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HOM > Digestive Physiology > Flashcards

Digestive Physiology Flashcards

1
Q

what is digestion?

A

the physiological process whereby the nutritive part of the food consumed is, in the stomach and intestines, rendered fit to be assimilated by the system

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2
Q

what does the basic histological structure of the gut tube consist of?

A

mucosa, submucosa, muscularis externa, serosa, simple squamous epithelium

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3
Q

what does the mucosa consist of?

A

consists of the epithelium, lamina propria and muscularis mucosae

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4
Q

what is the innermost layer of the gut tube?

A

mucosa

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5
Q

what is the lamina propria?

A

loose connective tissue containing glands, lymph nodules and capillaries

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6
Q

what is the muscularis mucosae?

A

thin layer of smooth muscle which throws the mucosa into folds

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7
Q

what are villi?

A

finger-like projections in the SI which increase the internal SA

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8
Q

what does the submucosa contain?

A

blood vessels, nerves, glands, the submucosal plexus (Meissner’s plexus)

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9
Q

what are the layers of the muscularis externa?

A

inner circular and outer longitudinal smooth muscle, myenteric plexus (Auerbach’s plexus) located between the 2 layers

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10
Q

what is the serosa?

A

outermost layer of connective tissues, covered by simple squamous epithelium

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11
Q

what is the splanchnic circulation?

A

the blood supply to the stomach, intestines, liver, spleen and pancreas

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12
Q

how much of the splanchnic circulation passes via the intestines to the liver in the hepatic portal vein?

A

around 75%

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13
Q

how much of the splanchnic circulation passes directly to the liver via the hepatic artery?

A

around 25%

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14
Q

what is functional hyperaemia?

A

after a meal splanchnic blood flow increases up to around 2500mlmin-1

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15
Q

what is the resting value of splanchnic blood flow?

A

around 1200mlmin-1

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16
Q

what is responsible for functional hyperaemia?

A

metabolites which increase during digestive activity, certain gut hormones and absorbed substances

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17
Q

what effect can maximal sympathetic vasoconstriction have on splanchnic blood flow?

A

can reduce it to as little as 300mlmin-1

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18
Q

how much of the blood volume do the great veins of the gut hold at rest?

A

about 20%

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19
Q

which direction do arterial and venous blood supply to each SI villus travel in?

A

arterial supply ascends from the base, venous supply descends towards the base- counter-current arrangement

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20
Q

how much blood can venoconstriction add into general circulation from the mesenteric veins and from the liver?

A

about 400ml from the mesenteric veins plus around another 200ml from the liver to the general circulation

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21
Q

where do the products of fat digestion go in the intestinal villi?

A

enter the lacteals within the villi

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22
Q

how are the central lacteals of the intestinal villi emptied into the lymphatic system?

A

irregular contractions of smooth muscle within the lamina propria of the villus stimulated by increased interstitial fluid pressure, help empty the central lacteals by squeezing. valves in submucosal lymph vessels prevent backflow

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23
Q

what is the gut epithelium comprised of?

A

single layer of columnar epithelial cells

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24
Q

why do the gut epithelium cells have a high turnover rate?

A

vital in preventing microbial invasion and very vulnerable to mechanical damage

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25
Q

how often is the entire gut epithelium estimated to be replaced?

A

every 2-6 days

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26
Q

how are the cells of the SI epithelium replaced at such a high rate?

A

old epithelial cells shed from the villus tips, replaced by new ones moving up the sides of the villus in conveyor-belt like fashion. new cells arise from stem cell population in the crypts of Lieberkuhn, before old cells shed new tight junctions formed under them between their neighbours to ensure barrier function of gut isn’t compromised

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27
Q

what are the crypts of Lieberkuhn?

A

blind-ending tubules projecting into the gut lining between villi

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28
Q

what make up the ENS?

A

the submucosal and the myenteric plexi which extend from the middle of the oesophagus to the colon

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29
Q

main function of the submucosal plexus?

A

co-ordinates motility

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30
Q

what are the inputs for the ENS?

A

sensory cells in gut wall, ANS fibres synapsing on ENS fibres

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31
Q

how does the ANS innervate the gastrointestinal tract?

A

forms synapses with ENS fibres

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32
Q

where is ANS input to the ENS particularly important?

A

proximal gut and rectum, ENS and hormones more important in between

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33
Q

where do sympathetic nerve fibres synapse outside the CNS

A

only synapse once, either in one of the paravertebral ganglia of the sympathetic chain or in a separate prevertebral ganglion within the abdominal cavity

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34
Q

what sort of fibres are postganglionic sympathetic nerve fibres normally?

A

noradrenergic

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35
Q

effect of sympathetic stimulation on gut motility and secretion, and on sphincter contraction?

A

inhibitory to gut motility and secretion, stimulates sphincter contraction

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36
Q

what carries parasympathetic supply to the gut?

A

the vagus

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37
Q

what sort of fibres are the postganglionic parasympathetic nerve fibres predominantly, where is the synapse between the pre and post-ganglionic fibres usually?

A

fibres are cholinergic, synapse between pre- and post-ganglionic fibres is within ENS

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38
Q

what is the effect of parasympathetic stimulation on gut motility, secretion and sphincters?

A

stimulates gut motility and secretion, may relax sphincters via inhibitory post-ganglionic fibres which often release VIP

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39
Q

what do the pelvic nerves supply?

A

distal colon, rectum and anus

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40
Q

are the pelvic nerves sympathetic or parasympathetic?

A

sympathetic

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41
Q

where are the sensory fibres of the gut located?

A

IPANs are entirely within the ENS, general visceral afferent fibres have cell bodies in PNS, IFANs- sensory fibres with cell bodies in ENS that have axons that synapse in the sympathetic chain

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42
Q

what are IPANs?

A

intrinsic primary afferent neurons- sensory fibres located entirely within the enteric nervous system. form the afferent limbs of local reflexes including those responsible for peristalsis, mixing and secretion

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43
Q

what are the general visceral afferent fibres?

