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Medicine Sem 4 > Case 1 > Flashcards

Case 1 Flashcards

1
Q

What layers does the GI tract include?

A
  • serosa or adventitia (visceral peritoneum)
  • muscularis propria (externa): (lets peristalsis happen)
  • longitudinal smooth muscle
  • (Auerbach’s (myenteric) plexus)
  • circular smooth muscle
  • submucosa (meisnner’s (submucosal) plexus)
  • mucosa:
  • muscularis mucosa
  • lamina propria
  • epithelium
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2
Q

what is the enteric nervous system?

A

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

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3
Q

what is the ENS involved in? what does it work dependently or independently with?

A

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).

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4
Q

what is the ENS composed of? where is this situated?

A
  1. A submucosal plexus/ Meissner’s plexus that lies in the submucosa
  2. A myenteric plexus lying between the longitudinal and circular muscle layers
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5
Q

what does the Meissner’s plexus control?

A

mainly gastrointestinal secretion and local blood flow

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6
Q

what does the myenteric plexus control?

A

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.
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7
Q

what neurones does the ENS consist of and what do these do?

A

The enteric nervous system includes 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.

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8
Q

what are the two types of movements that occur in the GI tract?

A
  1. Propulsive movements

2. Mixing movements

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9
Q

peristalsis - what can stimulation at any point in the gut cause?

A

a contractile ring to appear in the circular muscle, and this ring then spreads along the gut tube.

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10
Q

what is the usual stimulus that causes a contractile ring to appear? (peristalsis) what does this stimulus cause?

A

distention of the gut

That is, if a large amount of food collects at any point in the gut, the stretching of the gut wall stimulates the enteric nervous system to contract the gut wall behind this point, and a contractile ring appears that initiates a peristaltic movement.

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11
Q

what else is a stimuli for peristalsis?

A
  • Other stimuli that can initiate peristalsis include irritation of the epithelial lining in the gut.
  • Also, strong parasympathetic nervous signals to the gut will elicit strong peristalsis.
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12
Q

what does peristalsis require?

A

an active myenteric plexus

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13
Q

describe the movement of peristalsis, what actually happens?

A
  • The contractile ring causing the peristalsis normally begins on the orad side of the distended segment and moves toward the distended segment, pushing the intestinal contents in the anal direction for 5-10cm before dying out.
  • At the same time, the gut sometimes relaxes several centimetres downstream toward the anus, which is called “receptive relaxation,” thus allowing the food to be propelled more easily toward the anus than toward the mouth.
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14
Q

what are the different stages of swallowing?

A
  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
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15
Q

what is the cephalic stage?

A

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

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16
Q

what is the oral stage?

A
  1. Chewing (mastication)
  2. Salivation – lubricate the bolus and begin the process of digestion
  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.
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17
Q

mastication

  • what is this
  • what does it do
  • how does this happen
  • what muscles are involved - what innervation
  • what causes chewing
  • what happens to the food
A

• Mastication/ Chewing – this is the process by which food is crushed and ground by teeth.
 It is the first step of digestion.
• Mastication increases the surface area of foods to allow more efficient break down by enzymes.
• During the mastication process, the food is positioned by the cheek and the tongue between the teeth for grinding.
• There are 4 muscles of mastication: masseter, temporalis, lateral pterygoid, medial pterygoid.
 These are innervated by the mandibular branch (V3) of Trigeminal Nerve.

• 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.
• These muscles move the jaws to bring the teeth into intermittent contact, repeatedly occluding and opening.
• As mastication continues, the food is made softer and warmer, and the process of salivation begins.

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18
Q

what is the chewing reflex?

A
  • The presence of bolus of food in the mouth initiates reflex inhibition of the muscles of mastication, which allows the lower jaw to drop.
  • The drop in turn initiates a stretch reflex of the jaw muscles that leads to rebound contraction.
  • This causes raising of the jaw to cause closure of the teeth, but it also compresses the bolus again against the linings of the mouth, which inhibits the jaw muscles once again, allowing the jaw to drop and rebound another time.
  • This leads to the physical break down of food, which is important for the digestion of many carbohydrates (fruits and raw vegetables because these have indigestible cellulose membranes, that must be broken before the food can be digested.
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19
Q

what happens when the bolus of food enters the posterior mouth and pharynx?

A
  • 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
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20
Q

what are the pharyngeal muscle contractions that take place?

A

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.

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.

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.

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.

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21
Q

in summary what happens in the pharyngeal stage? how long does the process last?

A

 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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22
Q

what does the upper oesophageal sphincter consist of?

A

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

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23
Q

what is the innervation of the UES?

A

UES innervation is the vagus nerve, whereas the innervation to the musculature acting on the UES to facilitate its opening during swallowing comes from the fifth, seventh, and twelfth cranial nerves.

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24
Q

what is the UES like at rest? what causes this?

A

The UES remains closed at rest owing to both its inherent elastic properties and neurogenically mediated contraction of the cricopharyngeus muscle.

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25
Q

what does it take for the UES to open?

A

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.

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26
Q

what is at the centre of the swallowing system?

A

Brainstem Central Programme Generator (CPG)

central pattern generator for peristalsis

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27
Q

where is the CPG? and where does it extend? what else is involved?

A
  • 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.
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28
Q

how is the cortex involved in swallowing?

A
  • The cortex communicates with the brainstem salivatory nuclei.
  • These send signals via motor neurons to the muscles of swallowing.
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29
Q

how many muscles are required in the entire swallowing process?

A

26 pairs

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30
Q

what receptors are involved in the swallowing process? what do they do? what are the most powerful inducers of a swallow?

A

• 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.

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31
Q

is swallowing a reflex?

A

no it’s a patterned response

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32
Q

what afferents are involved in the swallowing response?

A

• 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.

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33
Q

how are breathing and swallowing linked?

A
  • 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.
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34
Q

what types of peristaltic movements does the oesophagus exhibit?

A
  1. Primary peristalsis

2. Secondary peristalsis

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35
Q

what is primary peristalsis?

A

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.

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36
Q

what is secondary peristalsis? when is it used? what are they initiated by?

A
  • 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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37
Q

what type of muscle is the pharyngeal wall?

A

striated muscle

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38
Q

what type of muscle is the oesophagus?

A

upper 1/3 = striated muscle

lower 2/3 = smooth muscle

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39
Q

what are peristaltic waves in the pharyngeal wall and upper 1/3 of oesophagus controlled by?

A

skeletal nerve impulses from the glossopharyngeal and vagus nerves from the nucleus ambiguus.

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40
Q

what is the muscle of the lower 2/3 of oesophagus controlled by?

