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Gastric Physiology Flashcards

1
Q

Functions of the stomach

A

Store and mix food
Dissolve and continue digestion
Regulate emptying into duodenum
Kill microbes
Secrete proteases
Secrete intrinsic factor
Activate proteases
Lubrication
Mucosal protection

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2
Q

Key cell types in a stomach

A

Mucous cells
Parietal cells
Chief cells
Enteroendocrine cells

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3
Q

Gastric acid secretion

A

Hydrochloric acid by parietal cells
Energy dependent
Neurohumoural regulation

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4
Q

Approximate production of HCl per day

A

2 litres/day

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5
Q

[H+] of gastric acid secretion

A

[H+] > 150mM

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6
Q

Cephalic phase stimulation

A

Parasympathetic nervous system- vagus nerve
Sight, smell, taste of food and chewing

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7
Q

Cephalic phase net effect

A

Increased acid production

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8
Q

Cephalic phase mechanism

A

Acetylcholine release
ACh acts directly on parietal cells
ACh triggers release of gastrin and histamine

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9
Q

Purpose of intrinsic factor

A

Binds to vitamin B12
Aids absorption in terminal ileum
Moderated by same regulators of gastric acid secretion

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10
Q

Gastric phase net effect

A

Increased acid production

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11
Q

Gastric phase mechanism

A

Activates chemoreceptors to stimulate G cells
Gastrin release
Gastrin acts directly on parietal cells
Gastrin triggers release of histamine
Histamine acts directly on parietal cells

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12
Q

Gastric phase stimulation

A

Gastric distension
Presence of peptides and amino acids

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13
Q

Histamine in gastric acid secretion

A

Acts directly on parietal cells
Also mediates effects of gastrin and acetylcholine

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14
Q

Gastric acid secretion

A

water (H2O) and carbon dioxide (CO2) combine within the parietal cell cytoplasm to produce carbonic acid (H2CO3), which is catalysed by carbonic anhydrase. Carbonic acid then spontaneously dissociates into a hydrogen ion (H+) and a bicarbonate ion (HCO3–).

The hydrogen ion that is formed is transported into the stomach lumen via the H+– K+ ATPase ion pump. This pump uses ATP as an energy source to exchange potassium ions into the parietal cells of the stomach with H+ ions.

The bicarbonate ion is transported out of the cell into the blood via a transporter protein called anion exchanger which transports the bicarbonate ion out the cell in exchange for a chloride ion (Cl–). This chloride ion is then transported into the stomach lumen via a chloride channel.

This results in both hydrogen and chloride ions being present within the stomach lumen. Their opposing charges leads to them associating with each other to form hydrochloric acid (HCl).

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15
Q

Which nerve is stimulated in cephalic phase

A

Vagus nerve

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16
Q

Gastric distension

A

Acts on stomach stretch receptors
Stimulates local and vagovagal reflexes

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17
Q

Protein in the stomach

A

Direct stimulus for gastrin release
Proteins in the lumen act as a buffer, mopping up H+ ions, causing pH to rise

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18
Q

Effect of rise in pH of gastric acid

A

Decreased secretion of somatostatin
More parietal cell activity (lack of inhibition)

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19
Q

Inhibitin of cephalic phase

A

Lack of vagal stimulation
Result of decreased appetite and depression

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20
Q

Inhibition of gastric phase

A

Low luminal pH (high [H+])
- directly inhibits gastrin secretion
- indirectly inhibits histamine release via gastrin
- stimulates somatostatin release which inhibits parietal cell activity

Negative feedback loop

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21
Q

Causes of inhibition of gastric phase

A

Excessive acidity
No food in the stomach to buffer
Reduce parietal cell activity by reducing channel expression
Emotional distress: sympathetic overrides parasympathetic stimulation

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22
Q

Intestinal phase of gastric acid secretion

A

Chyme in duodenum

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23
Q

Inhibition of gastric secretion by intestinal phase stimulation

A

Duodenal distension
Low luminal pH
Hypertonic luminal contents
Presence of amino acids and fatty acids

