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Gastro physiology Flashcards

1
Q

What are the functions of the liver (6)

A
  1. Gluconeogenesis, glycogenolysis
  2. Protein metabolism
    - Break down protein converting ammonia to urea, 50% of which is excreted by the kidneys
  3. Fat metabolism
    - Converts free fatty acids to ketones
    - Synthesis of VLDL
    - Processes chylomicron remnants from the blood
    - Formation & secretion of bile
    - Processes fat soluble vitamins
  4. Synthesis
    - IGF-1/ somatomedin
    - plasma proteins: acute phase proteins, albumin, clotting factors, steroid binding & other hormone-binding proteins
  5. Inactivation
    - Toxins
    - Steroids (chemical modification and excretion of thyroxine)
  6. Immunity
    - Kuppffer cells
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2
Q

How is glutamate produced and what is it.

A

Glutamate is an excitatory neurotransmitter. Which serves as a substrate for the production of A ketodehydrogenase.

Formed by converting GLUTAMINE to GLUTAMATE
- This is done by the enzyme GLUTAMINASE.

  • This enzyme is abundant in renal tubular cells (which is why ammonia is made in the kidney).
  • GLUTAMINE is found in the glia.
  • Glutamic acid/ glutamate is taken up by the brain.
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3
Q

What causes the abnormally high blood ammonia levels found commonly in hepatic coma

A
  1. porto-systemic shunting of blood
  2. reduced capacity for urea synthesis in the liver i.e. ammonia can’ t be converted to urea
  3. bacterial production of ammonia in the gut
  4. decreased hydrogen ion excretion by the kidney
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4
Q

What is the composition of bile

A

97% water
0.7% bile salt
0.2% bile pigment

Bile salts
- Na, K

Bile pigments
- Responsible for yellow colour
- From glucuronides, bilirubin & biliverdin by breakdown of RBCs

Other substances
- Cholesterol
- Inorganic salts
- Fatty acids
- Lecithin
- Fat
- Alkaline phosphatase

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5
Q

What would you see predominantly if you analyzed bile chemically

A

Bile salts

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6
Q

What does the cholesterol solubility of bile depend on

A

Presents of bile salts and lecithin

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7
Q

How much bile do we secrete a day, where from and what causes secretion of more

A

liver secretes 500ml of bile daily some excreted in faeces & urine, some gets reabsorbed & re-secreted (enterohepatic
circulation)

Reabsorption of bile salts from the intestine leads to further secretion of bile

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8
Q

What are the 4 types of bile acids

A
  1. Primary (formed in the liver)
    - Cholic acid 50%
    - Chenodeoxycholic acid 30%
  2. Secondary (made elsewhere e.g in the colon and converted by bacteria)
    - Cholic acid -> Deoxycholic acid (15%)
    - Chenodeoxycholic acid -> lithocholic acid (5%)
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9
Q

How are bile acids converted to bile salts

A

Conjugated with taurine & glycine to form bile salts

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10
Q

What is the function of bile salts

A

They are amphipathic (hydrophilic and hydrophobic) and form micelles.

  • To reduce surface tension
  • Assist in fat emulsification, digestion and absorption in the small intestine (in conjunction with phospholipids & monoglycerides)
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11
Q

What is required for the formation of micelles

A

A certain concentration of bile salts is required for the formation of micelles.

Bile salts contain bile acids, which are made from cholesterol.

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12
Q

Does steatorrhoea follow resection of the terminal ileum and if so why.

A

Steatorrhoea may follow resection of the terminal ileum

BECAUSE

95% of the bile salts are absorbed in the terminal ileum & recycled by the enterhepatic circulation

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13
Q

Where are bile salts absorbed and how are they re-circulated.

A
  • 95% small intestine (mainly terminal ileum). This is done by a Na-bile salt co transported, powered by Na-K basolateral ATPase
  • Some are absorbed by non-ionic diffusion along the way.
  • The remaining 5-10% then enter the colon where they are converted to deoxycholic acid and lithocholic acid.
  • Lithocholate is relatively insoluble, mostly excreted in stools; only 1% is absorbed.
  • Deoxycholate is absorbed
  • The absorbed bile salts are transported back to the liver in the portal vein -> re-excreted in bile (enterohepatic circulation)
  • Those lost in stool are replaced by synthesis in liver
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14
Q

What happens when enterohepatic circulation is interrupted e.g terminal ileum resection, Chron’s

A
  1. 50% of ingested fat will appear in the feces because liver cannot increase rate of bile salt production fast enough
  2. severe malabsorption of fat-soluble vitamins
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15
Q

What are bile salts synthesised from and where are they concentrated

A

Synthesised from cholesterol and concentrated in the GB

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16
Q

What are the clinical manifestations of excess bile salts

A

Make the skin jaundice and skin itchy

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17
Q

What are the primary bile salts and what are they conjugated with in the liver.

A

The primary bile salts are cholate & chenodeoxycholate & are conjugated with glycine or taurine in the liver

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18
Q

Where is Bilirubin formed

A

formed in the reticuloendothelial system & BM; when RBCs breakdown (life span ~120days)

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19
Q

When do we get an increase in un-conjugated bilirubin

A

When there is excessive destruction of RBC’s (haemolysis)

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20
Q

How do we make Bilirubin and how to we get rid of it.

A

Macrophages engulf old erythrocytes and degrade them.

Erythrocytes release Hb, which is broken down into haem and globin.

