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Phoebe's GI > Physiology > Flashcards

Physiology Flashcards

1
Q

Function of mouth

A

Chops and lubricates food
Starts carb digestion
Propels food to oesophagus

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2
Q

Oesophagus

A

Propels food to stomach

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3
Q

Stomach

A

Stores and churns food
Continuous carb digestion
Regulates delivery of chyme to duodenum

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4
Q

Small intestine

A

Duodenum, jejunum and ileum

Site of digestion and absorption of nutrients

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5
Q

Large intestine

A

Caecum, appendix and colon

Colon reabsorbs fluids and electrolytes, stores faecal matter before delivery to rectum

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6
Q

Rectum and Anus

A

Regulates expulsion of faeces

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7
Q

Mucosa

A

Mucous membrane
Lamina propria
Muscularis mucosae

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8
Q

Submucosa

A

Connective tissue
Larger blood and lymph vessels
Glands
Submucous plexus

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9
Q

Muscularis externa

A

Circular muscular layer
Myenteric plexus
Longlitudinal muscle layer

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10
Q

Serosa

A

Connective tissue

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11
Q

Motility

A

Mechanical activity mostly involving smooth muscle

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12
Q

Secretion

A

Secretion into lumen of digestive tract occurs from itself and accessory structures in response to the presence of food, hormonal and neural signs

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13
Q

Digestion

A

Chemical breakdown by enzymatic hydrolysis of complex foodstuffs to smaller absorbable units

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14
Q

Absorption

A

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

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15
Q

Circular muscle contraction

A

lumen becomes narrower and longer

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16
Q

Longitudinal muscle contraction

A

intestine becomes shorter and fatter

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17
Q

Muscularis mucosa contraction

A

Change in absorptive and secretory area of mucosa

Mixing activity

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18
Q

Electric coupling

A

Adjacent smooth muscles are coupled by gap junctions, electrical currents flow from cell to cell
Hundreds of cells are depolarised and contract at the same time as a synchronous wave

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19
Q

Spontaneous activity across coupled cells is driven by

A

specialised pacemaker cells

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20
Q

Spontaneous activity across coupled cells is modulated by

A

Intrinsic and extrinsic nerves

Hormones

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21
Q

Slow wave electrical activity determines

A

frequency, direction and velocity of rhythmic contraction

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22
Q

Slow wave electrical activity is driven by

A

ICC’s

Interstitial Cells of Cajal

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23
Q

ICC’s

A

Pacemaker cells located largely between circular and longitudinal muscle layers

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24
Q

True of False:

Depolarising waves always cause contraction

A

FALSE
Contraction only occurs if the slow wave amplitude is sufficient to reach a threshold to trigger smooth muscle cell calcium action potentials

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25
Q

Force of contraction is related to

A

Number of action potentials discharged

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26
Q

Wether a slow wave reaches the threshold depends on

A

Neuronal stimuli
Hormonal stimuli
Mechanical stimuli

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27
Q

Parasympathetic Innervation - excitatory influence

A

Increased gastric, pancreatic and small intestine secretion

Increased blood flow and smooth muscle contraction

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28
Q

Parasympathetic Innervation - inhibitory influence

A

Relaxation of sphincters

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29
Q

Sympathetic innervation - excitatory influence

A

Increased sphincter tone

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30
Q

Sympathetic innervation - inhibitory influence

A

Decreased motility, secretion and blood flow

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31
Q

where are cell bodies of enteric nervous system located

A

Ganglia

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32
Q

Local reflex

A

Peristalsis

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33
Q

Short reflex

A

Intestino-intestinal inhibitory reflex

Local distension activates sensory neurones, inhibits muscle activity

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34
Q

Long reflex

A

Gastrolineal Reflex

Increase in gastric activity causing propulsive activity

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35
Q

Peristalsis

A

Wave of relaxation followed by contraction
Precedes short distance along gut in aboral direction
Triggered by distension of gut wall

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36
Q

Segmentation

A

Rhythmic contractions of circular muscle layer that mix and divide luminal content

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37
Q

Colonic mass movement

A

Powerful sweeping contraction that forces faeces into rectum

Occurs a few times a day

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38
Q

Migrating motor complex (MMC)

A

Powerful sweeping contraction from stomach to terminal ileum
Inhibited by feeding and vagal activity
Triggered by motolin

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39
Q

Tonic contraction

A

Sustained contractions
Low pressure = organs with storage functions
High pressure = sphincters