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24
Q

Inhibition of gastric secretion by intestinal phase mechanism

A

Triggers release of entergastrones
- secretin
- Cholecystokinin
And short and long neural pathways, reducing ACh release

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25
Q

Secretin

A

Inhibitis gastrin release
Promotes somatostatin release

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26
Q

Stimulation of intestinal phase

A

Low pH
Partially digested food present
Release of intestinal gastrin
Overall effect = increased acid secretion

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27
Q

4 chemicals that regulate gastric acid secretion by second messengers

A

Gastrin
Acetylcholine
Histamine
Somatostatin - inhibition

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28
Q

Regulation of gastric acid secretion overview

A

Controlled by brain, stomach, duodenum
1 (parasympathetic) neurotransmitter (ACh +)
1 hormone (gastrin +)
2 paracrine factors (histamine +, somatostatin -)
2 key enterogastrones (secretin -, CCK -)

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29
Q

Peptic ulcers

A

An ulcer is a breach in a mucosal surface
Caused by action of gastric acid

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30
Q

Causes of peptic ulcers

A

Helicobacter pylori infection
Drugs - NSAIDS
Chemical irritants- alcohol, bile salts, dietary factors
Gastrinoma

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31
Q

How does the gastric mucosa defend itself

A

Alkaline mucus- bicarbonate-rich
Tight junctions between epithelial cells
Replacement of damaged cells
Feedback loops

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32
Q

Helicobacter pylori lives in…

A

Lives in gastric mucus

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33
Q

Helicobacter pylori mechanism

A

Secretes urease, splitting urea into CO2 and ammonia
Ammonia + H+ = ammonium
Ammonium, secreted proteases, phospholipases and vacuolating cytotoxic A damage gastric epithelium
Inflammatory response
Reduced mucosal defence

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34
Q

Where do peptic ulcers occur

A

Stomach, duodenum, oesophagus

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35
Q

NSAIDs examples

A

Aspirin
Ibuprofen

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36
Q

NSAIDs

A

Non-steroidal anti-inflammatory drugs
Mucus secretion is stimulated by prostaglandin
Cyclo-oxygenase 1 needed for prostaglandin synthesis
NSAIDs inhibit cyclo-oxygenase 1
Reduced mucosal defence

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37
Q

Peptic ulcers- bile salts

A

Duodeno-gastric reflux
Regurgitated bile strips away mucus layer
Reduced mucosal defence

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38
Q

Treating peptic ulcer disease- Helicobacter pylori

A

Eradicate the organism
Triple therapy:
1 Proton pump inhibitor
2 Antibiotics eg clarithromycin, amoxicillin, tetracycline, metronidazole

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39
Q

Treating peptic ulcer disease- NSAIDs

A

Prostaglandin analogues - misoprostol
Reduce acid secretion

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40
Q

Proton pump inhibitors in parietal cells

A

Omeprazole
Lansoprazole
Esmeprazole

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41
Q

H2 receptor (histamine) antagonists in parietal cells

A

Cimetidine
Ranitidine

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42
Q

What produces pepsinogen

A

Chief cells

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43
Q

Zymogen

A

Pepsinogen- Inactive form of pepsin
Synthesised by chief cells

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44
Q

What mediates pepsinogen

A

Input from enteric nervous system (ACh)

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45
Q

Protease secretion

A

Secretion parallels HCl secretion
Luminal activation

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46
Q

Protease activation

A

Conversion of pepsinogen to pepsin is pH dependent
Most efficient when pH<2
Positive feedback loop - pepsin also catalyses the reaction
Pepsin only active at low pH- irreversible inactivation in small intestine by HCO3 -

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47
Q

A 27 year old man presents to his General Practitioner with a three week history of worsening epigastric pain. The pain is made worse in between meals, and is relieved by antacids. The GP suspects the patient has a peptic ulcer.
Which of the following is a neurotransmitter that up-regulates the secretion of gastric acid by parietal cells?.