Globin is broken down into amino acids.

The haem is broken down into unconjuagted bilirubin and iron.

Iron is re used for erythropoiesis.

Un-conjugated bilirubin needs to be removed. It is lipid soluble, needs to be bound to albumin to travel in blood (some does float freely unbound).

Un-conjugated bilirubin is carried to the liver.

In the liver bilirubin is conjugated by the addition of glucoronic acid.

This conjugated bilirubin is now water soluble.

This occurs in the sER and is done by glucuronyl transferase.

Conjugated bilirubin can now be excreted in bile (against a concentration gradient) then into the small intestine.

In the ileum/ beginning of large bowel it is converted by gut bacteria into URObilinogen (this is also lipid soluble)

URObilinogen 10-15% reabsorbed by the blood and bound to albumin. Some of this makes it back to the liver and enters the enterohepatic circulation (secreted as bile)

The other 5% is transported to the kidneys where it is converted to urobilin and peed out.

85-90% is oxidised to form sterocobolin (brown) excreted as poop.

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21
Q

What level of billirubin is required for jaundice to occur

A

34

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22
Q

Where does excess bilirubin accumulate

A

Blood
Skin
Sclera
Mucus membranes

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23
Q

What causes hyperbilirubinemia (physiological not diseases)

A
  • Too much production (haemolytic anaemia)
  • Not enough uptake into liver cells
  • Not conjugated properly
  • Conjugated bilirubin can’ t be released into bile canaliculi
  • Obstruction of bile flow   inside & outside of liver
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24
Q

Do people with obstructive jaundice have a tendancy to bleed and if so why

A

Patient who has obstructive jaundice due to gallstone may have an increased tendency to bleed

BECAUSE

In obstructive jaundice, decreased absorption of vitamin K occurs in the gut

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25
Q

Compare haemolytic anaemia to obstructive jaundice with respect to plasma findings

A
  • In obstructive jaundice you get bile salt retention which contains ALP and cholesterol, therefore these levels increase as well
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26
Q

Describe what the Gallbladder does to bile.

A

It concentrates it by actively transported NaCl out of the gallbladder.

Gallbladder actively re absorbs Na. CL, bicarb and water passively follows. This decreases the water content out bile from 97 to 89%.

This concentrates the bile. Liver bile 10-20mmol/L; GB50-200mmol/L

Gallbladder also adds acid to it.
Liver bile pH 7.8-8.6, GB pH 7-7.4

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27
Q

How do we control our biliary secretion

A

When FFA and AA enter the duodenum we release CCK.

CCK stimulates the GB to contract.

This squeezes the bile into the second part of the duodenum.

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28
Q

What 2 things increases the production of bile
(neuronal and hormonal)

A

Stimulation of the vagus nerve
Secretin - Increases the water and bicarb content of bile

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29
Q

What are cholagogues and choleretics (what is the most potent choleretic)

A

Cholagogues are things that cause contraction of GB, e.g. CCK

Choleretics are things that increase secretion of bile, e.g. bile salts. The most potent stimulators of bile salts secretion are the bile salts themselves

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30
Q

How much pancreatic juice to we secrete a day

A

1.5L

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31
Q

What is the pH of the duodenum and how

A

Pancreatic, intestinal and bile secretions neutralise gastric acid. Raises pH 6.0 – 7.0

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32
Q

What does pancreatic juice contain

A

ALKALINE

Cation
- NA
- K
- Ca
- Mg
- pH ~8.0

Anions
- HCO3
- CL
- SO4
- HPO4

Digestive enzymes
- amylase
- lipase
- trypsin
- chymotrypsin
- elastase
- ribonuclease
- deoxyribonuclease
- peptidase
- Proelastase
- Phospholipase A
- a bile salt activated lipase capable of hydrolyzing cholesterol esters

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33
Q

What happens if trypsin is not controlled, and how do we control it

A

It acts on phospholipase A2, which splits of FA from lecithin producing lysolecithin.

This damages the cell membrane and causes the pancreatitis.

To control this we have a trypsin inhibitor

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34
Q

What does trypsin do and how is it secreted

A

Trypsin is secreted by the pancreas as trypsinogen, is activated by enterokinase in the duodenum, and hydrolyzes protein molecules to peptides and amino acids.

Trpysin acts as a positive feedback on itself, converting more trypsinogen to trypsin.

It also converts chymotripsinogens to chymotrypsins and prlolastase to elastase.

(Which break down protein and amino acids respectively)

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35
Q

Is enterokinase a GIT hormone

A

No it is an enzyme on the brush border that converts trypsinogen to trypsin.

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36
Q

Serum amylase may be elevated during…

A
  • Acute renal insufficiency
  • Administration of morphine
  • Acute perforation of a duodenal ulcer
  • Mumps
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37
Q

How do we regulate pancreatic juice secretion, neuronal or hormonal

A

Both but mainly hormonal
- CCK and Secretin

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38
Q

What happens when you inject someone with IV secretin

A
  • Volume of pancreatic juice increases
  • Amount of HCO3 in the juice increases significantly
  • [Cl] in the juice decreases
  • level of amylase is reduced
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39
Q

What is secretins role in pancreatic exocrine function

A

secretin via increasing intracellular cAMP
- (+) pancreatic ducts to make lots of very alkaline pancreatic juice, rich in HCO3 and poor in enzymes
- (+) bile secretion

HCO3 rich pancreatic juice is secreted ONLY in response to secretin, & nothing else

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40
Q

What is CCK and vagal stimulations role in pancreatic exocrine function.

