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year 1 > GI - physiology > Flashcards

GI - physiology Flashcards

1
Q

what regulates gastric emptying

A

pyloric sphincter

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2
Q

what regulates flow from ileum to caecum

A

ileocaecal sphincter

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3
Q

what opens the ileocaecal sphincter and what closes it

A

ileal distension opens

proximal colon distension closes it

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4
Q

what 2 spinchters are skeletal muscle

A

upper oesophageal

external anal

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5
Q

how does vomiting cause reflux of gastric and duodenal contents

A

relaxes pyloric sphincter

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6
Q

what causes gastrooesophageal reflux

A

lower oesophageal sphincter not closing properly

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7
Q

from what does the exocrine pancreas secrete digestive enzymes

A

acinar cells

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8
Q

from what does the exocrine pancreas secrete aqueous salt solution

A

duct cells

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9
Q

what is motility

A

mechanical activity mostly involving smooth muscle

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10
Q

what is digestion

A

biochemical breakdown of complex foodstuffs into smaller absorbable units

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11
Q

what is absoprtion

A

transfer of absorbable products of digestion from digestive tract to blood or lymph

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12
Q

how are slow waves in the stomach, small intestine and large intestine spread

A

gap junctions

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13
Q

what are the pacemaker cells of the gut called

A

interstitial cells of cajal

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14
Q

what causes the upstroke in the AP of ICC

A

Ca influx

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15
Q

what determines the basic electrical rhythm of the GI tract

A

slow waves

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16
Q

where are tonic contractions in the GIT

A

sphincters

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17
Q

what is colonic mass movement

A

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

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18
Q

PS cranial outflow is via what nerve

A

vagus

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19
Q

PS sacral outflow is via what nerve

A

pelvic nerves

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20
Q

where do parasympathetic nerves synapse

A

post ganglionic neurones are intrinsic to ENS

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21
Q

where do sympathetic nerves synapse

A

prevertebral ganglia

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22
Q

what is an example of a local reflex reaction

A

peristalsis

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23
Q

what is a local reflex reaction

A

sensory neurone synapses with interneuron at the myenteric or submucosal plexus

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24
Q

where does the synapse occur in a short reflex

A

prevertebral ganglia

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25
Q

what is an example of an inshort reflex

A

intestino-intestinal inhibitory reflex

over distension in one area of intestine causes relaxation in rest of intestine

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26
Q

what is the gastrocolic reflex

A

strong peristalsis in colon triggered by meals

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27
Q

what is the defection reflex

A

triggered by rectal distension

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28
Q

where does the synapse occur in a long reflex

A

dorsal motor nucleus of the vagus in the medulla oblongata

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29
Q

What is an example of a long reflex

A

Gastroileal reflex

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30
Q

what is the gastroileal reflex

A

when food enters stomach causing vigorous mechanical activity to occur - causes increased motility in the ileum and the opening of the ileocaecal valve to clear previous food remnants from the small intestine
triggers segmentation of ileum through release of gastrin

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31
Q

what is peristalsis

A

orderly wave of contraction to push food distally

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32
Q

what triggers peristalsis

A

distension of gut wall

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33
Q

what happens to the muscle behind the food bolus in peristalsis (propulsive segment)

A

circular muscle contracts - ACh + substance P

longitudinal muscle relaxes - VIP and NO

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34
Q

what happens to the muscle infront of the food bolus in peristalsis (receiving segment)

A

circular muscle relaxes (VIP and NO)

longitudinal muscle contracts (ACh + substance P)

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35
Q

when does peristalsis occur

A

in small intestine between meals

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36
Q

what is the name of the strong peristaltic contraction passing from the pyloric sphincter to the ileocaecal valve that clears the small intestine

A

Migrating motor complex/housekeeping mother reflex

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37
Q

what triggers the migrating motor reflex

A

hormone motilin

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38
Q

what suppresses the migrating motor reflex

A

gastrin

CCK

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39
Q

what is the term for rhythmic contractions of circular muscle layer that mixes and divides luminal contents

A

segmentation

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40
Q

in segmentation how many points of circular muscle contraction are there

A

2

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41
Q

what is the name of the lymphoid tissue on the side of the pharynx

A

palatine tonsils

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42
Q

what reflex causes the jaw to open

A

masseteric

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43
Q

what reflex causes the jaw to close

A

digastric reflex

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44
Q

stimulation from pressure from food bolus gets —– receptors to send ——– ——– to the swallowing centre in the ——

