Flashcards in case 1 Deck (156):
1
layers of the GI tract
Serosa, longditudinal muscle, circular muscle (myenteric plexus), submucosa (meissners plexus), mucosa, epithelial lining.
• Electrical signals that initiate muscle contractions can travel readily from one fibre to the next within each bundle using gap junctions.
2
enteric nervous system
• The enteric nervous system is part of the autonomic nervous system that is found in the lining of the GI Tract, beginning at the oesophagus and extending down to the anus.
• It is involved in the coordination of reflexes (although it receives innervation by the autonomic nervous system, it can work independently of the brain and the spinal cord).
3
two main plexuses of the enteric nervous system
1. A submucosal plexus/ Meissner’s plexus that lies in the submucosa - controls mainly gastrointestinal secretion and local blood flow.
2. A myenteric plexus lying between the longitudinal and circular muscle layers - controls motility.
This also secretes vasoactive intestinal polypeptide. The resulting inhibitory signals are especially useful for inhibiting some of the intestinal sphincter muscles that impede movement of food.
4
neurons in the enteric nervous system
afferent neurons, interneurons and efferent neurons.
Sensory neurons report on mechanical and chemical conditions.
Through intestinal muscles, the motor neurones control peristalsis and churning of intestinal contents.
5
two types of movement in the GI tract
propulsive and mixing movements
6
Propulsive movements-peristalsis
stimulation cause contractile ring in circular muscle which spreads along gut. Stimulus-distention of gut. stretch stim ENS to contract behind it. also stim by irritation of epithelial lining. Parasymp NS to gut elicit peristalsis. requires an active myenteric plexus. starts orad side, moves toward segment, pushing in anal direction 5cm before dying out. there is receptive relaxation down stream allowing food propelled through.
7
4 stages of swallowing
1. Cephalic Stage
2. Oral Stage (Voluntary stage)
3. Pharyngeal stage – involuntary and constitutes passage of food through the pharynx into the oesophagus
4. Oesophageal stage – involuntary phase that transports food from pharynx to the stomach
8
cephalic stage
• This is the point where one is thinking about having a meal:
All of this is part of the process of which would induce the activity of swallowing
9
oral stage
1. Chewing (mastication)
2. Salivation – lubricate the bolus and begin the process of digestion (discussed later)
3. Movement of bolus
The bolus is pushed against the hard palate.
The rugae on the hard palate help move the bolus posteriorly into the back of the mouth into the pharynx.
10
mastication
first step digestion, food ground by teeth, inc surface area food more efficient breakdown by enzymes, food positioned by cheek and tongue between teeth for grinding, 4 muscles-masseter temporalis, lat and medial pterygoid. innervated mandibular branch trigeminal. Stimulation of specific reticular areas in the brain stem taste centres will cause rhythmical chewing movements.
Also, stimulation of areas in the hypothalamus, amygdala, and even the cerebral cortex near the sensory areas for taste and smell can often cause chewing food made softer and warmer and process salivation begins.
11
teeth and mastication
• The anterior teeth (incisors) provide a strong cutting action.
• The posterior teeth (molars) provide a strong grinding action.
12
process of mastication - chewing reflex
presence of bolus in mouth initiates reflex inhibition of muscles of mastication so jaw drops, the drop makes stretch reflex rebound contraction. this compresses the bolus against lining of mouth making inhibition again to jaw drop, this causes break down of food, important for digestion carbs as have indigestible cellulose membranes.
13
pharyngeal stage
•After the voluntary stage, the bolus of food enters the posterior mouth and pharynx.
•Here, it stimulates the epithelial swallowing receptor areas all around the opening of the pharynx, especially on the tonsillar pillars.
•Impulses from these pass to the brain stem to initiate a series of automatic pharyngeal muscle contractions:
14
contractions of the soft patate and palatopharyngeal folds in the pharyngeal stage
1)The soft palate is pulled upward to close the posterior nares, to prevent the reflux of food into the nasal cavities (nasopharynx) 2)The palatopharyngeal folds on each side of the pharynx are pulled medially to approximate each other. In this way, the folds form a sagittal slit through which the food must pass into the posterior pharynx. This slit performs a selective action, allowing food that has been masticated sufficiently to pass with ease. Because this stage lasts less than 1 second, any large object is usually impeded too much to pass into the oesophagus.
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15
contractions of the vocal cords in the pharyngeal phase
3) The vocal cords of the larynx are closed, and the larynx is pulled upward and anteriorly by the neck muscles. These actions, combined with the presence of ligaments that prevent upward movement of the epiglottis, cause the epiglottis to swing backward over the opening of the larynx.
All these effects acting together prevent passage of food into the nose and trachea. Most essential is the tight approximation of the vocal cords, but the epiglottis helps to prevent food from ever getting as far as the vocal cords.
16
changes to the larynx in the pharyngeal phase
4) The upward movement of the larynx also pulls up and enlarges the opening to the oesophagus. At the same time, the upper 3-4cm of the oesophageal muscular wall, called the upper oesophageal sphincter (also called the pharyngoesophageal sphincter) relaxes, thus allowing food to move easily and freely from the posterior pharynx into the upper oesophagus. Between swallows, this sphincter remains strongly contracted, thereby preventing air from going into the oesophagus during respiration.
The upward movement of the larynx also lifts the glottis out of the main stream of food flow, so that the food mainly passes on each side of the epiglottis rather than over its surface; this adds still another protection against entry of food into the trachea.
17
changes to the pharynx in the pharyngeal phase
5) Once the larynx is raised and the pharyngoesophageal sphincter becomes relaxed, the entire muscular wall of the pharynx contracts, beginning in the superior part of the pharynx, then spreading downward over the middle and inferior pharyngeal areas, which propels the food by peristalsis into the oesophagus.
18
summary of changes in the pharyngeal phase
Trachea is closed.
Oesophagus is opened.
Fast peristaltic wave initiated by the nervous system of the pharynx forces the bolus of food into the upper oesophagus.
The entire process is less than 2 seconds
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upper Esophageal sphincter
consists of the cricopharyngeus muscle, the adjacent inferior pharyngeal constrictor, and the proximal portion of the cervical oesophagus. innervated by vagus, innervation of musculature on UES to facilitate opening is 5,7,12 nerve. • The UES remains closed at rest owing to both its inherent elastic properties and neurogenically mediated contraction of the cricopharyngeus muscle. For the UES to open, it is important that the cricopharyngeus muscle has to relax. This occurs due to cessation of vagal excitation. UES opening is also aided by simultaneous contraction of the suprahyoid and geniohyoid muscles that pull open the UES + upward and forward displacement of the larynx + pulling forward of the hyoid bone
20
neurophysiology of swallowing
At the centre of the swallowing system is the Brainstem Central Programme Generator (CPG). This is mainly in the medulla and extends into the pons and houses a vast array of neurones and interneurons which link together to produce the activity of swallowing. The interneurons consist of excitatory and inhibitory ones.