A

Acetylcholine

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48
Q

The GP prescribes the patient a drug that increases gastric mucus production. Which drug has this action?

A

Misoprostol

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49
Q

Which of the following is a hormone that increases gastric acid secretion by parietal cells?

A

Gastrin

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50
Q

Passage of chyme into the duodenum triggers a reduction in gastric acid secretion. Which of the following duodenal factors triggers the release of enterogastrones?

A

Presence of luminal fatty acids

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51
Q

Which of the following is an enterogastrone that causes gastric parietal cells to downregulate gastric acid secretion?

A

Cholecystokinin

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52
Q

To activators of pepsin activation

A

Low pH (HCl)
Pepsin- positive feedback loop

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53
Q

Role of pepsin in protein digestion

A

Not essential
Accelerates protein digestion
Normally accounts for 20% of total protein digestion
Breaks down collagen in meat - helps shred meat into smaller pieces with greater surface area for digestion

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54
Q

Gastric motility- volume of empty stomach

A

50mL

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55
Q

Total volume of food stomach can accommodate

A

1.5L with little increase in luminal pressure
Due to receptive relaxation of smooth muscle in body and fundus

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56
Q

Receptive relaxation of stomach

A

Mediated by parasympathetic nervous system on enteric nerve plexuses

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57
Q

Coordination of receptive relaxation

A

Afferent input via vagus nerve

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58
Q

What mediates receptive relaxation

A

Nitric oxide and serotonin released by enteric nerves

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59
Q

Peristalsis - body of stomach

A

Peristaltic waves begin in gastric body
Weak contraction in body (little mixing)

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60
Q

Peristalsis- gastric antrum and pylorus

A

More powerful contraction in gastric antrum
Pylorus closes as peristaltic wave reaches it

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61
Q

Peristalsis - retroperistalsis

A

Little chyme enters duodenum
Antral contents forced back towards body (mixing)

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62
Q

Pace of basic electrical rhythm of peristalsis

A

3/minute

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63
Q

What determines frequency of peristaltic waves

A

Pacemaker cells in muscularis propria
Pacemaker cells undergo slow depolarisation- repolarisation cycles
Depolarisation waves transmitted through gao junctions to adjacent smooth muscle cells
Do not cause significant contraction in empty stomach

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64
Q

Strength of peristaltic contractions varies

A

Excitatory neurotransmitters and hormones further depolarise membranes
Action potentials generated when threshold reached

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65
Q

Interstitial cells of Cajal

A

Pacemaker cells of the stomach in muscularis propria

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66
Q

Strength of peristaltic contractions increased by:

A

Gastrin
Gastric distension mediated by mechanoreceptors

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67
Q

Strength of peristaltic contractions decreased by:

A

Duodenal distension
Increased duodenal luminal fat
Increased duodenal osmolarity
Decreased duodenal luminal pH
Increased sympathetic NS action
Decreased parasympathetic NS action

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68
Q

Gastric emptying

A

Capacity of stomach > capacity of duodenum

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69
Q

Dumping syndrome

A

Overfilling of duodenum by a hypertonic solutiom

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70
Q

Dumping syndrome signs and symptoms

A

Vomiting
Bloating
Cramps
Diarrhoea
Dizziness
Fatigue
Weakness
Sweating

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71
Q

Gastroparesis

A

Delayed gastric emptying

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72
Q

Causes of gastroparesis

A

Idiopathic
Autonomic neuropathies (e.g. in Diabetes mellitus)
Drugs
Abdominal surgery
Parkinson’s disease
Multiple sclerosis
Scleroderma
Amyloidosis
Female gender

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73
Q

Gastrointestinal agents- gastroparesis

A

Aluminium hydroxide antacids
H2 receptor antagonists
Proton pump inhibitors
Sucralfate

