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GSSE - Physiology > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What are the main functions of saliva?

A
  1. Digestion initiation - amylase mainly for digestion of complex carbohydrates (starches)
  2. Lubrication - mucins which enable the food bolus to pass into the oesophagus and keep the whole mouth moist facilitating comfort and movement for speech
  3. Antimicrobial activity - with immunoglobulin A and lysozymes to protect the oral cavity from bacteria
  4. Solvent for taste esters
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2
Q

What is the pH of saliva relative to gastric secretions?

A

saliva is slightly more alkaline in order to neutralise reflux gastric secretions into the upper GIT.

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3
Q

Which part of the salivary gland does saliva exit from?

A

The blind end of the glands known as acini.

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4
Q

How much saliva is produced by each gland at maximal stimulation?

A

Each gland is capable of producing an amount of saliva equivalent to its own weight per minute at maximal stimulation.

On average, 1 to 1.5 litres of saliva is drained into the mouth per day.

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5
Q

How does the composition of saliva change as it moves from the acini to the duct to the mouth?

A

In the duct the electrolytes int he saliva are changed. NaCl is absorbed whilst K+ is excreted which renders the final product slightly hypotonic to plasma.

As secretion rate ramps up there is less time for NaCl absorption so overall it tends to be less hypotonic but still most so relative to plasma.

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6
Q

How is salivary secretion controlled?

A

The parasympathetic nervous system controls salivary secretion.

The sympathetic nervous system has some influence on the composition of saliva only, not volume.

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7
Q

What stimulates salivary secretion?

A

There are numerous phases in the stimulation of saliva.

Centrally acting triggers such as the thought of food or seeing and smelling food cause increased secretion. (cephalic phase)

Physical triggers such as chewing increase secretion,

Nausea increases salivary secretion.

Fear and sleep decrease salivary secretion.

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8
Q

What are the main cells in the body of the stomach (including fundus)?

A
  1. Parietal (oxyntic cells) secrete hydrochloric acid and intrinsic factor
  2. Chief cells (zymogen. peptic) secrete pepsinogens
  3. Goblet cells secrete bicarbonate and mucous
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9
Q

Which three hormones stimulate gastric secretions?

A
  1. Gastrin - release from G cells in the gastric antrum in response to oligopeptides and also gastrin releasing peptide from enteric nerve endings
  2. Histamine - Once gastrin acts via the bloodstream on to parietal (and probably chief cells) it causes these cells to secrete histamine from the fundic glands. The fundic glands also have enterochromaffin-like cells which also secrete histamine
  3. Acetylcholine - from enteric nerve endings around the fundus
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10
Q

Which hormone inhibits the secretion of G cells and ECL cells?

A

Somatostatin

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11
Q

By what mechanism does gastrin and acetylcholine promote secretion?

A

They both increase free calcium within the cell.

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12
Q

By what mechanism does histamine promote secretion?

A

Histamine increase cAMP within the cell.

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13
Q

How much does gastric secretion add to the daily intestinal contants?

A

2.5 litres on average, most of which is probably excessive and not required.

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14
Q

What are the names of the pancreatic ducts?

A

The main is also known as the duct of Wirsung.

The accessory duct is also known as the duct of Santorini.

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15
Q

How much pancreatic juice is secreted per day?

A

1.5 litres

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16
Q

Which hormones regulate pancreatic secretion?

A
  1. Secretin - primary acts on the pancreatic ducts to produce copious amounts of alkaline pancreatic juice rich in HCO3 but has little enzyme activity
  2. Cholecystokinin (CCK) - stimulates the release of the zymogen granules from acinar cells
  3. Acetylcholine - also causes zymogen release in the pancreas via vagally controlled response
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17
Q

What are the main constituents of pancreatic juice?

A
  1. HCO3 - neutralises the gastric secretions in conjunction with bile and the mucous secretion from the GIT
  2. Digestive enzymes - majority of which are inactive. The major activating enzyme is TRYPSIN, which is initially release as trypsinogen. The pancreas unsurprisingly secretes a trypsin inactivating enzyme should it be release in the pancreas itself
    - Remember trypsinogen itself is activated by enteropeptidase
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18
Q

What are the main functions of bile?

