Flashcards
GI Tract
Cards in this deck (132)
- 1GI TractContiuous hollow tube
8m from oesophagus to rectum
Mouth and Parynx
Oesophagus
Stomach
Small intestine
Large intestine (Colon, Cecum, Rectum)
Anus - 2Accessory proteinsControl secretions for breakdown of food
Teeth and tongue
Salivary glands
Gall bladder -> lies below liver, stores/releases bile, emulsifies fats
Liver -> produces bile
Pancreas -> digestive enzymes - 3FunctionTo break down ingested food into small molecules which can be taken into body tissue
Digestion -> process of breaking food into absorbable nutrients
Chemical -> secretions of enzymes
Mechanical -> motility (mixing, grinding)
Absorption -> passage of nutrients from GI tract into either the blood or lymph - 4OesophagusMuscular tube - 25cm in length, 2cm in diameter
It extends from the parynx to the stomach
Fast transport -> food in the oesophagus for less than 10 seconds - 5Stomach"J" shaped organ
Two openings
4 regions:
Fundus
Cardia
Body
Pylorus
Main roles:
Stores food
Mechanically breaks down food - chyme
Begins digestion - 6Sections of the stomach (diagram)
- 7Small intestineAbsorptive epithelium - Where most absorption takes place
3 regions
1) Duodenum
"C" shaped
Neutralises acid stomach contents (alkali mucus)
Further digestion
2) Jejunum and 3) Ilium
Highly coiled
4-6 metres long
No definable junction
Highly folded - plicae
Larger surface area
D - 8Large surface areaHelp to increase efficiency of digestion/absorption
3 orders (strata) of folding increases the area available for absorption
Villi
Microvilli - 9Large intestine1.5m length
No nutrients in chyme
Removes water, salts, sugar and vitamins
5 regions:
Cecum (compresses material into faecal matter)
Ascending, transverse and descending colon
Sigmoid colon
Tightly packed mucosa -> goblet cells for mucus secretion
Areas of lymphoid tissue - peyer's patches -> for local immune protection - 10Control mechaniams1. Autonomic NS
2. Enteric NS (gut's own NS)
3. Hormones - 11Control mechanism 1) Autonomic NSSpeeds up or slows down system
Sympathetic nerves -> inhibit digestion
Parasympathetic nerves -> stimulates digestion
'Fight or flight' vs. 'rest and digest' - 12Control mechanism 2) Enteric NS2 nerve plexus:
- Myenteric (Allerbach's)
- Submucus (Meissner's)
Work together to form small nerve network
Plexus in gut wall
- 'senses' luminal contents
- controls muscle and glands
100 million neurones (as many as the spinal cord)
"2nd brain" - 13Control mechanism 3) HormonesIn excess of 22 hormones and paracrine hormones (different locations in tract)
Secreted by Etervendocrine cells in the mucosa
Eg. Gastrin -> stomach, duodenum, jejunum
Secretin -> duodenum, jejunum, ilium - 14Intestinal 'taste' cellsPacked with vesicles
Enteroendocrine:
Single cells scattered through GI tract
Link between luminal contents and capillaries
Densely packed with vesicles
Sense luminal contents and responds via release of peptides transmitters:
Hormonal
Paracrine -> affects/communicates with nearby cells - 15Movement through GI tract 1) Sphincter contractionControlled movement of material through the tract
Maintains ordered sequence of events - Compartmentalisation
Upper oesophageal sphincter (UOS)
Lower oesophageal sphincter (LOS)
Pyloric -> monitors how much chyme enters the gut -> prevent overloading of intestine
Ileocaecal
Internal and external anal - 16Movement through GI tract 2) PeristalsisMovement throughout the GI tract - peristalsis
Most obvious in oesophagus -> food actively moves
Mediated by neurones in myenteric plexus (ENS)
Distention by bolus of chyme - stimulates peristalsis
Law of Bayliss and Starling:
Bolus is moved towards anus
'Law of the intestine'
Vomiting is an exception
Independent from CNS -> occurs in isolated intestine - 17Movement through GI tract 3) SegmentationPredominantly small and large intestine
