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Digestion Flashcards

1
Q

What are the 2 parts of the enteric nervous system?

A
  1. Myenteric (Auerbach’s) plexus: Located in muscularis externa.
  2. Submucosal (Meissner’s) plexus: Located in the submucosa.
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2
Q

What are the neurones in the ENS?

A
  1. Sensory (afferent) neurones: Detects mechanical/chemical stimuli in the lumen of the GI tract.
  2. Interneurones: Relays information from sensory to motor neurones.
  3. Secretomotor (efferent) neurones: Stimulate wide range of effectors such as smooth muscle, glands, blood vessels…
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3
Q

What is the clinical significance of the ENS?

A
  • The ENS allows the digestive system to be functionally independent from the CNS.
  • This allows bowel transplantation to occur.
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4
Q

What are the general effects of sympathetic stimulation in the GI tract?

A
  • Usually inhibits digestion.
  • Decreases gut motility.
  • Decreases secretion.
  • Decreases blood supply.
  • Causes sphincter constriction.
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5
Q

What are the general effects of parasympathetic stimulation on the GI tract?

A
  • Usually promotes digestion.
  • Increases gut motility.
  • Increases gut secretion.
  • Causes sphincter relaxation.
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6
Q

What are the main neurotransmitters used in ENS communication?

A
  1. Acetylcholine (ACh): Causes smooth muscle contraction and stimulates glandular secretion.
  2. Nitric oxide: Relaxes smooth muscles.
  3. Vasoactive intestinal peptide (VIP): Relaxes smooth muscle and stimulates glandular secretion.
  4. Noradrenaline (NAd): Released by sympathetic neurones and have the effect of causing sphincter & vascular smooth muscle contraction.
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7
Q

What are some additional NTs used by the ENS?

A
  • Enkephalins
  • Somatostatins
  • Substance P
  • ATP
  • CGRP (Calcitonin gene related peptide)
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8
Q

What are the types of proteins present in saliva?

A
  1. α-amylase
  2. Glycoproteins
  3. Proline-rich proteins
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9
Q

What are the types of saliva?

A
  1. Serous: Secreted by parotid glands
  2. Seromucous: Secreted by subinguinal & submandibular glands
  3. Mucous: Secreted by minor salivary glands in the submucosa of the oral cavity
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10
Q

What are the functions of saliva?

A
  1. Lubrication: Glycoproteins called mucins in saliva produced by mucous-secreting cells aid in lubrication of food. This facilitates taste, speech and swallowing.
  2. Defence: Lysosomes break down bacterial cells. Lactoferrin sequesters free Fe ions needed for bacterial growth. Proline-rich proteins neutralise plant tannins.
  3. Buffering: HCO3- in saliva helps neutralise acidic foods in order to protect teeth.
  4. Digestion: Salivary amylase (α-amylase) breaks down starch. Protected by bolus from the acidic environment of the stomach so that it continues to be active inside the bolus. It can digest up to 75% of ingested starch.
  5. Thermoregulation: Evaporation of saliva can be used to remove heat.
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11
Q

What is the process of salivary secretion?

A
  1. Active transport of Na+ out of the acinar cells by Na+/K+-ATPase creates high [Na+​] in ECF, which facilitates secondary active transport of Cl- ions into the cytoplasm of acinar cells through NKCC1 transporters (in ratio of Na+-2Cl—K+).
  2. Diffusion of Cl- out of cell through channels into the secretory duct lumen results in accumulation of Cl- in the lumen. –ve charge in lumen results in paracellular diffusion of Na+ into the lumen, followed by water. Acinar cells also secrete proteins into the lumen. This produces primary secretion, which is isotonic to plasma.
  3. Primary secretion is modified by salivary duct cells. Cl- is exchanged for HCO3- and Na+ is exchanged for K+. Salivary duct cells also secrete some proteins into the lumen, such as EGF and nerve growth factor.
  4. Reabsorption of NaCl by the salivary duct cells exceeds secretion of HCO3- and K+. Watertight junctions between the salivary duct cells mean that the duct walls are impermeable to water. This results in hypotonic saliva being produced.
  5. Secretion of saliva is mainly driven by bulk flow, but is aided by the contraction of myoepithelial cells in the salivary ducts.
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12
Q

What happens to the composition of saliva as flow rates increase?