A

‘concentrated’ juice, low volume, but high in acid content, so low pH

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41
Q

What impact does the sympathetic nervous system have on the pancreas

A

the sympathetic nerve supply of the pancreas is vasoconstrictive, and has minimal effect on exocrine secretion

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42
Q

How do we get a vagally mediate section of pancreatic juice and what blocks this affect

A
  • Vagally mediated conditioned reflex secretion of pancreatic juice occurs in response to the sight or smell of food
  • This effect is blocked by atropine and by denervation of the pancreas
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43
Q

In the absence of pancreatic enzymes does the faeceas contain more fat and why

A

In the absence of pancreatic enzymes, the faeces contain more fat MAINLY because there is little enteric lipase in the epithelial
cells of the small intestine

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44
Q

What impact does somatostatin have on glucagon secretion

A

Decreased

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45
Q

What impact does cholinergic stumulation have on insulin secretion

A

Increased

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46
Q

What impact does secretin have on HCO3 and CL (including concentrations)

A
  • [HCO3] being 80mmol/l normally, rising to 150 on stimulation by secretin
  • [Cl-] being 55mmol/l normally, decreases with stimulation by secretin
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47
Q

Two main anions of pancreatic juice

A

HCO3 and Cl

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48
Q

How much saliva do we secrete a day

A

1.5L

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49
Q

What is the pH of saliva

A

normally 7.0, but during active secretion, can go up to 8.0

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50
Q

What does saliva contain (7)

A
  • Lingual lipase
  • Salivary A-amylase
  • Mucins > glycoprotein that lubricate food, bind to bacteria & protect oral mucosa
  • IgA
  • Lysozyme > attack bacteria walls
  • Lactoferrin > binds iron & is bacteriostatic
  • Proline-rich proteins   > protect tooth enamel & bind toxic tannins
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51
Q

What is the function of saliva (6)

A
  • Helps swallowing
  • Keeps mouth moist
  • Serves as a solvent for molecules that stimulate taste buds
  • Helps speech by lubricating tongue
  • Keeps mouth & teeth clean
  • Antibacterial action
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52
Q

What happens in a patient with deficient salivation

A

Xerostomia > higher dental caries

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53
Q

What are the 3 types of salivary glands and wha do they secrete

A

Parotid
- serous cell
- secrete ptyalin
- watery secretions
- 20% contribution to daily saliva.

sublingual
- mucous cells
- secrete mucin
- viscous
- 5% contribution

submandibular
- mixed serous & mucous cells
- moderately viscous secretions
- 70% contribution

remaining 5% is contributed by lingual & other minor glands in the oral cavity

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54
Q

How do we control our salivary secretions (neural vs hormonal)

A

Neural control

Parasympathetic control
- Profuse secretion of water saliva, little organic material

Sympathetic control
- Vasoconstriction + small amounts of saliva rich in organic consituents from submandibular glands

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55
Q

What blocks saliva secretion

A

Atropine

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56
Q

What produces secretion of saliva (neural inputs)

A
  • Food in the mouth > reflex secretion
  • Parasympathetics > vagal stimulation
  • Vagal afferent stimulation at the gastric end of eosophagus
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57
Q

What are the 3 components of the lower oesphageal sphincter and what control are they under

A
  • The smooth muscle of LES is the intrinsic sphincter, under parasympathetic control by vagus/ach
  • Crural parts of the diaphragm. Extrinsic sphincter controlled by phrenic nerve of diaphragm, hence respiration
  • Oblique or sling fibres of the stomach wall
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58
Q

Is the oesophagus normally open or closed

A

Closed at both ends

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59
Q

Compare the activity of the LES with the body of the oesphagus

A
  • The LES exhibits tonic muscular activity unlike the body of the esophagus
  • But not 5mmHg above gastric pressure in resting
    state
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60
Q

What causes acahlasia and what are a couple of treatment options

A

Due to increased resting LES tone & incomplete relaxation on swallowing thus food accumulates in esophagus   therefore esophagus dilates.

This is because the myenteric plexus of the oesophagus is deficient at the LES and the release of NO and VIP is defective.

Can be treated by dilation, myotomy. Or you can inhibit Ach by botox.

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61
Q

Outline 4 physiological properties of the stomach (incuding what is secretes)

A
  1. receptive relaxation when bolus is coming from oesophagus, myenteric inhibitory nerve (+) stomach relaxes
  2. control of the rate of access of food to the small intestine
  3. secretion of a lipase, amylase, gelatinase
  4. secrete intrinsic factor which are essential for VitB12 absorption and thus erythrocyte formation
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62
Q

What cells types are present in the stomach, where are they located and what do they secrete (8)

A
  1. parietal (oxyntic) cells -
    -HCL
    - Intrinsic factor
    - Lie closer to gland opening
    - More located in fundus and body.
  2. chief (zymogen, peptic)
    - Pepsinogens and peptic lipase.
    - Lie deep within gland.
    - More located in fundus and body.
  3. ECL cells (enterochromaffin-like cells)
    - secrete histamine
  4. Goblet cells- secrete mucus
  5. surface epithelial cells - produce HCO3 rich secretions
  6. G cells
    - Secrete Gastrin
    - Located in the antrum
  7. D cells
    - Secrete somatostatin
    - Present in the antrum
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63
Q

Impact of vagal stimulation on stomach secretions

A

Increases secretion of acid and pepsin

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64
Q

Impact of vagotomy on stomach secretion

A
  • It diminishes (but does not abolish) acid secretion
  • It diminishes (but does not abolish) gastric motiliy
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65
Q

What is the respiratory quotient of the stomach during secretion of gastric juice

A

<1 BECAUSE the stomach takes up more CO2 from
arterial blood than it puts into the venous blood

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66
Q

Describe the relationship between Gastrin levels and a gastric bypass operation.

