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Gastrointestinal > Physiology and Pharmacology > Flashcards

Physiology and Pharmacology Flashcards

1
Q

what is the purpose of sphincters?

A

keep food moving aborally, prevent it from going the wrong way

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2
Q

what are the accessory structures of the digestive system?

A

salivary glands
pancreas
the liver and the gall bladder (hepatobiliarry system)

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3
Q

what are the 4 main digestive processes?

A

motility
secretion
digestion
absorption

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4
Q

what are the 3 types of mechanical activity within the GI system?

A

propulsive movements
mixing movements
tonic contractions

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5
Q

what are the 2 groups within secretions in the GI tract?

A

digestive secretions

protective secretions

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6
Q

what is the process of digestion?

A

biochemical breakdown of complex foodstuffs into smaller, absorbable units

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7
Q

what type of enzymes break down carbohydrates?

A

amylases and diasaccharidases

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8
Q

what type of enzymes break down proteins?

A

proteases and dipeptidases

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9
Q

what type of enzymes break down fats?

A

lipases

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10
Q

what is absorption within the GI tract?

A

transfer of absorbable products of digestion (+ water, electrolytes and vitamins) from the digestive tract to the blood or lymph

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11
Q

what are the 4 main layers of the digestive tract wall?

A

mucosa
submucosa
muscularis externa
serosa

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12
Q

what does the mucosa of the GI tract consist of?

A 
epithelial cells
exocrine cells
endocrine gland cells
lamina propria
muscularis mucosa
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13
Q

what does lamina propria of the mucosa of the GI tract consist of?

A

capillaries,
enteric neurones,
immune cells

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14
Q

what does the submucosa of the GI tract consist of?

A

connective tissue
larger blood and lymph vessels
sub mucous plexus (nerve network)

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15
Q

what does the muscularis externa of the GI tract comprise of?

A 
circular muscle layer
myenteric plexus (nerve network)
longitudinal muscle layer
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16
Q

what does the serosa of the GI tract comprise of?

A

connective tissue

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17
Q

which of the GI sphincters are made of skeletal muscle?

A

upper oesophagus sphincter

external anal sphincter

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18
Q

what does contraction of the circular muscle of the muscularis externa do to the GI tract?

A

lumen becomes narrower and longer

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19
Q

what does contraction of the longitudinal muscle in the muscularis externa do in the GI tract?

A

tract becomes shorter and fatter

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20
Q

what does contraction of the muscularis mucosa do to the GI tract?

A

causes changes in the absorptive and secretory area of mucosa

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21
Q

how are adjacent smooth muscle cells coupled in order to allow the spread of electrical currents?

A

by gap junctions

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22
Q

what 3 things modulate the spontaneous activity of the smooth muscle of the GI tract?

A

intrinsic nerves- enteric
extrinsic nerves- autonomic
hormones

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23
Q

what type of spontaneous electrical activity occurs in the stomach, small intestine and large intestine?

A

slow waves

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24
Q

what are the pacemaker cells within the stomach, small intestine and large intestine which drive the slow wave electrical activity?

A

interstitial cells of Cajal

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25
Q

what has to happen for a slow wave in the stomach, small intestine and large intestine to cause an action potential?

A

slow wave has to meet the threshold

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26
Q

what is force of contraction of the smooth muscle within the GI tract related to?

A

the number of action potentials discharged

ie the length of time that the slow wave was above threshold

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27
Q

where are interstitial cells of Cajal located?

A
  • between longitudinal and circular muscle layers

- submucosa

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28
Q

when does slow wave activity in the GI tract generally remain in the background and not reach thresholds?

A

between meals

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29
Q

what is the basic electrical rhythm (BER) of the GI tract determined by?

A

slow wave

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30
Q

what are the factors which determine whether a slow wave amplitude reaches threshold/for how long it remains above threshold?

A

neuronal stimuli
hormonal stimuli
mechanical stimuli

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31
Q

using basic electrical rhythm (BER), explain why chyme moves from oral to aboral direction within the small intestine?

A

higher BER in the duodenum than the terminal ileum

more vigorous mechanical activity proximally pushes food distally in the small intestine

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32
Q

using the basic electrical rhythm (BER), explain why the colon is able to hold contents for a long period of time?

A

higher BER in the distal colon than the proximal colon

(more vigorous actiivty distally favours retention of luminal contents(

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33
Q

why is it important that the colon holds food for a long period of time?

A

to allow for absorption of enough water and electrolytes

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34
Q

what neurones is the enteric nervous system made of?

A

sensory neurones
interneurones
effector neurones

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35
Q

where are the ganglia that the parasympathetic supply to the GI tract synapse at?

A

within the ENS

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36
Q

what excitatory influences does parasympathetic supply to GI tract have?

A

increases secretions
increases blood flow
generally increases smooth muscle contraction

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37
Q

what inhibitory influences does parasympathetic supply to the GI tract have?

A

relaxation of some sphincters

receptive relaxation of stomach

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38
Q

where are the ganglia that the sympathetic supply to the GI tract synapse at?

A

prevertebra ganglia

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39
Q

what inhibitory influences does the sympathetic supply to the GI tract have?

A

decreased motility
decreased secretions
decreased blood flow

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40
Q

what triggers the receptive relaxation of the stomach?

A

food entering the oesophagus

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41
Q

where does the sensory neurone synapse with the interneurone in a local reflex of the GI tract?

A

within the myenteric plexus or submucous plexus

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42
Q

where does the sensory neurone synapse with the interneurone in a short reflex of the GI tract?

A

at a preverterbal ganglion

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43
Q

where does the sensory neurone synapse with the interneurons in a long reflex of the GI tract?

A

at a dorsal motor nucleus of the vagus in the medulla oblongota

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44
Q

what type of GI reflex is peristalsis?

A 
local reflex
(intrinsic)
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45
Q

what type of GI reflex is a interstino-intestinal inhibitory reflex?

A

short reflex

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46
Q

what type of GI rexles is a gastroileal reflex?

A

long reflex

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47
Q

what is the gastroileal reflex?

A

occurs when food enters the stomach causing vigorous mechanical activity in the stomach.
this sends a reflex response to cause contraction of the ileum to remove the previous food remnants from the small intestine

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48
Q

what is peristalsis?

A

an orderly wave of contraction (squeeze from behind bolus, relax in front) to push food in the aboral direction

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49
Q

what is peristalsis reflexively triggered by?

