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GI Physiology > GI Physiology > Flashcards

GI Physiology Flashcards

1
Q

How many litres of fluid pass through the small intestine every day?

A

8/9 L.

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2
Q

What channels are found in the small intestine?

A

Absorptive cells:

Basolateral side - NaKATPase
Luminal side - HCO3/Cl (Cl into cell), H+Na+ (Na+ into cell)

Secretory cells:

Basolateral side - NaKATPase
Luminal side - Cl- into lumen.
Passive movement of Na+ and water between secretory cells.

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3
Q

What channels are found in the large intestine?

A

Absorptive cells:

Basolateral side - NaKATPase
Luminal side
- HCO3/Cl- (Cl into cell)
- H+Na+ (Na into cell)
- Na channel (influenced by aldosterone)
- H+K+ ATPase (K into cell)
- HCO3/SCFA (SCFA into cell)
Secretory cells:
Basolateral side - NaKATPase
Luminal side
- CFTR - Cl- transporter (into lumen)
- K+ into lumen
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4
Q

What do I cells produce? Where are they found?

A

I cells in the duodenum in response to lipids.

Produce CCK.

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5
Q

What causes gallbladder contraction and relaxation?

A

Contraction - CCK

Relaxation - sympathetic nerves, VIP and somatostatin

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6
Q

How are carbohydrates absorbed?

A

Glucose and galactose - SGLT1 channels

Fructose - GLUT 5 channels

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7
Q

What happens to carbohydrates that aren’t digested?

A

They are fermented in the colon to produce SCFA and gas

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8
Q

What does salivary a-amylase do?

A

Breaks down a1,4 glucosidic bonds to a limit dextrin, sucrose, lactose and maltose.

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9
Q

What brush border enzymes break down carbohydrates in the small intestine?

A

Lactase (lactose –> glucose and galactose)

Sucrase-isomaltase
(sucrose –> fructose and glucose)
(maltose –> glucose)
(a limit dextrins –> glucose)

Maltase-glucoamylase
(maltose, maltotriose –> glucose)

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10
Q

What is the action of pepsin?

A

Breaks down proteins to proteases, peptones and polypeptides.

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11
Q

How are proteins broken down in the small intestine?

A

Enterokinase (brush border peptidase) converts trypsinogen into trypsin, which activates pancreatic zymogens.

   e.g. proelastate to elastase
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12
Q

How are proteins absorbed?

A

Amino acids - 7 Na+ linked carriers

Di and tripeptides - PEPT1 with H+ ions

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13
Q

How is acute pancreatitis prevented?

A
  • Enzymes released as zymogens
  • Trypsin inhibitor secreted by acinar cells
  • Trypsin has an autolysis mechanism
  • Fluid secretion by duct cells flush enzymes into duodenum
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14
Q

How are fats digested?

A

Fats are emulsified by bile acids.

Pancreatic lipase then breaks down triglycerides to monoglycerides and fatty acids, which are combined with bile salts and phospholipids to form micelles.

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15
Q

How are fats absorbed?

A

Micelles release FA and monoglycerides at the surface of enterocytes, where they pass through.
Within enterocytes, they are repackaged into TAGs and combined with cholesterol and fat-soluble vitamins to form chylomicrons.

Chylomicrons then pass into lacteals before eventually entering the circulation.

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16
Q

How are vitamins absorbed?

A

Fat soluble vitamins - ADEK and B-carotene - absorbed alongside lipid carriers.

Water-soluble vitamins - similar transport to monosaccharides.

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17
Q

How are sodium, potassium and calcium absorbed?

A

Sodium - 99% in jejunum alongside glucose, galactose and some amino acids.

Potassium - in jejunum and ileum

Calcium - throughout small intestine - active in duodenum and passive in jejunum and ileum (through tight junctions)

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18
Q

How is iron absorbed?

A

Haem iron passes into enterocytes easily.

Non-haem iron (Fe) is converted from its ferric to ferrous form (Fe3+ to Fe2+) by dCytB1.
- Fe2+ then passes through DMT1 channels into enterocytes

Iron is either stored in the cell as ferritin or is transported into plasma via ferroportin, where it is bound to transferrin.

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19
Q

What enzyme converts Fe3+ to Fe2+? What else can influence this reaction?

A

Duodenal cytochrome B1.

Influenced by vitamin C.

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20
Q

What percentage of transferrin is normally saturated with iron?

A

Around 30%.

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21
Q

What are dietary sources of iron?

A

Haem iron - red meat

Non-haem iron - white meat, green veg, cereals etc

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22
Q

How is iron stored?

