GI Flashcards Preview

Phase 1 Medicine > GI > Flashcards

Flashcards in GI Deck (253):
1

Is stage 1 of swallowing voluntary or involuntary?

Voluntary.

2

What happens in stage 1 of swallowing?

Food is compressed against the roof of the mouth and is pushed to the oropharynx by the tongue.

3

Is stage 2 of swallowing voluntary or involuntary?

Involuntary.

4

What happens in stage 2 of swallowing?

The nasopharynx closes off due to soft palate elevation. The trachea is closed off by the epiglottis. Elevation of the hyoid bone shortens and widens the pharynx.

5

Is stage 3 of swallowing voluntary or involuntary?

Involuntary.

6

What happens in stage 3 of swallowing?

The pharyngeal constrictor muscles sequentially contract producing peristaltic waves. This propels the bolus of food down the Oesophagus. This is followed by depression of the hyoid bone.

7

Name 6 muscles/groups of muscles that are involved in swallowing.

1. Buccinator.
2. Suprahyoids.
3. Muscles of the palate.
4. Muscles of the floor of the mouth.
5. Infrahyoids.
6. Pharyngeal constrictor muscles.

8

Which muscle(s) manipulate food in chewing. Elevate the hyoid bone and flatten the floor of the mouth?

Buccinator and Suprahyoids.

9

What is the function of the muscles of the soft palate in swallowing?

They act to tense and elevate the soft palate.

10

What is the function of the muscles of the floor of the mouth in swallowing?

They raise the hyoid bone and larynx.

11

What is the function of the infrahyoids?

To depress the hyoid bone and larynx.

12

What is the function of the pharyngeal constrictor muscles?

They contract sequentially producing peristaltic waves which drive food into the oesophagus.

13

Do parotid glands have mainly serous or mainly mucous acini?

Mainly serous acini.

14

What is serous acini secretion composed of?

alpha amylase - this is needed for starch digestion.

15

Do sublingual glands have mainly serous or mainly mucous acini?

Mainly mucous acini.

16

What is mucous acini secretion composed of?

Mucin - needed for lubrication.

17

Do submandibular glands have mainly serous or mainly mucous acini?

They have serous and mucus acini.

18

Which of the main salivary glands is constantly active?

Submandibular.

19

What is the function of saliva?

It acts as a lubricant for chewing, swallowing and speech. It is important in oral hygiene; has a role in immunity, wash and it can also act as a buffer.

20

What is the optimum oral pH?

7.2

21

What is the pH range of saliva?

6.2 - 7.4

22

Name 4 factors that can affect the composition of saliva.

1. Stimulus.
2. Age.
3. Gender.
4. Drugs.

23

Are serous acini dark staining or pale staining on a histological slide?

Dark staining.
(Mucus acini = pale staining).

24

What is the epithelium lining of intercalated ducts?

Simple cuboidal epithelium.

25

What is the function of intercalated ducts?

They connect acini to larger striated ducts.

26

What ions are reabsorbed at striated ducts?

Na+ and Cl-

27

Is saliva hypotonic or hypertonic?

Hypotonic - water reabsorption and ion secretion.

28

What is the importance of the striated duct basal membrane being highly folded?

It is folded into microvilli for the active transport of HCO3- against its concentration gradient.

29

What organelle is abundant in striated ducts and why?

Mitochondria. For the active transport of ions.

30

Name 2 ions that striated ducts secrete.

K+ and HCO3-

31

Name 2 ions that striated ducts reabsorb.

Na+ and Cl-

32

What ducts do striated ducts lead on to?

Interlobular (excretory) ducts.

33

What is the epithelium lining of interlobular ducts?

Simple columnar epithelium.

34

What is the parasympathetic innervation of the Parotid gland?

Cn 9 - glossopharyngeal.

35

What is the parasympathetic innervation of the Sublingual gland?

Cn 7 - facial.

36

What is the parasympathetic innervation of the Submandibular gland?

Cn 7 - facial.

37

What nerve passes through the parotid gland but does not innervate it?

The facial nerve (Cn 7) gives rise to its 5 terminal branches in the parotid gland.

38

What artery ascends through the parotid gland?

The external carotid artery.

39

Does parasympathetic innervation stimulate or inhibit salivary secretion?

Stimulates.