A

by the vagus nerves acting through connections with the oesophageal myenteric nervous system.

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41
Q

what are the two high pressure zones of the oesophagus?

A

 The UES - pressure can reach up to 100mmHg

 The LES - pressure is around about 20mmHg (can be higher in pathological conditions)

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42
Q

what is the pressure of the inside of the oesophagus? why is this important? what causes this pressure?

A

• 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.

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43
Q

what is the pressure in the stomach? what is important about this pressure?

A

• 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.

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44
Q

what is receptive relaxation of the stomach during oesophageal peristalsis?

A
  • 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.
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45
Q

what is the LES/gastroesophageal sphincter normally like/pressure?

A

It normally remains tonically constricted with an intraluminal pressure in the oesophagus of 30mmHg.

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46
Q

what happens to the LES when a peristaltic swallowing wave passes down the oesophagus?

A

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.

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47
Q

what is achalasia?

A

dysfunction of the LSE

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48
Q

what are stomach secretions like? how is the oesophagus affected by these secretions or not?

A
  • The stomach secretions are highly acidic and contain many proteolytic enzymes.
  • The esophageal mucosa, except in the lower one eighth of the esophagus, is not capable of resisting for long the digestive action of gastric secretions.
  • 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.
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49
Q

which neurotransmitters cause constriction and relaxation of the muscles involved with sphincters and muscles involved in peristalsis?

A
  • Acetylcholine causes constriction of muscles that will close sphincters and also those muscles that aid peristalsis.
  • Nitric oxide causes relaxation of these muscles.
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50
Q

what are the 4 protective mechanisms to prevent oesophageal injury from the reflux of gastric acid?

A

Anti-reflux barrier:

  • involves LES and diaphragm
  • limits frequency of reflux

Oesophageal clearance:

  • involves gravity and peristalsis
  • limit duration of acid contact

Acid neutralisation:

  • involves saliva (HCO3) and HCO3 (secreted and blood)
  • limit duration of acid contact

Tissue resistance:

  • cell junctions + membranes, Na/H exchange, epithelial restitution, blood flow
  • protect epithelium during acid contact
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51
Q

throughout the alimentary tract, the secretory glands have two functions?

A
  1. Secretion of Digestive enzymes

2. Secretion of Mucus - provides lubrication and protection to alimentary tract

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52
Q

what are digestive secretions dependent on?

A
  • 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.
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53
Q

what are the different types of glands? whre are each found? what do each produce?

A

• 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.
• 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.
• Tubular Glands
 These are found in the stomach and the upper duodenum.
 These secrete substances such as acid and pepsinogen in the stomach.
• Salivary Glands/ Liver/ Pancreas
 These provide secretions for digestion or emulsion of food.

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54
Q

what is the effect of contact of food with the epithelium in the GI tract?

A
  • 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.

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55
Q

what does stimulation of parasympathetic nerves innervating the glands in the GI tract cause? where is this particularly true?

A

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.

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56
Q

what do some glands in the distal large intestine increase secretions in response to?

A

• 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.

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57
Q

what does the remainder of the GI tract secrete secretion as a result of?

A

due to local neural and hormonal stimuli in those particular segments of the tract.

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58
Q

what is the effect of stimulation of sympathetic nerves innervating the glands in the GI tract?

A

• 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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59
Q

hormonal regulation of secretion of glands

  • what does it regulate
  • where particularly important
  • where liberated and response in to what
  • what happens to the hormones
  • what secretion particularly important for
A
  • 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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60
Q

what are the two things that secretory glands secrete mainly?

A
  1. Organic substances (enzymes etc).

2. Water and electrolytes.

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61
Q

describe the process of organic substance secretion

- how are the substances formed inside and cell and how is it released

A
  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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62
Q

describe the process of water and electrolyte secretion

A
  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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63
Q

what is mucus? what composed of?

A

• Mucus is a 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)

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64
Q

what are the functions of mucus?

A

 Lubrication of the GI tract

 Protection of the GI tract

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65
Q

desribe and explain what mucus does - its properties

A
  • 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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66
Q

where is saliva secreted from? and what type of secretion does each secrete?

A

 Parotid glands – serous secretion only (mainly serous acinar cells)
 Submandibular glands – serous and mucus secretion
 Sublingual glands – serous and mucus secretion (mainly mucus acinar cells)
 Buccal glands – mucus secretion only

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67
Q

what is the amount of daily secretion of saliva?

A

800-1500ml (average = 1000ml).

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68
Q

saliva contains two major types of protein secretions - what are these? what do they contain?

A
  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.
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69
Q

what is the pH of saliva? why?

A

between 6.0-7.0 (a favourable range for the digestive action of ptyalin).

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70
Q

what ions does saliva contain?

A
  • 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
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71
Q

what do salivary glands contain?

A

acini and salivary ducts.

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72
Q

salivary secretion is a two stage process - what is the first stage?

A
  1. Acini – “primary secretion”
     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.
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73
Q

what is the second stage of salivary secretion?

A

 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.

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74
Q

summarise the salivary duct stage of secretion

A

 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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75
Q

What transporters are present in acinar cells? what do each do?

A

Na+, K+-ATPase (P-type pump):

  • maintains concentration gradients for Na+ and K+
  • small direct contribution to membrane potential

Na+, K+, 2Cl- cotransporter:

  • electrically neutral
  • uses inward gradient for Na+ to drive Cl- up its gradient - secondary active transport

K+ channels:
- recycles K+ and maintains membrane potential

Ca2+ activated Cl- channel:
- allows Cl- efflux down its electrochemical gradient

Aquaporin 5 wager channel:
- allows H2O efflux driven by a small osmotic gradient

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76
Q

what is the concentration of ions in resting salivation compared to that of plasma? |

A
  • 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.
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77
Q

what happens to different concentrations of ions during maximal salivation? why?

A
  • 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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78
Q

describe the function of saliva for oral hygiene - what exactly in saliva does this?

A

• 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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79
Q

how are salivary glands controlled? what stimulates this?

A

• 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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80
Q

what happens to saliva when there is parasympathetic stimulation? what nerves? what nuclei? what receptors?

A

 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.

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81
Q

what causes the changes that parasympathetic innervation brings about?

A

 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. (has an effect on chloride ion channel in apical membrane and potassium ion channel in basolateral membrane)

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82
Q

what happens to saliva when there is sympathetic stimulation? what nerves? what ganglion? what receptors?

A

 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).

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83
Q

does sympathetic stimulation increase salivation?

A

a slight amount, much less so than parasympathetic stimulation.

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84
Q

what does salivation also occur in response to? what does saliva do once swallowed?

