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Physiology Flashcards

1
Q

What is the function of the mouth and oropharynx?

A

chops and lubricates food, starts carbohydrate digestion, propels food to oesophagus.

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2
Q

What is the function of the oesophagus?

A

propels food to the stomach.

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3
Q

What is the function of the stomach?

A

stores/churns foods continues carbohydrate digestion, starts protein digestion, regulates delivery of chyme to duodenum.

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4
Q

What is the function of the small intestine?

A

principle site of digestion and absorption of nutrients.

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5
Q

What is the small intestine made of?

A

duodenum, jejunum and ileum

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6
Q

What is the function of the large intestine?

A

colon reabsorbs fluid and electrolytes, stores faecal matter before delivery to rectum

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7
Q

what is the large intestine made of?

A

caecum, appendix and colon

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8
Q

What is the function of the rectum and anus?

A

regulated expulsion of faeces

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9
Q

What are the four major functions of the alimentary canal?

A
  • Motility (movement)
  • secretion
  • digestion
  • absorption
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10
Q

What type of muscle is mostly involved in motility?

A

smooth muscle

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11
Q

where would skeletal muscle be found which assists motility?

A

mouth, pharynx, upper oesophagus and external anal sphincter

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12
Q

what is secretion of the alimentary canal required for?

A

digestion, protection and lubrication

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13
Q

what chemical process are foods digested by?

A

enzymatic hydrolysis

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14
Q

what happens during circular muscle contraction?

A

lumen becomes narrower and longer

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15
Q

what happens during longitudinal muscle contraction?

A

intestine becomes shorter and fatter

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16
Q

what happens during muscularis mucosae contraction?

A

change in absorption and secretory area of mucosa, mixing activity.

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17
Q

what are adjacent smooth muscle cells coupled by?

A

gap junctions, electrical currents flow from cell to cell.

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18
Q

what is a synchronous wave?

A

hundreds of cells are depolarised and contract at the same time as a single unit smooth muscle.

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19
Q

what is spontaneous activity across the coupled cells driven by?

A

specialised pacemaker cells and modulated by intrinsic and extrinsic nerves and hormones.

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20
Q

what does slow wave electrical activity determine?

A

frequency, direction and velocity of rhythmic contractions

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21
Q

what is slow wave electrical activity driven by?

A

interstitial cells of cajal (ICCs) - pacemaker cells located between circular and longitudinal muscle layers.

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22
Q

where do ICCs sometimes form bridges?

A

between nerve endings and smooth muscle cells

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23
Q

when does contraction of the intestines occur?

A

when the slow wave amplitude is sufficient to reach a threshold to trigger smooth muscle cell calcium action potentials.

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24
Q

what factors affect whether slow wave amplitude threshold is reached?

A

neuronal stimuli
hormonal stimuli
mechanical stimuli

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25
Q

what excitatory influences are due to parasympathetic stimulation?

A
  • increased gastric, pancreatic and small intestinal secretion
  • blood flow and smooth muscle contraction
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26
Q

what inhibitory influences are due to parasympathetic stimulation?

A

relaxation of some sphincters, receptive relaxation of stomach

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27
Q

what is the parasympathetic nerve supply?

A

preganglionic fibres (releasing Ach.) synapse with ganglion cells within the enteric nervous system (ENS)

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28
Q

where is the symapthetic innervation?

A

preganglionic fibres (reelasinf ACh) synapse in the prevenertebral ganglia.

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29
Q

what excitatory influences are due to sympathetic stimulation?

A

increased spincher tone

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30
Q

what inhibitory influences are due to sympathetic stimulation?

A

decreased motility secretion and blood flow

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31
Q

what is peristalsis?

A

a wave of relaxation, followed by contraction, that normally proceeds a short distance along the gut in an aboral direction triggered by distension of the gut wall.

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32
Q

what is segmentation?

A

rhythmic contractions of the circular muscle that mix and divide luminal contents.

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33
Q

where does segmentation occur?

A

in the small intestine (in the fed state)

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34
Q

what is segmentation called in the large intestine?

A

haustration

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35
Q

what is colonic mass movement?

A

powerful sweeping contraction that forces faeces into the rectum - occurs a few times a day

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36
Q

what is migrating motor complex (MMC)?

A

powerful sweeping contraction from stomach to terminal ileum

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37
Q

How many sphincters are there in the GI tract?

A

6 excluding the sphincter of Oddi

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38
Q

what are sphincters?

A

act as one way valves by maintaining a positive resting pressure relative to two adjacent structures

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39
Q

what does the upper oesophageal sphincter do?

A

relaxes to allow swallowing, closes during inspiration

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40
Q

what is the upper oesophageal sphincter made of?

A

skeletal muscle

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41
Q

what does the lower oesophageal sphincter do?

A

relaxes to permit entry of food to stomach, closes to prevent reflux of gastric contents to the oesophagus

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42
Q

what does the pyloric sphincter do?

A

regulates gastric emptying, usually prevents duodenal gastric reflux

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43
Q

what does the iloecaecal valve do?

A

regulates flow from ileum to caecum

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44
Q

what are the internal and external anal sphincters regulated by?

A

defaecation reflex

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45
Q

what does the myenteric plexus do?

A

mainly regulates motility and sphincters

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46
Q

what does the submucous plexus do?