40

What is the volume of an empty stomach?

50ml

41

What is the maximum volume of the stomach?

1.5L

42

What is receptive relaxation?

Smooth muscle in the body and fundus of the stomach relaxes prior to the arrival of food, this allows the stomach volume to increase. There is afferent input from Cn 10. NO and serotonin also influence relaxation.

43

Where do peristaltic waves begin?

In the gastric body.

44

Where in the stomach are peristaltic contractions the most powerful?

In the gastric antrum.

45

Why is the pyloric sphincter closed as the peristaltic wave reaches it?

This prevents chyme entering the duodenum and so the gastric contents are forced back and mixed together in the body of the stomach.

46

On average, how many peristaltic waves are there a minute?

3 (slow repol/depol cycles).

47

Name 2 factors that can increase the strength of peristaltic contractions.

1. Gastrin.
2. Gastric distension.

48

Name 5 factors that can decrease the strength of peristaltic contractions.

1. Duodenal distension.
2. Low pH in duodenum lumen.
3. Increased duodenal osmolarity.
4. Increased sympathetic action.
5. Decreased parasympathetic action.

49

What do parietal cells secrete?

HCl and intrinsic factor.

50

What do chief cells secrete?

Pepsinogen and gastric lipase.

51

What cells secrete Gastrin?

Enteroendocrine cells / G cells.

52

What cells secrete somatostatin?

D cells.

53

What cells secrete histamine?

Enterochromaffin like cells.

54

On average, how much gastric acid do we secrete a day?

2L

55

What is the hydrogen ion concentration of gastric acid?

>150mM

56

Where does the H+ come from in gastric acid?

In parietal cells: H2O + CO2 = HCO3- + H+

57

What is the mechanism of the H+/K+ ATPase proton pump?

It pumps H+ into the stomach lumen and K+ into the parietal cell.

58

What ions are exchanged on the side of the parietal cell in contact with the capillaries?

Cl- is pumped into the parietal cell and HCO3- moves out of the parietal cell into the capillary.

59

What is the importance of HCO3- being exchanged for Cl-?

HCO3- moving out of the cell increases the rate of the forward reaction and so more H+ are produced. Cl- moving into the cell then moves into the stomach lumen via Cl- channels and combines with H+ to form HCl.

60

What are the 4 phases important in regulating gastric acid secretion? Do these phases turn secretion on or off?

1. Cephalic phase - turning ON.
2. Gastric phase - turning ON.
3. Gastric phase - turning OFF.
4. Intestinal phase - turning OFF.

61

Regulating gastric acid secretion: What stimuli are involved in the cephalic phase?

Sight, smell, taste of food. Chewing.

62

Regulating gastric acid secretion: What stimuli are involved in the gastric ON phase?

Gastric distension, presence of peptides and amino acids in the stomach.

63

Regulating gastric acid secretion: What stimuli are involved in the gastric OFF phase?

Low pH in gastric lumen.

64

Regulating gastric acid secretion: What stimuli are involved in the intestinal phase?

Low pH in duodenal lumen, duodenal distension, presence of amino acids and fatty acids in the duodenum.

65

Briefly describe the cephalic phase.

The parasympathetic nervous system is triggered by stimuli. This releases Ach. Ach acts on parietal cells and on gastrin and histamine. HCl secretion increases.

66

Briefly describe the gastric ON phase.

Gastrin is released in response to the stimuli. This acts on parietal cells and triggers release of histamine (histamine then acts on parietal cells too). HCl secretion increases.

67

Briefly describe the gastric OFF phase.

Gastrin is inhibited in response to stimuli and histamine is therefore indirectly inhibited. Somatostatin is also released and this inhibits parietal cells. HCl secretion decreases.

68

Briefly describe the intestinal phase.

The enterogastrones secretin and CCK are released in response to stimuli. Secretin inhibits gastrin and stimulates further somatostatin release. HCl secretion decreases.

69

What neurotransmitter is involved in regulating gastric acid secretion?

Ach.

70

What hormone is involved in regulating gastric acid secretion?

Gastrin.

71

What paracrine factors are involved in regulating gastric acid secretion?

Histamine and Somatostatin.

72

What enterogastrones are involved in regulating gastric acid secretion?

Secretin and CCK.

