Gastrointestinal Physiology Flashcards
What are the layers of muscle of the gi tract
Outer longitudinal
Middle circular
Inner submucosal
Where does the enteric nervous system sit in relation to gi muscles
Myenteric plexus between the circular and longitudinal layers
Submucosal plexus between submucosal and circular layers
What is the basal electrical rhythm of the gi tract.
Where does it effect
How is it controlled and transmitted
Effects gi tract beneath oesophagus.
Spontaneous variation of transmembrane potential from -70 to -40 in smooth muscle cells. On reaching -40 depolarise and contract. Determines maximum rate contraction can occur.
Controlled by interstitial cells of cajal
Transmitted through gap junctions.
What is the term for how the smooth muscle of the gi tract contracts in coordination joined by gap junctions
Syncytium l
What alters the frequency and amplitude of the basal electrical rhythm?
Location in the bowel
Modulation by the nervous system
Hormonal control
Drugs
What is the effect of acetylcholine on basal electrical rhythm of the gi tract
Adrenaline?
Ach Raises cell membrane potential stimulating contraction
Adrenaline hyperpolarises inhibiting contraction
What is peristalsis
Where does it occur
Type of reflex
Reflex response to gut wall stretch. When wall stretched causes a contraction behind that point and a relaxation in front.
Occurs throughout gi tract
Polysynaptic reflex - 2 interneurones, one triggering efferent contraction, the other relaxation
What areas of gi tract motility involve the somatic nervous system
Swallowing
External anal sphincter control (defication)
Where is swallowing controlled
Swallowing centre in the reticular system of medulla and lower pons
Inputs to the swallowing centre
Trigeminal
Glossopharyngeal
Superior laryngeal
Recurrent laryngeal
Vagus
Motor output from swallowing centre
Vagus
Stages of swallowing
Oral
Pharyngeal
Oesophageal
Events of oral stage of swallowing
Voluntary
Masticated food pushed into pharynx by upward backward pressure of tongue against hard palate
Events of pharyngeal stage of swallowing
Pressure detected on tonsillar pillars
Signal transmitted to swallowing centre
Soft palate elevates closing nasopharynx
Respiration halted
Vocal cords close and larynx moves anterior and cephalad with epiglottis covering glottis
upper oesophageal sphincter opens
Superior constrictor muscles of pharynx propel bolus into oesophagus
Events of oesophageal phase of swallowing
Primary peristaltic wave from pharynx moves bolus down oesophagus to lower oesophageal sphincter
Los relaxes allowing bolus into stomach.
What is the parasympathetic autonomic nerve supply to the gi tract
Effects
Vagus and sacral fibres
Increase motility, tone, force of contraction and gastric emptying, increase gastrin, salivary production and pancreatic/bile secretions
What is the sympathetic supply to the bowel
Effects
Spinal nerves via coeliac, mesentieric and pelvic ganglia
Increase salivary production, decrease motility and gastric emptying, vasoconstriction.
Length of oesophagus
30cm
What is the musculature of the upper oesophagus?
How does it differ from rest of gi tract
Upper 6cm striated skeletal with no autonomic activity
What forms the upper oesophageal sphincter
Innervation
Resting state
Cricopharyngeal and pharyngeal constrictor muscles
Vagus
Tonic contraction;
What forms the lower oesophageal sphincter
Functional zone of increased intralumnal pressure in distal 4cm of oesophagus from semicircular oesophageal muscle fibres on left and gastric sling fibres on right. Also crural fibres from diaphragm.
What is the barrier pressure of the lower oesophageal sphincter?
Pressure difference between los and intragastric pressure
Usually 15-25mmHg
What helps prevent reflux when intragastric pressure is raised?
Acute angle of los and encircling diaphragm creating a flutter valve
Types of muscle action in stomach?
When food enters stomach proximal stomach relaxes minimising increases in intergastric pressure.
When fed however, proximal stomach slowly contracts in sustained manner to fascilitate gastric emptying.
In antrum rhythmic contractions mix food with stomach contents (acid, pepsin etc) grinding it to chyme
Between meals strong synchronised contractions occur in bursts to open pyloric sphincter to eject indigestible material out of stomach.
How does the stomach empty?
Pylorus doesn’t fully close so small volumes of chyme squirt out in each contraction
What reduces stomach emptying
Pain
Anxiety
Stress
Medications
Sns
What occurs on distension if the stomach?