A
  1. Lipid absorption
  2. Excretory fluid by which the body excretes lipid soluble end products of metabolism
  3. Excretion of cholesterol either as direct native form or conjugation into bile acids.
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19
Q

What are the main constituents of bile?

A
  1. Bile acids

2. Bile pigments - bilirubin and biliverdin

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20
Q

How much bile is secreted on average per day?

A

500mL

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21
Q

How much average fluid is lost in the stools daily?

A

Only 200mL, 2% of roughly 9000mL that enters the GIT daily

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22
Q

How is fluid resorbed in the GIT?

A

Between meals, when nutrients are not int he lumen, the sodium and chloride are absorbed by an exchange transport known as the sodium / hydrogen exchanger and chloride bicarbonate exchanger in the apical membrane. The water follows the sodium to maintain osmotic equilibrium.

In the colon, additional electrogenic transporters encourage the diffusion of water through the epithelium via the epithelial sodium channel (ENaC), same as the chanbel found in the distal tubyule of the nephron.

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23
Q

What happens to potassium in the GIT?

A

Potassium is partially excreted as part of mucous. In addition there are numerous potassium channels in the basolateral membrane so that K+ can be secreted into the colon.
The K+ accumulation in the colon is offset by the hydrogen/potassium ATPase pump which transports potassium into the cells.

Chronic loss of colonic fluids in diarrhoea can lead to hypokalaemia by this mechanism.

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24
Q

Where does the majority of bilirubin the body come from?

A

Breakdown of haemoglobin. Formed in the reticuloendothelial system and bone marrow where dying RBCs come to go to pasture. They have a lifespan of 120 days roughly.

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25
Q

How are bile salts absorbed?

A

The majority of bile salts are absorbed in the small instestine, predominantly in the terminal ileum.

The main bile acids are cholic acid and chenodeoxycholic acid. These are conjugated with glycine and taurine to form bile SALTS.

The small remaining percentage is converted to other bile salts: deoyxcholic acid and lithocholic acid. Lithocholic acid is excreted in the stool whislt deoxycholic acid can be resorbed.

Once reabsorbed they are again secreted, forming the so called entero-hepatic circulation.

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26
Q

What happens when there is a disruption in enterohepatic circulation?

A

In pathologies where there may be loss of the terminal ileum where most of the bile salts are absorbed, the synthesis of bile salts is unable to keep up with the daily fat intake.

As a result, up to 50% of ingested fats may pass, unabsorbed, in to the stool. Consequently fat-soluble vitamins will not be absorbed as effectively and may lead to severe deficiency.

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27
Q

How does bilirubin reach the liver following RBC breakdown in reticuloendothelial system?

A

Two ways:

  1. Free bilirubin floats unbound in blood. It is less water soluble and able to enter hepatocytes more freely
  2. Albumin bound
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28
Q

What happens to serum unconjugated bilirubin when there is excessive RBC destruction?

A

It rises

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29
Q

What happens to unconjugated bilirubin once it reaches the liver?

A
  1. Reaches the smooth endoplasmic reticulum and is conjugated with glucuronyl transferase to become glucuronic acid. This is a rate limiting step and competitors for clucuronyl transferase can inhibit the conjugation process of bilirubin leading to accumulation and jaundice.
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30
Q

What happens to conjugated bilirubin once it has formed?

A

Conjugated bilirubin (glucuronic acid) does one of two things. The majory of it is actively transported into bile canaliculi.

A smaller amount makes it into blood where it is bound to albumin and ultimately excreted in urine.

For this reason, when we take the bilirubin level we are really looking at the free bilirubin predominantly, with only a small contribution from conjugated bilirubin.

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31
Q

What happens to bilirubin in the bile?

A

Bilirubin is pumped into the small intestine with the bile acid. The common bile duct meets the duct of Wirsung and empties into D2. At this point intestinal bacteria metabolise the bilirubin into urobilinogen (colourless).

The intestinal wall is only permeable to urobilinogens and unconjugated bilirubin so a small amount is reabsorbed via enterohepatic circulation.

Conjugated bilirubin can not be absorbed so it is excreted in the stools.

A small amount of reabsorbed urobilinogen is absorbed into the blood and excreted in the urine.

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32
Q

What are the components of the lower oesophageal sphincter?