73

Name the 4 main defence mechanisms against gastric acid secretion.

1. Alkaline mucous.
2. Tight junctions between epithelial cells.
3. Replacing damaged cells.
4. Feedback loops.

74

Define ulcer.

A breach in a mucosal surface.

75

Name 3 things that can cause peptic ulcers.

1. Helicobacter pylori.
2. NSAIDS.
3. Chemical irritants.

76

Why do NSAIDS cause peptic ulcers?

They inhibit cycle-oxygenase 1.
Cycle-oxygenase 1 is needed for prostaglandin synthesis, prostaglandins stimulate mucus secretion. Without cycle-oxygenase 1 there is less mucus and so the mucosal defence is reduced.

77

Why does helicobacter pylori cause peptic ulcers?

Helicobacter pylori lives in gastric mucus. It secretes urease. Urease breaks into CO2 and NH3. The NH3 combines with H+ to form NH4+. NH4+ damages the gastric epithelium, an inflammatory response is triggered and mucosal defence is reduced.

78

Name 2 drugs that can be used to reduce gastric acid secretion.

1. Proton pump inhibitors.
2. H2 receptor antagonists.

79

If water input is 9L, how much is reabsorbed and how much is excreted in the faeces?

8.8L is reabsorbed and 0.2L is excreted in the faeces.

80

How does water move across the small intestine?

It moves freely by osmosis and also via aquaporins.

81

How does Na+ move across the small intestine?

Na+ is actively transported from the lumen by pumps located in the cell membranes in the ileum and jejunum.

82

How does K+ move across the small intestine?

Via passive diffusion. Movement is determined by the potential difference between lumen and capillaries.

83

Where does Cl- and HCO3- reabsorption mainly take place?

In the ileum and colon.

84

What is the mechanism for Cl- and HCO3- reabsorption?

Cl- is actively reabsorbed in exchage for HCO3-. The intestinal contents therefore become more alkaline.

85

What enzyme digests starch in the small intestine?

Pancreatic amylase.

86

What bonds does pancreatic amylase break?

alpha 1-4 linkages.

87

What are the end products of starch digestion?

Maltose!
Also maltotriose, glucose polymers and alpha-dextrins.

88

Where in the small intestine are bile salts absorbed?

Jejunum.

89

What enzyme(s) hydrolyse peptide bonds in the stomach?

Pepsins.

90

What is the optimum pH for pepsins?

1.6-3.2

91

Why is pepsin action terminated in the small intestine?

The pH in the small intestine is too alkaline and so it denatures.

92

What enzyme(s) further break down peptides in the small intestine?

Pancreatic proteases.

93

What is the precursor molecule for pepsin?

Pepsinogen.

94

What activates pepsinogen?

Low pH.

95

What 2 groups can pancreatic proteases be divided into?

1. Endopeptidases e.g. trypsin.
2. Exopeptidases e.g. carboxy dipeptidases.

96

How do amino acids get absorbed into the blood?

Passive diffusion.

97

What enzyme(s) hydrolyse cholesterol esters in the intestinal lumen?

Pancreatic esterases.

98

What emulsifies lipids?

Bile salts.

99

What is the advantage of emulsifying lipids?

It increases the SA for digestion and so digestion is more efficient.

100

What digests lipids in the small intestine?

Pancreatic lipases.

101

Are lipids hydrophobic or hydrophilic?

Hydrophobic.

102

What are the end products of fat digestion?

Free fatty acids and monoglycerides.

103

What triglyceride bonds is pancreatic lipase able to hydrolyse with ease?

1 and 3 bonds (the 2 bond is hydrolysed at a slower rate).

104

What protein binds pancreatic lipase to the surface of the lipid?

Co-lipase. This is essential, pancreatic lipase can not work without it.

105

The end products of fat digestion combine with bile salts and cholesterol to form what?

Mixed micelles.

106

What is the function of mixed micelles?

Lipid transport systems.

107

How are chylomicrons formed?

Triglycerides, phospholipids and cholesterol combine with proteins inside the epithelial cell forming chylomicrons.

108

Is vitamin A fat or water soluble?

Fat soluble.

109

What are the functions of vitamin A?

Vitamin A is needed for cellular growth and differentiation. It is also important for eyesight and lymphocyte production.

