Intestinal Movements and Liver Function Flashcards
Chewing (what and why?)
- A voluntary process but also has a reflex component;
- Food in the mouth inhibits chewing muscles – lower jaw drops
- Stretch reflexes of jaw muscles leads to rebound contraction – teeth close
- Food is compressed against lining of mouth jaw drops again
- Process repeated
- Prevents airway obstruction
- Mixes with saliva for lubrication and digestion
- Increases surface area for further GI secretions
Swallowing (3 phases…)
Oral (voluntary) phase: food is forced back on pharyngeal wall initiating swallowing centre
Pharyngeal phase: food passes into the oesophagus, epiglottis deflects food away from laryngeal opening and glottis closes preventing food entering the respiratory tract
Oesophageal phase: peristaltic wave of contraction drives food from the oesophagus into the stomach
Receptive relaxation of stomach
Vagovagal reflex Receptive relaxation as food comes in stomach stretches signals sent to brain which then tells musculature to relax thereby permitting the entry of more food.
The proximal part (orad portion) and distal parts (caudad portion) of the organ have different patterns of motility to allow for;
- accommodation of ingested material
- regulation of gastric emptying
During swallowing the orad portion of the stomach relaxes at the same time as the lower oesophageal sphincter
Intraluminal pressures in both regions fall due to the active relaxation of smooth muscle
After passage of the bolus the pressure of the stomach returns to what is was
Small Intestine
- Constitutes ~3/4 of GI tract
5 metres in length - Majority of digestion in proximal 50%
- Typical chyme transit time of 2-4 hours
- Duodenum – first 5 %, no mesentery
- Jejunum – proximal 40 % of small bowel
- Ileum – remaining distal portion ~55 %
Contractions of the small intestine;
- mix ingested foodstuffs with digestive secretions and enzymes
- circulate intestinal contents to facilitate contact with the intestinal mucosa
- propel intestinal contents in an aboral direction
Duodenal contractions of small intestine
- phasic
- around 12 per minute
- seldom occur in a continuous manner
- isolated or small groups of contractions are the norm
- not always peristaltic most are segmentation
- either impede or facilitate the emptying of contents from the stomach
- controlled by ANS via the myenteric (Auerbach) plexus
- Parasympathetic contribution- stimulatory increases intestinal contractions and sphincter relaxation; Ach muscarinic receptors in muscle layers
Segmentation contractions of small intestine
spontaneous mechanical activities initiated by stretch and responsible for the mixing chyme
Contraction is influenced by parasympathetic stimulation (increases) and sympathetic nerves and circulating catecholamines (decreases)
Peristalsis of small intestine
- Main propulsive force
- Travel slowly & only a few cm to allow time for digestion
- Initiated by stretch, irritation, parasympathetic activation and mediated by the myenteric plexus, gastroenteric reflex & GI hormones
Migratory motor complexes of small intestine
- Occur when absorption is complete (in a fasted state)
- Bursts of electrical activity from stomach to ileum
- Sweep remaining intestinal contents into large intestine & inhibit migration of colonic bacteria & limit bacterial overgrowth
- Motilin increases vagal impulses
- Suppressed by eating
Vomiting Reflex
occur when GIT is:
- irritated
- over distended
- over excitable
Sensory signals can originate in the pharynx, oesophagus, stomach & upper small intestine
Vagal & sympathetic stimulation to multiple regions in brain and the vomiting centre in the medulla oblongata
Motor impulses sent to lower GIT, abdominal muscles and diaphragm (vagal & sym. nerves)
loss of NaCl, H2O and H+ lead to dehydration and metabolic alkalosis
Emptying of Small Intestine
Ileocecal valve – prevents faecal backflow
Resistance to emptying <2L
chyme/day
Opening promoted by local peristalsis and via gastroileal reflex
Regulated by pressure, chemical irritation
The Large Intestine
2 functions:
- absorption of H2O and electrolytes - proximal portion
- storage of faeces - distal portion
Maintains a slow rate of contraction (2-4/hour)
Propulsive movements (mass movement) especially after eating triggered by gastrin & gastrocolic reflex
Force contents into rectum causing distension
Leads to defecation reflex
The Defecation Reflex
Mediated by parasympathetic nervous system
Stretch receptors in the rectal wall stimulate parasympathetic nerves in the sacral spinal cord
This increases the contraction of the colon while relaxing the smooth muscle of the internal anal sphincter
Somatic nerves to the striated muscle of the external anal sphincter are inhibited (it relaxes)
Rectal distension gives rise to a conscious awareness of the urge to defecate
Diarrhoea
causes:
- enteritis/colitis
- bacterial toxins
- emotion
- increased intestinal motility
- increased intestinal secretion
- malabsorption
leads to:
- dehydration
- hypokalaemia
- metabolic acidosis
Functions of liver
- filtration and storage of blood
- metabolism of carbohydrates, fats, proteins, hormones and foreign chemicals
- formation of bile
- storage of vitamins and iron
- formation of coagulation factors
Has a dual blood supply;
- hepatic artery – carries oxygenated blood
- portal vein - transports nutrient rich blood from the GIT
Mixed hepatic arterial and portal venous blood passes along the hepatic sinusoids to the central vein in each liver lobule which eventually transports the blood to the inferior vena cava via the hepatic vein.
