GI and Liver Physiology Flashcards
Function of GI tract
Provides continual supply of water, electrolytes, vitamins and nutrients
Secrete digestive juices (digests food)
Move food through tract
Circulate blood around tracts to carry away products of digestion
Smashes up food both physically and chemically, so it may be absorbed together with water
How are functions of GI tract controlled?
By local (e.g. food), nervous (enteric) and humoral systems
Upper GI tract contains
Buccal cavity
Oropharynx/ oesophagus
Stomach
Duodenum
Small intestine contains
Duodenum
Jejenum
Ileum
Lower GI tract contains
Caecum
Rectum
Anal canal
Buccal cavity function
Mastication:
Mechanical breakdown of food and mixes with saliva - ‘soft bolus’ of food, lubricated and readily swallowed
Digestion begins here
Oropharynx/ oesophagus function
Conveys food from mouth to stomach - upper sphincter controls entry into oesophagus
Muscular layer of oesophagus performs peristaltic movements to push bolus of food into stomach
Stomach function
Elastic bag that holds masticated food, adds gastric acid and digestive enzymes
Releases proteases and HCl, former begins smashing up proteins, latter is bactericidal
Churns its contents through peristalsis producing in 40-60 mins
Releases chyme, in small quantities, into duodenum
Duodenum function
1st portion of small intestine
Bulk of digestion
Digestive enzymes and intestinal juice secreted
Enzymatic breakdown of chyme
Regulates control of stomach emptying via hormones-secretin and cholecystokinin
Caecum function
Ileum pushes chyme into it through eleo-caecal valve
Absorbs fluids and salts remaining after intestinal digestion
Mixes with mucous
Rectum function
Electrolytes/ water absorbed
Faeces thickened and mucous added
Strectching of rectal walls stimulates stretch receptors and causes desire to defecate
Voluntary retention of faeces pushes it back into colon where more water extracted, making it harder (may lead to constipation)
Anal canal function
Continence organ
Regulates defecation
Lubricates and transmits faeces from rectum to outside world
Muscles of mastication
Masseter
Temporalis
Pterygoids
-innervated by V3 of trigeminal (CNV)
Saliva contains what to help digest
Alpha-amylase which begins breaking down starches in bolus
Some people have more than others
Oesophagus
Conduit between oropharynx and stomach
Fibromuscular tube about 20-25cm long
Passes posterior to trachea and heart, pierces diaphragm and enters fundus of stomach
Consists of layers of muscles, mucosa, submucosa and connective tissue
Stomach
Bag-like, dilated section of GI tract which can hold about 1L of food
Lies in upper left of abdominal cavity, against the diaphragm
Duodenum
25-38cm C-shaped structure lying adjacent to stomach
Four distinct sections, each with its own distinct function
Jejenum function
Much absorption occurs here
Inner surface consists of finger-like villi projections which > SA of jejenum allowing for > absorption of nutrients
pH > 7
Villi epithelium is ‘brush border’ made up of microvilli
Nutrient transport across epithelial cells is passive for sugar fructose but active for a.as, small peptides, vitamins, and most glucose
Ileum function
Absorbs vitamin B12, bile salts and products of digestion not absorbed by jejenum
Ileum and jejenum differences
Diameter of lumen of ileum smaller and has thinner walls
Ileum has more fat inside the mesentery
Abundant Peyer’s patches in ileum, encapsulated lymphoid nodules that contain large numbers cells of immune system (develops antibodies to different substances e.g. nut allergies in West)
Ileum absorbs vitamin B12, bile salts and products of digestion not absorbed by jejenum
Functions of the large intestine (colon)
Absorb remaining water and electrolytes from indigestible food matter
Accept and stores food remains that were not digested in small intestine
Eliminate solid waste (faeces) from body
Caecum
Pouch-like structure that is considered to be the beginning of the large intestine
Larger in herbivorous animals where cellulose-digesting bacteria are housed
Smaller or even absent in carnivorous animals and replaced by appendix
Rectum
Temporary store for faeces
Final part of large intestine connecting to anus
Approximately follows shape of sacrum
End expands into rectal ampulla where faeces if stored before defication
Why do we chew?