A

Mostly intracellular as ferritin or haemosiderin.

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23
Q

What is the action of hepcidin?

A

Hormone that acts to reduce iron levels in the body by binding to and inhibiting ferroportin.

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24
Q

What protein causes the conversion of iron to haem in erythroblastic mitochondria?

A

ALA-S2

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25
Q

What substances are present in salvia and what are their functions?

A

Mucus - lubrication
Amylase - break down starch
Bicarbonate - neutralise acid
Thiocyanate and lysosomes - bactericidal agents

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26
Q

Where is the swallowing centre found?

A

Reticular formation of the brain

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27
Q

Where is the pacemaker zone of the stomach found? What is its role?

A

Fundus on the greater curvature.

Sets the BMR of the stomach, leading to continuous contractions.

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28
Q

What are the 4 phases of the MMC?

A

Phase I - prolonged period of quiescence
Phase II - increased frequency of contraction
Phase III - a few minutes of peak electrical and mechanical activity
Phase IV - declining activity (progress to phase 1)

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29
Q

What is the role of the migrating motor complex?

A

Cyclic contraction sequence that occurs every 90 minutes.

Cleanse the stomach and intestine to rid of food particles and bacteria.

30
Q

What controls the MMC?

A

Motilin (secreted by endocrine M cells)

31
Q

What is the role of gastrin and CCK in gastric motility?

A

Both relax proximal stomach and enhance contractions in the distal stomach.

32
Q

Describe the times taken for gastric emptying.

A

Solids - empty completely over 3-4 hours (fats take longest, carbs quickest)

Liquids - inert liquids - 20 minutes

33
Q

At what size do particles leave the stomach?

A

When they are less than 1-2mm.

34
Q

Describe the phases of gastric acid secretions.

A

Cephalic Phase
- sight/smell/taste of food –> vagus nerve activates parietal and gastrin cells –> moderate stimulation of HCl

Gastric Phase
- distension of the stomach&proteins in antrum –> vago-vagal reflex –> parietal cell activation

Intestinal Phase

  • proteins in duodenum –> gastrin release (stimulatory)
  • lipids in duodenum –> release of peptide YY (inhibitory)
  • HCl in duodenum –> secretin release (inhibitory)
  • distension of duodenum –> enterogastric reflex (inhibition
35
Q

What stimulates acid secretion?

A

Histamine
Acetylcholine
Gastrin

36
Q

What inhibits acid secretion?

A

When the volume and pH in stomach decrease, gastrin release is inhibited and somatostatin is stimulated.
GIP, secretin and CCK are also released into the duodenum (inhibitory)

37
Q

What is the proton pump and how is it regulated?

A

A H+/K+ ATPase on the apical surface of parietal cells.

When the pH is less than 3, D cells are activated, inhibiting gastrin release.

38
Q

Discuss motility of the small intestine.

A

Segmentation - mix and bring contents to intestinal wall

Peristalsis - contraction of longitudinal muscle to move contents to anus

39
Q

How is motility controlled in the small intestine?

A

MMC - vagus and motilin
Segmentation - myenteric plexus
Peristalsis - ACh and substance P
Relaxation - NO and VIP

40
Q

Discuss motility in the large intestine?

A 
Segmental (or haustral) contractions
Peristalsis
Mass movements
    - a few times per day
    - intense and prolonged peristaltic contraction
41
Q

What is the defecation reflex?

A

Increased faecal matter in the rectum leads to distension and activation of mechanoreceptors.

These send an impulse to the sacral region of the spinal cord, and to higher centres of the brain to make a voluntary decision on whether defecation is appropriate.

If appropriate, PNS afferents cause relaxation of external sphincter and puborectalis muscle –> defecation.

42
Q

What happens to the products of Hb when broken down?

A

Globins
- Broken down to constituent amino acids.
Haem
- Fe is recycled
- Porphyrin ring is converted to bilirubin

43
Q

Describe conversion of haem to bilirubin.

A

Haem –> biliverdin by haem oxygenase

Biliverdin –> bilirubin (unconjugated) by bilverdin reductase

44
Q

What must unconjugated bilirubin be bound to in the blood?

A

Albumin

45
Q

What happens to unconjugated bilirubin when it enters the hepatocyte?

A

It is conjugated by UDP glucoronyl transferase

46
Q

What happens to conjugated bilirubin in the intestines?

A

It is converted to unconjugated bilirubin by B-glucoronidase.

