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P1: GI > Transport Along and Across the GI Tract > Flashcards

Transport Along and Across the GI Tract Flashcards

1
Q

How does gastric accommodation occur?

A

→ Decrease in cholinergic activity

→ VIP / NO promote accommodation

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2
Q

Where do tonic contractions start from?

A

→ The top of the antrum

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3
Q

What does the stomach do to store food and why?

A

→ The proximal stomach relaxes to store food at low pressure while it is acted on by acid and enzymes mechanically

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4
Q

Why is gastric emptying carefully regulated?

A

→ It ensures adequate acidification/neutralization
→ Action of enzymes, mechanical breakdown
→ avoid swamping the duodenum

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5
Q

What is a disorder of gastric emptying?

A

→ Gastric stasis

gastroparesis

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6
Q

What is gastric emptying dependent on?

A

→ Propulsive force generated by the tonic contractions of the proximal stomach
→ The stomachs ability to differentiate types of meals ingested and their components

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7
Q

What decreases the force and rate of gastric emptying?

A

→ Fatty, hypertonic and acidic chyme in the duodenum

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8
Q

How do liquids pass?

A

→ in spurts

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9
Q

How do solids pass?

A

→ Broken down into 1-2mm sizes

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10
Q

How do large indigestible materials pass?

A

→ Cleared by migrating motor complex

→ or vomiting

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11
Q

How are liquids emptied?

A

→ Rapidly disperse

→ Empty without a lag time

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12
Q

What is the rate of liquid emptying dependent on?

A

→ The rate of emptying is influenced by nutrient content

→ Nutrient rich liquids are retained for longer

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13
Q

How many phases are there in solid emptying?

A

→ 2 phases ( lag time and linear phase)

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14
Q

What is the duration of the lag time related to in solid emptying?

A

→ Duration of the lag time is related to the size of the particle

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15
Q

How are solids emptied?

A

→ Trituration of larger particles to smaller ones
→ Pylorus regulated the passage of material
→ (60 mins for a typical solid-liquid meal)

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16
Q

What is the order of highest gastric motility to lowest?

A

→ carbohydrates > proteins > fatty foods > indigestible solids

Liquefy at body temperature; float on top of liquid layer and empty slowly

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17
Q

What are the determinants of gastric motility?

A

→ Types of food eaten
→ Osmotic pressure of duodenal contents
→ Vagal innervation upon over distension
→Hormones

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18
Q

What hormones inhibit emptying?

A

→ Somatostatin
→ CCK
→ Secretin
→ GIP

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19
Q

What does injury to the intestinal wall and bacterial infections cause?

A

→ Decrease in motility

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20
Q

How does the osmotic pressure of duodenal contents affect gastric motility?

A

→ Hyperosmolar chyme decreases gastric emptying

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21
Q

What is BER?

A

→ Intrinsic basic electrical rhythm

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22
Q

What does BER allow?

A

→ smooth muscle cell to depolarize and contract rhythmically when exposed to hormonal signals

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23
Q

What do the stomach cells produce from resting potential?

A

→ Electrical depolarizations

→ Move ripples towards the antrum

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24
Q

What control is the fundus under?

A

→ Vagal excitatory control

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25
Q

What is an ICC?

A

→ Cajal cells

→ Pacemaker cells in the wall of the stomach, small intestine and large intestine

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26
Q

What produces the BER?

A

→ Regular migrating ripples from the ICC

reduced by sympathetic innervation- NA

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27
Q

What are the depolarizations due to?

A

→ Entry of K+ and Ca2+

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28
Q

What mediates a decrease in fundic motor activity?

A 
→ Cholecystokinin
→ Secretin
→ VIP
→ Somatostatin
→Duodenal distension
→ Gastrin releasing peptide
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29
Q

What increases fundic contractions?

A

→ Motilin

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30
Q

What initiates and maintains peristalsis in the small intestine?

A

→ Hormonal and nervous factors

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31
Q

What decreases activity in the small intestines?

A

→ Secretin

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32
Q

What does antral over distension cause?

A

→ Inhibitory signals

→ Vago- vagal reflex

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33
Q

What does distension of the fundus cause?

A

→ Excitatory effects in the antrum

→ Antrum contracts

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34
Q

What happens during duodenal over distension and chemical stimulation?