A

mainly modulates epithelia and blood vessels

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47
Q

what is an example of the local reflex?

A

peristalsis

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48
Q

what is an example of short reflex?

A

intestino-intestinal inhibitory reflex

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49
Q

what is an example of long reflex?

A

gastroileal reflex

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50
Q

what is energy homeostasis?

A

physiological process whereby energy intake is matched to energy expenditure over time

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51
Q

what are some consequences of metabolic stress?

A 
metabolic syndrome 
central obesity
dyslipidemia 
insulin resistance 
type 2 diabetes
cardiovascular disease
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52
Q

how do you calculate body mass index?

A

weight (kg) / square of . height (m)

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53
Q

what does the brain do when you try to lose weight?

A

brain views extra weight sd normal and dieting may be a threat to body survival e.e defends new weight

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54
Q

how does the CNS influence energy balance and body weight?

A

behaviour - feeding and physical activity
ANS activity - regulates energy expenditure
neuroendocrine system - secretion of hormones

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55
Q

what is the site of integration?

A

brain

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56
Q

which part of the brain is responsible for energy homeostasis

A

hypothalamus

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57
Q

which part of the hypothalamus causes obesity?

A

lesioning ventromedial hypothalamus

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58
Q

which part of the hypothalamus causes leanness?

A

lesioning lateral hypothalamus

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59
Q

what basic concepts underlie control of energy intake and body weight?

A
  1. satiety signalling
  2. adiposity negative feedback signalling
  3. food reward
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60
Q

which hormone is the hunger hormone?

A

Ghrelin

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61
Q

which two hormones report fat status to brain?

A

leptin and insulin

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62
Q

what molecules are responsible for digestion?

A

pepsin and HCL

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63
Q

what molecule is responsible for carbohydrate digestion in the stomach?

A

salivary amylase

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64
Q

what does food mixed with gastric secretions produce?

A

semi-liquid chyme

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65
Q

what are the two mechanical regions of the stomach?

A

orad and caudad stomach

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66
Q

what is the relaxation of the orad region of the stomach driven by?

A

vagas nerve

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67
Q

what does orad region not have that the caudad region does?

A

no slow wave activity

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68
Q

why are tonic contractions in the orad region weak?

A

due to thin musculature

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69
Q

how are contents propelled to the claudad region?

A

by low amplitude tonic contractions of about 1 minute duration - stomach size decreases after

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70
Q

what does gastrin do?

A

decrease contractions and hence the rate of stomach emptying

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71
Q

how many slow waves are produced by the caudad region of the stomach?

A

3 waves per minute

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72
Q

do contractions occur from every slow wave in the caudad region in the stomach?

A

no, only contract when threshold is reached

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73
Q

what are phasic peristalic contractions driven by?

A

suprathreshold slow waves

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74
Q

what do the phasic peristalic contractions do?

A

progress from midstomach to gastroduodenal junction propelling contents towards pylorus through which a very small volume of chyme flows into the duodenum

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75
Q

what is retropulsion?

A

velocity of contraction increases towards junction, overtaking the movement of chyme that rebounds against constricted distal antrum back into the relaxed body of the stomach

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76
Q

what does retropulsion do?

A

mixes gastric contents reducing chyme to small particles that pass through the pylorus

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77
Q

what determines the escape of chyme through the pyloric sphincter?

A

strength of antral wave

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78
Q

what factors effect how much chyme escapes the stomach?

A

gastric factors and duodenal factors

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79
Q

why does distension increase motility in the stomach?

A

stretch of smooth muscle, stimulation of intrinsic nerve plexuses, increased vagus nerve activity and gastrin release

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80
Q

what gastric factors are there that affect chyme rate?

A

rate of emptying proportional to volume of chyme in stomach and consistency of chyme

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81
Q

what neuronal response delays stomach emptying?

A

the enterogastric reflex - decreases antral activity by signals from intrinsic nerve plexuses and the ANS

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82
Q

what hormonal response delays stomach emptying?

A

release of enterogastrones e.g. cholecystokinin CCK from dueodenum inhibits stomach contraction

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83
Q

what stimuli within the duodenum drive the neuronal and hormone responses?

A
  • fat
  • acid
  • hypertonicity
  • distension
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84
Q

why does fat delay gastric emptying?

A

required for digestion and absorption in small intestine

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85
Q

why does acid delay gastric emptying?

A

time is required for neutralisation of gastric acid by bicarbonate secreted from the pancreas - important for optimal pancreatic digestive enzyme function

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86
Q

why does hypertonicity delay gastric emptying?

A

products of carbohydrate and protein digestion are osmotically active and draw water into the small intestine - danger of reduced plasma volume and circulatory disturbances (e.g. dumping syndrome)

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87
Q

what are the two secretion regions of the stomach?

A

oxyntic gland area and pylorlic gland area

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88
Q

what is the gastric mucosa composed of?

A

surface lining the stomach, pits, invaginations of the surface, glands, at the base of the pits responsible for several secretions

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89
Q

what is the function of HCL?

A
  • activates pepsinogen to pepsin
  • denatures protein
  • kills most micro-organisms ingested with food
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90
Q

what is the function of pepsinogen?

A
  • inactive precursor of the peptidase, pepsin.
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91
Q

what is the function of intrinsic factor and gastroferrin?