A

after the operation of high gastro-jejunostomy (gastric bypass) for obesity, the level of plasma gastrin may rise following a
meal

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67
Q

What happens to stomach acid secretions if you resect large segment of small intestine

A

increases

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68
Q

What happens to stomach acid secretion if you remove the pylorus i.e antrum

A

Would be expected to reduce acid secretion

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69
Q

Which part of the stomach secretes the most acid

A

Body and fundus

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70
Q

Volume of gastric secretions per day

A

2.5L

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71
Q

What is the function of HCL secretion

A
  • Kills many ingested bacteria
  • Provide necessary pH for pepsin to start protein digestion
  • Stimulates flow of bile
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72
Q

Content of gastric acid secretions

A

cations
- Na
- K
- Mg
- H+
- pH ~1.0

anions
- Cl
- HPO4
- SO4

Pepsins
Lipases
Mucus
Intrinsic factor

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73
Q

What is the purpose of the mucus secreted by the stomach and what stimulates its release

A

Traps HCO3 ions, and protect underlying epithelial cells from lysing
mucus secretion is stimulated by prostaglandins

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74
Q

What is the function of gastric lipase

A

Fat digestion

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75
Q

What is the function of IF

A
  • Essential for VitB12 absorption in terminal ileum
  • Normal daily secretion can bind 10-50 times the amount of B12 needed for the day
  • Secretion is depressed in gastric atrophy if untreated   can lead to pernicious anaemia
76
Q

What reduces secretion of stomach acid

A

the secretion of acid from the stomach is reduced when chyme enters the duodenum

77
Q

What is the function of pepsin and what pH does it work best at

A

works best at pH2-3, formed from pepsinogens they initiate breakdown of proteins to aa

78
Q

Are gastric drainage procedures required post truncal vagotomy and high selective vagotomy

A

Just truncal

79
Q

Give one negative feedback mechanism for gastric secretions

A

Acid in the antrum inhibits gastric secretion via a feedback mechanism involving somatostatin

80
Q

What are the 3 phases involved in gastric secretion and describe how gastric acid secretion is shut off.

A

Cephalic phase
- Vagal input (thinking about food etc) stimulates the release of Ach and GRP.
- Triggering release of gastrin before food even enters the stomach

Gastric phase
- Meal enters stomach, heaps of gastrin released.
- Stomach is also stretched increases vagal activity.

Food that enters the stomach buffers acid. Which would normally start acting as a negative feedback.
Somatostatin is released from D cells which acts on both G cells, EC cells and parietal cells themselves. In other words gastric secretion is terminated after the meal goes from the stomach to the small intestine.

81
Q

Where is the main terminal branch of the anterior vagus nerve

A

Crosses the stomach distal to the incisura angularis ~5-6 cm from the pylorus.

Some vagal fibres traveling to the parietal cell mass may sink into the muscular wall at the oesophagus some distance above the cardia

82
Q

What is pyloric stenosis and what causes it

A

Gastric outlet obstruction
May be due to benign duodenal/ prepyloric ulcer or by a stomach cancer.

83
Q

Metabolic effects that occur as a result of pyloric stenosis

A

Prolonged vomiting occurs which essentially results in metabolic alkalosis.

However, if the dehydration is severe enough, paradoxical aciduria may occur

  • Serum bicarbonate rises & serum chloride falls, with a rise in blood pH
  • The kidneys then waste bicarb to maintain homeostasis. A large bicarb load is presented to the kidney (an amount which exceeds the PCT’s capacity to reabsorb it).
  • An osmotic diuresis ensues as Na and therefore water follows bicarb.
  • Volume depletion stimulates the release of aldosterone and Na is exchanged for K+ (so we lose K+ too)
  • K+ loss is exacerbated as we try to increase blood pH by retaining H+ and secreting K+.

-######

  • correction requires iv isotonic saline with added K
84
Q

Volume of small intestine secretions per day (and how much makes it into the stool)

A

9L a day
2L from dietary sources
7L from GIT secretions
only 1-2 L go to the colon
100-200ml in stools

85
Q

What does the intestinal mucosa below the duodenum produce

A
  • Mucus
  • Secretin
  • CCK
  • Isotonic intestinal secretion
86
Q

What is maximally absorbed in the upper part of the small intestine and what isnt

A
  • iron
  • Calcium
    NOT bile salts and NOT vit B12 (these are maximally absorbed in the terminal ileum)
87
Q

What sort of metabolic disturbance can diarrhoea produce

A

hypo K

88
Q

Where are mucosal cells located in the small intestine.