A

pharyngeal receptors
afferent impulses
medulla

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45
Q

what happens to the larynx when you swallow

A

elevates

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46
Q

what happens to the epiglottis when you swallow

A

tilts

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47
Q

what happens to the vocal cords when you swallow

A

close across larynx opening

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48
Q

what happens to the respiratory centre in brain (medulla oblongata) when you swallow

A

inhibited

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49
Q

what happens to the upper oesophageal sphincter when food enters oesophagus

A

closes

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50
Q

what happens in food becomes lodged during swallowing

A

local pressure receptors stimulate a second wave of peristalsis more forceful than the first and increase saliva secretion

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51
Q

what gland produces the most saliva

A

submandibular

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52
Q

where are the parotid glands

A

over masseter, below ears

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53
Q

what kind of mucus do sublingual glands produce

A

thick viscous

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54
Q

what 2 nerves control the parasympathetic innervation of saliva production

A

facial and glossopharyngeal

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55
Q 
what is the function of the following saliva components
lysozyme
lactoferrin
IgA
amylase
Bicarbonate
A

antibacterial
lysozyme
lactoferrin
IgA

digest carbohydrates
amylase

neutralise acid
Bicarbonate

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56
Q

what pH is the oral cavity

A

alkaline

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57
Q

what is the functional unit of a salivary gland

A

salivon

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58
Q

from what does primary secretion of saliva occur and what is it composed of

A

acinus cells in a salivon
primary secretion with Na K Cl and HCO3 - similar to plasma
+ mucus and amylase

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59
Q

what are the 2 types of acinar cell

A

serous - alpha amylase

mucous - thicker

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60
Q

how do duct cells modify saliva

A

remove Na+ and Cl-
add K and HCO3
no movement of water

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61
Q

true false

as saliva flow rate increases HCO3 content decreases

A

false

as saliva flow rate increases HCO3 content also increases

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62
Q

what is the simple saliva reflex

A

saliva increased in response to food in mouth - pressure receptors in mouth

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63
Q

what is the conditioned (learned) saliva reflex

A

saliva increased in response to stimulus that suggests food is coming

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64
Q

where do afferent impulses travel in the simple reflex

A

salivary centre in medulla

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65
Q

where do afferent impulses travel in the conditioned reflex

A

activates cerebral cortex which activates salivary centre in medulla

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66
Q

what kind of stimulation produces
large volume
enzyme rich
watery saliva

A

parasympathetic

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67
Q

what kind of stimulation produces
small volume
mucus rich
thick

A

sympathetic

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68
Q

what receptors are responsible for PS saliva production

A

M3

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69
Q

what receptors are responsible for S saliva production

A

B1

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70
Q

what is retropulsion

A

process by which food in the body of the stomach is propelled forward by peristaltic waves - chyme hits the pyloric sphincter and bounces back - churning

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71
Q

true/false

fat in the duodenum can delay stomach emptying

A

true - time needed for digestion and absorption in small intestine

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72
Q

what are enterogastrones

A

inhibit stomach contraction and delay emptying of stomach
CCK
Secretin

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73
Q

true/false

alkali in the duodenum can delay stomach emptying

A

false
acid in the duodenum delays stomach emptying - time required for neutralisation of gastric acid by bicarbonate secreted from the pancreas

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74
Q

true/false

hypertonicity in the duodenum delays stomach emptying

A

true

products of CHO and protein digestion osmotically active and draw water into the small intestine

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75
Q

what does acid in the duodenum stimulate the release of

A

secretin

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76
Q

what does fat in the duodenum stimulate the release of

A

CCK

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77
Q

what is the name of the reflex which delays stomach emptying due to signal from duodenum that it has enough chyme

A

enterogastric reflex

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78
Q

what are the 3 secreting cells within the pyloric gland area of the antrum of the stomach

A

D cells
G cells
Mucosal cells

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79
Q

what do D cells secrete

A

somatostatin

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80
Q

what does somatostatin do

A

inhibits the release of gastrin - inhibits HCl secretion

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81
Q

how is somatostatin release inhibited

A

cholinergic stimulation

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82
Q

what do G cells secrete

A

gastrin

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83
Q

what does gastrin do

A

stimulates HCl and histamine secretion

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84
Q

what do mucosal cells secrete

A

mucous to protect mucosa from ulcer formation - prevents pepsin/HCl reaching apical surface of cells