A
  • 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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85
Q

does blood supply to the glands affect saliva production? why? what causes changes in blood supply?

A

• 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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86
Q

what are oesophageal secretions like in character? and what do they do?

A

entirely mucous in character and principally provide lubrication for swallowing.

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87
Q

what glands is the oesophagus lined with at different parts? why different in different parts? ?

A

• The main body of the oesophagus is lined with many simple mucous glands.
• At the gastric end and to a lesser extent in the initial portion of the oesophagus, there are also many 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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88
Q

what is dysphagia? what can it affect if severe?

A

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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89
Q

epidemiology of dysphagia - age

A

 16-22% over 50 years old

 55% over 70 years old

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90
Q

what are the complications of dysphagia?

A 
	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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91
Q

what are the signs and symptoms of dysphagia?

A

 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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92
Q

what are the two types of dysphagia based on cause?

A
  • 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.
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93
Q

what are the two types of dysphagia based on position?

A

• Dysphagia is classified into two types:

1) Oropharyngeal Dysphagia
2) Oesophageal Dysphagia

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94
Q

what is oropharyngeal dysphagia? what does it result in?

A

difficulty emptying material from the oropharynx into the oesophagus.

• 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.

  • Abnormal bolus transfer to the oesophagus
  • Difficulty initiating a swallow
  • Only one manifestation of the primary disease (e.g. stroke)
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95
Q

what are causes of oropharyngeal dysphagia?

A

Anatomic e.g. Zenker’s diverticulum: decreased compliance of cricopharyngeus

Neurologic e.g. stroke: weak pharyngeal contraction, incoordination of UES and pharyngeal contraction

Muscular e.g. myasthenia gravis: weak pharyngeal contraction

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96
Q

what are 1/3 of oropharyngeal dysphagia cases a result of? how does positioning and size of lesion affect the resulting dysphagia?

A

• 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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97
Q

what is oesophageal dysphagia? what does it result from?

A
  • Oesophageal dysphagia is difficulty passing food down the oesophagus.
  • It results from either a motility disorder or a mechanical obstruction.
  • Abnormal bolus transport through the oesophagus
  • Food stops after initiation of swallow
  • Oesophagus is location of the primary disease (e.g. achalasia – LES fails to open during swallowing, which leads to a backup of food within your oesophagus)
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98
Q

what are the different treatments for dysphagia? depending on type and does dysphagia improve after stroke?

A

• Treatment of dysphagia depends on both the locus and the specific etiology.
• Oropharyngeal dysphagia most commonly results from functional deficits caused by neurologic disorders.
 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.
• Aspiration risk may be reduced by altering the consistency of ingested food and liquid.
• Dysphagia resulting from a stroke (in 50% of people) usually, but not always, 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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99
Q

what are interventions for dysphagia?

A
  • Postural modifications
  • Manoeuvres
  • Head postures
  • Biofeedback
  • Sensory stimulation – pharyngeal electrical stimulation
  • Combinations
  • Dietary modifications – viscosity matters
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100
Q

what is the management of dysphagia?

A
  • 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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101
Q

dysphagia and stroke

  • how common
  • how affect mortality
  • what is most common complication
  • recovery?
  • treatment options
A
  • 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).
102
Q

what is VFSE and FEES?

A

VFSE = video fluoroscopy swallowing exam

FEES = fiberoptic endoscopic examination swallowing - visualise any residues in the laryngeal inlet

103
Q

what is parenteral and enteral nutrition? which is prefered?

A

• 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.

104
Q

what are the different routes of feeding? and reasons for each?

A

 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.

105
Q

what are the problems in dysphagia? (what causes dysphagia?)

A
  • 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.
106
Q

what is achalasia?

A

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

107
Q

what is the pathophysiology of achalasia?

A

 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.

108
Q

what does the loss of inhibitory innervation in the LOS cause?

A

 The basal sphincter pressure to rise.
 Sphincter muscle incapable of normal relaxation.
 Oesophageal body smooth muscle aperistalsis.

109
Q

what is the aetiology of achalasia?

A

 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)

110
Q

epidemiology - sex, age, incidences

A

 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.

111
Q

what is the clinical presentation of dysphagia?

A

 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

112
Q

what is involved in the diagnosis of achalasia?

A
  • clinical history
  • endoscopy
  • radiology
  • manometry
113
Q

how can endoscopy help diagnose achalasia?

A

 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.

114
Q

how can radiology help diagnose achalasia? what reveals an absence of peristalsis?

A

 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.
- Fluoroscopy reveals the absence of peristalsis
 Purposeless, spastic contractions can be observed (“vigorous achalasia”).

115
Q

how can manometry help diagnose achalasia?

A

 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.

116
Q

what is treatment for achalasia?

A

 No treatment can restore muscular activity to the denervated oesophagus in achalasia.

 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.
- for people that are frail and old

 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.

 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.
- better if you’re younger - lasts longer

117
Q

what is most important in diagnosis of achalasia?

A

barium swallow and manometry

118
Q

what is aspiration?

A

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

119
Q

what is penetration?

A

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

120
Q

what is aspiration pneumonia?

A

results from inhalation of stomach contents or secretions of the oropharynx leading to lower respiratory tract infection.

121
Q

what can aspiration cause? what is the resultant pneumonia caused by? what are the most common sites of spillage?

A

 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.

  • 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.
122
Q

what are the clinical signs of aspiration pneumonia?

A 
	Fever
	Tachycardia
	Tachypnoea
	Hypoxia
	Coarse crackles right base lung
	Decreased percussion right base lung
123
Q

what are measures of functioning generally called?

A

activity-of-daily-living scales (ADLs)

124
Q

what is the conceptual framework of measures of quality of life?

A

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.

125
Q

what are unidimensional meaures?

A

 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

126
Q

what are multidimensional measures of quality of life?

A

 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.

127
Q

what are individual quality of life measures?

A

 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.
 Examples:
 Schedule for Evaluating Individual Quality of Life (SEIQoL)
o This 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.

128
Q

what is the self-regulatory model of illness cognition?

A 
Stage 1: interpretation 
-	Symptom perception 
-	Social messages – deviation from norm 
Stage 2: coping 
-	Approach coping 
-	Avoidance coping 
Stage 3: appraisal 
-	Was my coping strategy effective?
Representation of health threat:
-	Identity 
-	Cause 
-	Consequences 
-	Time line 
-	Cure/control 
Emotional response to health threat:
-	Fear
-	Anxiety 
-	Depression
129
Q

what is the doctrine of double effect?

A

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.

‘it’s morally indefensible to intend to harm an innocent person, but it is morally defensible to perform actions with good intended consequences, where harm is a foreseen but unintended consequence’

130
Q

what are examples of red flags?

