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GI Flashcards

1
Q

Is stage 1 of swallowing voluntary or involuntary?

A

Voluntary.

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2
Q

What happens in stage 1 of swallowing?

A

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

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3
Q

Is stage 2 of swallowing voluntary or involuntary?

A

Involuntary.

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4
Q

What happens in stage 2 of swallowing?

A

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.

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5
Q

Is stage 3 of swallowing voluntary or involuntary?

A

Involuntary.

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6
Q

What happens in stage 3 of swallowing?

A

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.

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7
Q

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

A
  1. Buccinator.
  2. Suprahyoids.
  3. Muscles of the palate.
  4. Muscles of the floor of the mouth.
  5. Infrahyoids.
  6. Pharyngeal constrictor muscles.
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8
Q

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

A

Buccinator and Suprahyoids.

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9
Q

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

A

They act to tense and elevate the soft palate.

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10
Q

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

A

They raise the hyoid bone and larynx.

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11
Q

What is the function of the infrahyoids?

A

To depress the hyoid bone and larynx.

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12
Q

What is the function of the pharyngeal constrictor muscles?

A

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

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13
Q

Do parotid glands have mainly serous or mainly mucous acini?

A

Mainly serous acini.

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14
Q

What is serous acini secretion composed of?

A

alpha amylase - this is needed for starch digestion.

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15
Q

Do sublingual glands have mainly serous or mainly mucous acini?

A

Mainly mucous acini.

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16
Q

What is mucous acini secretion composed of?

A

Mucin - needed for lubrication.

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17
Q

Do submandibular glands have mainly serous or mainly mucous acini?

A

They have serous and mucus acini.

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18
Q

Which of the main salivary glands is constantly active?

A

Submandibular.

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19
Q

What is the function of saliva?

A

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.

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20
Q

What is the optimum oral pH?

A

7.2

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21
Q

What is the pH range of saliva?

A

6.2 - 7.4

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22
Q

Name 4 factors that can affect the composition of saliva.

A
  1. Stimulus.
  2. Age.
  3. Gender.
  4. Drugs.
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23
Q

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

A

Dark staining.

Mucus acini = pale staining

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24
Q

What is the epithelium lining of intercalated ducts?

A

Simple cuboidal epithelium.

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25
Q

What is the function of intercalated ducts?

A

They connect acini to larger striated ducts.

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26
Q

What ions are reabsorbed at striated ducts?

A

Na+ and Cl-

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27
Q

Is saliva hypotonic or hypertonic?

A

Hypotonic - water reabsorption and ion secretion.

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28
Q

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

A

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

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29
Q

What organelle is abundant in striated ducts and why?

A

Mitochondria. For the active transport of ions.

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30
Q

Name 2 ions that striated ducts secrete.

A

K+ and HCO3-

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31
Q

Name 2 ions that striated ducts reabsorb.

A

Na+ and Cl-

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32
Q

What ducts do striated ducts lead on to?

A

Interlobular (excretory) ducts.

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33
Q

What is the epithelium lining of interlobular ducts?

A

Simple columnar epithelium.

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34
Q

What is the parasympathetic innervation of the Parotid gland?

A

Cn 9 - glossopharyngeal.

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35
Q

What is the parasympathetic innervation of the Sublingual gland?

A

Cn 7 - facial.

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36
Q

What is the parasympathetic innervation of the Submandibular gland?

A

Cn 7 - facial.

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37
Q

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

A

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

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38
Q

What artery ascends through the parotid gland?

A

The external carotid artery.

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39
Q

Does parasympathetic innervation stimulate or inhibit salivary secretion?

A

Stimulates.

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40
Q

What is the volume of an empty stomach?

A

50ml

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41
Q

What is the maximum volume of the stomach?

A

1.5L

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42
Q

What is receptive relaxation?

A

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.

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43
Q

Where do peristaltic waves begin?

A

In the gastric body.

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44
Q

Where in the stomach are peristaltic contractions the most powerful?

A

In the gastric antrum.

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45
Q

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

A

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

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46
Q

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

A

3 (slow repol/depol cycles).

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47
Q

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

A
  1. Gastrin.