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85
Q

what are the 3 secreting cells within the oxyntic mucosa of the funds and body of stomach

A

chief cells
enterochromaffin-like cells
parietal cells

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86
Q

what do chief cells secrete

A

pepsinogen (inactive precursor of pepsin)

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87
Q

what do enterochromaffin-like cells secrete

A

histamine

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88
Q

what does histamine do

A

stimulates HCl secretion from parietal cells

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89
Q

what receptors work on Enterochrommaffin cells and what does their stimulation cause

A

M1 receptors

M1 stimulation causes increased histamine secretion

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90
Q

what do parietal cells secrete

A

HCl and intrinsic factor

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91
Q

what does intrinsic factor do

A

binds to vitamin B12 which allows its absorption in the terminal ileum

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92
Q

CO2 and H2O combine under enzyme ——— which dissolves to form – and –

  • — is transported out of the cell via antiporter in exchange for — which is driven out into the ——
    • is secreted into canaliculus via proton pump and combines with – to form —
A

CO2 and H2O combine under enzyme carbonic anhydrase
which dissolves to form H+ and HCO3
HCO3 is transported out of the cell via anti porter in exchange for Cl
Cl is driven out into the canaliculus
H+ is secreted into the canaliculus via proton pump where it combines with Cl to form HCl

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93
Q

what receptors are present in parietal cells and what happens when they are stimulated

A

M3 receptors

M3 stimulation increases HCl secretion

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94
Q

parietal cells express PGE2 which inhibits/stimulates secretion

A

inhibits

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95
Q

where in parietal cells are the ion ATPase pumps when resting

A

within cytoplasmic tubulovesicles

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96
Q

where do PPs move in response to secretogogues

A

active state in apical membrane of parietal cell

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97
Q

what are the 3 phases of gastric secretion

A

cephalic
gastric
intestinal

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98
Q

when is the cephalic phase of gastric secretion

A

before food enters the stomach

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99
Q

during the cephalic phase how does the vagus nerve activate parietal cells

A
  • release ACh to directly activate parietal cells
  • release of histamine from ECL cells which locally activates parietal cells
  • release of GRP (gastrin releasing peptide) causing release of gastrin into systemic circulation activating parietal cells
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100
Q

when is the gastric phase of gastric secretion

A

when food is in the stomach

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101
Q

during gastric phase amino acids cause what

A

stimulate G cell production of gastrin

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102
Q

during gastric phase food buffering pH inhibits what

A

D cells

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103
Q

during gastric phase acid secretion is caused by what

A

distension of stomach activating mechanoreceptors

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104
Q

when is the intestinal phase of gastric secretion and what happens

A

when good has left stomach

gastric secretions are switched off - secretin, CCK, somatostatin

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105
Q

what is pepsinogen activated by

A

HCl

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106
Q

enteric neurones release ACh which acts on D cells to

A

decrease somatostatin

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107
Q

enteric neurones release ACh which acts on ECL cells to

A

increase histamine

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108
Q

enteric neurones release GRP which acts on

A

G cells

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109
Q

increase in gastrin in the blood increases/decreases parietal cell secretion

A

increases

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110
Q

Full activity of pancreatic lipase requires

  • what cofactor
  • what pH
  • what metal ion
  • 2 other things
A
  • colipase cofactor
  • alkaline
  • Ca2+
  • bile salts and fatty acids
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111
Q

pancreatic lipase is secreted from – cells of pancreas in response to — which also ———

A

pancreatic lipase is secreted from acinar cells of pancreas in response to CCK which also stimulates bile flow

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112
Q

how is a suitable pH for pancreatic lipase achieved

A

HCO3 in pancreatic juice

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113
Q

where does pancreatic lipase hydrolyse the TAGs

A

1 and 3 position

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114
Q

digestion by pancreatic lipase gives

A

monoglyceride + 2 FAs

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115
Q

what are 2 additional lipases

A

carboxyl ester hydrolase

phospholipase A2

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116
Q

what stops the cephalic phase

A

decreased vagal nerve activity due to

  • cessation of eating and stomach emptying
  • pain
  • nausea
  • negative emotions
117
Q

at the end of the gastric phase what happens to the pH of the antrum

118
Q

is somatostatin released from D cells at the end of the gastrin phase

A

yes - this decreases gastrin secretion

119
Q

what is continually secreted by gastric mucosa to reduce histamine and gastrin-mediated HCl secretion

A

Prostaglandin E2 (PGE2)

120
Q

ranitidine and cimetidine are examples of what drug

how are they administered?