A
  • Loss of appetite
  • Weight loss
  • Night sweats
  • Fatigue
  • Lumps and bumps
  • Bleeding
131
Q

what are different types of bias with diagnosing?

A

Anchoring bias = locking onto a diagnosis too early and failing to adjust to new information
Availability bias = thinking that a similar recent presentation is happening in the present situation
Confirmation bias = looking for evidence to support a pre-conceived opinion, rather than looking for information to prove oneself wrong
Diagnosis momentum = accepting a previous diagnosis without sufficient scepticism

132
Q

which types of induced deaths are legal?

A
  • voluntary passive euthanasia

- non-volutnary passive euthanasia may be legal

133
Q

what is manslaughter gross negligence?

A

A failure to meet the appropriate standard of care, resulting in death, through action (or omission) sufficiently negligent to amount to a crime

134
Q

what is CANH?

A

clinically-assisted nutrition and hydration

135
Q

what are the guidelines for withdrawing treatment?

A
  • You can withdraw any treatment which is no longer in a patient’s best interest (or of ‘overall benefit’)
  • Clinically assisted nutrition or hydration is no different
  • Basic care does not stop just because you withdraw clinically assisted nutrition
136
Q

what is the oral cavity lined by?

A

Lined by oral mucosa, a thick stratified squamous epithelium that is resistant to abrasion

137
Q

what does the oral cavity produce? what does this do?

A

Produces defensins to inhibit bacterial growth

138
Q

what are the adult teeth?

A
  • Incisors (2I) = slice and cut
  • Canines (1C) = tear and rip
  • Premolars (2PM) = grind and crush
  • Molars (3M) = grind and crush (mostly grind)
139
Q

how many permanent teeth?

A

32

140
Q

what does saliva consist of? what does each component do?

A
  • 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
  • Lysozyme
  • Immunoglobulins (esp. IgA)
  • Electrolytes
  • Calcium and phosphate (dental repair)
141
Q

describe the control of salivation

A
  • Saliva is secreted continuously, but salivation is controlled by salivatory nuclei in the medulla and pons of the brainstem
  • Mechanoreceptors and chemoreceptors in the mouth stimulate production of saliva with a high-water content – mechanoreceptors are not food specific (non-food objects induce salivation) – but in response to food being present in your mouth, you produce a more enzyme-rich saliva
  • Input from higher brain centres (thinking about food) and lower digestive tract (irritation) can also induce salivation
142
Q

what runs in the mesentery?

A

nerves, arteries and veins

143
Q

what can you see between longitudinal muscle coat and circular muscle coat?

A

nerve cell bodies

144
Q

who are particularly suscpetible to damage to gut brain?

A

people with diabetes

145
Q

what are the pacemaker cells in the gut?

A

interstitial cells of Cajal

146
Q

msuscularis externa:

  • what does it consist of
  • what is the function of each part
  • what sets activity and what modulates this activity
A
  • With the exception of some parts of the stomach (3 layers) consists of inner circular and outer longitudinal layers
  • 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 Cajal have ‘pacemaker’ activity
  • Enteric neurones or extrinsic neurones modulate this basic activity
147
Q

what can loss of the cells of Cajal lead to?

A

gut motor dysfunction disorders

148
Q

how long is the oesophagus?

A

25cm

149
Q

what state is the oesophagus normally in?

A

Normally closed – highly folded mucosa

150
Q

oesophagus:

  • what does the submucosa contain
  • what is it lined by and why
  • describe the muscularis layer
  • describe the outer layer - what attached to
A
  • Submucosa contains blood vessels, lymphatics, nerves, lymphoid tissue and mucus glands
  • Lined by stratified squamous epithelium to resist abrasion
  • Muscularis layer: 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
151
Q

what is the histology of the gastroesophageal junction?

A

Lining changes from squamous to columnar epithelium (glandular)

152
Q

what is Barrett’s oesophagus?

A

Metaplasia: Barrett’s oesophagus – change of epithelium from stratified squamous to gastric due to repeated damage from gastric reflux – oesophagus starts to take on a stomach like appearance, but not very organised -> more likely to go to develop oesophageal cancer

153
Q

where does peristalsis take place in the stomach?

A

confined to the lower part

154
Q

what is the rate of gastric emptying? why? what is the rate controlled by?

A
  • The action of peristalsis and the pyloric valve result in vigorous churning of contents and relatively slow gastric emptying
  • The rate of gastric emptying is controlled to some extend by the caloric value of the contents of the duodenum
155
Q

what’s the lining of the stomach like?

A

Thick mucosal and submucosal layers form numerous longitudinal folds (rugae)

156
Q

what happens in the small intestine after a meal?

A

there are small irregular contractions

157
Q

what happens in the small intestine in the inter-digestive state?

A
  • In the inter-digestive state, 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)

MMC = distinct pattern of electromechanical activity observed in gastrointestinal smooth muscle during the periods between meals - it is thought to serve a ‘housekeeping’ role and sweep residual undigested material through the digestive tube

158
Q

what are the signals to stop this interdigestive activity?

A

The signal to stop this interdigestive (not much digestion) activity is ingestion of food, and this can be mimicked by gastrin and by cholecystokinin (CCK), which are released from the stomach and intestine, respectively

159
Q

what is CCK? what’s it released in response to?

A

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 (CCK released in response to chyme hitting the duodenum) – digests what it already has and make sure the stomach doesn’t release too much for it to handle

160
Q

when is the colon active?

A
  • Active almost continuously, although increased activity can be elicited by particular stimuli
161
Q

what is transit time in the colon?

A

2-3 days

162
Q

what is the major component in terms of transit time in colon?

A
  • Transverse colon is the major component in terms of transit time (dehydration, storage)
163
Q

what do contraction of the circular muscle in the colon cause?

A

haustra (not like peristalsis)

  • As one haustrum fills and distends this induces contractions that push food into the next
164
Q

what is the gastrocolic reflex?

A

Powerful propulsive contractions (of the colon) can be elicited by the introduction of food to the stomach (gastrocolic reflex) – if you put food in, some food has to be eliminated

165
Q

what is long loop reflex activity?

A
  • For good reason, food entering the upper end of the gut must to some extent displace faeces at the lower end
  • Such effects are mediated by reflexes that must (for geographic reasons) be long loop
166
Q

what is the physiology of the stomach? what absorbed here?

