Physiology Flashcards

1
Q

What is the function of lips,cheeks and tongue?

A

to keep food moving and place it in the optimal position for effective chewing.

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2
Q

What are the main muscles involved for food to be masticated (chewed)?

A

Masseter and temporalis- bring lower jaw up against upper jaw

Pterygoids- open jaws, keeps them aligned and moves them up down and side to side.

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3
Q

What nerve controls the muscles of mastication?

A

Trigeminal nerve (vth cranial)

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4
Q

Describe the roles of the different teeth in the mouth.

A

Incisors- sharp edges to cut tough food

canines- sharp end to to grind food

premolars and molars- complex surfaces that capture small bits of food and crush food.

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5
Q

what does the term sublingually mean?

A

Under the tongue

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6
Q

What are the advantages of sublingual prescription?

A

the need to swallow drug is avoided and so bypasses the liver and avoids hepatic first-pass metabolism.

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7
Q

What are the salivary glands?

A

parotid,submandibular and sublingual glands.

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8
Q

Saliva is hypertonic true or false?

A

false its hypotonic

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9
Q

What nerves are responsible sending impulses from the brainstem salivary nuclei for salivary secretion and what fibres are involved?

A

Facial (vii cranial)

Glossopharyngeal (IXth cranial)

Parasympathetic fibres

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10
Q

What is xerostomia and why does it occur with antidepressants, tranquilizers and opiate analgesics?

A

Xerostomia- dry mouth

These drugs inhibit parasympathetic nerve activity which therefore inhibits salivation.

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11
Q

What are the main roles of salivation?

A
  1. Moisten and lubricate the mouth to form bolus
  2. Dissolve food molecules so they can react with taste receptors
  3. Ease swallowing of bolus
  4. Begin digestion- contains alpha amylase which breaks down of polysaccharides
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12
Q

How does saliva help against infection and tooth decay?

A
  1. Coats teeth with proline-rich protein(pellicle) as protective barrier on its surface.
  2. Contains immunoglobulins and antimicrobials that maintain control of the residen bacterial flora of the mouth and prevent serious infection.
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13
Q

Describe the formation of saliva

A
  1. Stimulation of acinar epithelial cells cause ca2+ dependent activation of K+ and CL- channels.
  2. Efflux of cl- cause Na+ to move through the glandular ducts via paracellular route. Creating concentration gradient for water to move into luminal space via osmosis.
  3. Na+ and CL- are reabsorbed by ENaC and CL- HCO3- exchange.
  4. HC03- and K+ are secreted- creates hypotonic saliva.
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14
Q

Which nerve innervates the tongue muscle?

A

hypoglossal (XIIth cranial) nerve.

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15
Q

Sensory fibres from the tongue travel through which nerves?

A

Glossopharyngeal (IXth cranial) nerve

and chorda tympani branch of facial (VIIth cranial) nerve

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16
Q

What are the functions of the tongue?

A

directs and retrieves food between the teeth

clears obstructions

propels food posteriorly to initiate pharyngeal phase of swallowing

speech

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17
Q

What are the major modalitlies of taste?

A
  1. Sweet
  2. sour
  3. salt
  4. bitter
  5. umami
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18
Q

What nerve runs alongside the oesophagus and innervates oesophageal muscle?

A

Vagus nerve.

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19
Q

What is the role of the submucosal venous plexus?

A

Drains venous blood from the oesophagus avoiding the hepatic portal vein and liver.

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20
Q

What happens to oesophageal veins during portal hypertension?

A

Collateral veins divert gastric blood to oesophageal veins, which enlarge and form varices.

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21
Q

What is peristalsis?

A

a coordinated wave of contraction behind the bolus of food, with relaxation ahead of it, propelling bolus forward. Down the oesophagus

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22
Q

What causes peristalsis to occur?

A

along with controlling sphincter movement, vagus nerve and the enteric nervus plexus, which is in the tract itself. controls peristalsis

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23
Q

How does vomiting occur?

A

When peristalsis waves move in the opposite direction. i.e towards the mouth

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24
Q

Describe the stages of swallowing.

A
  1. Tongue forces bolus down into oropharynx. UOS closed
  2. This initiates a reflex which raises the soft palate thus sealing off the nasopharynx preventing food entering the nasal cavity. This inhibits respiration
  3. Superior and middle pharyngeal constrictor force the bolus down in the hypopharynx and the glottis closes.
  4. Epiglottis is forced backwards and downwards
  5. this prevents food from entering the trachea.
  6. The UOS relaxes and these changes reverse. Larynx opens allowing breathing to occur.
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25
Q

What controls swallowing?

A

swallowing centres in the medulla

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26
Q

What is the difference between the first two waves of peristalsis?

A
  1. primary peristaltic wave, which occurs when the bolus enters the oesophagus during swallowing. The primary peristaltic wave forces the bolus down the oesophagus and into the stomach in a wave lasting about 8–9 seconds. The wave travels down to the stomach even if the bolus of food descends at a greater rate than the wave itself, and continues even if for some reason the bolus gets stuck further up the oesophagus.
  2. In the event that the bolus gets stuck or moves slower than the primary peristaltic wave (as can happen when it is poorly lubricated), stretch receptors in the oesophagal lining are stimulated and a local reflex response causes a secondary peristaltic wave around the bolus, forcing it further down the oesophagus, and these secondary waves continue indefinitely until the bolus enters the stomach.
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27
Q

What is the third wave of peristalsis?

A

it is a pathogenic caused form.

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28
Q

What are the main functions of the stomach?

A

store food

digest food

regulate the release of chyme

secrete the intrinsic factor.

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29
Q

What is the role of the intrinsic factor

A

Binds to Vitamin B12 protecting it from being absorbed in the proximal intestine.

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30
Q

What is the volume of the stomach when empty vs it being fully distended?

A

50 ml vs 4 L

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31
Q

Why is the storage of food important in the stomach?

A

As the stomach can ingest food more rapidly than it can digest it.

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32
Q

What are proteins broken down into and what type of enzyme does this?

A

Proteins are broken down into polypeptides

Pepsin is the type of enzyme.

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33
Q

What is the inactive form of pepsins called?

A

pepsinogen.

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34
Q

Where are pepsinogens found?

A

Produced by chief cells found in the gastric mucosa’s glands.

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35
Q

How are pepsinogens activated?

A

HCL

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36
Q

What cells produce HCL in the stomach to lower the pH?

A

Parietal cells.

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37
Q

What else do parietal cells produce?

A

Intrinsic factor.

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38
Q

Where are parietal cells found in the stomach?

A

Found in the gastric mucosa’s glands.

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39
Q

Describe the formation of HCL inside the parietal cells.

A
  1. H+ ions are made by H2O being broken down via hydrolysis
  2. H+ ions are transported out of the cell on the apical surface via a Proton pump ( h+-K+ ATPase protein) entering the lumen
  3. CL- enters the cell on the basolateral side in exchange for HCO3- via another proton pump
  4. CL- then via an apical chloride channel enters the lumen
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40
Q

Describe the formation of HCO3- in the parietal cells?

A

CO2 and H20 internally bind via carbonic anhydrase to form carbonic acid ( h2co3)

This breaks down into H+ and HCO3-

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41
Q

What is the main role of HCO3- in the stomach

A

Used to raise the pH in the alkali tide after the stomach has secreted acid.

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42
Q

What are the three stages of gastric secretion?

A

Cephalic phase

Gastric phase

intestinal phase

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43
Q

What causes the cephalic phase to occur?

A

the sight, smell, taste and mastication of food

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44
Q

When does gastric phase occur?

A

when food reaches the stomach

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45
Q

What stimulates acid secretion during the cephalic phase?

A

activation of the vagus nerve via the medulla oblongata and its actions on the enteric plexus.

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46
Q

how does vagal stimulation cause the release of HCL and pepsin?

A

the postganglionic parasympathetic fibres cause the release of Acetylcholine.

It also releases GRP which causes the release of Gastrin from G cells.

Causes release of histamine from ECL cells.

inhibits D cells- this, in turn, reduces the inhibitory effect of somatostatin on G- cells.