Conctraction of circular muscles
Movement in both directions
Mixing and churning
Mixing with digestive enzymes - 18Peristalsis
- 19Hirschsprung's DiseaseCongenital disorder
All or part of the colon has no innervation
1:5000 children affected
Severity differs - based on how much innervation there is
May result in surgical removal of the colon - 20Transit timesOesophagus -> 10 secs
Stomach -> 3-4 hours
Small intestine -> 3-6 hours
Large intestine -> 1-2 days
Some foods require longer to digest
eg. if it is larger - 21Function of salivaNormal production is 0.5-1.5 litres per day
1) cleanse and protect teeth
2) digestion
3) lubrication
4) swallowing
5) speech
6) taste
7) antimicrobial function - 22Salivary glands (diagram)
- 23Salivary glandsMajor:
1) Parotid
2) Submandibular
3) Sublingual
Minor:
4) Buccal
5) Lingual
6) Palate - 24Stimulated vs. unstimulatedChemical or physical stimuli
Contribution from salivary gland differs if saliva is stimulated or unstimulated
Unstimulated -> 65% submandibular
Stimulated -> 50% parotid - 25Components of salviaWater
Mucous
Proteins
Enzymes
eg. alpha amylase released from the parotid gland which initiates carbohydrate digestion
eg. lipase is secreted within glands of the mucosa of the tongue (linguinal) - 26Secretory structure Acinus12 or more acinar cells are arranged radially around a central lumen
Zymogen granules -> inactive enzyme to stop breakdown of own tissues - stops autodigestion
Mucus cells
Myoepithelial cells - 27Secretory structure DuctsIntercalated
Striated
Excretory - 28Saliva production1) Anicar cells produce primary saliva
Water, enzymes, mucus, NaCl
Passes through the intercalated duct and the striated duct
2) Ductal cells modify saliva
NaCl reabsoption, HCO3 secretion (bufferer of acids)
Myoepithelial cells (stimulated by neural input) contract to eject saliva into mouth. Also the thought/sight of food. - 29Secretory structure of salivary glands
- 30Rate of flow and composition of salivaAlways hypotonic
NaCl and HCO3 concentration increases with flow
Due to amount of time spent in duct
Largest flow rate saliva is least like plasma, high K+, low NaCl
Highest flow rate saliva resembles primary saliva and plasma - 31SwallowingSwallowing/deglutition = process by which food passes from mouth to stomach
Chewing -> jaw opening and closing and movement of the tongue
Breakdown of food into smaller particles and mixing with saliva for taste
Binding of particles into bolus foe deglutition
3 phases - 323 phases of swallowing: 1) Oral phaseTongue moves upwards
Compression of bolus against hard palate. Respiration inhibited
Retraction of tongue forces bolus into pharynx - 333 phases of swallowing: 2) Pharyngeal phaseInvoluntary mechanism
Bolus pushed from pharynx into oesophagus
Soft palate reflected back closing nasal pharynx
Epiglottis covers opening of larynx
Opening of UOS - 343 phases of swallowing: 3) Oesophageal phaseUpper oesophageal sphincter relaxes and bolus moves into oesophagus
Start primary wave of peristaltic wave (vagal)
Secondary peristaltic wave (enteric)
LOS relaxes -> allows bolus to move into the stomach - 35Oesophageal manometryDetecting pressure changes
Thin catheters with sensors is passed through the oesophagus into the stomach - patient swallows
Oesophageal manometry measures oesophageal motility
Diagnose abnormalities in oesophageal contractions, strength of the muscle or LOS - 36Lower oesophageal sphincter3-4cm long sphincter
Tonically contracted
Prevents reflux of material back into oesophagus - 37GERD 'Gastro-esophageal reflux disease'Retrograde flow of gastric contents into oesophagus:
Abnormal peristalsis
Weak LOS contraction
Increase in thoraco-abdominal pressure
Leads to:
Pain/discomfort (heartburn)
Mucousal damage
Dysphagia (difficulty swallowing)