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74
Q

Anticholinergic medications- gastroparesis

A

Diphenhydramine (Benadryl)
Opioid analgesics
Tricyclic antidepressants

75
Q

Miscellaneous drugs- gastroparesis

A

Beta-adrenergic receptor agonists
Calcium channel blockers
Interferon alpha
Levodopa

76
Q

Mechanisms to prevent duodenal overfilling

A
  1. Increased acidity/fat/amino acids, hypertonicity and distension
  2. Increased secretion of enterogastrones AND stimulate neural receptors
  3. Decreased gastric emptying:
    - increased plasma enterogastrones
    - short neural reflexes via enteric neurons act on stomach directly
    - long neural reflexes increases sympathetic efferents and decreases parasympathetic efferents
77
Q

Signs and symptoms of delayed gastric emptying

A

Nausea
Early satiety
Vomiting undigested food
GORD
Abdominal pain and bloating
Anorexia

78
Q

Gastric motility and emptying regulated by

A

Same factors that regulate HCl production

79
Q

Which of the following cells secretes pepsin?

A

No cells

80
Q

What cells produce intrinsic factor

A

Parietal cells

81
Q

A 74 year old man has his stomach removed to treat a stomach cancer. He worries that he will not be able to digest food after the operation. What proportion of protein digestion normally takes place in the stomach?

A

20%

82
Q

Which cells in the stomach act as pacemakers, regulating the rhythm of gastric peristalsis?

A

Interstitial cells of Cajal

83
Q

Which of the following will lead to a decrease in the strength of gastric peristaltic contractions?

A

Increased sympathetic stimulation

84
Q

What is cholecystokinin responsible for

A

Contraction of the gallbladder and release of stored bile into the duodenum
(Released in response to fatty acids in chyme)

85
Q

Why do proteins act as a buffer

A

They are negatively charged so can accept H+

86
Q

A 23 year old patient complains of stomach pains after taking a Non-steroidal anti-inflammatory analgesic (NSAID).

How do NSAIDs irritate the stomach?

A

inhibition of gastrointestinal mucosal cyclo-oxygenase (COX) activity

NSAIDs inhibit COX-1 and COX-2 (COX = cyclo-oxygenase).

COX-2 is the target enzyme and blockade of this will inhibit production of inflammatory and nociceptive-enhancing prostaglandins.

Inhibition of COX-1 will prevent production of gastro-protective prostaglandins.

87
Q

The parietal cells within the stomach produce Intrinsic factor.

What is the function of Intrinsic Factor?

A

Intrinsic Factor is a glycoprotein produced by the parietal cells of the stomach and is essential for the absorption of Vit B12.

It binds with Vit B12 and forms a complex that resists digestion by gastric enzymes.

The Vit B12 complex then passes through the stomach where it absorbed in the terminal ileum, transported to the liver and stored.

88
Q

The stomach contains a variety of cell types.

Which of these substances is secreted by G cells?

A

Gastrin

89
Q

The porta hepatis forms part of the liver.

Which of the following structures is NOT present in the Porta Hepatis?

A

Hepatic vein

Porta hepatis is a fissure on the underside of the liver. It has several structures running through it, the hepatic artery proper, portal vein, hepatic bile duct, Vagus nerve branches, sympathetics and lymphatics.

90
Q

The stomach contains a variety of cell types.

Which of these substances is secreted by Chief cells?

A

Pepsinogen

91
Q

The proton pump is part of the parietal cell.

What is the function of the proton pump with regard to ion exchange across the cell membrane?

A

K+ into cell, H+ out of cell

92
Q

Which of the following statements is correct regarding the function of the Vagus nerve and its action on parietal cells?

A

Vagus nerve is part of the parasympathetic system and releases acetylcholine onto parietal cells

93
Q

The stomach contains a variety of cell types.

Which of these substances is secreted by D cells?

A

Somatostatin

94
Q

Omeprazole is routinely prescribed for acid reflux.

What is the mechanism of action of Omeprazole on the GI tract?

A

Inhibition of Proton Pump to reduce acid secretion

95
Q

Regarding the embryology of the GI tract.