A

Saliva becomes more isotonic with a greater NaCl content because transporters in salivary ducts don’t have enough time to absorb sufficient amounts of NaCl.

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13
Q

What are the roles of the parasympathetic nervous system in the control of salivation?

A
  • PNS stimulation involves the release of ACh/VIP.

Effects include:

  1. Vasodilation/increased blood supply to salivary glands.
  2. Promotes growth of salivary glands.
  3. Open more channels in acinar cells to promote secretion of saliva.
  4. Stimulates salivation at sight/smell of food as part of feed-forward response.
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14
Q

What are the roles of the sympathetic nervous system in the control of salivation?

A
  • SNS stimulation involves the release of NAd.
  • Effects are:
    1. Vasoconstriction/decreased blood supply to salivary glands.
    2. Stimulates contraction of myoepithelial cells.
    3. Stimulates exocytosis in acinar cells, promoting protein secretion.
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15
Q

What are slow waves?

A

Periodic depolarisations of the gut smooth muscle with amplitudes of 10-50 mV.

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16
Q

What are the differences between slow waves and APs?

A
  1. Unlike APs, slow waves do not depolarise beyond 0 mV.
  2. Unlike APs, the time course of one wave is in the magnitude of seconds, not milliseconds.
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17
Q

Which cells are responsible for producing slow waves?

A

Interstitial cells of Cajal (ICCs)

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18
Q

How is the amplitude of slow waves increased?

A
  1. Increased Ca2+ release from internal stores.
  2. Increased number of open plasma membrane Ca2+ channels.
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19
Q

How is the amplitude of slow waves decreased?

A

Opening of hyperpolarising PM K+ channels.

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20
Q

What is segmentation?

A

Contraction of smooth muscle in alternating segments of the gut aid in the mixing of food.

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21
Q

What causes segmentation?

A

Slow waves (with modifying nervous and hormonal inputs)

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22
Q

What are the effects of nervous inputs on segmentation?

A
  • Sympathetic stimulation inhibits segmentation.
  • Parasympathetic stimulation promotes segmentation.
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23
Q

What is the peristaltic reflex?

A
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24
Q

What are the 3 types of sensory neurones associated with the GI tract?

A
  1. Intrinsic primary afferent neurones (IPANs)
  2. Vagal sensory neurones
  3. Intestinofugal afferent neurones (IFANs)
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25
Q

What is the location and function of IPANs?

A
  • Location: Located entirey in ENS.
  • Function: Short distance ENS reflexes (e.g. peristaltic reflex)
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26
Q

What is the location and function of vagal sensory neurones?

A

Location: Cell bodies in vagal dorsal root ganglia and axons in branches of vagus nerve.

Function: Transfers information from the GI tract to the CNS and coordinates reflexes (e.g. vagovagal reflexes).

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27
Q

What is the location and function of IFANs?

A

Location: Cell bodies located in ENS but axons travel with sympathetic fibres.

Function: Long distance reflexes.

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28
Q

What is function of feedback reflexes in the GI tract?

A

Prevent sfood from moving through GI tract too quickly.

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29
Q

What is the function of feedforward reflexes in the GI tract?

A

Increases motility in distal parts of the GI tract in response to food in the proximal parts, ensuring there’s enough space.

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30
Q

What is the ileal break reflex?

A

Feedback: Reduced motility in proximal GI tract on detection of fat and nutrients in the ileum. This reflex is mediated by hormones (PYY and GLP-1) and neurones.

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31
Q

What is the gastrocolic reflex?

A

Feedforward: Increased motility of the colon in response to food entering the stomach.

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32
Q

What is the sequence of events that occur during swallowing?

