digestion post midterm Flashcards

1
Q

the enterogastric reflex involves the activation of what?

A

receptors in the duodenum via the ENS and ANS to inhibit signal

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2
Q

what can inhibit ENS neurons in the enterogastric reflex?

A

Parasympathetic input from vago-vagal input

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3
Q

what will the sympathetic input inhibit in the enterogastric reflex?

A

inhibit excitatory neurons

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4
Q

what is the purpose of the enterogastric reflex?

A

Purpose is to slow down the rates of peristalsis

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5
Q

what are some factors that contribute to enterogastric reflex?

A

o Distension as the meal enters the duodenum
o Ph < 3.5 signals to slow down peristalsis
o Chemical composition
o High osmolarity
o Fats» proteins > carbs

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6
Q

what does the enterogastrone hormone complex contribute to?

A

antral peristalsis

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7
Q

what is the gastric emptying due to?

A

due to a balance between gastric and duodenal conditions

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8
Q

what happens do the duodenal and gastric factors in gastric emptying?

A

Duodenual factors will decrease motility

Gastric factors increase motility

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9
Q

what causes vomiting?

A

• Results from an increase in intrabdominal pressure due to the concerted action of the diaphragm and abdominal muscles

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10
Q

what happens to the abdomen and diaphragm during vomiting?

A

The diaphragm will lower

Abdominal muscles contract

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11
Q

is the GIT active or passive during vomiting?

A

passive process

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12
Q

is their resistance to flow at the level of the LES?

A

no

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13
Q

what happens to the force of vomiting if the pressure increases?

A

greater force

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14
Q

what are some factors that may stimulate/trigger vomiting?

A
  • pharygeal stimulation
  • GIT or urogenital distention
  • pain, cardiac ischemia
  • biomechanical disequlibrium
  • vestibular signals
  • psychogenic factos
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15
Q

is the chemoreceptor trigger zone the same as the vomiting center?

A

they are distinct but both part of the medulla.

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16
Q

what is the function of the chemoreceptor trigger zone

A

it signals the vomiting center

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17
Q

what happens if the CTZ is removed?

A

vomiting can persist

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18
Q

where is the CTZ located?

A

Sits at the forth ventricle, outside the blood brain barrier

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19
Q

what happens when the vomiting center is activated?

A
  • widespread autonomic discharge
  • nausea
  • retching
  • emesis
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20
Q

how does the widespread autonomic discharge affect the para/sympathetic System?

A

Leads to imbalances between the parasympathetic and sympathetic system which a continuously activated and disactivating leading to accompanying symptoms

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21
Q

what are some symptoms that will accompany the widespread autonomic discharge in vomiting?

A
  • Sweating
  • Vasoconstriction
  • Salivation
  • Alternating bradycardia & tachycardia
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22
Q

what causes nausea?

A

unknown cause

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23
Q

what is retching?

A

incomplete contraction of muscles which leads to  Abrupt, uncoordinated respiratory movements with glottis closed

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24
Q

how are the teeth protected during vomiting?

A

increase salivation to protect teeth from the high acidity

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25
Q

what type of experience is nausea described as?

A

A psychic experience

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26
Q

what is emesis?

A

Actual expulsion of contents of the upper GIT

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27
Q

what is the function of the SI?

A

site where all digestion and absorption of the nutrients occurs

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28
Q

what is the SI divided up into?

A

o duodenum
o jejunum
o ileum

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29
Q

what does the Upper SI neutralize?

A

the chyme comming from the stomach due to its high acidity

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30
Q

will the chybe be isotonic or isomostic as it leaves the duodenum?

A

isotonic (process known as osmotic equilibration)

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31
Q

what motor activities take place in the SI?

A

Effective mixing

Slow propulsion

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32
Q

what governs intestinal contractions?

A

electrical characteristics of the smooth muscles

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33
Q

what controls the frequency of intestinal contractions?

A

the BER

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34
Q

what are the ERA spikes initiated by?

A

by stretch or increased release of ACh

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35
Q

what is the amplitude of contraction of the SI related to?

A

Related to the number of spikes/bursts of the ERA

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36
Q

how does the frequency of the BER differ in the SI compared to the somach?

