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Y1 GI > Physiology + Pharmacology of absorption > Flashcards

Physiology + Pharmacology of absorption Flashcards

1
Q

What 2 modifiable factors contribute to obesity?

A

Higher calorie intake

Sedentary lifestyle

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2
Q

What medical condition is most strongly associated with obesity?

A

Type 2 diabetes

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3
Q

Which area of the brain is associated with obesity?

A

Hypothalamus

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4
Q

What 3 neurological processes contribute to obesity?.

A

Satiety signalling
Adiposity negative feedback signalling
Food reward

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5
Q

What is satiation?

A

The feeling of fullness generated during a meal

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6
Q

What is satiety?

A

The period of time between the termination of one meal and the initiation of the next

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7
Q

What is adiposity?

A

The state of being obest

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8
Q

Give the 5 ways satiation is signalled.

A 
Cholecystokinin
Peptide YY
Glucagon-like peptide 1
Oxyntomodulin
Obestatin
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9
Q

How does cholecystokinin signal satiation?

A

Secreted from I cells within the duodenum and jejunum
Released in proportion to lipids and proteins in a meal.
Signals via sensory nerves to the hindbrain and stimulates the hindbrain directly (at NTS)

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10
Q

How does peptide YY signal satiation?

A

Secreted from L-cells of GI tract.
Levels increase rapidly post-prandially.
Inhibits the gastric motility and slows emptying and reduces food intake by action on the hypothalamus

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11
Q

How does Glucagon-like peptide 1 signal satiation?

A

Released from L cells and is a product of the pro-glucagon gene
Released in response to food ingestion
Inhibits the gastric emptying and reduces the food intake.

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12
Q

How does oxyntomodulin signal satiation?

A

Released from oxyntic cells and L-cells and is a product of the pro-glucagon gene.
Acts to suppress the appetite by an unknown mechanism

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13
Q

How does obestatin signal satiation?

A

Released from the cells lining the stomach and small intestine and is a product of the genes encoding ghrelin.
Possibly an antagonist to Ghrelin but this is unclear.

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14
Q

Explain Ghrelin.

A

Ghrelin is the signal for hunger.
Produced and secreted by Gh cells through the GI tract.
Ghrelin levels are raided by fasting and hypoglycaemia
Ghrelin increases food intake through the hypothalamus and decreases the utilization of fat

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15
Q

Name the 2 hormones that inform the brain about the amount of fat on the body.

A

Leptin (made and released from fat cells)

Insulin (made and released from pancreatic cells)

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16
Q

What happens to the levels of leptin in a patient with high levels of body fat?

A

Leptin increases with body fat

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17
Q

How does leptin work for obesity control?

A

Circulate and enter the brain.
Bind to leptin receptors in the hypothalamus leading to inhibition of food intake and a decrease in body weight.
Also does lots of other stuff

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18
Q

How does insulin work for obesity control?

A

Circulates and enters the brain

Binds to insulin receptors in the hypothalamus leading to inhibition of food intake and a decrease in body weight

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19
Q

Explain the idea of food reward?

A

Food causes the release of dopamine which improves mood

Leads some to eat more

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20
Q

What is leptin resistance?

A

In those who suffer from diet-induced obesity, there are 2 major theories that occur
Defective leptin transport to the brain
Altered signal transduction following leptin binding to its receptor

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21
Q

Explain the 2 types of mechanical activity within the stomach?

A 
Orad stomach (fundus and proximal body) have a tonic action
Caudad stomach (distal body and antrum) have a phasic action
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22
Q

Explain the mechanical activity of the orad stomach region

A

This is the fundus and proximal body
Relaxation driven by the vagus occurring during swallowing to permit the storage of ingested material
No slow wave activty, when tonic contractions occur are weak
Content propelled intermittently to caudad region by low amplitude tonic contraction

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23
Q

Explain the mechanical activity of the caudad stomach region

A

Due to slow wave (only those reaching threshold elicit contraction)
Phasic peristaltic contractions from suprathreshold slow wave, mid stomach to gastroduodenal junction propelling contents towards pylorus through which some chyme passes to duodenum
Mixing occurs by increased speed approaching the pylorus causing retropulsion

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24
Q

What is the purpose of retropulsion in the stomach

A

Mixing the gastric contents to reduce the size of the chyme particles so they better pass through the pylorus

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25
Q

What 2 factors influence stomach emptying?