Fruit and veg which have indigestible walls around nutritious bits
Enzymes work on surface of food particles to smaller particles -> larger SA: volume ratio
Finer particles of food prevent excoriation of GI tract and > ease food emptied from stomach
Chewing reflex
Presence of bolus in mouth initiates reflex inhibition of MoM - mandible drops –>
This initiates stretch reflex of muscles of mastication that leads to rebound contraction and elevation of mandible and closure of teeth –>
This compresses bolus against lining of mouth which inhibits MoM once again allowing mandible to drop and rebound another time
How much force do we exert when we chew?
24kg on incisors
90kg on molars
Oesophagus
20cm long, muscular tube lined with mucosa
Upper 1/3: skeletal muscle
Lower 2/3: smooth muscle
Runs posterior to trachea, heart and lungs anterior to vertebrae and pierces diaphragm before entering stomach
Peristaltic waves of skeletal muscle controlled skeletal nerve impulses from CNIX and CNX
Smooth muscle controlled by CN X
Primary peristalsis
Continuation of peristaltic wave that commences in oropharynx and spreads to oesophagus
Pharynx to stomach: 8-10s
Gravity assist - 5-8s
Secondary peristalsis
Sweeps down any remaining food
Trigger is distension of oesophagus
Barrett’s Oesophagus
Metaplasia (abnormal change) of cells lining the lower oesophagus
Exposure to stomach acid in reflux oesophagitis
Normal SS epithelium replaced by simple columnar epithelium with goblet cells (lower GIT cells)
Strong association with oesopohageal adenocarcinoma - virulent form of cancer
-85% mortality rate
-premalignant condition
Barrett’s oesophagus symptoms
None in themselves but associated with acid reflux
- heartburn
- dysphagia
- haemtemesis
- sub-sternal pain
- erosion of teeth due to acid exposure
Barrett’s oesophagus management
Proton pump inhibitor
Endoscopic surveillance
Resection of oesophagus
Stomach
‘J-shaped’, muscular, elastic pouch which churns and partly digests masticated food
Stomach volume
1L but can relax and expand to hold greater volume
Where does food enter stomach
Food enters stomach and forms concentric circles in orad portion of stomach
-old food by wall, newest food in opening of oeophagus
Learn parts of stomach from lecture
Learn parts of stomach from lecture
How does stomach store more food?
Food stretches stomach and vagovagal reflex from stomach to brainstem and back to stomach reducing muscular tone and allowing stomach to bulge outwards and accommodate more food to max of 0.8-1.5L
Stomach digestion mechanism
Gastric juice secreted by gastric glands that cover almost entire lumen of stomach
Weak mixing waves churn food and gastric secretions
Beginning in mid/upper portion of stomach, reaching antrum in 15-20s
Become more powerful towards pylorus - squeezing food out like toothpaste tube
Only few mm squirted out through pylorus into duodenum with each wave
Pylorus slightly tonically contracted thus acting as sphincter –> open enough to allow fluids to pass directly into duodenum –> but prevents food particles passing until they are well mixed and fluid-like –> opening and closing of pylorus controlled by nervous and hormonal signals from stomach and duodenum
(LOOK AT PIT AND GLAND DIAGRAM)
Control of stomach emptying
Duodenum provides the most potent signals for stomach emptying
Rate is never greater than the rate the chime can be digested and absorbed in the small intestines
Factors increasing rate of stomach emptying
> food volume in stomach stretches walls eliciting ‘myenteric reflexes’
Gastrin - hormone produced by G-cells in antral mucosa
Mainly causes production of highly gastric juice
Also mild stimulatory effects on motor activity of ‘pyloric pump’
Factors decreasing rate of stomach emptying
Stretch of duodenal wall –>
- directly inhibits pyloric pump via enteric NS in gut wall
- via extrinsic nerves –> prevertebral, sympathetic ganglia –> back to stomach via inhibitory sympathetic fibres
- vagus nerves to brainstem –> inhibit excitatory signals to stomach through vagi (a bit)