There are also nuclei which include the dorsal vagal motor nucleus and the nucleus ambiguus alongside the CN nuclei of CN 5, 7, 9, 10 and 12. All of these CN combine together with the interneurons to allow the sequence to take place. The cortex communicates with the brainstem salivatory nuclei. These send signals via motor neurons to the muscles of swallowing. 26 pairs of muscles are required in the entire swallowing process
21
different types of receptors in swallowing
Sensory receptors in the oropharynx, larynx and oesophagus detect changes and send signals back to the brainstem and the cortex via CN 5, 7, 9, 10 and 12. Chemical receptors – stimulus (acid); response (feedback control)
Thermal receptors – stimulus (hot/cold); response (non-painful sensation) Mechanical receptors – stimulus (distention); response (burning/pain) – MOST POWERFUL INDUCERS OF A SWALLOW. These help mediate the swallowing response.
Swallowing is not a reflex, but a patterned response.
22
vagal and spinal afferents
send different types of sensations back into the system via the:
Nadose ganglion of the vagus afferents
Dorsal root ganglion of the spinal afferents
The vagus afferents then go via the thalamus and into the cortex via the medulla.
For spinal afferents, the system involved is the anterolateral system (spinithalamic tract) for nociception and mechanoreception.
23
cortical input in swallowing
•It has been shown through studies that there are many areas of the cortex that help regulate the swallowing response.
•Cortical dysfunction (i.e. in stroke for example) results in dysphagia.
24
brainstem and swallowing
• During the process of swallowing, the epiglottis closes off the larynx to prevent aspiration.
For this period swallowing period, respiration is stopped.
The salivatory nuclei are situated close to, if not exactly in the same location, as those nuclei controlling breathing.
They work together to carry out this intricate procedure during swallowing.
25
Oesophageal stage
• The oesophagus exhibits two types of peristaltic movements:
1. Primary peristalsis
2. Secondary peristalsis
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primary peristalsis
• This is a continuation of the peristaltic wave that begins in the pharynx and spreads into the oesophagus during the pharyngeal stage of swallowing.
• This is quicker in someone sitting up/standing up, due to the influence of gravity
27
secondary peristalsis
•If the primary peristaltic wave fails to move all the food into the stomach, secondary peristaltic waves result from distention of the oesophagus itself by the retained food.
•These waves continue until all the food has emptied into the stomach.
•The secondary peristaltic waves are initiated partly by intrinsic neural circuits in the myenteric nervous system and partly by reflexes that begin in the pharynx and are then transmitted upward through vagal afferent fibres to the medulla and back again to the oesophagus through glossopharyngeal and vagal efferent nerve fibres.
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musculature of oesophagus
•Pharyngeal wall and the upper 1/3 of oesophagus = striated muscle.
Peristaltic waves in these regions are controlled by skeletal nerve impulses from the glossopharyngeal and vagus nerves from the nucleus ambiguus.
•Lower 2/3 of oesophagus = smooth muscle.
This is also strongly controlled by the vagus nerves acting through connections with the oesophageal myenteric nervous system
29
pressure zones of the Oesophagus
• There are 2 high pressure zones:
The UES - pressure can reach up to 100mmHg
The LES - pressure is around about 20mmHg (can be higher in pathological conditions)
•The inside of the oesophagus had a negative pressure of about -5mmHg.
This acts to help the bolus to be pulled through from the pharynx which is at atmospheric pressure (0mmHg) through the sphincter and into the oesophagus.
The reason why it is negative is because of the lungs and the pleura and there is the mediastinal pleura which pulls against the oesophagus creating this negative pressure.
•In the stomach, there is a slightly higher pressure of +5mmHg than the oesophagus
This doesn’t overcome the LES pressure so reflux is prevented.
•The reason why continuous reflux is prevented is because the pressure in the LES is higher than in the stomach.
30
receptive relaxation of the stomach
•When the oesophageal peristaltic wave approaches toward the stomach, a wave of relaxation, transmitted through myenteric inhibitory neurons, precedes the peristalsis.
•Furthermore, the entire stomach and, to a lesser extent, even the duodenum become relaxed as this wave reaches the lower end of the esophagus and thus are prepared ahead of time to receive the food propelled into the esophagus during the swallowing act
31
lower eosophageal sphincter
• This sphincter is found at the lower end of the oesophagus.
• It normally remains tonically constricted with an intraluminal pressure in the oesophagus of 30mmHg.
• When a peristaltic swallowing wave passes down the oesophagus, there is “receptive relaxation” of the lower oesophageal sphincter ahead of the peristaltic wave, which allows easy propulsion of the swallowed food into the stomach.
• Dysfunction of the LSE is called achalasia•Fortunately, the tonic constriction of the lower esophageal sphincter helps to prevent significant reflux of stomach contents into the esophagus except under very abnormal conditions.
32
Neurotransmitters on sphincters
• Acetylcholine causes constriction of muscles that will close sphincters and also those muscles that aid peristalsis.
• Nitric oxide causes relaxation of these muscles.
33
protective mechanisms to prevent oesophageal injury from reflux of gastric acid
anti reflux barrier: LES, diaphram, limit frequency of reflux.
Oesophageal clearance: gravity, peristalsis, limit duration of acid contact
Acid neutralization: saliva (HCO3) HCO3 (secreted and blood) limit duration of acid contact
Tissue resistance: cell junctions + membranes, Na/H exchange, Epithelial resitution, blood flow. Protect epithelium during acid contact.
34
secretory functions of the alimentary tract
•Throughout the alimentary tract, the secretory glands have two functions:
1.Secretion of Digestive enzymes
2.Secretion of Mucus - provides lubrication and protection to alimentary tract
•The digestive secretions are dependent on the presence of food in the alimentary tract.
•In parts of the GI tract, the digestive enzymes secreted are specific to certain foods
35
goblet cells/mucous cells
These are single-cell mucous glands.
These function mainly in response to local irritation of the epithelium.
They secrete mucous directly onto the epithelial surface to act as a lubrication that also protects the surfaces from excoriation and digestion.
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pits
These represent invaginations of the epithelium into the submucosa.
In the small intestine, these pits are called crypts of Lieberkuhn. These are deep and contain specialized secretory cells
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TUBULAR GLANDS
These are found in the stomach and the upper duodenum.
These secrete substances such as acid and pepsinogen in the stomach
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salivary glands, liver, pancreas
These provide secretions for digestion or emulsion of food.
39
effect of contact of food with the epithelium
•The presence of food in a particular segment of the GI tract causes the glands to secrete large quantities of juices.
•Direct contact of food with the glandular cells causes this local secretion in the GI tract.
•This local epithelial stimulation also activates the enteric nervous system of the gut wall:
The types of stimuli that do this are:
Tactile stimulation/ Chemical irritation/ Distention of the gut wall
•The resulting nervous reflexes stimulate both the mucous cells on the gut epithelial surface and the deep glands in the gut wall increase their secretion.
40
autonomic stimulation-parasympatheric
•Stimulation of parasympathetic nerves innervating the glands in the GI tract strongly increases the rate of alimentary glandular secretion.
•This is particularly true in the upper GI tract (innervated by the glossopharyngeal and vagus parasympathetic nerves), e.g. Salivary glands and oesophageal glands.
•Some glands in the distal large intestine (innervated by the pelvic parasympathetic nervous system) secrete secretion as a response to the mechanical presence of food.
•The remainder of the GI tract result in secretion due to local neural and hormonal stimuli in those particular segments of the tract.
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autonomic stimulation - sympathetic
•Stimulation of sympathetic nerves innervating the glands in the GI tract has a dual effect:
1.Increase in the amount of secretion.