A
  • Mixes food
  • Acts as a reservoir
  • Starts digestion (protein, nucleic acids)
  • Activates some enzymes (pH 1-2)
  • Destroys some bacteria
  • Synthesises intrinsic factor (B12 absorption) – the only truly ‘essential’ function of the stomach
  • Absorbs:
  • alcohol (although most is absorbed in the SI)
  • some water
  • some vitamin B12
167
Q

what cells are lining the stomach at different parts?

A
  • Mainly mucous cells – top part – cardia (sphincter – more of a kink)
  • All cell types – main part – body of stomach
  • Mucous cells & enteroendocrine, cells producing gastrin, tightly coiled – end part – pylorus (pyloric sphincter – true sphincter)
168
Q

what is intrinsic factor?

A

substance secreted by the stomach which enables the body to absorb vitamin B12 – it’s a glycoprotein

169
Q

what are gastric secretions? - exocrine and endocrine

A

Exocrine:

  • Hydrochloric acid
  • Mucus
  • Pepsinogen
  • Intrinsic factor

Endocrine:

  • Gastrin
  • Somatostatin
170
Q

what cells are in the stomach?

A
  • goblet cells
  • mucous cells
  • parietal cells
  • chief cells
  • G cells
  • D cells
171
Q

what do goblet cells secrete?

A

an alkaline mucus

172
Q

what do mucous cells secrete?

A

mucus and pepsinogens

173
Q

what do parietal cells secrete?

A

gastric acid and intrinsic factor

174
Q

what do chief cells secrete?

A

pepsin and gastric lipase

175
Q

what do G cells secrete?

A

gastrin

176
Q

what do D cells secrete? where found?

A

somatostatin - antrum

177
Q

what does HCl do in the stomach?

A

acidifies lumen, produces pepsin from pepsinogen, kills bacteria

178
Q

what does mucus do in the stomach?

A

protects mucosal surface being damaged by HCl (protect from autodigestion)

179
Q

what does pepsinogen do?

A

precursor of pepsin (which acts as an endopeptidase)

180
Q

what does intrinsic factor do?

A

important in the absorption of vitamin B12 (later, in the terminal ileum) and erythropoiesis

181
Q

what does gastrin do in the stomach? what stimulates it?

A
  • stimulated by distention of stomach
  • relax cardia
  • increase antral activity
  • increase gastric acid secretion
182
Q

what does somatostatin do?

A

inhibits release of gastrin

183
Q

what controls pepsinogen secretion in stomach?

A

Acetylcholine (i.e. vagal input)

184
Q

what controls HCl secretion in stomach?

A
  • Acetylcholine (i.e. vagal input)
  • Gastrin (from G cells)
  • Histamine (from enterochromaffin cells)
  • Other hormones
185
Q

what inhibits gastric acid secretion? and how?

A
  • Somatostatin (via decreased gastrin release)
  • Secretin (via decreased gastrin secretion)
  • Gastric inhibitory peptide and other enterogastrones (directly on parietal cells)
186
Q

what is gastric acid composed of?

A

HCl, KCl and NaCl

187
Q

what are the phases of gastric secretion?

A
  • cephalic
  • gastric
  • intestinal
188
Q

describe the cephalic phase of gastric secretion

  • what stimulus for what
  • how much of gastric acid secretion occurs in this phase?
A
  • Thought, smell, sight, taste of food releases ACh, stimulating the parietal cells and also the G cells
  • Vagally mediated, about 40% of gastric acid secretion occurs here
189
Q

describe the gastric phase of gastric secretion

  • what stimulus for what
  • how much of gastric acid secretion occurs in this phase?
A
  • Distention and reflex activation of enteric neurones and vagal outflow 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
190
Q

describe the intestinal phase of gastric secretion

  • what stimulus for what
  • how much of gastric acid secretion occurs in this phase?
A

(essentially a mopping up phase – if duodenum senses a lot of amino acids – get a bit more gastric acid secretion)

  • Amino acids present in the bloodstream (products of protein digestion) directly stimulate the parietal cells
  • About 10% of gastric acid secretion occurs here
191
Q

what are the two mechanisms for inhibition of gastric secretion?

A

Gastric mechanism:

  • If proteins are present in the stomach, they act as buffers to keep luminal pH > 3
  • As the stomach empties, therefore, the luminal pH falls below 3: D cells release somatostatin to inhibit gastrin release and thereby reduce acid secretion

Duodenal mechanism:

  • Acidification of the duodenal lumen releases secretin, which inhibits gastrin secretion
  • Acidification of the duodenal lumen and the presence of fatty acids and salt in the duodenum release gastric inhibitory peptide, which acts directly on parietal cells to inhibit HCl secretion
192
Q

where is motilin produced? what does it do?

A

duodenum

  • increase gastric acid secretion
  • increase stomach activity
193
Q

where is gastric inhibitory peptide produced? what does it do?

A

small intestine

- decrease gastric acid secretion

194
Q

where is CCK produced? what does it do?

A

small intestine

  • relax stomach
  • contract gallbladder
  • increase pancreatic secretion
195
Q

where is secretin produced? what does it do?

A

small intestine

  • relax stomach
  • increase HCO3- secretion by pancreas
196
Q

where is vasoactive intestinal peptide (VIP) produced? what does it do?

A

glands and nerves
- increase intestinal electrolyte secretion
(- decrease gastric acid secretion)

197
Q

why is plasma membrane impermeable to ions and polar molecules?

A

due to hydrophobic tails

198
Q

what are the three main categories of membrane transport proteins?

A
  • channels – passive transport – driven by gradients
  • carriers – passive transport – driven by gradients
  • pumps – active transport – ATP hydrolysis (ATPases) – against concentration gradient

gas – oxygen, CO2 – can freely diffuse (simple diffusion = passive transport), most other things need transporters

199
Q

describe transport for regulation of following:

  • gradient maintenance
  • acid extrusion
  • base extrusion
  • regulatory volume increase
  • regulatory volume decrease
A
  • Gradient maintenance – K+/Na+ pump mainly – K+ in, Na+ out
  • Acid extrusion – H+ out, Na+ in
  • Base extrusion – HCO3- out, Cl- in
  • Regulatory volume increase – Na+, K+, Cl- in
  • Regulatory volume decrease – Cl-, K+ out
200
Q

sodium pump

  • what is it
  • where expressed
  • what does it do
A
  • Na+, K+ -ATPase (the sodium pump) – expressed in virtually all cell types
  • Uses energy from ATP hydrolysis
  • Transports 3Na+ out for every 2K+ in
  • Creates and maintains electrochemical gradients:
  • K+ gradient generates the membrane potential (approx. -60mV)
  • Na+ gradient drives other passive transporters – secondary active transport
201
Q

ions channels

  • what is ion flow driven by
  • what may be gated by
A
  • Ion flow is driven by concentration gradient and membrane potential: electrochemical gradient – passive transport
  • May be gated by intracellular or extracellular messengers, or by membrane potential changes (voltage-gated)
202
Q

the action of which ions channels underpins action potentials?