A
  1. The soft palate is pulled up to prevent food from entering the nasal cavity.
  2. The larynx is pulled up and against the epiglottis, closing its entrance.
  3. Swallowing centre inhibits respiratory centre and stops respiration during swallowing, causing deglutition apnoea.
  4. The UOS relaxes and sequential contraction of the pharynx pushes the bolus into the oesophagus.
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33
Q

What are the processes that mediate peristalsis in the oesophagus?

A
  • Swallowing initated primary peristaltic wave
  • Secondary wave produced (by ENS and vagovagal reflexes as a result of oesophageal distension) if primary wave fails.
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34
Q

What are the activities of the lower oesophageal sphincter during swallowing?

A
  1. LOS relaxes as a feedforward response in the swallowing reflex.
  2. Swallowing triggers vagus nerve reflex that promotes activity of inhibitory ENS fibres.
  3. Inhibitory ENS fibres secrete NO, which causes smooth muscle in the sphincter to relax
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35
Q

What is the sequence of events that occur during the vomiting (emesis) reflex?

A
  1. Increased salivation (to protect teeth against stomach acid).
  2. Retroperistalsis in small intestine to move food back into stomach and neutralise stomach acid.
  3. Lowering of intrathoracic pressure (inspiration against closed glottis).
  4. Increased intra-abdominal pressure (contraction of abdominal muscles).
  5. Relaxation of the LOS and propulsion of food into the oesophagus as a result of pressure gradient.
  6. UOS relaxes and the vomitus is expelled through the mouth.
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36
Q

What is Sjögen syndrome?

A

Autoimmune disease resulting in the destruction of salivary acini and the inability to salivate.

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37
Q

What is Chagas’ disease?

A

Parasitic disease causing damage to the ENS

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38
Q

What are the stimuli of vomiting?

A
  1. Mechanical receptors in the GI tract in response to overeating.
  2. Chemoreceptors in the ‘chemoreceptor trigger zone’, which is outside the BBB and so can detect blood-borne emetics.
  3. Touching back of throat.
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39
Q

What are the consequence of excess vomiting?

A
  1. Teeth erosion
  2. Metabolic alkalosis
  3. Hypovolaemia
  4. Hypokalaemia
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40
Q

What are the functions of the pyloric sphincter?

A
  1. Controls rate of gastric emptying
  2. Prevention of duodenal-gastric reflex
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41
Q

What is receptive relaxation?

A

Stretch in the walls of the oesophagus causes vagovagal reflex that relaxes the fundus and body of the stomach, allowing it to expand and accommodate the food.

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42
Q

How do slow waves in the stomach help break down food?

A
  1. Propagation of the slow wave down the stomach and sequential contraction of the stomach pushes the food towards the pyloric sphincter. This is called propulsion.
  2. As the slow waves reach the pyloric sphincter, APs propagate to the smooth muscles in it and cause constriction.
  3. Because the sphincter is constricted, pressure builds up in the antrum and the food is propelled back towards the body of the stomach. This is called retropulsion.
  4. This process repeats and is termed the ‘antral mill”, as it helps grind up food particles and reduce their size.
  5. Between slow waves, the pyloric sphincter is relaxed and allows the passage of small amount of food into the duodenum.
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43
Q

What is the migrating myoelectric complex (MMC)?

A

In the fasting state, the stomach is quinescent but displays periods (~10 minutes) of intense electrical activity every 90-120 minutes.

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44
Q

What initiates the MMCs?

A

Motilin through the ENS.

45
Q

What is the significance of the MMC?

A

Helps push food particles larger than 2mm through the GI tract so that they can be excreted.

46
Q

How is gastric emptying brought about?

A

Relaxation of the pyloric sphincter caused by NO release through the MMC.

47
Q

What substances, when detected by the duodenum, inhibits gastric emptying?

A
  1. Low pH
  2. High lipid content
  3. Amino acid and partially digested proteins
  4. Hyperosmotic solutions
48
Q

How can gastric emptying be delayed?