A

binds vitamin B12 and Fe2+ respectively, facilitating subsequent absorption

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92
Q

what is the function of histamine?

A

stimulates HCL secretion

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93
Q

what is the function of mucus in the stomach?

A

protective

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94
Q

what is the function of gastrin?

A

stimulates HCL secretion

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95
Q

what is the function of somatostatin?

A

inhibits HCL secretion

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96
Q

what is a secretagogue?

A

an agent that causes secretion

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97
Q

what are the three important secretagogue that induce acid secretion from the parietal cells?

A

acetylcholine (ACh)
gastrin
histamine

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98
Q

how do the secretagogue work in the direct pathway?

A

ACh, gastrin and histamine stimulate the parietal cell, triggering the secretion of H+ into the lumen

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99
Q

how do the secretagogue work in the indirect pathway?

A

ACh and gastrin also stimulate ECL cell, resulting in secretion of histamine. the histamine then acts on parietal cells

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100
Q

which molecules are responsible for sending satiation signals?

A
  • cholecystkinin (CKK)
  • Peptide YY
  • glucagon-like peptide 1
  • oxyntomodulin (OXM)
  • obestatin
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101
Q

where is gherlin produced?

A

oxyntic cells in the stomach

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102
Q

what are the functions of leptin?

A
  • food intake/energy expenditure/fat deposition
  • peripheral glucose homeostasis
  • maintenance of immune system
  • maintenance of reproductive system
  • angiogenesis
  • tumourigenesis
  • bone formation
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103
Q

During the resting state of the parietal cell where is H+/K+ATPase?

A

within the cytoplasmic tubulovesicles

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104
Q

where is H+/K+ATPase during the stimulated phase of the parietal cell?

A

traffics to the apical membrane taking residence in extended microvilli

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105
Q

what are the three phases of gastric acid secretion?

A
  • cephalic phase
  • gastric phase
  • intestinal phase
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106
Q

when does the cephalic phase of gastric acid secretion happen?

A

when the stomach is preparing to receive food

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107
Q

what is the cephalic phase driven by?

A

CNS and vagus nerves

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108
Q

when does the gastric phase of gastric acid secretion happen?

A

when food is in the stomach - involves both physical and chemical mechanism

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109
Q

when does the intestinal phase of gastric acid secretion happen ?

A

after food has left stomach- chyme entering the upper small intestine causes weak stimulation of gastric section via neuronal and hormonal mechanisms

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110
Q

what are some other stimulants of G cells apart from amino acids?

A

Ca2+
caffeine
alcohol

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111
Q

how is gastric acid secretion inhibited during the cephalic phase?

A

vagal activity decreases upon cessation of eating and following stomach emptying.

pain, nausea and negative emotions also decrease vagal nerve activity which reduces gastric acid secretion

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112
Q

How is gastric acid secretion inhibited during the gastric phase?

A

pH falls when food exits stomach - release of somatostatin from D cells recommences, decreasing gastrin secretion

prostaglandin E2 works to reduce histamine and gastrin mediated HCL secretion

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113
Q

How is gastric acid secretion inhibited during the intestinal phase?

A

factors that reduce gastric motility also reduce gastric secretion e.g. neuronal reflexes, enterogastrones

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114
Q

what do prostaglandins (PGE2 and PGI2) do?

A
  • reduce acid secretion
  • increase mucus and bicarbonate secretion
  • increase mucosal blood flow
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115
Q

What things does the small intestine receive from other organs?

A
  • chyme from stomach
  • pancreatic juice from pancreas
  • bile from gall bladder
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116
Q

what liquid does the small intestines secrete?

A

intestinal juice (succus entericus)

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117
Q

what does the small intestine move residue to the large intestine via?

A

ileocaecal valve

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118
Q

Where is gastrin released from?

A

G cells of gastric antrum and duodenum

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119
Q

what peptide hormones does the small intestine secrete?

A 
gastrin
cholecystokinin (CCK)
secretin 
motilin
glucagon-like insulinotropic peptide (GIP)
glucagon-like peptide-1 (GLP-1)
Ghrelin
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120
Q

where is CCK released from?

A

from I cells of duodenum and jujunum

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121
Q

where is secretin released from?

A

from S cells of duodenum, released in response to H+ and fatty acids in lumen

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122
Q

where is motilin released from?

A

from M cells of duodenum and jejunum

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123
Q

where is GIP released from?

A

from K cells of duodenum and jejunum

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124
Q

where is GLP-1 released from?

A

from L cells of the gut

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125
Q

where is ghrelin released from?

A

from Gr cells of the gastric antrum, small intestine and elsewhere

126
Q

what do all various peptide hormones secreted in the small intestines work on?

A

G-protein coupled receptors

127
Q

what control mechanisms enhance secretions of the small intestine?

A
  • distension/irritation
  • gastrin
  • CCK
  • secretin
  • parasympathetic nerve activity
128
Q

what control mechanisms decrease secretions of the small intestine?

A

sympathetic nerve activity

129
Q

why do secretions contain aqueous salt?

A

for enzymatic digestion

130
Q

what is segmentation in the empty ileum triggered by?

A

gastrin from the stomach (gastroileal reflex)

131
Q

what is strength of segmentation enhanced by?

A

parasympathetic activity

132
Q

what is strength of segmentation decreased by?

A

sympathetic activity

133
Q

what does the migrating motor complex (MMC) do?