A

sensory fibres of gut with cell bodies in dorsal root ganglia or homologous ganglion of the vagus. axons transmit signals from gut to spinal cord/brainstem and are involved in certain stomach reflexes, pain, defecation reflexes

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44
Q

what % of fibres in sympathetic nerves to the gut and what % of vagal fibres to the gut are general visceral afferent fibres?

A

50% in sympathetic nerves, 75% of vagal fibres

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45
Q

what are vagovagal reflexes?

A

reflexes in which both afferent and efferent arms are carried by the vagus nerve

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46
Q

what are IFANs?

A

intestinofugal afferent neurons, sensory fibres of gut with cell bodies in ENS that send axons with the sympathetic nerves to synapse in the prevertebral sympathetic ganglia. fibres often form afferent limbs of long-range inhibitory reflexes used to coordinate activity of different parts of gut

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47
Q

how do the long range reflexes of the GI tract work?

A

GI hormones contribute both directly and by stimulating vagal afferent fibres to elicit a neural response. the long range reflexes usually involves a synapse in the prevertebral ganglia. responsible for overall coordination of activities of GI tract

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48
Q

what is the ileal brake mechanism?

A

example of a long range reflex of the GI tract. refers to the effect of nutrients which have reached the ileum without being absorbed reducing the motility and secretion of more proximal parts of the digestive tract. may involve peptide hormones PYY and LGP-1 as well as nerve fibres

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49
Q

what is the gastrocolic reflex?

A

example of a long range reflex of the GI tract. where food entering the stomach promotes the motility of the colon which may result in urge to defecate

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50
Q

how can voluntary control be exerted over swallowing and defecation?

A

striated muscle is present at each end of the digestive tract

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51
Q

how is smooth muscle in the GI sphincters controlled?

A

tonically contracted for durations of minutes to hours. relaxes when required

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52
Q

typical contraction of smooth muscle in walls of stomach and intestines?

A

phasic contraction- slow and rhythmic. wave of depolarisation spreads through gap junctions, cells are also mechanically coupled allowing coordinated contraction. smooth muscle in which cells electrically coupled= single unit smooth muscle

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53
Q

excitation-contraction coupling in smooth muscle?

A

calcium inside the cell bind to calmodulin- complex activates MLCK which phosphorylates a regulatory light chain on myosin allowing it to bind with actin and undergo cross-bridge cycle. when calcium level falls the myosin is dephosphorylated by MLC phosphatase which prevents further cycling

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54
Q

what is peristalsis?

A

gut motility patterns which propel food in the anal direction

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55
Q

what is the peristaltic reflex?

A

type of peristalsis which occurs when stretching of gut wall elicits contraction of the longitudinal and circular muscle behind a bolus (mediated by ACh) and relaxation of the muscle in front of the bolus (mediated by NO) propelling the food onwards

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56
Q

does the peristaltic reflex require extrinsic innervation?

A

no, mediated entirely within the ENS

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57
Q

how is food detected in the peristaltic reflex?

A

may be via mechanical stretch receptors in the myenteric plexus or mechanical or chemical stimuli to the mucosa promoting serotonin (5-HT) release from enterochromaffin cells which stimulates local sensory neurons

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58
Q

what controls peristalsis in the striated muscle portion of the oesophagus?

A

somatic motor neurons causing sequential contractions of the striated muscle

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59
Q

what causes peristalsis in the antrum of the stomach and in the MMC?

A

slow wave activity

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60
Q

range of the resting MPs of smooth muscle cells of the gut?

A

from around -70 to -40mV

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61
Q

amplitude of slow waves of electrical activity in the smooth muscle of the gut?

A

between 10-50mV

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62
Q

what is the tone of the smooth muscle of the gut?

A

basal level of tension between slow waves of depolarisation

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63
Q

what are the pacemakers in the gut?

A

the ICCs (interstitial cells of Cajal)

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64
Q

what are the ICCs?

A

specialised smooth muscle cells containing a few contractile elements located mainly between the longitudinal and circular muscle layers. innervated by ENS, acts as pacemakers for gut smooth muscle

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65
Q

how do the ICCs act as pacemakers?

A

gap junctions with each other and nearby smooth muscle cells in both circular and longitudinal layers: slow waves propagated within the ICC network and spread from there to the smooth muscle cells

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66
Q

what does depolarisation of smooth muscle cells by slow waves originating in the ICCs do?

A

results in opening of L-type VGCaCs in their plasma membranes so calcium enters cell- if enough enters then the muscle will contract, APs may be generated if it exceeds a certain threshold- spike potential

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67
Q

which are longer, spike potentials in smooth muscle or APs in a nerve?

A

spike potential is up to 20ms longer

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68
Q

how do excitatory substances (e.g.. ACh) increase amplitude of slow waves in gut smooth muscle?

A

opening cation channels which contribute to the depolarisation- more depolarisation means more spikes, more calcium entering cell, stronger contraction

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69
Q

how do inhibitory substances (eg. NA) decrease amplitude of slow waves in gut smooth muscle?

A

opening of hyperpolarising K+ channels resulting in weaker contraction/no contraction if amplitude under contraction threshold

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70
Q

what causes tonic contraction of sphincter muscle?

A

can be caused by continuous sequence of APs, partial depolarisation of the smooth muscle cell membrane without APs or other mechanisms resulting in sustained levels of intracellular Ca2+

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71
Q

what is segmentation?

A

where different regions of the circular muscle of the gut contract to aid mixing

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72
Q

what drives and modulates segmental contraction in the gut?

A

driven by slow waves initiated in the ICCs, modulated by nerves and hormones (e.g. gastrin)- excitatory parasympathetic stimulation and inhibitory sympathetic stimulation

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73
Q

what is neurocrine transmission?

A

when nerve terminals release a transmitter onto a target cell or into blood

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74
Q

what receptors does ACh act on in the gut? effect of this?