A

distension of the gut wall

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50
Q

what 2 neurotransmitters released from an inhibitory motoneurone cause smooth muscle within the muscularis externa to relax?

A

VIP (vasoactive peptide)

NO (nitrate)

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51
Q

what neurotransmitter released from an excitatory motoneurone causes smooth muscle within the muscularis externa to contract?

A

ACh

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52
Q

in peristalsis, what do the muscle layers within the muscularis externa do to cause contraction behind the bolus?

A

circular muscle contracts (under ACh control)

longituidinal muscle relaxes (under VIP and NO control)

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53
Q

in peristalsis, what do muscle layers within the muscularis externa do to cause relaxation in front of the bolus?

A

circular muscle relaxes (under VIP and NO control)

longituidinal muscle contracts (under ACh control)

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54
Q

what is sementation?

A

rhythmic contractions of the circular muscle layer that mixes and divides luminal contents

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55
Q

where does segmentation occur?

A

in small intestine (fed state)

in large intestine

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56
Q

what is segmentation called within the large intestine?

A

haustration

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57
Q

what type of contractions do sphincter muscles of the GI tract go through?

A

tonic contractions

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58
Q

how does segmentation occur?

A

circular muscle layer is contracted at 2 points

between these 2 points the muscle is relaxed

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59
Q

why does a sphincter open?

A

if proximal pressure is greater than distal pressure

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60
Q

what are the 6 sphincter of the GI tract? (excluding sphincter of oddi)

A 
upper oesophageal sphincter
lower oesophageal sphincter
pyloric sphincter
ileocecal sphicter
internal anal sphincter
external anal sphincter
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61
Q

why does vomiting cause the reflux of duodenal gastric contents?

A

vomitting relaxes the pyloric sphincter

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62
Q

why does the upper oesophageal sphincter close during inspiration?

A

to prevent large amounts of air entering the oesophagus

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63
Q

what disease occurs in the lower oesophageal sphincter doesn’t function properly?

A

gastro-oesophageal reflux disease

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64
Q

what is the function of the palate of the mouth?

A

separates mouth from nasal passages to allow breathing and chewing simultaneously

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65
Q

what is the function of the uvula?

A

helps seal off nasal passages during swallowing

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66
Q

what is the function of the tongue?

A

guides food, important in speech and swallowing, major location of taste buds

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67
Q

what are the tonsils on the side walls of the pharynx?

A

lymphoid tissues

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68
Q

what is mastication?

A

chewing

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69
Q

what is the function of the masseteric reflex?

A

jaw opening

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70
Q

what is the function of the diagastric reflex?

A

jaw closing

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71
Q

what stimulates the pharyngeal receptors to send an afferent impulse to the swallowing centre in the medulla?

A

pressure from the food bolus

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72
Q

what happens to the soft palate, tongue, uvula during swallowing and why?

A

soft palate raises
tongue presses against the hard palate
uvula presses against back of throat
(to prevent food entering nasal passages)

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73
Q

what happens to the larynx, epiglottis, vocal cords during swallowing and why?

A

larynx elevates
epiglottis tilts
vocal cords close across the larynx opening
(to prevent food entering the trachea)

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74
Q

what centre in the brain does the swallowing centre inhibit during swallowing and why?

A

the respiratory centre

to prevent food entering the trachea

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75
Q

where is the swallowing centre within the brain?

A

medulla oblongata

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76
Q

once the food bolus has entered the oesophagus, what triggers the closure of the upper oesophageal sphincter?

A

swallowing centre

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77
Q

what do local pressure receptors within the oesophagus stimulate when food has become lodged?

A

stimulate a secondary peristaltic wave (more forceful than primary)
increase saliva production

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78
Q

what are the 3 major salivary glands that saliva is secreted from?

A

parotid gland
submandibular gland
sublinual gland

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79
Q

what are the 6 important functions of saliva?

A 
lubrication
solvent
antibacterial
digestion of complex carbohydrates
neutralisation of acid
facilitates sucking by infants
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80
Q

what is the solvent function of saliva important for?

A

taste

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81
Q

what 3 important antibacterial substances does saliva contain?

A

lysozyme
lactoferrin
immunoglobulins

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82
Q

what is the job of lactoferrin?

A

binds iron needed for bacterial replication

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83
Q

what important salivary substance is important in the digestion of complex carbohydrates?

A

amylase

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84
Q

what important salivary substance is important in the neutralisation of acid?

A

bicarbonate

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85
Q

how does saliva facilitate sucking by infants?

A

fluid seal

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86
Q

what are the 2 stages of the formation of saliva?

A

primary secretion

secondary modification

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87
Q

what cells are important in the primary secretion phase of saliva formation?

A

acinus

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88
Q

what cells are important int he secondary modification phase of saliva formation?

A

duct cells

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89
Q

what occurs in the primary secretion phase of saliva formation?

A

acinus cells produce a primary secretion with Na+, K+, Cl- and HCO3- content similar to plasma, plus mucus and amylase

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90
Q

what occurs in the secondary modification phase of saliva formation?

A

duct cell modify acinus secretion by removing Na+ and Cl- (and to a lesser extent adding K+ and HCO3-)
there is no movement of H2O, but there is an overal diluting phase

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91
Q

why is there no movement of water in the secondary modification phase of saliva formation?

A

epithelium is impermeable to water

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92
Q

why is important that the NaCL content of saliva is much lower than plasma?

A

to allow detection of salty taste

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93
Q

as the flow rate of saliva increases, what happens to the concentration of HCO3- within it?

A

as saliva flow rate increases HCO3- content of saliva increases

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94
Q

what are the 2 types of reflexes which increase the rate of saliva formation?

A 
simple reflex (saliva increased in response to food in mouth)
conditioned reflex (saliva increased in response to a certain stimuli which suggests food is coming-acquired)
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95
Q

in normal saliva production which section of the autonomic nervous system has a dominant role?

A

parasympathetic stimulation

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96
Q

what type of saliva is produced when parasympathetic stimulation has a dominant role?

A

a large volume of enzyme rich, watery saliva

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97
Q

what receptors mediate the parasympathetic control on saliva production?

A

M3 muscarinic acetylcholine receptors

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98
Q

during stressful times which section of the autonomic nervous system has dominant control?

A

sympathetic system

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99
Q

what type of saliva is produced when sympathetic stimulation has a dominant role?

A

a small volume of mucus rich, thick saliva

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100
Q

what receptors mediate the sympathetic control on saliva production?

A

B1-adrenoceptors

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101
Q

what are the 4 main areas of the stomach?