2.Constriction of the blood vessels that supply the glands.
•Sympathetic stimulation alone usually slightly increases secretion.
•But, if parasympathetic or hormonal stimulation is already causing abundant secretion by the glands, superimposed sympathetic stimulation usually reduces the secretion, sometimes significantly so, mainly because of vasoconstrictive reduction of the blood supply
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hormonal regulation
•The hormones in the help regulate the volume and character of the secretions.
•They are particularly important in the stomach and the intestine.
•They are liberated from the GI mucosa in response to the presence of food in the lumen of the gut.
•The hormones are then absorbed into the blood and carried to the glands, where they stimulate secretion.
•This type of stimulation is particularly valuable to increase the output of gastric juice and pancreatic juice when food enters the stomach or duodenum.
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basic mechanism of secretion by glandular cells
• The secretory glands secrete two things mainly:
1. Organic substances (enzymes etc).
2. Water and electrolytes
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organic substance secretion
1.The nutrient material needed for the formation of the secretion must first diffuse or be actively transported by the blood in the capillaries into the base of the glandular cell.
2. Mitochondria located inside the glandular cell near its base use oxidative energy to produce ATP.
3.Energy from ATP, along with the appropriate substrates provided by the nutrients, is then used to synthesise the organic secretory substances.
The synthesis occurs in the ER and golgi complex of the glandular cell.
Ribosomes adherent to the ER are responsible for the synthesis of the proteins that are secreted.
4.The secretory materials are transported through the tubules of the ER to the golgi complex.
5.Golgi complex – materials are modified, added to, concentrated, and discharged into the cytoplasm in secretory vesicle, which are stored in the apical end of the glandular cells.
6.Nervous or hormonal signalling causes exocytosis of these vesicles. It happens in the following way:
The control signals increase the cell membrane permeability to calcium ions, and calcium enters the cell.
The calcium causes the vesicles to fuse with the apical cell membrane.
The apical cell membrane breaks open, thus emptying the vesicles via exocytosis.
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water and electrolyte secretion
• Water and electrolytes are secreted along with the organic substances.
1.Nerve stimulation of the basal portion of the cell membrane causes an influx of chloride ions.
2.The resulting increase in electronegativity induced inside the cell by excess negatively charged chloride ions then causes an influx of positive ions (e.g. sodium ions).
3.Due to the influx of ions (both positive and negative) an osmotic gradient is created, therefore water enters the glandular cells.
This increases the cell volume and hydrostatic pressure inside the cell, causing the cell itself to swell.
4.The pressure in the cell then initiates minute openings of the secretory border of the cell, causing flushing of water, electrolytes and organic materials out of the secretory end of the glandular cell.
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mucus
thick secretion composed mainly of:
Water
Electrolytes
Mixture of several glycoproteins (which themselves are composed of large polysaccharides bound with much smaller quantities of protein)
•Functions:
Lubrication of the GI tract
Protection of the GI tract
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mucus functions
•Mucus adheres tightly to the food or other particles and spreads as a thin film over the surfaces.
•It has sufficient body that it coats the wall of the gut and prevents actual contact of most food particles with the mucosa.
•Mucus has a low resistance for slippage, so the particles can slide along the epithelium with great ease, thus preventing excoriative or chemical damage to the epithelium.
•Mucus causes faecal particles to adhere to one another to form the faeces that are expelled during a bowel movement.
•Mucus is strongly resistant to digestion by the GI enzymes.
•The glycoproteins of mucus have amphoteric properties (able to react both as an acid and an alkali). This allows them to buffer small amounts of either acids or alkalis; also, mucus often contains moderate quantities of bicarbonate ions, which specifically neutralize acids.
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saliva is secreted by
Parotid glands – serous secretion only
Submandibular glands – serous and mucus secretion
Sublingual glands – serous and mucus secretion (mainly mucus)
Buccal glands – mucus secretion only
• Daily secretion of saliva = 800-1500ml (average = 1000ml).
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two major types of protein secretion in saliva
1.Serous secretion
Contains ptyalin (α-amylase), which is an enzyme for digesting starches.
2.Mucus secretion
Contains mucin for lubricating and for surface protective purposes.
•Saliva has a pH of between 6.0-7.0 (a favourable range for the digestive action of ptyalin).
50
secretion of ions in saliva
•Saliva contains large amounts of potassium and bicarbonate ions.
•Saliva also contains small amounts of sodium and chloride ions. There is a higher concentration of these ions in the plasma as opposed to the saliva.
•The salivary glands contain acini and salivary ducts.
•Salivary secretion is a two stage process
51
primary secretion of saliva-acini
This contains ptyalin and/or mucin in a solution of ions in concentrations similar to that of the extracellular fluid.
The ions secreted by the acini into the salivary duct are sodium ions (Na+), chloride ions (Cl-) and small amounts of bicarbonate ions (HCO3-).
Sodium ions enter the lumen via tight junctions too.
Water is also added to the salivary duct as a result of osmosis.
This leads to an isotonic, plasma-like primary secretion.
52
salivary ducts, reabsorption of Nacl
Sodium ions are actively reabsorbed from all the salivary duct lumen and small amounts of potassium ions are actively secreted into the lumen in exchange for the sodium.
The sodium ion concentration of the saliva becomes greatly reduced, whereas potassium ion concentration becomes increased.
There is excess reabsorption of sodium ions over potassium ions.
This creates electrical negativity (around -70mV) in the salivary ducts.
As a result, chloride ions are passively reabsorbed from the lumen (to make the lumen more positive).
Chloride ion concentration in the salivary fluids is greatly reduced, matching the ductal decrease in sodium ion concentration.
Small amounts of bicarbonate ions are secreted by the ductal epithelium into the lumen of the duct. This is caused by the passive exchange of bicarbonate for chloride ions.
53
summary of salivary duct stage of secretion
There is reabsorption of sodium ions and chloride ions (NaCl) from the duct.
There is some secretion of potassium ions and bicarbonate ions into the duct.
The cell membranes of the epithelial lining of the duct have low water permeability (less aquaporins) and so hardly any water enters the duct via osmosis. This leads to the final saliva being hypotonic.
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resting salivation
• Sodium chloride concentration of the saliva (15 mEq/L) is about 1/7 to 1/10 of their concentration in the plasma.
• The concentration of potassium ions (30 mEq/L) is 7 times as great as the plasma.
• The concentration of bicarbonate ions (50-70 mEq/L) is about 2-3 times as great as the plasma
55
maximal salivation
• During maximal salivation, the salivary ionic concentrations change considerably because the rate of formation of primary secretion by the acini can increase as much as 20x.
• This acinar secretion then flows through the ducts so rapidly that the ductal reabsorption of NaCl is considerably reduced.
• Therefore, when copious quantities of saliva are being secreted, the sodium chloride concentration in the saliva rises only to 1/2 or 2/3 that of plasma (normally 1/7 to 1/10), and the potassium concentration rises to only 4 times (normally 7 times) that of plasma.
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what 3 muscles make the UES
cricopharyngeus muscle, the adjacent inferior pharyngeal constrictor, and the proximal portion of the cervical oesophagus
57
membrane transport
phospholipid bilayer impermeable to ions and polar molecules. channels and carrier transporters are passive down conc gradient, pumps are active against conc gradient.