A
  • Voltage-gated Na+ channels open – Na+ enters cell

- Voltage-gated K+ channels open – K+ leaves cell

203
Q

what is terminology for transporters?

A
  • Facilitated diffusion (uniport)
  • Cotransport (symport)
  • Countertransport (exchange) (antiport)

FACILITATED DIFFUSION

  • Highly selective carrier protein in the membrane
  • Substrate has to bind so different to a channel
  • Transport is passive
204
Q

what does SLC stand for? what is it? give examples.

A

SOLUTE CARRIER (SLC) FAMILIES

  • 52 families, 395 members (excludes channels & pumps)
  • SLC1, SLC2 etc.
  • SLC1 = high-affinity glutamate and neutral amino acid transporter
  • SLC2 = facilitative GLUT transporter
205
Q

what are the glucose transporters? how is each different?

A

GLUT1, GLUT2, GLUT3, GLUT4, GLUT5

  • Different transports will be expressed in different cell types
  • They have different affinities and specificities for glucose
  • GLUT2 – liver and intestine (basolateral membrane of intestinal cells) (transport glucose and fructose)
  • GLUT4 – adipocytes, muscle (insulin-sensitive glucose transporter)
206
Q

what is the alternating access model?

A
  • Ligand-bound occluded
  • Inward open
  • Outward open
  • Ligand-free occluded
207
Q

give example of a symporter/cotransporter

- explain it

A
  • Na+, K+, Cl- cotransporter (symporter)
  • NKCC2 transporter
  • Inward movement of Na+ drives uptake of Cl- against its gradient
  • 2Cl- for every Na+ and K+
  • Uses Na+ gradient that’s been established by Na+/K+ ATPase to bring Na+ in by moving down its concentration gradient, which moves Cl- and K+ against their concentration gradients
208
Q

describe an antiporter/exchanger

- explain it

A
  • Na+/H+ exchanger (antiporter)

- Inward movement of Na+ drives extrusion of H+ against its gradient

209
Q

what kind of transport are the NKCC2 and Na+/H+ transporters an example of?

A

These both examples of secondary active transport – no ATP hydrolysis but they’re strictly passive as they’re using the previously established gradients that have required hydrolysis of ATP

210
Q

which SCL transporter mutation implicated in a human disease?

A

Polymorphism can be associated with human disease

- e.g. SLC22A4 – inflammatory bowel disease

211
Q

what are example of transporters as drug targets?

A

Omeprazole

  • proton pump inhibitor – decrease stomach acid secretion
  • H+ out, K+ in = pump

Lidocaine

  • Voltage-gated Na+ channel blocker
  • Block nerve impulse generation and propagation

Frusemide

  • Diuretic targeting NKCC2 transporter (and other SLC12 family transporters)
  • Decreases sodium reabsorption in the kidney
  • Increases urine production and decreases blood volume
212
Q

aquaporins

  • what are they
  • how selective to water
  • which one important in salivary secretion
A
  • Water channels
  • Pore is highly selective to water
  • Aquaporin 5 is important in salivary secretion
  • Water flow is driven by osmosis
213
Q

paracellular pathway

  • what are tight junctions like
  • what is permeability determined by
  • what is this dependent on
A
  • 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 proteins – they interact and form a pore
  • Tightness of junctions depends on the function of that epithelia – in transport epithelia, such as in the gut, there’s a degree of leakiness to those channels – they will allow ions and movement through
  • In epithelia where primary function is a barrier, such as skin, those junctions will be much tighter and much more impermeable
214
Q

how is glucose absorbed from lumen of intestine into blood?

A
  • Start with Na+/K+ ATPase generating gradients at basolateral membrane
  • NA+ and glucose uptake – SGLT transporter (sodium-dependent glucose cotransporters) – apical membrane – use sodium gradient to uptake glucose against gradient
  • Glucose exits by facilitated diffusion via GLUT2 in the basolateral membrane
215
Q

what is the percentage that each salivary gland contributes to salivary secretion when unstimulated and stimulated?

A

Unstimulated:

  • parotid = 25%
  • submandibular = 60%
  • sublingual = 7-8%
  • minor glands = 7-8%

Stimulated:

  • parotid = 50%
  • submandibular = 25%
  • sublingual = 7-8%
  • minor glands = 7-8%
216
Q

how dark are the cells fo the salivary glands?

A
  • parotid cells darker

- sublingual cells very pale - mucous doesn’t stain

217
Q

describe the inorganic components of saliva when stimulated and unstimulated

A 
When unstimulated:
-	Primary K+ 
-	Low levels of Na+, HCO3-, Cl- 
When stimulated:
-	Large increase in Na+ (particularly), HCO3- (important in making more alkaline), Cl- secretion 
-	Decrease in K+ secretion

Plasma also has high levels of Na+ and Cl-, but much lower levels of HCO3-

218
Q

first stage of salivary secretion

  • from where
  • what secreted
  • what result in (osmolarity)
A

Acinus:

  • Secretion of Na+, Cl- & HCO3 by active transport
  • High water permeability
  • Results in isotonic (same concentration of ions in fluid secretion as in intracellular, extracellular fluids), plasma-like primary secretion
219
Q

second stage of salivary secretion

  • from where
  • what secreted
  • what result in (osmolarity)
A

Duct:

  • Reabsorption of NaCl
  • Some secretion of K+ and HCO3-
  • Low water permeability – not reabsorbing water, therefore solution becomes more hypotonic
  • Results in hypotonic final saliva
220
Q

describe primary secretion by acinar cells (transporters)

A
  • Start with Na+/K+ ATPase – establishing ion gradient (basolateral)
  • NKCC1 transporter, transports K+ and Cl- into cell by secondary active transport, using Na+ gradient (basolateral)
  • K+ recycling through K+ channel – getting rid of build up of K+ (basolateral)
  • Cl- channel on apical membrane – allows transcellular transport of Cl
  • In lumen of acinar cell, generating a more negative potential
  • This draws Na+ through paracellular junctions into lumen
  • Aquaporins in basolateral and apical membranes – means water will move transcellularly
221
Q

give a summary of the transporter used in primary acinar secretion

A

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 coupled uptake of Cl-
  • Secondary active transport

K+ channels (BK & IK1)

  • Recycles K+
  • Maintains membrane potential

Ca2+-activated Cl- channel (TMEM16A)

  • Allows Cl- efflux down its electrochemical gradient
  • Small negative potential in lumen drives Na+ secretion via paracellular pathway

Aquaporin 5 water channel (AQP5)
- Allows H2O efflux driven by a small osmotic gradient

222
Q

how does parasympathetic nerve stimulation trigger salivatory secretion?