A

clears small intestine of debris, mucus and sloughed epithelial cells between meals

134
Q

what is the migrating motor complex inhibited by?

A

feeding and vagal activity

135
Q

what is the MMC triggered by?

136
Q

what is the MMC suppressed by?

A

gastrin and CCK

137
Q

what are the endocrine pancreatic secretions?

A

insulin and glucagon

138
Q

what are the exocrine pancreatic secretions?

A

digestive enzymes (acinar cells), aqueous NaHCO3- solution (duct cells) - secreted to the duodenum collectively as pancreatic juice

139
Q

what does the pancreatic fluid do?

A
  • neutralises acidic chyme entering duodenum
  • provides optimum pH for pancreatic enzyme function
  • protects the mucosa from erosion by acid
140
Q

what can pancreatic enzymes do in the absence of all other enzymes?

A

completely digest food

141
Q

how is the cephalic phase of control of pancreatic secretion mediated?

A

by the vagal stimulation of mainly the acinar cells

142
Q

what does the gastric phase of control of pancreatic secretion evoke? what does this cause?

A

a vagovagal reflex resulting in parasympathetic stimulation of acinar and duct cells

143
Q

define digestion

A

enzymatic conversion of complex dietary substances to a form that can be absorbed

144
Q

what is luminal digestion mediated by?

A

pancreatic enzymes secreted into the duodenum

145
Q

what is membrane digestion mediated by?

A

enzymes situated at the brush border of epithelial cells

146
Q

what is absorption?

A

process by which the absorbable products of digestion are transferred across the atpical and basolateral membranes of enterocytes

147
Q

what is assimilation?

A

overall process of digestion and absorption

148
Q

what does secretin do?

A

promotes secretion of pancreatic and biliary HCO3-

149
Q

what does CCK do?

A
  • inhibits gastric emptying
  • causes secretion of pancreatic enzymes required for digestion
  • stimulates relaxation of sphincter of Oddi and contraction of gall bladder to eject bile into duodenum, - - - potentiates the action of secretin
150
Q

what must dietary carbohydrates be converted to before absorption?

A

monosaccharides

151
Q

what does GIP do?

A
  • simulates release of insulin from pancreatic Beta cells

- inhibits gastric emptying

152
Q

what is the function of alpha- amylase?

A

breaks down linear internal alpha-1,4 linkages but not terminal alpha-1,4 linkages. hence, no production of glucose

153
Q

what are the products of alpha-amylase?

A

linear glucose oligomers (maltotriose, maltose) and alpha-limit dextrins

154
Q

what are oligiosaccharidases?

A

integral membrane proteins with a catalytic domain that faces the lumen of the GI tract

155
Q

what does lactase do?

A

breaks down lactose to glucose and galactose

156
Q

what do all oligosaccharidases apart from lactase do?

A

cleave the terminal alpha-1,4 likages of maltose, maltotriose and alpha-limit dextrins

157
Q

what is sucrase specifically responsible for?

A

hydrolysing sucrose to glucose and fructose

158
Q

why is isomaltase unique?

A

only enzyme that can split the branching alpha-1,6 linkages of alpha-limit dextrins

159
Q

what can maltase do?

A

degrade the alpha-1,4 linkages in straight chain oligomers up to nine monomers in length

160
Q

what is lactose intolerance a consequence of?

A

inability to adequately digest lactose caused by lactase insufficiency

161
Q

what is primary lactase deficiency (primary hypolactasia)?

A

due to lack of the lactase persistence (LP) allele

162
Q

what is secondary lactase deficiency?

A

caused by damage to/infection of/ the proximal small intestine

163
Q

what is congenital lactase deficiency?

A

rare autosomal recessive disease - no ability to digest lactose from birth

164
Q

what does the ileum colonic microflora from the colon produce when lactose is delivered in a lactose intolerant person?

A

short-chain fatty acids
hydrogen
carbon dioxide
methane

165
Q

what do the by products of the ileum colonic microflora in lactose intolerant people cause?

A

bloating
abdominal pain
flatulence

166
Q

what does undigested lactose cause?

A
  • acidification of the colon

- an increased osmotic load: loose stool and diarrhoea

167
Q

where does the digestion of the final products of carbohydrate digestion occur?

A

duodenum and jejunum

168
Q

what happens during the absorption of the final products of carbohydrate digestion?

A
  • two step process involving entry and exit from the enterocytes via the apical and basolateral membranes
169
Q

what is glucose and galactose absorbed by?

A

secondary active transport mediated by SGLT1

170
Q

what is fructose absorbed by?

A

facilitated diffusion mediated by GLUT5

171
Q

what is exit for all monosaccharides mediated by?

A

facilitated diffusion by GLUT5

172
Q

how does SGLT1 work?

A
  1. 2 Na+ binds
  2. affinity for glucose increases, glucose binds
  3. Na+ and glucose translocate from extracellular to intracellular
  4. 2 Na+ dissociate, affinity for glucose falls
  5. glucose dissociates
  6. cycle is repeated
173
Q

what must proteins be digested to for efficient absorption?

A

oligopeptides and amino acids

174
Q

how many different pathways are there for protein digestion?

175
Q

how much daily energy intake is from protein assimilation?

176
Q

which pancreatic proteases in the duodenum act as endopeptidases?