A

muscarinic receptors. excites smooth muscle and stimulates secretion of many glands

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75
Q

what do NO and vasoactive internal peptide (VIP) do in the gut?

A

typically relax smooth muscle, VIP stimulates secretion

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76
Q

what does NA do in the gut?

A

released by sympathetic neurons, typically inhibitory but promotes contraction of sphincters and vascular smooth muscle

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77
Q

what is paracrine transmission?

A

involves a locally-produced substance diffusing through the ECF to work on neighbouring cells of a different cell type

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78
Q

what is endocrine transmission?

A

involves transmitters travelling via the blood

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79
Q

what sort of hormones are all GI hormones?

A

peptides secreted by the enteroendocrine cells which are scattered throughout the gut epithelium

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80
Q

role of the apical membrane on most enteroendocrine cells?

A

has receptors that detect luminal conditions and stimulate hormone release in response

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81
Q

what cells secrete secretin and why?

A

S cells of the duodenum in response to the presence of acid

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82
Q

roles of secretin?

A

stimulates pancreatic growth HCO3- and water secretion, inhibits gastric acid secretion and motility, promotes constriction of the pyloric sphincter

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83
Q

what cells release gastrin and why?

A

G cells of the gastric antrum and duodenum in response to nervous stimulation + presence of peptides and amino acids

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84
Q

roles of gastrin?

A

stimulates gastric acid secretion by parietal cells, promotes growth of the oxyntic mucosa

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85
Q

what cells release cholecystokinin (CCK)?

A

I cells in the duodenum and jejunum in response to long chain FFAs and mono-glycerides

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86
Q

roles of cholecystokinin?

A

stimulates gall-bladder contraction, pancreatic secretion and growth, inhibits gastric emptying and appetite

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87
Q

what are the incretins? what is their function?

A

GIP (glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like peptide 1). augment insulin release from pancreas following a meal

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88
Q

what secretes GIP? what secretes GLP-1?

A

K cells in the upper SI secrete GIP, L cells in Si and Li secrete GLP-1

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89
Q

role of GLP-1 agonists as a drug?

A

used to treat type II diabetes

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90
Q

what secretes motilin, what controls this release?

A

M cells in upper SI, under neural control, cyclical release during fasting

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91
Q

what is the only know action of motilin?

A

initiates migrating myoelectric complex

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92
Q

what secretes grehlin? when?

A

endocrine cells of the stomach in response to fasting

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93
Q

role of grehlin?

A

works on hypothalamus to stimulate appetite and promotes GH release from pituitary gland

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94
Q

what is potentiation?

A

when the response of a cell with receptors for more than 1 type of messenger/different types of receptor for the same messenger exceeds the sum of the responses to each messenger delivered individually causing activation of different pathways with same end point

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95
Q

what is the difference between the secretion produced by the parotid vs the sublingual and submandibular glands

A

parotid only produces serous secretion, sublingual and submandibular produce mixed mucous/serous secretion

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96
Q

major functions of saliva?

A

lubrication, defence, buffering, digestion

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97
Q

how does saliva provide lubrication?

A

glycoproteins called mucins produced by mucus secreting glands.

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98
Q

how does saliva provide defence?

A

contains isozyme, lactoferrin and antibodies (IgA). proline rich proteins bind to and neutralise the effects of plant tannins in humans + herbivores

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99
Q

how does saliva provide buffering?

A

HCO3- ions raise pH of saliva- from slightly acidic at basal secretion level to around 8 during active secretion

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100
Q

how does saliva provide digestion?

A

contains amylase (not in cats, dogs or horses) which breaks down starch to oligosaccharides. inhibited by low pH in stomach, when protected inside bolus of food activity can continue for up to 1/2 an hour, has time to digest up to 75% of the starch in a meal

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101
Q

what produce the primary secretion of salivary glands? what is its composition?

A

the acinar cells. it is isotonic to plasma and high in NaCl

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102
Q

how is water drawn into the acinar lumen?

A

osmosis due to the accumulation of NaCl in the lumen

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103
Q

what do the acinar cells secrete?

A

the primary secretion, plus salivary enzymes and other proteins by exocytosis

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104
Q

what helps to empty saliva into ducts?

A

contraction of myoepithelial cells

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105
Q

what happens to the primary secretion as it proceeds through the ducts?

A

modified by the duct cells, becomes more hypotonic, ion exchange of Na+ for K+ and HCO3-

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106
Q

what does aldosterone promote in the salivary ducts?

A

ion exchange

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107
Q

what mediates almost the entire control of salivation?

A

the ANS

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108
Q

what is the cephalic phase of digestion?

A

anticipatory response to prospect of food which promotes salivation

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109
Q

role of parasympathetic output to the salivary glands?

A

ACh and VIP promote vasodilatation and increase blood supply, metabolism and growth. also causes contraction of the myoepithelial cells and opens more of the acinar cell channels increasing volume of saliva secreted

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110
Q

role of sympathetic output to the salivary glands?

A

promote myoepithelial cell contraction and via cAMP promotes exocytosis increasing protein content

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111
Q

what is the overlap between the sympathetic and parasympathetic pathways in the acinar cells of the salivary glands?

A

crossover between the cAMP (sympathetic) and Ca2+ (parasympathetic) pathways

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112
Q

what initiates swallowing?

A

when food is pushed towards the back of the mouth by the tongue, touch receptors in the pharynx initiate the swallowing (deglutition) reflex, coordinated in swallowing centre in medulla and lower pons

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113
Q

what is deglutition apnoea?

A

respiratory system of the medulla is directly inhibited by the swallowing centre for the brief time it takes to swallow

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114
Q

muscles of upper, middle and lower 1/3 of human oesophagus?

A

upper 1/3 is striated, middle is mix of striated and smooth, lower 1/3 is entirely smooth

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115
Q

peristalsis in the oesophagus?

