Wk 1 - Physiology: Mouth, Stomach and Secretion Flashcards

1
Q

What two plexuses make up the enteric nervous system?

A
  • Myenteric plexus
    • Located between the inner and outer layers of muscularis externa
    • Responsible for increasing tone of gut
    • Controls velocity and intensity of contractions
  • Submucosal plexus
    • Located in the submucosal layer
    • Responsible for secretions and absorption in the gut
    • Controls local muscle movements as well
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2
Q

Where is the myenteric plexus located?

A

Between the inner and outer layers of the muscularis externa

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3
Q

Where is the submucosal plexus located?

A

In the submucosal layer

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4
Q

List the structures that make up the enteric nervous system.

A
  1. myenteric plexus
  2. submucosal plexus
  3. mucosal plexus
  4. deep muscle plexus
  5. sensory neurones
  6. internurones
  7. motor neurones
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5
Q

What is the function of the enteric nervous system?

A
  • Constantly receiving sensory info from the GI tract
  • Responds via local control of motor functions + secretions
  • Feedback mechanism in a way
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6
Q

List the structures that make up the sympathetic nervous system.

A

Post ganglionic fibres from :

  • coeliac
  • superior mesenteric plexi
  • inferior mesenteric plexi
  • hypogastric

Some direct to blood vessels

Some to secretory cells

Many synapse with enteric plexi

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7
Q

What is the function of the sympathetic nervous system on the GI tract?

A

Mostly inhibitory on GI function

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8
Q

List the structures that make up the parasympathetic nervous system.

A
  • Vagus as far as transverse colon
  • Pelvic nerves via Hypogastric plexi
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9
Q

What is the function of the parasympathetic nervous system on gut function?

A

Mostly stimulatory

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10
Q

What are the main salivary glands?

A
  1. Submandibular gland (mixed secretion) produces 75% of secretions
  2. Parotid gland (serous) produces 20% of secretions
  3. Sublingual gland (mixed) produces 5% of secretions - produces lipase
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11
Q

What is the total flow from glands per day?

A

About 1000ml (1L) per day (nb at maximum stimulation a gland can produce 1ml per minute per gram of gland)

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12
Q

Describe the structure of the glands.

A
  • Salivary glands are made up of secretory acini (acini - means a rounded secretory unit) and ducts. The acini can either be serous, mucous, or a mixture of serous and mucous.
  • The secretory units merge into intercalated ducts, lined by simple low cuboidal epithelium, and surrounded by myoepithelial cells.
  • These ducts continue on as striated ducts. These have a folded basal membrane, to enable active transport of substances out of the duct. Water resorption, and ion secretion takes place in the striated ducts, to make saliva hypotonic (reduced Na,Cl ions and increased carbonate, and potassium ions).
  • The striated ducts lead into interlobular (excretory) ducts, lined with a tall columnar epithelium.
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13
Q

What controls the ionic composition of saliva?

A

Saliva flow

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14
Q

What is saliva composed of?

A
  • Enzymes: amylase (breakdown of starch), lipase (breakdown of fat imp in children whose pancreas has not yet fully developed) and lysosomes (kill bacteria - mouth imp source on infection)
  • Inorganic: Na, K, Cl and HCOs + little bit of phosphate and Ca
  • Organic: urea, citrate, amino acids, steroid hormones at same conc as plasma (exact equilibrium of free hormone)*, ABO antigens, mucin (ie mucous), kallikrein (indicator that vasodilation system is working - produce bradykinin)

*Useful to detect hormones eg ovulation in women salivary progesterone

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15
Q

What are the 4 functions of saliva?

A
  1. Moistens food
  2. Digests food (amylase and lipase - which continue to digest the food bolus into the stomach)
  3. Lysozyme activity (protect teeth and mouth from infection)
  4. Buffer action (but saliva generally more acidic)
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16
Q

What controls salivary gland secretion?