A

trypsin, chymotrypsin and elastase

177
Q

which pancreatic proteases in the duodenum act as exopeptidases?

A

procarboxypeptidase A and procarboxypeptidase B

178
Q

what is the product of endopeptidases?

A

oligopeptides

179
Q

what is the product of exopeptidase?

A

single amino acids

180
Q

what is pepsin?

A

an endopeptidase

181
Q

what does pepsin prefer?

A

bonds between aromatic and larger neutral amino acids

182
Q

where are the additional proteases present?

A

at the brush border and within the cytoplasm of the enterocyte

183
Q

what do brush border peptidases have an affinity for?

A

larger oligopeptides (3-8 amino acids)

184
Q

what are bursh border peptidases?

A

numerous, either endopeptidases or exopeptidase, the latter comprising both aminopeptidases and carboxypeptidases

185
Q

what do cytoplasmic peptidases do?

A

primarily hydrolyse dipeptides and tripeptides

186
Q

how are amino acids transported across the apical membrane?

A

via a variety of amino acid transporters some of which are Na+ dependant and others Na+ independant

187
Q

how are oligopeptides transported across the apical membrane?

A

the H+/oligopeptide co-transporter, pepT1

188
Q

how are oligopeptides within the cytoplasm hydrolysed to amino acids?

A

by peptidases within the enterocyte

189
Q

how do amino acids exit the enterocyte across the basolateral membrane?

A

by several, Na+ independent transporters

190
Q

How much of the daily energy requirement is provided by ingested lipids?

191
Q

why do ingested lipids cause problems for digestion and absorption?

A

they are either insoluble or poorly soluble

192
Q

What must ingested lipids be converted to?

A

emulsion of small oil droplets suspended in water

193
Q

what does emulsion of small oil droplets occur by?

A
  • mouth: chewing
  • stomach: gastric churning and squirting through the narrow pylorus. content mixed with digestive enzymes from mouth and stomach
  • small intestine: segmentation and peristalsis mix the luminal content with pancreatic and biliary secretions
194
Q

How are emulsion droplets stabilised?

A

by the addition of a ‘coat’ of amphiphilic molecules that form a surface layer that includes certain products of lipid digestion, biliary phospholipids, cholesterol and bile salts.

195
Q

what is the name of the enzyme which digests food in the stomach during the gastric phase?

A

gastric lipase (lingual lipase in saliva)

196
Q

when is gastric lipase secreted?

A

in response to gastrin from chief cells

197
Q

what is the main lipid digestive enzyme in adults during the intestinal phase?

A

pancreatic (TAG) lipase

198
Q

when is pancreatic lipase secreted?

A

from acinar cells of pancreas in response to CCK which also stimulates bile flow

199
Q

what does the full activity of pancreatic (TAG) lipase require?

A
  • colipase co-factor
  • alkaline pH
  • Ca2+
  • bile salts
  • fatty acids
200
Q

what does digestion by lipase produce?

A

2-monoacylglycerol and free fatty acids

201
Q

where does pancreatic lipase mainly hydrolyse TAGs?

A

at the 1 and 3 positions

202
Q

when are bile salts released?

A

into the duodenum in bile from the gall bladder in response to CCK

203
Q

what is the role of bile salts?

A

act as detergents to help emulsify large lipid droplets to small droplets (they are amphipathic)

204
Q

what does failure to secrete bile salts result in?

A
  • lipid malabsorption - steatorrhoea (fat in feaces)

- secondary vitamin deficiency due to failure to absorb fat soluble vitamins (A,D,E,K)

205
Q

what do bile salts do?

A

increase surface area for attack by pancreatic lipase, but block access of the enzyme to the TAGs

206
Q

what is colipase secreted as?

A

inactive procolipase which is activated by trypsin

207
Q

what does colipase do?

A

binds to bile salts and lipase allowing access by the latter to tri- and di-acylglycerols

208
Q

what happens hen TAGs towards the surface of the emulsion droplets are hydrolysed?

A

they are replaced, by TAGs within the core, decreasing droplet size until a mixed micelle results

209
Q

what do short chain (<6 carbon) and medium (8-12 carbon) fatty acids do during lipid absorption?

A

diffuse through the enterocyte, exit through the basolateral membrane and enter the villus capillaries

210
Q

what do long chain (>12 carbon) fatty acids and monoglycerides do during lipid absorption?

A

they are resynthesized to triglycerides in the endoplasmic reticulum and are subsequently incorporated into chylomicrons

211
Q

how is cholesterol absorbed?

A
  • due to transport by endocytosis in clatherin coated pits by niemann-picj C1-like 1 (NPC1L1) Protein
212
Q

How is cholesterol absorption prevented?

A
  • ezetimibe binds to NPC1L1, Prevents internalisation and thus cholesterol absorption.
213
Q

how is Ca2+ absorbed?

A

occurs by passive (i.e. paracellular; whole length of small intestine) and active (i.e. transcellular; mainly duodenum and upper jejunum) transport mechanisms

214
Q

what is active Ca2+ regulated by?

A

1,25-dihydroxyvitamin D3 (calcitriol) and parathyroid hormone (increases 1,25-dihydroxyvitamin D3 synthesis)

215
Q

what does a deficiency of iron result in?

216
Q

what does an excess of iron result in?

217
Q

what is Fe3+ reduced to Fe2+ by?