Which of the following structures is classified in embryology as part of the ‘foregut’?

A

Pancreas, Gallbladder, proximal 2 parts of the duodenum and the lower third of the oesophagus

96
Q

You are trying to design a drug to act on histamine receptors on parietal cells to help patients with reflux disease.

What would be the mechanism of this drug?

A

Inhibits Histamine 2 receptors to reduce acid secretion

97
Q

The digestive tract has a rich blood supply.

Which of the following vessels supplies arterial blood to the Jejunum?

A

Superior mesenteric artery

98
Q

The stomach contains a variety of cell types.

Which of these substances is secreted by Enterochromaffin-like (ECL) Cells

A

Histamine

99
Q

A 40 year old has been diagnosed with gallstones, one of which is in the common bile duct.

Where does the Common Bile Duct drain into?

A

Duodenum

100
Q

The stomach contracts to aid mixing of the ingested food.

How many layers of muscle are present in the stomach wall?

A

3
Longitudinal
Circular
Oblique

101
Q

Digestion of the different dietary components occurs in different parts of the GI tract.

What is the first location that fat is acted upon by Lipase enzymes when passing through the GI tract?

A

Oral cavity

102
Q

A 56 year old man has a long standing history of gastro-oesophageal reflux.

What is the change in cell-type (‘metaplasia’) seen in the lower oesophagus after prolonged reflux of acid?

A

Stratified squamous to columnar

103
Q

Function of D cells

A

Release somatostatin

104
Q

Function of G cells

A

Release gastrin, HCl

105
Q

Function of enterochromaffin-like cells

A

Release histamine

106
Q

Function of chief cells

A

Produce pepsinogen

107
Q

Function of parietal cells

A

Produce gastric acid and intrinsic factor

108
Q

Function of mucous cells

A

produce mucous at entrance to gland
Forms a barrier between the gastric acid and gastric mucosa
Rich in HCO3 - (bicarbonate)

109
Q

Stimulation of Cephalic phase

A

Vagus

110
Q

Stimulation of gastric phase

A

Local nervous secretory reflexes
Vagal reflexes
Gastrin-histamine stimulation

111
Q

Stimulation of intestinal phase

A

Nervous mechanisms
Hormonal mechanisms

112
Q

Luminal secretion of lower oesophageal sphincter and stomach cardia

A

Mucus
HCO3 -

113
Q

Luminal secretion of Fundus and body of stomach

A

H+
Intrinsic factor
Mucus
HCO3 -
Pepsinogens
Lipase

114
Q

Luminal secretion of antrum and pylorus of stomach

A

Mucus
HCO3 -

115
Q

Motility of lower oesophageal sphincter and cardia of stomach

A

Prevention of reflux
Entry of food
Regulating of belching

116
Q

Motility of Fundus and body of stomach

A

Reservoir
Tonic force during emptying

117
Q

Motility of antrum and pylorus of stomach

A

Mixing
Grinding
Sieving
Regulation of emptying

118
Q

Function of gastric acid

A

Activates pepsin
Kills bacteria

119
Q

Function of intrinsic factor

A

Complexes with vitamin B12 to permit absorption

120
Q

Function of histamine

A

Stimulate gastric acid secretion

121
Q

Function of somatostatin

A

Inhibits gastric acid secretion

122
Q

APUD cells

A

Amine precursor uptake decarboxylation cells
Dispersed amongst epithelial cells

123
Q

Superficial to deep order of cells in stomach lining

A

Mucus neck cells
Parietal cells
Enterochromaffin-like cells
Chief cells
D cells
G cells

124
Q

What neurotransmitter activates parietal and chief cells to initiate receptive relaxation

A

ACh

125
Q

Inhibition of Cephalic phase

A

Lack of vagal stimulation
Result of decreased appetite and depression

126
Q

Cephalic phase direct effect

A

On parietal cells
Increases channel expression

127
Q

Cephalic phase indirect phase

A

On G cells and ECL cells
Increase release of gastrin and histamine which act on parietal cells to increase the number of H/K ATPase on the apical membrane