Ach, gastrin and histamine stimulate release of H+ from parietal cells.

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47
Q

What pathways are used to stimulate HCL in the cephalic phase?

A

Direct- Ach, gastrin and Histamine act on M2 muscarinic and H2 receptors to stimulate parietal cells

indirect- ACH and gastrin stimulate ECL cell resulting in release of histamine acting on LOCAL. parietal cells.

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48
Q

What are the main stimuli for the gastric phase?

A

distention of stomach

chemical composition of the food.

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49
Q

What does the distention of the stomach do to the mechanoreceptors?

A

they are stretched thus making longer vagovagal reflexes and setting up local myenteric reflexes

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50
Q

How does the break down of proteins affect gastric secretion?

A

the release of peptides and free amino acids directly stimulate G cells to relase Gastrin

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51
Q

Why is gastrin described as self-regulating?

A

at pH 3 or below gastrin stops being produced. This occurs due to decreased buffering of HCL. Therefore when there is no food there is a low pH and so gastrin is inhibited via release of somatostatin from D cells.

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52
Q

What is chyme?

A

it is semi-fluid material which food is converted into after the stomach.

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53
Q

How is histamine regulated?

A

PGE2 continually secreted by the gastric mucosa in the gastric phase acts locally to reduce histamine.

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54
Q

What is the effect of chyme when in the pyloric antrum?

A

it causes the duodenum to distend

Antral contraction

opening of pyloric sphincter

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55
Q

What increases the rate of gastric emptying?

A

Volume of chyme in the antrum

fall in pH of chyme.

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56
Q

What decrease rate of gastric emptying?

A

Distention of duodenum

Presence of fats and decrease of pH in the duodenum lumen. Needs to be neutralised and fat to be absorbed

Hypertonicity - products of carbs ad protein digestion draw water into small intestine- danger of reduced plasma volume and circulatory disturbances (e.g. ‘dumping syndrome’)

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57
Q

How does duodenum delay gastric emptying?

A

Neuronal response- enterogastric reflex which decreases activity by signals from intrinsic nerve plexuses and the ANS

Hormonal response- release of enterogastrones inhibits stomach contractions

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58
Q

What are the two sections of the stomach based on its mechanical activity?

A

Orad stomach

caudad stomach

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59
Q

Does the Orad region have slow-wave activity true or false?

A

false

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60
Q

What type of contractions occur in orad region?

A

tonic contractions

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61
Q

Why are the tonic contractions weak?

A

Because of the thin musculature in that region

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62
Q

What makes up the orad stomach?

A

fundus and proximal body

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63
Q

What makes up the caudad region?

A

distal body and antrum

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64
Q

what is gastric slow wave?

A

Rhythmic electric activity in the caudad stomach produces regular peristaltic waves (3min-1)

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65
Q

What are the three sections of the small intestine?

A

Duodenum,jejunum and ileum

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66
Q

What happens when chyme first enters the duodenum?

A

Intestinal phase:

continuation of gastric secretion due to duodenal G cells

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67
Q

What does the small intestine receive from other organs?

A

chyme- stomach

Pancreatic juice - pancreas

bile - liver and gall bladder

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68
Q

What is segmentation?

A

Mixing of chyme in the digestive state in a circular motion

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69
Q

How does segmentation occur?

A

alternating contraction and relaxation of circular muscle are initiated by pacemaker cells which cause the basal electrical rhythm (BER)

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70
Q

When is segmentation in the duodenum initiated?

A

when BER has hit the threshold which occurs when duodenum distends.

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71
Q

compare segmentation contractions between duodenum, jejunum and ileum.

A

Duodenum and jejunum has more frequent contractions then ileum

duodenum and jejunum = 12 min-1

Ileum = 9 min-1

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72
Q

When is segmentation in the ileum initiated?

A

Triggered by gastrin in the stomach via gastroileal reflex

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73
Q

What is the role of secretin in the duodenum?

A

inhibits the release of gastrin

stimulates the release of pancreatic and biliary HCO3-

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74
Q

What cells produce secretin?

A

S cells in the duodenum

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75
Q

What cells produce CCK?

A

I cells in the duodenum and jejunum

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76
Q

When is secretin released?

A

in response to detection of H+ and fatty acid in the lumen

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77
Q

What are the two types of contractions in the small intestine?

A

Mixing (segmentation)

propulsive (peristalsis)

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78
Q

What happens during segmentation?

A

A portion of SI becomes distended with chyme

Intestinal wall elicit localised concentric contractions spaced at intervals along the tract.

spaced segments form along the intestine

as a set relaxes another segmentation contracts usually between the two old points.

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79
Q

What are the principal effects of the myenteric plexus when it is stimulated?

A
  1. increased tonic contraction of the gut wall
  2. increased intensity of the rhythmical contractions
  3. Slightly increased rate of the rhythm of contraction
  4. Increased velocity of conduction of excitatory waves along the gut wall, causing more rapid movement of the gut peristaltic waves
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80
Q

What are the two main plexuses which makes up the ENS?

A
  1. Myenteric plexus

2. Submucosal plexus

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81
Q

What is the main role of the submucosal plexus?

A

Regulates epithelial cell and submucosal blood vessel function

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82
Q

What are the three types of GI reflexes?

Give examples of each

A
  1. Local reflexes Integrated entirely within the gut wall ENS- mainly involved in movement

examples
secretion,
peristalsis

  1. short reflexes from the gut to the prevertebral sympathetic ganglia and then back to GI tract

examples

gastrocolic reflex ( stomach to colon) or enterogastric reflexes ( inhibit gastric motlilty from colon and SI)

  1. Long reflexes from the gut to the spinal cord/brain stem and then back to tract-:

These include stomach to brain stem to stomach for gastric motor and secretory activity

examples

Pain reflexes

Defecation reflexes ( gastro ileal)

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83
Q

Discuss the pathway of chyme in the small intestine via peristalsis.

A

propels chyme from the pylorus to the ileocaecal valve

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84
Q

What is the role of peristalsis in the small intestine?

A
  1. move chyme through tract

2. Spread chyme out along the intestinal mucosa

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85
Q

What stimulates peristalsis in the SI?

A
  1. Greatly increased after a meal
  2. Gastroenteric reflex
  3. gastrin, CCK, insulin and serotonin increase intestinal motility
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86
Q

What inhibits peristalsis

in SI?

A
  1. No chyme present
  2. Secretin
  3. Glucagon
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87
Q

What is the difference between segmentation and peristalsis ?

A
  1. Segmentation pushes chyme in both directions but net movement is slightly aboral

Peristalsis pushes chyme in one direction (aborally)

  1. Segmentation relies on circular muscular contraction

Peristalsis relies on rhythmic longitudinal muscular contraction

  1. segmentation doesn’t occur in oesophagus and stomach
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88
Q

What is the peristaltic rush?

A

strong waves of contraction which is caused by intense irritation of the intestinal mucosa.

These powerful contractions travel long distances sweeping the contents of the intestine into the colon relieveing it of chyme and excessive distention.

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89
Q

What is the role of the ileocecal valve?

A

prevents backflow of chyme into the ileum

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90
Q

What is the effect of the gastroileal reflex on the ileocecal valve?

A

ileocecal may prevent food entering the cecum until the person may eat another meal

Gastroileal reflex intensifies the peristalsis waves forcing the remaining chyme through.

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91
Q

Discuss how the cecum controls the ileocecal sphincter and ileal peristalsis

A
  1. When cecum becomes distended - sphincter becomes intensified

This leads to ileal peristalsis being inhibited

  1. irritation of cecum delays emptying
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92
Q

What is the migrating motor complex?

A

Strong peristaltic contractions which clear debris and mucus and sloughed epithelial cells between meals.

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93
Q

what stimulates MMC?

A

Molitin

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94
Q

What inhibits MMC?

A

feeding and vagal activity

Gastrin and CCK

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95
Q

What is CCK released in response to?

A
Release of :
monoglycerides
free fatty acids
Amino acids
Small peptides
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96
Q

What is the role of CCK?