110

Name 3 sources of vitamin A.

1. Oily fish.
2. Dairy.
3. Liver

111

What is the recommended daily intake of vitamin A for men and women?

Women - 600µg. Men - 700µg.

112

What are the consequences of vitamin A deficiency?

Night blindness, growth retardation, increased susceptibility to infection.

113

What are the consequences of vitamin A toxicity?

Anorexia, vomiting, headache, reduced bone density, conjunctivitis.

114

Is vitamin C fat or water soluble?

Water soluble (easily lost when boiled).

115

What are the functions of vitamin C?

Synthesis of collagen, neurotransmitters and carnitine. It has an antioxidant ability and can absorb non-haem iron.

116

Name 4 sources of vitamin C.

1. Citrus fruits.
2. Green leafy veg.
3. Potatoes.
4. Kidney.

117

What is the recommended daily intake of vitamin C?

40mg.

118

What are the consequences of vitamin C deficiency?

Weakness, shortness of breath, aching, bleeding gums, thickening of skin.

119

What are the consequences of vitamin C toxicity?

Diarrhoea, nausea, renal stone formation.

120

Are B vitamins fat or water soluble?

Water soluble.

121

How many B vitamins are there?

8.

122

What are B vitamins important for?

Cell metabolism and energy production.

123

How long do glycogen stores in a 70Kg adult last?

About 12 hours.

124

How long do lipid stores in a 70Kg adult last?

3 months.

125

What percentage of BMR do these organs use?
a) Brain.
b) Liver.
c) Muscle.

a) 20%.
b) 21%.
c) 22%.

126

What fuels does the brain use?

Glucose and ketone bodies.

127

What fuels does the liver use?

Glucose, amino acids, fatty acids.

128

What fuels does muscle use?

Glucose, ketone bodies, amino acids and triacylglycerol.

129

What are free sugars and starch associated with effecting?

They can cause shifts in blood glucose and insulin due to their rapid absorption. This can strain the pancreas.

130

What type of starch is the most desirable and why?

Slowly digestible starch. It is slowly digested and absorbed and so has little influence on blood glucose and insulin.

131

What is the cause of lactose intolerance?

A deficiency in lactase.

132

Give 3 symptoms of lactose intolerance.

1. Bloating.
2. Diarrhoea.
3. Pain.

133

Explain the mechanism that produces the symptoms of lactose intolerance.

Lactose intolerance has an osmotic effect. H2O and fermentable sugars enter the the large intestine lumen and cause diarrhoea, bloating and pain.

134

Why might someone with enterocyte loss be unable to break down lactose?

Enterocytes at villi contain lactase. If the enterocytes are lost they may have lactase deficiency.

135

Define BMR.

The energy needed to stay alive at rest, usually 24kcal/kg/day.

136

Where does the foregut begin and end?

Mouth to the major duodenal papilla. (In the embryo - oropharyngeal membrane to the liver bud).

137

Where does the midgut begin and end?

Major duodenal papilla to 2/3 along the TC. (In embryo - liver bud to 2/3 along TC).

138

Where does the hindgut begin and end?

Distal 1/3 of TC to anal canal. (In embryo - distal 1/3 of TC to cloacal membrane).

139

Why are the foregut, midgut and hindgut divisions different in the adult compared to in the embryo?

It changes due to the formation of the ampulla of vater.

140

Are the pharyngeal clefts formed in the endoderm or ectoderm?

Ectoderm.

141

Are the pharyngeal pouches formed in the endoderm or ectoderm?

Endoderm.

142

How many pharyngeal arches are there?

5 (4 pharyngeal clefts and pouches).

143

What does the first pharyngeal arch form?

Muscles for mastication. Innervation: Cn 5.

144

What does the second pharyngeal arch form?

Muscles for facial expression. Innervation: Cn 7.

145

What does the third pharyngeal arch form?

Stylopharyngeus muscle. Innervation: Cn 9.

146

What does the fourth pharyngeal arch form?

Cricothyroid muscle. Innervation: External branch of superior laryngeal nerve (Cn 10).

147

What does the sixth pharyngeal arch form?

Intrinsic muscles of the Larynx. Innervation: Recurrent laryngeal nerve (Cn 10).

148

Why is the stomach the shape it is?