58
functions of transport proteins
uptake nutrients substrates and cofactors like glucose, Na amino acid transporter, and export waste like urea and lactate- H+.
Regulate ions PH and vol. Gradient maintanence by K+ Na+. volume inc by Na, K, Cl in. Vol dec Cl and K out. Acid extrusion by Na in H+ out. base extrusion Cl in HCO3 out.
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aquaporins
Pore is highly selective to water
•Aquaporin 5 is important in salivary secretion
•Water flow is driven by osmosis
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k+ channels
Four subunits arranged around a central pore
•Important in maintaining membrane potential
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voltage gated Na channel
Single polypeptide chain
•24 transmembrane domains
•Important in nerve conduction
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carrier proteins - classification
facilitator-uniport. cotransporter-symport. exchanger-antiport.
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primary secretion by acinar cells
Na+,K+-ATPase (P-type pump) Maintains concentration gradients for Na+ and K+ Small direct contribution to membrane potential
Na+,K+,2Cl- cotransporter (NKCC1, SLC12A2) Electrically neutral Uses inward gradient for Na+ to drive Cl- up its gradient – secondary active transport
K+ channels (BK & IK1) Recycles K+ and maintains membrane potential
Ca2+-activated Cl- channel (TMEM16A) Allows Cl- efflux down its electrochemical gradient
Aquaporin 5 water channel (AQP5) Allows H2O efflux driven by a small osmotic gradient
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paracellular pathway
Tight junctions in some epithelia are ‘leaky’ to small ions and water
•In others they are ‘tight’ and impermeable
•TJ permeability is determined by claudin family protein
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oral/buccal cavity
Lined by oral mucosa, a thick stratified squamousepithelium that is resistant to abrasion
•Produces defensinsto inhibit bacterial growth
•Teeth lie in sockets in the mandible and maxilla, covered by the gums
•Deciduous teeth (n=20) appear within the first 6-24 months of life, these are gradually replaced in childhood as the permanent teeth erupt (finished by approx age 12)
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adult teeth
Incisors (2I): ‘slice’ and cut
•Canines (1C): tear and rip
•Premolars (2PM): grind and crush
•Molars (3M): grind and crush (mostly grind)
•NB: Numbers in the dental formula refer to each side of the mouth, with upper jaw over lower jaw.
•Mastication = Chewing
•Cavitiesor Dental cariesresult from gradual demineralisation as a result of acid production from bacteria in plaque
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saliva
Mostly water (approx 99%)
•Lingual lipases and alpha-amylase
•Slightly Acidic (pH 6.75-7) to provide reasonably optimal conditions for enzyme function
•Mucoproteins(mucin) act as lubricants
•Lysoszyme
•Immunoglobulins(esp. IgA)
•Electrolytes
•Calcium and phosphate
(dental repair)
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control of salivation
Saliva is secreted continuously but salivation is controlled by salivatorynuclei in the medulla and ponsof the brainstem:
•Mechanoreceptors and chemoreceptorsin the mouth stimulate production of saliva with a high water content
•Mechanoreceptors are not food specific! (non food objects induce salivation)
•Input from higher brain centres (thinking about food) and lower digestive tract (irritation) can also induce salivation
69
muscularis externa
With the exception of some parts of the stomach (3 layers) consists of inner circular and an outer longitudinallayers
Contraction of circular smooth muscle: squeezes gut contents
Contraction of longitudinal muscle: shortens that portion of the gut
Smooth muscle layers in the gut are spontaneously active –interstitial cells of Cajalhave ‘pacemaker’ activity
Enteric neurones or extrinsic neurones modulate this basic activity
Loss of the cells of Cajalcan lead to gut motor dysfunction disorders
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oesophagus
Pharynx to stomach (~25cm)
•Normally closed -highly folded mucosa
•Submucosa contains blood vessels, lymphatics, nerves, lymphoid tissue and mucus glands
•Lined by stratified squamous epithelium to resist abrasion
•Muscularislayer: skeletal in first third (voluntary), Smooth in last third (involuntary), mixed in middle third
•Outer layer is mostly adventitia
•fixed to adjacent structures by connective tissue.
•Last part beyond the diaphragm covered with serosa
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small intestine motor activity
After a meal, there are small irregular contractions of the small intestine.
•In the interdigestivestate,the small intestine exhibits the migrating motor complex (MMC), which can take up to 2 hours to pass along the small intestine.
•Thought to have a housekeeping role (sweeps material through the gut).
•The signal to stop this interdigestiveactivity is ingestion of food, and this can be mimicked by gastrinand by cholecystokinin(CCK), which are released from the stomach and intestine, respectively.
•CCK is a potent inhibitor of gastric emptying in response to high caloric value in the duodenum, an example of local integration of activity to meet demand
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physiology of the stomach
Gobletcells–secrete an alkaline mucus
•Mucouscells-secrete mucus and pepsinogens
•Parietalcells-secrete gastric acid and intrinsic factor
•Chiefcells–secrete pepsinandgastric lipase
•Gcells–gastrin
•D cells(found in antrum) –somatostatin
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functions of gastric secretions
Exocrine:
•Hydrochloric acid –acidifies lumen, produces pepsin from pepsinogen.
•Mucus –protects mucosal surface being damaged by HCl.
•Pepsinogen–precursor of pepsin (which acts as an endopeptidase).
•Intrinsic factor –important in the absorption of vitamin B12(later, in the terminal ileum) and erythropoiesis.
•Endocrine:
•Gastrin–stimulates acid production.
•Somatostatin–inhibits release of gastrin
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control of gastric secretion
Gastric acid secretion is inhibited by:
•Somatostatin (via decreased gastrin release)
•Secretin(via decreased gastrinsecretion)
•Gastric inhibitory peptide and other enterogastrones(directly on parietal cells)
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phases of gastric secretion
Cephalic phase:
•Thought, smell, sight, taste of food releases ACh, stimulating the parietal cells and also the G cells –vagallymediated, about 40% of gastric acid secretion occurs here
Gastric phase:
•Distension and reflex activation of enteric neurones and vagaloutflow stimulate the parietal cells and the G cells. Digested proteins in stomach also stimulate the G cells –about 50% of gastric acid secretion occurs here
Intestinal phase:
•Amino acids present in the bloodstream (products of protein digestion) directly stimulate the parietal cells –about 10% of gastric acid secretion occurs here
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three phases of a swallow
Oral-striated muscle, control in the cortex/medulla, full voluntary control. Pharyngeal-striated muscle, control in the medulla, some voluntary control. Esophageal phase smooth muscle near end, medulla and ENS control. No voluntary control.
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sensory receptors in the swallowing tract
chemical-stimulated by acid, feedback control responce.
Thermal receptor to hot cold stim, non painful sensation.
Mechanical receptor-stimulated by distention, burning pain.
78
esophageal sensation transmitted via vagal and spinal afferents
vagal afferents like chemo, mechano and nociception-nodose ganglion-parabrachial nucleas-thalamus-cortex-medulla nucleus of solitary tract-anterolateral system spinothalamic tract-spinal cord dorsal horn
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the central pattern generator for esophageal peristalsis is initiated two ways:
swallowing-primary peristalsis
Distention-secondary peristalsis
clears solids and liquids from esophagus
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oropharyngeal dysphagia
abnormal bolus transfer to esophagus, difficult initiating swallow, can be caused by stroke
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esophageal dysphagia
abnormal bolus transport through esophagus, food stops after initiation of swallow. achalasia
82
achalasia
failure of ring of muscle fibres, such as a sphincter of oesophagus to relax. Achalasia results from the degeneration of neurons in the esophageal wall (ganglion cells) in the myenteric plexuses, and the ganglion cells that remain often are surrounded by lymphocytes and, less prominently, by eosinophils.