A

fundus
body
antrum
pylorus

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102
Q

what happen to the rugae when the stomah fills up?

A

they smooth out

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103
Q

what is retropulsion with respects to the mixing of contents in the stomach?

A

food in the body of the stomach is propelled forward by peristaltic waves. chyme hits the pyloric area and bounces back

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104
Q

what hormone stimulated the release of HCl?

A

gastrin

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105
Q

how can duodenum delay emptying?

A

neuronal response

hormonal responce

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106
Q

what is the function of the enterogastric reflex?

A

decreases antral peristaltic activity to delay emptying of the stomach

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107
Q

what does the release of enterogastrones (secretin, CCK) from the duodenum do to the emptying of the stomach?

A

release of enterogastrones inhibit stomach contraction and so delay emptying of the stomach

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108
Q

what 4 things within the duodenum drive neuronal and hormonal responses to delay gastric emptying?

A

fat
acid
hypertonicity
distension

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109
Q

what major secreting cells are within the pyloric gland area (PGA) in the antrum of the stomach?

A

D cells
G cells
mucosal cells

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110
Q

what do D cells within the pyloric gland area in the antrum of the stomach secrete?

A

somatostatin

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111
Q

what do G cells within the pyloric gland area in the antrum of the stomach secrete?

A

gastrin

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112
Q

what secreting cells are within the oxyntic mucosa (OM) in the fundus and body of the stomach?

A

chief cells
enterochromaffin-like cells
parietal cells

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113
Q

what do chief cells within the oxyntic mucosa in the fundus and body of the stomach secrete?

A

pepsinogen

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114
Q

what do enterochromaffin-like cells within the oxyntic mucosa in the fundus and body of the stomach secrete?

A

histamine

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115
Q

what do parietal cells within the oxyntic mucosa in the fundus and the body of the stomach secrete?

A

hydrocholic acid

intrinsic factpr

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116
Q

what is the function of HCl secreted from parietal cells of the oxyntic mucosa?

A
  1. activates pepsinogen to pepsin
  2. denatures protein
  3. kills most micro-organisms
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117
Q

what is the function of pepsinogen secreted from chief cells of the oxyntic mucosa?

A

inactive precursor of pepsin

once pepsin is formed it is autocatalytic and so activated pepsinogen

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118
Q

what is the function of intrinsic factor secreted from parietal cells of the oxyntic mucosa?

A

binds to vitamin B12 allowing absorption in terminal ileum

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119
Q

what is the function of histamine secreted from enterochromaffin-like cells of the oxyntic mucosa?

A

stimulates HCl secretion from parietal cells

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120
Q

what is the function of gastrin secreted from the G cells of the pyloric gland area?

A

stimulates HCl secretion from parietal cells

stimulates histamine production from enterochromaffin-like cells

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121
Q

what is the function of somatostatin secreted from D cells of the pyloric gland area?

A

inhibits secretion of gastrin from G cells to decrease HCl production from parietal cells

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122
Q

why is somatostain important?

A

reduced concentrations of acid going into the duodenum

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123
Q

what is the function of mucus secreted from mucosal cells of the pyloric gland area?

A

protect the mucosa

otherwise ulcers can form

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124
Q

what type of secretions are somatostatin and gastrin?

A

endocrine (into blood stream)

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125
Q

what is the function of prostaglandin (PGE2) on parietal cells?

A

inhibits parietal cell secretions

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126
Q

what is the effect of cholinergic stimulation of M1 receptors on enterochromaffin-like cells?

A

increase histamine secretion

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127
Q

what is the effect of cholinergic simulation of M3 receptors on parietal cells?

A

increase HCl secretion

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128
Q

where are the ion ATPase pumps in a resting parietal cell?

A

within cytoplasmic tubulovesicles

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129
Q

where are the ion ATPase pumps in a stimulated parietal cell?

A

they trafficked to the apical membrane and sit in the extended microvilli

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130
Q

what are the 3 phases of gastric secretion?

A

cephalic
gastric
intestinal

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131
Q

when is the cephalic phase of gastric secretion?

A

before food reaches the stomach

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132
Q

when is the gastric phase of gastric secretion?

A

when food is in the stomach

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133
Q

when is the intestinal phase of gastric secretion?

A

after food has left the stomach

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134
Q

what is the effect of cholinergic simulation of M receptors on D cells?

A

decreased somatostatin production

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135
Q

what is the main effect off the intestinal phase on acid secretion?

A

switches it off

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136
Q

what 3 classes of drugs decrease hydrochloric acid secretion?

A

muscarinic receptor competitive antagonists (no longer used)
H2 histamine receptor competitive antagonists
Proton-pump inhibitors

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137
Q

how do proton-pump inhibitors work?

A

covelent modification of a K+/H+ ATPase on the apical membrane of parietal cells

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138
Q

what class of drugs increases hydrochloric acid secretion?

A

NSAIDs (eg aspirin, ibuprofen etc)

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139
Q

how do NSAIDs work to increase HCl secretion?

A

by blocking COX irreversibly which results in decreased prostaglandins

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140
Q

what is the function of PGE2 and PGI2 in the stomach? (locally produced prostaglandins)

A

reduced acid secretion
increase mucus secretion
increase bicarbonate secretions
increase mucosal blood flow

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141
Q

what 2 things can NSAIDs trigger due to the fact they reduce prostaglandins?

A

ulceration

bleeding

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142
Q

how can gastric damage due to long-term NSAID treatment be prevented?

A

using a stable PGE1 analogue (eg misoprostol)

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143
Q

what do PGE1 analogues do?

A

inhibit basal and food-stimulated gastric acid formation

maintains/increases secretion of mucus and bicarbonate

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144
Q

what bacterium can cause chronic infection of the gastric antrum and is associated with peptic ulcers?

A

Helicobacter pylori

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145
Q

why does H. pylori predispose to peptic ulcers?

A

causes persistent inflammation that weakens the mucosal barrier leaving the submucosa subject to attack by HCl and pepsin

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146
Q

why are PPIs called prodrugs?

A

because they are inactive at neutral pH but change conformation in a strongly acidic environment

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147
Q

how do PPI’s get to the secretory cannaliculi?

A

absorbed from the GI tract and delivered via the systemic circulation

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148
Q

what are ranitidine and cimetidine?

A

H2 receptor antagonists

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149
Q

how are H2 receptor antagonists administered?

A

PO

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150
Q

what is sucralfate?