A

mucosal cells are formed from undifferentiated cells in the crypts of Lieberkuhn

89
Q

How does motility differ in the jejunum compared to the ileum

A

the frequency of slow waves decreases from the jejunum to the ileum

Peristalsis is not the only form of movement demonstrated

90
Q

What increases the surface area in the small intestine

A

The absorptive surface of the small intestine is increased 600 fold by the valvulae conniventes, villi & microvilli

However, the single most important factor is the microvilli

91
Q

How does the colon and small intestine handle K+ and Na

A
  • K is absorbed by small intestine & secreted by large intestine
  • Ative absorption of Na from the colon is accompanied by water absorption
92
Q

How much of the small intestine has to be resected for malabsorption to occur

A

> 50%

93
Q

What impact does a small intestine resection have on bile salts

A

resection of ileum prevents absorption of bile acids
- leading to deficient of fat absorption malabsorption of fat soluble vitamins ADEK
- malabsorption of vit B12

94
Q

Which part of the ileum being resected leads to the greatest degree of malabsorption

A

Distal small bowel resection.

95
Q

Complications from a small bowel resection include (7)

A
  • Lowered serum calcium
  • Hyperuricemia - increased likelihood of renal stone
  • Hypergastinaemia
  • Lowered serum protein
  • Intractable diarrhoea
  • Arthritis
  • Fatty infiltration of the liver, followed by cirrhosis
96
Q

Are patients who undergo massive resection of the proximal small bowel likely to develop peptic ulcer disease and if so why.

A

Yes, BECAUSE in such patients
1. there is hypersecretion of gastric acid
2. there is decreased secretion of secretin & GIP

97
Q

5 Features of colonic function

A
  1. constancy of faecal content despite variation in diet
  2. active transport of Na out of the colonic mucosa water follows
  3. sterile contents at birth
  4. secretion of K & HCO3 into lumen
  5. absorption is so good that rectal drug administration is ideal
98
Q

What is blind loop syndrome

A

Also known as stagnant loop syndrome, can occur as a surgical complication.
Get an outpouching of bowel (a bit like a diverticula) that becomes stagnant, this has several significant flow on effects.

  • Bacterial overgrowth
  • Malabsorption
  • Macrocytic anaemia (not enough B12 absorbed)
  • Metabolic derrangements.
  • Steattoreha: Bacteria hydrolyse conjugated bile
99
Q

What is more likely to produce symptoms a narrowed segment of the distal third of colon or the proximal third of the colon and why.

A

A narrowed segment of the distal third of colon is more likely to produce symptoms than a narrow in proximal third BECAUSE

Faecaes are more fluid in the proximal third of the colon than they are in the distal third

100
Q

How much isotonic chyme enters the colon each day from the ileum

A

1-2L

101
Q

Describe the feedback mehcanism involved in gastric secretions.

A

Gastrin release is stimulated by…
- Neurotransmitter (GRP, which is released by Vagus nerve)
- Presence of oligopeptides (amino acids)

Once Gastrin is released it acts on
- Parietal cells to secrete HCL
- Likely chief cells (to secrete pepsinogen)
- EC cells to release histamine which acts on an H2 receptor.

Ach again released by the vagus nerve can also act on EC cells and parietal cells. Ach acts on an M3 receptor.

Gastrin, histamine and ACh all work on distinct receptors.
- Gastrin and ACh both increase cystolic calcium
- Histamine increases cAMP
- All of these work synergistically together

102
Q

Explain how HCL is secreted

A

H/K ATPase on apical membrane pumps out H+ against its concentration gradient (K+ comes into cell).

Secretion of protons is associated with release of bicarcb into the blood stream, which neutralises the acid once gastric function is complete. (Cl- is exchanged for bicarb)

103
Q

Describe the influence of CCK , secretin and Ach on pancreatic and bile secretions

A

Secretin
- Lots of alkaline fluid thats poor in enzymes
- Affect is due to increase in cAMP
- Also stimulates bile secretion

CCK
- Releases zymogen granules and production of panc juice that has lots of enzymes but low in volume.
- Promotes contraction of GB, relaxation of Oddi
- Effect mediated by phospholipase C

BY acting together they add enzymes to panc juice and ensure they are washed out in the intestine.

ACh works the same as CCK

104
Q

Stimuli that affect gastrin secrretion
(Luminal, neural, blood, other)

A

Increased
- Luminal -Peptides and amino acids, distention
- Neural - Increased vagal discharge via GRP
- Blood borne - Calcium and epinephrine
- After a small bowel resection

Decreased
- Luminal - Acid and somatostatin
- Bloodborne - Secretin, GIP, VIP, glucagon, calcitonin

105
Q

Why do bile salts form Micelles

A

Bile acids are amphipathic they have hydrophobic and hydrophilic domains.
They form micelles with their hydrophilic portions facing out and their hydrophobic portions facing in.

106
Q

What GIT hormones are structurally similar.

A

VIP
GIP
Secretin
Glucagon

All have a portion of similar amino acid sequence

107
Q

Where is Gastrin found/ secreted from

(Lots beyond primary site)

A

Produced by G cells in
- Gastric antrum
- First part of duodenum

Also found in
- Pancreatic islet cells
- Pituitary
- Hypothalamus
- Medulla
- Vagus
- Sciatic nerve

108
Q

What are the functions of gastrin (4)

A
  • Acts on both oxynitic and peptic cells (HCL and pepsin)
  • Trophic effect on stomach, small and large intestinal mucosa.
  • Improves gastric motility
  • Promotes insulin secretion, however only after a protein meal and not a CHO meal.
109
Q

Outline the similarities between Gastrin and CCK

A

They are functionally and structurally related.

