case 1

Question 1

layers of the GI tract

Answer 1

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.

Question 2

enteric nervous system

Answer 2

• 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).

Question 3

two main plexuses of the enteric nervous system

Answer 3

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.

Question 4

neurons in the enteric nervous system

Answer 4

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.

Question 5

two types of movement in the GI tract

Answer 5

propulsive and mixing movements

Question 6

Propulsive movements-peristalsis

Answer 6

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.

Question 7

4 stages of swallowing

Answer 7

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

Question 8

cephalic stage

Answer 8

• 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

Question 9

oral stage

Answer 9

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.

Question 10

mastication

Answer 10

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.

Question 11

teeth and mastication

Answer 11

• The anterior teeth (incisors) provide a strong cutting action.
• The posterior teeth (molars) provide a strong grinding action.

Question 12

process of mastication - chewing reflex

Answer 12

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.

Question 13

pharyngeal stage

Answer 13

• 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:

Question 14

contractions of the soft patate and palatopharyngeal folds in the pharyngeal stage

Answer 14

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.
.

Question 15

contractions of the vocal cords in the pharyngeal phase

Answer 15

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.

Question 16

changes to the larynx in the pharyngeal phase

Answer 16

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.

Question 17

changes to the pharynx in the pharyngeal phase

Answer 17

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.

Question 18

summary of changes in the pharyngeal phase

Answer 18

 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

Question 19

upper Esophageal sphincter

Answer 19

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

Question 20

neurophysiology of swallowing

Answer 20

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

Question 21

different types of receptors in swallowing

Answer 21

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.

Question 22

vagal and spinal afferents

Answer 22

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.

Question 23

cortical input in swallowing

Answer 23

• 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.

Question 24

brainstem and swallowing

Answer 24

• 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.

Question 25

Oesophageal stage

Answer 25

• The oesophagus exhibits two types of peristaltic movements:

1. Primary peristalsis
2. Secondary peristalsis

Question 26

primary peristalsis

Answer 26

• 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

Question 27

secondary peristalsis

Answer 27

• 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.

Question 28

musculature of oesophagus

Answer 28

•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

Question 29

pressure zones of the Oesophagus

Answer 29

• 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.

Question 30

receptive relaxation of the stomach

Answer 30

• 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

Question 31

lower eosophageal sphincter

Answer 31

• 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.

Question 32

Neurotransmitters on sphincters

Answer 32

• Acetylcholine causes constriction of muscles that will close sphincters and also those muscles that aid peristalsis.
• Nitric oxide causes relaxation of these muscles.

Question 33

protective mechanisms to prevent oesophageal injury from reflux of gastric acid

Answer 33

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.

Question 34

secretory functions of the alimentary tract

Answer 34

•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

Question 35

goblet cells/mucous cells

Answer 35

 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.

Question 36

pits

Answer 36

 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

Question 37

TUBULAR GLANDS

Answer 37

 These are found in the stomach and the upper duodenum.

 These secrete substances such as acid and pepsinogen in the stomach

Question 38

salivary glands, liver, pancreas

Answer 38

 These provide secretions for digestion or emulsion of food.

Question 39

effect of contact of food with the epithelium

Answer 39

•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.

Question 40

autonomic stimulation-parasympatheric

Answer 40

• 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.

Question 41

autonomic stimulation - sympathetic

Answer 41

•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

Question 42

hormonal regulation

Answer 42

• 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.

Question 43

basic mechanism of secretion by glandular cells

Answer 43

• The secretory glands secrete two things mainly:

1. Organic substances (enzymes etc).
2. Water and electrolytes

Question 44

organic substance secretion

Answer 44

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.

Question 45

water and electrolyte secretion

Answer 45

• 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.

Question 46

mucus

Answer 46

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

Question 47

mucus functions

Answer 47

• 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.

Question 48

saliva is secreted by

Answer 48

 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).

Question 49

two major types of protein secretion in saliva

Answer 49

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).

Question 50

secretion of ions in saliva

Answer 50

• 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

Question 51

primary secretion of saliva-acini

Answer 51

 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.

Question 52

salivary ducts, reabsorption of Nacl

Answer 52

 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.

Question 53

summary of salivary duct stage of secretion

Answer 53

 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.

Question 54

resting salivation

Answer 54

• 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

Question 55

maximal salivation

Answer 55

• 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.