A
  • HCL
  • Vitamin C
  • brush border cytochrome B ferric reductase
218
Q

what does Fe2+ bind to in the stomach?

A

gastroferrin

219
Q

what is expression of divalent metal transporter 1 (DMT1 aka SLC11A2) increased/reduced by?

A

increased - blood loss

reduced- human haemochromatosis protein (HFE)

220
Q

what is the storage form of iron called?

221
Q

what is ferroportin 1 (aka SLC40A1) negatively regulated by?

A

the hormone hepcidin released from liver when body iron are high

222
Q

how is vitamin B12 (cobalamin) absorbed?

A
  1. vitamin B12 ingested in food bound to proteins
  2. stomach acid releases vitamin B12 from protein
  3. haptocorin, secreted in saliva binds vitamin b12, Released in stomach
  4. stomach parietal cells release intrinsic factor
  5. pancreatic proteases digest haptocorin in small intestine, vitamin B12 release
  6. vitamin B12 binds to intrinsic factor in small intestine
  7. Vitamin B12 intrinsic factor complex absorbed in terminal ileum by endocytosis
223
Q

which group of people are susceptible to vitamin B12 deficiency?

A

vegans - no vitamin B12 in vegetables

224
Q

what does absorption of fat soluble vitamins require?

A

adequate bile secretion and an intact intestinal mucosa

225
Q

how are fat soluble vitamins usually transported?

A

passively into enterocytes

226
Q

what are fat soluble vitamins incorporated into?

A

chylomicrons or VLDLs

227
Q

what are fat soluble vitamins distributed by?

A

intestinal lympathics

228
Q

how are water soluble vitamins transported?

A

may be either Na+ dependant or Na+ independant

229
Q

what are the water soluble vitamins?

A

B complex vitamins (not B12), C and H

230
Q

what is the longitudinal smooth muscle layer in caecum and colon divided into?

A

three strands - the taeniae coli

231
Q

when is smooth muscle thickened in the large intestine?

A

at the internal anal sphincter, which is surrounded by the skeletal muscle of the external anal sphincter

232
Q

what does activity of the taeniae coli and circular muscle layers in colon cause?

A

‘sac-like’ bulges - the haustra - that very slowly change in location

233
Q

what does the caecum normally receive?

A

approx. 1-2l of material (undigested residues, unabsorbed biliary components, unabsorbed fluid) per day from the terminal ileum

234
Q

how is entry into the caecum permitted?

A

by the gastroileal reflex in reponse to gastrin and CCK through the ‘one way’ ileocaecal valve

235
Q

How does the ileocaecal valve act by?

A
  • maintaining a positive resting pressure
  • relaxing in response to distension of the duodenum
  • contracting in response to distension of the ascending colon
  • being under the control of the vagus nerve, sympathetic nerves, enteric neurones and hormonal signals
236
Q

what is the appendix?

A

a blind-ended tube with extensive lymphoid tissue connected to the distal caecum via the appendiceal orifice

237
Q

how is appendicitis caused?

A

appendiceal orifice obstructed by a faecalith

238
Q

what are the primary functions of the colon?

A
  • absorption of Na+, Cl- and H20 to condense ileocaecal material to solid or semi solid stool
  • absorption of short fatty acids
  • secretion of K+, HCO3- and mucus
  • reservoir of storage of colonic contents
  • periodic elimination of faeces
239
Q

what does the mucosa of the colon have that increases its surface area?

A

colonic folds, crypts and microvilli

240
Q

what do surface epithelial cells (colonocytes) of the colon do?

A

mediate electrolyte absorption which, by osmosis, drives absorption of H20

241
Q

what do crypt cells in the colon do?

A

mediate ion secretion

242
Q

what do goblet cells in the colon secrete?

A
  • copious mucus containing glycosaminoglycans

- trefoil proteins involved in host defence

243
Q

what is Na+ absorption and K+ secretion enhanced by?

A

aldosterone

244
Q

when might significant loss of K+ in the faeces occur?

A

secretory diarrhoea

245
Q

what are the patterns of motility in the large intestine?

A
  • haustration
  • peristaltic propulsive movements
  • defaecation
246
Q

what is haustration?

A
  • haustra are saccules caused by alternative contraction of the circular muscle
  • disappear before and reappear a mass movement
  • probably generated by slow wave activity
  • mixes content - allows time for fluid and electrolyte reabsorption
247
Q

what is mass movement of the colon?

A

simultaneous contraction of large sections of the circular muscle of the circular muscle of the ascending and transverse colon, powerfully drives faeces into distal regions

248
Q

what does mass movement in the distal colon do?

A

propels faeces in the rectum triggering the defaecation reflex in response to rectal stretch

249
Q

why are the bacteria in the colon beneficial?

A
  • increase intestinal immunity by competition with pathogenic microbes
  • promote motility and help maintain mucosal integrity
  • synthesise vitamin K2 and free fatty acids that are absorbed
  • activate some drugs
250
Q

where does gas in the colon arise from?

A
  • swallowed air that enters the small intestine is either absorbed or passed onto colon
  • bacteria in the colon which attack forms of carbohydrate that are indigestible to humans
  • gas that is not absorbed in the large intestine is expelled through the anus
251
Q

what is constipation?