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40
Q

How many sphincters in GI tract

A

6

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41
Q

Sphincters in GI tract

A 
Upper oesophageal
Lower oesophageal 
Pyloric
Ileocaecal 
Internal anal sphincter
External anal sphincter
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42
Q

Upper oesophageal sphincters

A

Relaxes to allow swallowing

Closes during inspiration

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43
Q

Lower oesophageal sphincter

A

Relaxes to permit entry of food to stomach

Closes to prevent reflux of gastric contents

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44
Q

Pyloric sphincter

A

Regulates gastric emptying

Prevents duodenal gastric reflux

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45
Q

Internal and External anal sphincters

A

Regulated by defecation reflex

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46
Q

normal BMI

A

20 - 25

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47
Q

Overweight BMI

A

25-30

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48
Q

Obese BMI

A

30-40

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49
Q

Morbidly obese BMI

A

Over 40

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50
Q

Lesioning ventromedial hypothalamus

A

obesity

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51
Q

Lesioning lateral hypothalamus

A

leanness

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52
Q

Satiation

A

Sensation of fullness generated during a meal

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53
Q

Satiety

A

Period of time between termination of one meal and initiation of next

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54
Q

Adiposity

A

State of being obese

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55
Q

Satiation signals increase

A

during meal to limit size

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56
Q

Satiation signals

A 
CCK
Peptide YY
Glucagon-like peptide
OXM
Obestatin
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57
Q

Glucaogon-like peptide 1

A

Released from L cells in response to food ingestion

Inhibits gastric emptying and reduces food intake

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58
Q

OXM

A

Oxyntomodulin
Released from oxyntic cells and L cells
Acts to suppress appetite

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59
Q

Grehlin

A

Hunger signal

Increases before meals, decreases after

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60
Q

Glutamate, Gaba and opioids

A

Increase food intake when injected into hypothalamus centre

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61
Q

Monoamines

A

Suppress food intake

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62
Q

2 hormones report fat status to brain

A

Leptin

Insulin

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63
Q

Leptin

A

made and released from fat cells

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64
Q

Insulin

A

Made and released from pancreatic cells

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65
Q

Stomach shape

A

J shaped bag

Relaxes to accommodate food from oesophagus

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66
Q

What nerve causes stomach to relax

A

Vagus

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67
Q

2 regions of stomach

A

Orad

Caudad

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68
Q

Orad region

A

Fundus and proximal body

Degree of tone and maintained contractile activity

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69
Q

Caudad region

A

Distal body and antrum body

Rhythmic patterns or contractions, intermittent

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70
Q

Orad contraction

A

No slow wave electrical activity
Tonic, weak contractions
As stomach empties, size slowly decreases
Gastrin decreases contractions and hence rate of stomach emptying

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71
Q

Caudad contraction

A

Slow waves occur

Phasic peristaltic contraction

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72
Q

Retropulsion

A

Pyloric end of stomach acts as a pump that delivers small amounts of chyme into the duodenum
Simultaneously forces most of its contained material backward into stomach

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73
Q

Strength of antral wave determines …

A

strength of chyme in stomach

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74
Q

Strength of antral wave is determined by

A

Gastric Factors

Duodenal Factors

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75
Q

Gastric factors

A
  1. Rate of emptying proportional to volume of chyme in stomach
  2. Consistency of chyme
    (thinner chyme is quicker)
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76
Q

Distension increases motility due to

A

Stretching smooth muscle
Stimulation of intrinsic nerve plexuses
Increased vagus nerve activity and gastrin release

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77
Q

Duodenal Factors

A
  1. Duodenum ready to receive chyme

2. Stimuli within duodenum that drive neuronal and hormonal response

78
Q

When chyme enters it stimulates

A

ANS

79
Q

Duodenum releases

A

CCK

80
Q

2 gland areas

A

Oxyntic

Pyloric

81
Q

Gastric mucosa is made up of

A

Surface lining
Pits
Glands (at the base of pits)

82
Q

Secretions from oxyntic mucosa

A 
HCl
Pepsinogen
Intrinsic factor and gastroferrin
Histamine
Mucus
83
Q

Pyloric gland area secretions

A

Gastrin
Somatostatin
Mucus

84
Q

HCl

A

Activates pepsinogen to pepsin
Denatures protein
Kills micro-organisms ingested with food

85
Q

Pepsingogen

A

Inactive precursor of pepsin

Pepsin once formed activates pepsinogen (autocatalytic)