A

primary peristaltic wave starts just below UOS, sweeps bolus downwards at 3-5cm/sec. if doesn’t manage to be moved all the way to stomach secondary peristaltic wave initiated by persistent distension of oesophagus- initiated partly by local reflex, partly through vagovagal reflex

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116
Q

what is the lower oesophageal sphincter?

A

region of specialised circular smooth muscles at the bottom of oesophagus, controlled by ENS fibres which receive input from ANS. tonically contracted, feed-forward vagal reflex means relaxes before food has even arrived- relaxation believed to be promoted by NO

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117
Q

importance of the LOS?

A

preventing the acid contents of the stomach from entering the oesophagus (gastro-oesophageal reflux)

118
Q

how much mucus does the oesophagus secrete, what is its function?

A

only small amounts, used to lubricate food when swallowing and protect mucosa against acid reflux

119
Q

where is emesis (vomiting) coordinated?

A

vomiting centre in the medulla oblongata

120
Q

what is the chemoreceptor trigger zone for vomiting?

A

receptors on the floor of the 4th ventricle of the brain, stimulation of which leads to vomiting. lies outside blood brain barrier (so can be stimulated by blood-borne drugs)

121
Q

where can emetic drugs target?

A

can either travel in blood to chemoreceptor trigger zone for vomiting in the brain or work in GI tract sending signals to brain via vagus

122
Q

what does vomiting entail?

A

increased salivation, retroperistalsis (from middle of SI) sweeping contents up digestive tract into stomach through relaxed pyloric sphincter, lowering of intrathoracic pressure + increase in abdominal pressure as abdominal muscles contract, stomach contents propelled into oesophagus. lower oesophageal sphincter relaxes. if UOS stays contracted person retches, if UOS relaxes stomach contents are expelled

123
Q

general functions of the stomach?

A

acts as reservoir for food to be eaten quickly, releasing contents at controlled rate. facilitates digestion including initiating protein digestion, destroys some ingested microbes with acid, helps regulate appetite through feedback on brain, helps regulate activity of later parts of gut through feed-forward mechanisms

124
Q

what causes stomach fundus and body relaxation when oesophagus or stomach stretches?

A

vagovagal reflex

125
Q

which region of the stomach performs more forceful contractions?

A

the antrum- has thicker muscular walls

126
Q

what does the antrum lead into?

A

the pylorus

127
Q

what forms the pyloric sphincter?

A

circular muscles of the pylorus- it isn’t anatomically discrete from pylorus

128
Q

what limits rate of stomach opening?

A

narrow opening of pyloric sphincter

129
Q

describe gastric motility

A

ICCs in pacemaker zone of stomach body generate slow waves (around 3 per min), these propagate down towards pylorus, stop there as pyloric sphincter region lacks ICCs. towards antrum APs may be superimposed of plateaus of gastric slow waves

130
Q

what increases chance of gastric APs and therefor contractions in the fed state?

A

substances including ACh and gastrin increasing duration of the plateau phase of gastric slow waves

131
Q

what is retropulsion?

A

following meal contractions sweep down stomach body and antrum becoming increasingly powerful, as wave of contraction approaches pylorus the pyloric sphincter contracts to prevent passage of ingesta forcing stomach contents back towards middle of stomach. results in antral mill

132
Q

what is the antral mill?

A

movement of stomach contents towards pyloric sphincter and then back to middle of stomach (retropulsion), functions to break up larger particles

133
Q

what is chyme, how is it formed?

A

mix of food and gastric secretions formed in stomach during antral mill movement of stomach contents

134
Q

how are contents allowed to pass into the duodenum out of the stomach?

A

pylorus relaxes between stomach contractions allowing contents out- only liquid and particles under 2mm diameter

135
Q

control of gastric emptying?

A

tone of pyloric sphincter controlled by ENS, ANS and circulating hormones. relaxation promoted by inhibitory fibres in ENS releasing NO. MMC promotes empting of residual particles, neural and hormonal reflexes involved in slowing emptying of stomach contents by inhibiting gastric motility/tightening the pyloric sphincter

136
Q

what causes slowing of gastric emptying as a response?

A

excess acid (duodenal pH below 4), fat digestion products in duodenum, peptides and amino acids in duodenum, duodenal stretch, the ileal brake

137
Q

what are the glands of the stomach mucosa?

A

cardiac glands near entrance of oesophagus, oxyntic glands in fundus and body, pyloric glands in antrum

138
Q

what do the cardiac glands secrete?

A

mainly mucus

139
Q

what do the oxyntic glands secrete?

A

oxyntic/parietal cells secrete HCl + IF, chief/peptic cells secrete pepsinogens + prochymosin, mucus secreting cells line the necks

140
Q

what do the pyloric glands secrete?

A

mucus from mucus secreting cells, G cells which secrete gastrin

141
Q

what promotes secretion of pepsinogens from chief cells?

A

vagal ACh and a cholinergic reflex in response to acidity

142
Q

effect of acidity on pepsinogens?

A

catalyses cleavage of active pepsinogens to form pepsins which digest proteins + peptides, pepsins can then also cleave pepsinogens. pepsins require low pH to work properly

143
Q

effect of acidity on prochymosin?

A

catalyses its cleavage to form active chymosin (rennin)

144
Q

effect of chymosin in neonatal mammals?

A

curdles milk converting the soluble protein caseinogen into insoluble casein, allows the milk protein to remain in stomach long enough to be acted on by pepsins

145
Q

what is responsible for milk curdling in human neonates?

A

pepsins- the prochymosin gene is inactive in human neonates unlike other mammal neonates

146
Q

what protects vitamin B12 from stomach acidity?

A

binds to haptocorrin, secreted in saliva

147
Q

what does B12 bind to in the SI once released by haptocorrin?

A

binds to intrinsic factor (glycoprotein secreted by stomach)

148
Q

what does the B12-IF complex do?

A

resists digestion by proteases, is taken up into the epithelial cells of the ileum by receptor mediated endocytosis

149
Q

what is the only gastric function essential to human life?