A
  • Parasympathetic nervous system: stimulation of saliva flow associated with powerful vasodilation
  • Sympathetic nervous system: if stimulated in isolation, leads to profound vasoconstriction - leading to dry mouth (characteristic of stressful situations. If alongside PNS, it stimulates enzyme secretion
  • If sympathetic innervation is stimulated same time as parasympathetic then PNS vasodilation OVERRIDES the SNS vasoconstriction
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17
Q

Describe the different phases of saliva secretion.

A
  1. Cephalic phase: triggered by sight, smell or thought of food. This is a learned (conditional) response
  2. Reflex phase: triggered by presence of food in mouth (by rubbing gums and/or chewing. This is a hardwired (unconditional) reponse

Resting flow falls during sleep - imp as otherwise would choke on own saliva.

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18
Q

Describe the muscles found in the oesophagus.

A
  • Upper portion (5%) is voluntary muscle
  • Middle portion (35-40%) is a mixture of voluntary and smooth muscle
  • Lowest portion (55-60%) is smooth muscle
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19
Q

What are the two sphincters of the oesophagus?

A
  • Upper oesophageal sphincter (UOS) is an “anatomical” structure
  • Lower oesophageal sphincter (LOS) is physiological (cannot see it anatomically)
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20
Q

What is the function of the upper oesophageal sphincter?

A

Prevents air swallowing

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21
Q

What is the function of the lower oesophageal sphincter?

A

Prevents acid reflux (acid reflux usually worse when lying down). More of a problem as would lead to inflammation and maybe Barrett’s oesophagus.

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22
Q

How does food pass down through the oesophagus?

A

Through primary (and if necessary secondary) peristaltic wave - the wave goes down the whole of the oesophagus until the stomach.

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23
Q

Explain the mechanism of swallowing food.

A
  1. Voluntary phase:
    • Mastication leads to a bolus of food being produced, during this stage the back of the tongue is elevated and the soft palate pulled anteriorly against it.
    • Following this, inspiration is inhibited (i.e. close nasal opening) and the bolus of food is moved to the pharynx by the tongue.
  2. Pharyngeal phase:
    • Pressure receptors are activated in the palate and anterior pharynx.
    • This signals swallowing centre in brainstem which inhibits respiration, raises the larynx, closes the glottis, opens the upper oesophageal sphincter.
    • The true vocal cords close to prevent aspiration.
    • The bolus is moved towards the oesophagus via peristalsis of the pharyngeal constrictor muscles.
  3. Oesophageal phase:
    • At the beginning of this phase, the larynx lowers, returning to its normal position.
    • The cricopharyngeus muscle then contracts to prevent reflux and respiration begins again.
    • Bolus is moved down the oesophagus via peristalsis (initiated by UOS contraction), which is coordinated by extrinsic nerve.
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24
Q

List the main functions of the stomach.

A
  1. Sterilisation of food (with fluid pH of 2/3)
  2. Storage of food (receptive relaxation - tone of stomach decreases as more food goes in)
  3. Mechanical disruption of food
  4. Digestion
  5. Control of release of material to duodenum (water-permeable so if pyloric sphincter is not working –> gastric dumping –> blood volume drops. People with this condition faint after eating)
  6. Secretion of intrinsic factor (imp in absorption of Vit B12)
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25
Q

What is the ‘pacemaker’ zone in the stomach?

A

The pacemaker cells in the fundus of the stomach establish a basal electrical rhythm continuously that spread down to the pyloric sphincter, creating a rate of approximately three to eight contractions per minute.

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26
Q

List the phases of gastric motility and acid secretion.

A
  1. Cephalic Phase: mediated entirely by activity in the vagus nerve initiated by the sight, smell or thought of food and by chewing and swallowing
  2. Gastric phase: mediated by the presence of food in the stomach which stimulates mechanoreceptors (inducing local and central reflexes) as a result of distension and chemical receptors which also mediate gastrin secretion directly.
  3. Intestinal Phase: the presence of chyme in the duodenum brings about neural and endocrine responses which first stimulate (via duodenal distension initiating local reflexes and by duodenal gastrin secretion) and then inhibit acid secretion and gastric motility. Inhibition predominates as duodenal pH falls and secretin is released.
27
Q

What mediates the cephalic phase?