86
Q

Instrinsic factor and Gastroferrin

A

Bind vitamin B12 and Fe2+

Facilitates absorption

87
Q

Histamine

A

Stimulates HCl secetion

88
Q

Mucus

A

Protective

89
Q

Gastrin

A

stimulates HCl secretion

90
Q

Somatostatin

A

Inhibits HCL secretion

91
Q

Secretion of HCL by gastric parietal cell

A
  1. CA combines with Co2 to form unstable carbonic acids
  2. Rapidly dissociates to H+, Na+ and HCO3-
  3. H+ transports across membrane to lumen of gastric pit
  4. H+ pumped out is swapped for a K+ which ‘enters cell’
  5. HCO3- goes out to plasma via antiporter in exchange of Cl- which enters cytoplasm
  6. Cl- eventually leaves cell through CFTR channel
  7. H+ and Cl- combine in lumen and canaliculus creates HCl
92
Q

Secretagogues

A

3 stimuli helping acid secretion

Cause trafficking in proton pumps to canalicular area where the become active

93
Q

3 secretagogues

A

ACh
Gastrin
Histamine

94
Q

3 phases of gastric secretion

A

Cephalic
Gastric
Intestinal

95
Q

Cephalic phase

A

In head, before food reaches stomach, preparing it to receive food

96
Q

Gastric phase

A

When food is in stomach

97
Q

Intestinal phase

A

After food has left stomach, chyme enters SI causing weak stimulation of gastric secretion

98
Q

Steps of the gastric phase

A
  1. Stimuli (sight smell)
  2. Causes activation of vagus nerve
  3. Drives acid secretion
99
Q

Mechanisms of acid secretion in gastric phase

A
  1. Stimulates neurones present in enteric part of stomach, neurotransmitter released, works of G cells, release gastrin into blood, acid secretion
  2. Stimulates neurones, releases ACh, acts on muscarinic cells, increased acid secretion
  3. Stimulates neuornes, releases ACh, releases Histamine, increased acid secretion
  4. Stimulates neurones, release ACH, somatostatin inhibited, increased acid secretion
  5. Food arrives at stomach, distension, recognised by mechanoreceptor, ACh etc.
  6. Food arrives at stomach, distension, G cells release gastrin, etc.
  7. Pepsin in stomach, hydrolyses proteins, releases digestive products, phenylamine activates G cells, low pH = release somatostatin etc.
100
Q

Drugs that can affect acid secretion

A

PPI
H2 receptor antagonists
Muscarinic receptor antagonists
NSAIDS

101
Q

PPI

A

Inhibits M3, G and H2
Irreversibly
Decreases secretion

102
Q

Example of PPI

A

Omeprazole

103
Q

H2 receptor antagonist

A

Block histamine H2 receptors
Comp and reversibly
Decreases sec secretion

104
Q

Example of H2 receptor antagonists

A

Ranitadine

105
Q

Example of Muscarinic receptor antagonist

A

Pirenzepine

106
Q

NSAIDS

A

PGE2 produced, decreases acid secretion
Formed by arachidonic acid
CXO used to convert
If CXO inhibited, acid secretion increases

107
Q

Why doesn’t the stomach digest itself?

A

Some gastric glands, pits and surface mucosa secrete a mucosa gel layer Prevents protons and acid from reaching surface stomach cells
Gel layered buffered, creating pH gradient, 2 at top, 7 at bottom

108
Q

PGE2

A

Reduce acid secretion in parietal cells
Increase mucous and HCO3- secretion
Increase mucosal blood flow to wash away H+

109
Q

Drug treatment of peptic ulcer aims to

A

Reduce acid secretion
Increase mucosal resistance
Eradicate H. Pylori

110
Q

Side effect of NSAIDS

A

Trigger gastric ulceration
Cause bleeding
Can be prevented with PGE1

111
Q

Mechanisms of anti-secretory activity

A

Irreversible inhibition of PPI
Competitive antagonism of Histamine H2 receptors
Competitive antagonism of M1 and M3 ACh receptors
Antagonism of CKK2 receptors

112
Q

3 parts of small intestine

A

Duodenum
Jejunum
Ileum

113
Q

Small intestine receives

A

Chyme from stomach
Pancreatic juice from pancreas (via pyloric sphincter)
Bile from liver and gall bladder
(via sphincter of oddi)

114
Q

Small intestine secretes

A

Intestinal juices

115
Q

Motility in SI causes

A

Mixing of chyme with digestive juices
Slow propulsion of chyme aborally (peristalsis)
Removal of undigested residues to large intestine via ileocaecal valve