Question 56

what 3 muscles make the UES

Answer 56

cricopharyngeus muscle, the adjacent inferior pharyngeal constrictor, and the proximal portion of the cervical oesophagus

Question 57

membrane transport

Answer 57

phospholipid bilayer impermeable to ions and polar molecules. channels and carrier transporters are passive down conc gradient, pumps are active against conc gradient.

Question 58

functions of transport proteins

Answer 58

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.

Question 59

aquaporins

Answer 59

Pore is highly selective to water
•Aquaporin 5 is important in salivary secretion
•Water flow is driven by osmosis

Question 60

k+ channels

Answer 60

Four subunits arranged around a central pore

•Important in maintaining membrane potential

Question 61

voltage gated Na channel

Answer 61

Single polypeptide chain
•24 transmembrane domains
•Important in nerve conduction

Question 62

carrier proteins - classification

Answer 62

facilitator-uniport. cotransporter-symport. exchanger-antiport.

Question 63

primary secretion by acinar cells

Answer 63

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

Question 64

paracellular pathway

Answer 64

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

Question 65

oral/buccal cavity

Answer 65

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)

Question 66

adult teeth

Answer 66

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

Question 67

saliva

Answer 67

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)

Question 68

control of salivation

Answer 68

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

Question 69

muscularis externa

Answer 69

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

Question 70

oesophagus

Answer 70

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

Question 71

small intestine motor activity

Answer 71

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

Question 72

physiology of the stomach

Answer 72

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

Question 73

functions of gastric secretions

Answer 73

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

Question 74

control of gastric secretion

Answer 74

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)

Question 75

phases of gastric secretion

Answer 75

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

Question 76

three phases of a swallow

Answer 76

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.

Question 77

sensory receptors in the swallowing tract

Answer 77

chemical-stimulated by acid, feedback control responce.
Thermal receptor to hot cold stim, non painful sensation.
Mechanical receptor-stimulated by distention, burning pain.

Question 78

esophageal sensation transmitted via vagal and spinal afferents

Answer 78

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

Question 79

the central pattern generator for esophageal peristalsis is initiated two ways:

Answer 79

swallowing-primary peristalsis
Distention-secondary peristalsis
clears solids and liquids from esophagus

Question 80

oropharyngeal dysphagia

Answer 80

abnormal bolus transfer to esophagus, difficult initiating swallow, can be caused by stroke

Question 81

esophageal dysphagia

Answer 81

abnormal bolus transport through esophagus, food stops after initiation of swallow. achalasia

Question 82

achalasia

Answer 82

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

Question 83

three manometry findings for achalasia

Answer 83

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.

Question 84

botulinum toxin

Answer 84

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.

Question 85

pneumatic dilation

Answer 85

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

Question 86

hellers myotomy

Answer 86

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

Question 87

function of saliva for oral hygiene

Answer 87

•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.

Question 88

nervous regulation of salivary secretion

Answer 88

•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.

Question 89

parasympathetic stimulation of saliva

Answer 89

 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

Question 90

sympathetic stimulation of saliva

Answer 90

 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

Question 91

reflexes affecting saliva

Answer 91

• 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

Question 92

blood supply affecting saliva

Answer 92

• 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.

Question 93

oesophageal secretion

Answer 93

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.

Question 94

dysphagia

Answer 94

• 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

Question 95

epidemiology of dysphagia

Answer 95

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

Question 96

complications of dysphagia

Answer 96

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

Question 97

signs and symptoms of dysphagia

Answer 97

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?

Question 98

screening for dysphagia

Answer 98

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

Question 99

classification of dysphagia

Answer 99

•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

Question 100

oropharyngeal dysphagia

Answer 100

• 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

Question 101

anatomic oropharyngeal dysphagia

Answer 101

eg zenkers diveticulum-dec compliance of cricopharyngeus.

Question 102

neurologic oropharyngeal dysphagia

Answer 102

stroke-weak pharyngeal contraction, incoordination of UES and pharyngeal contraction

Question 103

muscular oropharyngeal dysphagia

Answer 103

myasthenia gravis-weak pharyngeal contraction

Question 104

signs of oropharyngeal dysphagia

Answer 104

• 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.