Pathologies of stomach
Peptic ulcer
Gastric cancer
Peptic ulcer
Damage to wall of stomach by stomach acid
Can affect duodenum and lower oesophagus
Peptic ulcer symptoms
Gnawing, burning, upper abdominal pain that worsens on eating (secreting more acid)
Indigestion, ‘heartburn’, nausea
Peptic ulcer causes
Helicobactor pylori 60% of gastric and up to 50-75% of duodenal ulcers
Causes chronic inflammation in antral mucosa
Acid secretion leads to erosion of gastric wall
Non-steroidal anti-inflammatory drug such as ibuproefn or aspirin - long time or at high doses
Peptic ulcer treatment
Proton pump inhibitor (PPI) - reduces acid to nearr zero allowing ulcer to heal naturally
‘Triple therapy’ if caused by H.pylori - amoxillin, clarithromycin and PPI Nobel Prize
Gastric cancer
Develops from lining of stomach
Average age of diagnosis = 69 years
Gastric cancer symptoms
Pain or burning sensation on swallowing Food may stick in throat or chest Weight loss Upper abdominal pain Persistent dyspepsia and burping Feeling full after even small amounts Nausea and vomiting Bleeding (-> dark stools), tiredness and breathlessness
Gastric cancer causes
All the usual carcinogenic things
Rest of GI tract functions (aside oesophagus and stomach)
Absorption of nutrients and water
Limiting factor for absorption is SA over which this occurs
Folds of Kerckring
Folds that > absorptive SA by 3x
Well developed in duodenum and jejenum protruding 8mm into lumen
Villi
Project from very surface of mucosa by 1mm
Numbers decrease toward distal end of GI tract
Microvilli
Each epithelial cell has many 1000s of 1µm extensions
Brush border
20x increase in SA
How much SA of small intenstines
250m2
LOOK AT VILLI PICTURE ON LECTURE
LOOK AT VILLI PICTURE ON LECTURE
Fat absorbed to lacteal
Small intestine daily turnover
Several hundred g carbs 100g+ fat 50-110 of amino acids 50-100g ions 7-8L of water
Small intestine capable turnover
Several kg carbs
500g fat
500-700g protein
20L+ water
Small intestine - water
Transported entirely by diffusion going from high to low concs
If chyme is dilute enough, water absorbed from mucous villi to blood entirely by osmosis
Can also go in other direction if chyme is hyperosmotic but within minutes chyme will be diluted to make it isosmotic with plasma
Mostly occurs at tight junctions between apical borders of epithelial cells (‘paracellular route’) but also through cells (transcellular route)
Osmotic movement of water creates flow of fluid into and through the paracellular spaces and into the blood of the villus
Small intestine - ions
Na is actively transported across intestinal membrane
20-30g Na secreted in intestinal secretions/day. We eat 5-8g/day thus intestine must absorb25-35g/day
<0.5% of intestinal Na lost in faces since it is rapidly absorbed through intestinal mucosa
If significant amounts of intestinal secretions are lost to the exterior (diarrhoea). Na reserves can be depleted to lethal levels in hours
Small intestine (cellular level) apical cell. How is sodium absorption powered?
By active transport using ATP
Na+ / K+ ATPases
Small intestine (cellular level) apical cell. Where does the sodium go? What does this lead to?
Travels from inside the epithelial cells through the basal and lateral walls of the epithelial cells
Cl- ions ‘dragged’ along by their attraction to the positive Na+ (to balance electronegativity)
Active transport of Na+ across basolateral membrane reduces cellular [Na+] to low value (50mEq/L)
Chyme cellular concentration value
142mEq/L
What happens to Na+ because of chyme gradient?
Moves down steep electrochemical gradient from chyme through brush border into epithelial cell cytoplasm
Na+ also co-transported via different transporters
Sodium co-transporters
Sodium-amino acid co-transporter
Sodium-glucose co-transporter
Sodium-hydrogen exchangers
Won’t function until other site on transporter is filled
Highest proportion of nutrients one absorbs
Starches
-broken down into monosaccharides
How are monosaccharides absorbed?