A
  1. Relaxing and inhibiting motor activity of the fundus
  2. Inhibiting motor activity of the antrum
  3. Contracting the pyloric sphincter
49
Q

What types of glands are found in the stomach?

A
  • Cardiac glands: Found in cardia and secretes mucous but does not contain acid-secreting cells.
  • Oxyntic glands: Found in the fundus and body of the stomach and contain:
    1. Parietal cells
    2. Chief cells
    3. Mucous-secreting cells
    4. Endocrine cells
  • Pyloric glands: Found in the antrum of the stomach and conain:
    1. Mucous-secreting cells
    2. G-cells
50
Q

What are the secretions of the gastric glands?

A
  1. HCl
  2. Pepsinogens: Precursor to pepsin.
  3. Prochymosin: Curdles milk.
  4. Intrinsic factor: Binds to vitamin B12 and prevents breakdown, aiding in its absorption.
  5. Histamine: Controls acid secretion.
51
Q

What is the function of intrinsic factor?

A

Aids in absorption of vitamin B12

52
Q

What are the cells that secrete histamine?

A

Enterochromaffin-like cells (ELCs)

53
Q

What are the functions of stomach acid?

A
  1. Delays gastric emptying (on detection of low pH by the duodenum)
  2. Aids in absorption of Fe and Ca
  3. Helps release vitamin B12 from haptocorrin
  4. Catalyses breakdown of pepsinogens into pepsins
  5. Destroys pathogens
54
Q

What is the sequence of events that occur during the process of acid secretion?

A
  1. H+/K+-ATPase on the luminal membrane of parietal cells actively transport H+ ions out of the parietal cells into the lumen of the stomach in exchange for K+.
  2. K+ ions diffuse back out of the parietal cell into the gastric lumen through channels, and so are recycled.
  3. Active pumping of H+ out of parietal cells increases the pH in the cytoplasm, which shifts p.o.e. for the reaction CO2 + H2O ⇋ HCO3- + H+ the right in favour of H+ production. This reaction is catalysed by carbonic anhydrase.
  4. HCO3- exits parietal cell in exchange for Cl- by HCO3-/Cl- exchangers on the basolateral membrane, down electrochemical gradient. Cl- is thus pumped into parietal cells by secondary active transport.
  5. Cl- diffuses out of the parietal cells and into the lumen of the stomach through channels on the basolateral membrane.
55
Q

Where are H+ transport proteins located in the parietal cells in the stomach at rest?

A

In tubulovesicular membranes in the cytoplasm.

56
Q

What are the agonists of stomach acid secretion?

A
  1. Gastrin (endocrine)
  2. ACh (neurocrine)
  3. Histamine (paracrine)
57
Q

What promotes gastrin secretion?

A
  1. Local stretch reflexes (via ENS and ACh)
  2. Vagal reflexes (using gastin-releasing peptide - GRP)
  3. Presence of amino acids, Ca2+ in lumen
58
Q

How does gastrin promote stomach acid secretion?

A
  1. Indirect (main role): Promotes histamine secretion by ELCs.
  2. Direct: Binds to CCKB receptors and via the PKC pathway, increases intracellular [Ca2+], promoting H+/K+-ATPase activity (possibly via calmodulin-dependent protein kinase).
59
Q

How does ACh promote stomach acid secretion?

A
  1. Indirect: Promotes histamine secretion by ELCs, gastrin release and inhibits somatostatin secretion.
  2. Direct: Binds to M3 (muscarinic) ACh receptors and via the PLC pathway, increases intracellular [Ca2+], promoting H+/K+-ATPase activity.
60
Q

What promotes histamine secretion?

A
  1. Gastrin
  2. ACh
61
Q

How does histamine promote stomach acid secretion?

A

It binds to H2 receptors and via the cAMP pathway, promotes the activity of H+/K+-ATPase (probably by phosphorylation).

62
Q

What is Zollinger-Ellison syndrome?