A

presence of hard faeces within the colon (results from delay in defaecation and enhanced absorption of H2O)

252
Q

what are some causes of constipation?

A
  • ignoring/suppressing, the urge to defaecate
  • decreased colonic motility
  • obstruction of faecal movement
  • paralytic ileus following abdominal surgery
  • impairment of motility/defaecation reflex
253
Q

what symptoms may arise from constipation?

A
  • abdominal discomfort
  • headache
  • loss of appetite
  • general malaise (caused by prolonged distension of the large intestine - not toxins)
254
Q

if hardened, calcified, faecal matter gets into the appendix what may happen?

A

causes appendicites

255
Q

what is nausea?

A

subjective, highly unpleasant, sensation - normally felt in throat and stomach as ‘sinking’ sensations

256
Q

what does nausea usually involve?

A
  • pallor, sweating excessive salvation and relaxation of stomach and lower oesophagus
  • upper intestinal contractions, forcing intestinal contents by reverse peristalsis into the stomach
257
Q

what does retching involve?

A
  • rhythmic reverse peristalsis of the stomach and oesophagus
  • forceful, involuntary, contraction of abdominal muscles and the diaphragm
  • upper intestinal contractions, forcing intestinal contents by reverse peristalsis into the stomach
  • pallor, sweating excessive salvation
258
Q

what is the medical term for vomiting?

259
Q

how does vomiting commence?

A

with forceful inspiration, reflex closure of the glottis and elevation of the soft palate to close off the airways and nasal passages

260
Q

what is vomiting co-ordinated by?

A

by the vomiting centre (VC) in the medulla oblongata of the brain stem

261
Q

what is the steps of the vomiting cycle?

A
  1. suspension of intestinal slow wave activity
  2. retrograde contractions from ileum to stomach
  3. suspension of breathing (closed glottis - prevents aspiration)
  4. relaxation of LOS-contraction of diaphragm and abdominal muscles compresses stomach
  5. ejection of gastric contents through open UOS
  6. Repeat of cycle
262
Q

what is vomiting often preceded by?

A
  • profuse salvation
  • sweating
  • elevated heart rate
  • sensation of nausea
263
Q

What is the pathway of vomiting when induced by toxics?

A
  1. toxin materials in gut lumen/ systemic toxins
  2. stimulate enterochromaffin cells in mucosa (release of mediators)
  3. depolarisation of sensory afferent terminals in mucosa
  4. action potential discharge in vagal afferents to brainstem (CTZ and NTS)
  5. co-ordination of vomiting by the ‘vomiting centre’
264
Q

What does mechanical stimuli (e.g. pharynx); pathology within the GI tract (e.g. gastritis) or other visceral organs (e.g. myocardial infarction) stimulate that causes vomiting?

A

vagal afferents to brainstem (CTZ and NTS)

265
Q

what do absorbed toxic materials and drugs in blood stimulate that causes vomiting?

A

CTZ within the AP of brainstem (lacks an affective BBB)

266
Q

what does the vestibular system (e.g. motion sickness) signal through to cause vomiting?

A

vestibular nuclei > CTZ

267
Q

what does stimuli within the CNS (e.g. pain, repulsive sights and odours, fear, anticipation, psychological factors) signal through to cause vomiting?

A

cerebral cortex, limbic system > medulla

268
Q

what is the ‘vomiting centre’?

A

a group of interconnected neurones within the medulla that are driven by a central pattern generator (CPG) that receives input from the NTS

269
Q

what are the consequences of severe vomiting?

A
  • dehydration
  • loss of gastric protons and chloride (causes hypocholoraemic metabolic alkalosis, raising blood pH)
  • hypokalaemia
  • rarely, loss of duodenal bicarbonate may cause metabolic acidosis
  • rarely, oesophageal damage (mallory-weiss tear)
270
Q

what is absorption of water?

A

a passive process driven by the transport of solutes (particularly Na+) from the lumen of the intestines to the blood stream

271
Q

what is diarrhoea?

A

loss of fluid and solutes from the GI tract in excess of 500ml per day

272
Q

How is the osmotic force for reabsorption of water provided?

A

by the reabsorption of Na+

273
Q

where does the Na+/glucose co-transport and the Na+/amino acid co-transport occur?

A

throughout the small intestine and is the most important in the postprandial period (also occurs in the colon in the new born)

274
Q

where does Na+/H+ exchange occur? what is it stimulated by?

A

in the duodenum and jejunum and is stimulated by the alkaline environment of the lumen due to the presence of luminal HCO3-

275
Q

where does the parallel Na+/H+ and Cl-/HCO3- exchange occur?

A

ileum and colon most important in the interdigestive period

276
Q

where does epithelial Na+ channels (ENaC) occur?

A

in the colon (distal particularly)

277
Q

what are Na+/glucose co-transport and the Na+/amino acid co-transport examples of?

A

secondary active transport

278
Q

what does electorgenic mean?

A

producing a change in the electrical potential of a cell

279
Q

what does the overall transport of Na+ generate in the Na+/glucose co-transport and the Na+/amino acid co-transport?

A

a transepithelial potential (VTE) in which the lumen is negative - this drives the parallel absorption of Cl-

280
Q

what is the parallel Na+/H+ and Cl-/HCO3- regulated by?

A

intracellular cAMP, cGMP and Ca2+, all reduce NaCl absorption

281
Q

what does reduction in NaCl absorption cause?