A

3 components:

  1. Smooth muscle forming the intrinsic sphincter - increased tone by way of acetylcholine from vagus
  2. The crus of right diaphragm loops over to the left to support the posterior portion of the sphincter
  3. Oblique sling fibres from the wall of the stomach
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33
Q

Describe the tone of the oesophagus during different periods of swallowing

A

The lower oesphageal sphincter is tonically active to prevent reflux in the resting state. It is relaxed during swallowing.

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34
Q

Describe the pathophysiology of achalasia

A

Achalasia means failure to relax. Achalasia occurs when there is excessive lower oesphageal sphincter pressure and food is unable to pass into the stomach, thus accumulating in the oesophagus and causing massive dilatation. The deficiency in relaxation occurs due to a lack of myenteric plexus cells.

Relaxation of the lower oesphageal sphincter occurs through nitrous oxide and vasoactive intestinal peptide (VIP).

35
Q

What are the main functions of GASTRIN?

A
  1. Produced by the G cells in the gastric antrum and D1
  2. Actions:
    - Enhance gastric acid secretion and pepsin
    - Growth effect on stomach, promotes mucosal growth
    - Increases gastric motility
    - Causes oxyntic (parietal) cells to secrete HCl and intrinsic factor
    - Causes chief (pepsin) cells to secrete pepsinogen
    - Enhances insulin secretion after protein meal!
36
Q

What stimulates gastric secretions?

A
  1. Cephalic phase of digestion
  2. Distension of the gastric antrum
  3. Presentation of amino acids to the antrum, espcially tryptophan and phenylalamine
  4. Increased vagal tone and acetylcholine secretion
  5. Hypercalcaemia or adrenaline in blood
  6. Following SB resection (no absorption /production of inhibitory agents
37
Q

Which situations are there high circulating levels of gastrin?

A
  1. Zollinger-Ellison syndrome (gastrinoma)
  2. Pernicious anaemia
  3. Hypercalcaemia
  4. Following small bowel resection
38
Q

Where does cholecystokinin come from?

A

CCK by I cells in the mucosa of the upper small intestine.

39
Q

What is the main function of cholecystokinin?

A

Basically wants to get bile and pancreas juice into the small intestine. So firstly it is stimulate by the small intestine.

It acts on 3 things:

  1. Gall bladder - causes contraction for which the hormone was named
  2. Causes small amounts of highly concentrated pancreatic juice to be secreted which contains high concentrations of zymogens
  3. Causes relaxation of the Sphincter of Oddi to permit secretion of juices into the small intestine

It has secondary functions too :
1. Enhances the effects of secretin on the pancreas to produce HCO3 rich juice

40
Q

Where does secretin come from?

A

It is secreted by S cells in the deep glands of the mucosa in the upper portion of the small intestines.

41
Q

What is similar between VIP, GIP, secretin and glucagon?

A

The only thing similar between them is that they all have similar amino acid sequences.

42
Q

What is the main function of secretin?

A

Secretin has a few main functions:

  1. Stimulate bicarb rich juice from pancreas and BILE DUCT too
  2. Decrease gastric motility (it actually decreases entire GIT motility to some degree to allow digestion of food
  3. Decrease gastric acid secretion by a gastrin feedback loop
  4. Augments the function of CCK to produce enzyme rich pancreatic juice
43
Q

What increases secretin release?

A
  1. Acid in the duodenum
  2. Amino acids in the small intestine

It is NOT stimulated by the vagus nerve.

44
Q

What does secretin do to chloride in pancreatic juice?

A

Chloride is one of the two main ions in pancreatic juice, the other being bicarbonate.

Chloride concentration in bowel normally sits at around 55mmol/L, and decreases with stimulation from secretin!

45
Q

Where does somatostatin come from?

A

D(delta) cells in the pancreas and D cells in the GIT.

Also a hypothalamic hormone which inhibits growth hormone production.

REMEMBER, somatostatin means -body stop- because it is also known as growth hormone inhibiting hormone.

46
Q

What stimulates somatostatin release?

A

The main fuels in the GIT:

  1. Glucose
  2. Amino acids, mainly arginine and leucine.

Additionally, CCK stimulates somatostatin release (think that somatostatin wants to stop the absorption of food products. somatoSTATIN (STOP)

47
Q

What does VIP do (vasoactive intestinal peptide)?