2. Gastric distension.

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48
Q

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

A
  1. Duodenal distension.
  2. Low pH in duodenum lumen.
  3. Increased duodenal osmolarity.
  4. Increased sympathetic action.
  5. Decreased parasympathetic action.
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49
Q

What do parietal cells secrete?

A

HCl and intrinsic factor.

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50
Q

What do chief cells secrete?

A

Pepsinogen and gastric lipase.

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51
Q

What cells secrete Gastrin?

A

Enteroendocrine cells / G cells.

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52
Q

What cells secrete somatostatin?

A

D cells.

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53
Q

What cells secrete histamine?

A

Enterochromaffin like cells.

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54
Q

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

A

2L

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55
Q

What is the hydrogen ion concentration of gastric acid?

A

> 150mM

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56
Q

Where does the H+ come from in gastric acid?

A

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

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57
Q

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

A

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

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58
Q

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

A

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

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59
Q

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

A

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.

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60
Q

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

A
  1. Cephalic phase - turning ON.
  2. Gastric phase - turning ON.
  3. Gastric phase - turning OFF.
  4. Intestinal phase - turning OFF.
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61
Q

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

A

Sight, smell, taste of food. Chewing.

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62
Q

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

A

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

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63
Q

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

A

Low pH in gastric lumen.

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64
Q

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

A

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

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65
Q

Briefly describe the cephalic phase.

A

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

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66
Q

Briefly describe the gastric ON phase.

A

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.

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67
Q

Briefly describe the gastric OFF phase.

A

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.

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68
Q

Briefly describe the intestinal phase.

A

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

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69
Q

What neurotransmitter is involved in regulating gastric acid secretion?

A

Ach.

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70
Q

What hormone is involved in regulating gastric acid secretion?

A

Gastrin.

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71
Q

What paracrine factors are involved in regulating gastric acid secretion?

A

Histamine and Somatostatin.

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72
Q

What enterogastrones are involved in regulating gastric acid secretion?

A

Secretin and CCK.

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73
Q

Name the 4 main defence mechanisms against gastric acid secretion.

A
  1. Alkaline mucous.
  2. Tight junctions between epithelial cells.
  3. Replacing damaged cells.
  4. Feedback loops.
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74
Q

Define ulcer.

A

A breach in a mucosal surface.

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75
Q

Name 3 things that can cause peptic ulcers.

A
  1. Helicobacter pylori.
  2. NSAIDS.
  3. Chemical irritants.
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76
Q

Why do NSAIDS cause peptic ulcers?

A

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.

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77
Q

Why does helicobacter pylori cause peptic ulcers?

A

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.

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78
Q

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

A
  1. Proton pump inhibitors.

2. H2 receptor antagonists.

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79
Q

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

A

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

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80
Q

How does water move across the small intestine?

A

It moves freely by osmosis and also via aquaporins.

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81
Q

How does Na+ move across the small intestine?

A

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

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82
Q

How does K+ move across the small intestine?

A

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

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83
Q

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

A

In the ileum and colon.

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84
Q

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

A

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

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85
Q

What enzyme digests starch in the small intestine?

A

Pancreatic amylase.

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86
Q

What bonds does pancreatic amylase break?

A

alpha 1-4 linkages.

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87
Q

What are the end products of starch digestion?

A

Maltose!

Also maltotriose, glucose polymers and alpha-dextrins.

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88
Q

Where in the small intestine are bile salts absorbed?

A

Jejunum.

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89
Q

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

A

Pepsins.

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90
Q

What is the optimum pH for pepsins?

A

1.6-3.2

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91
Q

Why is pepsin action terminated in the small intestine?

A

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

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92
Q

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

A

Pancreatic proteases.

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93
Q

What is the precursor molecule for pepsin?

A

Pepsinogen.

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94
Q

What activates pepsinogen?

A

Low pH.

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95
Q

What 2 groups can pancreatic proteases be divided into?

A
  1. Endopeptidases e.g. trypsin.

2. Exopeptidases e.g. carboxy dipeptidases.

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96
Q

How do amino acids get absorbed into the blood?

A

Passive diffusion.

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97
Q

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

A

Pancreatic esterases.

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98
Q

What emulsifies lipids?

A

Bile salts.

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99
Q

What is the advantage of emulsifying lipids?