Question 105

causes of oropharyngeal dysphagia

Answer 105

• 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

Question 106

oesophageal dysphagia

Answer 106

• Oesophageal dysphagia is difficulty passing food down the oesophagus.
• It results from either a motility disorder or a mechanical obstruction

Question 107

treatment for dysphagia

Answer 107

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.

Question 108

managment of dysphagia

Answer 108

• 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

Question 109

dysphagia after stroke

Answer 109

• 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

Question 110

psychological impacts on patients

Answer 110

•Health anxiety and worry
•Concern leading to vulnerability
•Depression
•Frustration
•Embarrassment
Choking-fear-stress and fear death-food avoidance-malnutrition.

Question 111

assessment of dysphagia in stroke

Answer 111

•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

Question 112

enteral nutrition

Answer 112

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

Question 113

problems in dysphagia

Answer 113

• 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.

Question 114

achalasia

Answer 114

the failure of a ring of muscle fibres, such as the lower oesophageal sphincter (LOS), to relax

Question 115

pathophysiology of achalasia

Answer 115

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.

Question 116

mechanism of achalasia

Answer 116

 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

Question 117

aetiology of achalasia

Answer 117

 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)

Question 118

prevalence of achalasia

Answer 118

 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

Question 119

clinical presentation of achalasia

Answer 119

 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

Question 120

diagnosis of achalasia

Answer 120

 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”).

Question 121

manometry use to diagnose achalasia

Answer 121

 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.

Question 122

treatment of achalasia

Answer 122

 No treatment can restore muscular activity to the denervated oesophagus in achalasia
botulinum toxin, pneumatic dilation, hellers myotomy

Question 123

botulinum toxin

Answer 123

 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.

Question 124

pneumatic dilation

Answer 124

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

Question 125

hellers myotomy

Answer 125

 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

Question 126

assessing responce to treatment

Answer 126

 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.

Question 127

summary of achalasia

Answer 127

 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

Question 128

aspiration

Answer 128

the passing of any foreign substance, such as saliva or gastric content, through the vocal cords and entering the respiratory tract

Question 129

penetration

Answer 129

refers to the presence of foreign substances above the vocal cords (they haven’t managed to pass through the vocal cords).

Question 130

aspiration pneumonia

Answer 130

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.

Question 131

consequences of aspiration

Answer 131

 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

Question 132

clinical signs

Answer 132

	Fever
	Tachycardia
	Tachypnoea
	Hypoxia
	Coarse crackles right base lung
	Decreased percussion right base lung

Question 133

patient journey of a stroke

Answer 133

• 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.

Question 134

neuroregeneration

Answer 134

•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

Question 135

endogenous repair mechanisms

Answer 135

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.

Question 136

neuroplasticity/neurogenesis

Answer 136

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.

Question 137

neurogenesis in the subgranular zone of dentate gyrus

Answer 137

 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

Question 138

neurogenesis in the subventricular zone

Answer 138

 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.

Question 139

angiogenesis

Answer 139

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

Question 140

inflamation

Answer 140

• 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

Question 141

glial scarring-neurotoxic

Answer 141

• 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

Question 142

neuroprotective

Answer 142

• 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

Question 143

Ongoing Stroke Management and Rehabilitation

Answer 143

• 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.

Question 144

Current Guidelines for Rehabilitation

Answer 144

• 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

Question 145

Management of a Dysphagic Patient

Answer 145

• 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

Question 146

mortality rates

Answer 146

• 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.

Question 147

morbidity rates

Answer 147

• 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’

Question 148

Measures of Functioning

Answer 148

• 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.

Question 149

sunjective health status

Answer 149

• 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?

Question 150

quality of life

Answer 150

 ‘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’

Question 151

measures of quality of life

Answer 151

[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.

Question 152

unidimensional measures of quality of life

Answer 152

 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

Question 153

Multiidimensional measures of quality of life

Answer 153

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

Question 154

individual quality of life measures

Answer 154

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

Question 155

self regulatiry model of illness cognition

Answer 155

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

Question 156

principles of ethics

Answer 156

1. Autonomy
2. Beneficence
3. Non-maleficence
4. Justice
    Futility – interventions that are unlikely to produce any significant benefit for the patient.
   Acts and omissions – killing and letting die.
   Double effect – if doing something morally good has a bad side-effect it’s ethically Ok to do it providing the bad side-effect wasn’t intended.
   Basic care and medical treatment
   Ordinary and extraordinary treatment