It is then converted to mesobilinogen, stercobilinogen, urobilinogen by microbes in the small intestine.

These are converted to mesobilin, stercobilin and urobilin in the large intestine.

20% goes to the liver via the portal vein and ends up in the kidneys where urobilinogen is oxidised to urobilin and excreted in the urine.

47
Q

What is the total daily need of iron?

A

1-2mg

48
Q

How is iron stored in the body?

A

Ferritin
- cellular ferritin - iron is readily available from here

Haemosiderin
- conglomerates of ferritin - iron is slowly available

49
Q

How can serum ferritin be used as a biological marker of disease?

A

Serum ferritin is normally very low.

High serum ferritin signifies iron overload (or potentially inflammation as this is an acute phase protein)

Low serum ferritin signifies IDA.

50
Q

What are food sources of iron?

A

Haem iron - red meat

Non-haem iron - white meat, green vegetables, cereals

51
Q

How is iron excreted?

A

No excretory mechanism.

52
Q

How and where is iron primarily absorbed?

A

Haem iron
- Can pass through into enterocyte through a transporter.

Non-haem iron
- Must first be converted from its ferric to ferrous form (Fe3+ –> Fe2+) by duodenal cytochrome b1. It then passes into the enterocyte via the DMT1 channel.

When in the cell, these can be stored as ferritin/haemosiderin, or used by mitochondria to produce enzymes etc.

It is then absorbed into plasma via the ferroportin channel.

53
Q

What is the role of hepcidin?

A

Binds to and inhibits ferroportin, therefore decreasing the release of iron from the RES.

54
Q

What gene is responsible for hepcidin production?

A

HFE gene.

55
Q

What must iron be bound to in the blood for transport?

A

Transferrin.

56
Q

How saturated is transferrin with iron in a healthy patient?

A

Around 30%

57
Q

What gene/protein is responsible for the conversion of iron to haem in the mitochondria?

A

ALA-S2.

58
Q

What is the CFTR channel?

A

The cystic fibrosis transmembrane protein.

- secretes Cl- ions, which creates a gradient attracting Na+, therefore attracting water.

59
Q

Where are absorptive, and where are secretory cells found in the small intestine?

A

Absorptive cells - villi

Secretory cells - crypts

60
Q

What is the function of HCO3 secreted by enterocytes?

A

Neutralise acidic products in the lumen

61
Q

What are the functions of the large bowel?

A 
Motility
Absorption of water
Vit K production (bowel flora) and absorption
Breakdown of fibre
Store and eliminate waste
Ammonia production (bowel flora)
62
Q

What happens to nitrogen in the body?

A

It is converted into urea in the liver and excreted by the kidneys.

63
Q

Where is ammonia produced?

A

In the liver and large bowel.

64
Q

What are the main constitutes of bile?

A 
Bile salts
Water
Electrolytes
Cholesterol
Phospholipids 
Conjugated bilirubin
65
Q

How are bile salts synthesised and what are they made from?

A

Synthesised from cholesterol.

Primary bile acids are cholic acid and chenodeoxycholic acid.

These are conjugated with an amino acid group (taurine or glycine) to form secondary bile acids.

Secondary bile acids leave hepatocytes by active transport and are dehydroxylised by intestinal bacteria, forming secondary bile salts.

66
Q

What is the difference between bile acids and bile salts?

A

Bile salts are better at emulsifying fats, as they are amphiphatic. The terms are interchangeable however.

67
Q

What is the function of bile acids/salts?

A

Emulsification and micelle formation.

Enhance absorption of fat-soluble vitamins.

Enhances cholesterol excretion.

Exerts a hormone-like effect on intestinal metabolic pathways.

68
Q

How is bile acid secretion regulated?

A

Between meals, the SOI is contracted which increases pressure in the common bile duct - bile travels into GB for storage and concentration.

When a meal is consumed, FA and amino acids in the duodenum cause CCK release –> GB contraction and SOI relaxation. Bile is therefore released into the biliary system.

69
Q

What does acidic chyme in the duodenum cause?

A

Secretin release - HC03 is released into bile to neutralise bile, and bile production is also upregulated.

70
Q

What causes relaxation of the GB?

A

VIP, somatostatin and the sympathetic nervous system.

71
Q

What is the enterohepatic circulation?

A

A way by which 95% of bile acids recirculate.

They are carried in bile into the duodenum. Most are reabsorbed in the ileum by active transport into the portal circulation.

The other 5% is lost in the faeces.

72
Q

Where are bile acids produced?

A

In the liver

GI Physiology (1 decks)

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