A

a mucosal strengthener

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151
Q

what is bismuth chealate?

A

a mucosal strengthener which is also toxic towards H. pylori

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152
Q

what drug is bismuth chealate usually administered with?

A

ranitidine

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153
Q

what type of carbohydrates are indigestible in humans?

A

cellulose

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154
Q

what are the 2 sub-groups of starch?

A

amylose

amylopectin

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155
Q

what type of carbohydrates are sucrose and lactose?

A

disaccharides

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156
Q

what endogenous sources of proteins are also ingested?

A

digestive enzymes (ie once role has been fufilled) and dead cells from GI tract

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157
Q

what are the 3 main digestive processes that occur in the small intestine?

A

luminal digestion
membrane/brush border digestion
intracellular digestion (in enterocyte)

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158
Q

what is luminal digestion in the small intestine mediated by?

A

pancreatic enzymes secreted into the duodenum

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159
Q

what is membrane/brush border digestion in the small intestine mediated by?

A

enzymes situated at the brush border of enterocytes

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160
Q

what are enterocytes?

A

absorptive cells of the intestinal epithelium

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161
Q

assimilation =

A

digestion + absorption

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162
Q

what is the movement of substances across the epithelial tight junctions called?

A

paracellular movement

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163
Q

what is the movement of sybstances through enterocytes called?

A

intracellular movement

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164
Q

what substances can actually move through the tight junctions between the enterocytes?

A

ions

165
Q

what type of carbohydrates are glucose and fructose?

A

monosaccharides

166
Q

compare amylose and amylopectin in terms of linkages?

A

amylose- linear straight chain: a1-4 linkages

amylopectin- branched chain: a1-4 and a1-6 linkages

167
Q

which is more highly branched? (glycogen or amylopectin)

A

glycogen

glycogen has more a1-6 linkages than amylopectin

168
Q

in sucrose, what are glucose and fructose linked by?

A

a1-2 linkages

169
Q

in lactose, what are glucose and galactose linked by?

A

b1-4 linkages

170
Q

in an alpha glucose molecule, on C1, where is the hydroxyl group?

A

below

171
Q

in a beta glucose molecule, on C1, where is the hydroxyl group?

A

above

172
Q

what must dietary carbohydrates be converted to for absorption into the enterocyte?

A

monosaccharides

173
Q

what type of digestion do polysaccharides (eg starch) go through to form oligosaccharides?

A

intraluminal hydrolysis

174
Q

what type of digestion do oligosaccharides (eg sucrose and lactose) go through to form monosaccharides?

A

brush border hydrolysis

175
Q

what enzymes are involved in the intraluminal hydrolysis of polysaccharides (eg starch)?

A

salivary a-amylase

pancreatic a-amylase

176
Q

what 4menzymes are involve in the brush border digestion of oligosaccharides?

A

oligosaccharidases:
lactase
maltase
sucrase-isomaltase

177
Q

what is maltose made of?

A

2 glucose monomers

178
Q

what is maltotriose made of?

A

3 glucose monomers

179
Q

what is special about sucrase-isomaltase?

A

2 different enzymes with 2 different substrates but in the form of one combines macro-molecule

180
Q

what linkages can a-amylase break down?

what linkages can it not break down?

A

a1-4 internal linkages
(not a-1-4 terminal linkages or a1-6 linkages or a1-4 linkages adjacent to branch points:
this is why monosaccharides aren’t formed)

181
Q

what is an endoenzyme?

A

only breaks down internal linkages but not terminal linkages

eg a-amylase

182
Q

what is the unique function of lactase?

A

breaks down lactose to glucose and galactose

b1-4 bond hydrolysis

183
Q

what is the unique function of sucrase?

A

breaks down sucrose to glucose and fructoase

a1-2 bond hydrolysis

184
Q

what is the unique function of isomaltase?

A

breaks down a1-6 linkages

185
Q

what 3 oligosaccharides, in addition to their unique function, can cleave terminal a1-4 terminal linkages?

A

maltase

sucrase-iso-maltase

186
Q

what is the rate-limiting step of assimilation for maltase, sucrase and isomaltase?

A

transport process

187
Q

what is the rate-limiting step of assimilation for lactase?

A

the hydrolysis of lactose

188
Q

what is lactose intolerance caused by?

A

lactase insufficiency

189
Q

what is primary lactase deficiency? (primary hypolactasia)

A

lactose intolerance due to lack of lactase persistence (LP) allele

190
Q

what is secondary lactase deficiency?

A

lactose intolerance due to damage to proximal small intestine

191
Q

what is congenital lactose deficiency?

A

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

192
Q

why are some humans able to digest lactose after weaning?

lactase activity is generally lost in mammals after weaning- primary lactase deficiency

A

these individuals have a variable degree of lactase persistance due to polymorphisms

193
Q

when does hypolactasia cause problems?

A

lactose-containg food is consumed in amounts that overwhelm the activity of remaining lactase

194
Q

if lactose is delivered to the colon in a person with hypolactasia what happens?

A

colonic microflora feed on the lactose and produce:
short chain fatty acids (which can be absorbed)
hydrogen
carbon dioxide
methane

195
Q

what is the result of the products produced by colonic microflora feeding on lactose?

A

bloating
abdominal pain due to distension
flatulence

196
Q

what 2 things does undigested lactose cause?

A

acidification of the colon

an increased osmotic load causing diarrhoea

197
Q

where does absorption of monosaccharides take place?

A

duodenum

jejunum

198
Q

how are glucose and galactose absorbed across the apical membrane of an enterocyte?

A

secondary active transport mediated by SGLT1

199
Q

how is fructose absorbed across the apical membrane of an enterocyte?

A

facilitated diffusion mediated by GLUT 5

200
Q

how do all monosaccharides exit the basal membrane of an enterocyte?

A

facilitated diffusion mediated by GLUT 2

201
Q

what is secondary active transport?

A

the movement of a substance coupled to the movement of ions in the ATPase

202
Q

which type of glucose can be absorbed?

A

ring glucose not linear glucose

203
Q

how far must protein be digested to enable absorption into enterocyte?

A

to oligopeptides and amino acids

204
Q

what are the 3 pathways for protein digestion?

A
  1. a) protein digested to amino acids by luminal enzymes
  2. a) protein digested to peptides by luminal enzymes
    b) peptides digested to amino acids by brush border enzymes
  3. a) protein digested to peptides by luminal enzymes
    b) peptides digested to amino acids by intracellular hydrolysis
205
Q

what are the 5 pancreatic proteases?