A

Action potentials -> ACh -> acts at receptor muscarinic M1 and M3 receptors (G-coupled protein receptors) -> coupled to phospholipase 3 -> increase in IP3 concentration -> Ca2+ release from endoplasmic reticulum -> calcium then goes and affects other ion channels, particularly Cl- and K+ channels -> more Cl- movement across apical membrane -> more Na+ movement -> more water movement -> increase in amount of fluid that we’re secreting

223
Q

describe the modification of primary saliva (transporters)

A
  • Isotonic primary saliva passes through duct (lumen)
  • Na+/K+ ATPase – basolateral membrane (blood)
  • Na+ channel – apical membrane – Na+ absorbed (ENaC)
  • Build-up of positive charge in blood
  • Draws Cl- from lumen through cell to blood – Cl- channel and Cl-/HCO3- exchanger
  • HCO3- comes from carbonic anhydrase breaking down CO2 + H2O -> HCO3- + H+
  • HCO3- through basolateral membrane and H+ through apical membrane
  • H+ leaves cell through basolateral membrane into blood, by H+/Na+ exchanger
  • Ductal cells relatively impermeable to water
  • Leads to hypotonic final saliva
  • Na+ enters the cell passively via ENaC (epithelial sodium channel) channels
  • Na+ leaves across the basolateral membrane via Na+, K+ -ATPase
  • Small positive potential on the blood side draws Cl- through the cell via Cl- channels
  • Cl- also taken up from saliva in exchange for HCO3- via apical Cl-/HCO3- exchangers (intracellular HCO3- is generated from CO2 and water by the enzyme carbonic anhydrase)
  • Basolateral Na+/H+ exchangers extrude H+
  • Low water permeability ensures little water reabsorption
224
Q

what do carriers include?

A

facilitators, exchangers and cotransporters

225
Q

describe the muscle, neutral control and voluntary control for all phases of swallow

A

oral:

  • striated muscle
  • cortex/medulla control
  • full voluntary control

pharyngeal:

  • striated muscle
  • medulla control
  • some voluntary control

oesophageal:

  • striated/smooth muscle
  • medulla/ENS control
  • no voluntary control
226
Q

preparation of bolus and initiation of swallowing occurs in oral phase - component, function and effectors?

A

chewing:

  • prepare solid food for transfer through pharynx
  • teeth, jaws, masseter muscles

salivation:

  • lubricate bolus and begin digestion
  • mucus, amylase, lipase, water, HCO3-

movement of bolus:

  • deliver prepared bolus to oropharynx
  • tongue
227
Q

how long does it take for the bolus to be transfered from mouth to the oesophagus?

A

1.2 seconds = very quick

228
Q

bolus transfer from the mouth to the oeosphagus requires multiple events - what are these?

A 
Bolus in mouth:
-	Tongue thrust up and back 
-	Then nasopharynx closed – stop regurgitation 
-	Then larynx elevated 
-	Then airway closed 
Bolus moves through pharynx and UES (upper oesophageal sphincter):
-	Larynx still elevated 
-	Airway still closed 
-	UES opens
-	Then pharynx contracts 
Bolus enters oesophagus:
-	Airway still closed but then opens 
-	Larynx still elevated but then descends
229
Q

what has a higher pressure the oesophagus or the stomach? what does this mean?

A

Stomach has a slightly higher pressure that the oesophagus (due to the diaphragmatic and abdominal muscles), therefore it is promoting slight reflux, which is why you need the sphincter

230
Q

how is the central pattern generator for oesophageal peristalsis initiated?

A

Two ways:
- Swallowing -> primary peristalsis
Or
- Distention -> secondary peristalsis
-reflux phenomenon – if you refluxate something from your stomach into your oesophagus, your oesophagus detects that due to some degree of distention
-produce clearance of solids and liquids from the oesophagus

231
Q

which are the afferent and efferent nerves that control swallowing?
- where nuclei

A
  • Swallowing centre (medulla) -> motor -> V, VII, IX, X, XII -> control of tongue, palate, pharynx and upper oesophagus
  • Sensory -> V, IX, X -> swallowing centre (medulla)
  • Nuclei in swallowing centre = nucleus solitarius, nucleus ambiguus, dorsal vagal nucleus
  • allow reflex to occur
  • also input from the brain
232
Q

how do efferent neural pathways differ in striated and smooth muscle regions of the oesophagus? why?

A
  • Nucleus ambiguus – predominantly the upper oesophagus
  • Dorsal motor nucleus – predominantly the lower oesophagus
  • much more mixed pathway because it uses both vagal and spinal pathways, where is nucleus ambiguus is entirely vagal
  • Control striated and non-striated muscle
  • They nuclei interact in the middle – important for coordination of sensation, motor, visceral and chemical sensitivity
    Vagus = 90% sensory, 10% motor
    Many parts of the brain are involved in control of swallowing – much more complicated than a pure reflux
233
Q

what are the causes of dysphagia?

A
  • Neurological – including diseases/injuries or abnormalities of the CNS, anterior horn cell, PNS and/or neuromuscular junction
  • Physical – related to head and neck impairments such as cancer and or surgery – e.g. glossectomy
  • Respiratory disease e.g. COPD
  • Psychological
    In both children and adults dysphagia can present as acute or chronic, and within these categories static or progressive in its presentation
    It’s frequently associated with the following disorders:
  • Stroke
  • Head/neck cancer
  • Acquired brain injury
  • Brain or CNS cancer
  • Respiratory conditions (including COPD or post-polio syndromes)
  • Following cervical spinal surgery
  • Progressive neurological diseases, including MS, PD and dementia
  • Developmental disorder (carried on into adulthood)

PREVALENCE OF NEUROGENIC DYSPHAGIA

  • Stroke – most common (in western world)
  • Neuro-degenerative disease
  • Motor neurone disease
  • Parkinson’s disease
  • Head injury
  • MS
  • Other
234
Q

what is videofluoroscopy (VFS) used for?

A
  • Used to investigate oropharyngeal dysphagia
  • Barium test
  • Looking for aspiration – into trachea
235
Q

what is FEES used for?

A

FIBEROPTIC ENDOSCOPIC EXAMINATION OF SWALLOWING

  • Visual the upper airway
  • Don’t have to give barium – quite difficult to swallow
236
Q

why do dysphagia stroke patients recover swallowing function?