•This inflammatory degeneration preferentially involves the nitric oxide-producing, inhibitory neurons that effect the relaxation of oesophageal smooth muscle
•The cholinergic neurons that contribute to LES tone by causing smooth muscle contraction are relatively spared
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three manometry findings for achalasia
Elevated resting LES pressure - Above 45 mmHg
–Incomplete LES relaxation - This manometric finding distinguishes achalasia from other disorders associated with aperistalsis
–Aperistalsis - In the smooth muscle portion of the body of the oesophagus. For most patients, low amplitude; in some cases, however, the simultaneous esophageal contractions have higher amplitudes (eg, >60 mmHg). Such patients are said to have "vigorous" achalasia.
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botulinum toxin
Endoscopic injection of botulinum toxin (type A) into the lower oesophageal sphincter
–Botulinum toxin inhibits the calcium-dependent release of acetylcholine from nerve terminals, thereby countering the effect of the selective loss of inhibitory neurotransmitters
•It is initially effective in relieving symptoms in about 85% of patients. Symptoms recur in more than 50% of patients within 6 months, possibly because of regeneration of the affected receptors.
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pneumatic dilation
Pneumatic dilation is the most effective non-surgical treatment option for patients with achalasia
•It involves placing a balloon across the lower oesophageal sphincter, which is then inflated to a pressure adequate to tear the muscle fibres of the sphincter
•50–93% of patients obtain good to excellent relief of symptoms
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hellers myotomy
Surgical myotomy for achalasia involves carrying out an anterior myotomy across the lower oesophageal sphincter (Heller's myotomy)
•However, whether myotomy should be combined with an antireflux procedure (loose Nissen fundoplication, incomplete Toupet, or Dor fundoplication) is a cause for debate
•Myotomies are usually done laparoscopically through the abdomen with a 1–2 cm distal myotomy onto the stomach
•Good to excellent results are reported in 80–100% of patients
•The major complication is uncontrolled gastro-oesophageal reflux in about 10% of patients
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function of saliva for oral hygiene
•During sleep, little secretion occurs.
•This secretion maintains healthy oral tissues.
•The flow of saliva itself helps wash away pathogenic bacteria, as well as food particles that provide their metabolic support.
•Saliva contains several factors that destroy bacteria:
Thiocyanate ions: These enter bacteria and become bactericidal.
Proteolytic enzymes (lysosome)
Attack the bacteria.
Aid the thiocyanate ions in entering the bacteria.
Digest food particles, thus helping further to remove the bacterial metabolic support.
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nervous regulation of salivary secretion
•Salivary glands are controlled mainly by parasympathetic nervous signals all the way from the superior and inferior salivatory nuclei in the brainstem.
•The salivatory nuclei are excited by tactile stimuli from the tongue and other areas of the mouth and pharynx.
•Salivation can also be stimulated or inhibited by nervous signals arriving in the salivatory nuclei from higher centres of the CNS.
E.g. smelling liked foods increases salivation. This is caused by the appetite area of the brain.
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parasympathetic stimulation of saliva
An increase in the secretion of watery saliva (water and electrolyte secretion) is mediated by CN 7 & 9 from the superior and inferior salivatory nuclei in the brain stem via muscarinic receptors.
Parasympathetic nerve stimulation occurs via the IP3 intracellular pathway, whereby calcium released in this pathway activates the relevant channels and transport proteins to cause this increase in secretion
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sympathetic stimulation of saliva
Mediated by β-adrenergic receptors and causes an increase in secretion of viscous saliva (via T1-T3 nerves of the superior cervical ganglion which travel along the surfaces of blood vessel walls to the salivary glands).
Sympathetic stimulation increases salivation a slight amount, much less so than parasympathetic stimulation
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reflexes affecting saliva
• Salivation also occurs in response to reflexes originating in the stomach and upper small intestines - particularly when irritating foods are swallowed.
• The saliva, when swallowed, helps to remove the irritating factor in the gastrointestinal tract by diluting or neutralizing the irritant substances
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blood supply affecting saliva
• Blood supply to the glands affects saliva production. This is because secretion always requires adequate nutrients from the blood.
• The parasympathetic nerve signals that induce copious salivation also moderately dilate the blood vessels.
• In addition, salivation itself directly dilates the blood vessels, thus providing increased salivatory gland nutrition as needed by the secreting cells.
Part of this additional vasodilator effect is caused by kallikrein secreted by the activated salivary cells, which in turn acts as an enzyme to split one of the blood proteins, to form bradykinin, a strong vasodilator.
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oesophageal secretion
entierly mucous on character and provide lubrication for swallowing. main body is lined simple mucous glands. in gastric end compound mucous glands. Upper oesophagus compound mucous glands - The mucus secreted by these prevents mucosal excoriation by newly entering food.
Oesophagogastric junction compound mucous glands - protect the oesophageal wall from digestion by acidic gastric juices that often reflux from the stomach back into the lower oesophagus.
Despite this protection, a peptic ulcer at times can still occur at the gastric end of the oesophagus.
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dysphagia
• Dysphagia is the symptom of difficulty of swallowing.
• Dysphagia refers to problems with the transit of food or liquid from the mouth to the laryngopharynx or through the oesophagus.
• Severe dysphagia can compromise nutrition, cause aspiration, and reduce quality of life
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epidemiology of dysphagia
16-22% over 50 years old
55% over 70 years old
More than 900,000 people in England, with half of these dependent on other people foe help with everyday activities, suffer from dysphagia as a result of stroke
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complications of dysphagia
Aspiration, penetration
Pneumonia
Nutritional compromise
Increased length to hospital stay (people suffering from dysphagia as a symptom post-stroke are likely to stay in hospital for twice as long as those patients who do not have dysphagia post-stroke)
Poorer outcomes
Reduced quality of life
NHS costs
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signs and symptoms of dysphagia
Reduced appetite/ refusing to eat?
Weight loss?
Food modification?
Food residue after eating?
Drooling/ dry mouth/ coughing/ throat clearing?
Change in voice/ changes in respiratory status (breathless)/ changes in temperature?
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screening for dysphagia
can they sit up are they awake? no-artificial support. yes-keep mouth clean-sit patient give 3 teaspoons water observe absent swallow, cough, throat clear, delayed cough, altered voice. if ok observe drink continuously 1/3 glass. then go to soft food. if abnormal refer SLT
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classification of dysphagia
•Dysphagia caused by an oversized bolus or a narrow lumen is called structural dysphagia.
•Dysphagia due to abnormalities of peristalsis or impaired sphincter relaxation after swallowing is called propulsive dysphagia.
•Dysphagia is classified into two types:
1)Oropharyngeal Dysphagia
2)Oesophageal Dysphagia
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oropharyngeal dysphagia
• Oropharyngeal dysphagia is difficulty emptying material from the oropharynx into the oesophagus.