Stimulation of vagus
Increased acid secretion
Increased peristaltic activity
Increased gastric emptying
What happens if the stomach empties too quickly
Activation of duodena receptors (stretch, acid, osmolarity or fatty acid concentration) activating reflex to decrease gastric emptying
What’s is the implication of the decrease in gastric emptying caused by increased duodenal fatty or amino acid concentrations
Carb meals leave stomach fastest
Then protein meals
Then fatty meals the slowest
Length of small bowel
5m
What key vitamin is produced by large bowel bacteria
Vit k
Functions of large bowel
Water absorption
Faeces storage
Vitamin production
Electrolyte absorption
How much saliva is produced per day
0.5 to 1.5L
Factors that decrease los tone
Antimuscarinics
Dopamine
Cholecystokinin
Alpha blockade
Beta stimulation
Secretin
Prostaglandin E1
Thiopental
Alcohol
Functions of saliva
Lubrication
Solvent for taste
Buffering of irritants
Antimicrobial
Digestion of starch by amylase
Digestion of fats by lipase
Volume of gastric juice secretions
Ph
1.5 - 2.5L per day
Ph 1 to 3.5
Function of gastric secretions
Protein digestion
Activation of. Pepsinogen to pepsin
Optimal ph for pepsin
Improve solubility of dietary iron
Antimicrobial
Stimulate biliary and pancreatic secretions.
Glandular cell types in stomach - what do they release
Mucus - mucus and bicarb
Parietal - hydrochloric acid and intrinsic factor
Chief - pepsinogens and gastric lipase
G - gastrin
D - somatostatin
Enterochromaffin like cells - histamine
How is gastric acid secreted
Other ion changes in cell
From parietal cells via HKATPase pumps
H out for k in
H created in cells from breakdown of h2CO3 - bicarbonate then excreted into plasma
Chloride enters cell from plasma and secreted along with the h
What stimulates gastric acid secretion via what receptors
Gastrin - gastrin receptor
Ach - M1 muscarinic
Histamine - H2
What is the effect of gastric acid production on bicarb and co2
Bicarb tide released at time of peak acid production causing alkali urine
Co2 consumption high in stomach giving a negative respiratory quotient!
Enzyme pathway for breaking down proteins
Pepsinogen released by chief cells converted to pepsin in acid conditions
Pepsinogen stored in secretory granules and released by same triggers for acid release
What is gastric mucus
Release?
Glycoproteins, water, electrolytes and sloughed cells
Released from mucus cells stimulated by vagus, gastrin, prostaglandins
What is secreted along with acid from parietal cells? What is it? Function
Intrinsic factor
Glycoprotein
B12 absorption in terminal ilium
Phases of gastric acid secretion
Cephalic - anticipation of food causes vagal stimulation to stomach increasing mobility, gastin and histamine release with increased gastric acid
Gastric - stomach distension and luminal peptides promote local and vagal reflexes increasing gastrin secretion and thus acid. When pH reaches 2 acid secretion stopped by somatostatin
Intestinal - chyme reaches duodenum feedback mechanisms including somatostatin inhibit gastric secretions. Stimulation from other factors also decreases.
How much pancreatic juice is produced per day?
What does it contain
1500ml
Proenzymes - trypsinogen (to trypsin), proelastase (to elastin)
Enzymes - amylase, lipase
Alkali
What stimulates pancreatic secretions? Where are they released from? Trigger?
Secretin (s cells of upper small intestine, released due to acid) - causes bicarb rich pancreatic fluid
Cholecystokinin (duodenal mucosa, released due to amino acids, peptides and fat) - triggers pancreatic enzyme release
Acetylcholine - vagus nerve - triggers Pancreatic enzyme release
Where are pancreatic enzymes stored
Zymogen granules
How much bile is produced per day?
How much is stored in gallbladder?
500-1000ml
30-60ml
Composition of bile
Bile salts
Pigments
Inorganic compounds
What is the stored amount of bile salts?
How is this managed
3.5g
Recycled via enterohepatic circulation twice per meal!