A

→ Vago-vagal reflex and hormones

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35
Q

What does the pyloric sphincter contract in response to?

A

→ Antral or duodenal rhythms

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36
Q

What do fatty acids in the duodenum cause?

A

→ Contraction of the pylorus

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37
Q

What promotes the relaxation of the pyloric sphincter when the duodenum has no food in it?

A

→ NO and VIP

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38
Q

What causes the pylorus to relax?

A

→ Descending inhibitory reflex

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39
Q

What are the types of movements in the intestine?

A

→ Segmentation (mixing contractions)
→ Peristalsis propulsive): in stomach (3 waves/min)

→ Migrating Motor Complex
→ Mass movements

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40
Q

What are the phases of motor activity in the small intestine?

A

→ Phase 1 : quiescent/ quiet period
→ Phase 2 : Irregular propulsive contractions
→ Phase 3 : Burst of uninterrupted phasic contractions

41
Q

Where does segmentation originate?

A

→ In the pacemaker cells (ICC)

42
Q

What is segmentation and why is it needed ?

A

→ Divisions and subdivisions of chyme

→ Brings chyme into contact with intestinal walls

43
Q

What does segmentation cause?

A

→ Slow migration of chyme towards the ileum
→Contractions per minute dies down as it approaches the ileum
→allows enzymes to be mixed with the chyme so that digestion can occur
→bring the chyme close to the gut mocosa

44
Q

How long are the contractions in the jejunum/duodenum?

A

→ 10-12 contractions per min

45
Q

How long are the contractions in the ileum?

A

→ 8-9 contractions per min

46
Q

What is peristalsis?

A

→ The propagating contraction of successive sections of circular smooth muscle preceded by relaxation/dilatation

47
Q

What is the difference between segmentation and peristalsis?

A

→ Peristaltic contractions spread the food out allowing digestive enzymes to mix with it
→ Push food towards the anus (global movement)

→ Segmenting contractions primarily churn the food but also propel it towards the anus

48
Q

When does the migrating motor complex occur and where does it start?

A

→ Between meals when the stomach/intestine are empty

→ Starts in the lower portion of the stomach

49
Q

What is phase 3 of motor activity in the intestines?

A

→ Burst of high frequency large amplitude contractions that migrate along the length of the intestine and die out

50
Q

What are the functions of the MMC?

A

→ Intestinal housekeeper
→ Indigestible residues are moved out by large contractions and wide opening of the pyloric sphincter during phase III
→ Removes dead epithelial cells by abrasion
→ Prevents bacterial overgrowth
→ prevents colonic bacteria entering small intestine

51
Q

What inhibits motility in the intestine?

A

→ Increased sympathetic activity

52
Q

What stimulates motility in the intestine?

A

→ Increased parasympathetic activity

53
Q

What emotions decreases motility?

A

→ Pain and fear

54
Q

What is the large intestine for?

A

→ Storage while water is absorbed from the contents

→ Intensive mixing and slow movement of waste and indigestible material aborally

55
Q

What are the fermenting chambers for in the large intestine?

A

→ Hydrolysis of fibre and indigestible nutrients

56
Q

What mixes the contents in the large intestine?

A

→ Segmental or haustral contractions

57
Q

What are the features of motility in the large intestine?

A

→ Intensive mixing
→ Fermentation
→ Slow propagating aboral flow

58
Q

What is mass movement?

A

→ Powerful contraction of mid-transverse colon that sweeps colon contents into rectum

59
Q

What is diarrhoea?

A

→ Frequent discharge of liquid feces

→ 3x a day

60
Q

What is constipation?

A

→ Difficulty/ constraint in opening bowels

61
Q

What are adaptations of the small intestine to absorb food?

A

→ Epithelial folds
→ Villi + microvilli
→ Increase SA

62
Q

What is absorbed when it enters the upper small intestine?

A

→ Dietary nutrients
→ Water
→ Electrolytes

63
Q

What is in the crypt cells?

A

→ Stem cells

found at the base of the crypts, which divide continuously to replace enterocytes

64
Q

What are the two modes of transport across enterocytes?

A

→ Transcellular- glucose

→ Paracellular- Na+, Cl-, H2O

65
Q

How can carbohydrates be absorbed?