A

Mediated by activity in the vagus nerve, which is initiated by:

  • Sight, smell or thought of food
  • Chewing and swallowing food
28
Q

What mediates the gastric phase?

A

Presence of food in stomach stimulates mechanoreceptors (as a result of distention) and chemical receptors

29
Q

What mediates the intestinal phase?

A

Presence of chyme in the duodenum brings about neural and endocrine responses which:

  • First, stimulate (via duodenal distension initiating local reflexes and by duodenal gastrin secretion)
  • Then inhibit acid secretion and gastric motility
  • Inhibition predominates as duodenal pH falls and secretin is released
30
Q

What is gastrin?

A
  • Main hormone involved in increasing acid production
  • Secreted from G cells in the stomach (activated by vagus nerve)
  • Activation of the G cells leads to the production of gastrin which is released into the blood and travels through the blood until it reaches the parietal cells
  • Gastrin secretion is inhibited by low stomach pH (which happens when the stomach starts emptying –> build-up of acid)
31
Q

What are the parietal cells (aka oxyntic cells) in the stomach?

A

Epithelial cells that secrete hydrochloric acid (HCI) and intrinsic factors

32
Q

Describe how parietal cells (aka oxyntic cells) produce acid and secrete it into the stomach.

A
  • Acid producing cells + ATP-dependent secretion into lumen (pH is about 2 –> vs body is pH 7 so need large amount of energy)
  • Secreting HCl into stomach - secretes protons into stomach lumen in exchange for potassium
  • Protons come from CO2 - comes into cell from blood side - reacts with OH from the water found in these cells to release H
  • For each H (HCl) into stomach, there is HCO3 going into blood

This exchange is associated with metabolic alkalosis. Vomiting is major cause of metabolic alkalosis (as losing acid and need to produce more so have more of this exchange)

33
Q

How does the stomach protect itself from its very acidic nature + release of HCl via parietal cells?

A
  1. Stomach lumen lined by mucous –> protection
  2. Stomach epithelium secreting bicarbonate –> protection
  3. Stomach epithelium rapid turnover rate
  4. Stomach lining high blood flow –> if there is damage then blood flow will wash acid away
34
Q

How is the acid (gastric) secretion in parietal cells controlled?

A

Gastric secretion is stimulated chiefly by three chemicals: acetylcholine (ACh), histamine (secreted by ECL cells), and gastrin:

  • Acetylcholine (ACh). This is secreted by the parasympathetic nerve fibers of both the short and long reflex pathways.
  • Histamine. This is a paracrine secretion from the enteroendocrine cells in the gastric glands.
  • Gastrin. This is a hormone produced by enteroendocrine G cells in the pyloric glands.

ACh and gastrin increase Ca into cells which increases proton pumps (H/K pump) on lumen layer, while histamine activates cAMP cascade to promote proton pump action.

Below pH of 2, stomach acid inhibits the parietal cells and G cells; this is a negative feedback loop that winds down the gastric phase as the need for pepsin and HCl declines!

35
Q

What initiates vomiting?

A

The vomiting centre

36
Q

Where is the vomiting centre located?

A

Vomiting centre (VC) is in the dorsal aspect of the lateral reticular formation. It coordinates afferent information and initiates vomiting.

37
Q

List some factors that induce vomiting?

A

Vomiting may be induced by:

  1. Bloodborne chemical stimuli (including some emetic drugs) which are identified by the chemical trigger zone. This is in the area postrema which is outside the blood brain barrier and close to but separate from the VC.
  2. Physiological triggers include uraemia and acidosis eg diabetic ketoacidosis or those with severe COPD (?corrective)
  3. Gastrointestinal mucosal irritants (some emetics including strong saline, toxins, drugs, radiation damage eg cancer pts due to damage to GI mucosa where cells divide rapidly which radiation blocks)
  4. Distension of hollow viscera
  5. Gastrointestinal blockage (eg ulcerative colitis)
  6. Stimulus of labyrinthine system of inner ear – motion sickness
  7. Smells, tastes, sights
38
Q

Describe the mechanism/sequence of events in vomiting.