• Anatomic, neurologic, and muscular defects can cause oropharyngeal dysphagia. Treatment focuses on utilizing postures or maneuvers devised to reduce pharyngeal residue and enhance airway protection learned under the direction of a trained swallow therapist
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anatomic oropharyngeal dysphagia
eg zenkers diveticulum-dec compliance of cricopharyngeus.
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neurologic oropharyngeal dysphagia
stroke-weak pharyngeal contraction, incoordination of UES and pharyngeal contraction
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muscular oropharyngeal dysphagia
myasthenia gravis-weak pharyngeal contraction
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signs of oropharyngeal dysphagia
• It results in poor bolus formation and control so that food has prolonged retention within the oral cavity and may seep out of the mouth.
Drooling and difficulty in initiating swallowing are other characteristic signs.
• Poor bolus control also may lead to premature spillage of food into the laryngopharynx with resultant aspiration into the trachea or regurgitation into the nasal cavity.
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causes of oropharyngeal dysphagia
• 1/3 of oropharyngeal dysphagia cases are as a result of unilateral hemispheric strokes.
The lesion size is more important than the location, because there are many areas in the brain that control swallowing and so a larger lesion is like to damage more of these areas.
Anterior lesions and lesions in subcortical white matter may experience high risk of aspiration.
Dysphagia tends to be less severe after hemispheric stroke and remains prominent in the rehabilitation brainstem stroke
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oesophageal dysphagia
• Oesophageal dysphagia is difficulty passing food down the oesophagus.
• It results from either a motility disorder or a mechanical obstruction
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treatment for dysphagia
postures and maneuvers. •Aspiration risk may be reduced by altering the consistency of ingested food and liquid.
•Dysphagia resulting from a stroke (in 50% of people) can spontaneously improves within the first few weeks after the event. More severe and persistent cases may require gastrostomy and enteral feeding. Feeding by a nasogastric tube or a percutaneous endoscopic gastrostomy (PEG) tube may be considered for nutritional support; however, these maneuvers do not provide protection against aspiration of salivary secretions or refluxed gastric contents.
•The majority of causes of esophageal dysphagia can be treated by esophageal dilation.
•A common symptom is a gurgly/wet voice that worsens after drinking water.
•Soft Diet - The soft diet for dysphagia eliminates all foods that may be difficult to chew.
•The goal of dysphagia therapy – safe, adequate, independent, satisfying, nutritional and hydrational needs.
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managment of dysphagia
•Swallow assessment within 4 hours or arrival in hospital.
•Nil By Mouth (NBM) if unable to swallow.
•Intravenous infusion (IVI)
•SALT (Speech and language therapy) assessment.
•Feeding by alternative route.
•Nutritional assessment for ALL including weight
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dysphagia after stroke
•Common (50% of all stroke patients).
•30% increased risk of mortality.
•Aspiration is the most important complication.
•Natural (swallowing) recovery in majority.
•Decisions about alternative feeding (optimal timing, method of delivery).
•Treatment options limited (SALT).
•Brainstem stroke – lower motor neurons
•Cerebellar stroke – ataxia, hypotonia
•Subcortical stroke – motor and sensory pathways
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psychological impacts on patients
•Health anxiety and worry
•Concern leading to vulnerability
•Depression
•Frustration
•Embarrassment
Choking-fear-stress and fear death-food avoidance-malnutrition.
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assessment of dysphagia in stroke
•History
•Clinical observations
•Cognitive screening
•Cranial nerve assessment
•Oral cavity inspection
•Test swallows
•Mealtime observations, posture diet level, self-feeding, respiratory changes
•Videofluoroscopy (barium meal)
•Fiberoptic Endoscopic Examination Swallowing (FEES)
This is to visualise any residues in the laryngeal inlet
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enteral nutrition
nasogastric, nasoduodenal, gastrostomy, jejunotomy.
•Parenteral refers to the infusion into the bloodstream via a peripheral vein.
•Enteral refers to feeding via a tube placed into the gut.
This is the preferred route because of benefits derived from maintaining the digestive, absorptive, and immunologic barrier functions of the gastrointestinal tract.
•Feeds can be given by various routes:
By mouth (food supplements with multiple benefits).
By nasogastric tube – easy to insert; may be uncomfortable; can get dislodged; can be misplaced - require re-siting and can lead to aspiration pneumonia.
Percutaneous endoscopic gastrostomy (PEG) – needs two doctors to insert at endoscopy, more comfortable, can be permanent if necessary. It is useful for patients who need enteral nutrition for a prolonged period (e.g. more than 30 days). A catheter is placed percutaneously into the stomach under endoscopic control
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problems in dysphagia
•Reduced ability to initiate a saliva swallow.
•Delayed triggering of pharyngeal swallow.
•Incoordination of oral movements in swallow.
•Increased transit time.
•Reduced pharyngeal contraction.
•Residue of the bolus.
•Aspiration.
•Upper Oesophageal Sphincter (UES) dysfunction.
•Impaired lower oesophageal sphincter relaxation.
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achalasia
the failure of a ring of muscle fibres, such as the lower oesophageal sphincter (LOS), to relax
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pathophysiology of achalasia
Achalasia results from the degeneration of neurons in the oesophageal wall (ganglion cells) in the myenteric plexuses, and the ganglion cells that remain often are surrounded by lymphocytes and, less prominently, by eosinophils.
This inflammatory degeneration occurs of the inhibitory neurons. The inhibitory neurons usually release nitric oxide causing the sphincter to relax.
The cholinergic neurons that contribute to LES tone by causing smooth muscle contraction are relatively spared.
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mechanism of achalasia
Loss of inhibitory innervation in the LOS causes:
The basal sphincter pressure to rise.
Sphincter muscle incapable of normal relaxation.
Oesophageal body smooth muscle aperistalsis
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aetiology of achalasia
Not known
Associated with HLA-DQw1
Circulating antibodies to enteric neurons suggest that achalasia may be an autoimmune disorder.
It may result from chronic infections with herpes zoster or measles viruses (unconfirmed).
It may also be due to malignancy, Chagas Disease, Infiltrative Disorders (e.g. Sarcoid Amyloid)
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prevalence of achalasia
Annual incidence of approximately 1 case per 100,000.
Likely to occur in men and women all the same.
Onset before adolescence unusual.
Usually diagnosed between the ages of 25 and 60 years
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clinical presentation of achalasia
Long history of intermittent dysphagia, characteristically for both liquids and solids from the onset.
Regurgitation of food from the dilated oesophagus occurs, particularly at night, and aspiration pneumonia is a complication.
Weight loss
Difficulty breathing
Chest pain
Heartburn
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diagnosis of achalasia
Clinical history
Endoscopy
May reveal dilated oesophagus containing residual material/ May appear normal.
Oesophageal stasis predisposes to candida infection that may be apparent.
Can be an oesophagogastroduodenoscopy (OGD) or a colonoscopy.
Radiology
Barium swallow diagnostic accuracy is around 95%.
Dilated oesophagus with beak-like narrowing.
Dilation may be so profound that the oesophagus assumes a sigmoid shape.
Purposeless, spastic contractions can be observed (“vigorous achalasia”).
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manometry use to diagnose achalasia
This is usually required for confirmation.
Manometry is performed by passing a catheter through the nose into the oesophagus and allowing the patient to swallow on either saline or a jelly-like substance.