128
Q

Why do proteins and amino acids stimulate an increase in gastrin

A

Molecules act as a buffer for H+ therefore pH rises

129
Q

Inhibition of gastric phase

A

Excessive acidity inhibits gastrin secretion and increases somatostatin secretion
Can occur when there is no food in the stomach to buffer
Reduce parietal cell activity by reducing channel expression
Emotional distress

130
Q

Parasympathetic neurotransmitter stomach physiology

A

ACh

131
Q

Hormone stomach physiology

A

Gastrin

132
Q

Paracrine stomach physiology

A

Histamine
Somatostatin

133
Q

Enterogastrins stomach physiology

A

Secretion
Cholecystokinin (CCK)

134
Q

Stimulation of intestinal phase

A

Low pH
Partially digested food present
Release of intestinal gastrin

135
Q

Inhibition of intestinal phase

A

Duodenal distention
Hypertonic solutions
Presence of amino acids and fatty acids
Leads to entero-gastric reflex
Release of intestinal hormones
Secretin inhibits gastrin release and promotes somatostatin release

136
Q

Function of secretin

A

Inhibits gastrin release
Promotes somatostatin release

137
Q

Stomach lining damage- chemical irritants

A

Alcohol and bile salts
Duodenal-gastric reflux- bile enters the stomach
Alkaline bile strips away gastric mucosal layer resulting in reduced defence

138
Q

Zollinger-Ellison Syndrome/ gastrinoma

A

Rare tumour of G cells
Excessive gastrin release
Increased attack on the gastric mucosa leading to ulcers

139
Q

Duodenal absorption occurs by

A

Simple diffusion
Facilitated diffusion
Active transport
Endocytosis
Paracellular transport

140
Q

Small intestine digestion

A

In lumen by secreted enzymes
Cell surface of enterocytes by membrane bound enzymes

141
Q

3 ways that peptides modulate GI tract function

A

Endocrine
Paracrine
Neurocrine

142
Q

Which cells release secretin

A

Duodenal S cells

143
Q

Primary effects of secretin

A

Increasing secretion of:
Bile from the liver and gall bladder
Secretion of HCO3- and enzymes from the oancreas

144
Q

Secondary effects of secretin

A

Reducing gastric motility
Reducing gastric secretory rates

145
Q

Primary effects of Gastric inhibitory peptide (GIP)

A

Inhibits gastric activity
Increases insulin release

146
Q

Secondary effects of Gastric inhibitory peptide (GIP)

A

Stimulating duodenal gland activity
Stimulating lipase synthesis
Increasing glucose use by skeletal muscle

147
Q

Which cells release cholecystokinin

A

I cells in duodenum, Jejunum and less so from the ileum

148
Q

Pancreatic effects of cholecystokinin

A

Accelerates release of enzymes
Increases HCO3- secretions

149
Q

Liver and gallbladder effects of cholecystokinin

A

Sphincter of Oddi relaxation
Gallbladder contraction
Increasing secretions

150
Q

High CCK levels

A

Inhibit gastric activity
Feeds to CNS to reduce sensation of hunger

151
Q

Vasoactive intestinal peptide

A

Stimulated the secretion of intestinal glands
Dilates regional capillaries
Inhibits acid production in the stomach
Dilation of capillaries allows more efficient absorption

152
Q

Direct causes of release of duodenal regulators

A

Nervous input from the brain or luminal contents eg acid

153
Q

Indirect causes of release of duodenal regulators

A

Distention of the gut
Release of another hormone

154
Q

Negative feedback loop in duodenal digestion

A

Acid activates D cells which release somatostatin and this acts to reduce the further release of acid
Inhibits G cells production of gastrin
Inhibits enterchromaffin-like cells release of histamine
Directly inhibits the release of acid from parietal cells
Stops the chief cells production of pepsinogen