A

Highly coordinated sequence of events, often preceded by nausea, sometimes preceded by salivation (overflow from VC to glossopharyngeal and facial nerves).

Sequence of events:

  1. Retching may occur – (rhythmic contractions of the diaphragm and abdominal muscles against a closed glottis thus one gets forced inspiratory thoracic activity combined with forced abdominal expiratory activity. The mouth remains closed gastric contents may be retropulsed into the oesophagus)
  2. Stomach - tone in the fundus and general peristaltic activity is decreased
  3. Duodenal tone and proximal jejeunal tone is increased such that duodenal contents may reflux into the stomach and further (bile in vomitus)
  4. There is some direct evidence for reverse peristalsis in the intestine in cats and dogs and intestinal contents can appear in vomitus in humans
  5. Finally strong antral contractions occur, the LOS opens, the mouth opens and the nasal passages are (hopefully) closed off by the soft palate
39
Q

What keeps the nasal passages closed during vomiting?

A

The soft palate

40
Q

What happens in the stomach during vomiting?

A

Tone in fundus and general peristaltic activity is decreased

41
Q

Describe what happens to the duodenum and jejunum during vomiting.

A

Duodenal and jejunal tone is increased such that duodenal contents may reflux into stomach

42
Q

List some of the consequences of vomiting.

A
  1. Hypochloraemic metabolic alkalosis due to loss of gastric juice
  2. Hypovolaemia which activates the renin-angiotensin system promotes renal sodium retention and potassium excretion
  3. Hypokalaemia (due to decreased intake and increased loss)
  4. Hyponatraemia (due to decreased intake and secondary to bicarbonate excretion due to the severe alkalosis)
  5. Damage to teeth
  6. Malnutrition
  7. Injury to oesophagus stomach junction (Mallory Weiss tears)
  8. Fatigue
  9. Low mood
43
Q

A consequence of protracted vomiting is _______ (hypochloraemic metabolic alkalosis or hyperchloremic metabolic acidosis)?

A

Hypochloraemic metabolic alkalosis due to loss of gastric acid - a compensatory mechanism where stomach produces more acid HCl so more HCO3 into the bloodstream as a result*.

Need more H and Cl into parietal cell –> hypochloraemic

*Hydrogen ions may be lost through the kidneys or the GI tract. Vomiting or nasogastric (NG) suction generates metabolic alkalosis by the loss of gastric secretions, which are rich in hydrochloric acid (HCl). Whenever a hydrogen ion is excreted, a bicarbonate ion is gained in the extracellular space.

44
Q

________ (hypovolaemia or hypervolaemia) is a consequence of protracted vomiting.

A

Hypovolaemia

45
Q

What does hypovolaemia (fluid loss) as a result of vomiting lead to?

A

Activation of the renin-angiotensin-aldosterone* system which promotes renal sodium retention and potassium excretion.

*The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system within the body that is essential for the regulation of blood pressure and fluid balance.

46
Q

There is _____ (hypokalaemia or hyperkalaemia) as a result of protracted vomiting.

A

Hypokalaemia due to decreased intake (in stomach/GI due to vomiting) and increased loss (via RAAS activation - K excretion in kidney/renal system).

47
Q

Due to protracted vomiting, there is ______ (hyponatraemia or hypernatraemia).

A

Hyponatraemia. Due to decreased intake (vomited out) and secondary to bicarbonate excretion (Na lost in kidney despite RAAS activation, bicarbonate not reabsorbed so Na taken with it) due to severe alkalosis.

48
Q

Mallory-Weiss Tears are a consequence of protracted vomiting, what are these tears?