A

Found in the neurons of the GIT, brain and autonomic nerves.

Functions:

  1. Stimulates secretion of electrolytes in the GIT and water
  2. Relaxation of intestine, vasodilatation
  3. Relaxation of intestinal sphincters
  4. Inhibits gastric acid secretion
  5. Potentiates action of acetylcholine in the GIT
48
Q

What is the precursor to VIP?

A

pre-pro vasoactive intestinal peptide (preproVIP)

49
Q

What is somatostatin’s main function in relation to gastric acid secretion?

A

Stimulates the release of bicarbonate rich juice.

50
Q

What are the main monosaccharides by which carbonhydrates are absorbed?

A

Glucose
Galactose
Fructose

Disaccharides are broken down by brush border enzymes (disaccharidases)

51
Q

Which part of the GIT has the greatest percentage of monosaccharide absorption?

A

Duodenum and jejunum

52
Q

How are carbohydrates absorbed?

A

Most of the monosaccharides are absorbed before they reach the terminal ileum.

Glucose absorption is dependent on intraluminal sodium concentration. High concentration encourages absorption whilst low concentration inhibits it. This is due to the fact that sodium and glucose share the same co-transporter.

This transporter is known as the sodium-glucose linked transporter (SLGT). Sodium moves across its concentration gradient (low intracellular concentration) and along with it comes a glucose into the cell.

Subsequently a GLUT2 transporter allows the glucose to move from the intracellular space to the interstitial space and then into capillaries.

53
Q

What are the two types of SGLT?

A

1: present in gastrointestinal epithelium to facilitate intracellular transport of sodium and glucose.
2. Present in renal tubules to facilitate glucose transport OUT of the tubule

54
Q

Which monosaccharide is not transported by SGLT 1?

A

Fructose. Has its own mechanism of absorption

55
Q

How is fructose absorbed?

A

Fructose absorption is independent of sodium absorption and it enters cells via facilitated diffusion with the GLUT 5 transporter.
Like the other monosaccharides it is transported into the interstitium via the GLUT 2 transporter.

56
Q

How does insulin affect intestinal carbohydrate transport?

A

It basically has no effect. Similarly to the kidney where glucose resorption out of the tubules is independent of insulin and are normal in diabetes.

The maximal rate of glucose absorption from the GIT is 120 grams per hour!

57
Q

Where are antigens absorbed in the GIT?

A

Antigens are immune proteins and as such are absorbed largely in the proximal small intestine.

There are specialised microfold cells (M cells) that sit over the lymphoid patches (Peyer’s patches). Microfold cells absorb and pass the antigens to the lymphoid patches where they activate waiting T lymphocytes. These lymphocytes then enter systemic circulation and later return to secrete the same antigens to protect the host.

58
Q

How are lipids absorbed in the mouth?

A

Lingual lipase is secreted by the Ebner’s glands on the dorsal aspect of the tongue.

59
Q

How are lipids absorbed in the stomach?

A

The stomach secretes a gastric lipase. Remember, the release of other digestive enzymes is sometimes dependent on the presence of free fatty acids so it makes sense that the stomach secretes a lipase to accelerate the release of these hormones for later on.

60
Q

Where does the majority of fat DIGESTION take place?

A

Duodenum by way of pancreatic lipase.

61
Q

What are the main enzymes involved in lipid metabolism?

A

Lipase from the tongue, stomach and pancreas. Pancreatic lipase is probably the most potent and acts only on emulsified fats. It acts in conjunction with colipase to act on emulsified fats, even in the absence of bile salts.

Cholesterol has its own special lipase knwon as cholesterol esterase which is essential in cholesterol and fat-soluble vitamin digestion.

62
Q

What is the role of bile acids on lipid metabolism?

A

Bile acids emulsify lipids into micelles. Micelles are cylindrical and make lipids more water soluble to allow their transport into enterocytes.

This allows them to cross via their concentration gradient through the unstirred layer to the brush border.

When the micelles reach the brush border the lipids diffuse out and are catalyzed by the brush border enzymes.

63
Q

How are fats ABSORBED in the GIT?

A
  1. Passive diffusion, intracellular lipids are quickly esterified which maintains the concentration gradient
  2. Active carriers
64
Q

What happens to different fatty acids in the enterocytes?

A

Depends on their size.