A

secretion of IF by the parietal cells

150
Q

functions of gastric acid?

A

delays gastric emptying, solubilises so improves absorption of Ca2+ and Fe, helps to release vitamin B12 from food, activates pepsinogens, destroys ingested microbes

151
Q

what does gastric juice contain more of between meals?

A

NaCl

152
Q

what happens when the parietal cells are stimulated?

A

tubules and vesicles with membranes containing transport proteins fuse with the luminal membrane of the parietal cell, at maximal stimulation gastric juice becomes largely isotonic solution of HCl

153
Q

why are the pumps of the gastric glands working against a large concentration gradient during maximum secretion?

A

intracellular pH is 7 and pH within gastric gland can be as low as 0.8

154
Q

how are protons generated and secreted by parietal cells?

A

generated from the intracellular reaction of CO2 with water under the influence of carbonic anhydrase (CA), secreted by the H+/K+-ATPAse pumps (proton pumps) on luminal membrane of parietal cells

155
Q

what else is formed in the reaction to generate H+ in parietal cells, how is this secreted?

A

H2O + CO2 -> HCO3- + H+, exchanged into ECF for Cl- by secondary active transporter on the basolateral membrane using energy from the electrochemical gradient for HCO3-

156
Q

how is Cl- secreted by the parietal cells?

A

enters from basolateral side in exchange for HCO3-, exits down electrochemical gradient through channels in luminal membrane

157
Q

effect on blood plasma as acid is secreted by gastric glands?

A

CO2 removed from plasma and bicarbonate added, gastric venous blood becomes more alkaline

158
Q

controllers of acid secretion by parietal cells?

A

1 endocrine transmitter (gastrin), 1 paracrine transmitter (histamine), and 1 neurocrine transmitter (ACh)

159
Q

how does gastrin promote acid secretion by parietal cells?

A

released by G cells in antrum and duodenum, travels in blood to parietal cells. promotes histamine production and release from ECL cells, and increases free Ca2+ in parietal cell

160
Q

how is gastrin release stimulated?

A

local stretch reflexes via ACh, vagal stimulation via gastrin releasing peptide (GRP), peptides, a.a.s and Ca2+ in the stomach lumen

161
Q

how does histamine promotes acid secretion by parietal cells?

A

released from enterochromaffin-like cells in the gastric glands (so is paracrine transmitter), is agonist of HCl secretion, acts on H2 receptors to increase cAMP

162
Q

how does ACh promote acid secretion by parietal cells?

A

released from nerve terminals, promotes release of acid, histamine and gastrin, inhibits somatostatin release, increases free Ca2+ in parietal cell

163
Q

what is required for maximum secretion of HCl?

A

activation of Ca2+ and cAMP pathways

164
Q

what mediates inhibition of acid secretion from parietal cells?

A

somatostatin, secretin and prostaglandins

165
Q

how does somatostatin inhibit parietal cell acid secretion?

A

paracrine transmitter released from D cells in response to luminal acidity, inhibits parietal cells

166
Q

how does secretin inhibit parietal cell acid secretion?

A

released from S cells in response to acid in duodenum, inhibits acid secretion indirectly by stimulating vagal afferent fibres. reflexes elicited reduce gastrin release from G cells

167
Q

how do prostaglandins inhibit parietal cell acid secretion?

A

paracrine transmitters which promote bicarbonate and mucus production

168
Q

acid secretion in the cephalic phase of digestion?

A

acid secretion increases but negative feedback through somatostatin release and neural reflexes limits any pH change. accounts for around 30% of total secretion

169
Q

acid secretion in the gastric phase of digestion?

A

protons buffered by proteins in food, luminal pH rises to around 6, releases secretory mechanisms from inhibition so dramatic rise in acid secretion, compounded by stretch of stomach wall causing vagovagal and local reflexes to increase gastrin and acid release, and peptides and amino acids stimulating G cells to increase gastrin secretion

170
Q

acid secretion in the intestinal phase of digestion (when chyme enters duodenum)?

A

duodenal stretch initially triggers vagovagal relfexes increasing acid secretion by stomach, and peptides and amino acids cause gastrin release from duodenal G cells- as duodenal contents become increasingly acidic acid secretion by the stomach is decreased

171
Q

how is the stomach mucosa protected from acid and ulcer formation?

A

by secretion of mucus and bicarbonate by the mucous cells forming the epithelial lining of the stomach and in the necks of the gastric glands, which forms alkaline lining the gastric mucosal barrier which helps maintain the luminal surface of the stomach at pH 6-7

172
Q

how are the mucous cells that form the gastric mucosal barrier maintained?

A

epithelial mucous cells continually lost from stomach surface and replaced by mucous cells from necks of the gastric glands which migrate upwards and over the surface. neck mucous cells replaced as stem cell deeper within the glands divide and differentiate

173
Q

what causes gastric ulcers?

A

if the gastric mucosal barrier is compromised the surface of the stomach can be attacked by acid and pepsins causing a gastric ulcer

174
Q

how can gastric ulcers be treated?

A

with drugs that suppress acid secretion, including H2 receptor antagonists and H+/K+-ATPase proton pump inhibitors. if caused by Helicobacter pylori requires antibiotic treatment as well

175
Q

predisposing factors for ulcer formation?

A

overuse of NSAID drugs such as aspirin, presence of gram-negative bacterium Helicobacter pylori which inflames the stomach wall

176
Q

what does the pancreas secrete?

A

produces an endocrine secretion (insulin and glucagon) and an exocrine secretion which enters the duodenum and is HCO3- rich, as well as having enzymes like amylase, lipases, proteases, ribonucleases + deoxyribonucleases

177
Q

how do pancreatic acinar cells secrete enzymes?

A

exocytosis, proteases secreted as inactive zymogens

178
Q

how is pancreatic secretory trypsin inhibitor (PSTI) secreted?

A

in zymogen granules with trypsinogen

179
Q

role of pancreatic secretory trypsin inhibitor?

