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(7) GIT (Secretion/Digestion/Absorption
A lot of water secreted in GIT…
(7) GIT
Secretion/Digestion/Absorption
- A lot of water secreted in GIT daily
- Most of absorbed fluid are secretions
Stomach
Secretion Rate
- Basal 1-5mM/hr Maximum 6-40mM/hr
- Gastric ulcer (Lower, protectionary)
- Duodenal ulcer (Higher causes ulcer)
- Pernicious anemia; loss of cells producing intrinsic factor (Lower)
Secretion
- HCL (Parietal)
- Intrinsic factors (Parietal) for Vit B12 absorption, forms complex resistant to digestion, absorbed at ileum. Trigger same as HCL but not linked to acid secretion
- Pepsinogen (Chief) activated by acid (Highest activity pH 3), 10-20% protein, inactive at duodenal pH
- Gastrin regulate HCL secretion (Hormone)
- Mucus Insoluble in acidic pH (Interdigestive state), Soluble in less acidic pH (digestion). Acetylcholine regulates (like HCL), mechanical stimulation
- Renin & Gastric lipase (Children)
*Faster secretion, higher [H+]
*[K+] always higher than in plasma (vomiting causes Hypokalemia)
Digestion
Carbohydrate
- Depends on salivary a-amlyase (Stop at low pH)
-
Fat
- Minimal
- High acidity prevents emulsification
Absorption
- Very little absorption takes place
- Only highly lipid-soluble substance (eg. ethanol)
Regulators of HCL secretion
Note CCK no effect
Inhibitors:
- Omeprazole
- Protaglandin
Stimulate mucus, HCO3, phospho
Enhance mucosal blood flow
Stimulate mucosal cell turnover
Deficiency leads to injury (NSAIDS/Aspirin)
- H2 antagonist
- Anticholinergic
- Gastrin antagonist
-
Second Messengers:
- Calcium (Maintenance)
- cAMP (Rapid response); most drugs
Regulation Mucosal Barrier
- Against abrasion, HCL. pepsin
- Thick (1mm) mucous (mucins & HCO3)
- Max HCO3 = 10% HCl secretion
- High cell turnover 1-3days
- Repair rate 48hrs to 3-5months
Inhibitors of HCO3
- Adrenergic agonist (Stress ulcers)
- Aspirin & NSAID
-
Ulcer therapy
- Neutralizing HCl
- Prevent acid release
- Antibiotics
- Prostaglandin agonist
Intestinal
Secretion (2-3L/day, net absorption of fluid)
- Function: Makes chyme fluid & alkaline
- Mucus (stimulated by Gastrin, Cholecystokinin, Secretin & Parasym)
- Enzymes (Not secreted by by cell degeneration / turnover 2/3days)
Maltase / Sucrase / Lactasae / L - Glucosidase /
- Enterokinase (Exclusively intestinal): Converts trypsinogen to trypsin (Pancreas)
- Secretion is isotonic to plasma, higher HCO3, lower Cl
Absorption
- Primary Sites: Dupdenum & Upper Jejunum
- Folds, Villi, Microvilli
- Absorbs 99% of water (Dependent on movement of solutes)
- Vitamins (A,D,E,K) are absorbed together with fats. fat soluble
- 95% bile salts reabsorbed into distal ileum through ASBT (apical sodium-dependent bile transporter
- Fats by Simple & Facilitated Diffusion
- K+ by solvent drag through paracellular routes
- Folate absorbed near ileum and cecum
Regulation: (Stimulation)
- Mechanical irritation
- Distension
- Acetylcholine / Gastrin ( Ca2+ )
- Secretin / CCK / GIP (cAMP)
pH & drug absorption:
- pH affects % of drug un-ionised (Lipid soluble)
Secretion
- Mucus
- Intestinal Juice (High K+ & HCO3) pH 8-.4
Buffer against H+ produced by bacterial fermentation
Pathological Absorption
- Absorption of electrolyte (Congenital Cl- diarrhoea)
lack Cl/HCO3 exchanger. Retention of HCO3 causes alkalosis
- Absorption of nutrient (Carbohydate malabsorption)
- Hypermotility of intestine less time for absorption
- Enhanced secretion of water & electrolyte diarrhoea
*Requires glucose SGLT to solvent drag water and electrolytes back into cell
-
Regulation (Stimulation)
- Parasympathetic impulses
- Sympathetic (decrease secretion)
- Mechanical/Chemical irritation
-
Absorption:
- Bacteria in colon convert primary bile salts to secondary.
- Also absorb secondary passively.