A

in duodenum ~ 12/minutes and in ileum ~ 8/minute (declines as we move trhough the SI) vs 3/minutes in the stomach

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37
Q

what caused for the frequency of the cells of SI to change?

A

Changes along the length due to groups of pacemaker cells which drive ~1000 cells

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38
Q

excitability of the smooth muscle cells of the SI is greater in the proximal or distal SI?

A

proximal

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39
Q

what part of the SI has the thickest smooth muscle?

A

greater in the proximal stomach

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40
Q

what does the greater thickness of the smooth muscle in the proximal SI caused?

A

oth the Frequency and the amplitude of contractions will be greater in the proximal portion of the small intestine

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41
Q

what is the most common type of contractile in the SI after a meal?

A

segmentation and peristalsis

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42
Q

what is segmentation?

A

circular muscles which contract at different points

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43
Q

what is the use of segmentation?

A

Effective at mixing the contents within the intestine

aids in absorption due to greater contact with luminal contentes

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44
Q

what is segmentation caused by?

A

myogenic response to distention

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45
Q

what coordinates and organizes contraction over the length of the SI?

A

ENS

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46
Q

what happens to the para/sympathetic systems in response to hormones during segmentation?

A

parasympathetic signal will increase,

sympathetic decreases

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47
Q

what does segmentation also contribute to?

A

slow propulasion; Forward movement of the contents in the aboral direction

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48
Q

how are peristaltic contractions in the SI defined as?

A

infrequent and irregular, weak and shallow

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49
Q

do peristaltic contractions travel over large distances in the SI?

A

no, short distances

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50
Q

what is peristalsis mediated by in the SI?

A

a series of local reflexes

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51
Q

what gastric motility involves the interaction of longitudinal and circular muscles

A

peristalsis

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52
Q

the max frequency of peristalsis cannot exceed the max frequency of what?

A

the max frequency of the BER

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53
Q

integrity of what is needed in SI peristalsis?

A

integrity of the ENS

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54
Q

what is peristalsis modulated by?

A

by the ANS and hormones

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55
Q

following the law of the intestines; what happens to the muscle contraction ahead of the bolus?

A

contraction of longitudinal muscles and relaxation of circular muscles AHEAD of the bolus [path becomes shorter]

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56
Q

following the law of the intestines; what happens to the muscle contraction behind of the bolus?

A

contraction of the circular muscle and relaxation of the longitudinal muscles BEHIND the bolus [increase pressure behind bolus, while decreasing pressure and length ahead of the bolus]

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57
Q

contents from the SI move into the colon through what?

A

the ileocecal valve

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58
Q

is the the ileocecal valve generally open or closed?

A

closed

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59
Q

how does the action of the colon differ from the SI

A

• The muscular activity in the colon is similar to that of the SI, but slower, more sluggish and irregular.

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60
Q

what is the main fucntion of the colon?

A

absorb water and ions

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61
Q

how many L of water chyme leaves the SI and enters the colon daily?

A

1.5L/day

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62
Q

how much of the water chyme that enters the colon is excreted as fecal matter?

A

200 mL

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63
Q

what is the function of the colon?

A

mixing to promote absorption of water and ions
propulsion
storage

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64
Q

what rate does propulasion in the colon take place?

A

slow, takes about 50-60H for chyme to be converted to feces in the colon

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65
Q

what motor activity occurs in the colon?

A

Segmentation & peristalsis

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66
Q

what controls the motor activity in the colon?

A

BER

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67
Q

how often does emptying of the large intestine occur daily?

A

2-3x daily

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68
Q

what does small intestine emptying increase?

A
  • increase gastoileal reflex (ileum)
  • opening of the ilocecal valve to push contents into the colon
  • increases gastrocolic reflex
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69
Q

what does the emptying of the intestine allow?

A

room to accomodate new meals

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70
Q

what does an increased gastrocolic reflex

A

leads to defecation reflex

due to increased activity in the distal part of the colon

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71
Q

what is GI motility organized into?

A

organized into intense pattern of cyclic myoelectric (motor) activity

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72
Q

what intervals does the cyclic pattern of GI motility occur?

A

~90 minutes

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73
Q

at what speed does the interdigestive period sequential motility occur?