A
  1. Inhibit gastric emptying (inhibits release of gastrin and acid)
  2. Cause secretion of pancreatic enzymes
  3. stimulates relaxation of the sphincter of Oddi
  4. Stimulates contraction of the gall bladder to eject bile from the duodenum
  5. potentiates the action of secretin
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97
Q

Where is GIP produced?

A

K cells of duodenum and jejunum

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98
Q

What is GIP released in response to?

A

Presence of
Glucose

amino acids

fatty acids

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99
Q

What is the role of GIP?

A

Stimulate release of insulin

Inhibit gastric emptying

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100
Q

Where is GLP-1 produced?

A

L cells

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101
Q

What is GLP-1 produced in response to?

A

presence of food in SI.

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102
Q

What is the role of GLP-1?

A

Stimulates insulin secretion

Inhibits glucagon secretion

Decrease gastric emptying and appetite

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103
Q

Where is Motilin produced?

A

M CELLS of duodenum and jejunum

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104
Q

What is motilin secreted in response to?

A

secreted during a fasting state

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105
Q

What is the role of motilin?

A

initiates MMC

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106
Q

What type of receptor do all peptide hormones act on?

A

G-protein coupled receptors.

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107
Q

Where is ghrelin produced?

A

Gr cells of the gastric antrum

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108
Q

What is the role of ghrelin?

A

Stimulates appetite.

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109
Q

where is vitamin b12 absorbed?

A

Terminal ileum

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110
Q

What is succus entericus?

A

intestinal juices

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111
Q

What is the role of the Brunner’s glands?

A

Produces alkaline mucus to prevent digestion of duodenal wall from highly acidic gastric juices.

It also produces the mucus as it contains a large number of bicarbonate ions which is used to neutralise the HCL as well

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112
Q

What stimulates the Brunner’s glands?

A
  1. Tactile or irritating stimuli on the duodenal mucosa
  2. vagal stimulation - increase in stomach secretion= increase in brunner’s gland secretion
  3. GI hormones e.g. CCK, gastrin especially SECRETIN
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113
Q

What inhibits the Brunner’s glands

A

Sympathetic stimulation- suggests why very excitable people have peptic ulers in the duodenal bulb

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114
Q

What are the properties of the crypt of lieberkuhn which make it effective with intestinal secretion?

A
  1. contains goblet cells- secrete mucus which lubricates and protects intestinal surfaces
  2. Contains enterocytes which secrete large quantities of water and electrolytes. Eventually reabsorbing them with end products of digestion. Also absorb carbohydrates,proteins fats and vitamins.
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115
Q

What does the small intestine absorb?

A
  1. water
  2. electrolytes
  3. carbohydrates
  4. amino acids
  5. minerals
  6. fats
  7. vitamins
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116
Q

What enzymes are released from enterocytes in the brush border?

A
  1. peptidases e.g. carboxypeptidase and aminopeptidase

2. sucrase, maltase, isomaltase and lactase

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117
Q

What are the properties of the small intestine which make it adapted for absorption?

A
  1. large surface area - plicae circulae - transverse folds

villi which are finger-like projections of lumen

microvilli which are finger-like projections of the apical surfaces of the enterocytes

  1. rich blood supply- each villus contains a capillary network
  2. epithelial cells are replaced every 6 days
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118
Q

Discuss the ways sodium ions are move into the mucosa.

A
  1. Na+/glucose co-transport
  2. Na+/amino acid co-transport
  3. Na+/H+ exchange
  4. Parallel Na+/H+ and Cl-/HCO3- exchange
  5. epithelial Na+ channels ( ENaC)
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119
Q

What two ways can water enter the blood?

A
  1. transcellular

2. paracellular

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120
Q

For na+/H+ exchange in the jejunum, what antiporters are used?

A
  1. Apical side - NHE2 and NHE3

2. Basolateral NHE1

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121
Q

what stimulates the exchange of the apical membranes in the jejunum?

A

the alkaline environment of the lumen (low H+ concentration)

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122
Q

Parallel Na+/H+ and Cl-/HCO3- exchange occurs where and when?

A
  1. in the ileum and proximal colon

2. Interdigestive period

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123
Q

What are the differences between Parallel Na+/H+ and Cl-/HCO3- exchange and cotransport exchange?

A
  1. Cotransport is electrogenic while the parallel exchange is electroneutral
  2. Cotransport is not regulated by intracellular cAMP
  3. co-transport mainly occurs in the jejunum while parallel is in the ileum
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124
Q

Where do ENaC help in absorption of NA+?

A

distal colon

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125
Q

How does aldosterone help in absorption of Na+

A

Released when feeling dehydrated

  1. Open ENaC channels
  2. Inserts more into the apical membrane from intracellular vesicle pool
  3. increases the synthesis of ENaC and Na+/K+ Atpase
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126
Q

Discuss the formats in which chloride ions are absorbed into the intestines.

A
  1. diffuse via transcellular or paracellular. Exchange systems are also used
  2. Small intestine- lumen has negative potential due to transport of sodium
  3. Large intestine - lumen has negative potential due to ENaC movement of Na+
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127
Q

where are CL- ions are secreted from?

A

Crypt enterocytes

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128
Q

Discuss the secretion of CL-

A
  1. chloride ions are absorbed from the blood into the cell via low intracellular Na+ which causes a drive of sodium , potassium and chloride ions via NKCC1
  2. High conc of Cl- means that diffuses out of cell through apical membrane via CFTR
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129
Q

What activates CFTR

A
  1. Bacterial enterotoxins- diarrhoea causing
  2. Hormones and neurotransmitters
  3. Immune cells products
  4. cAMP
  5. gGMP
  6. Ca 2+
  7. some laxatives
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130
Q

Discuss the reabsorption of water via the small intestine.

A
  1. Sodium ions are actively transported on the basolateral side of the villus cells via Atpase (3 for 2 K+)
  2. Creates conc gradient for Na+ to diffuse into cell via apical membrane
  3. high conc of K+ in the cell means it diffuses back out of cell via basolateral membrane along with Cl-. creating ionic enviromment in the blood
  4. creates an osmotic enviroment in the lumen causing water to be reabsorbed ( released from crypt first).
  5. Water diffuses down the gradient into the cell and then transported into the blood.
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131
Q

What is the role of paneth cells?

A

they are involved in protein synthesis,secretion and contain antibacterial proteins such as lysozyme,phospholipase A2 and defensins

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132
Q

What is the role of acinar cells in the pancreas?

A

It secretes the pancreatic juice

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133
Q

What is pancreatic juice secreted in response to?

A

the detection of chyme.

Hormone release of CCK

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134
Q

What is the pancreatic juice made up of?

A
  1. Bicarbonate ions
  2. Water
  3. Enzymes
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135
Q

What enzymes are present in the pancreatic juice?

What are their functions?

A
  1. Pancreatic amylase- breaks down carbohydrates into monosaccharides
  2. Pancreatic lipase- breaks down fats into glycerol and fatty acids.
  3. ribonuclease and deoxyribonuclease- break down nucleic acids and free mononucleotides
  4. PROTEOLYTIC ENZYMES- MOST IMPORTANT. This includes trypsin, chymotrypsin and carboxypeptidase.

Trypsin and chymotrypsin break down proteins into peptides of various size but not individual amino acids

carboxypeptidase splits peptides into individual amino acids

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136
Q

What are the names of the inactive forms of:

  1. trypsin
  2. chymotrypsin
  3. carboxypeptidase
A
  1. Trypsinogen
  2. chymotrypsinogen
  3. procarboxypeptidase
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137
Q

How are the three main proteolytic enzymes activated?

A

trypsinogen is activated by the enzyme enterokinase. This is secreted by the intestinal mucosa when chyme is detected

Trypsinogen can also be autocatalytically activated by trypsin

Chymotrypsinogen and procarboxypeptidase are activated by trypsin

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138
Q

Where is the trypsin inhibitor produced?

A

the cytoplasm of the glandular cells of the pancreas

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139
Q

what secretes water and bicarbonate ions from the pancreas?

A

epithelial cells of the ductules and ducts which lead from the acini.

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140
Q

discuss the secretion of bicarbonate ions and water from epithelial cells.