116
Q

Longest part of SI

A

Jejunum

117
Q

Smallest part of SI

A

Duodenum

118
Q

Mixing and propulsion of chyme

A
  1. Segmentation
  2. Peristalsis occuring as few localised contractions
    (MMC)
119
Q

Secretion of SI

A 
Gastrin
Secretin
CCK
Glucose Dependant Insulinotropic
GLP-1
Motilin
Grehlin
120
Q

Gastrin

A

From G cells of gastric antrum
Stimulates H+ secretion by gastric parietal cells
Stimulates growth of parietal cells

121
Q

Secretin

A

From S cells of duodenum
Released in response to H+ and fatty acids in lumen
Promotes secretion of pancreatic and biliary HCO3-

122
Q

CCK

A

From I cells of duodenum and jejunum
Released in response to monoglycerides, free fatty acids, aa’s in lumen
Inhibits gastric emptying
Causes secretion of pancreatic enzymes needed for digestion
Stimulates relaxation of shpincter of Oddi
Potentiates action of secretin

123
Q

Glucose dependant insulinotropic

A

From K cells
Released in response to glucose, aa’s and fatty acids
Stimulates release of insulin from pancreatic B cells
Inhibits gastric emptying

124
Q

GLP-1

A

From I cells
Stimulates insulin secretion
Inhibits glucagon secretion
Decreases gastric emptying and appetite

125
Q

Motilin

A

From M cells
Secretes during fasting
Initiates MMC

126
Q

Ghrelin

A

From Gr cells

Stimulates appeptite

127
Q

All peptide hormones act on what receptors

A

G-protein couples

128
Q

Pancreatic secretion

A

Endocrine

Exocrine

129
Q

Endocrine secretions

A

Insulin and glucagon - secreted to blood

130
Q

Exocrine secretion

A

Digestive enzymes, NaHCO3-, secreted to duodenum collectively

131
Q

Why do duct cells secrete alkaline fluid into duodenum

A

Neutralises acidic chyme
Provides optimum pH for pancreatic enzymes
Protects mucosa from erosion by acid

132
Q

Luminal digestion

A

Mediated by pancreatic enzymes secreted into duodenum

133
Q

Membrane digestion

A

Mediated by enzymes situated at brush border of epithelial cells

134
Q

Assimilation

A

Overall process of digestion and absorption

135
Q

Alpha amylase

A

Breaks down internal 1-4 linkages but not terminal ones so no glucose created

136
Q

How are glucose and galactose absorbed

A

Secondary active transport mediated by SGLT1

137
Q

How is fructose absorbed

A

Secondary active transport mediated by GLUT5

138
Q

How do monosaccharides get absorbed

A

Through GLUT2

139
Q

Digestion in stomach

A

HCL denatures proteins

Pepsin cleaves proteins into peptides

140
Q

Digestion in duodenum

A

Uses 5 pancreatic proteases

141
Q

Trypsin, chymotrypsin and elastase

A

Endopeptidases

142
Q

Procarboxypeptidase A

Procarboxypeptidase B

A

Exopeptidases

143
Q

Main lipid digestive enzymes in adults

A

TAG lipase

144
Q

Failure to secrete bile salts results in

A 
Lipid malabsorption (Steatorrhea)
Secondary vitamin deficiency
145
Q

Role of bile salts

A

Increase surface area for attack by pancreatic lipase

Block TAG’s

146
Q

Colipase

A

Binds to bile salts and allows TAG’s

147
Q

How is cholesterol absorbed

A

By endocytosis in clatherin coated pits (NPC1L1)

148
Q

Ezetimibe

A

Binds to NPC1L1 to prevent internalisation

149
Q

How is Fe2+ absorbed

A

Binds to gastroferrin in stomach

150
Q

How is B12 absorbed

A
  1. B12 ingested in food, bound to proteins
  2. Stomach acid releases B12 from protein
  3. Haptocorcin, from saliva binds, with B12
  4. Stomach parietal cells release intrinsic factor
  5. Pancreatic proteases digest haptocorcin, B12 released
  6. B12 binds to intrinsic factor
  7. B12/intrinsic factor absorbed by endocytosis
151
Q

What is B12 not present in

A

Vegetables

152
Q

Who is susceptible to a B12 deficiency

A

Vegans

153
Q

Haustra

A

Sac like bulges in large intestine

Caused by taenia coli and circular muscle layers

154
Q

Colon function

A 
Absorp Na+, Cl-, H20 
and fatty acids
Secrete K+, HCO3- and mucous 
Stores colonic content 
Eliminate faeces
155
Q