Acidic environment of stomach in oesophagus -> can be very serious and damaging to the oesophagus - 38Gastric functions: 1) MotilityGastric accommodation - temporary storage reservoir
Tituration - dissolve, mix and grind food particles (mechanically breaking down food)
Gastric emptying - Control delivery to small intestine - 39Gastric functions: 2) DigestionInitiate digestive process (proteins) via gastric secretion
- 40Gastric functions: 3) ProtectionForeign invasion (acid/proteases)
Mechanical abrasion (mucous)
Prevents autodigestion (mucous) - 41Gastric functions: 4) AbsorptionAbsorbs alcohol and fat soluble drugs (diffusion)
(Why you get drunk quickly) - 42Gastric juice1) Water and ions
2) HCl
Provides low pH
Prevents bacterial growth
Catalyses cleavage of pepsinogens to pepin
3) Pepsinogens
Proenzyme of pepsin
Pepsin breaks down proteins into peptides
4) Intrinsic factor
Glycoprotein
Binds to vitamin B12 - allowing digestion in the ilium
5) Mucous
Protects gastric mucosa
6) Gastrin
From 'G' cells
Regualtes acid secretion - 43Gastric glandsCardiac glands - Mucous, HCl
Oxyntic (acid secreting) - mucous, HCl, pepsinogen, intrinsic factor
Pyloric - mucous, pepsinogen - 44Gastric pit cell types
- 45Gastric pit cell types 1) Mucous neck cellMucins:
High molecular weigh glycoproteins
Hydrophilic
Low solubility
High viscosity
High elasticity
Strong adhesiveness
Bicarbonate ion secretion (preventing damage from the acid)
Unstirred layer - 46Gastric mucosal barrier Mucous entraps alkali fluid Alcohol, vinegar and bile can disrupt barrier
- 47Gastric pit cell types 2) Chief cellZymogen granules:
Inactive pepsinogen
Acid splits of part of the molecule -> active pepsin
Starts digestion of protein
20% of protein in a meal - the rest is broken down in the small intestine using another method - 48Gastric pit cell types 3) Endocrine cellsHighly regulated
G cells:
Secrete gastrin
D cells:
Secrete somatostatin which inhibits gastrin secretion
Enterochromaffin-like (ECL) cells:
Secrete histamine which stimulates gastric acid secretion - 49Gastric pit cell types 4) Parietal cellBranching canaliculi
Unstimulated vs. stimulated vells
Responsible to releasing acid
H+ and Cl- secretion against concentration gradient
100,000:1 against gradient
Lots of energy required - 50Gastric acid secretionH+/K+ ATPase:
'Proton pump'
Acid secretion against the concentration gradient - therefore process required energy
Cl/HCO3- exchanger:
When H+ is pumped out - excess of HCO3 is left behind
Removed by HCO3- exchanger
During acid secretion blood pH is high - 'Alkaline tide' - 51Control of acid secretionParietal cell:
1) Receptors
Gastrin from G cell
ACh from vagus
Histamine from ECL cell (prostaglandins inhibit histamine stimulated secretion)
2) Increased intracellular Ca2+
3) Activation of proton pump - 52Gastric/peptic ulcersBreak in mucousal barrier exposing underlying tissue to corrosive action (acid, proteases)
Symptoms:
Abdominal pain
Bloating
Nausea
Bleeding - haemorrhage and anaemia - 53Ulcer formationProduced by imbalance:
Decreased mucous and/or HCO3
Increased acid production
Endogenous factors (arising from body):
1) Anxiety - parasympathetic output (ACh, gastrin) -> increased acid
2) Stress - sympathetic output (Ad) -> decreased HCO3/mucous
Exogenous factors:
1) Diet - alcohol (damages cells, stimulates parietal cells) and coffee (stimulates parietal cells)
2) Non-steroidal anti-inflammatory drugs (NSAIDs) - reduce protective mechanism
3) H. pylori
Buffering system
Releases proteases and endotoxins that break down tissues
Also linked to gastric cancer - 54Ulcer treatment Aimed at reducing acid environment to allow regeneration of cells or killing H. pylori1) Diet - avoid acid containing food and beverages (alcohol, coffee)
2) Antacids - neutralise lumen acid
3) Parietal vagotomy (almost obsolete now) - reduce ACh