A 
trypsin
chymotrpin
elastase
procarboxypeptidase A
procarboxypeptidase B
206
Q

which pancreatic proteases are endopeptidases (target internal bonds) and which are exopeptidase (target terminal bonds)?

A

endopeptidase- trypsin, chymotrypsin, elastase

exopeptidase- procarbosypeptidase A, procarboxypeptidase B

207
Q

what are the products of endopeptisases?

A

oligopeptides (2-6 amino acids chain)

208
Q

what are the products of exopeptidases?

A

single amino acids

209
Q

are aminopeptidases exopeptidases of endopeptidases?

A

exopeptidase

210
Q

how many different amino acid absorption mechanisms are present at the brush border of the enterocyte?

A

7
5 Na dependent (Secondary active transport)
2 Na independent

211
Q

how many different amino acid transport mechanisms are present at the basal membrane of the enterocyte?

A

5 (bidirectional)
3 Na independent and mediate efflux
2 Na dependent and mediate influx

212
Q

how are oligopeptides transported across the apical membrane of an enterocyte?

A

via H+ dependent mechanisms (secondary active transport)

213
Q

what is the lingual phase of digestion?

A

when food is in the mouth

214
Q

why is HCO3 in pancreatic juice important for the digestion of fats?

A

neutralises stomach acid to provide a suitable pH for pancreatic lipase

215
Q

what hormone is bile secreted in response to?

A

CCK

216
Q

what is the function of bile salts?

A

emulsification of large lipid droplets to small lipid droplets
(increased surface area for action of lipase)

217
Q

what does failure to secrete bile salts result in?

A
  1. lipid malabsorption

2. secondary vitamin deficiency due to failure to absorb lipid vitamin

218
Q

what stool sign indicated the patient has lipid malabsorption?

A

steatorrhoea

219
Q

why is co-lipase important?

A

because without co-lipase bile salts block access of lipase to the lipid- co-lipase binds to both bile salts and lipase to allowing access to the lipids

220
Q

where is co-lipase produced?

A

pancreas

221
Q

what are the final products of lipid digestion (eg fatty acids, monoglycerides, phospholipids) stored in?

A

mixed micelles

222
Q

how do micelles enter the enterocyte?

A

passive diffusion

223
Q

what apolipoprotein joins the forming chylomicron?

A

apo-B48

224
Q

what transport protein carries cholesterol across the enterocyte apical membrane?

A

NPC1L1

225
Q

what is the function of ezetimibe?

A

binds to NPC1L1 to prevent internalisation of cholesterol

226
Q

how does the absorption of Ca++ occur?

A

passive transport

active transport

227
Q

what does the passive transport of calcium across the epithelium involve?

A

paracellular movement

228
Q

where does paracellular movement of Ca++ occur in the GI tract?

A

whole length of the small intestine

229
Q

what does active transport of calcium across the epithelium involve?

A

transcellular movement through a calcium channel

230
Q

where does transcellular movement of Ca++ occur in the GI tract?

A

duodenum and upper jejunum

231
Q

when there is a low lumenal concetration of calcium what way is calcium transported?

A

transcellular movement (Calcium channels)

232
Q

when there is a high lumenal concentration of calcium what way is calcium transported?

A

paracellular movement

233
Q

how is iron transported across the epithelium of the intestines?

A

transcellularly by metal transporter

234
Q

how is haem transported across the epithelium of the intestines?

A

transcellularly by haem transporter

235
Q

what form does iron need to be in to be transported into the enterocyte by the metal transporter?

A

Fe2+

236
Q

what reduces the iron from Fe3+ to Fe2+ in the gut?

A

vitamin C

237
Q

how does Fe2_ leave the enterocyte?

A

via feroportin

238
Q

what is the function of hepcidin?

A

it is released from the liver when body iron levels are high and negatively regulates ferroporitin

239
Q

what causes vitamin B12 to be released from food?

A

stomach acid

240
Q

what binds to the vitamin B12 once released in the stomach?

A

haptocorrin

241
Q

where is haptocorrin produced?

A

salivary glands

242
Q

what happens to the haptocorrin-vitB12 complex in the small intestine?

A

pancreatic proteases digest the haptocorrin and vitamin B12 is released

243
Q

what binds to vitamin B12 in the small intestine?

A

intrinsic factor

244
Q

what is the function of intrinsic factor?

A

forms a complex with B12 and allows it to be absorbed in the terminal ileum by endocytosis

245
Q

how are fat soluble vitamins absorbed across the epithelium of the intestine?

A

incoporated into mixed micelles and passively transported into enterocytes

246
Q

once inside the enterocyte, what is the journey of fat-soluble vitamins?

A

incorporated into chylomicrons and distributed by lymphatics

247
Q

how are water soluble vitamins absorbed across the epithelium?

A

active transport

248
Q

what cause motion sickness?

A

sensory conflict regarding position of body in space

inner ear senses movement but brain thinks we have not moved

249
Q

why is pregnancy-induced nausea and vomiting (in the first trimester) an adaptive advantage?

A

encourages picky eating during a time of rapid foetal growth

250
Q

what type of pregnancy-induced vomiting outlasts first trimester and can be extremely damaging to both mum and baby?

A

hyperemesis gravidarum

251
Q

what is emesis (vomiting)?

A

the forceful propulsion of gastric contents out of the mouth

252
Q

during emesis, what state are the stomach, oesophagus and associated sphincter in?

A

relaxed state

253
Q

what part of the medulla oblongata in the brain stem co-ordinates vomiting?

A

the vomiting centre

254
Q

describe the vomiting cycle?

A
  1. suspension of intestinal slow wave activity
  2. retrograde contractions from ileum to stomach
  3. deep inhalation
  4. suspension of breahing
  5. relaxation of LOS + contraction of diaphragm and abdominal muscles
  6. ejection of gastric contents through open UOS
  7. repeated until relief is felt
255
Q

why during emesis is breathing suspended and the rima glottis closed?

A

to prevent aspiration

256
Q

during emesis, what is the purpose of the contraction of diaphragm and abdominal muscle?

A

increases pressure in abdominal cavity and compresses stomach

257
Q

what usually precedes vomiting?

A

profuse salivation
sweating
elevated heart rate/force
nausea

258
Q

what is retching?

A

the mechanical process of vomiting but no substance (stomach is already empty)

259
Q

what do toxic materials in the gut/systemic toxins causes the release of?