A
  1. CO2 diffuses from the blood into the cell.
  2. carbonic anhydrase combines water and CO2 to form carbonic acid
  3. carbonic acid dissociates into bicarbonate ions and H+
  4. More HCo3- ions diffuse into the cell via cotransport with Na+
  5. bicarbonate ions leave cell on luminal border via secondary active transport with chloride ions
  6. chloride ions reenter the cell via CFTR channels
  7. H+ ions are actively exchanged with na+ on the basolateral side of the cell. K+/ H+ ATPase are also used.
  8. Na+ ions diffuse from blood to negative voltage lumen via tight junctions between cells as well
  9. Bicarbonate and sodium ions create an osmotic gradient for water to diffuse paracellular and transcellular.
  10. Isosmotic bicarbonate environment in the lumen forms
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141
Q

pancreatic amylase and lipase are active in the acinar cells true or false?

A

TRUE!

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142
Q

What are the three hormones responsible for stimulating pancreatic secretion

A
  1. Acetylcholine, which is released from the parasympathetic vagus nerve endings and from other cholinergic nerves in the enteric nervous system
  2. Cholecystokinin (CCK), which is secreted by the duodenal and upper jejunal mucosa when food enters the small intestine
  3. Secretin, which is also secreted by the duodenal and jejunal mucosa when highly acidic food enters the small intestine
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143
Q

What is the main difference between acetylcholine and CCK vs secretin?

A

Acetylcholine and CCK stimulate the release of pancreatic enzymes

secretin stimulates the release of water and electrolytes which are required to move the enzymes into the duodenum

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144
Q

What are the three phases of a pancreatic secretion called?

A
  1. cephalic
  2. gastric
  3. intestinal
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145
Q

What happens in the cephalic stage?

A

20 % of pancreatic enzymes are secreted due to acetylcholine after vagal stimulation (mainly acinar cells)

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146
Q

What happens in the gastric stage?

A

5-10% of pancreatic enzymes are secreted due to gastric distention. Caused by a vagovagal reflex. (acinar and duct cells)

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147
Q

What happens in the intestinal phase?

A

Secretin
chyme enters the duodenum. Secretin is released which stimulates the release of pancreatic juice. It is released in response to HCL in chyme

The sodium bicarbonate neutralises the HCL in the chyme to form NaCl and H2Co3 ( carbonic acid). The carbonic acid immediately dissociates with the co2 being expelled via the lungs. Thus raising the pH in the duodenum.

CCK
Chyme enters the duodenum. it is secreted in response to fatty acids and proteins

This stimulates the release of pancreatic enzymes in the acinar cells.

This results in the digestion of the fatty acids and proteins

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148
Q

Which cells secrete insulin in the pancreas?

A

beta cells

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149
Q

Which cells secrete glucagon in the pancreas?

A

alpha cells

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150
Q

which cells secrete somatostatin in the pancreas?

A

D cells

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151
Q

What is the role of the sphincter of oddi?

A

to control the secretion of pancreatic juice and bile

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152
Q

What is the role of the liver?

A

Metabolism

  1. Carbohydrate metabolism
  2. Fat metabolism
  3. Protein metabolism
  4. Hormonal metabolism

Exocrine function

  1. Storage
  2. secretion of bile
  3. synthesis of protein
  4. Detoxification
  5. Protection
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153
Q

Give examples of carbohydrate metabolism in the liver

A
  1. gluconeogenesis – to produce glucose from amino acids
  2. glycolysis – to form pyruvate thence lactate (anaerobic conditions), or acetyl-coA (aerobic conditions)
  3. glycogenesis – to store polymerised glucose, as glycogen
  4. glycogenolysis – to release glucose, as required
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154
Q

Give examples of fat metabolism in the liver.

A
  1. processing of chylomicron remnants
  2. synthesis of lipoproteins (e.g. VLDLs, HDLs; for export) and cholesterol (for steroid hormone and bile acid synthesis)
  3. ketogenesis (in starvation) – important for neuronal function
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155
Q

Give examples of protein metabolism in the liver.

A
  1. synthesis of plasma proteins
  2. transamination and deamination of amino acids
  3. conversion of ammonia to urea
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156
Q

Give examples of hormonal metabolism in the liver

A
Inactivation of:
insulin
glucagon
anti-diuretic hormone (ADH, vasopressin)
steroid hormones

Activation of:

Thyroid hormone: Thyroxine to triiodothyronine

Vitamin D to conversion of vitamin D to 25-hydroxyvitamin D2 (calcifediol) – further activation to 1,25-dihydroxyvitamin D3 occur s in kidney

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157
Q

Give examples of molecules stored by the liver.

A
  1. Glycogen
  2. Water soluble vitamins: A,D,E and K.
  3. Fat soluble vitamins: B12
  4. Iron and copper.
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158
Q

What cells store vitamin A in the liver?

A

ito cells

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159
Q

What cells store vitamins D,E and K in the liver?

A

Hepatocytes

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160
Q

What proteins are synthesised in the liver?

A
  1. Albumin
  2. complement proteins
  3. apolipoproteins
  4. carrier proteins
  5. coagulation factors II, VII, IX and X
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161
Q

How does the liver help in protecting the body?

A
  1. Detoxification of ethanol and drugs
  2. contains Kupfer cells
  3. Acts as a blood resevoir
  4. produce host defense proteins
  5. Maintains blood glucose concentration

Hypoglycemia=neuroglycopenia

Hyperglycemia= diabetes mellitus

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162
Q

What is bile made out of?

A
  1. Bile salts
  2. bile pigments
  3. Cholesterol
  4. Lecithin
  5. mucus
  6. Bilirubin
  7. IgA
  8. Water
  9. electrolytes
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163
Q

What does the bile acid- dependent fraction consist of?

A
  1. Bile salts
  2. bile pigments
  3. Cholesterol
  4. Lecithin
  5. mucus
  6. Bilirubin
  7. IgA
164
Q

What does the bile acid- independent fraction consist of ?

A

water and electrolytes

165
Q

Where is the bile acid-dependent fraction secreted?

A

Hepatocytes

166
Q

Where is the bile acid- independent fraction secreted from?

A

cholangiocytes-epithelial cells lining the bile duct

167
Q

What causes the hepatic acute phase response?

A

Inflammation which causes the release of interleukin 6

168
Q

What occurs during the hepatic acute phase response?

A

Synthesis of host defense proteins

reduces albumin synthesis

169
Q

Give examples of acute defense proteins.

A
  1. CRP
  2. serum amyloid A
  3. secretory phospholipase A2
170
Q

What is the role of bile?

A
  1. Emulsify and break down fats
  2. Used in absorption of fats
  3. bile serves as a means for excretion of several important waste products from the blood e.g. bilirubin and excess cholesterol
171
Q

What is the role of the gallbladder?

A

stores bile

172
Q

How can the gallbladder hold up to 450 millilitres despite having a volume of only 30-60 ml?

A

As it can absorb the water and the electrolytes into its mucosa thereby storing the rest of the bile components?

173
Q

How does the gall bladder absorb the electrolytes and water?

A

Most of this gallbladder absorption is caused by active transport of sodium through the gallbladder epithelium, and this transport is followed by secondary absorption of chloride ions, water, and most other diffusible constituents.

174
Q

How does this effect the bile concentration in comparison to hepatic bile?

A

this makes bile salts , bilirubin ,cholesterol and lecithin more concentrated

175
Q

What is the role of cck for bile secretion?

A
  1. Opening of the sphincter of oddi

2. Gall bladder contraction.

176
Q

What causes gall bladder contractions?

A
  1. CCK

2. Vagal stimulation

177
Q

What is the role of secretin on bile secretion?

A

Increases the secretion of bile acid-independent fraction of bile

178
Q

Why is it useful that bile is alkaline?

A

Neutralises chyme

protects duodenum mucosa

acts as a pH adjustment for digestive enzymes.

179
Q

Discuss how cholesterol forms into bile salts.

A

The cholesterol is first converted to cholic acid or chenodeoxycholic acid via hepatocytes. These acids in turn combine principally with glycine and to a lesser extent with taurine to form glyco- and tauro-conjugated bile acids.

180
Q

What is the function of bile salts?