A

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

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100
Q

What digests lipids in the small intestine?

A

Pancreatic lipases.

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101
Q

Are lipids hydrophobic or hydrophilic?

A

Hydrophobic.

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102
Q

What are the end products of fat digestion?

A

Free fatty acids and monoglycerides.

103
Q

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

A

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

104
Q

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

A

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

105
Q

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

A

Mixed micelles.

106
Q

What is the function of mixed micelles?

A

Lipid transport systems.

107
Q

How are chylomicrons formed?

A

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

108
Q

Is vitamin A fat or water soluble?

A

Fat soluble.

109
Q

What are the functions of vitamin A?

A

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

110
Q

Name 3 sources of vitamin A.

A
  1. Oily fish.
  2. Dairy.
  3. Liver
111
Q

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

A

Women - 600µg. Men - 700µg.

112
Q

What are the consequences of vitamin A deficiency?

A

Night blindness, growth retardation, increased susceptibility to infection.

113
Q

What are the consequences of vitamin A toxicity?

A

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

114
Q

Is vitamin C fat or water soluble?

A

Water soluble (easily lost when boiled).

115
Q

What are the functions of vitamin C?

A

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

116
Q

Name 4 sources of vitamin C.

A
  1. Citrus fruits.
  2. Green leafy veg.
  3. Potatoes.
  4. Kidney.
117
Q

What is the recommended daily intake of vitamin C?

A

40mg.

118
Q

What are the consequences of vitamin C deficiency?

A

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

119
Q

What are the consequences of vitamin C toxicity?

A

Diarrhoea, nausea, renal stone formation.

120
Q

Are B vitamins fat or water soluble?

A

Water soluble.

121
Q

How many B vitamins are there?

A

8.

122
Q

What are B vitamins important for?

A

Cell metabolism and energy production.

123
Q

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

A

About 12 hours.

124
Q

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

A

3 months.

125
Q

What percentage of BMR do these organs use?

a) Brain.
b) Liver.
c) Muscle.

A

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

126
Q

What fuels does the brain use?

A

Glucose and ketone bodies.

127
Q

What fuels does the liver use?

A

Glucose, amino acids, fatty acids.

128
Q

What fuels does muscle use?

A

Glucose, ketone bodies, amino acids and triacylglycerol.

129
Q

What are free sugars and starch associated with effecting?

A

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

130
Q

What type of starch is the most desirable and why?

A

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

131
Q

What is the cause of lactose intolerance?

A

A deficiency in lactase.

132
Q

Give 3 symptoms of lactose intolerance.

A
  1. Bloating.
  2. Diarrhoea.
  3. Pain.
133
Q

Explain the mechanism that produces the symptoms of lactose intolerance.

A

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

134
Q

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

A

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

135
Q

Define BMR.

A

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

136
Q

Where does the foregut begin and end?

A

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

137
Q

Where does the midgut begin and end?

A

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

138
Q

Where does the hindgut begin and end?

A

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

139
Q

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

A

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

140
Q

Are the pharyngeal clefts formed in the endoderm or ectoderm?

A

Ectoderm.

141
Q

Are the pharyngeal pouches formed in the endoderm or ectoderm?

A

Endoderm.

142
Q

How many pharyngeal arches are there?

A

5 (4 pharyngeal clefts and pouches).

143
Q

What does the first pharyngeal arch form?

A

Muscles for mastication. Innervation: Cn 5.

144
Q

What does the second pharyngeal arch form?

A

Muscles for facial expression. Innervation: Cn 7.

145
Q

What does the third pharyngeal arch form?

A

Stylopharyngeus muscle. Innervation: Cn 9.

146
Q

What does the fourth pharyngeal arch form?

A

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

147
Q

What does the sixth pharyngeal arch form?

A

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

148
Q

Why is the stomach the shape it is?

A

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

149
Q

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

A

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

150
Q

What are the axis of stomach rotation?

A

Longitudinal and anteroposterior.

151
Q

What does the dorsal mesentery become?

A

The greater omentum.

152
Q

What does the ventral mesentery become?

A

The lesser omentum.

153
Q

What are the 5 stages of midgut development?