BOTH gastrin and CCK are stimulated by a protein meal and both stimulate glucagon secretion ###

110
Q

What syndromes are Gastrin levels high in

A

Zollinger Ellison
Pernicious anaemia

111
Q

Where is CCK secreted from

A
  • I cells in the small bowel mainly but also found in NERVES of distal ileum and colon
112
Q

What promotes secretion of CCK

A

AA and FA

113
Q

What are the functions of CCK (8)

A
  • Stimulate pancreatic enzyme secretion
  • Contract GB + relax sphincter of oddi = bile into small bowel
  • Augment Secretin
  • Inhibit gastric emptying
  • Reduce gastric acid secretion
  • Trophic effect on pancreas
  • Increase synthesis of enterokinase
  • Enhance motility of small intestinse and colon
114
Q

Where is Secretin released from

A

S cells
- Deep in glands of upper small intestine and mucosa of duodenum

115
Q

What the is action of Secretin (6)

A
  • Lots of alkaline rich fluid from biliary tract and pancreas
  • Augments CCK
  • Decrease Gastric acid secretion
  • May cause contraction of pyloric sphincter
  • Inhibits gastric motility
  • Powerful stimulant of pancreatic enzyme
116
Q

What stimulates release of secretin (2)

A
  • Acid in the duodenum
  • AA in the upper small intestine
117
Q

Feedback mechanism of secretin

A

Alkaline pancreatic juice enters duodenum which neutralises acid in stomach and reduces further secretin

118
Q

What is Secretin structurally similar to (and what is it not similar to)

A

GLI, VIP, GIP and glucagons

(CCK and gastrin)

119
Q

Where is somatostatin released from

A

D cells in the pancreas and by similar D cells in gastrointestinal tract.

Exists in 2 forms
- 14 and 28 which are found in various parts of the brain as a neurotrasmitter

120
Q

What stimulates Somatostatin release

A

Acid in lumen
Glucose
Amino acids
CCK

121
Q

What is somatostatin actions

A
  • Inhibit Gastrin release
  • Inhibits parietal cell function
  • Inhibit release of insulin, glucagon, CCK and pancreatic polypeptide.
  • Gastric motility
  • inhibits absorption of glucose, amino acids and triglycerides.
  • Inhibits gallbladder contraction
  • Secretes bicarcb
122
Q

What do people with somatostatinomas develop

A

hyperglycemia
gastroparesis
gallstones

123
Q

Where is GIP produced

A

K cells of duodenum and jejunum

124
Q

What stimulates the release of GIP

A

Glucose and fat in duodenum

125
Q

Actions of GIP

A
  • Inhibits gastric secretion and motility in large doses
  • Increases the sensitivity of insulin response to raised BGL
126
Q

Why do patients who undergo resection of the proximal small bowel develop peptic ulcer disease

A

Because there is decreased secretion of secretin and GIP

127
Q

Where is VIP found

A

Nerves in GIt
Brain and in many autonomic nerves

128
Q

What stimulates the release of VIP

A

Fat

129
Q

What is the action of VIP (4)

A
  • Markedly (+) intestinal secretion of electrolytes & hence of water
  • Relaxation of intestinal smooth muscle, including sphincters
  • Dilation of peripheral blood vessels
  • Inhibition of gastric acid secretion
130
Q

What do VIPomas cause

A

Severe diarrhoea

131
Q

Where is enteroglucagon produced

A

L cells in distal ileum and colon

132
Q

Compare enterogloucagon to gluacgon

A

Similar structure but different function

133
Q

What stimulates the release of enteroglucagon

A

Presence of glucose and fat in the ileum

134
Q

What is the action of enteroglucagon

A
  • Inhibits gastric and intestinal motility
  • Has trophic effect on intestinal crypt cells
135
Q

How are carbohydrates digested

A

We eat polysacharides
disaccharides and monosacarides.

Polysaccarides get broken down into discarraides by amylase in saliva, stomach and small intestine, these then subsequently get broken down into monosaccaraides (by things like maltase, sucrase, lactase)

Overall brush border digestion of carbohydrates generates monosaccharides (glucose, galactose and fructose) at high concs at the exact location they need to be digested.

136
Q

How are cardbohydrates absorbed (glucose and galactose)

A

Monosaccharides are readily absorbed across the wall of the small intestine

Largely in the duodenum and upper jejunum.

Most of the monosachs are removed before the meal reaches the terminal part of the ileum.

The transport of glucose and galactose via SLGT depends on sodium in the intestinal lumen. This is because it is a co transporter.

Na is exported basolaterally by Na/K ATpase.

Whilst any glucose not used by the cell is diffused out by GLUT2 into the interstitium then blood.

An example of indirect active transport.

137
Q

Symptoms of oligosacharidases deficiency

A

Diarrhoea
Bloating
Flatulance
All after the ingestion of sugar

138
Q

How is fructose absorbed

A

Occurs independently of Na.
Facilitated diffusion via GLUT5 and into interstitium via GLUT2

139
Q

What is the maximal rate of glucose absorption from the intestine

A

120 g/h

140
Q

Does insulin affect intestinal transport of sugars

A

Little effect

141
Q

Similarities between renal and gut glucose absorption

A
  • neither require phosphorylation
  • both are essentially normal in diabetes
  • both are depressed by drug phlorhizin
142
Q

How is protein digested and where

A

Starts in the stomach where pepsin cleaves some of the peptide linkages (particularly phenylalaine/ tyrosine) into POLYPEPTIDES.

Pepsin works best at 1.6-3.2 so it gets inhibited when gastric contents are mixed with alkaline fluid within the small intestine.