A
  1. acts as emulsifier for fat gobules

2. Form micelles in lipids which allow them to be absorbed in the mucosa

181
Q

Discuss the process of enterohepatic circulation.

A
  1. Bile salts either are absorbed in the duodenum by diffusion. Or absorbed in the distal ileum via active transport
  2. a small fraction of bile salts are broken down by intestinal bacteria in the lumen into secondary bile acids. Secondary bile acids once in the liver conjugate with glycine or taurine to form bile salts
  3. Carried by portal vein to liver
  4. 5% of bile is lost in feces however this is made up by the the synthesis of bile via hepatic cholesterol
182
Q

What are the two main lipoproteins exported from the liver?

A
  1. Very low density lipoproteins (VLDL)

2. high density lipoproteins ( HDL)

183
Q

Give examples of resin agents.

A

Colveselam, colestipol, colestyramine

184
Q

What are the benefits of resin agents?

A

Bind to bile acids preventing their reabsorption.

This increases hepatic cholesterol synthesis which is required to turn bile acids into salts

Thus reducing amount of lower plasma LDL cholesterol which is being used up . Decreasing risk of atherosclerosis.

185
Q

What are the benefits of lower plasma LDL cholesterol in the blood?

A

indirectly:
1. promote hepatic conversion of cholesterol to bile acids

  1. increase cell surface expression of LDL-receptor in hepatocytes
  2. increase clearance of LDL-cholesterol from plasma
186
Q

Why are statins effective against hypercholesterolaemia?

A

Inhibits HMG-CoA reductase which is a rate limiting enzyme in cholesterol synthesis.

This in turns reduces cholesterol synthesis and increases LDL receptors thus lowering LDL plasma concentrations

187
Q

What is the role of drug metabolism?

A
  1. Convert parent drugs into more polar metabolites- facilitates excretion and prevents reabsorption in the kidneys
  2. Convert drugs to metabolites that are usually pharmacological less active than the parent compound.
188
Q

What occurs in phase 1 of drug metabolism?

A
  1. Hydrolysis
  2. oxidation
  3. reduction

These all make drugs more polar allowing for conjugation

189
Q

What occurs in phase 2 of drug metabolism

A

Conjugation- enzymes covalently link drugs with water-soluble moieties e.g. glucuronate,sulphate or alkyl group.

Makes them more water soluble and easier to excrete

190
Q

What are the two main types of digestion in the small intestine?

A

Luminal digestion

Membrane digestion

191
Q

What occurs in luminal digestion?

A

pancreatic enzymes break down large particles into smaller ones in the duodenum

192
Q

What occurs in membrane digestion?

A

enzymes situated at the brush border of the enterocytes break down particles to be absorbed

193
Q

How do humans store glucose as?

A

glycogen

194
Q

What is sucrose made out of?

A

Glucose and fructose via alpha 1,2 linkage

195
Q

What is lactose made of?

A

Glucose and galacatose via beta 1,2 linkages

196
Q

What is the difference between amylopectin and glycogen?

A
  1. Amylopectin is used as storage in plants while glycogen is for animals
  2. Glycogen is more branched
197
Q

What type of enzymes hydrolyse polysaccharides?

A

alpha-amylase

198
Q

Where are the two types of alpha amylase used in breaking down polysaccharides?

A
  1. Salivary glands amylase

2. pancreatic amylase

199
Q

What are the products of hydrolysis of starch with alpha amylase?

A

produces mainly linear gluocse ogliomers
1. Maltose (mainly)

  1. Maltotriose
  2. limit dextrins

Lactose and sucrose will present in the diet but not broken down by amylase

200
Q

What stops salivary amylase from continuing the break down of starch in the stomach?

A

pH below 4.0 makes amylase inactive.

201
Q

Why do we have pancreatic amylase?

A

Not all of the starch has been hydrolysed into maltose due to the salivary amylase being inactive in the stomach.

Need to convert starch into ogliosaccharides for membrane digestion.

202
Q

Why can alpha amylase not produce glucose from polysaccharides?

A
  1. cannot break down terminal alpha 1,4 linkages only internal ones
203
Q

Why are alpha limit dextrins a product of hydrolysis by alpha amylase?

A
  1. Because it cannot break down alpha 1,6 linkages at branch point
  2. cannot break down 1,4 linkages adjacent to these branch points
204
Q

What are the ogliosaccharidases?

A
  1. lactase
  2. sucrase
  3. maltase
  4. isomalatase (alpha dextrinase)
205
Q

where are ogliosaccharidases produced and where are they found ?

A

Produced by enterocytes and are found in the brush border of the mucosa of the small intestine

206
Q

What is the co transporter involved in the absorption of Glucose and galactose in the duodenum and jejunum?

A

SGLT1 - sodium-glucose co- transporter

207
Q

What transporter is required for the absorption of fructose?

A

GLUT5

208
Q

what is the difference between the the absorption of glucose/galactose and fructose?

A
  1. SGLT1 is a co transporter while GLUT5 isnt

2. Glucose and galactose enter via secondary active transport while fructose enters via facilitated diffusion

209
Q

Describe the process of the absorption of monosaccharides.

A
  1. Basolateral Na+/k+ pump actively removes 3 sodium ions from the enterocyte
  2. creates a concentration gradient for sodium which enters via SGLT1 with glucose and galacatose in the apical membrane
  3. Fructose enters in enterocyte due to already high concentration in the lumen
  4. Conc gradient allows for all three forms to diffuse into blood via GLUT 2
210
Q

What transporter is used in the facilitated diffusion of the monosaccharides on the basolateral side of the enterocytes?

A

GLUT2

211
Q

What is the optimum pH for pepsin?

A

1.8-3.5

212
Q

What are the differences between endopeptidases and exopeptidases

A

endopeptidases cleave at non terminal bonds

exopeptidases cleave at terminal bonds

213
Q

Give examples of endopeptidases

A
  1. pepsin
  2. Trypsin
  3. chymotrypsin
  4. elastase
214
Q

Give examples of exopeptidases

A
  1. Procarboxypeptidase A

2. Procarboxypeptidase B

215
Q

What are the products of a endopeptidase reaction?

A

ogliopeptides

216
Q

What are the products of a exopeptidase reaction?

A

amino acids and ogliopeptides

217
Q

What bond is broken between proteins during hydrolysis? (primary structure)

A

peptide bonds

218
Q

What is the role of enterokinase?

A

To activate tryspinogen

219
Q

what are the main forms of peptides which enter the duodenum and the brush border?

A

tri and dipeptides

220
Q

What does pepsin convert proteins into ?

A
  1. polypeptides
  2. proteoses
  3. peptones
221
Q

What are the two types of enzymes found in the brush border?

A
  1. Aminopolypeptidase

2. dipeptidases

222
Q

what do are the role of the brush border peptidases>?

A

convert few remaining polypeptides to tri and dipeptides

223
Q

What is the role of cytoplasmic peptidases?

A

convert the di and tri peptides intosingle amino acids

224
Q

where are the cytoplasmic peptidases found?

A

in the cytoplasm of the enterocyte

225
Q

Discuss the amino acid absorption at the brush borders.

A
  1. 5 different Na+ dependent co transporters - neutral, aromatic, imino, positively and negatively charged amino acids
  2. 2 different Na+ sodium independent co transporters
226
Q

Give example of a na+ dependent transporter at the brush border.

A

SLCA19 - used for neutral amino acid

227
Q

Give example of Na+ independent transporter at brush border?

A

SLC7A(- ussed for cationic aminoacids

228
Q

Discuss the amino acid absorption at the basolateral membrane of the enterocyte.

A

3 mediate efflux of amino acids- Na+ independent

2 mediate influx - Na+ dependent - enterocytes need amino acids !

net movement is bidirectional

229
Q

Discuss the ogliopeptides absorption at bush border.

A

H+ dependent pathways using the transporter e.g. PepT1 and SLC15A

They are then hyrdolysed into amino acids

230
Q

what bond is broken between polysaccharides during hydrolysis?

A

glycosidic bonds

231
Q

What is the name given to the lymphatic channel which are found in the villi?