155
Q

Which hormone inhibits gastrin

A

GIP

156
Q

What is mainly responsible for gastric-inhibitory peptide (GIP) secretion

A

Presence of glucose in duodenum

157
Q

What cells are found at the bottom of the Crypt of Lieberkuhn in intestinal mucosa

A

Proliferating stem cells

158
Q

What causes Zollinger-Ellison syndrome

A

A gastrin secreting tumour- leading to excessive gastric acid secretion

159
Q

Which hormone delays gastric emptying to prevent unabsorbed nutrients entering the lower ileum

A

Gastric inhibitory peptide

160
Q

What reduces gastric acid production

A

Somatostatin
Enterogastric reflex
Cholecystokinin
Secretin

161
Q

What effect does initiation of the Cephalic phase have on gastric secretion

A

Directly: chief cells and parietal cells
Indirectly: G cells

162
Q

Where are S cells found

A

Mainly in duodenum and partially in Jejunum

163
Q

What stimulates gastric acid release

A

Gastrin
Acetylcholine
Enterochromaffin-like cells (secrete histamine)

164
Q

Which neurotransmitters cause contraction of smooth muscle above a food bolus during peristalsis

A

Acetylcholine and substance P

165
Q

During vagal stimulation of G cells, which neurotransmitter triggers release of gastrin from G cells

A

Gastrin releasing peptide

166
Q

What are the main functions of motilin

A

Increases gastrointestinal motility
Promotes gastric emptying

167
Q

Which hormone is produced in excess in Zollinger-Ellison syndrome

A

Gastrin

168
Q

How is procolipase activated

A

By trypsin in the small intestine

169
Q

Where are glucagon-like peptide-1 and glucagon-like peptide-2 hormones released from

A

Enteroendocrine L cells in the ileum and colon

170
Q

Risk factors of GORD

A

Pregnancy
Hiatus hernia
Smoking and alcohol
Stress and anxiety

171
Q

Histological change associated with GORD

A

Barrett’s oesophagus
Stratified squamous —> simple columnar

172
Q

Forms of mucosal defence

A

Alkaline secretions
Tight junctions
Rapid cell replacement
Feedback loop for gastric acid secretion

173
Q

Where is vitamin b12 absorbed and how

A

Terminal ileum bound to intrinsic factor

174
Q

Function of vitamin b12

A

DNA synthesis
Brain development
Erythrocytes formation

175
Q

Macroscopic differences between small and large bowel

A

Smaller / larger
Longitudinal muscle layer is continuous/ not continuous but is 3 muscles called tense coli
No appendices epiploe/has
Wall smooth/sacculated (haustrations)
Villi/no villi

176
Q

A 22 year old medical student develops profuse watery diarrhoea whilst on his elective in Bangladesh. Although he is drinking approximately 2 litres of fluid per day, he is passing 8-10 litres of liquid stools per day. He sees a doctor, who diagnoses cholera infection. Which part of the gastrointestinal tract normally absorbs the most fluid?

A

Jejunum

177
Q

A dietician is prescribing total parenteral nutrition for a severely malnourished patient. Which of the following vitamins is fat-soluble?

Biotin
Folic acid
Retinol
Riboflavin
Niacin

A

Retinol

178
Q

What nutrients are absorbed in the stomach

A

Water
Copper
Iodide
Fluoride

179
Q

What nutrients are absorbed in the duodenum

A

Iron
Fat-soluble vitamins
Calcium
Magnesium

180
Q

What nutrients are absorbed in the Jejunum

A

Thiamine
Riboflavin
Calcium
Phosphorus
Iron

181
Q

What nutrients are absorbed in the ileum

A

Vitamin C
Vitamin B12
Votamin D
Folate
Vitamin K

182
Q

What nutrients are absorbed in the colon

A

Water
Vitamin K
Biotin
Sodium
Chloride
Potassium

183
Q

Which vitamin can only be found in meat products

A

Vitamins B12

GI (12 decks)

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