Within the small intestine polypeptides are further digested by the proteolytic enzymes of the pancreas and intestinal mucosa (trypsin etc).

These polypeptides are then broken down into amino acids, some of this occurs in the lumen, some at the brush border, and some are transported into the intestinal cells before being hydrolyzed.

143
Q

How is protein absorbed (amino acids and peptides)
including where

A

Absoprtion of amino acids occurs rapidly in the duodenum and jejunum, little absorption occurs in the ileum.

It occurs via 7 different transport systems
- 5 of which require Na co transport
- 2 of those 5 also require Cl
- 2 of the systems occur independently of Na

Peptides
- Transported via PepT1 which requires H+ not Na. They are then hydrolyzed into amino acids. Very little of this occurs after the neonatal period.
-

144
Q

Where is our protein sourced from

A

Protein gets broken down into peptides or amino acids.
~50% from ingested food
~ 25% from gut secretions
~ 25% from desquamated epithelial cells

145
Q

How much protein that enters the small intestine escapes digestion and absorption

A

2-5%
Some of which gets digested by bacteria in the colon.

146
Q

Compare infant to adult protein digestion

A

Whole protein is absorbed from the alimentrary canal (largely as igA)

147
Q

Why does ingestion of protein foods provoke antibody formation in infants

A

Because in infants there is absorption of whole protein from the alimentary canal.

(these whole foreign protein enter the circulation and provoke antibody formation)

148
Q

Why do we absorb the same amount of calories from protein and carbs despite protein being more calorific

A

Because the oxidation of protein is incomplete (i.e not all digested)

149
Q

What is our daily protein requirement for parenteral nutrition and when should we consider reducing this dose.

A

1.2 - 1.5 g/kg/day.

When there is a rise in blood urea level that exceeds 100mg/dL or a rising blood ammonia level that is a/w with clinical encephalopathy.

Dont need to reduce in AKI, but you do in CKD.

150
Q

What is the benefit of nucleic acids in parenteral nutrition.

A

Nutritional reqiurement has not been established.
Possibly have the following benefits
- Proliferation of intestinal crypts
- Lymphocyte proliferation
- Cellular DNA and RNA synthesis

151
Q

What is the half life of albumin

A

28 days

152
Q

What is a convenient source of nitrogen in parenteral nutrition

A

Glycine as it is a simple amino acid.

153
Q

How quickly does haemodyalsis and haemofiltration remove amino acids

A

3 to 5 g/hr

Need to consider these losses when adjusting amount of protein administered.

154
Q

How much of fat do we eat in a day, how much of this is absorbed, compare this to infants

A

150g a day, 5g to faeces and the rest is absorbed
>95% is absorbed
Infants <90%

155
Q

How is fat digested

A

Begins with 2 preliminary lipases, one in the saliva (secreted from Ebner glands) and one in the stomach.

Both contribute only a little to fat digestion other than in the setting of PEI. (saliva ~30%)

But they might make FFA (medium and short chains) that begin to stimulate release of CCK.

Most of true fat digestion begins in the duodenum by pancreatic lipase. This produces fatty acids and monoglycerdies Lipase is stablised by colipase and is critical for its action.

Fats are insoluble so it is difficult for them to reach the mucosal layer of cells. Therefore they are furhter emulsififed by bile acids and lecithin. This produces micelles which can be absorbed (bile salt + monoglyceride + FA = micelle).

Micelles essentially give them a way to transport themselves to the enterocyte.

156
Q

Outline how fat absorption occurs (starting from the micelle)

A
  • Greatest in the upper intestine.
  • Micelles get close to luminal membrane then FFAs & monoglycerides leave the micelles and diffuse across.

-Micelles DOES NOT get actively absorbed across the lumen.

Once inside the mucosal cell the fate of the FA depends on their size.

<10-12 carbons i.e short and medium chain
- Small enough to circulate

> 12 carbon i.e large FA
- Too large to circualte
- Get re-esterified to triglyceride to form chlyomicrons (with cholesteroll, protein and phospholipid) which leave the cell by exocytosis.

157
Q

What is the make up of a chylomicron and where is it fomed

A

Formed in golgi apparatus
Triglyceride 87%
Phospholipids 9%
Cholesterol ester 3%
Apoprotein 1%

+ fat soluble vitamin and free cholesterol.

158
Q

How do chylomicrons get into the blood

A

They are too big to enter the portal circulation
They enter the lymph channel by the thoracic duct therefore bypassing the liver.

159
Q

How much of our fat is transported as a chylomicron

A

80-90%

160
Q

What is the fate of the chylomicron

A

Enter the blood via the thoracic duct, makes its way to adipose tissue and muscle.

Apoprotein CII that is within it activates lipoporotein lipase and FFA/ monoglycerides are released entering the adipose tissue and muscle cell.

The remaining chylomicron makes its way back to the liver.

In other words dietary triglycerides are delivered to peripheral tissues whilst cholesterol is delivered back to the liver.