- SCFA stimulate water absorption
Pancreatic
Secretion
Exocrine
- Enzymes (Acinus):
Peptidase: Trypsinogen, Chymotrypsin, Carboxypeptidase, Secreted inactive
Lipase: All are secreted active. Water insoluble require bile salts
a-amylase
Nucleases
Failure: malabsorption
- Electrolyte (ductal): Pancreatic juices (HCO3)
Failure: Duodenal ulcers
- Mucin (goblet)
-
Aqueous Component
- Na+ / HCO3
- Inverse proportion of HCO3/Cl
Regulation
- Inhibited by sympathetic
- Stimulated by parasympathetic
-
-
- Gastric stimulation: 10-20% Gastric distension; Gastrin produces low volume, high-enzyme pancreatic secretion
- VIP stimulates pancreatic HCO3- secretion
Salivary Secretion
- 1-1.5L a day
- High metab & blood flow (x10 of skeletal muscles)
- Mucin, a-amylase, lactoferrin, lysozyme, histidine
Through ducts: Na+ reabsorbed, K+ secreted, Cl- follows Na and is reabsorbed, HCO3- secreted. HCO3- is in highest conc
Hormones
Gastrin: (Stimulated by vagal/sight smell)
- Secreted by Stomach
- Travel through body back to Stomach
- Stimulate release of HCL
- Stimulate release of pepsinogen
- Increase gastric motility / chyme
- Increase ileum motility & relaxation of ileocecal sphincter
- Negative Feedback: pH 3, reduce gastrin
- Opposed by secretin
Regulation:
Release
- Distension of antrum
- Hypercalcemia
- Proteins & Fats in stomach
- Vagal Stimulation
Inhibiting
- Calcitonin
- Somatostatin
- Secretin
- GIP / VIP
- Glucagon
- Acid in stomach
-
-
-
General Functions
- Exercise: Better lipid profile
- For CVS and obesity
-
3) Integration with
- Hepatobiliary
- Cardiovascular / Respiratory
- Renal
-
Heartburn
- Increased gastric acid secretion
- Chyme into esophagus
- Causes: Overeating, smoking, fatty food, coffee, alcohol, lying down, tight clothing
Food Types
Carbohydate
Luminal
- a-amylase (more than salivary, concentrated in duodenum
Carbohydrates ---> Oligosaccharides
-
Absorption
- Major: Duodenum & Upper jejunum
- Not regulated
- Failure to absorb results in diarrhea & gas
-
-
Lactose Intolerance
- Lactase 5-10% of childhood
- Diseases affect lactase
Proteins
Digestion Enzymes
- Gastric Pepsin (10-15%)
- Pancreatic Protease
- Enterocyte Peptidase (50%)
- 20-50% reaches ileum
- 10% reaches colon (Digested by micro-organisms)
- Brush Border Peptidases
-
Lipids
Digestion
Bile:
- Excretion of water-insoluble (Cholesterol & bilirubin)
- Formed by liver & bile duct cells
- Released by CCK
- Stored in gall bladder
- Bile pigment (From hemoglobin)
- Reabsorbed in terminal ileum 80-90%
- Composition
- Phospholipid: Mostly Lecithin (Fat)
- Electrolytes (HCO3 > Plasma)
- Convert bilirubin into urobilinogen (intestines)
- urobilinogen (Urine)
Subtypes:
- Secondary Bile Acids
- Deoxycholic & lithocholic acids
-Deconjugaed/hydroxylated by colon bacteria
- Primary Bile Acids
- Cholic & Chenodeoxychlic
- Active transport at ileum
- More soluble than cholesterol
- Conjugation of Bile Acids
- Become bile salts with Glycine & Taurine (more significant)
- Bile salts are more amphiphatic
Gastric Lipase
- 20-30% of lipid digestion
- Increases if pancreatic lipase secretion decreases
- Secreted by Chief Cells
Lingual Lipase
- 0.015% of gastric lipase activity
Intestinal Lipase
- Akaline pH
- Ca2+
- Bile salts
- Lecithin
- Lipolytic Enzymes
Pancreatic Lipase
- Glycerol Ester Hydrolase
- Cholesterol Esterase
- Phospholipase A2
Absorption
- Rate Limiting step: Migration of Micelles from Chyme to Microvilli surface
-
-
-
Sodium
- Glucose Na+ coupled
- Amino acid Na+ coupled
Motility (Pg 1- 35)
Types
Segmentation
- Non-propulsive
- Small & Large intestine
-
Tonic Contraction
- Sphincters that divide gut into function segments (e.g. stomach
- Muscular Tone: Continuous, Passive, Partial Contraction
Areas
Esophagus
Upper Esophageal Spincter (UES)
- Skeletal muscles
- Controlled by swallowing centre
Lower Esophageal / Cardiac Spincter (LES)
- Smooth muscles
- Modulated by swallowing centre
Increase tone:
- Cholinergic agonist (Mimic acetylcholine)
- a-adrenergic agonist (Selectively stimulate a receptors)
- Gastrin (Stimulates the production of gastric acid / HCL
- Substance P (Pain)
Decrease tone:
- b-adrenergic agonist (Selectively stimulate b receptors)
- Dopamine
- CCK (Produced by duodenum, hunger suppressant)
- Nicotine, tea, coffee, cola
One way flow
- Gastric contents damaging to esophageal epithelium
- Tonic contraction prevents reflux
Stomach/Gastric
Functions:
- Interdigestive period: Clear undigested & sloughed cells
- After meal: Relaxes to accommodate ingested food
- Further digestion: Delivered to duodenum at optimal rate for digestion in intestine
Accommodate food entry
-
Receptive Relaxation (Fundus): Food passing down pharynx and esophagus
- Occurs within 10s of swallowing
- Mediated by mechanoreceptors in gastric wall
Gastric Reflexes
Gastro-duodenal reflex: Chyme duodenum hormonal response intestine cells
- Secretin released into bloodstream (Response to Acidity)
- 1) Pancreas release Bicarbonate to neutralize
- 2) Inhibit gastric motility
- 3) Acid & pepsinogen secretion (oppose gastrin)
- Cholecystokinin released into bloodstream (Response to Fat & AA)
- 1) Pancreas release pancreatic enzymes (eg. lipase)
- 2) Gall bladder contraction, pump bile
- 3) Inhibit gastric motility
- Both inhibit gastric motility to give time for digestion
-
Emptying Triggers
- T1/2 from 8- 18mins
- Initial lag phase (1 hour)
- First Order wrt to volume
Promote emptying:
1) Parasympathetic stimulation (Happiness)
2) Hypotonic
3) High volume & High fluidity
4) Anger/Agression (Neural)
5) Gastrin (Hormonal)
Inhibit emptying:
1) Sympathetic stimulation
2) Hypertonicity
3) Low volume & fluidity
4) Fat/Protein-rich meal (CCK effect, reduce motility)
Fructose less potent than glucose
L-Trytophan most effective A.A
- Pain/Fear/Depression (Neural)
- CCK/Secretin/GIP (Hormonal)
- Duodenal acidic pH / Distention
- Low volume, Low fluidity / High solidity
Abnormal Emptying: Vomiting
- Vomit centre (Medulla)
- e.g Injury / Inc intracranial pressure (No nausea)
- Activated by afferent nerves from GIT
- e.g. Apomorphine / copper sulfate (Nausea)
- Prevent blood from being drawn out of GIT
- Salivation before vomiting, help to neutralize
Gastro-entero reflex:
- Stomach & Intestine too much acid
- Reduces Gastrin
- Consequently, HCL & Motility reduced
Intestinal
- Spinchter of Oddi (Ampulla of vater)
Types
-
Migrating motor complex
- Interdigestive period
- Inhibit migration of colon bacteria into ileum
-
Function
- Movement cadually (2-4hours)
- Digestion & Absorption
- Interdigestive period (Cleansing)
Regulation
- Gastrin stimulates ileum motility, relax ileocecal spinchter
- Intestino-intestinal reflex: Injury inhibits motility
- Ileogastric reflex: Distension of ileum inhibit gastric motility
- Gastroileal reflex: Chyme in stomach trigger increase ileum motility
Colonic
- Slow and variable transit
- 0.5-2.5L of chyme
- Storage
-
Aided by:
- Microbial digestion of SCFA
- Reabsorption of water
- Small absorptive S/A (no villi)
Regulation:
- Gastro-colic and Duodeno-colic reflex
- Opiates decrease mass movement
- Distention of rectal wall
*Causes relax internal spincter, contract external spincter (Voluntary), elevate intra-abdominal pressure
Abnormal Motility
Incontinence:
- Incompetence of IAS
- Weakening of EAS / pelvic muscles (Surgical trauma)
Diarrhoea:
- Increase motility due to inflammation
- Failure to absorb effectively
- Excess secretion by small intestine
Constipation:
- Inadequate fibre
- Lack of exercise
- Slow passage exacerbate problem
- Voluntary inhibition of defecation reflex
Reflexes: Entero-gastric for example. If thing is after but worded before, it inhibits the thing after (gastric)
-
Gastric Glands
Mucous Cells/Goblet Cells: Mucus
Parietal Cells: HCL & Intrinsic Factor
G-Cells: Gastrin (Stimulates HCL production)
Chief Cells: Pepsinogen & Lipase