10-12 carbon atom size: are water soluble enought to pass through enterocytes without esterification and be actively transported into circulation.

12 or greater carbon atoms in size: are too large to simple diffuse through and must be re-esterified back into triglycerides. They are mixed with esterified cholesterol and packed in a protein and phospholipid box to form a chylomicron. The chylomicron can then be absorbed into lymphatics where they are transported around the body.

Chylomicra are too large to diffuse directly into capillaries from enterocytes.

65
Q

What proportion of proteins in the GIT come from ingested food?

A

50% from food
25% from GIT secretions
25% from desquamated epithelium

66
Q

Protein has a higher caloric value than carbohydrates, why is it they have similar value in the body?

A

Protein metabolism is incomplete

67
Q

Where are chylomicrons formed?

A

WITHIN enterocytes which aids the transport of lipids in the lymphatic system.

68
Q

Where is most of the dietary sodium absorbed?

A

The majority is in the small intestine with 10% absorbed in the colon.

Breaking it down further, the jejunum and ileum exhibit the most sodium absorption:
Duodenum: 60mmol
Jejunum: 140mmol
Ileum:140mmol
Colon: 40mmol
69
Q

How is sodium absorbed?

A

It is absorbed via cotransporters with glucose, amino acids and in a hydrogen / sodium exchange symporter.

70
Q

How are iron losses controlled?

A

One cannot control the amount of iron lost in the healthy individual, we can only modify the iron intake.
Men lose 0/6mg/d of iron whilst women lost about twice as much. Predominantly this is vai menstruation, in men iron loss occurs via the stool.

71
Q

How is iron absorbed?

A

Almost all iron absorption is in the duodenum. All iron that is absorbed is in its ferrous form Fe2+

It is transported into enterocytes by divalent metal transporter 1 (DMT1).

When the iron enters the enterocyte it may be stored as ferretin otherwise it is transpoted out of the basolateral membrane via a transporter called ferroportin 1.

72
Q

How is iron transported in the body?

A

Fe2+ (ferrous iron) is converted to Fe 3+ (ferric iron) and bound to transferrin.

70% of the iron in the body is in haemoglobin!
3% in myoglobin
The remainder is in ferritin.

73
Q

What factors affect iron absorption?

A
  1. Current state of iron store in the body - low stores = increase iron absorption
  2. State of erythropoeisis in the body - high EPO leads to increased absorption
  3. Ascorbic acid - chelates the iron
  4. Acid gastric juices which converts ferric iron to ferrous iron (Fe3 to Fe2)
  5. Recent dietary intake
74
Q

What factors inhibit iron absorption?

A
  1. Phytic acid in cereals
  2. Basic pH such as that of pancreatic juice
  3. Phosphates
  4. Oxalic acid
75
Q

What factors may increase serum amylase?

A
  1. AKI
  2. Morphine
  3. Perforated duodenal ulcer
  4. Mumps
76
Q

How much parenteral protein is required per day?

A

1.2 - 1.5 grams

AKI is not a contraindication to administration or cause for dose titration.

77
Q

What is the halflife of albumin?

A

28 days

78
Q

What is cobalt deficiency associated with?

A

Megaloblastic anaemia

79
Q

What is chromium insufficiency associated with?

A

Insulin resistance

80
Q

What is the role of branched chain amino acids in surgical patients?

A

BCAAs are leucine, isoleucine and valine, the essential amino acids required for protein synthesis.

They are metabolised in the skeletal muscles rather than the liver.
They improve nitrogen retention and increased protein synthesis and thus the quality and quantity of polyribosomes in muscles.
BCAA are good for patients who may have hepatic encephalopathy because they allow greater protein intake without affecting the encephalopathy.

81
Q

What is arginine?

A

Essential amino acid.
Made in the kidney from citrulline.
Important in urea synthesis, proliferation of lymphocytes and wound healing.
Can be a substitute for production of nitric oxide.

82
Q

What is glycine?

A

Inhibitory amino acid in the spinal cord
Mediates its inhibitory function by hyperpolarising neurons in the CNS.
Acts with arginine and methionine for creatinine synthesis in muscles
Is not affected by atropine

83
Q

What is glutamine?

A

Essential amino acid used predominantly in cells undergoing rapid proliferation.

GSSE - Physiology (8 decks)

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