The pressures generated by the muscles in the UOS, the muscles of the oesophagus and the LOS are monitored as the object passes down the oesophagus.
Three primary findings:
1. Elevated resting LES pressure (above 45mmHg)
2. Incomplete LES relaxation – this manometric finding distinguishes achalasia from other disorders associated with aperistalsis.
3. Aperistalsis – in the smooth muscle portion of the body of the oesophagus. For most patients, low amplitude; in some cases, however, the simultaneous oesophageal contractions have higher amplitudes (eg, >60 mmHg). Such patients are said to have "vigorous" achalasia.
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treatment of achalasia
No treatment can restore muscular activity to the denervated oesophagus in achalasia
botulinum toxin, pneumatic dilation, hellers myotomy
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botulinum toxin
Endoscopic injection of botulinum toxin (type A) into the lower oesophageal sphincter:
o Botulinum toxin inhibits the calcium-dependent release of acetylcholine from nerve terminals, thereby countering the effect of the selective loss of inhibitory neurotransmitters.
It is initially effective in relieving symptoms in about 85% of patients. Symptoms recur in more than 50% of patients within 6 months, possibly because of regeneration of the affected receptors.
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pneumatic dilation
Most effective non-surgical treatment option for patients with achalasia.
It involves placing a balloon across the LOS, which is then inflates to a pressure adequate to tear the muscle fibres of the sphincter.
50-93% of patients obtain good to excellent relief of symptoms.
The clinical response improves proportionally with increasing balloon diameter.
The procedure can be done on an outpatient basis, recovery is rapid, and discomfort is short-lived.
About 30% of patients might require subsequent dilations.
The main adverse event with pneumatic dilation, which occurs at a cumulative rate of 2%, is oesophageal perforation
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hellers myotomy
Surgical myotomy involves carrying out an anterior myotomy across the lower oesophageal sphincter.
o This means cutting the muscles in the anterior part of the LOS, thus allowing food and liquids to pass to the stomach.
It is unclear if this procedure should be combined with an anti-reflux procedure.
Myotimies are usually done laproscopically through the abdomen with a 1-2cm distal myotomy onto the stomach.
Good to excellent results are reported in 80-100% of patients.
The major complication is uncontrolled gastro-oesophageal reflux in about 10% of patients
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assessing responce to treatment
Symptom improvement is used to assess the success of pneumatic dilation or surgical myotomy.
However, up to 30% of patients can feel better and still have poor oesophageal emptying.
Simple objective testing such as follow-up manometry or a timed barium swallow might help to define objective improvement after treatment.
Studies may suggest that patients with good oesophageal emptying have better long-term symptom relief.
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summary of achalasia
Low but important prevalence.
Symptoms may be initially vague.
Barium swallow and manometry most useful in diagnosis.
Data suggest pneumatic dilatation is most cost effective treatment, with myotomy reserved for failed procedures
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aspiration
the passing of any foreign substance, such as saliva or gastric content, through the vocal cords and entering the respiratory tract
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penetration
refers to the presence of foreign substances above the vocal cords (they haven’t managed to pass through the vocal cords).
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aspiration pneumonia
inhalation of stomach contents or secretions of the oropharynx leading to lower respiratory tract infection.
•In many healthy adults, very small quantities of aspiration occur frequently but the normal defence mechanisms (cough, lung cilia) remove the material with no ill effects.
•Aspiration pneumonia occurs in markedly debilitated patients or those who aspirate gastric contents either while unconscious or during repeated vomiting.
These patients have abnormal gag and swallowing reflexes that predispose to aspiration.•The resultant pneumonia is partly chemical because of the extremely irritating effects of the gastric acid, and partly bacterial (from the oral flora).
•Because of the bronchial anatomy, the most usual sites for spillage are the apical and posterior segments of the right lower lobe
This type of pneumonia is often necrotizing, pursues a fulminant clinical course, and is a frequent cause of death. In those who survive, lung abscess is a common complication.
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consequences of aspiration
Chemical pneumonitis: chemical irritation of the lungs.
Obstruction: large volumes of aspirated material may lead to obstruction of the respiratory tract.
Bacterial infection (pneumonia): infection of the lower airways may lead to empyema, lung abscess, acute respiratory failure and acute lung injury.
Persistent aspiration pneumonia is often due to anaerobes and it may progress to lung abscess or even bronchiectasis
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clinical signs
Fever
Tachycardia
Tachypnoea
Hypoxia
Coarse crackles right base lung
Decreased percussion right base lung
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patient journey of a stroke
• Primary Prevention – doctors and the patient act towards reducing risk of stroke, by controlling/reducing the person’s risk factors.
•If this fails or is inefficient, this will result in a stroke.
•Following a stroke, the patient undergoes acute treatment.
This is will be dependent on the type of stroke, but in the case of ischaemic stroke, the patient is administered a thrombolysis (tPA).
There has been research done for neuroprotective treatment, however this has failed.
•Following this, the patient undergoes secondary prevention (reduces stroke risk) and rehabilitation (restores functionality).
Rehabilitation is the current interest in terms of clinical management.
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neuroregeneration
•Neuroregeneration begins days/weeks/months after the acute injury.
•Neuroregeneration is more restricted in those animals that have a more complex nervous system and a more complex immune system, such as in humans.
• Neural repair is most efficient by the combination of:
Neuroplasticity
Behavioural activity/ neurorehabilitation
Drug and cell-based therapies
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endogenous repair mechanisms
1) Neuroplasticity/ Neurogenesis – restoration of the neuronal network, including the migration of the new cells out of the area.
2) Angiogenesis – restoration of the blood supply.
3) Inflammation –neurorepair role of other brain immune cells (microglia), and the expression of growth factors.
4) Glial Scarring – protection of non-injured brain structures.
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neuroplasticity/neurogenesis
in 2 locations in the brain:
Subgranular Zone (SGZ) of the dentate gyrus
Subventricular Zone (SVZ). Neural stem cell proliferation into neural precursor cells.
Precursor cells then do 4 things:
1.Perpetuation
2.Differentiation - into glial cells (astrocytes/ oligodendrocytes/ microglia), neurones
3.Integration – neurones integrate with other parts of the body
4.Migration
•Neurogenesis can play a vital role in re-establishing memory.
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neurogenesis in the subgranular zone of dentate gyrus
The neural stem cells proliferate in the SGZ of the hippocampal dentate gyrus.
These differentiate into neurones whilst migrating from the SGZ to the inner granule cell layer in the hippocampal dentate gyrus.
Here the neurones re-establish the function
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neurogenesis in the subventricular zone
In the normal brain, neural progenitors migrate from SVZ to olfactory bulb via Rostral Migratory Steam (RMS).
Following injury, neural progenitors from SVZ leave RMS and migrate laterally towards the damaged area.
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angiogenesis
biological process involved in the growth of new blood vessels from pre-existing vessels, in order to restore blood supply to an area.
•Angiogenesis is involved in wound-healing to restore the blood supply to an injured tissue.
•It is also a characteristic feature of tumour development.
•Factors involved in angiogenesis after brain injury:
Cytokines
Chemokines
Integrins/ ECM
Growth Factors
•Angiogenesis is mediated in many ways, via many pathways:
The pathway involved in repair is as follows:
Vascular Endothelial Growth Factor (VEGF)
VEGFR2 (in all endothelia)
Repair
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inflamation
• Inflammation has a dual role:
Loss of function (e,g. multiple sclerosis)
Recovery
This occurs by increasing the expression of growth factors which help in neurogenesis.