A

Gastric factors: volume of chyme, consistency of chyme

Duodenal factors: neuronal response, hormonal response

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26
Q

How does the volume and consistency of chyme affect the rate of stomach emptying?

A

Volume:
Stretch of the smooth muscle
Stimulation of intrinsic nerve plexuses
Increased vagus nerve activity and gastrin release

Consistency:
Thin liquid chyme moves through the pylorus more easily

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27
Q

Explain the enterogastric reflex.

A

Occurs in the duodenum

Decreases the antral activity by signals from intrinsic nerve plexus and the ANS

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28
Q

Explain enterogastrones. (context of gastric emptying)

A

Chemicals released from the stomach can inhibit the stomach contractions

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29
Q

Explain factors in the duodenum that delay gastric emptying.

A

Fat, delays gastric emptying required for digestion and absorption in the small intestine
Acid, time is required for neutralization of gastric acid by bicarbonate secreted from the pancreas (important for enzyme function)
Hypertonicity, osmotically active products (carb and protein) draw water in
Distention of the duodenum delays gastric emptying

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30
Q

What are the 2 gland areas of the stomach?

A

The oxyntic gland area (proximal stomach including fundus and body)
The pyloric gland area (distal stomach, designated the antrum)

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31
Q

What type of cells are found in the oxyntic gland area, and what do they release?

A

Chief cells: pepsinogen
Parietal cells: HCl
Enterochromaffin-like cell: histamine

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32
Q

What type of cells are found in the pyloric gland area, and what do they release?

A

D cells: Somatostatin

G cells: Gastrin

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33
Q

What is the function of HCl in the stomach?

A

Denatures proteins
Kills most micro-organisms ingested with food
Activates pepsinogen to pepsin

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34
Q

What is the function of pepsinogen?

A

An inactive precursor molecule to the peptidase pepsin

Note that pepsin stimulates pepsinogen to pepsin so is termed autocatalytic

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35
Q

What is the function of the intrinsic factor?

A

Binds to Vit.B12 facilitating absorption in the terminal ileum

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36
Q

What is the function of gastroferrin?

A

Bind Fe2+ facilitating absorption later

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37
Q

What is the function of histamines? (stomach)

A

To stimulate HCl secretion

38
Q

What is the function of mucus?

A

To be protective

39
Q

What is the function of gastrin?

A

To stimulate HCl secretion

40
Q

What is the function of somatostatin?

A

To inhibit HCl secretion

41
Q

What 3 factors increase the acid secretion?

A

PANS: M3 on the parietal cells directly, M1 on enterochromaffin-like cells to stimulate histamine release
Gastrin: Through CCK2 receptors directly, CCK2 on enterochromaffin-like cells to stimulate histamine release
Histamine: Through H2 receptors directly

42
Q

How are proton pumps expressed?

A

Proton pumps sit preformed in tubulovesicles
Through stimulation by M3, CCK2 and H2 receptors acting on protein kinases traffic the tubulovesicles to the apical membrane

43
Q

What are the 3 phases of gastric acid secretion?

A 
Cephalic phase (before food in the stomach)
Gastric phase (when food is in the stomach)
Intestinal phase (after food has left the stomach)
44
Q

Explain the cephalic phase of gastric acid secretion.

A

Vagus stimulation through the enteric nervous system
Release ACh stimulating parietal cells
Release of gastrin-releasing peptide leading to gastrin release
Release of histamines
Inhibition of D cells to decrease the effect of somatostatin on G cells

45
Q

Explain the gastric phase of gastric acid secretion

A

Stomach distension stimulates reflexes for acid secretion
Food buffers the pH leading to D cell inhibition (less somatostatin so more gastrin)
Amino acids stimulate G cells

46
Q

Explain the intestinal phase of gastric acid secretion

A

This is inhibitory

The enterogastric reflex along with the enterogastrones lead to decreased action secretion

47
Q

How is the stomach mucosa protected from acids?

A

Locally produced prostaglandins lead to
Reduced acid secretion
Increased mucus and bicarbonate secretion
Increased mucosal blood flow

48
Q

What is luminal digestion?