A

seretonin from enterochromaffin cells in mucosa

260
Q

what does the seretonin released in response to a toxin cause?

A

depolarisation of sensory afferent terminals in mucosa via 5-HT3 receptors causing an vagal afferent action potential discharge to brainstem

261
Q

what particular areas in the brainstem are vagal vomiting-inducing afferent discharges sent to?
(these cause co-ordination of vomiting by the vomiting centre)

A

CTZ-chemoreceptor trigger zone

NTS- nucleus tractus solitarius

262
Q

how can toxic materials within the blood stimulate the chemoreceptor trigger zone to cause vomiting without APs?

A

CTZ lacks an effective blood brain barrier so the toxic materials can stimulate it directly

263
Q

what 2 types of stimuli can send vagal afferents to the brain stem to cause the co-ordination of the vomiting centre?

A 
chemical stimuli (via 5HT3 receptors)
mechanical stimuli
264
Q

how does the vestibular system signal to the vomiting centre to cause the co-ordination of vomiting? (motion sickness)

A

signalls through vestibular nuclei to chemoreceptor trigger zone
and then to vomiting centre

265
Q

what type of stimuli can cause co-ordination of vomiting by the vomiting centre via the medulla and cerebral cortex limbic system?

A

stimuli within the CNS itself

eg pain, repulsive sights/odours, fear etc

266
Q

what are the 5 consequences of severe vomiting?

A
  1. dehydration
  2. hypochloraemic metabolic alkalosis
  3. hypokalaemia
  4. (Rarely) metabolic acidosis
  5. (rarely) malloey-weiss tear
267
Q

why does severe vomiting cause hypochloraemic metabolic alkalosis?

A

loss of gastric protons and chloride (ie HCL)

268
Q

why does severe vomiting cause hypokalaemia?

A

proton loss causes the kidneys to excrete potassium

269
Q

why can severe vomiting sometime cause metabolic acidosis?

A

because of los of duodenal bicarbonate

270
Q

why does cancer chemotherapy and radiotherapy cause nausea and vomiting?

A

induces release of 5-HT and substance P from enterochromaffin cells in the gut

271
Q

why can medications used in parkinsons disease cause nausea and vomiting?

A

because these drugs have high dopamine activity

dopamine D2 receptors are prevalent in the chemoreceptor trigger zone

272
Q

why can anti-depressants such as selective serotonin reuptake inhibitors cause nausea and vomiting?

A

because they enhance 5-HT function

5HT3 receptors are prevalent in the chemoreceptor trigger zone

273
Q

what are the 6 major classes of antiemetic drugs?

A 
5HT3 receptor antagonists
Muscarinic ACh receptor antagonists
Histamine H1 receptor antagonists
Dopamine receptor antagonists
NK1 receptor antagonists
Cannabinoid receptor agonists
274
Q

how do 5HT3 receptor antagonists work in the prvention of emesis?

A

block peripheral and central 5HT3 receptors

275
Q

what are 5HT3 receptor antagonists used for?

A
  • to supress chemothrapy and radiation induced emesis

- to reduced post-operative emesis

276
Q

5HT3 receptor antagonists become less effective during subsequent treatments, how is function improved?

A

by the addition of a corticosteroid and NK1 receptor antagonist

277
Q

How do muscarinic acetylcholine receptor antagonists work in the prevention of emesis?

A
  • block muscarinic acetylcholine receptors at multiple sites (eg vestibular nuclei, NTS, vomiting centre)
  • direct inhibition of GI movement
278
Q

what are anti-emetic muscarinic acetylcholine receptor antagonists used for?

A

prophylaxis and treatment of motion sickness

transdermal or PO

279
Q

what are the adverse effects of antiemetic muscarinic acetylcholine receptor antagonists?

A

many unwanted effects from parasympathetic blockade

centrally-mediated sedation

280
Q

how do H1 receptor antagonists work?

A

block of histamine receptor 1 in vestibular nuclei and NTS

H1 receptors are important in allergic effect and emetic effect

281
Q

what are anti-emetic H1 receptor antagonists used for?

A

prophylaxis and treatment of motion sickness

282
Q

what are the adverse effects of anti-emetic H1 receptor antagonists?

A

CNS depression and sedation

283
Q

how do dopamine receptor antagonists work?

A

centrally block dopamine D2 and D3 receptors in the CTZ

284
Q

compare the adverse effects of domperidone and metoclopramide?

A

domperidone doesn’t cross blood brain barrier unlike metoclopramide so has less unwanted effects

285
Q

what are dopamine receptor antagonists used for?

A

drug-induced vomiting

and vomiting in GI disorders

286
Q

when should dopamine receptor antagonists be avoided?

A

in children

287
Q

how do NK1 receptor antagonists work?

A

antagonism of substance P

288
Q

when are cannabinoid receptor agonists used?

A

in cytotoxic chemotherapy that is unresponsive to other anti-emetics

289
Q

what are the adverse effects of cannabinoid receptor agonists

A

drowsiness, dizziness, dry mouth, mood changes

290
Q

what is the name for the intestinal juice that the small intestine secretes?

A

succus entericus

291
Q

where do the bile duct and pancreatic duct meet?

A

ampulla of Vater

292
Q

where is gastrin produced in the duodenum?

A

from G cells

293
Q

where is cholecystokinin produced?

A

from I cells of duodenum and jejunum

294
Q

where is secretin produced?

A

from S cells of the duodenum

295
Q

where is motilin produced?

A

from M cells of the duodenum and jejunum

296
Q

where is glucagon-like insulinotropic peptide (GIP- gastric inhibitory peptide) produced?

A

from K cells of duodenum and jejunum

297
Q

where is glucacon-like peptide-1 (GLP-1) produced?

A

from L cells of the gut

298
Q

where is ghrelin produced?

A

from Gr cells of the gastric antrum and small intestine

299
Q

what are incretins?

A

hormones which act upon the beta-cells of the pancreas in a feed-forward way to stimulate the release of insulin

300
Q

which hormones produced from the duodneum are incretins?

A

glucagon-like insulinotropic peptide (GIP- gastric inhibitory peptide)
glucagon-like peptide-1 (GLP-1)

301
Q

when are incretins (GIP and GLP-1) from the duodenum released?

A

in response to chyme entering the duodenum

302
Q

what does the succus entericus contatin?

A

mucus
aqueous salts
(no digestive enzymes)

303
Q

where is mucus from the duodenum produced?

A

goblet cells

304
Q

where are the aqueous salts secreted in the duodenum from?

