastric reflex

Food entering duodenum causes release of secretin, CCK and GIP

All inhibit gastrin and parietal cell activity

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Vomiting reflex

Coordinated by vomiting centre in the medulla

Impulses along
-CN V
-CV VII
-CV IX
-CN XII
-Intercostals
-Diaphragm
-Andominal muscles

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

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