A

Mediated by pancreatic enzymes secreted into the duodenum

49
Q

What is membrane digestion?

A

Mediated by enzymes situates at the brush border of epithelial cells

50
Q

What is the process of digestion?

A

The enzymatic conversion of complex dietary substances to a form that can be absorbed

51
Q

What is absorption?

A

The processes by which the absorbable products of digestion are transferred across both the apical and basolateral membrane of enterocytes

52
Q

What is the overall process of digestion and absorption?

A

Assimilation

53
Q

By what mechanism are carbohydrates digested

A

Break down by enzymes
Amylose: straight chain
Amylopectin: branches chain

All dietary carbohydrates must be converted to monosaccharides for absorption

54
Q

What is the sequence of carbohydrate digestion?

A

Intraluminal hydrolysis forms oligosaccharides
Membrane digestion forms monosaccharides

Absorption happens after this

55
Q

What is the function of alpha-amylase?

A

The breakdown of internal alpha-1,4 glycosidic bonds

Cannot clear alpha-1,6 linkages

56
Q

What are oligosaccharidases?

A

Intergral membrane proteins with an enzymatic function into the GI tract lumen
Break down oligosaccahrides

57
Q

How are monosaccharides absorbed into the gut wall?

A 
Monosaccharides are moved in through secondary active transport by SGLT1 carriers a type of Na+ co-transport proteins (The Na+/K+ pump acts on the basolateral membrane to maintain a Na+ gradient)
Fructose is an exception as it moves through GLUT5 in a passive manner.
All monosachharides (fructose included) are moved through GLUT 2 cariers in the basolateral membrane
58
Q

Explain the MoA of SGLT1?

A

2Na+ bind
Affinity for glucose increases, glucose binds
Na+ and glucose translocate from extra to intracellular
2Na+ dissociate and the affinity for glucose thus falls
Glucose dissociates
(Re-sets the cycle)

59
Q

Briefly explain the 4 major pathways of protein digestion

A

Luminal enzymes break down proteins to amino acids which are moved through the enterocytes
Luminal enzymes break down proteins to peptides which are broken down to amino acids by brush border enzymes. The amino acids are then moved through the enterocytes
Luminal enzymes break down the proteins to peptides which are moved into the enterocytes. Intracellular hydrolysis forms amino acids which are moved through the basolateral membrane
A peptide can be moved from the enterocyte without intracellular hydrolysis but this is uncommon

60
Q

What % of the daily energy intake is due to proteins?

A

10-15%

61
Q

What is the major difference between an endopeptidase and an exopeptidase?

A

Endopeptidases form oligopeptides

Exopeptidases form single amino acids

62
Q

Explain protein absorption.

A

Brush borders: 5Na+ dependant co-transporters and 2 Na+ independent transporters
Basolateral membrane: at least 5 mechanisms 3 for efflux and 2 for influx
Di, tri and tetrapeptides are by H+ dependent mechanisms at the brush border which further hydrolyse to amino acids within the enterocyte
Na+ independent systems at the basolateral membrane

63
Q

What % of the daily energy requirement is due to lipids?

A

55-60 %

64
Q

Why are lipids made to smaller droplets as part of digestion?

A

This increases the surface area for action by enzymes such as lipases.

65
Q

How are droplets stabilized in the digestive tract?

A

Addition of a coat of amphiphilic molecules that form a surface layer.

66
Q

What components help to form the amphiphilic coat of lipid molecules?

A

Products of the lipid digestion: fatty acids and monoacylglycerols
Biliary phospholipids
Cholesterol
Bile salts (When unilamellar or mixed micelle)

67
Q

What are the phases of lipid digestion?

A

Lingual phase
Gastric phase
Intestinal phase

68
Q

Explain the lingual phase of lipid digestion

A

Relatively unimportant in humans

69
Q

Explain the gastric phase of lipid digestion

A

Done by gastric lipase (and lingual lipase)
More important in infants and those without a pancreas
Gastric lipase if released in response to gastrin from chief cells

70
Q

What is the optimum pH of gastric lipase?

A

4

71
Q

When does gastric lipase stop working?

A

In the duodenum due to digestion by pancreatic enzymes and the unfavoured pH

72
Q

What is the preferred hydrolysis position of gastric lipase

A

Hydrolysis of TAGs at the 3 position

73
Q

Explain the intestinal phase of lipid digestion.