A

helps protect acinar cells from inappropriate trypsin activation

180
Q

what cells secrete the exocrine pancreatic secretion?

A

acinar cells secrete small amount of NaCl rich solution into acinus lumen, pancreatic duct cells secrete bulk of aqueous component of pancreatic juice in the form of HCO3- rich solution

181
Q

how is pancreatic secretion stimulated?

A

parasympathetic nerves, enteric neurons passing from stomach and duodenum. in cephalic phase secretion stimulated by feedforward control, in gastric phase occurs in response to vagovagal and local neural reflexes, in intestinal phase secretin stimulates HCO3- and water secretion from pancreatic duct cells to increase secretion

182
Q

main stimulus for cholecystokinin release?

A

fat digestion products in the duodenum

183
Q

effect of CCK on pancreatic exocrine secretion?

A

stimulates enzyme secretion from acinar cells, potentiates effects of secretin on duct cells

184
Q

effects of ACh, CCK, secretin and VIP on pancreatic cells?

A

ACh and CCK increase intracellular [Ca2+] whereas secretin and VIP increase intracellular [cAMP]- both augment secretion

185
Q

effect on cAMP on acinar and duct cells and therefore secretion?

A

opens the luminal chloride channels (in duct cells this is the cystic fibrosis transmembrane conductance regulator) increasing secretion

186
Q

what does the most common form of cystic fibrosis result in?

A

impaired water and electrolyte secretion into the pancreatic duct system

187
Q

effect of clogged pancreatic ducts?

A

leads to severe maldigestion and nutrient deficiency, combined with premature activation of proteolytic enzymes can cause pancreatic damage

188
Q

what is secreted by the gut epithelium?

A

NaCl by the intestinal crypts of Lieberkuhn and other epithelial cells

189
Q

effect of cholera toxin?

A

permanently high [cAMP] leading to excessive secretion of Cl- with Na+ and water following leading to potentially life-threatening diarrhoea

190
Q

how much doe the mucosal folds of Kerckring increase the SI SA?

A

around 3x

191
Q

how much do villi increase the SI SA?

A

10x

192
Q

how much does the brush border formed by microvilli increase the SI SA?

A

20x

193
Q

role of the crypts of Lieberkuhn between the villi?

A

secrete fluid and also contain the stem cells for the replacement of desquamated epithelial cells that are continuously lost from the gut

194
Q

how often is the entire SI epithelium replaced?

A

every 3-6 days

195
Q

how much fluid is secreted by the SI, pancreatic secretion and biliary secretions each day?

A

up to 2 litres from SI, matched by the other 2

196
Q

what do salivary and pancreatic amylase do? what can’t they do?

A

cleave the internal α-1,4 bonds in starch. can’t cleave the α-1,6 branching links or the α-1,4 bonds next to them

197
Q

result of amylase breakdown of starch?

A

smaller chains of glucose molecules (oligosaccharides) mostly 2 or 3 units long plus α-limit dextrins which contain the branch points

198
Q

what completes carbohydrate digestion after action of amylase?

A

enzymes on brush border of duodenum and jejunum

199
Q

what breaks down the α-1,4 bonds within glucose oligosaccharides?

A

glucoamylase

200
Q

what breaks down the α-1,6 bonds within glucose oligosaccharides?

A

α-dextrinase

201
Q

what digests lactose?

A

lactase

202
Q

what digests sucrose?

A

sucrase

203
Q

what digests trehalose?

A

trehalase

204
Q

what transporter on the apical membranes of duodenal and jejunal epithelial cells takes up glucose and galactose?

A

SGLT1 (sodium-glucose transport protein 1)

205
Q

what transporter on the apical membranes of duodenal and jejunal epithelial cells takes up fructose?

A

GLUT5 - facilitated diffusion transporter

206
Q

what is export of glucose, galactose and fructose into the ECF from the duodenal and jejunal basolateral membrane via?

A

GluT2

207
Q

how much of protein digestion do pepsins contribute? what in particular are they useful in digesting?

A

up to 15%, particularly useful in digesting collagen

208
Q

what are more important than pepsins in protein digestion?

A

pancreatic proteases

209
Q

what converts trypsinogen to active trypsin?

A

enteropeptidase on the brush border of the upper SI, trypsin itself, other pancreatic proteases (chymotrypsin, elastase), the carboxypeptidases

210
Q

role of pancreatic proteases?

A

digest proteins to peptides to be digested further by brush border peptidases

211
Q

where are brush border peptidases located?

A

apical membranes of epithelial cells in the upper SI

212
Q

how are the products of brush border peptidases (di and tripeptides) taken up into cells?

A

facilitated diffusion and secondary active transport

213
Q

what happens to di- and tripeptidases once within the intestinal cells?

A

further digested into amino acids which are released from the cells by facilitated diffusion or secondary active transport, some amino acids then used within the intestinal cells themselves

214
Q

what reduces calcium and iron availability in the SI?

A

their binding to other dietary constituents (e.g. phytate anions) to yield insoluble salts

215
Q

main mechanisms for calcium absorption in SI?

A

uptake both transcellularly and paracellularly, secreted into ECF by CA2+ pump and Na+/Ca2+ exchange pump

216
Q

how is iron absorbed in the SI?

A

iron reductase on duodenal brush border reduces Fe3+ to Fe2+ which is taken up via the proton-Fe2+ cotransporter DMT1, Fe2+ may also be taken up as haem. excreted into ECF by ferroportin

217
Q

how does iron travel in the blood (other than as part of haem)?

A

bound to the protein transferrin

218
Q

what happens to iron efflux into the ECF from duodenal cells in the presence of peptide hormone hepcidin? how does the body use this?

A

efflux is reduced, excess iron trapped in cell bound to ferritin- when epithelial cell shed the iron is lost. body increases hepcidin production to fight infection as bacteria need iron to grow

219
Q

where is sodium absorption greatest in the GI tract? why?