A

lacteal

232
Q

What promotes emulsification in the GI tract?

A
  1. Chewing ( not that important)
  2. gastric churning
  3. peristalsis and segmentation
233
Q

What is a saturated fatty acid?

A

Fatty acid with only single carbon bonds

234
Q

What is an unsaturated fatty acid?

A

Fatty acid with at least one double carbon bond

1 double carbon bond = monounsaturated

2 or more = polyunsaturated

235
Q

What is the methyl end of a fatty acid called?

A

omega end.

This is used to distinguish where the double bond is in the fatty acid in relation to the methyl end e.g. omega 3

236
Q

Give examples of amphiphilic molecules

A

biliary phospholipids (lecithin)
cholesterol
bile salts

237
Q

What are the roles of amphilphilic molecules?

A

Form emulsion droplets which help break down dietary lipids by increasing the surfarce area to volume ratio

238
Q

What is gastric lipase secreted in response to?

A

gastrin

239
Q

Where does gastric lipase break triglycerides into?

A

Diglyceride and free fatty acid

240
Q

What is the importance of the free fatty acid?

A

Stimulates the release of CCK which stimulates the production of pancreatic lipase

241
Q

What position does gastric lipase normally break down triglycerides?

A

At position 3

242
Q

What environment is required for pancreatic lipase to act at their most optimum activity?

A
  1. Colipase co-factor
  2. Alkaline pH
  3. Ca2+
  4. Bile salts
  5. fatty acids
243
Q

What points do pancreatic lipase mainly hydrolyse triglycerides at?

A

position 1 and 3

244
Q

Give examples of dietary lipids

A
  1. Triglycerides
  2. phospholipds
  3. Cholesterol and cholesterol esters
  4. free fatty acids
245
Q

What type of fatty acids are absorbed in the stomach?

A

short and medium fatty acids

246
Q

What lipase are present in the stomach.

A

gastric lipase

lingual lipase

247
Q

What are the primary products of hydrolysis of triglycerides by pancreatic lipase?

A
  1. Fatty acids

2. 2-monoglycerides

248
Q

What is the role of bile salts?

A

Form mixed miscelles

249
Q

What is the role of colipase?

A

Allow lipase to bind to the triglycerides which the bile salts blocked.

250
Q

What is the inactive form colipase

A

procolipase

251
Q

What activates procolipase?

A

trypsin

252
Q

Discuss the formation of mixed micelles.

A

Triglycerides on the surface of the emulsion droplets are broken down into their products.

These emulsion droplets reduce in size as these lipids are broken down.

the final products are the micelles

253
Q

which enzyme hydrolyse cholesterol ester?

A

Cholesterol ester hydrolase

254
Q

Which enzyme hydrolyse phospholipids?

A

phospholipase A2

255
Q

what are the digested lipids which enter the enterocytes?

A
  1. Fatty acids
  2. monoglycerides
  3. cholesterol
256
Q

How do digested lipids enter the enterocytes?

A
  1. passive diffusion

2. facilitated diffusion via fatty acid translocases, fatty acid bind proteins and fatty acid-transport proteins

257
Q

Discuss the difference in lipid absorption between short /medium chained fatty acids and long chained fatty acids.

A

short/medium chain diffused into cytoplasm of enterocyte and then straight into the villus capillaries via basolateral end

Long chain

Long chain are re-esterified to triglycerides and then complexed with apolipoproteins in the endoplasmic reticulumv to form chylomicrons

Chylomicrons then enter the lacteal (lymph system)

258
Q

Discuss how cholesterol is absorbed.

A

Endocytosis in clatherin coated pits by NPC1L1 protein

259
Q

Discuss the pathways the different for Calcium ions to be absorbed

A
  1. Acitve transport in the duodenum (transcellular)

2. diffusion whole of small intestine ( paracellular)

260
Q

Where are parathyroid hormones released from?

A

parathyroid glands

261
Q

what is the role of parathyroid hormones?

A

Activates Vitamin D

262
Q

What is the role of vitamin D in regards to absorption of Ca2+?

A

Stimulates the synthesis of calcium binding and transporting in the enterocytes e.g. calblindin and intestinal membrane calcium-binding protein

263
Q

Give examples of dietary iron

A
  1. Fe 3+
  2. Haem
  3. inorganic iron
  4. Ferratin
264
Q

Where is haem absorbed?

A

duodenum

265
Q

What is the role of vitamin C in regards to Ferric iron (3+)

A

Acts as a reducing agent to Reduce Fe3+ to Fe2+

266
Q

Where is gastroferrin secreted from?

A

gastric parietal cells.

267
Q

What is the role of gastroferrin?

A

Binds to Fe2+ prevents it binding to anions thus allowing it to be absorbed.

268
Q

Give other examples of molecules trying to promote reduction of Fe3+ to Fe2+

A
  1. HCl within the stomach

2. a ferric reductase, duodenal cytochrome B (Dctyb), present on the brush border membrane of enterocytes

269
Q

Why is Fe2+ important

A

Ferric (3+) cannot be absorbed only ferrous (2+) can

270
Q

What transport protein is involved in the absoprtion of Fe2+ in the enterocytes?

A

DMT- Divalent metal transporter . This couples Fe2+ with H+

271
Q

How is haem absorbed?

A

uncertain mechanism.

However either Haem carrier protein 1 (aka SLC48A1), or endocytosis )

272
Q

Discuss how iron can be stored in enterocytes.

A
  1. Fe 2+ is oxidised to Fe3+ in the cytoplasm

2. Binds to apoferratin to form ferratin

273
Q

What happens once haem enters the enterocytes?

A

degraded by haem oxidase to form Fe2+

Biliverdin is also formed

274
Q

What channel proteins are responsible for the efflux of Iron from enterocytes?

A

Mobilferrin which carried Fe2+ in cell to ferroportin

275
Q

What is the role of Hephaestin?

A

Oxidises Fe2+ to Fe3+ at the basolateral surface of the enterocytes

276
Q

What occurs to Fe3+ once it is circulating in the blood?

A

Binds with apotransferrin to form transferrin.

277
Q

What increases DMT expression?

A

blood loss

278
Q

What decreases DMT expression?

A

HFE protein

Excess body iron stores

279
Q

What is the role of hepcidin?

A

Binds to ferroportin

released from liver when body iron levels are high) – major control on iron absorption

280
Q

What is haptocorin?

A

It is a type of transcobalamin which binds to vitamin b12 in the stomach

It is secreted in the saliva

Pancreatic proteases break it down in the duodenum

Intrinsic factor then binds to Vitamin B12

281
Q

What is Vitamin b12 present in?

A

meat,eggs ,milk- watch out vegans

282
Q

What is Vitamin B12 used for?

A

methylation reactions

283
Q

Where is folic acid absorbed?

A

jejunum

284
Q

What is the role of folic acid?

A

methylation reactions

285
Q

List fat soluble vitamins

A

A,D,E,K

286
Q

List water soluble vitamins

A

B (not b12)
C
H

287
Q

What do fat soluble vitamins rely on to be absorbed?

A

an adequate bile slat secretion and intact small intestinal mucosa

288
Q

What is the function of vitamin A?

A

Critically important for vision

289
Q

What is the function of Vitamin D?

A

Calcium homeostasis and bone formation

290
Q

What is the function of E?

A

antitoxidant

291
Q

What is the function of K?

A

required for post-translational modification

292
Q

where is Vitamin A stored in the liver?

A

ito cells

293
Q

Where is Vitamin D and K stored in the liver?

A

Hepatocytes

294
Q

What is the difference between the absorption of fat soluble vitamins and water soluble vitamins?

A

Fat soluble

Incorporated into mixed micelles
Usually passively transported into enterocytes
Incorporated into chylomicrons, or VLDLs
Distributed by intestinal lymphatics

Water soluble

Transport processes in the apical membrane are similar to those described for monosaccharides, amino acids and di- and tri-peptides. May be either Na+-dependent, or Na+-independent

295
Q

What is the function of copper?

A

essential co factor for oxidative enzymes

296
Q

Where is copper stored?

A

In the liver bound to copper-binding proteins

297
Q

What happens to excess copper?