A

Mostly by pancreatic lipase

Secreted from acinar cells of the pancreas in response to CCK (CCK also stimulates bile flow)

74
Q

What factors are needed for full activation of pancreatic lipase?

A 
Colipase co-factor
Alkaline pH
Ca2+
Bile salts
Fatty acids
75
Q

What is the function of bile salts?

A

Bile salts act as emulsifiers to break down large lipid droplets to smaller lipid droplets
This increases the surface area for the attack of lipases

76
Q

What causes a release of bile salts?

A

In response to CCK

77
Q

What is the function of colipase?

A

Colipase binds to bile salts and lipase allowing access of lipase to the tri/di-acylglycerols

78
Q

What is colipase and where is it from?

A

An amphipathic polypeptide secreted with lipase by the pancreas

79
Q

What is a mixed micelle?

A

A micelle formed of fatty acids, bile salts, cholesterol, acylglycerols and phospholipids

80
Q

State the ways lipids are moved into the enterocytes?

A

By passive diffusion &/or membrane fatty-acid translocases, fatty-acid binding proteins and fatty-acid transport proteins

81
Q

How are lipids moved from the enterocytes?

A

Short and medium chain fatty acids (<6C, 8-12C respectively) diffuse through the enterocyte and exit through the basolateral membrane and enter the villus capillaries
Long chain fatty acids (>12C) and monoglycerides are synthesised to triglycerides by the SER and are subsequently incorporated into chylomicrons.

82
Q

Briefly explain how chylomicrons are formed

A

TAGs are synthesised in the SER
TAGs, cholesterol esters and phospholipids combine to form a nascent chylomicrons
Nascent chylomicrons join with Apolipoproteins (ApoB-48) to form chylomicrons.

(Chylomicrons are exocytosed to be carried in the lymph system to the circulatory system)

83
Q

Explain the movement of cholesterol into a cell

A

Cholesterol binds to Niemann-Pick C1-like protein in clathrin-coated pits
A clathrin structure is used to carry the NPC1L1 and cholesterol complex into the cell

84
Q

How is Ca2+ absorbed into enterocytes

A

Is a passive process
Occurs through a Ca2+ channel with low luminal Ca2+
Occurs paracellularly with high luminal Ca2+

The channel is regulated by 1,25-dihydroxyvitamin D3 and parathyroid hormone (Up regulates the synthesis of 1,25-dihydroxyvitamin D3)

85
Q

How is Ca2+ moved out of the cell?

A

Through a Ca2+ ATPase (increased by 1,25-dihydroxyvitamin D3)
Through a sodium/calcium exchanger

86
Q

How is iron absorbed into enterocytes?

A

Only Fe2+ can be absorbed
This is by divalent metal transporter 1 (coupled to H+

Haem is absorbed through Haem carrier protein 1
Haem is oxidised from Fe3+ to Fe2+ by haem oxidase

87
Q

What can happen to Fe2+ once it is within the cell

A

Apoferratin + Fe2+ form ferratin a storage form of iron

Mobilferrin through ferroportin 1 moves Fe2+ into the lumen of the blood vessel

88
Q

What happens to Fe2+ once it is in the blood

A

Fe2+ binds to transferrin

This forms transferrin-Fe2+ to be carried around the body

89
Q

Explain the absorption of Vit.B12

A

Vit.B12 is in food bound to animal proteins
Stomach acid releases Vit.B12 from proteins
Haptocorin secreted in saliva binds to Vit.B12 released in the stomach
Parietal cells of the stomach release intrinsic factor
Pancreatic enzymes digest haptocorin to release Vit.B12
Vit.B12 binds to the small intestine
Vit.B12-intrinsic factor complex is absorbed in the terminal ileum by endocytosis

90
Q

Explain the absorption of fat-soluble vitamins

A

Incorporated into mixed micelles
Usually passively transported into enterocytes or incorporated to chylomicrons
Distributed by the intestinal lymphatics

91
Q

List the fat soluble vitamins

A

A
D
E
K

92
Q

Explain the absorption of water-soluble vitamins

A

Transport in the apical membrane by either Na+-dependant or Na+-indepentant carriers

Y1 GI (7 decks)

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