Factors that control bile release? Location of release and trigger
Secretin - s cells in proximal small bowel, triggered by acid - create watery bicarb rich bile
Cholecystokinin - duodenal mucosa in response to amino acids, fats and peptides, - stimulates gall bladder contraction and sphincter of oddi relaxation
Acetylcholine - vagus nerve - gallbladder contraction
Bile salts - from bile, if increased in portal circulation trigger increased bile secretion
Carbohydrate breakdown pathways to absorbable monomers
Lactose - [lactase] - galactose and glucose
Starch - [amylase] - alpha dextrins, maltose - [alpha dextrinase, maltase] - glucose
Sucrose - [sucrase] - fructose and glucose
How are carbohydrates absorbed
Small intestine only
Galactose and glucose through SGLT-1 (sodium dependant glucose co- transporter-1) on luminal membrane then through GLUT-2 to plasma
Fructose through GLUT-5 on luminal border and again into plasma
Maximal carbohydrate absorption rate
Glucose 100g/hr
Fructose 50g/hr
Why can cellulose not be broken down
Beta glucose linkages
Breakdown of proteins in gi tract
Stomach = Protein - [pepsin] - polypeptides
Duodenum = polypeptides [exopeptidase, trypsin, chemotrypsin, elastase] - free amino acids and mono/di/tripeptides
Duodenum and epithelial cells = mono/di/tripeptides - [peptidases] - free amino acids
Absorption of amino acids and short peptides in gi tract
Efficiency
Free amino acids in transporter with na
Short peptides through pept-1 with hydrogen ions.
Very efficient <5% protein escapes absorption
Absorption of lipids in gi tract
Triglycerides - [lipase] - free fatty acids and monoglycerides
Fat soluble vitamins + fatty acids + cholesterol - [bile salts] - micelle
Micelle fuses with epithelial cells leading to absorption and either fatty acids into portal vein or reform triglycerides then into chylomicrons into lymph
How much water per day is absorpbed in the intestine
How much is lost in faeces
Where is most water reabsorbed
10l
200ml
Most in the small intestine, around 1.5 litres in the large
How much Na is absorbed in the intestine each day? Where does this come from?
35g
Most reabsorbed from secretion, only about 5-8g from diet
Effect of aldosterone on gi tract
Increases na channels in epithelium and basolateral nak pumps resulting in increased sodium and thus increased water absorption.
How are fat soluble vitamins absorbed in the gi tract
In micelles with bile salts and fat
Examples of water soluble vitamins
Vit c
Folic acid
B12
How are Vit c and folic acid absorbed in the bowel
Active transport
Vit c - passive transport
Folic acid - na independent transport
How is Vit b12 absorbed
Intrinsic factor released in stomach then active sodium independent transport (Pinocytosis) in terminal iliu
How and where is iron absorbed in the bowel
How much of dietary iron is absorbed
Pinocytosis in duodenum and jejunum
3-6%
How and where is calcium absorbed
Controlling factors
How much absorbed
Duodenum, active transport facilitated by proteins
Regulated by 1.25 dihydroxycholcalciferol
30-80%
Where and how is magnesium absorbed in the bowel
Small and large
active and passive transport, facilitated by protein
What is vomiting
Forceful expulsion of contents of the upper gi tract
Where is vomiting controlled
The vomiting centre - a number of interconnected areas in the brainstem
Phases of vomiting with description
Pre-ejection - nausea, sympathetic upregulation, reduced gastric acid secretion, reduced salivation, stomach relaxes, peristalsis of small bowel reverses, retrograde giant contraction begins in mid small bowel pushing contents back into stomach, deep inspriatory breath, closure of glottis
Ejection - retching, contraction of abdominal wall and diaphragm producing increased abdominal pressure, perioesophageal diaphragm relaxes opening los, contents of stomach expelled from mouth. Respiration temporerally ceases to protect airway.
Areas involved in nausea and vomiting and links.
Chemoreceptor trigger zone activates nucleus tractus solitarius, and both CTZ and NTS activate brainstem vomiting centre triggering vomiting response.
Triggers to vomiting
Pain/ distress - higher centres - vomiting centre
Motion/vertigo - labyrinth organs - cerebellum - vomiting centre
Drugs and hormones - chemoreceptor trigger zone - vomiting centre
Gastric irritants - vagus nerve - chemoreceptor trigger zone + nucleus tractus solitarius - vomiting center
Pharyngeal irritation - glossopharyngeal nerve - nucleus tractus solitarius - vomiting centre