Detoxification and Phagocytosis
- Removal of ammonia - via the urea cycle and the resulting urea is released into the systemic circulation where it is excreted by the kidney
- Removal of ethanol – alcohol dehydrogenase facilitates the conversion of ethanol into acetaldehyde and reduced nicotinamide adenine dinucleotide. These two products can be converted into acetyl co-enzyme A by peripheral tissue such as skeletal muscle
- Drug metabolism – the first pass effect of the liver can be a problem i.e. aspirin inhibits platelet function, hydrolysed to salicyclic acid, anti inflammatory but not antiplatelet activity. Some prodrugs take advantage of 1st pass effect i.e. enalapril (an ACE inhibitor) hydrolysed to active form - enalaprilat
- Hormone removal – one of the ways that hormones are removed from the plasma is their excretion by the liver into the bile
- Küppfer cells phagocytic cells forming part of reticuloendothelial system
Protein Metabolism
Deamination of amino acids:
- required before they can be used for energy or converted to fats or carbohydrates
- Results in the amino group being removed, the formation of ammonia and the resulting carbon skeleton being available for energy metabolism.
- Certain deaminated amino acids are similar to substrates that are used by cells (mainly liver cells) to synthesise glucose or fatty acids
- The conversion of amino acids into glucose or glycogen is called gluconeogenesis and the conversion of amino acids into fatty acids is call ketogenesis
Urea formation:
- Large amounts of urea are formed from the deamination process and by the gut bacteria which is absorbed into the blood
- Toxic if not removed
- Ammonia released during the deamination will be removed from the blood by the liver and converted to urea
Formation of plasma proteins:
- All the plasma proteins except the gamma globulins (antibodies formed by the lymph tissue) are formed by the hepatic cells of the liver
Vitamin storage by the liver
Vitamin A – up to 10 months worth
- Retinol helps vision in dim light
- Strengthens immune system
- Keeps skin & some body linings healthy
Vitamin D – up to 3-4 months worth
- Calcium homeostasis
Vitamin B12 – 1-4 years worth
- DNA synthesis & regulation
- Red blood cell formation
Lipid Metabolism (the liver)
Degrades fatty acids into smaller compounds to be used for energy
Synthesises triglycerides from carbohydrates and proteins
Synthesises cholesterol and phospholipids from fatty acids
Large amounts of triglycerides appear in the liver when fat is being used for energy rather than carbohydrate
Transported from adipose tissue to liver in the blood as free fatty acids
Fat degradation occurs depending on how much energy is needed
Contains large quantities of cholesterol and phospholipids which are continually synthesised by the liver
Principal source of unsaturated fatty acids required for cell structures
Functions of phospholipids
- essential for the formation and function of lipoproteins in the blood
- involved in the synthesis of thromboplastin
- large quantities of sphingomyelin are present in the nervous system as this is one of the substances that make up the myelin sheath
- donate phosphate radicals when they are necessary for certain chemical reactions
- essential in the formation of structural elements, mainly membranes
Lipoproteins
Chylomicrons – are the least dense and largest lipoproteins, transport products from dietary fat digestion to peripheral tissues
Chylomicron remnants
Very Low Density Lipoproteins (VLDLs) – these contain high concentrations of triglycerides and moderate concentrations of both cholesterol and phospholipids, main source of triglycerides exported from the liver to muscle and adipose tissue
Intermediate Density Lipoproteins (IDLs) – are particle remnants of VLDLs from which some of the triglycerides have been removed, so the concentration of cholesterol and phospholipid is increased. They are precursors of low density lipoproteins
Low Density Lipoproteins (LDLs) – are derived from intermediate density lipoproteins and have almost all the triglycerides removed, leaving an especially high concentration of cholesterol and a moderately high concentration of phospholipids. LDLs are the main cholesterol carrier, carrying cholesterol to the liver and peripheral tissues
High Density Lipoproteins (HDLs) – are synthesised in the liver and intestines. They carry cholesterol from adipose tissue directly to the liver (reverse cholesterol transport) and to tissues that synthesis steroid hormones (adrenal glands, ovaries and testes)
Dyslipidaemias
- disorders of chylomicron and VLDL metabolism – underlying genetic factors which are poorly understood
- disorders of LDL metabolism (hypercholesterolaemia) – underlying genetic factors
- combined hyperlipidaemia (hypercholesterolaemia and hypertriglyceridaemia) - underlying genetic factors
- secondary hyperlipaemia – can be associated with diabetes, hypothyroidism and liver disease (particularly alcohol related)
- disorders of HDL metabolism (Tangier disease) - underlying genetic factors
Atherosclerosis
The vascular endothelium becomes damaged
Circulating monocytes and LDLs accumulate at the site of injury
Monocytes cross the endothelium and enter the intima (middle layer) of the vessel wall and become macrophages
Macrophages become foam cells
Fatty streaks grow and proliferate forming plaques
Macrophages release substances promoting inflammation and proliferation of smooth muscle and fibrous tissue
Fibroblasts cause sclerosis
Calcium salts precipitate with cholesterol; Causing hardening of the arteries