4) Antibacterial drugs - amoxicillin and clrithromycin; bismuth
5) H2 antagonists - inhibition of parietal cell stimulation by histamine (cimetidine, ranitide)
6) Proton pump inhibitors - inhibition of parietal cell activiation (omeprazole) - 55Lecture 1: OverviewLecture 1: Overview
- 56Lecture 2: Gastro-oesophageal functionLecture 2: Gastro-oesophageal function
- 57Lecture 3: Gastroduodenal functionLecture 3: Gastroduodenal function
- 58StomachActs as:
1) Reservoir
2) Preparatory chamber
3) Emptying regulator - responds to feedback from duodenum. controls rate of calorie, H+ and particles into the duodenum - 594 Anatomical regions
- 602 functional/motor regions
- 61Stomach motility after a meal
- 62Feedback regulationOptimal digestion and absorption
Prevent overload of intestine
Controls delivery of calories and sugar
Gastric emptying influenced by composition of chyme in stomach, duodenum, ilium and colon
Physical composition (particle size <1mm)
Chemical compostion (acid, osmolality, nutrients) - 63Rate of gastric emptyingLiquids:
Empty faster than solids
2-3mins
Solids:
Lag time due reduction of particle size
Solid food requires more breaking down
1mm diameter - 64Delivery of sugar into the intestineHigher sugar content takes longer
To prevent hyperglycaemia - 65Feedback regulation
- 66PancreasExocrine gland (85%) - Acinus:
Similar to salivary gland
1) Water and ions
2) Bicarbonate
Neutralise duodenal contents to prevent damage and pH for enzymes
3) Enzymes - essential for digestion
Endocine glands (2%) - islets of Langerhans:
alpha - glucagon
beta - insulin - 67Pancreas: FeaturesAcinar cells
Centroacinar cells
Intercalated ducts
Intralobular duct
Islet of langerhans - 68Pancreas: Enzymes1) Proteins:
Trypsinogen - trypsin
Chymotrypsinogen - chymotrypsin
Proelastase - elastase
Procarboxypeptidase - carboxypeptidase
2) Fats: lipase and phospholipase
3) Nucleic acids: nucleases
4) Carbohydrates: alpha-amylase - 69Exocrine pancreasAcinar cells produce a small amount of protein (enzyme rich) fluid
->
Passed through the intercalated duct - duct cells and centroacinar cells secret bicarbonate, water and ions - 70Pancreas (diagram)
- 71Acinar secretion (diagram)
- 72Ductal secretion
- 73Cystic fibrosisCFTR (Cl- transmembrane protein) defective
Ductal secretion is defective
Alteration in pH therefore enzymes aren't activated
Consequences of CF:
Less negative lumen
Less Na+ and water
Less secretion
Less enzyme action in gut (pH too low)
Malabsorption/malnutrition - 74Duodenal feedback:Digestion:
Nutrients in chyme ->
Cholecystokinin (CCK) release into blood stream in response to proteins and fats ->
Pancreatic acinar cell secretion
Buffer:
HCl in chyme ->
Secretin release into bloodstream in response to pH <5 ->
Pancreatic ductal secretion - 75Liver (diagram)
- 76Liver: FunctionsMetabolic powerhouse of the body, 500 vital functions
Protein synthesis - particularly albumin and clotting fibres (eg. fibrinogen)
Storage - triglycerides, glycogen, some vitamins (eg. vit A)
Gluconeogenesis - conversion of lipids and amino acids to glucose
Toxins - conjugation and breakdown
Bile - Synthesis and secretion of bile acids and bilirubin - 77Liver lobules
- 78Functional anatomy (diagram)
- 79Function anatomyHepatocytes (normal liver cells) surrounded by blood filled sinusoids
Bile flows through cancaliculus - opposite direction to blood - 80Bile: Secretion250ml - 1000ml per day
Dependent on what has been eaten
Concentrated in the gall bladder for storage (15-60ml volume) - 81Bile: Main functions1) Adequate pH -> to control enzyme activation and efficiency
2) Facilitate fat digestion/emulsification
3) Excretion of waste products (cholestrol) - 82Bile: Composition1) water and ions - alkali
2) Bile acids - digestion and absorption of dietary fats (micelle formation) - 70%