A
  1. Elongation.
  2. Herniation.
  3. Rotation.
  4. Retraction.
  5. Fixation.
154
Q

What connects the midgut to the yolk sac?

A

The Vitelline duct.

155
Q

What happens in the elongation stage of midgut development?

A

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
Q

What happens in the herniation stage of midgut development?

A

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

157
Q

What happens in the rotation stage of midgut development?

A

The elongated intestinal loop rotates 270 degrees anticlockwise.

158
Q

What happens in the retraction stage of midgut development?

A

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

159
Q

What happens in fixation of midgut organs?

A

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

160
Q

What are the 4 layers of the GI tract?

A
  1. An innermost mucosa.
  2. A sub-mucosa.
  3. An external muscle coat (muscularis externa)
  4. A serosa.
161
Q

What is the innermost mucosa layer composed of?

A
  • A folded epithelium.
  • Lamina propria (connective tissue).
  • Muscularis mucosa (ring of smooth muscle).
162
Q

What is the submucosa layer composed of?

A

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
Q

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

A

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
Q

What is the serous layer composed of?

A

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

165
Q

What enzyme are parietal cells abundant in?

A

Carbonic anhydrase.

166
Q

Give 5 functions of hepatocytes.

A
  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
Q

What are the 2 key stages for fat digestion?

A
  1. Emulsification.

2. Triglyceride hydrolysis.

168
Q

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

A

Pale and smelly faeces.

169
Q

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

A

Bruising.

170
Q

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

A

Swollen ankles.

171
Q

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

A

In the submucosa.

172
Q

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

A

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

173
Q

Name the abdominal retroperitoneal organs.

A

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

174
Q

Name the abdominal intraperitoneal organs.

A

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

175
Q

What is the arcuate line?

A

The lower limit of the posterior rectus sheath.

176
Q

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

A

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

177
Q

What envelopes the rectus abdominis above the arcuate line?

A

It is enveloped by the internal oblique aponeurosis.

178
Q

What is the anterior layer of rectus sheath formed from?

A

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

179
Q

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

A

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

180
Q

What forms the anterior rectus sheath below the rectus abdominis?

A

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

181
Q

What vertebral level does the umbilicus mark when lying down?

A

L3.

182
Q

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

A

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

183
Q

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

A
  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
Q

Name 3 structures that cross the transpyloric plane.

A
  1. The pylorus of the stomach.
  2. The gall bladder.
  3. The pancreas.
185
Q

At what vertebral level is the transpyloric plane?

A

L1.

186
Q

What is the intercristal plane?

A

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

187
Q

At what vertebral level is the intercristal plane?

A

L4/5.

188
Q

What is the intertubercular plane?

A

A line that joins the tubercles of the iliac crests.

189
Q

At what vertebral level is the intertubercular plane?

A

L4.

190
Q

What is the subcostal plane?

A

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

191
Q

At what vertebral level is the subcostal plane?

A

L2.

192
Q

Where is the swallowing centre found?

A

Medulla oblongata.

193
Q

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

A

HCl.

194
Q

Give 3 functions of HCl in the stomach.

A
  1. Solubilisation of food particles.
  2. Kills microbes.
  3. Activates pepsinogen forming pepsin.
195
Q

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

A

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

196
Q

What type of cells are secretin and CCK?

A

Enterogastrones.

197
Q

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

A

Gastric lipase.

198
Q

Name 3 monosaccharides.

A
  1. Glucose.
  2. Fructose.
  3. Galactose.
199
Q

Name 3 disaccharides.

A
  1. Sucrose (glucose and fructose).
  2. Lactose (glucose and galactose).
  3. Maltose (glucose and glucose).
200
Q

Name 3 polysaccharides.

A
  1. Starch.
  2. Cellulose.
  3. Glycogen.
201
Q

Where does the majority of complex polysaccharide digestion occur?

A

In the large intestine via gut bacteria.

202
Q

Where is the first site of starch digestion?

A

In the mouth via salivary amylase.

203
Q

Briefly describe starch digestion.

A

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
Q

What are proteins digested into?

A

Dipeptides, tripeptides and amino acids.

205
Q

What enzyme is responsible for protein digestion in the stomach?

A

Pepsin.

206
Q

What is the optimum pH for pepsin action?