Due to differences in growth rates. The greater curvature grows faster than the lesser curvature.

149

Why does the left vagus nerve become the anterior vagal trunk and the right vagus become the posterior vagal trunk?

Due to the 90 degrees clockwise rotation of the stomach in its longitudinal axis.

150

What are the axis of stomach rotation?

Longitudinal and anteroposterior.

151

What does the dorsal mesentery become?

The greater omentum.

152

What does the ventral mesentery become?

The lesser omentum.

153

What are the 5 stages of midgut development?

1. Elongation.
2. Herniation.
3. Rotation.
4. Retraction.
5. Fixation.

154

What connects the midgut to the yolk sac?

The Vitelline duct.

155

What happens in the elongation stage of midgut development?

Rapid elongation forms the primary intestinal loop. The proximal part of the loop forms the small intestine and the distal part forms the large intestine up to 2/3 TC.

156

What happens in the herniation stage of midgut development?

The rapid growth of the intestinal loop means it is pushed into the extra embryonic cavity in the umbilical cord.

157

What happens in the rotation stage of midgut development?

The elongated intestinal loop rotates 270 degrees anticlockwise.

158

What happens in the retraction stage of midgut development?

In the 10th week the herniated midgut returns into the expanded abdominal cavity. Th jejunum is first to return.

159

What happens in fixation of midgut organs?

This is when some regions of the gut lose their dorsal mesentery. These regions become retroperitoneal.

160

What are the 4 layers of the GI tract?

1. An innermost mucosa.
2. A sub-mucosa.
3. An external muscle coat (muscularis externa)
4. A serosa.

161

What is the innermost mucosa layer composed of?

- A folded epithelium.
- Lamina propria (connective tissue).
- Muscularis mucosa (ring of smooth muscle).

162

What is the submucosa layer composed of?

Loose connective tissue containing glands and lymph tissue. Many blood vessels and a rich plexus of nerves that is part of the enteric nervous system (Meissner's plexus) are also found in the submucosa.

163

What is the muscular externa composed of? What is its function?

Composed of 2 layers of smooth muscle: circular and longitudinal. Nerves that are part of the enteric nerve plexus are also present here (Aurebach's plexus). Contraction of the muscle helps to break down and food and propel it along the GI tract.

164

What is the serous layer composed of?

Composed of a simple squamous epithelium that covers the outside surface of the gut tube facing the peritoneal cavity.

165

What enzyme are parietal cells abundant in?

Carbonic anhydrase.

166

Give 5 functions of hepatocytes.

1. Creation and storage of energy in the form of glycogen.
2. Synthesise and secrete plasma proteins.
3. Remove amino groups from amino acids for the production of urea. (Deamination).
4. Uptake, synthesis and excretion of bilirubin and bile acids.
5. Detoxification and inactivation of drugs and toxins.

167

What are the 2 key stages for fat digestion?

1. Emulsification.
2. Triglyceride hydrolysis.

168

What clinical feature would you see in a patient with fat malabsorption?

Pale and smelly faeces.

169

What clinical feature would you see in a patient with vitamin K malabsorption?

Bruising.

170

What clinical feature would you see in a patient with protein malabsorption?

Swollen ankles.

171

Where in the layers of the GI tract would Meissner's plexus be found?

In the submucosa.

172

Where in the layers of the GI tract would Auerbach's plexus be found?

In the muscularis externa between the circular and longitudinal layers of muscle.

173

Name the abdominal retroperitoneal organs.

Supradrenal glands, Aorta, IVC, Duodenum (except cap), Pancreas (except tail), Ureters, Colon (ascending and descending), Kidneys, Oesophagus, Rectum.

174

Name the abdominal intraperitoneal organs.

Spleen, Small intestine, Appendix, Liver, Transverse colon, Stomach, Sigmoid colon.

175

What is the arcuate line?

The lower limit of the posterior rectus sheath.

176

What happens to the posterior rectus sheath below the arcuate line?

It is absent. The rectus abdominis is in direct contact with the transversalis fascia.

177

What envelopes the rectus abdominis above the arcuate line?

It is enveloped by the internal oblique aponeurosis.

178

What is the anterior layer of rectus sheath formed from?

External oblique aponeurosis and the anterior lamina of the internal oblique aponeurosis.