A

H2 histamine receptor competitive antagonists

orally

121
Q

Omeprazole is an example of what kind of drug

how is it administered

A

PPI

oral OD

122
Q

how do proton pump inhibitors work

A

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

123
Q

how do PPIs reach the secretory cannaliculi

A

absorbed from GI tract and delivered via systemic system

124
Q

aspirin and ibuprofen are examples of what drugs

125
Q

what do NSAIDs block irreversibly

A

COX1 - increase HCl secretion

126
Q

what does blockage of COX1 cause

A

decreased prostaglandins

127
Q

what is the role of PGI2 and PGE2 in stomach

A

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

128
Q

what is given if using NSAIDs longterm

A

PGE1 analogue e.g. misoprostol

129
Q

what does misoprostol do

A

inhibits basal and food stimulated gastric acid secretion

maintains/increases secretion of mucus and bicarbonate

130
Q

name 2 mucosal strengtheners

A 
sucralfate (oral)
Bismuth chelate (oral) (also H.pylori toxic)
131
Q

sucralfate increases…

A

mucosal blood flow
mucus
bicarb
prostaglandin production

132
Q

what are the 2 subgroups of starch

A

amylose

amylopectin

133
Q

what is the structure of amylose

A

straight chain

alpha-1,4 only

134
Q

what is the structure of amylopectin

A

branched chain

alpha-1,4 and alpha-1,6

135
Q

what is more branched amylopectin or glycogen

136
Q

sucrose and lactose are

A

disaccharides

137
Q

sucrose is made up of

A

glucose and fructose

alpha-1,2 links

138
Q

lactose is made up of

A

glucose and galactose

beta-1,4 links

139
Q

glucose and fructose are

A

monosaccharides

140
Q

in alpha/beta glucose the hydroxyl group is above/below C1

A

alpha - below

beta - above

141
Q

what enzymes cause intraluminal hydrolysis of polysaccharides to oligosaccharides (sucrose and lactose)

A

salivary a-amylase

pancreatic a-amylase

142
Q

what enzymes cause brush border hydrolysis of oligosaccharides to monosaccharides

A

lactase
maltase
sucrose-isomaltase

143
Q

maltose is made up of

144
Q

what is the rate limiting step of hydrolysis of CHOs

A

transport process

145
Q

where does intracellular digestion occur

A

enterocytes

146
Q

how do ions move between cells

A

paracellular - across epithelial tight junctions

147
Q

true / false

a-amylase can break a-1,4 INTERNAL linkages only and is therefore an endozyme

148
Q

what enzyme breaks down lactose to glucose and galactose and what bonds are hydrolysed

A

lactase

B-1,4

149
Q

what is the rate limiting step of lactase action

A

hydrolysis of lactose

150
Q

what enzyme breaks down sucrose to glucose and fructose and what bonds are broken

A

sucrase

a-1,2

151
Q

what enzyme breaks down a-1,6 bonds

A

isomaltase

152
Q

how are glucose and galactose absorbed into enterocytes

A

secondary active transport

SGLT1

153
Q

what does facilitated diffusion by GLUT5 absorb

154
Q

how do all monosaccharides exit the basolateral side of an enterocyte

A

facilitated diffusion by GLUT2

155
Q

can ring or linear glucose be absorbed

156
Q

how are proteins digested to amino acids

A

luminal enzymes

or to peptides by luminal enzymes then AA by brush border enzymes or intracellular hydrolysis

157
Q

trypsin
chymotrypsin
elastase
are examples of what enzymes

A

endopeptidases - produce oligopeptides (2-6 AA)

158
Q

procarboxypeptidase A and B are examples of what enzymes

A

exopeptidases - produce single AA

159
Q

how many of the 7 AA absorption mechanisms are Na dependent

A

5 (secondary active transport)

160
Q

AA transport mechanisms at basal side

  • Na independent and mediate —
  • Na dependent and mediate –
A

3 Na dependent and mediate efflux

2 Na independent and mediate influx

161
Q

how are oligopeptides transported across the apical membrane of an enterocyte

A

H+ dependent mechanisms (secondary active transport)