161
Q

What impact does fat in the duodenum have on stomach emptying

A

It delays it because fat in the duodenum releases CCK, secretin and GIP

162
Q

What 2 hormones decrease plasma cholesterol levels

A

Thyroxine
Oesotrogens

163
Q

What is the role of VLDL

A

Transported endogenously derived triglyceride.
It is increased by carbohydrate excess in diet
(as VLDL and LDL are both made by glucose > cholesterol > lipoprotein by HMG-COA)
It is removed from circulation by muscle and adipose tissue (where it is stored or used as an energy source)

164
Q

Where is sodium absorbed

A

90% small intestine
10% colon

60mmol duodenum
140 jejunum
140 ileum
40 colon

165
Q

How is sodium absorbed

A

Secondary active transport
- NA/ glucose
- NA /amino acid co transport
- Na/H exchange

Therefore Na absorption is enhanced by glucose and amino acids

Thats why it is important to drink sugar water with severe diarrhoea/ vomiting as it will help with Na absorption

It is absorbed into the interstitial fluid by primary transport.

166
Q

What does Vitamin B12 absorption require (x2) and what does it not require (x2)

A

IF binding with B12 in the small intestine
Trypsin which facilitates efficient absorption

Not high oral intake of B12
Not pepsin

167
Q

4 things that pernicious anaemia is typically associated

A
  • A reduced packed cell volume
  • Megaloblastic marrow
  • Gastric atrophy
  • Thrombocytopenia
168
Q

Why is scurvy associated with blood vessel fragility

A

Because ascorbic acid is an essential co factor for the synthesis of collagen

169
Q

What fibre should we use in enteral nutrients and what is the rationale.

A

Butyrate

Endogenous products of fibre fermention are important for colonocyte integrity and function.
But provision of fibre has not clearly demonstrated a clinical advantafe

170
Q

Why is glutamine not included in parenteral nutrition

A

Because it is unstable in solution and breaks down to form toxic amounts of pyroglutamate and ammonia.

171
Q

What cells use glutamine for fuel

A

It is the main fuel consumed by rapidly dividing cells.

e.g. gut mucosa, immunocytes, and some tumours

172
Q

Does glutamine improve outcomes in catabolic patients

A

Remains unclear

173
Q

What might cobalt deficiency cause

A

Megaloblastic anaemia

174
Q

What might chromium deficiency cause

A

Insulin resistance

175
Q

Why might artic explorers get a headache, diarrhoea and dizziness if they eat polar bear liver

A

Lots of vitamin A

176
Q

Diarrhoea during enteral tube feeding may be due to

A
  1. excess volume of feed
  2. hyperosmolarity of feed
  3. malabsorption
  4. short bowel syndrome
177
Q

What is the daily requirement for CHO for parenteral administration

A

25 kcal/kg /day
appears adequate for most patients.

178
Q

Proportion of calories per day that can be given as CHO for parenteral nutrition

A

30-70%

179
Q

What BGL do you try to maintain whilst giving CHO for parenteral nutrition and what can you do if it exceeds this

A

<225 mg/dL
May be desirable to administer insulin

180
Q

What should the calorie to nitrogen ratio be for parenteral nutrition

A

150kcal per gram of nitrogen (about 6.25gm of protein contains 1gm of nitrogen)

181
Q

What sources should and shouldn’t be used in parenteral nutrition

A
  • Glycerol
  • Sorbitol

NOT maltodextrins
NOT starch

182
Q

How is arginine produced

A

Synthesized in the kidney from gut derived citrulline.

Small intestine converts dietary amino acids including gutamine to citruline.

183
Q

What is the function of arginine

A

Substrate for production of NO, present in many tissues and cells including endothelium and inflammatory cells.

Participates in a variety of metabolic functions
- Urea synthesis
- Lymphocytes proliferation
- Wound healing

184
Q

What is the role of arginine in critically ill patients and how much should they be given.

A

Exact role remains to be defined.

Might be helpful with immune function when combined with fish oil and nucleic acids

up to 30g a day

185
Q

Compare hormones (Gastrin, CCK, Secretin, GIP) present in
- Antrum
- Duodenum
- Jejunum
- Ileum

A

Gastrin
- Antrum
- Duodenum
- Jejunum

CCK
- Duodenum
- Jejunum
- Ileum

Secretin
- Duodenum
- Jejunum
- Ileum

GIP
- Duodenum
- Jejunum

186
Q

Outline how ammonia is metabolised and excreted.

A

Ammonia is insoluble and toxic to the CNS and freely permeable across the BBB. The liver is the only organ which completes the urea cycle by converting ammonia to urea which can then be excreted in the urine.

Ammonia comes from the colon and kidneys + a small amount from RBC breakdown and metabolism in muscles.

Proteins are broken down into amino acids (which contain an amino group).

Free ammonium ions/ammonia (NH4+) are not transported to the liver by themselves given their toxicity.

2 steps occur before the urea cycle begins.

  1. Transamination
    - Amino group in an amino acid which contains a nitrogen is taken from the amino acid and given to another molecule (like alpha ketoglutarate which is a nitrogen scavenger) which converts it into GLUTAMATE.
    This is catalysed by GLUTAMIC DEHYDROGENASE.
  2. Oxidative deamination
    - When GLUTAMATE reaches the liver it under goes oxidative deamination (i.e the amino group is removed). Glutamate is the only amino acid that undergoes a significant amount of oxidative deamination.

The ammonia that has been liberated in the mitochondria by oxidative deamination is converted to urea by the urea cycle.

UREA CYCLE 5 step cycle
1. Ammonia + CO2
- Carbomyl phosphatase
- Mitochondria

  1. Carbomyl phosphate + Ornithine
    - Citrulline.
    - Mitochondria
  2. Citrulline is ultimately converted to Urea through a few more enzymatic streps.

GSSE (15 decks)

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