A

excreted in bile

298
Q

What is the role of zinc?

A

a co factor for many enzymes and transcription factors

299
Q

What causes the opening fo the ileocaecal vale?

A

distention of the terminal ileum

300
Q

What causes the closing of the ileocaecal valve?

A

distention of the caecum

301
Q

What is the proximal colon sometimes refered to as?

A

the absorbing colon

302
Q

What is the distal colon sometimes refered to as?

A

the storage colon

303
Q

What are the main roles of the large intestine?

A
  1. absorption of water and electrolytes
  2. absorption of fatty acids
  3. storage of colonic contents
  4. periodic elimination of faeces
304
Q

Which cells are responsible for the absorption of water and electrolytes in the large intestine?

A

colonocytes

305
Q

Discuss how water and electrolytes are absorbed in large intestine

A
  1. Atpase at basolateral surface actively switches 2 K+ for 3 Na+
  2. Removal of Na+ creates conc gradient which causes Na+ to diffuse into cell similar to small intestine methods
  3. efflux of Hco3- occurs at apical membrane which swaps it with chloride ions to maintain net charge
  4. Also increases osmosity gradient for h20 to diffuse into cell and then into blood supply
306
Q

What is the role of bicarbonate ions in the lumen?

A

The bicarbonate helps neutralize the acidic end products of bacterial action in the large intestine

307
Q

What are the roles of the large intestine goblet cells?

A

secrete:

copious mucus containing glycosaminoglycans – hydrated to form a slippery surface gel

trefoil proteins involved in host defence

308
Q

what are the effects of aldosterone on the large intestine?

A

aldosterone greatly enhances sodium transport capability ( increase sodium conc gradient)

309
Q

What are the forms of movement in the large intestine?

A
  1. Mixing ( haustration)
  2. propulsion ( mass movements)
  3. defaecation
310
Q

Discuss what occurs in haustration.

A

Haustra are saccules which form. The shunting of these saccules is called haustra shunting. This increases the exposure of chyme to the mucosa increasing absorption of electrolytes and water.

311
Q

What causes mass movement to occur?

A

gastrocolic and duodenocolic reflexes. Via Extrinsic autonomic nerves

These reflexes result from distention of the stomach and duodenum after a meal

312
Q

Discuss what occurs in mass movement

A
  1. constrictive ring occurs in response to a distended or irritated point in the colon
  2. Then, rapidly, the 20 or more centimeters of colon distal to the constrictive ring lose their haustrations and instead contract as a unit, propelling the fecal material in this segment en masse further down the colon

pushes stool to rectum

313
Q

What are the differences between the internal anal sphincter and the external anal sphincter?

A

Internal sphincter-circular smooth muscle and is involuntary

External sphincter- striated smooth muscle and is voluntary

314
Q

which nerve supplies the external anal sphincter?

A

pudendal nerve

315
Q

What triggers defecation?

A

Distention of the rectal wall which is triggered by faecal matter in the rectum

316
Q

What is the role of the intrinsic myenteric defecation reflex?

A

after distention of rectum, afferent signals sent to myenteric plexus (ENS)

efferent signals sent to sigmoid colon to increase peristaltic waves and increase pressure in rectum

relaxes internal anal sphincter

317
Q

What is the role of the parasympathetic defecation reflex?

A

Afferent signals sent to SPINAL CHORD

greatly increase the peristaltic waves in the colon. help intirinsic myenteric defecation reflex

Also relax internal anal sphincter

318
Q

Which nerves are involved in the parasympathetic defecation reflex?

A

Pelvic nerves

319
Q

What occurs if the there is prolonged distention of the rectum?

A

Reverse peristalsis

320
Q

What other physiological effects occur when the defecation signals enter the spinal chords?

A
  1. Deep breath
  2. contraction of abdominal muscles
  3. closure of glottis
  4. pelvic floor to relax and pull outward on the anal ring
321
Q

What are the benefits of Gut microflora?

A

Involved in
1. synthesis of vitamin K and B12

  1. synthesis of thiamine and riboflavin
  2. Breakdown of primary to secondary bile acids
  3. conversion of bilirubin to non-pigmented metabolites
  4. activate some drugs
  5. maintain mucosal integrity
  6. Intestinal immunity by competition with pathogenic microbes
322
Q

What is flatus?

A

intestinal gas

323
Q

What is eructation?

A

burping

324
Q

What happens to intestinal gas?

A

Either absorbed in the large intestine or expelled through the anus

325
Q

where is the myenteric plexus?

A

Between the circular and longitudinal layers of the intestine

326
Q

Where is the submucosal plexus?

A

lies in the submucosa

327
Q

Give examples of when the myenteric plexus is used for an inhibitory effect.

A

Sphincters muscles can be relaxed allowing food/chyme to move into the next stage of the GI tract

328
Q

Give examples of ENS neurotransmitters.

A
  1. Acetylcholine
  2. Noradrenaline
  3. ATP
  4. serotonnin
  5. CCK
  6. somatostatin
  7. Dopamine
329
Q

What do voluntary nerves control in the GI tract?

A
  1. Lips
  2. Tongue
  3. muscles of mastication
  4. pelvic floor muscles
  5. external anal sphincter
330
Q

Where do cranial parasympathetic nerve fibres control?

A

Foregut and mid-gut structures

331
Q

What do the sacral parasympathetic nerve fibres control

A

distal half of the large intestine and all the way to the anus

332
Q

Where does the sacral parasympathetic nerve fibres originate from?

A

second, third, and fourth sacral segments of the spinal cord

333
Q

Where are postganglionic neurons of the GI parasympathetic system normally found?

A

in the intrinsic plexuses

334
Q

Where do the sympathetic fibres to the GI tract originate from?

A

between T5 and L2 of the spinal chords

335
Q

What does stimulation of the sympathetic fibres normally cause in the GI tract?

A

Inhibits Gi tract activity

336
Q

What are the main ways sympathetic fibres inhibit GI tract activity?

A
  1. Inhibit smooth muscle due to secretion of noradrenaline

2. Inhibit the neurons of the entire ENS

337
Q

What are the main examples which cause stimulation of sensory afferent nerves?

A
  1. irritation of gut mucosa
  2. excessive distention of the gut
  3. Presence of specific chemicals in gut
338
Q

What transmitters do afferent nerves use?

A

Substance P and CGRP

339
Q

Where do visceral afferents send signals to?

A

Hypothalamas

340
Q

What is the main role of parasympathetic activity in the GI tract?

A

Stimulates ENS

341
Q

What does the innate defense of the GI tract include?

A
  1. Constant movement of intestinal products
  2. pH and chemical composition of intestinal secretion ( e.g. Stomach acid and bile salts)
  3. Antibacterial enzymes and peptides
  4. Mucins- form a tough slippery mucous gel
  5. Paneth cells
  6. Mast cell,s eosinophils, neutrophils,macrophages and dendritic cells in the lamina propria
342
Q

What does the adaptive immune system of GI tract include?

A
  1. Lamina propria lymphocytes
  2. Intra-epithelial lympthocytes
  3. Peyer’s patches
  4. Tonsils
343
Q

What do paneth cells secrete?

A

defensins

344
Q

Where are paneth cells found?

A

small intestine ( not in large)

345
Q

What does saliva contain which can be used in the mucosal immune system?

A

Contain lysozyme

346
Q

Where are intra-epithelial lymphocytes found?

A

predominantly in the small intestine.

347
Q

What makes intra-epithelial T lympthocytes different to other lympthocytes?

A
  1. Resident in their position and don’t migrate
  2. express different T cell receptor
  3. React to lipid antigens present on CD1 cell surface molecule rather than peptide MHC class I or II molecules
  4. special role responding to proteolipid antigens in bacterial cell membranes
348
Q

Where are peyer’s patches found?

A

Predominantly in the terminal ileum ( not large intestine)

349
Q

What do peyer’s patches contain?

A
macrophages
dendritic cells
intra-epithelial lymphocytes
effector T cells
IgA secreting plasma cells
innate lymphoid cells
stromal cells (eg fibroblasts)
350
Q

What makes up the epithelial lining of Peyer’s patches?