162
Q

what is primary lactase deficiency

A

lack of lactase persistence allele (LP)

- can happen to a varying degree due to polymorphisms

163
Q

what is secondary lactase deficiency

A

lactose intolerance due to damage to proximal small intestine

164
Q

what is congenital lactase deficiency

A

infants unable to break down lactose

165
Q

undigested lactose causes

A

acidification of colon
increased osmotic load –> diarrhoea
food for microflora –> produce SCFAs, H, CO2 and methane

166
Q

what is bile secreted in response to

167
Q

Co-lipase is produced where

168
Q

why is collapse necessary

A

without it bile salts block access of lipase to lipid

169
Q

where is bile stored and concentrated

A

gallbladder

170
Q

what are the final products of lipid digestion stored in

A

mixed micelles - emulsified fat globule containing monoglyceride, FAs, phospholipid, bile salt and cholesterol

171
Q

how do short and medium chain (-12C) FAs enter the villus capillaries

172
Q

what happens to LCFAs (12C+) and monoglycerides

A

resynthesised into triglycerides in the ER and incorporated into chylomicrons

173
Q

what carries cholesterol across the enterocyte apical membrane

174
Q

how does cholesterol bound to NPC1L1 move around cell

A

myosin runners

175
Q

what drug binds to NPC1L1 to prevent internalisation of cholesterol

176
Q

how does absorption of Ca2+ occur

A 
passive transport (paracellular movement in whole small intestine)
active transport (transcellular movement through calcium channel in duodenum and upper jejunum)
177
Q

what vitamin increases the expression of calcium channels

178
Q

how is iron transported

A

transcellularly by metal transporter across epithelium of intestine
can also be absorbed through harm

179
Q

what form is iron transported in

180
Q

what vitamin stabilise the ferrous ion (Fe2+)

181
Q

how is the ferrous ion absorbed

A

cotransporter - H+ ion coupled with its transport

H+ dependent transport

182
Q

how is iron stored

183
Q

how does ferrous ion leave enterocyte

A

ferroportin

184
Q

what is released from liver when body iron levels get too high which negatively regulates ferroportin

185
Q

how is haem transported

A

transcellularly by haem transporter

taken up and degraded by haem oxidase

186
Q

what is NCX1

A

transporter that couples exit of Ca2+ and entry of sodium in enterocytes

187
Q

what does haptocorrin bind to

A

vitamin B12

188
Q

where is haptocorrin produced

A

salivary glands, released in the stomach

189
Q

what do pancreatic proteases digest in small intestine to release Vit B12

A

haptocorrin-B12 complex

190
Q

what binds to B12 in small intestine to allow it to be absorbed in terminal ileum

A

intrinsic factor

191
Q

what vitamins are incorporated into mixed micelles and passively transported into enterocytes

A

fat soluble ADEK

192
Q

what joins the forming chylomicron

A

apolipoprotein apob48

193
Q

how are water soluble vitamins absorbed

A

active transport - may be Na dependent

194
Q

where is the sodium potassium chloride co-transporter (1 Na, 2Cl, 1 K enter cell)

A

basolateral side of enterocyte - build up intracellular conc of Cl so that it can move out apical side

195
Q

how does Cl move out of apical side

A

CFTR channels

196
Q

what illness causes CFTR channels to be overactive

197
Q

cAMP, cGMP and Ca2+ —— CFTR channels

A

up regulate

198
Q

true/false

SGLT1 Na/glucose channel is not affected by diarrhoea

199
Q

what 2 Na transport systems occur throughout small intestine

A

Na/glucose

Na/amino acid

200
Q

luminal HCO3 stimulates what transport of Na - duodenum and jejunum

201
Q

where does parallel Na/H and Cl/HCO3 exchange occur

A

ileum and colon

202
Q

what Na channel is most important in the inter digestive period

A

Na/H Cl/HCO3

203
Q

where are epithelial Na channels

A

distal colon

204
Q

what hormone regulates epithelial Na channels

  • opens them
  • inserts more from intracellular vesicles into membrane
  • increases synthesis of them and Na+/K+ ATPase
A

aldosterone

205
Q

intracellular cAMP, cGMP and Ca2+ —- absorption of NaCl through —–

A

decreases

Na/H+ Cl/HCO3 exchange

206
Q

what does E.Coli enterotoxin do

A

activates adenylyl cyclase which increases intracellular cAMP - reduced NaCl absorption - diarrhoea