A

2-10cm/minute

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74
Q

where does the migrating myoelectric complex take place?

A

begins at the distal part of the stomach & moves down sequentially until the distal ileum

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75
Q

what initiates the MMC ?

A

unknown cause most probably the ENS

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76
Q

how does the propagation of the MMC occur?

A

• via the ENS with modulation via ANS & Gut peptides

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77
Q

when is the MMC disrupted?

A

the intake of a meal

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78
Q

how long does the 1st phase of MMC last?

A

60 minutes

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79
Q

what happens during the first phase of MMC?

A

not much;
• no spike potentials
• no contractions of the muscles

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80
Q

how long does the 2nd phase of MMC last?

A

~20 minutes

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81
Q

what occurs during the 2nd phase of MMC?

A

• irregular spike potentials and contractions

82
Q

how long does the 3rd phase of MMC last?

A

~10 minutes

83
Q

what happens during the 3rd phase of MMC?

A

• Regular spike potentials and contractions at max frequency

84
Q

how does the MMC progress through out the MMC?

A

it gets delayed as it moves through the GIT

85
Q

what are the main functions of the MMC

A

-housekeeping function
constant cell turnover
gastric emptying of large, non-digestible particles

86
Q

what is found in the colon in exponential amounts?

A

bacteria

87
Q

what is the bacteria’s role?

A

its favorable for digestion

88
Q

how does the MMC function in bacterial control?

A

The MMC allows to push bacteria back into the colon if it ever reaches the SI.

89
Q

where do endocrine secretions travel?

A

into the blood stream

90
Q

where do exocrine secretions travel?

A

into the GIT

91
Q

how does digestion occur?

A

in a sequence of interdependent steps

92
Q

what are enzymes?

A

proteins

93
Q

what happens to enzymes in digestion?

A

they also need to be broken down

94
Q

what is digestion?

A

• chemical breakdown of food to progressively smaller molecules

95
Q

what causes for digestion to occur?

A

• results from the secretory activity of a large number of exocrine gland found within and in association with the GIT

96
Q

the digestive secretions are released into what?

A

into the lumen of the digestive tract

97
Q

what is amylase?

A

enzyme that breaks down CHO

98
Q

what is proteases?

A

enzyme that breaks down proteins

99
Q

what are lipases?

A

enzymes that break down fats

100
Q

what are secretion dependent on?

A

energy and blood flow

101
Q

what is the pattern of regulation throughout the GIT

A

it will vary along the GIT

102
Q

nervous system inputs are more important in the proximal or distal part of the GIT?

A

proximal

103
Q

what type of mechanism is responsible for secretion regulation at the distal part of the GIT?

A

hormonal mechanisms

104
Q

in the stomachs, more than half the inputs for secretory regulation are obtained from?

A

nervous and hormonal inputs

105
Q

what are the 3 large glands that produce saliva in the mouth?

A

paratoid gland
sublingual
submandibular

106
Q

what is secreted by the parotid gland?

A

mainly serous fluid

107
Q

what is secreted by the submandibular gland?

A

mixed fluid

108
Q

what is secreted by the sublingual gland?

A

• Mucin-rich fluid (thick-viscous secretion)

109
Q

the secretion by which salivary gland is essential to move the bolus via the GIT

A

subliginual

110
Q

what is the role of saliva?

A

aids in chemical digestion

111
Q

what is salivary amylase

A

it initiates the digestion of CHO

112
Q

what enzyme is produced in the mouth?

A

lingual lipase

salivary amylase

113
Q

how much saliva is produced daily?

A

0.5-1.5L/day

114
Q

what ions are present in saliva?

A

Na+, K+, Cl-, HCO3-

115
Q

what is the function of the ions in saliva

A

helps neutralize the food

116
Q

what is the pH of saliva?

A

6.5-7

117
Q

what is the function of mucin?

A

protects the mouth and lubricates food

118
Q

under what pH does lipase operate?

A

operates at a lower pH and continues to function bettwe in the stomach and duodenum as the pH is more acidic

119
Q

what is the function of lysozymes?

A

they break down bacterial cell wall

120
Q

what regulates the salivary gland

A

both parasympathetic and sympathetic NS

121
Q

what do the preganglionic parasympathetic fibers activate?