• The microglia contribute to CNS renewal:
CNS injury causes the resting microglia to undergo a change in their phenotype.
Initially (“primary activation”), they change to a M1 phenotype, where they bring about neurotoxic effects involved in tissue injury.
Then there is “delayed activation”, where the resting microglia change to a M2 phenotype which bring about tissue repair due to immune suppression
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glial scarring-neurotoxic
• Damage to the central nervous system (CNS) results in a glial reaction, leading eventually to the formation of a glial scar.
• In this environment, axon regeneration fails, and remyelination may also be unsuccessful.
• The glial reaction to injury recruits microglia, oligodendrocytes and myelin debris.
• Most of these cell types produce molecules that have been shown to be inhibitory to axon regeneration.
• Microglia produce free radicals, nitric acid and arachidonic acid derivatives.
• The glial scar itself is formed by astrocytes.
• This is the neurotoxic effect of the glial scarring
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neuroprotective
• The glial scar forms a barrier between the glial reaction (apoptotic) site and the health tissue surrounding it.
• This is the neuroprotective effect of glial scarring, thus preventing further damage to the brain
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Ongoing Stroke Management and Rehabilitation
• Risk factor management (hypertension, exclude AF, diabetes, hyperlipidaemia).
• Managing the neurological deficit.
• Managing complications (e.g. pneumonia).
• Managing emotional symptoms (anxiety, depression, hyperemotionalism).
• Monitoring recovery.
• Helping the patient and family.
• Planning discharge.
• Helping bridge the gap into the community.
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Current Guidelines for Rehabilitation
• Swallow assessment within 4 hours or arrival in hospital.
• Nil By Mouth (NBM) if unable to swallow.
• Intravenous infusion (IVI)
• SALT (Speech and language therapy) assessment.
• Feeding by alternative route
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Management of a Dysphagic Patient
• Monitor fluid balance, electrolytes, weight.
• Management of oral hygiene.
• Regular SALT review for recovery.
• Specific SALT techniques (limited evidence).
• Positioning Management of neglect, positioning, upper limb movement for feeding
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mortality rates
• Mortality rates are measured by counting the number of deaths in one year compared with either previous or subsequent years.
• An increase in mortality rate can be seen as a decrease in health status.
• A decrease in mortality rate can be seen as an increase in health status.
• In order to provide a more meaningful measure of health status, mortality rates are corrected for age and sex (males usually die younger than females).
• Furthermore, mortality rates can be produced to be either age specific, such as infant mortality rates, or illness or illness specific, such as sudden death rates.
• As long as the population being studied is accurately specified, corrected and specific, mortality rates provide an easily available and simple measure: death is a good reliable outcome.
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morbidity rates
• Morbidity rates are measured by prevalence rates involving large surveys of ‘caseness’ to simply count how many people within a given population suffer from a particular problem.
• It can also be measured by looking at sickness absence rates by counting the number of days lost due to illness and caseload assessments count the number of people who visit their GP or hospital within a given time frame.
• It is also measured for each individual using ‘Measures of Functioning’
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Measures of Functioning
• Measures of functioning are generally called activity-of-daily-living scales (ADLs).
• ADLs we initially developed to assess levels of functioning in the elderly
Developed for the therapist and/or carer to complete and ask the rater to evaluate the individual on a range of dimensions including bathing, dressing, continence and feeding.
• ADLs have also been developed for individuals themselves to complete and include questions such as: ‘Do you or would you have any difficulty: washing down/ cutting toenails/ running to catch a bus/ going up/down stairs?’
• Measures of functioning can either be administered on their own or as part of a more complex assessment involving measures of subjective health status.
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sunjective health status
• Over recent years, measures of health status have increasingly opted for measures of subjective health status, which all have one thing in common: they ask the individuals themselves to rate their health.
• Some of these are referred to as subjective health measures, while others are referred to as either quality-of-life scales or health-related quality-of-life scales.
• However, the literature in the area of subjective health status and quality of life is plagued by two main questions: ‘What is quality of life?’ and ‘How should it be measured?
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quality of life
‘The value assigned to duration of life as modified by the impairments, functional states, perceptions and social opportunities that are influenced by disease, injury, treatment or policy’ (Patrick and Ericson 1993).
‘A personal statement of the positivity or negativity of attributes that characterise one’s life’ (Grant et al. 1990).
‘A broad ranging concept affected in a complex way by the person’s physical health, psychological state, level of independence, social relationships and their relationship to the salient features in their environment’
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measures of quality of life
[Browne et al. (1997)]:
Standard-Needs Approach: ‘ a consensus about what constitutes a good or poor quality of life exists or at least can be discovered through investigation’
This assumes that needs rather than wants are central to quality of life and that these needs are common to all, including researchers.
Psychological Processes Perspective: ‘constructed from individual evaluations of personally salient aspects of life’
•Browne et al. conceptualised measures of quality of life being devised either by researchers or by individuals themselves.
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unidimensional measures of quality of life
These measures assess health in terms of one specific aspect of health.
They can be used on their own or in conjunction with other measures.
Examples:
General Health Questionnaire (GHQ) – assesses mood
McGill Pain Questionnaire – assesses pain levels
Self-esteem Scale/ Self-esteem Inventory – assesses self-esteem
Measures of Social Support
Measures of Satisfaction with Life
Measures of Symptoms
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Multiidimensional measures of quality of life
These measures assess health in the broadest sense.
These measures aren’t always long and complicated.
Doctors can simply as respondents to make a relative judgement about their health on a scale from ‘best possible’ to ‘worst possible’.
Due to the many definitions of Quality of Life, different measures have been developed.
Some focus on:
Particular populations (e.g. elderly/children/ those in the last year of life).
Specific illnesses (e.g. diabetes/heart disorder/ renal disease)
Also, generic measures of quality of life have been developed, which can be applied to all individuals.These help explore quality of life in different cultures, with different levels of health and different levels of economic security.
Examples:
Nottingham Health Profile (NHP)
WHOQoL-100
Generic measures have been criticised for being too broad and for being too focused or for potentially missing out aspects of quality of life that may be of specific importance to the individual concerned.
This has led to the development of individual quality-of-life measures
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individual quality of life measures
Measures of subjective health status ask the individual to rate their own health. This is in contrast to measures of mortality, morbidity and most measures of functioning, which are completed by carers, researchers or an observer.
Although these measures enable individuals to rate their own health, they do not allow them to select the dimensions along which to rate it.
For example, a measure that asks about an individual’s work life assumes that work is important to this person, but they might not want to work.
Individual quality-of-life measures not only ask the subjects to rate their own health status but also to define the dimensions along which it should be rated.
Schedule for Evaluating Individual Quality of Life (SEIQoL)
oThis asks the subjects to select five areas of their lives that are important to them, to weight them in terms of their importance and then to rate how satisfied they currently are with each dimension
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self regulatiry model of illness cognition
interpretation, symptom perception, social messages-deviation from norm
Representation of health threat. identity cause consequence time line cure.
Emotional responce to health threat, fear anxiety, depression.
Coping-avoidance or approach.
Appraisal, was coping effective
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