A

the SI, as movement down its electrochemical gradient into the SI cells is coupled to movement of monosaccharides via SGLT1 and some amino acids, as well as Na+/H+ antiporters

220
Q

what extra sodium transporters are present in the colon that aren’t in the SI?

A

epithelial sodium channels (ENaC)

221
Q

what provides the driving force for paracellular K+ uptake by the small intestine?

A

as water is absorbed potassium becomes concentrated

222
Q

net potassium flux in the colon?

A

normally net secretion via apical potassium channels

223
Q

chloride absorption in the digestive tract?

A

via paracellular pathway and via exchange with bicarbonate

224
Q

how does water enter the digestive tract?

A

through the ingesta (2l/day) and through GI secretions (saliva, stomach, pancreas, bile, crypts) (7l/day)

225
Q

how much of the normal 9l of water entering the digestive tract is absorbed by the SI, colon and lost in faeces? how much more can the gut take if necessary?

A

around 7.5 l in SI, around 1.4 in colon, so around 100ml lost in faeces. can take 2-3x more than this if necessary

226
Q

what is the standing gradient model of water uptake across an epithelium?

A

Na+ pumped into intercellular clefts by Na+ pumps concentrated around edges of the clefts on the basolateral membranes. anions follow. a solute concentration gradient is set up- highest near the tight junctions, decreasing towards the open ends where it becomes equal to the concentration in the bulk phase. due to high solute concentration within intercellular clefts water enters from the adjacent cells and from lumen via leaky tight junctions. rise in pressure drives flow across basement membrane whereupon water and salts taken up and removed by capillaries

227
Q

why is absorption in the SI isosmotic?

A

the SI epithelium is leaky

228
Q

why is much less water absorbed in the colon than the SI?

A

against a large osmotic gradient as tight junctions between cells are tighter limiting back-diffusion of ions

229
Q

how are the fat-soluble vitamins absorbed?

A

similarly to fat- transported mainly in lymph

230
Q

fat soluble vitamins?

A

A, D3, E, K

231
Q

how are the water-soluble vitamins absorbed?

A

in SI by diffusion or active transport

232
Q

how is vitamin B12 absorbed and how does it travel in blood?

A

absorbed via receptor-mediated endocytosis in ileum, exported from cells into blood, travels in blood bound to protein transcobalamin II

233
Q

size of liver lobules?

A

several mm long, up to 2mm diameter

234
Q

what is between liver lobules?

A

portal triads comprising branch of hepatic portal vein, branch of hepatic artery, branch of the bile duct

235
Q

what lines the sinusoids?

A

rows of hepatocytes

236
Q

what are bile canaliculi?

A

tiny channels that drain bile produced by hepatocytes lining sinusoids outwards towards the branches of bile duct that lie between lobules (bile flows countercurrent to blood)

237
Q

functions of the liver?

A

carbohydrate, protein and lipid metabolism (including cholesterol synthesis and excretion in bile directly/as bile acids), bile formation, vitamin + iron storage (A, D, E, K and B12), destruction and detoxification of hormones, drugs, toxins, filtration of blood (removal of effete erythrocytes + bacteria from gut), blood reservoir

238
Q

how does the liver take up monosaccharides from the portal vein?

A

GluT2 facilitated diffusion

239
Q

how much glycogen can accumulate in liver and muscle? how long can this provide for the body’s needs for?

A

up to 100g in liver, up to 400g in muscle cells. provides for body’s needs for up to 24 hours

240
Q

what happens to excess glucose in liver that can’t be converted to glycogen?

A

converted to triglycerides, exported as lipoproteins, stored as fat in adipocytes

241
Q

protein metabolism by liver?

A

extracellular proteins digested by macrophages, intracellular returned as amino acids to liver- which can interconvert amino acids, pyruvate and TCA cycle intermediates by transamination to synthesise non-essential amino acids. excess amino acids oxidised for energy directly or converted to glucose or ketone bodies. urea and glutamine produced and exported

242
Q

what does bile contain?

A

bile acids (65% of bile dry mass), phospholipids (20%), cholesterol (4%), bile pigments (0.3%)

243
Q

roles of bile?

A

promotion of fat absorption, excretion of waste, protection

244
Q

how does bile promote fat absorption

A

bile acids are surfactants, normally conjugated with glycine or taurine to increase their solubility, found as salts of cations like Na+. primary bile acids made from cholesterol in liver, some are converted to secondary bile acids by gut bacteria

245
Q

how does bile excrete waste

A

primary means of cholesterol excretion, also secreted excess heavy metals like copper and cadmium

246
Q

how does bile offer protection?

A

contains IgA, mucus and tocopherol (antioxidant)

247
Q

the role of the gall bladder

A

collection and concentration of bile before expulsion into digestive tract

248
Q

where is the sphincter of Oddi, what does it do?

A

at entrance to duodenum. contracts between meals so bile diverted into gallbladder. relaxed by CCK during a meal emptying gallbladder bile into duodenum

249
Q

role of CCK in gallbladder bile secretion?

A

during meal CCK relaxes sphincter of Oddi and contracts gall-bladder so bile empties into duodenum

250
Q

how are bile acids taken up in the terminal ileum and colon. how much is lost in faeces?

A

epithelial cells in terminal ileum take up bile acids by secondary active transport, most of rest absorbed passively in colon, 5% lost

251
Q

what happens to secondary bile acids in the hepatocytes?

A

some reconverted to primary bile acids. both secondary and primary then resecreted into bile canaliculi

252
Q

what is bilirubin?

A

bile pigment, yellow-coloured breakdown product of haem made in spleen, bone marrow and liver

253
Q

how does bilirubin travel around body?

A

travels in blood mainly bound to albumin, taken up by liver, rendered soluble by conjugation with glucuronic acid before excretion in the bile

254
Q

what happens to bilirubin in the distal ileum and colon?

A

bacteria break it down to urobilinogen, some of this is reabsorbed into blood and either resecreted in bile or secreted in urine, rest lost in faeces

255
Q

what happens to urobilinogen in urine and in the gut?