179

What is the posterior layer of the rectus sheath formed from?

The posterior lamina of the internal oblique aponeurosis and the transversus abdominis aponeurosis.

180

What forms the anterior rectus sheath below the rectus abdominis?

The external oblique, internal oblique and transversus abdominis aponeurosis' all form the anterior rectus sheath. There is no posterior rectus sheath.

181

What vertebral level does the umbilicus mark when lying down?

L3.

182

What abdominal plane would you refer to when carrying out a lumbar puncture?

The intercristal plane. It joins the highest points of the pelvis posteriorly and marks the space between L4 and L5.

183

Describe 2 ways in which the transpyloric plane can be drawn.

1. The midpoint between the suprasternal notch and the pubic symphysis.
2. Connects the two points marked by the insertion of the rectus sheath into the costal margin.

184

Name 3 structures that cross the transpyloric plane.

1. The pylorus of the stomach.
2. The gall bladder.
3. The pancreas.

185

At what vertebral level is the transpyloric plane?

L1.

186

What is the intercristal plane?

It connects the highest points of the pelvis at the lower back.

187

At what vertebral level is the intercristal plane?

L4/5.

188

What is the intertubercular plane?

A line that joins the tubercles of the iliac crests.

189

At what vertebral level is the intertubercular plane?

L4.

190

What is the subcostal plane?

A plane parallel to the lowest points of the costal margins.

191

At what vertebral level is the subcostal plane?

L2.

192

Where is the swallowing centre found?

Medulla oblongata.

193

What molecule is responsible for the activation of pepsinogen into pepsin?

HCl.

194

Give 3 functions of HCl in the stomach.

1. Solubilisation of food particles.
2. Kills microbes.
3. Activates pepsinogen forming pepsin.

195

Histamine is secreted by enterchromaffin like cells. What are enterochromaffin cells?

Enterchromaffin cells are located in the intestine and secrete serotonin, not histamine.

196

What type of cells are secretin and CCK?

Enterogastrones.

197

Chief cells secrete pepsinogen and and an enzyme. What is the enzyme?

Gastric lipase.

198

Name 3 monosaccharides.

1. Glucose.
2. Fructose.
3. Galactose.

199

Name 3 disaccharides.

1. Sucrose (glucose and fructose).
2. Lactose (glucose and galactose).
3. Maltose (glucose and glucose).

200

Name 3 polysaccharides.

1. Starch.
2. Cellulose.
3. Glycogen.

201

Where does the majority of complex polysaccharide digestion occur?

In the large intestine via gut bacteria.

202

Where is the first site of starch digestion?

In the mouth via salivary amylase.

203

Briefly describe starch digestion.

Begins in the mouth via salivary amylase. In the small intestine pancreatic amylases catalyse alpha 1-4 linkages forming maltose. The end products are further broken down by enzymes e.g. maltase on the luminal membrane; this forms monosaccharides. The products diffuse into the blood.

204

What are proteins digested into?

Dipeptides, tripeptides and amino acids.

205

What enzyme is responsible for protein digestion in the stomach?

Pepsin.

206

What is the optimum pH for pepsin action?

1.6 - 3.2

207

What does pepsin break proteins into?

Peptide fragments.

208

What enzymes are responsible for protein digestion in the small intestine?

Pancreatic proteases.

209

What are the 2 types of pancreatic proteases?

1. Endopeptidases.
2. Exopeptidases.

210

Give 2 examples of an endopeptidase.

1. Trypsin.
2. Chymotrypsin.

211

Give 2 examples of an exopeptidase.

1. Carboxypeptidases.
2. Aminopeptidases.

212

What is the function of endopeptidases?

They break peptide bonds between non-terminal amino acids.

213

What is the function of exopeptidases?

They break peptide bonds between terminal amino acids and so form monomers.

214

Which type of pancreatic protease can form monomers?

Exopeptidases.

215

By what process are the products of protein digestion absorbed into the intestinal epithelial cells?

Secondary active transport coupled to H+ or Na+.

216

What molecules make up phospholipids?

1 glycerol backbone, 2 fatty acids and 1 phosphate group.

217

What are triglycerides broken down into?

Monoglycerides and 3 fatty acids.

218

What enzyme is needed for fat digestion?

Pancreatic lipase.