3) Proteins - protect against infection
4) Bile pigments - breakdown products of haemoglobin (bilirubin)
5) Organic molecules -
Cholesterol (4%)
Phosopholipid-Lecithin (20%) - 83Bile Acids
- 84Micelle formationFunction -> To emulsify dietary fat for lipase breakdown
Bile salts
Cholesterol; Lecithin -> Solublised by bile salts
Micelles are lipid soluble -> can easily be taken up intestine wall -> goes into lymph system - 85Micelle formation (diagram)
- 86The GallbladderAbsorption -> Na+, Cl- and H20 concentrates bile
Secretion -> (H+, mucin) neutralise alkaline bile and protect epithelium of gall bladder
Motor -> no digestion - relaxation and storage
Digestion - contraction and delivery of bile - 87The Gallbladder: Under hormonal control1) Secretin
Stimulates production of bile
2) CCK
Relaxes sphincter of Oddi
Contracts the gallbladder - 88Lecture 4: Digestion and absorptionLecture 4: Digestion and absorption
- 89Small intestine: Goblet cellsWhite blobs on EM
Secrete mucous
- Protection
- Role in digestion as well
(Crypt -> new cells being developed) - 90Small intestine: Villus1mm long
Rich blood supply with central lacteal (fats go into lymph)
Short diffusion pathway
Enterocytes - continuous mitosis at crypt
Secretion of fluid -
Crypt cells -> NaCl
Paneth cells -> defensins
Goblet cells -> mucous
Endocrine cells -> hormones - 91Small intestine: Microvilli (brush border)Further increase in surface area
Glycocalyx (unstirred layer) - acts as barrier for protection
Brush border enzymes:
Additional surface for absorption
Eg. Maltase, lactase, sucrase, dipeptidases
Absorbed pancreatic enzymes
Advantages:
Limits rise in luminal osmolality
Close proximity to sire of absorption - 92Carbohydrate digestionStage 1 - Mouth:
Salivary amylase
Stage 2 - Duodenum:
Pancreatic amylase
Polysaccharides -> disaccharides
Stage 3 - Brush border:
Disaccharides -> monosaccharides - 93Carbohydrate digestion (diagram)
- 94Carbohydrate transportGlucose/galactose carrier:
Co-transport, Na+ dependent
Energy required to maintain Na+ gradient
Fructose:
Facilitated diffusion
GLUT 2
Fate:
Capillaries -> hepatic portal vein - 95Carbohydrate transport (diagram)
- 96Protein digestionStage 1 - Stomach:
Gastric pepsin
Stage 2 - Duodenum:
Pancreatic proteases
Stage 3 - Brush border:
Brush border or intracellular protease
(protease = generic name for the group of enzymes that break down proteins) - 97Protein transportCarriers:
More than 7
Na+ or H+ dependent
Intracellular peptidases/proteases:
Another method for digestion
Small peptides -> amino acids
Fate:
Capillaries -> hepatic portal vein - 98Protein transport (diagram)
- 99Lipid digestionStage 1 - Mouth:
Salivary lipase
Stage 2 - Duodenum
Bile salts emulsify fat
Stage 3 - Small intestine:
Pancreatic lipases - 100Fat transportMembrane soluble diffusion - doesn't require carrier proteins as it can pass through plasma membranes
Intracellular:
Products reconstituted - trigylcerides
Chylomicron formation
Fate:
Diffusion into lacteals - 101Fat transport (diagram)
- 102Absorption - key points (diagram)
- 103Water absorption in small intestine (water follows solutes and sodium)
- 104Absorption and secretionToo much secretion of water -> malabsorption, diarrhoea
Too much absorption of water -> constipation
Normally volume moving from blood to lumen is less than lumen to blood
ie. absorption greater than secretion - 105MalabsorptionAbsent or defective digestive enzymes
Defects in transporter proteins
Diseases and infections of small intestine
Symptoms:
Steatorrhea (frothy greasy stools), diarrhoea, weight loss
Examples:
Lactase deficiency - lactose intolerance
Coeliac disease - abnormal immune response to gluten, loss of mucosal epithelium
Can lead to malnutrition - 106Large intestinesTenna coli - 3 bands
Longitudinal muscles
Haustra - pockets undergoing segmentation