A

crypts of lieberkihn

305
Q

how does chloride get into the enterocytes?

A

sodium potassium chloride co-transporter on basolateral membrane
(Na, 2Cl, K enters cell)

306
Q

what is the function of the sodium potassium chloride co-transporters on the basolateral membrane?

A

to increase the intracellular concentration of chloride to allow chloride to move out through chloride channels (CFTR) on the apical membrane

307
Q

mutations of what channel cause cystic fibrosis?

A

CFTR

308
Q

what does cystic fibrosis do to the succus entericus?

A

decreases the amount

309
Q

what does cholera do to the CFTR channels?

A

causes them to become over active which causes secretory diarrhoea

310
Q

what hormone from the stomach triggers segmentation in the empty ileum?
(what is this reflex called?)

A

gastrin

gastroileal reflex

311
Q

when does peristalsis occur in the small intestine?

A

in the interdigestive state (between meals)

312
Q

what are the 2 forms of peristalsis in the small intestine?

A
  1. weak infrequent localised contractions

2. migrating motor complex

313
Q

what is the migrating motor complex?

A

a strong peristaltic contraction passing from pyloric sphincter to ileocaecal valve

314
Q

what is the function of the migrating motor complex?

A

cleans the the small intestine of undigested debris, unabsorbed electrolytes and dead cells

315
Q

what hormone, produced in the small intestine itself, triggers the migrating motor complex?

A

motilin

316
Q

what hormones supress the migrating motor complex?

A

gastrin, CCK

317
Q

what is CCK produced in response to?

A

fats

318
Q

what is the response of the gallbladder to CCK?

A

contraction

319
Q

what cells secrete digestive enzymes within the pancreas?

A

acinar cells

320
Q

what cells within the duodenum secrete enterokinase?

A

mucosal cells (brush border enzyme)

321
Q

why are pancreatic protease enzymes stored as pro-enzymes?

A

otherwise they would digest themselves and the pancreas wall

322
Q

how is trypsinogen activated into trypsin?

A 
enterokinase
trypsin (autocatalysis)
323
Q

how is chymotrypsinogen activated into chymotrysin?

A

trypsin

324
Q

how are procarboxypeptidase A and B activated into carboxypeptidase A and B?

A

trypsin

325
Q

what cells secrete an alkaline fluid into the duodenum?

A

duct cells of the pancreas

326
Q

what exchanger sits in the apical membrane of duct cells and allows the transfer of alkaline solution into the lumen of the small intestine?

A

Cl-/HCO3- exchanger

327
Q

what are the 3 phases of pancreatic secretion?

A

cephalic
gastric
intestinal

328
Q

what is the cephalic phase of pancreatic secretion mediated by?

A

vagal stimulation of acinar cells

329
Q

what is the gastric phase of pancreatic secretion mediated by?

A

gastric distension which evokes a vasovgal reflex. This results in parasympathetic stimulation of acinar and duct cells

330
Q

what hormone is released in response to acid in the duodenal lumen?

A

secretin from S cells

331
Q

what does secretin cause?

A

increased secretion of aqueous NaHCO3 solution from pancreatic duct cells

332
Q

what is CCKs role in the pancreas secretion?

A

increases secretion of digestive enzymes from acinar cells

333
Q

wat is the function of the ileocaecal valve?

A

stops regurgitation of the colonic content into the ileum

334
Q

what are the 5 main functions of the large intestine?

A
  1. absorption of water and electrolytes
  2. secretion of K+, HCO3- and mucus
  3. absorption of short chain fatty acids
  4. stores colonic contents
  5. periodic elimination of faeces
335
Q

why does the large intestine secrete HCO3-?

A

to neutralise acid produced by bacterial fermentation

336
Q

how do short chain fatty acids form in the colon?

A

unabsorbed carbohydrates are fermented by colonic flora to short chain fatty acids

337
Q

what are faeces made of?

A

indigestible residue
bacteria
bilirubin

338
Q

what is haustration of the colon?

A

non-propulsive segmentation of the colon (slow movement)

339
Q

what direction of movement does haustration cause?

A

orad movement
(oral direction)
to increase transit time for fluid and electrolyte reabsorption

340
Q

what does the contraction of taenia coli cause?

A

shortening of the colon

341
Q

what are the 3 patterns of motility in the large intestine?

A

haustration
peristaltic propulsion
defecation

342
Q

how does defecation occur?

A

mass movement driving faeces into rectum to trigger defaecation reflex

343
Q

what are the 4 main benefits of colonic symbiotic bacteria?

A
  1. increase intestinal immunity by competition with pathogenic microbes
  2. promote motility and help maintain mucosal integrity
  3. synthesis vitamin K2 and free fatty acids
  4. activate some drugs
344
Q

what is the difference between laxatives and purgatives?

A

laxatives are used to treat constipation

purgatives are used to clean bowel by promoting evacuation

345
Q

what are bulk laxatives?

A

indigestible polysaccharide polymers which improve stool consistency

346
Q

what are osmotic laxatives?

A

poorly absorbed solutes to improve stool consitency

347
Q

what purgatives are known to cause abdominal cramps?

A

stimulant purgatives

348
Q

what is the function faecal softners?

A

lubricate the stool to enable it to pass through intestines easier

349
Q

what is the main adverse effect of faecal softners?

A

anal sepage

350
Q

what drugs are used to clean bowels before colonoscopy?

A

stimulant purgatives

351
Q

when are glucocorticoids used in IBD?

A

for acute flate ups

352
Q

what do aminosalicylates release? (the active molecule)

A

5ASA

5-aminosalicylic acid

353
Q

what UC medications are cleaved by bacteria in order to become activated?

A

many aminosalicytes

sulfsalazine, olsalazine, balsalazide

354
Q

how is water transported from the lumen of the intestine to the bloodstream?

A

passive transport driven by the transport of solutes (particularly Na)

355
Q

what are the 5 ways Na+ gets transported from lumen of the GI tract to the bloodstream?

A
  1. Na+/glucose co-transport
  2. Na+/amino acid co-transport
  3. Na+/H+ exchange
  4. Parallel Na+/H+ and Cl-/HCO3- exchange
  5. epithelial Na channels (ENaC)
356
Q

where does Na+/glucose co-transport occur?

A

throughout small intestine

357
Q

when is Na+/glucose co-transport most important?

A

postprandially

358
Q

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

A

throughout the small intestine

359
Q

when is Na+/amino acid co-transport most important?