219

What mechanism speeds up the digestion of fats?

Emulsification - the surface area for lipase action is increased.

220

What substances emulsify lipids?

Bile salts and phospholipids.

221

What enzyme anchors lipase to the surface of an emulsified lipid droplet?

Colipase.

222

Name 4 molecules to make up micelles.

1. Fatty acids.
2. Monoglycerides.
3. Bile salts.
4. Phospholipids.

223

What molecule is produced that aids absorption?

Micelles.

224

What is the function of micelles?

They are lipid transport systems. They move to the epithelial brush border and release the fatty acids and monoglycerides for absorption.

225

What happens to the fatty acids and monoglycerides inside the intestinal epithelial cells?

They are re-synthesised into triglycerides in the smooth ER.

226

Why are fatty acids and monoglycerides re-synthesised into triglycerides inside the intestinal epithelial cells?

To maintain the concentration gradient for further absorption of fatty acids and monoglycerides.

227

Inside the intestinal epithelial cell, triglycerides combine with other lipids e.g. cholesterol to form what molecules?

Chylomicrons.

228

What are the functions of chylomicrons?

Chylomicrons move through the lymphatics and the blood stream to tissues.

229

How is vitamin B12 absorbed?

It binds to a protein, intrinsic factor. It is then absorbed in the terminal ileum via endocytosis.

230

What can cause pernicious anaemia?

If you have low levels of intrinsic factor you will have B12 deficiency. This will mean fewer RBC's will be formed leading to pernicious anaemia.

231

What can cause Barrett's oesophagus?

GORD.

232

Describe Barrett's oesophagus.

When the stratified squamous oesophageal epithelium changes to a simple columnar one at the lower end of the oesophagus. This can be caused by prolonged acid reflux from the stomach.

233

What is the function of the Vagus nerve in regards to parietal cells?

The vagus nerve stimulates the release of Ach which then acts on the parietal cells to increase HCl production.

234

Give 4 risk factors for GORD.

1. Obesity.
2. Pregnancy.
3. Hiatal hernia.
4. Smoking.
(Sedentary lifestyle is not a risk factor).

235

Where in the stomach are G cells most numerous?

In the antrum.

236

Name 2 areas of the body with a low pH to combat bacteria.

Stomach and vagina.

237

Name 3 organs that secrete digestive enzymes.

1. Stomach.
2. Pancreas.
3. Salivary glands.

238

What structure, visible microscopically, is primarily responsible for absorption?

Villi.

239

Name 3 physical mechanisms of absorption.

1. Endocytosis.
2. Diffusion/facilitated diffusion.
3. Active transport.

240

Name 2 diseases that can cause malabsorption.

1. Crohn's disease - loss of plicae circulares.
2. Coeliac disease - vili atrophy.

241

Define malnutrition.

A lack of nutrition due to not eating enough, being unable to absorb nutrients, eating the wrong things.

242

Why might an elderly person be at risk of malnutrition?

1. Immobility - unable to cook and eat.
2. Dental problems meaning its difficult to chew foods.
3. Decreased appetite.
4. Not eating the right things.

243

Name 3 physical tests for malnutrition.

1. BMI.
2. Amount of body fat.
3. Height.

244

Give 4 complications of malnutrition.

1. Apathy.
2. Depression.
3. Increased risk of infection.
4. Anaemia.

245

Why is endoscopy preferred to a barium meal?

Produces a better image and is more accurate. Also prevents exposure to radiation as a barium meal requires an X-ray.

246

What muscles contributes to the upper oesophageal sphincter?

Cricopharyngeus.

247

Where are the stem cells that replace the epithelium located?

The base of crypts.

248

What are the pacemaker cells of the small intestine called?

Interstitial cells of Cajal.

249

Name 2 endocrine secretions from the duodenum?

1. Secretin.
2. CCK.

250

Why are fatty acids and monoglycerides re-synthesised into triglycerides inside the epithelial cell?

To maintain a diffusion gradient allowing for further reabsorption.

251

Which papillae do not bear taste buds?

Filiform papillae.

252

Does the oesophagus have a serosa layer?

No!

253

What is refeeding syndrome?

Metabolic disturbances (hypokalemia, hypomagnesemia etc) that occur due to reinstitution of nutrition to patients who are starved/severley malnourished.