Slow movement of contents
No villi
High concentration of goblet cells - mucous secretion - 107Colon motility: Segmented contractions99% of the time
1) Retain material in the proximal colon (water reabsorption and fermentation)
2) Mixing contents - 108Colon motility: Gastric-colic response2-3 times per day
Mass movement of material into aboral end of colon - ready for defecation - 109Large intestine: Main functionsHigh mucous secretion - goblet cells
No carrier mediated transport of nutrients (absorption by diffusion rather than active transport)
Efficient water reabsorption
Follows Cl- and Na+ movement
HCO3 buffers acid produced by bacterial fermentation - 110Gut Flora10^14 microorgansims
More than human cells in the body
> 500 different species
3kg of bacteria in the gut
Gut microbiome forms hours after birth
Primes the guts immune system
Many functions
Symbiosis -> between host and bacteria - 111GI Tract FloraOral - Denstal care
Stomach - H. pylori
Large intestine - bacterial fermentation:
Short fatty acid chains (SFACs)
Synthesise essential nutrients - folic acid, vit K
Absorb B12 - 112Dietary fibre - fermentation (diagram)
- 113Dietary fibreIndigestible portion of plant foods - bulk
Motility:
Decrease in gastric emptying
Increase motility of the colon
Adsorption:
Holds water
Traps sugars, cholesterol, fats -> slows absorption
Slow absorption of enzymes and nutrients
Colonic bacteria substrate
Prevention and treatment of constipation, haemorrhoids and diverticulosis - 114Dietary fibreIndigestible portion of plant foods - bulk
Motility:
Decrease in gastric emptying
Increased motility of colon
Adsorption:
Holds water
Traps sugars, cholesterol and fats - slows absorption
Slows absorption of enzymes and nutrients
Colonial bacterial substrate
Prevention and treatment of constipation, haemorrhoids and diverticulosis - 115GI Gas1-4 pints of gas produced per day
Sources:
Swallowed air
Result of neutralisation of acid or bacterial metabolism
Diffusion from blood (small)
Bacterial fermentation - fibre:
Non-absorbable substrate -> beans (stachyose), onions, cabbage, prunes and nuts
Component gases:
Hydrogen, methane, (ammonia, hydrogen sulphide, indole, skatole, volatile amines)
Surgical explosions:
Avoid by fasting, enemas, inert gas perfusions - 116Lecture 5: Vomiting and defecationLecture 5: Vomiting and defecation
- 117The ileumImportant in digestion because of the ileal brake
Acts as a 'checkpoint'
Nutrients (lipids) detected in the terminal ileum and distension slow gastric emptying and small intestinal transit
Ensures adequate absorption and prevents loss of nutrients into the colon
Mediated by hormones (eg. GLP1) - 118Net absorptionStomach:
Alcohol
Fat soluble drugs
Small intestine:
100% protein
100% digestible carbohydrates
95% fats
Water, electrolytes, vitamins
Large intestine:
Fermentation products, esp. SCFAs (eg. buthyrate)
Water and electrolytes
Excreted:
Indigestible fibre, bacteria, inorganic material, fat derivatives, desquamated cells, mucous - 119DiarrhoeaIncrease in stool volume or increased frequency of defecation
Can be fatal - 2 million people die per year (eg. cholera)
1) Osmotic:
Increased solutes in lumen causes less water reabsorption
- Poorly absorbed substrate (ie. sorbitol)
- Malabsorption disorder (lactose intolerance)
2) Secretory:
Increased secretion of water into the lumen (when secretion exceeds absorption)
- Cholera toxin -> opening of Cl- channel, increase secretion of water
- Laxatives, hormones, drugs (antidepressants), caffeine
3) Inflammatory/infections:
Pathogens breach and damage the absorptive epithelium
4) deranged motility:
Altered transit time hence less time for water reabsorption - 120Defecation - ControlFaeces moved into the rectum, leading to distension. This activates stretch receptors-afferent signals to the spinal cord.