A

Constant secretion of gastrin causes over-secretion of stomach acid and low pH, promoting stomach ulcer formation.

63
Q

What are the antagonists of stomach acid secretion?

A
  1. Secretin (endocrine)
  2. Somatostatin (paractine)
  3. Prostaglandins (paracine)
64
Q

How does secretin inhibit stomach acid secertion?

A
  1. Inhibits gastrin release (via vagal stimulation)
  2. Stimulates somatostatin release
  3. Direct inhibition through parietal cells
65
Q

Where is somatostatin produced?

A

D cells in pyloric antrum (low pH)

66
Q

How does somatostatin inhibit stomach acid secretion?

A
  1. Direct: Binds to somatostatin receptors on basolateral membrane of parietal cells and inhibits activity of adenylate cyclase, decreasing intracellular [cAMP].
  2. Indirect: Inhibits secretion of histamine and gastrin (part of negative feedback regulation of gastrin release, which itself stimulates somatostatin secretion)
67
Q

How do prostaglandins inhibit stomach acid secretion?

A

Inhibits activity of histamine and activity of adenylate cyclase.

68
Q

What are the phases of digestion?

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
69
Q

How does the cephalic phase promote stomach acid secretion?

A
  1. Release of ACh from terminus of postganglionic vagus fibres stimulates parietal cells directly, increasing the rate of acid secretion.
  2. Release of ACh stimulates ELCs to secrete histamine, which promotes gastric acid secretion.
  3. Release of GRP from terminus of peptidergic postganglionic vagus fibres stimulates gastrin secretion from G cells, which promotes gastric acid secretion.
  4. Release of ACh inhibits somatostatin secretion from D cells, which normally inhibits gastric acid secretion, thus promoting gastric acid secretion
70
Q

How does the gastric phase promote stomach acid secretion?

A

Distension of the stomach walls causes vagal and ENS reflexes that stimulate gastrin release.

71
Q

What is the gastric secretion response during intestinal phase?

A
  • Initially, food in the proximal part of small intestines promote acid secretion.
  • Detection of low pH in duodenum then inhibits secretion of stomach acid.
72
Q

How is the gastric mucosa protected from acidic lumen?

A
  1. Secretion of mucous by epithelial mucous-secreting cells and mucous neck cells create a gastric mucosal barrier, which is relatively impermeable to H+ ions.
  2. Secretion of HCO3- by the mucous cells (possibly through vagus stimulation) into the gastric mucosal barrier neutralises any H+ ions that do manage to diffuse through the barrier.
73
Q

What is the name of the process by which parietal cells secrete acid through mucous layer?

A

Viscous fingering

74
Q

What is coeliac disease?

A

Autoimmune disease triggered by exposure to protein gliadin. Antibodies cause inflammation of the small intestine and thus loss of microvilli and shortening of villi.

75
Q

What are the mechanisms that control the ileocaecal valve?

A
  1. ENS: Distension of the terminal ileum causes the ileocaecal sphincter to relax and the contents of the ileum to empty into the colon
  2. Gastroineal reflex: Feed-forward reflex whereby distension of the stomach as a result of food ingestion results in relaxation of the ileocaecal valve. This increases the rate at which food moves through the small intestines and into the colon, making room for newly consumed food.
  3. Colonoileal reflex: Feedback reflex whereby distension of the colon due to overfilling results in contraction of the ileocaecal valve. This decreases the rate at which food moves into the colon and prevents further overfilling.
76
Q

What are the mechanisms in place to prevent the pancreatic proteases from autodigesting the pancreas?

A
  1. Pancreatic enzymes are secreted as zymogens.
  2. Pancreatic Secretory Trypsin Inhibitor (PSTI).
77
Q

What is the mechanism behind production of the primary pancreatic secretion?