A

excitatory ENS neurons

122
Q

the activation of excitatory ENS neurons releases what and causes what

A

releases ACh on muscarinic receptors

causes an increase of secretions & leads to vasodilation

123
Q

what is the most important system for salivary activation

A

parasympathetic NS

124
Q

what can atropine block in the salivary glands

A

its activation as it blocks parasympathetic NS

125
Q

do the para/sympathetic NS have opposing functions in salivary gland regulation?

A

no

126
Q

what is the main function of the sympathetic NS in salivary regulation?

A

causes vasoconstriction without however preventing saliva production and release

127
Q

can salivation be a conditionned reflex?

A

yes

128
Q

what is the cephalic phase of secretion?

A
  • psychic due to a conditionned reflex

- gustatory after tasting

129
Q

what is one of the functions of saliva related to taste?

A

saliva allows to bring the food in contact with the taste receptors of the tongue

130
Q

in what cases will the gastric and intestinal phases of secretion be activated?

A

in cases where very spicy food are eaten

131
Q

what type of secretion occurs in the stomach?

A

mixed gastric juices

132
Q

what volume of secretions is released in the stomach daily?

A

1.5-2L/day

133
Q

what ions are contained in gastric secretion?

A

Na+, K+, Cl-, H+

134
Q

what is the pH of gastric secretions?

A

1-2

135
Q

What is pepsinogen broken down to and what is its function?

A

o Broken down into pepsin which is needed to break down proteins

136
Q

where is pepsinogen released?

A

in the stomach

137
Q

what is the utility of intrinsic factor

A

allows to absorb B12

138
Q

what is the function of mucin in the stomach?

A

protects the gastric mucosa

139
Q

how are proteins broken down

A

broken down from proteins to polypeptides to peptides to AA

140
Q

what secretes mucous through out the GIT

A

• Surface epithelial cells

141
Q

What type of fluid is mucous

A

alkaline fluid

142
Q

what increases the amount of secretory cells in the stomach

A

the amount of tubular glands in the stomach which cause increase in surface area

143
Q

what do the Cardiac and Pyloric tubular glands secrete

A

an Alkaline, Mucin rich fluid

144
Q

what is released in the fondus of the stomach?

A

Acid, enzymes and intrinsic factors

145
Q

what are the 3 gastric glands found in the fondus and corpus of the stomach?

A

parietal cells
chief cells
mucous neck cells

146
Q

what is released by parietal cells

A

HCL

147
Q

what is a given ability of the parietal cells

A

Have the ability to increase their own surface area on its apical surface i

148
Q

what are the addition invaginations of the parietal cells known as?

A

intracellular canaliculus

149
Q

what is the function of the canaliculus?

A

• Each canaliculus is a pathways for acidic secretions to pass through the lumen of the stomach

150
Q

what is contained in the parietal cells that gives them energy

A

mitochondria

151
Q

why are mitochondria found in the stomach?

A

they require lots of energy to produce the HCl and pump it against concentration gradient

152
Q

what is the base of parietal cells in contact with?

A

capillaries

153
Q

what is the concentration of HCl pumped into the lumen vs in capillaries

A

The concentration of HCl pumped into the lumen is much greater than what is present in the capillary [4x10^-5 mEQ] vs 150 mEq H+ & 150 mEq Cl-] in the parietal cells (7M increase)

154
Q

what happens to HCO3- for every HCL pumped into the lumen?

A

1 HCO3- needs to be pumped out into the capillary

155
Q

what does the pump in HCL/ pump out HCO3 cause in blood?

A

alkalinizes the blood & o Production of the postprandial (urinary) alkaline tide

156
Q

when does the postprandial (urinary) alkaline tide occur?

A

Occurs primarily after ingestion of a protein rich meal

157
Q

what enzyme favours the pump in HCL/ pump out HCO3 cause in blood?

A

carbonic anhydrase

158
Q

what happens to the H+ produced by carbonic anhydrase

A

The H+ ions produces are pumped in the lumen by H+/K+/ATPase into the canalicular membrane

159
Q

what is the main target of the H+/K+ATPase pump?

A

main target in cases of ulcers as proton pump inhibitors

160
Q

what will pump sodium out and potassium into the parietal cell?