If it is convenient to defecate, voluntary motor nerves are inhibited allowing the external and sphincter to relax.
Sympathetic and parasympathetic - stimulate contraction of the rectum and relaxation of the internal anal sphincter. - 121Defecation - Control (diagram)
- 122Defecation - Control: StorageContinence:
Rectal accommodation
Sphincter closure
Incontinence:
Pelvic floor damage
Pudendal nerve damage - 123Defecation - Control: EmptyingDefecation:
Colorectal contraction
Raised abdominal pressure
Sphincter relaxation - internal (autonomic) and external (somatic)
Defecation failure:
Spinal injury
Outlet obstruction - 124Vomiting - EmesisProtective mechanism to prevent damage to the GI tract and ingestion of contaminated/toxic substances
However some vomiting can be inappropriate and have no useful purpose (pregnancy, motion sickness). Unwanted side effect in cancer therapy - 125Things that make us vomitFood poisoning
Bowel disease
Motion/vestibular disease
Pregnancy
Head injury
Radiation/chemotherapy
Surgery/anaesthesia
Drugs
Pain - 126Toxin detectionDetectors:
1) Pre-ingestion
Smell, sight, taste
2) Pre-absorption
Toxin detection in the lumen
Mechanoreceptors and chemoreceptors
Neutralisation/expulsion (vomiting)
3) Post-absorption
Chemoreceptive trigger zone - area postrema
Outside the blood brain barrier - samples toxins in the blood
Induces nausea to prevent further ingestion and activates vomiting centres
Can be activated directly with drugs (emetics) - 127NauseaVomiting is preceded by nausea
Pallor (paling of skin)
Sweating
Salivation
Irregular breathing
Increased heart rate
Retching (several, increased force)
Body is preparing itself for vomiting - 128GI motor correlates of nauseaExplusion caused by contractions of the diaphragm and abdominal wall
The proximal stomach relaxes to accommodate returning intestinal contents
Antral motility inhibited to prevent gastric emptying
Retrograde giant contractions return intestinal contents to the stomach - 129Act of VomitingDeep inspiration
Closure of glottis - protects respiratory tract
Air and saliva drawn into oesophagus - protection from stomach acid and to decrease oesophageal pressure
Soft palate elevated to prevent entry into nasopharynx
Expiration against closed glottis and abdominal contraction - increase intra abdominal pressure
Relaxation of the LOS
Passage of contents into oesophagus
Relaxation of the EOS
Violent expulsive force - stomach and abdominal contraction - 130Act of Vomiting - SummaryGI smooth muscle:
Relaxation of all areas from gastric body to upper oesophagus
Violent contractions of gastric antrum
Respiratory system:
Slow deep inspirations to decrease oesophageal pressure
Skeletal muscle:
Contraction of abdominal muscle
Retching:
UOS remains closed
Vomiting:
UOS opened - 131Origin of sensory triggersGI:
Distension (stomach and duodenum)
Irritation of back of throat
Chemical or toxin
Genitourinary system:
Injury/infection
Hypothalamus/cerebellum:
Stimulation/injury
Vestibular apparatus:
Motion sickness
Chemoreceptor trigger zone:
(4th ventricle in brainstem)
Anaesthesia
Drugs
Radiation
Toxins
Stimulated by some chemotherapy drugs - 132Inputs to the vomiting centres (diagram)
Information
- Description
- BSc Biomedical Science Year 1 Flashcards on GI Tract, created by rachel-chads on 09/06/2014.
- Created by
- rachel-chads
- Views
- 44
- Rating