Mucosa of colon

A

No villi

Has colonic folds, crypts and microvilli

156
Q

Colonocytes

A

Mediate electrolyte absorption

157
Q

Crypt cells

A

mediate ion absorption

158
Q

Goblet cells secrete

A

mucous

159
Q

Haustration

A

Non-propulsive segmentation

160
Q

Peristaltic propulsive movement

A

Mass movement

161
Q

Defection

A

Periodic egestion

162
Q

Defecation reflex

A
  1. Mass movement
  2. Activation of rectal stretch receptors
  3. Activation of pelvic nerve
  4. Activates parasympathetic efferents
  5. Contraction of smooth muscle of colon and rectum
163
Q

Pudenal Nerve

A

Keep your guts off the floor

Control defecation

164
Q

Colonic flora

A

Increase intestinal immunity by competition with pathogenic microbes
Promote motility
Synthesise vitamin K2 and fatty acids
Activate some drugs

165
Q

Retching

A

Rhythmic reverse peristalsis of stomach and oesophagus

166
Q

Vomiting

A
  1. Suspension of intestinal slow wave activity
  2. Retrograde contractions from ileum to stomach
  3. Suspension of breathing
  4. Relaxation of LOS, contraction of diaphragm and abdominal muscles compress stomach
  5. Ejection of gastric components through UOS
167
Q

Where is vomiting co-ordinated

A

Vomiting centre in the medulla oblongata of brain stem

168
Q

Where does Na+/glucose and Na+/amino acid co-transport occur

A

Small Intestine

169
Q

Where does Na+/H+ exchange occur

A

Duodenum and jejunum

Stimulated by luminal HCO3-

170
Q

Where does parallel Na+/H+ exchange and Cl+/HCO3- exchange occur

A

Ileum and colon

Regulated by cAMP

171
Q

SGLT1

A
  1. 2 Na bind
  2. Affinity for glucose increases, glucose binds
  3. Na+ and glucose translocate from extracellular to intracellular
  4. 2 Na+ dissociate, affinity for glucose fails
  5. Glucose dissociates
172
Q

Rehydration therapy exploits

A

SGLT1

Absorption of Na+ and glucose causes accompanying H20 to also be absorbed

173
Q

Role of liver in metabolism

A

Carbohydrate metabolism
Fat metabolism
Protein metabolism

174
Q

Role of liver in hormone metabolism

A

Deactivation (insulin, glucagon, ADH, steroid)

Activation

175
Q

Liver stores

A 
Fat soluble vitamins
Water soluble vitamin B12
Iron
Copper
Glycogen
176
Q

Bile between meals

A

Stored and concentrated in gall bladder

177
Q

Bile during meals

A

Chyme in duodenum stimulates gall bladder smooth muscle to contract
Sphincter of Oddi opens
Bile spurts into duodenum

178
Q

Laparascopic Cholecystectomy

A

Best treatment for symptomatic stones

179
Q

Ursodeoxycholic acid

A

For patients with unimpaired gall bladder function with small radioulcent stones

180
Q

Morphine/Buprenophine

A

Biliary colic
Constricts sphincter of oddi
Raises intrabiliary pressure

181
Q

Atropine or GTN

A

Relief of biliary spasm

182
Q

How much bile salts are lost in faeces

A

5%

Rest is absorbed in terminal ileum by active transport and undergoes enterohepatic recycling

183
Q

Bile acid sequestrants

A

Binds to bile acids preventing reabsorption

Lowers plasma conc indirectly

184
Q

When are bile acid sequestrants used

A

Hyperlipidaemia

Cholestatic jaundice

185
Q

Examples of bile acid sequestrants

A

Colveselam, colestipol, colestyramine

186
Q

Phase 1 of Drug Metabolsim

A

Right liver
Oxidation, reduction, hydrolysis
Makes drugs more polar, adds a chemically reactive group permitting conjugation

187
Q

Phase 2 of drug metabolism

A

Left liver
Conjugation
Adds endogenous compound increasing polarity

188
Q

CTP450

A

Metabolising enzyme in liver

Paracetamol and other drugs mess this up

189
Q

Hepatic Encephalopathy

A

Detoxification of NH3 to urea doesn’t occur in severe hepatic failure
Blood NH3 levels rise = coma

190
Q

Treat HE

A

Lactulose (converts ammonium which is not absorbed)

Antibiotics (minimally absorbed, suppress colonic flora and inhibit ammonia generation)

Phoebe's GI (24 decks)

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