207
Q

does odansetron help motion sickness

208
Q

what nerve regulates motion sickness

A

CN VIII

vestibulocochlear - found in ear

209
Q

what is the forceful propulsion of gastric contents out of the mouth

A

vomiting /emesis

210
Q

where is the vomiting centre in the brain

A

medulla oblongata

211
Q

during emesis the stomach oesophagus and sphincters are relaxed
true/false

212
Q

during emesis the abdominal muscles and diaphragm are relaxed
false/true

A

false - contract to increase pressure

213
Q

what do vagal efferents cause in the vomiting cycle

A

oesophagus shortens
stomach relaxes
small intestine retrograde contractions

214
Q

toxic materials in the gut stimulate the release of what from ECL cells

215
Q

what receptors does serotonin work by

216
Q

the depolarisation of sensory afferent terminals in mucosa by serotonin via 5HT3 receptors causes what

A

vagal afferent AP discharge to vomiting centre in medulla

217
Q

vagal vomiting-inducing afferent discharges are sent to …

A

CTZ (chemoreceptor trigger zone)

NTS (nucleus tractus solitaries)

218
Q

what cranial nerve supplies stomach and small intestine in vomiting

219
Q

true/false

vestibular system signals to the vomiting centre through vestibular nuclei to vomiting centre then to CTZ

A

false

vestibular systems signals to the vomiting centre through vestibular nuclei to CTZ and then to vomiting centre

220
Q

what is a mallory weiss tear

A

tear in mucous membrane where oesophagus meets stomach

221
Q

how does cancer therapy induce vomiting

A

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

222
Q

why would drugs with high dopamine activity cause nausea and vomiting
e.g. drugs used in parkinsons

A

dopamine D2 receptors are prevalent in the CTZ

223
Q

how can antidepressants cause sickness

A

enhance 5HT function (5HT3 receptors in CTZ)

224
Q

true/false

the CTZ lacks an effective BBB so toxic materials in blood can stimulate it directly

225
Q

what drug would be prescribed to suppress chemo radiation induced emesis and post op emesis

A

5HT3 receptor antagonist

226
Q

how can the function of 5HT3 receptor antagonists be improved

A

addition of a corticosteroid and a NK1 receptor antagonist

227
Q

what drug would be used to treat motion sickness/prophylaxis

A

Muscarinic ACh receptor antagonist e.g. hyoscine scopolamine (transdermal or PO) - direct inhibition of GI movement - can be seditive
Histamine H1 receptor antagonist - CNS depression and sedation e.g. cyclizine

228
Q

what do all serotonin antagonists end in

229
Q

what do dopamine receptor antagonists do

A

block dopamine D2 and D3 receptors in the CTZ

230
Q

what has more unwanted effects - domperidone or metoclopramide

A

metoclopramide as it crosses the BBB

both DRAs

231
Q

what drugs are used for drug induced vomiting and vomiting in GI disorders

A

dopamine receptor antagonists

232
Q

true/false

DRA can be used in children

A

false

avoid in children

233
Q

what do NK1 receptor antagonists do

A

antagonism of substance P e.g. aprepitant

used + 5HT3 receptor in chemo

234
Q

when are cannabinoid receptor antagonists used

A

cytotoxic chemotherapy which is unresponsive to other anti-emetics

235
Q

what are some side effects of cannabinoid receptor antagonists

A

drowsiness
dizziness
dry mouth
mood changes

236
Q

CCK is produced from what cells

A

I cells of duodenum and jejenum

237
Q

secretin is produced from what cells

A

S cells of duodenum

238
Q

what does secretin in response to acid in the duodenal ileum cause

A

increased secretion of NaHCO3 from pancreatic duct cells

239
Q

what is produced from M cells of duodenum and jejunum

240
Q

what is produced from K cells of duodenum and jejunum

A

GIP

gastric inhibitory peptide

241
Q

what is produced from L cells

A

glucagon-like peptide-1 (GLP-1)

242
Q

is gastrin produced from just the stomach

A

no

stomach and duodenum

243
Q

what 2 hormones report fat status to brain and increase in levels when more fat is stored

A

insulin and leptin

244
Q

alpha islet cells produce

245
Q

beta islet cells produce

246
Q

delta islet cells produce

A

somatosatin

247
Q

what hormone added GLUT4 transporters to membrane to increase permeability for glucose