Virtually all absorbed by secondary active transport processes
Final digestion products are monosaccharides –> glucose 80% and galactose (from milk) and fructose (20%)
Sodium co-transport mechanism
- Active transport of Na+ through basolateral membrane into interstitial fluid, this depletes Na+ inside epithelial cell
- Na+ from intestinal lumen enters cell by combining with transport protein - will not move Na+ unless other substance combines with it. Na+ & other substance both transported into cell
- Once inside epithelial cell, other transport proteins & enzymes facilitate diffusion of substance through basolateral membrane, into paracellular space and into blood
Fats are broken down into
Monoglycerides (MG) and fatty acids (FFA) which are then emulsified
MG and FFA emulsified by
Liver secretion (bile) into tiny 3-6nm bile secretions Highly charged exterior means they are soluble in chyme
MG and FFA as micelles
Highly charged exterior means they are soluble in chyme
Micelles carried to brush border of epithelial cells and penetrate recesses in between agitating microvilli
MG and FFAs diffuse out of micelle and into interior of epithalial cell (phospholipid bilayer)
Micelle remains in chyme and emulsifies more fats, acting as ‘ferry’
MG and FFA in cell
Taken up by SER, converted into triglycerides & released to form chylomicrons through basolateral membrane, up through thoracic lymph duct and emptied to blood
Which substances require secondary active transport systems?
Glucose and galactose –> monosaccharides –> facilitated diffusion –> blood
Secondary active transporter is Na
Which substance are absorbed by facilitated diffusion?
Fructose
Which substance are absorbed by diffusion?
Micelle –> chylomicrons in epithelial cell of villi –> lacteal
Which substance are absorbed by secondary active co-transport?
Amino acids (Na) –> diffusion –> blood and peptides (H)
Large intestine overview
1.5m length
No nutrients in chyme
Removes water, salts, sugar and vitamins
Can absorb 5-8L of fluid and electrolytes per day
Teeming with bacteria
High capacity for absorption of Na+ which drags Cl- with it (electrical potential)
Regions of large intestine
1) Cecum - compress material into faecal matter
2) Ascending colon
3) Transverse colon
4) Descending colon
5) Sigmoid colon
Peyer’s patchers
Areas of lymphoid tissue on large intestine for local immune protection
Large intestine muscle
Tenia coli - 3 bands of longitudinal muscle
Houstra
Pockets which give a segmented appearance
Squeezes in other way to muscles
Speed of movement in large intestine
Slow movement of contents as trying to absorb water
Villi and goblet cells in large intestine
No villi
High concentration of goblet cells - mucous secretion
Junction between ileum and caecum
Ileocaecal valve
Tight junctions between epithelial cells
Smaller in large intestine than small intestine
Prevents significant back-diffusion of ions allowing for more net Na+ absorption, especially in presence of aldosterone
Aldosterone
Greatly enhances Na+ absorption
When dehydrated, large amounts of aldosterone secreted by cortices of adrenal gland
Within 1-3 hours, > activation of enzyme and transport mechanisms for Na+ absorption by intestinal epithelium which leads to > Cl- and water absorption
Colon motility
Segmented contractions 99% of the time:
- Retain material in proximal colon (water reabsorption and fermentation)
- Mixing contents
Large intestine main functions
High mucous secretion - goblet cell
No carrier mediated transport of nutrients (absorption by diffusion)
Efficient water reabsorption - follows Cl and Na movement
HCO3 buffers acid produced by bacterial fermentation
Composition of faeces
3/4 water 1/4 solid matter: -3% protein -30% undigested roughage -10-20% inorganic matter -10-20% fat -30% dead bacteria
Normal brown colour of faeces
Caused by stercobilin and urobilin - derivatives of bilirubin
Odour of faeces
Caused by bacterial action and vary from one person to another depending upon colonic flora and types of food eaten
Odouriferous compounds: indole, skatole, mercaptans and hydrogen sulphide