A

Na+/K+-ATPase

161
Q

what is the pH of parietal cell secretions?

A

pH ~0.8

162
Q

the secretions of parietal cells are independent of what?

A

Secretion independent of type and magnitude of stimulus

163
Q

what modifies the pH of the contents of the stomach so it sits around 1-2

A

non-parietal alkaline gastric secretions

164
Q

what dictates the pH in the stomach?

A

the amount of parietal cells , higher amount = lower the pH

165
Q

how is Cl- entering the cell transported across what?

A

across the canalicular membrane

166
Q

H+ available from the dissociation of intracellular water is pumped where and for what?

A

actively pumped into the canaliculi in exchange for K+

167
Q

what do the H+ secretion leave an excess of in the cell?

A

leave an excess OH which increases intracellular pH

168
Q

what does the increase intracellular pH cause?

A

This causes more CO2 to diffuse in from the plasma combines with H20 in the presence of carbonic anhydrase, to produce H2CO3

169
Q

what happens to the H2CO3- produced by carbonic anhydrase?

A

diffuses into the circulation, thus restoring the intracellular status quo, and giving rise to an increased alkalinity in the venous blood.

170
Q

what are the main functions of HCl in the stomach

A

precipitates soluble proteins
denatures proteins into digestible structures
activates pepsin and provides optimal pH for pepsin activity

171
Q

what is the usefulness of precipitating soluble proteins?

A

Allows the proteins to remain longer in the stomach

172
Q

what is required to activate pepsin?

A

a low pH

173
Q

what is the only secretion of the stomach essential for life

A

intrinsic factor release

174
Q

what is intrinsic factors and what is it secretes by?

A

• It’s a glycoprotein that is secreted by the parietal cells

175
Q

what is released by chief cells?

A

pepsinogen

176
Q

what does pepsinogen get converted to?

A

pepsin

177
Q

what pH is needed to convert pepsinogen to pepsin?

A

low pH <6

178
Q

what is a specific property of pepsin?

A

it can autocatalyze pepsinogen into pepsin

179
Q

what pH is is needed for pepsin to break down proteins into peptides?

A

pH 2-3

180
Q

where does IF-B12 complex get absorbed?

A

in the ilieum

181
Q

what is IF deficency known as?

A

pernicious anemia

182
Q

what is released by mucous neck cells?

A

mucin

183
Q

mucin is produced by all what?

A

all surface epithelial cells

184
Q

what is mucin secreted by other than the mucous neck cells?

A

cardiac and pylori tubular glands

185
Q

where are mucous neck cells located?

A

in the fundus and corpus in the stomach

186
Q

what part of the GIT has the most mucous production?

A

in the stomach

187
Q

what is released by HCO3- and mucin

A

surface epithelial cells

188
Q

what does mucin produce?

A

mucous

189
Q

what is the pH of the lumen of the stomach?

A

pH ~2

190
Q

what is the pH of the epithelial cells and mucous gel

A

pH ~7

191
Q

what is the usefulness of mucous?

A

it protects the cell against acidic pH

192
Q

how can mucous protect against acidic pH?

A

entering HCO3- to be broken down into H20 & CO2 within the mucous gel layer and thus H+ entering the gel won’t reach the epithelium cells.

193
Q

what primary factor acts to protect the GIT from acidic damamge?

A

Gastric Mucosal Barrier (GMB)

194
Q

what is the GMB?

A

Specialization of the epithelial cells and their apical surfaces and the tight junctions that connect them in order to make them impermeable to the H+ ions

195
Q

what is rapid cell turnover important for?

A

in protecting the GIT from acidic content

196
Q

how many cells are replaced daily in the stomach

A

~1 million cells

197
Q

how can ulcers be formed?

A

weakening of barriers due to drugs (Asprin/NSAIDs) or by helicobacter pylori

198
Q

how does helicobacter function in the GIT?

A

colonizes the GIT

burrys between mucous layer and epithelial cells and releases toxin that breaks down epithelial cell

199
Q

how can the normal barrier be broken and cause for ulcers?

A

excessive HCl output

200
Q

how are gastric secretions inhibited?

A

release NANC onto the secretory cells in order to inhibit secretion