282
Q

what is epithelial Na+ channels (ENaC) regulated by?

A

increased by aldosterone

283
Q

what are the actions of aldosterone in epithelial Na+ channels (ENaC)?

A
  1. opens ENaC (seconds)
  2. inserts more ENaC into membrane from intracellular vesicle pool (minutes)
  3. increases synthesis of ENaC and Na+/K+-ATPase (hours)
284
Q

what is the driving force in the small intestine for Cl- absorption?

A

provided by lumen negative potential due to electrogenic transport of Na+ (Na+/glucose and Na+/amino acid)

285
Q

what is the driving force in the large intestine for Cl- absorption?

A

provided by the lumen negative potential due to electrogenic movement of Na+ through ENaC

286
Q

which cells secrete Cl-?

A

crypt cells

287
Q

what does low intracellular Na+ drive forward?

A

inward movement of Na+, K+ and Cl- via NKCC1

288
Q

why does little secretion of Cl- normally occur?

A

because apical CFTR is either closed or not present

289
Q

what is CFTR indirectly activated by?

A
  • bacterial enterotoxins (e.g. cholera toxin (V. cholerae), heat stable enterotoxin (E.coli), C. difficile toxin)
  • hormones and neurotransmitters (e.g. vasoactive intestinal peptide (VIP), guanylin, acetylcholine, bradykinin, 5-HT (serotonin)
  • immune cells products (e.g. prostaglandins, histamine)
  • some laxatives (e.g. bile acids)
290
Q

Activation of CFTR occurs indirectly as a result of the generation of second messengers, what do these include?

A

cAMP (e.g. cholera toxin, VIP, histamine)
cGMP (e.g. heat stable enterotoxin, guanylin)
Ca2+ (e.g. acetylcholine, bradykinin, 5-HT)

291
Q

what does the Cl- conductance mediated by CFTR result from?

A
  • opening of channels at the apical membrane

- insertion of channels from intracellular vesicles into the membrane

292
Q

what are the causes of diarrhoea?

A
  • infectious agents -viruses, bacteria
  • chronic disease
  • toxins
  • drugs
  • psychological factors
  • excess bile in colon
  • inflammation
  • congenital defects
  • impaired absorptions of NaCl
  • lactase deficiency
293
Q

what are the consequences of diarrhoea?

A

can result in dehydration (Na+ and H2O loss), metabolic acidosis (HCO3- loss) and hypokalaemia (K+ loss)
may be fatal if severe (e.g. cholera)

294
Q

what is the treatment of severe acute diarrhoea?

A
  • maintenance of fluid and electrolyte balance
  • use of anti-infective agents
  • use of non- antimicrobial antidiarrhoael agents
295
Q

what are the major metabolic functions of the liver?

A

regulation of carbohydrate, lipid and amino acid metabolism

296
Q

what is glycogenolysis?

A

to release glucose, as required

297
Q

what is included in fat metabolism?

A
  • processing of chylomicron remnants
  • synthesis of lipoproteins and cholesterol
  • ketogenesis
298
Q

what is included in protein metabolism?

A
  • synthesis of plasma proteins
  • transamination an deamination of amino acids
  • conversion of ammonia to urea
299
Q

which hormones are deactivated by the liver?

A
  • insulin
  • glucagon
  • anti-diuretic hormone (ADH, vasopressin)
  • steroid hormone
300
Q

which hormones are activated by the liver?

A
  • conversion of thyroid hormone

- conversion of vitamin D to 25-hydroxyvitamin D

301
Q

what does the liver store?

A
  • fat soluble vitamins
  • water soluble vitamin B12
  • iron, copper
  • glycogen
302
Q

which proteins are synthesised in the liver?

A
  • coagulation factors II,VII,IX and X
  • protein C and S
  • albumin
  • complement proteins
  • apolipoproteins
  • carrier proteins
303
Q

what do kupffer cells do?

A

digest/destroy particulate matter (e.g. bacteria) and senescent erythrocytes (metabolism of haemoglobin)

304
Q

what does the liver detoxify?

A 
many endogenous substances (e.g. bilirubin)
exogenous substances (xenobiotics) e.g. drugs and ethanol
305
Q

what does bile do between meals?

A

stored and concentrated in the gall bladder

306
Q

what does bile do during a meal?

A
  1. chyme in duodenum stimulates gall bladder smooth muscle to contract
  2. spinchter of oddi opens
  3. bile spurts into duodenum via cystic and common bile ducts
307
Q

what does neutral/ slightly alkaline bile assist?

A
  • micelle formation
  • neutralisation of chyme
  • pH adjustment for digestive enzyme action
  • protection of the mucosa
308
Q

what do hepatocytes do?

A

secrete primary juice into canaliculi which drain into biliary ductules and ducts

309
Q

what is the most common pathology of the biliary tract?

A

cholelithiasis

310
Q

what may cholesterol do over time in the gall bladder?

A

crystallise and grow into a gall stone

311
Q

what happens to bile salts that are not lost in feaces?

A

reabsorbed by active transport in the terminal ileum and undergoes enterohepatic recycling

312
Q

what do bacteria do to some primary bile acids?

A

dehydroxylate them to form secondary bile acids which return to the liver. they are then conjugated with glycine or taurine and recycled as bile salts

GI (10 decks)

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