A

Mallory-Weiss syndrome (MWS) is one of the common causes of acute upper gastrointestinal (GI) bleeding, characterised by the presence of longitudinal superficial mucosal lacerations (Mallory-Weiss tears). These tears occur primarily at the gastroesophageal junction; they may extend proximally to involve the lower or even mid oesophagus and at times extend distally to involve the proximal portion of the stomach.

49
Q

What are the main proteolytic enzymes secreted by the pancreas?

A

The proteolytic class of pancreatic enzymes secreted as inactive precursors into the duodenum consists of:

  1. Trypsinogen - becomes trypsin
  2. Chymotrypsinogen - becomes chymotrypsin
  3. Procarboxypolypeptidase A and B - becomes carboxypolypeptidase A and B
  4. Pro-elastase - becomes elastase
50
Q

What ‘produces’ the active form of trypsin (ie from trypsinogen to trypsin)?

A

Enteropeptidase –> n enzyme secreted from the brush border of the small intestine (in response to secretin and CCK). Enterokinase (ie peptidase) serves to activate trypsinogen to trypsin, which in turn converts many of the other proenzymes into their respective enzymatic forms for ongoing protein hydrolysis.

51
Q

Discuss the presence of Ca in pancreatic secretions.

A
  • Lower than plasma and partly associated with enzyme secretion
  • Pancreatic secretion has more HCO3 (bicarbonate) - to neutralise acids in GI lumen
  • Lack of protein to bind to Ca + high HCO3 –> Ca salt precipitation
52
Q

What controls pancreatic secretion?

A

The pancreas is controlled both by hormones and nerves!

  • Secretin (released from duodenum in response to acid presence) stimulates salt and water secretion
  • CCK (released from duodenum in response to fat) stimulates enzyme secretion
  • Gastrin (released from G cells in the lining of the stomach and upper small intestine/duodenum) shares a terminal tetrapeptide with CCK and has some CCK like activity
  • Vagus causes a powerful vasodilation
  • Vagus:
    • ACh causes enzyme secretion
    • VIP causes salt and water secretion
53
Q

What three hormones control pancreatic secretions?

A
  1. Secretin
  2. CCK
  3. Gastrin
54
Q

What nerve control pancreatic secretion?

A

The vagus nerve

55
Q

What is Secretin?

A

Polypeptide of 27 amino acids

56
Q

Where is Secretin produced?

A

Produced by cells in the crypts of Lieberkühn between the villi of the duodenum and jejunum

57
Q

What does Secretin do?

A
  1. Stimulates the production of salt and water by the pancreas
  2. Inhibits stomach acid secretion and motility to control food entry into duodenum
58
Q

What stimulates Secretin release?

A

Stimulus to release is low pH in lumen

59
Q

What is CCK (Cholecystokinin)?

A

Polypeptide of 33 amino acids

60
Q

Where is CCK produced?

A

Produced in cells in “pear-shaped” enteroendocrine glands which are situated in the intestinal mucosa and have apical processes which reach into the lumen of the duodenum (similar to G cells in stomach)

61
Q

What does CCK do?

A
  1. Stimulates gall bladder contraction
  2. Stimulates pancreatic enzyme secretion
  3. Has gastrin like activity
  4. Inhibits gastric emptying
62
Q

What stimulates CCK release?

A

Stimulus to release is food in the duodenum/jejunum especially fat - they can ‘taste’ the lumen

63
Q

List the main phases of pancreatic secretion.

A
  1. Cephalic phase mainly via the vagus from the nucleus tractus solitarius and the dorsal vagal nucleus - sight, smell and thought of food
  2. Gastric Phase – distension of the stomach via vagovagal reflexes. Gastrin has some CCK like activity
  3. Intestinal – secretin (salt and water secretion), CCK (enzyme secretion) and vagus (due to ENS activation - vasodilation)
64
Q

What is vagovagal stimulation?

A

AKA gastrointestinal tract reflex circuits where afferent and efferent fibers of the vagus nerve coordinate responses to gut stimuli via the dorsal vagal complex in the brain