A

postprandially

360
Q

where does Na+/H+ exchange take place?

A

duodenum and jejunum

361
Q

what is Na+/H+ exchange stimulated by?

A

luminal (pancreatic) HCO3-

362
Q

where does parallel Na+/H+ and Cl-/HCO3- exchange take place?

A

ileum and colon

363
Q

when is parallel Na+/H+ and Cl-/HCO3- exchange most important??

A

interdigestive period

364
Q

where does movement of Na+ through ENaC take place?

A

colon

365
Q

what is the movement of Na+ through ENaC regulated by?

A

aldosterone

366
Q

what do intracellular cAMP, cGMP and Ca2+ do to the movement of Na+ and Cl- through Na+/H+ and Cl-/HCO3- exchange?

A

decrease absorption of NaCl

367
Q

what is the mechanism of how E coli enterotoxin causes diarrhoea?

A

enterotoxin activates adenylate cyclase which increases intracellular cAMP. this reduces the NaCl absorption causing secretory diarrhoea

368
Q

what are the 3 roles of aldosterone within ENaC channel regulation?

A
  1. opens ENaCs
  2. inserts more ENaC into membrane from intracellular vesicle pol
  3. increases synthesis of ENaC and Na+/K+ATPase
369
Q

which occurs at the fastest rate: Cl- absorption or Cl- secretion in GI tract?

A

Cl- absorption occurs at a faster rate than Cl- secretion

370
Q

what is the effect of cAMP, cGMP and Ca2+ on CFTR channels?

A

up-regulation

371
Q

how does cholera cause diarrhoea?

A

cholera toxin causes increased activity of adenyl cyclase leading to increased intracellular cAMP, this enhances CFTR leading to hypersecretion of Cl- with Na+ and water following

372
Q

what are the 2 blood supplies to the liver?

A 
hepatic portal vein (nutrient rich, oxygen poor)
hepatic artery (oxygen rich)
373
Q

where does hepatic portal blood and hepatic artery blood mix?

A

within liver sinusoids

374
Q

what are the functional units of the liver?

A

hexagonal lobules

375
Q

what lies in the centre of a liver lobule?

A

hepatic vein

central vein

376
Q

a hepatic lobule has a portal triad at each of its six corners. what does this triad contain?

A

a branch of hte hepatic portal vein
a branch of the hepatic artery
a bile duct

377
Q

nutrients coming into the liver through sinusoids are received by what membrane of hepatocytes?

A

basolateral membrane

378
Q

what membrane of heaptocytes faces the canaliculi- where bile collects?

A

apical canaliculi

379
Q

what is the pericellular space between the capillaries (sinusoids) and basolateral membrane of the hepatocytes?

A

space of Disse

380
Q

what are the 3 types of cells within the sinusoidal space?

A

endothelial cells
kuppfer cells
stellate (Ito) cells

381
Q

what are kuppfer cells?

A

macrophages resident to the sinusoidal vascular space

382
Q

where do stellate (ito) cells reside within the sinusoidal space?

A

within space of Disse

383
Q

what is the main function of stellate (ito) cells?

A

storage of vitamin A

play a role in fibrosis and cirrhosis due to storage of collagen

384
Q

why are endothelial cells within the liver sinusoids fenestrated?

A

to allow for the free movement of solutes

385
Q

what is the pathway of bile from the canaliculi?

A 
canaliculi
terminal bile ductules
perilobular ducts
interlobular ducts
septal ducts
lobar ducts
2 hepatic ducts
common hepatic duct
386
Q

where is bile stored and concentrated?

A

gall bladder

387
Q

what causes the gall bladder smooth muscle to contract?

A

CCK and vagal impulses

388
Q

what 2 secretions does bile consist of?

A

secretion of hepatocytes

secretion of bile duct cells (cholangiocytes)

389
Q

what is the secretion from bile duct cells? (cholangiocytes)

A

an alkaline solution

390
Q

between meals the secretion from bile duct cells has an ionic composition similar to plasma, what causes the solution to become alkaline during meals?

A
  1. secretin released from S cells causes the flow rate to increase
  2. increased flow rate increases Cl-/HCO3- exchange, causing HCO3- content of solution to increase
391
Q

what is hepatic bile composed of?

A
  1. primary bile acids
  2. water and electolyes
  3. lipids and phospholipids
  4. cholesterol
  5. IgA
  6. bilirubin
392
Q

what is the only way cholesterol can be excreted from the body?

A

through bile

393
Q

what imbalance causes gall stones? (cholelithiasis)

A

excess cholesterol relative to bile acids may precipitate out and aggregate into gall stones

394
Q

what pharmacological therapy can be used to dissolve non-calcified cholesterol gallstones?

A

ursodeoxycholic acid

395
Q

how are bile salts secreted from apical membrane of hepatocytes into canalicula?

A

active transport

396
Q

how are bile salts absorbed in the ileum?

A

secondary active transport

397
Q

what is the synthesis of primary bile salts from cholesterol initially mediated by?

A

cholesterol 7alpha-hydroxylase

398
Q

what is rate of synthesis of bile salts dependent upon?

A

the hepatic portal blood concentration of bile salts

399
Q

what does low concentration of bile salts in the portal blood cause?

A

stimulates synthesis of bile salts

400
Q

what does high concetration of bile salts in the portal blood cause?

A

inhibits synthesis of bile salts

401
Q

what is the most common pathology of the biliary tract?

A

cholelithiasis

gallstones

402
Q

what is the usual management of cholelithiasis?

A

surgery

403
Q

what are the main drugs used for the pain of biliary colic?

A

morphine for analgesia

atropine or GTN for relief of biliary spasm

404
Q

what is the problem with using morphine fro biliary colic?

A

morphine can increase presure within biliary tree and constricts sphincter of Oddi

405
Q

what are the 4 mechanisms of drug metabolism within the liver?

A
  1. conversion to a metobilite less pharmacologically active
  2. concerstion from inactive prodrug to active compound
  3. unchanged activity
  4. conversion to a different spectrum of action
406
Q

what are the 2 phases of drug metabolism?

A

phase 1: oxidation, reduction, hydrolysis
phase 2: conjugation
(although remember some drugs are excreted unchanged)

407
Q

what is the function of phase 1 of drug metabolism?

A

makes drug more polar thus permitting conjugation

408
Q

what is the function of phase 2 of drug metabolism?

A

adds an endogenous compound to increase polarity

Gastrointestinal (15 decks)

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