A

M cells

enterocytes

351
Q

What does the specialised dome epithelium of the peyer’s patches not contain?

A

Villi and crypts

352
Q

Why are M cells specialised?

A

contain no Microvilli but membranous folds which enclose lymphocytes, macrophages and dendritic cells.

353
Q

What is the function of M cells?

A

transport intact peptides,viruses and bacteria across epithelium via endo and exocytosis and release them via the basolateral membrane where the antigens are detected by dendritic cells

354
Q

Where are Tonsils found?

A

Opening of hypopharynx

Stomach

colon

appendix

355
Q

Why must the immune system not react to food antigens?

A
  1. Allergies

2. Hypersensitivity

356
Q

what is the usual hypersensitivity response to food?

A
vomiting
diarrhoea
pruitis
urticaria
anaphylaxis (rarely)
357
Q

apart from in peyers patches, how else can antigen presentation in the gut occur?

ii. which cells are used in this?

A

directly across epithelium

ii. dendritic cells

358
Q

What occurs in Mucosal homing?

A
  1. T cells enter Peyers patches- directed in blood vessels by L selectin and CCR7
  2. Become activated by dendritic cells in peyers patches
  3. T cells now get drained via mesenteric lymph nodes and return to thoracic gut. Re enter bloodstream to the GI tract
  4. Activated T lymphocytes express Α4β7 and CCR9 home to the lamina propria and intestinal epithelium
  5. MADCAM-1 binds to the activated T lymphocytes on the endothelium of the blood vessel
  6. Gut epithelial cells release chemokines for gut homing T lymphocytes to bind to in the lamina propria
359
Q

What mediates mucosal homing?

A

Addressins interact with receptors on the blood vessels in the GI tract

360
Q

once a T cell has become activated by dendritic cells from peyers patches what integrin becomes expressed?

A

Α4β7

361
Q

What is the function of Α4β7 integrin molecule ?

A

binds MadCAM-1 ( addressin molecule)

362
Q

once a T cell has become activated by dendritic cells from peyers patches what chemokine becomes expressed?

A

CCR9

363
Q

What ligand is used for CCR9?

A

CCL25 - increases higher affinity by causing a conformational change

364
Q

What do two IgA molecules form?

A

polymeric IgA

365
Q

what forms when a pIgA binds to a secretor component?

A

Secretory dimeric immunoglobulin A

366
Q

What is the role of sIgA?

A

primarily acts by blockading epithelial receptors (e.g. by binding their ligands on pathogens), by sterically hindering attachment to epithelial cells, and by immune exclusion

Basically bind and neutralise antigens and toxins

367
Q

Where are IgA produced?

A

Plasma cells

368
Q

What joins to form an immunoglobulin dimer?

A

J chain

369
Q

How does sIgA get released from the mucosa?

A

crosses the cytoplasm (transcytosis) of the enterocyte and then released at the apical surface by proteolytic cleavage of the secretory component.

370
Q

How do sIgA enter the enterocyte?

A

endocytosis

371
Q

intraepithelial lympthocytes are CD8 positive true or false?

A

true

372
Q

What is the difference between humoral intestinal response and systemic humoral response?

A

Opposite in proportion of the different types of immunoglobulins produced

Intestine

80% IgA

15% IgM

5% IgG

systemic

80% IgG

15% IgM

5% IgA

373
Q

What does the lamina propria consist of in regards to the immune system? Not peyers patches

A
  1. Mast cells
  2. CD4 T cells
  3. mast cell
  4. dendritic cell
  5. Immunoglobulin A
  6. Plasma cells
374
Q

What does the epithelium of the intestine contain in regards to the immune system? Not peyers patches

A
  1. CD8 T lymphocyte (IEL)

2. Dendritic cells

375
Q

What happens when a mucosal intestinal epithelial cell becomes infected?

A

Displays viral peptide to CD8 Intra epithelial lymphocyte via MHC class 1

CD8 T Lymphocycte then kills cell via perforin and fas dependent pathway

376
Q

What do enterocytes produce when infected?

A

Express MIC-A and MIC-B

377
Q

What does an Intra epithelial cell bind MIC-A and MIC-B to?

A

NKG2D

378
Q

what type of spontaneous electrical activity occurs in the stomach, small intestine and large intestine?

A

slow wave

379
Q

what are the pacemaker cells within the stomach, small intestine and large intestine which drive the slow wave electrical activity?

A

interstitial cells of Cajal

380
Q

what has to happen for a slow wave in the stomach, small intestine and large intestine to cause an action potential?

A

slow wave has to meet the threshold

381
Q

what is force of contraction of the smooth muscle within the GI tract related to?

A

the number of action potentials discharged

ie the length of time that the slow wave was above threshold

382
Q

where are interstitial cells of Cajal located?

A
  • between longitudinal and circular muscle layers

- submucosa

383
Q

when does slow wave activity in the GI tract generally remain in the background and not reach thresholds?

A

between meals

384
Q

what is the basic electrical rhythm (BER) of the GI tract determined by?

A

slow waves

385
Q

what are the factors which determine whether a slow wave amplitude reaches threshold/for how long it remains above threshold?

A

neuronal stimuli
hormonal stimuli
mechanical stimuli

386
Q

using basic electrical rhythm (BER), explain why chyme moves from oral to aboral direction within the small intestine?

A

higher BER in the duodenum than the terminal ileum

more vigorous mechanical activity proximally pushes food distally in the small intestine

387
Q

using the basic electrical rhythm (BER), explain why the colon is able to hold contents for a long period of time?

A

higher BER in the distal colon than the proximal colon

more vigorous actiivty distally favours retention of luminal contents

388
Q

what neurones is the enteric nervous system made of?

A

sensory neurones
interneurones
effector neurones

389
Q

what inhibitory influences does parasympathetic supply to the GI tract have?

A

relaxation of some sphincters

receptive relaxation of stomach

390
Q

what excitatory influences does parasympathetic supply to GI tract have?

A

increases secretions
increases blood flow
generally increases smooth muscle contraction

391
Q

what inhibitory influences does the sympathetic supply to the GI tract have?

A

decreased motility
decreased secretions
decreased blood flow

392
Q

What is the role of the spleen?

A
  1. Breaks down RBCs - produces bilirubin
  2. Site for lymphocyte proliferation
  3. breaks down platelets
  4. recycles iron and globin
393
Q

Which part of the duodenum does the pancreatic juices and bile drain into?

A

2nd part

394
Q

What is the role of the hepatic portal vein?

A

Drains venous blood from absorptive parts of the GI tract and associated organs to the liver for cleaning

395
Q

what are the main properties of collateral veins in portal-systemic anastomoses?

A
  1. No valves
  2. blood flows either into systemic or portal system
  3. Very little blood flows within these veins
396
Q

what is the role of the ampulla of the rectum?

A

holds and accumulates fecal matter.

397
Q

What is the role of the levator ani muscles?

A

supports pelvic organs- tonically contracted most of the time.

Relax to allow defecation and urination ( pelvic diaphragm descends)

398
Q

Whats causes levator ani to actively contract?

A

Increase in intra abdominal pressure - caused by contraction of abdominal muscles and thoracic diaphragm (coughing/sneezing)

399
Q

What does contraction of the puborectalis muscle of the levator ani muscle do?

A

decreases the anorectal angle- acts like a sphincter to maintain continence

400
Q

what stimulates the contraction of the internal sphincter?

A

distention of the rectum ampulla

401
Q

What allows for the external sphincter to voluntarily contract?

A

internal sphincter relaxation

402
Q

what is the normal flora of the mouth?

A

strep viridans

neisseria

candida ( few)

staphylococci

403
Q

What is the normal flora of the stomach/duodenum

A

usually sterile

may have some candida and staphylococci

404
Q

What is the normal flora of the jejenum

A

coliforms - rod shaped aerobic gram negative which majority ferment lactose and live mainly in large bowel

anaerobes- don’t grow in presence of oxygen

405
Q

What is the normal flora of the colon?

A

coliforms ( loads)

anaerobes ( loads)

enterococcus fecalis

406
Q

What is the normal flora of the bile ducts?

A

usualy sterile