A
  • Swallowing is a bilaterally innervated system
  • Initially after stroke, they don’t have enough activity on both sides to amount to a swallow
  • As they start to recover you said a big increase in activity in the undamaged side of the brain
  • Therefore, think recovery is due to compensation
237
Q

what does conventional manometry study? what does it measure?

A
  • Study oesophageal motility

- Measure pressure in the oesophagus as bolus as swallow

238
Q

what is the manometry that we use now? what does it involve?

A

HIGH RESOLUTION MANOMETRY

  • What we use now
  • More precise measurement of upper GI motility
  • Catheters with multiple sensory <2cm apart (24+ arrays) – many more points where pressure measured
  • Spatiotemporal or topographic (location) plot of pressure date
  • Evolutionary technology

SPATIOTEMPORAL (CLOUSE) PLOT
- Display method can improve accuracy and speed of recognition of motility disorders even in manometry-naïve individuals
HRM (high resolution manometry) demonstrates segmental character of oesophageal motor function

239
Q

what is the chicago classification of oesophageal motility disorders?

A

Achalasia or other obstruction (disorders with EGJ outflow obstruction)
No ->
Major motility disorder (of peristalsis)
No ->
Minor motility disorder (of peristalsis)
No ->
Normal

240
Q

what does achalasia mimic?

A

oesophageal cancer

241
Q

what is the clinical presentation of achalasia? how differentiate from oesophageal cancer?

A
  • Dysphagia solids
  • Dysphagia liquids
  • Weight loss
  • Difficulty belching (expelling air from the stomach through the mouth (i.e. burping)
  • Chest pain
  • Regurgitation
  • Heartburn
  • Aspiration

Oesophageal cancer – often describe dysphagia for solids first and dysphagia for liquids later – cancer, it’s an anatomical blockage
In motility disorders they describe the two together – occurring at the same time – functional disorder, peristalsis is failing

242
Q

what are the achalasia subtypes?

A
  • Type 1 – no pressure – aperistaltic
  • Type II – pan pressurisation – contractions all simultaneously and together
  • Type III – LES hasn’t relaxed
    Types tends to predict outcome from treatment
  • Type III does better and to some extent type I
243
Q

what can achalasia lead to?

A

oesophageal cancer

244
Q

how is the swallowing motor cortex organised?

A

bilaterally organised, but crucially displays inter-hemispheric asymmetry (may be while patients with unilateral stroke develop dysphagia)

245
Q

what is the health belief model?

A

Individual perceptions:
- Perceived susceptibility of seriousness of disease

Modifying factors:

  • Age, sex, ethnicity, personality, socio-economics, knowledge
  • Perceived threat of disease
  • Cues to action: education, symptoms, media information

Likelihood of action:

  • Perceived benefits vs. barriers to behavioural change
  • Likelihood of behavioural change
246
Q

what are the muscles of mastication? innervation? action of each?

A
  • Temporalis, lateral pterygoid, medial pterygoid, masseter
  • Trigeminal nerve
  • Masseter – elevates mandible, closing the mouth
  • Temporalis – elevates mandible, closing the mouth – retracts the mandible, pulling the jaw posteriorly
  • Medial pterygoid – elevates mandible, closing the mouth
  • Lateral pterygoid – protract the mandible, pushing jaw forwards
247
Q

what are the risk factors for oesophageal cancer?

A
  • More common in men than women – 3 to 4 times more likely
  • Smoking
  • Persistent gastro-oesophageal reflux disease (GORD)
  • Barrett’s oesophagus
  • Alcohol
  • Overweight/obese
  • Age – 45-70 years
  • Achalasia
  • HPV
248
Q

what does ferritin test show?

A
  • Test to show how much iron your body is storing
  • If a ferritin test reveals that your blood ferritin level is lower than normal, it indicates your body’s iron stores are low you have iron deficiency
  • 12 to 300 ng/mL for males and 12 to 150 ng/mL for females
  • Ferritin is a blood cell protein that contains iron – it stores iron in the tissues
249
Q

what does ESR test show?

A
  • Type of blood test that measures how quickly erythrocytes settle at the bottom of a test tube that contains a blood sample
  • Normally, red blood cells settle relatively slowly
  • A faster-than-normal rate may indicate inflammation in the body
  • ESR can help determine if you have a condition that causes inflammation
  • Increased blood levels of certain proteins (such as fibrinogen or immunoglobulins, which are increased in inflammation, cause the red blood cells to fall more rapidly
  • Sometimes the ESR can be slower than normal – a slow ESR may indicate a blood disorder such as sickle cell anaemia
250
Q

MRI vs. CT?

A
  • Diagnose conditions – including damage to bones, injuries to internal organs, problems with flood flow, stroke, and cancer
  • Guide further tests or treatments – CT scans can help to determine the location, size and shape of a tumour before having radiotherapy, or allow doctor to take a needle biopsy
  • Monitor conditions – including checking the size of tumours during and after cancer treatment
  • Doctor may suggest MRI if CT scan hasn’t been able to give all the information they need
  • MRI is particularly good for brain tumours, primary bone tumours, soft tissue sarcomas, tumours affecting the spinal cord
  • MRIs provide more detailed information about the inner organs (soft tissues) such as the brain, skeletal system, reproductive system and other organ systems than is provided by a CT scan.
  • CT scans are most commonly used to view bone injuries, problems in the lungs or chest, and for detecting tumors. MRI’s, on the other hand, are better suited for examining soft tissue injuries, particularly in the ligaments or tendons. They’re also good for spinal cord injuries and brain tumors.
251
Q

what are the enterostomy feeding options?

A
  • percutaneous endoscopic gastrostomy (PEG) - need two doctors to insert at endoscopy, more comfortable, can be permanent if necessary – useful for patients who need enteral nutrition for a prolonged period – a catheter is placed percutaneously into the stomach under endoscopic control
  • percutaneous endoscopic jejunostomy (PEJ)
252
Q

what are the ethics of PEG ?

A
  • Unlike nearly every other method of feeding, PEG feeding does not require the cooperation or consent of the person being treated – in effect, PEG is a form of forced feeding
  • Patients shouldn’t be subjected to a PEG unless they are expected to require feeding for greater than 30 days
  • Those with a life expectancy of less than 30 days or who will only require short-term feeding should be fed via a nasogastric feeding tube
  • Complex issues particularly for patients near the end of life, where the decision to use or not use PEG is frequently made without the participation of the patient
  • There are two basic value systems: some people, perhaps based on religious beliefs, regard all life as valuable and worth preserving, others may value the quality of life preserved over the quantity of life preserved – prolonging unnecessary suffering

Medicine Sem 4 (23 decks)

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