A
  1. HCO3- pumped from the cytoplasm of duct cells into the lumen of the pancreatic duct by Cl-/HCO3 exchanger.
  2. Cl- is recycled back into the lumen by CFTR (Cystic Fibrosis Transmembrane conductance Regulator) Cl- channels.
  3. Reaction: CO2 + H2O ⇋ HCO3- + H+ in the presence of carbonic anhydrase in the cytoplasm.
  4. H+ produced by reaction of CO2 with H2O is pumped out of the duct cell cytoplasm via 2 mechanisms:
    - Na+/H+ exchangers on the basolateral membrane.
    - H+-ATPase (in some species).
78
Q

What are the promoters of pancreatic secretion?

A
  1. CCK
  2. Secretin
  3. VIP and ACh (promotes HCO3- secretion)
79
Q

What is the function of pancreatic amylase?

A

Breaks starch down to oligosaccharides

80
Q

What is the function of lactase?

A

Breaks lactose down to glucose and galactose

81
Q

What is the function of glucoamylase (maltase)?

A

Capable of hydrolysing terminal and intermediate α-1,4 bonds

82
Q

What is the function of sucrase-isomaltase?

A
  • Sucrase: Hydrolyses sucrose to glucose and fructose
  • Isomaltase: Hydrolyses α-1,6 bonds
83
Q

How are monosaccharides transported across the apical membrane?

A
  • Glucose and galactose are transported through SGLT1 transporters by secondary active transport
  • Fructose is transported through GLUT5 transporters by facilitated diffusion
  • All 3 are tranported across GLUT2 transporters
84
Q

What is the sequence of events that occur during protein digestion?

A
  1. Proteins are denatured by stomach acid, opening them up to attack by proteases.
  2. Chief cells in the stomach secrete pepsinogens that are then activated by stomach acid and converted into pepsins. These partially break down proteins into proteases, but are physiologically redundant (not required).
  3. Pancreatic juice contains 5 distinctive proteases. 3 are endopeptidases (trypsin, chymotrypsin, elastase) and only break proteins down to oligopeptides. 2 are exopeptidases (carboxypeptidase A, carboxypeptidase B) and break down proteins into amino acids.
  4. All pancreatic protease enzymes are secreted as zymogens. Trypsin is secreted as trypsinogen, which is activated by enteropeptidase on the jejunal brush border.
  5. Trypsin subsequently activates more trypsin and the other 4 pancreatic proteases.
  6. Oligopeptides are further broken down into amino acids by brush border and cytoplasmic peptidases.
85
Q

How are oligopeptides transported across the apical membrane?

A

PepT1 oligopeptide/H+ cotransporter

86
Q

How are amino acids transported across the apical membrane?

A

Facilitated diffusion and secondary active transport

87
Q

What are the functions of bile?

A
  1. Fat absorption: Primary bile acids (cholic and chenodeoxycholic acids) are synthesised by hepatocytes from cholesterol. They are amphipathic and act as good surfactants for breaking down fat into micelles.
  2. Excretion of waste: Bile is involved in secretion of substances not secreted by the kidneys; including cholesterol (directly or through bile acid), bile acid and bile pigments such as bilirubin.
  3. Stomach acid neutralisation: Bile contains HCO3-, which is involved in neutralising stomach acid.
  4. Protection: Bile contains IgA, mucous and antioxidants that are involved in protecting the gut mucosa.
88
Q

What is the main function of the gallbladder?

A

Stores and concentrates bile

89
Q

What is the enterohepatic circulation?

A

Process whereby bile is reabsorbed in the terminal ileum and colon to be re-used in digestion in the small intestine.

90
Q

What is the process of fat digestion in the duodenum?

A
  1. Partially digested fat triggers secretion of CCK from I cells. CCK stimulates bile secretion into the duodenum, which emulsifies fat into tiny droplets.
  2. CCK also stimulates secretion of pancreatic juice containing pancreatic lipase, which digests TAGs into 2 free amino acids and MAG, in the presence of cofactor colipase.
  3. Other lipases (e.g. carboxyl ester hydrolase) break down other lipids into free fatty acids and associated products.
  4. The action of lipases turns the fat droplets into a aggregates of free fatty acids, MAGs and other lipids called micelles.
91
Q

How is fat reabsorbed?