248
Q

what are incretins

A

hormones that act upon beta islet cells of pancreas in feed forward way to stimulate release of insulin

249
Q

give 2 examples of incretins

250
Q

when are incretins released

A

in response to chyme entering the duodenum

251
Q

what cells produce ghrelin

A

Gr cells of gastric antrum and small intestine and pancreas

252
Q

levels of gherkin —- before a meal and —- after

A

increase before a meal and decrease after

253
Q

what cells in the pancreas secrete digestive enzymes

A

Acinar cells

254
Q

—- cells in duodenum secrete —– which is a brush borer enzyme that activates —– to trypsin

A

mucosal cells in duodenum secrete enterkinase which is a brush border enzyme that activates trypsinogen to trypsin

255
Q

what activates procarboxypeptidase to carboxypeptidase

256
Q

what exchanger sits in the apical membrane of duct cells of pancreas to allow transfer of alkaline solution into the lumen of small intestine

A

Cl/HCO3 exchanger

257
Q

vagal stimulation of acinar cells mediates what stage of pancreatic secretion

258
Q

gastric distension which evokes a vasovagal reflex that results in PS stimulation of acinar and duct cells mediates what stage of pancreatic secretion

259
Q

CCK —- the secretion of digestive enzymes from acinar cells in pancreas

260
Q

what is xerostomia

A

dry mouth syndrome due to inadequate production of saliva

261
Q

what is the name for the intermittent circular muscle contraction in the large intestine

262
Q

in what direction does haustration cause food to move

A

oral - allow time for reabsorption

263
Q

contraction of the tenai coli causes what

A

shortening of the colon

264
Q

give an example of a time laxatives wouldn’t be used

A

bowel obstruction

265
Q

what is the mechanism of orlistat

A

inhibits pancreatic lipase to decrease triglyceride absorption in small intestine

266
Q

what are some side effects of orlistat

A

abdominal cramps
diarrhoea
steatorrhoea

267
Q

what are sulfasalazine, olsalazine and balsalazine examples of

A

aminosalicylates

268
Q

what do aminosalicylates do

A 
release 5ASA (5-aminosalicylic acid)
used in UC
269
Q

where does the hepatic artery and the hepatic portal vein blood mix in the liver

270
Q

what are the functional units of the liver

A

hexagonal lobules

271
Q

in a liver lobule
blood flows — through sinusoids towards central —-
bile flows — through cannaliculi towards —-

A

blood flows inwardly through sinusoids towards central vein

bile flows outwardly through cannaliculi towards bile duct

272
Q

what membrane faces the cannaliculi

273
Q

what is the space of disse

A

pericellular plasma containing space between capillaries (sinusoid) and basolateral membrane of hepatocyte

274
Q

what 3 cells are present in the space of disse

A

fenestrated endothelial cells
kuppfer cells - resident macrophages - remove bacteria and dead RBCs
Stellate cells - storage of vitamin A

275
Q

what pathology can stellate cells cause

A

fibrosis and cirrhosis due to storage of collagen

276
Q

what is the first stage of metabolism in the liver

A

1 - oxidation, reduction, hydrolysis - making the drug more polar therefore permitting conjugation

277
Q

what is the second stage of metabolism in the liver

A

conjugation - adds endogenous compound to increase polarity

278
Q

what is the fate of most bile entering the duodenum

A

reabsorbed in terminal ileum via secondary active transport

279
Q

how do bile salts reach the cannaliculi

A

secreted from apical membrane of hepatocytes via active transport

280
Q

what enzyme initiates the synthesis of primary bile salts from cholesterol

A

cholesterol 7-alpha-hydroxylase

281
Q

what does the rate of synthesis of bile depend on

A

hepatic portal blood concentration of bile salts

- high conc = low synthesis

282
Q

what can be given for relief of biliary spasm in biliary colic

A

GTN or atropine

283
Q

how do chylomicrons reach the LVA

A

thoracic duct

284
Q

what metabolises chylomicrons once in the blood

A

lipoprotein lipase

285
Q

what carries the free fatty acids and glycerol released by chylomicron degradation

286
Q

what does a chylomicron remnant consist of

A

cholesterol and phospholipid

287
Q

lesioning ventromedial hypothalamus

288
Q

lesioning lateral hypothalamus

289
Q

what makes up the small intestine in size order

A

duodenum - shortest
jejunum
ileum - longest

year 1 (45 decks)

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