A

→ In the form of monosaccharides

66
Q

What are complex carbohydrates reduced to and how?

A

→ Disaccharides and by amylases

67
Q

What converts disaccharides to monosaccharides?

A

→ Brush border enzymes

68
Q

What is the equation for the breakdown of sucrose?

A

Sucrose + sucrase → Glucose + fructose

69
Q

What is the equation for the breakdown of lactose?

A

lactose + lactase →Glucose + galactose

70
Q

What is the equation for the breakdown of glucose oligomers?

A

Glucose oligomers + glucoamylase → glucose

71
Q

How are glucose and galactose absorbed?

A

→ rapidly

→ by a secondary active transport process

72
Q

Describe the way glucose and galactose are transported

A

→ On the basolateral side Na+ is transported into the blood
→ Gradient is created for Na+ to come into the lumen
→ Driving force of Na+ allows glucose to come with it

73
Q

What is the glucose/galactose co-transporter called?

A

→ SGLT 1

74
Q

What are the transporters for glucose and fructose called?

A

→ F - GLUT-5- specific for fructose with no ability to transport glucose or galactose
→ G - GLUT-2

75
Q

How are polypeptides produced from proteins?

A

→ Action of pepsin

76
Q

How are di and tri peptides formed from polypeptides?

A

→ Action of pancreatic proteases

77
Q

How are amino acids completely digested?

A

→ Di-peptidases in the brush border

78
Q

How is pepsin secreted and how is it activated?

A

→ Secreted as a zymogen (pepsinogen)

→ HCl converts it into pepsin

79
Q

How are amino acids transported?

A

→ Na+ coupled carrier system
→ Separate carriers for different types of AA
→ Some di+tri peptides are transported using an inwardly directed H+ gradient
→process powered by the electrochemical potential difference of Na+across the membrane
active process

80
Q

What forms the majority of dietary lipids?

A

→ Triglycerides- 90%

81
Q

What do triglycerides include?

A

→ phospholipids
→ Cholesterol
→Fat soluble vitamins (A,D,E,K)

82
Q

What are dietary triglycerides broken down into?

A

→ Simpler units to facilitate absorption

83
Q

Where are most TGs digested?

A

→ In the small intestine

84
Q

What digests a small fraction of TGs?

A

→ Salivary lipase

85
Q

What must TGs be dissolved in before they can be digested?

A

→ Aqueous phase

86
Q

What is the digestion and absorption of lipids facilitated by?

A

→ Emulsification aided by bile salts

→ Micelle formation

87
Q

How much fat does gastric lipase break down and what is the remainder digested by?

A

→ 10-30% of fats

→ Pancreatic lipase

88
Q

What does lipase action require?

A

→ Emulsification of TGs by bile salts

89
Q

Where does pancreatic lipase bind?

A

→ To the surface of the small emulsion particles

90
Q

What does the duodenum detect?

A

→ Lipids which must be emulsified

91
Q

How do bile salts work?

A

→ They make the lipid molecules much smaller
→enzymes from the pancreas can break down the lipid and get to the core
→Bile salts ensure droplets do not stick together
→micelles is now small enough to be taken up by the enterocyte and into the lacteals

92
Q

How are lipids transported?

A

→ Micelles fuse with the gut mucosa
→ Resynthesis of TGs occurs on the SER
→ Lipoprotein is added
→ Chylomicrons are formed- cannot cross the basement membrane of the blood capillaries
→ This is transported and ends up in the blood
→Goes through lymphatic system

93
Q

Where do digestive components of lipids end up?

A

→ Do not end up directly in the blood they go via the lymphatic system

94
Q

Where do bile salts go?

A

→ Recycled by enterohepatic circulation

95
Q

What disorders can lead to fat malabsorption?

A

→ Crohns disease
→ Liver disease
→ Gallstones
→ Pancreatitis

96
Q

What is one of the causes of steatorrhea?

A

→ Having gall stones

97
Q

What is the effect of serotonin, insulin, and glucagon?

A

→Serotonin and insulin can increase motility

→Glucagon can decrease motility

98
Q

What happens in the ascending colon, transverse colon, and sigmoid colon of the LI?

A

→ Absorption of water and ions
→ Bacterial fermentation
→ Storage of waste and indigestible material

P1: GI (15 decks)

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