A

Micelles are reabsorbed in small intestines by simple diffusion.

92
Q

What are the breakdown products of bilirubin?

A
  • Urobilinogen (gut flora)
  • Stercobilin (faeces)
  • Urobilin (urine)
93
Q

How is water reabsorbed in the GI tract?

A

Standing gradient model

94
Q

How is Na+ reabsorbed in the GI tract?

A
  1. SGLT1 (glucose needed): Small intestine
  2. NHE: Small and large intestines
  3. ENaC: Large intestine
95
Q

How is K+ reabsorbed in the GI tract?

A
  • Paracellularly (as result of being concentrated by water reabsorption)
  • Secretion of K+ through apical channels causes net secretion of K+ in GI tract
96
Q

How is Cl- reabsorbed in the GI tract?

A
  • Paracellularly
  • HCO3-/Cl- exchanger
97
Q

What is the process of Ca2+ reabsorption in the duodenum?

A
  1. Ca2+ enters the epithelial cells through Ca2+ channels in apical membrane down electrochemical gradient.
  2. It is ferried across the cytoplasm by calbindin and is transported out of basolateral membrane by PMCAs.
98
Q

How does vitamin D3 (1,25-DHCC) upregulate Ca2+ absorption?

A
  • ↑ Ca2+ channels
  • ↑ Calbindin
  • ↑ Ca2+-ATPase
99
Q

What is the process of Fe absorption in the duodenum?

A
  1. Iron reductase in duodenal brush border reduces Fe3+ to Fe2+.
  2. Fe2+ is transported across the apical membrane through the Fe2+/H+-cotransporter DMT1.
  3. It is transported across the basolateral membrane by ferroportin.
100
Q

How is Fe transported in the blood?

A

Bound to transferrine

101
Q

What is mass movement?

A

Periods of extended contraction of the colon mediated by the ENS associated with relaxation of the haustra.

102
Q

What is the sequence of events that occur during defaecation?

A
  1. Internal anal sphincter relaxes (due to ENS and external innervation)
  2. Sensory neurones in rectum detects distension and causes propulsive movements of the colon by pelvic splanchnic nerves
  3. External anal sphincter voluntarily relaxed
  4. Pelvic floor muscles relax to straighten the anus
  5. Valsalva manoeuvre (breathing against closed glottis) aids in defaecation
103
Q

What is Hirschsprung’s disease?

A

ENS gangion cells lacking in descending colon and internal anal sphincter. This results in absence of reflex relaxation of the IAS and inability for defecation to occur.

104
Q

What is the function of the gut flora?

A
  • Metabolises unabsorbed carbohydrates and produce volatile fatty acids that can be source of energy for colic cells (colic salvage)
  • Synthesis of vitamin K and B
105
Q

What is the benefit of having blood-bile countercurrent in hepatocytes?

A

Allows gradient to be maintained between bood and bile for easy secretion.

106
Q

What are the functions of the liver?

A
  • Carbohydrate, protein, lipid metabolism.
  • Bile formation
  • Storage of vitamins
  • Destruction and detoxification of hormones
  • Filtration of blood (red blood cells, bacteria…)
  • Blood reservoir
107
Q

What is the process of lipid absorption in the small intestine?

A
  1. Micelles diffuse into the epithelial cells by simple diffusion.
  2. Fatty acids and cholesterol bind to fatty acid binding proteins (FABPs).
  3. They are transported to the ER where they are converted to chylomicrons.
  4. These are exported into lacteals by exocytosis and carried in lymph. This eventually drains into the blood.
108
Q

What causes insulin release?

A
  1. High blood [glucose]
  2. Parasympathetic stimulation in cephalic phase of digestion for feedforward insulin release
  3. Incretins (GIP and GLP-1)
109
Q

What inhibits insulin release?

A

Adrenaline

Homeostasis (15 decks)

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