A

in urine oxidised to yellow-coloured urobin, in gut some converted to urobilin and some to brown stercobilin which is responsible for colour of faeces

256
Q

how do bile salts work?

A

amphipathic- their hydrophobic domains bind to surface of fat globule and hydrophilic domains face outwards- so dietary triglycerides and other lipids emulsified into tiny emulsion droplets in duodenum

257
Q

how are fats digested and absorbed?

A

associate with bile salts to form tiny emulsion droplets- greatly increases SA for attack by lipases. pancreatic lipase (in association with helper protein colipase) hydrolyses triglyceride within emulsion droplet to 2 FFAs and 1 monoglyceride. + addition of more bile salts -> eventual production of micelles which ferry products of fat digestion to brush border and enter epithelial cells either by simple diffusion or transport proteins

258
Q

how does cholesterol enter enterocytes?

A

special transporters

259
Q

effect of plant sterols on cholesterol absorption?

A

prevent it by displacing cholesterol from mixed micelles

260
Q

export of fat from gut epithelial cells?

A

fat digestion products + cholesterol bind FA binding proteins within epithelial cells of SI and are delivered to ER where they are converted back into triglycerides- combined with apolipoproteins, phospholipids and cholesterol to form chylomicrons (type of lipoprotein particle). chylomicrons exported from Golgi apparatus, released by exocytosis to enter central lacteals of villi, enter venous circulation via thoracic duct

261
Q

location and role of lipoprotein lipase?

A

bound to capillary walls in tissues including muscle, fat, lactating mammary gland. catalyses hydrolysis of triglycerides within chylomicrons to release FAs that diffuse into cells + chylomicron remnants and glycerol that are taken up by liver

262
Q

what happens to most dietary triglyceride?

A

ends up in adipocytes. when blood glucose low some is hydrolysed to release FFAs

263
Q

why does liver secrete VLDLs when fasting?

A

means of exporting triglyceride and hepatic cholesterol to the tissues

264
Q

what are the ketone bodies?

A

acetone, acetoacetate, β-hydroxybutyrate

265
Q

length of human SI in vivo?

A

3-5 metres long

266
Q

how long does chyme take to pass through human SI?

A

2-5 hours

267
Q

what does terminal ileum empty into?

A

large intestine at junction of caecum and colon- projecting lips referred to as ileocaecal valve

268
Q

what happens in gastroileal reflex?

A

ileal motility enhanced in response to signals from a full stomach

269
Q

what happens in colonileal reflex?

A

inhibits movement through sphincter when colon is full

270
Q

parts of the large intestine?

A

caecum, ascending, transverse, descending, sigmoid colon, rectum, anal canal

271
Q

length of large intestine in humans?

A

1.5m long

272
Q

how many taenia does the colon have?

A

3

273
Q

where in colon is faeces stored?

A

transverse colon

274
Q

roles of large intestine?

A

store, mix and process contents, expose contents to microbes and absorb nutrients from microbial fermentation, expel waste as faeces

275
Q

large intestinal motility?

A

ICC within circular muscle generate 3-6 slow waves/minute- duration of these can be prolonged by ACh

276
Q

transit time through colon?

A

usually 1-2 days

277
Q

why is transit time through colon so slow?

A

most colonic movements are low-amplitude contractions, propel contents slowly in retrograde direction giving time for fluid absorption

278
Q

what are HAPCs in colon?

A

high-amplitude propagating contractions which accelerated forward movement of colon contents periodically. associated with relaxation of haustra

279
Q

what is the internal anal sphincter?

A

thickening of the circular smooth muscle just inside the anus- has own myogenic tone modulated by ANS

280
Q

what is the external anal sphincter?

A

made of striated muscle, under somatic motor control, tonically contracted- tone will increase with rise in intra-abdominal pressure

281
Q

what happens when the rectum fills?

A

sensory nerves send signals to sacral spinal cord- responds via autonomic fibres in pelvic nerves resulting in highly propulsive movements. internal anal sphincter relaxes, external sphincter may be voluntarily relaxed, relaxation of pelvic floor muscles lowers anus straightening angle between rectum and anal canal, defecation aided by Valsalva manoeuvre

282
Q

what is lacking in Hirschsprung’s disease?

A

ENS ganglion cells in descending colon and internal anal sphincter - so reflex relaxation of rectum and internal anal sphincter can’t occur when rectum fills- colon dilates and may perforate

283
Q

effect of opioid receptors in the GI tract?

A

when stimulated by endogenous transmitters such as β-endorphins promote effects including decreased propulsion, decreased secretion, increased sphincter tone

284
Q

gut bacterial metabolism

A

bacteria will metabolise any carbohydrate that gets through to colon and produce VFAs which represent energy source for colonic cells- represents colonic salvage of energy that would otherwise be lost. also synthesise Vitamin K + B vitamins

285
Q

what does a high-fibre diet do?

A

substrate for metabolism of beneficial gut bacteria, relieves constipation, promotes satiety, protects against bowel cancer

286
Q

why does lactose intolerance cause diarrhoea?

A

undigested lactose reaches colon, colonic bacteria thrive and produce metabolites that cause osmotic water retention, diarrhoea and excess gas (some H2 which is absorbed and exhaled on breath)

287
Q

role of appendix and caecum?

A

appendix has mucosal walls with lots of GALT- local defence against infection which may assist with maturation of B lymphocytes and production of IgA antibodies. may be store of beneficial microbes used to re-inoculate gut after diarrhoea

288
Q

what is flatus?

A

gas in the digestive tract

289
Q

average composition of flatus?

A

50% N2, very small amount of O2, 25% H2, 15% CO2, 10% methane. odour from hydrogen sulphide + methyl sulphides mostly

290
Q

constituents of faeces?

A

75% water. rest is around 40% bacteria, 15% fat, 2.5% protein, 15% inorganic matter and rest indigestible fibre

HOM (9 decks)

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