A

1.6 - 3.2

207
Q

What does pepsin break proteins into?

A

Peptide fragments.

208
Q

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

A

Pancreatic proteases.

209
Q

What are the 2 types of pancreatic proteases?

A
  1. Endopeptidases.

2. Exopeptidases.

210
Q

Give 2 examples of an endopeptidase.

A
  1. Trypsin.

2. Chymotrypsin.

211
Q

Give 2 examples of an exopeptidase.

A
  1. Carboxypeptidases.

2. Aminopeptidases.

212
Q

What is the function of endopeptidases?

A

They break peptide bonds between non-terminal amino acids.

213
Q

What is the function of exopeptidases?

A

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

214
Q

Which type of pancreatic protease can form monomers?

A

Exopeptidases.

215
Q

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

A

Secondary active transport coupled to H+ or Na+.

216
Q

What molecules make up phospholipids?

A

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

217
Q

What are triglycerides broken down into?

A

Monoglycerides and 3 fatty acids.

218
Q

What enzyme is needed for fat digestion?

A

Pancreatic lipase.

219
Q

What mechanism speeds up the digestion of fats?

A

Emulsification - the surface area for lipase action is increased.

220
Q

What substances emulsify lipids?

A

Bile salts and phospholipids.

221
Q

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

A

Colipase.

222
Q

Name 4 molecules to make up micelles.

A
  1. Fatty acids.
  2. Monoglycerides.
  3. Bile salts.
  4. Phospholipids.
223
Q

What molecule is produced that aids absorption?

A

Micelles.

224
Q

What is the function of micelles?

A

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

225
Q

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

A

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

226
Q

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

A

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

227
Q

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

A

Chylomicrons.

228
Q

What are the functions of chylomicrons?

A

They transport long chain triglycerides to the tissues via lymphatics and blood stream. They are lipoproteins.

229
Q

How is vitamin B12 absorbed?

A

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

230
Q

What can cause pernicious anaemia?

A

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
Q

What can cause Barrett’s oesophagus?

A

GORD.

232
Q

Describe Barrett’s oesophagus.

A

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
Q

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

A

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

234
Q

Give 4 risk factors for GORD.

A
  1. Obesity.
  2. Pregnancy.
  3. Hiatal hernia.
  4. Smoking.
    (Sedentary lifestyle is not a risk factor).
235
Q

Where in the stomach are G cells most numerous?

A

In the antrum.

236
Q

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

A

Stomach and vagina.

237
Q

Name 3 organs that secrete digestive enzymes.

A
  1. Stomach.
  2. Pancreas.
  3. Salivary glands.
238
Q

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

A

Villi.

239
Q

Name 3 physical mechanisms of absorption.

A
  1. Endocytosis.
  2. Diffusion/facilitated diffusion.
  3. Active transport.
240
Q

Name 2 diseases that can cause malabsorption.

A
  1. Crohn’s disease - loss of plicae circulares.

2. Coeliac disease - vili atrophy.

241
Q

Define malnutrition.

A

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

242
Q

Why might an elderly person be at risk of malnutrition?

A
  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
Q

Name 3 physical tests for malnutrition.

A
  1. BMI.
  2. Amount of body fat.
  3. Height.
244
Q

Give 4 complications of malnutrition.

A
  1. Apathy.
  2. Depression.
  3. Increased risk of infection.
  4. Anaemia.
245
Q

Why is endoscopy preferred to a barium meal?

A

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

246
Q

What muscles contributes to the upper oesophageal sphincter?

A

Cricopharyngeus.

247
Q

Where are the stem cells that replace the epithelium located?

A

The base of crypts.

248
Q

What are the pacemaker cells of the small intestine called?

A

Interstitial cells of Cajal.

249
Q

Name 2 endocrine secretions from the duodenum?

A
  1. Secretin.

2. CCK.

250
Q

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

A

To maintain a diffusion gradient allowing for further reabsorption.

251
Q

Which papillae do not bear taste buds?

A

Filiform papillae.

252
Q

Does the oesophagus have a serosa layer?

A

No!

253
Q

What is refeeding syndrome?

A

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

254
Q

What is the function of omeprazole on the GI tract?

A

Inhibition of proton pump to reduce acid secretion

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