Digestion Flashcards

1
Q

What is the ideal pH in the oral cavity, stomach and small intestine?

A
  • Stomach- 1-3.5
  • Oral cavity- 6.2-7.6
  • Small intestine- 6-9
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2
Q

What are the digestive and absorption function of each gastrointestinal section?

A
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3
Q

What two principal cell types is pancreatic juice made from?

A

Pancreatic acinar cells- enzyme secretion
Pancreatic duct cells- HCO3- seccretion and water

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4
Q

What does stimulation with acetylcholine or cholecystokinin cause in pancreatic acinar cells?

A

intracellular Ca2+ increases and stimulates the exocytosis of enzyme containing secretory granules (zymogen granules), also stimulates NaCl rich fluid secretion

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5
Q

What are zymogen granules?

A

Pancreatic enzymes are packaged within zymogen granules. The enzymes within the zymogen granules are inactive precursors (proenzyme) of the mature enzyme to prevent autodigestion of the cell. Zymogen granules can be secreted upon stimulation of the acinar cell. The interior of the zymogen granule is very acidic. The zymogen granules also contain serine protease inhibitors (e.g. SPINK1 gene) to guard against autodigestion. Serine protease inhibitors – disrupt active site of enzymes. Mutations of SPINK1 gene has been shown to lead to hereditary forms of pancreatitis

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6
Q

What is the action of proenzymes?

A
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7
Q

How is pancreatic lipase activated?

A
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8
Q

How is NaCl rich fluid secreted?

A
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9
Q

How does the pancreatic duct secrete HCO3- rich pancreatic fluid?

A
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10
Q

What does secretion of HCO3- do?

A
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11
Q

What is CFTR?

A

Cystic fibrosis transmembrane conductance- regulator plays a central role in the pancreatic ductal secretory functions by carrying Cl-and HCO3-ions across the apical membrane. Failure to synthesis this protein in its normal state or failure to insert it properly in the apical membrane results in cystic fibrosis and a severe decrease of ductal secretion. As a result protein containing acinar secretions become concentrated and precipitate within the duct lumen, blocking small ducts and eventually destroying the gland. The effects of impaired ion secretion by pancreatic ductal epithelial cells in CF can lead to exocrine pancreatic damage and pancreatic exocrine insufficiently

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12
Q

What syndrome is caused my stomach acid hypersecretion?

A

Zollinger-Ellison syndrome

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13
Q

What does acidic chyme do?

A

when it enters the duodenum -> stimulate S-cells to release secretin, if the luminal pH falls below 4.5

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14
Q

What does secretin do?

A

ultimately aids neutralisation of acidity

  • Role in HCO3 secretion from: pancreatic duct, stimulates Brunner’s gland and regulates secretion into duodenum from biliary ducts.
  • Stimulates bile (alkali) secretion from the biliary ducts.
  • Slows H+ secretion by stomach parietal cells (inhibits gastrin
    release)
  • Decreases motility of the stomach
  • Constriction of pyloric sphincter
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15
Q

What are the 3 phases of digestion?

A
  1. Cephalic - External environment and mouth
  2. Gastric - Stomach
  3. Intestinal - Intestines
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16
Q

What happens in cephalic phase?

A

The sight, smell and taste of food allows for an anticipatory response meaning the body can prepare the gastrointestinal tract to receive food e.g. for:
• lubrication with saliva
• ensuring acid is present in the stomach to digest food/kill bacteria
• bicarbonate is present to neutralise any acidic chyme escaping the
stomach
• to have active enzymes in place when the food arrives

  • Role of the stomach- The afferent nerve impulses are transmitted through the vagal nucleus and vagal efferent fibres to the stomach. The vagus nerve acts directly
    on:
    • parietal cells (acetylcholine is mediator) = acid secretion
    • antral G cells (gastrin releasing peptide GRP is mediator) = gastrin release
  • Role of the pancreas- Afferent impulses travel to the vagal nucleus. Vagal efferent transmissions to the pancreas stimulate both the duct and the acinar cells to secrete. Stimulation is mediated by ACh and has a greater effect on the enzymatic component than it does on the aqueous component
17
Q

What happens in gastric phase?

A
  • Distention- activates mechanoreceptors. Mucosal distention
    receptors send signals by vagal afferents -> vagal nucleus. Efferent signals are sent back to G cells and parietal cells by the vagal efferents. All distention reflexes are mediated cholinergically (activated by or capable of liberating acetylcholine)
  • Digestion of protein- G-cells in the stomach secrete gastrin in response to amino acids and peptides in the stomach. Gastrin stimulates acid secretion matches degree of secretion to predicted quantity of food ingested. pH <3 inhibits gastrin release in response to digested protein
18
Q

What happens in intestinal phase?

A

Gastric acid stimulate secretin release -> stimulating water and HCO3- release from duct cells. Fat and protein digestion
products stimulate Cholecystokinin (CCK) released from the I cells. CCK acts by stimulating vagal afferent receptors and initiating vagovagal reflexes (depends on cholinergic signalling). Stimulates the release of enzymes from the acinar cells. Active trypsin in the intestinal lumen inhibits CCK release

19
Q

Summarise the secretion and action of gastrin, CCK, secretin and GIP

A
20
Q

How are monosaccharides absorbed?

A

SGLT1 needed for the uptake of glucose. Energised by the electrochemical Na+ gradient. Maintained by the extrusion of Na+ across by the Na-K pump (secondary active transport).Facilitated diffusion mediated by GLUT5 is responsible for fructose absorption. Facilitated diffusion - GLUT2 mediates their efflux across the basolateral membrane into the interstitial space

21
Q

How are proteins absorbed?

A

Most peptides or amino acid molecules transport is supplied by a Na+ cotransport mechanism. After binding, the Na+ ion then moves down its electrochemical gradient to the interior of the cell and pulls the amino acid or peptide along with it = co-transport (secondary active transport). Oligopeptide uptake occurs via an H/oligopeptide
cotransporter known as PepT1 = secondary active transport

22
Q

How are fats absorbed?

A

Fatty-acid/bile-salt mixed micelles enter acidic microclimate generated by Na+/H+ exchange at the brush- border membrane. Fatty acids become protonated leave the micelle. Membrane proteins assist uptake of fatty acids:
• FAT or CD36
• FABPpm
• FATPs

23
Q

What is the absorption of lipids across the intestinal wall?

A
24
Q

What is the function of carbohydrates?

A

source of energy and fibre

  • 4 kcal/g
  • Functions: Energyproduction, Energystorage, Buildingmacromolecules, Sparingprotein, Lipidmetabolism
25
Q

What is the function of proteins?

A

structural building blocks

  • 4 kcal/g
  • Functions: Structureandmotion, Enzymes, Hormones, Acidbasebalance (intracellular proteins serve as buffers because they contain a large number of acidic or basic groups such as -COOH/-COO-or NH3* /-NH2), Transport, Protection (antibodies), Woundhealing (fibrin clot), Energyproduction
26
Q

What is the function of fats?

A

energy storage, cell repair

  • 9 kcal/g
  • Functions: Storingenergy (fats -> fatty acids and glycerol -> acetyl Co A and can be used in the Citric acid cycle = ATP), Regulatingandsignalling, Insulation andprotection (visceral fat for organs), Aidingdigestion
27
Q

What is the function of water?

A

solvent & lubricant, transport if nutrients, temperature regulation

  • 0 Kcal/g
  • Functions: Transport (blood and lymphatic fluid), Mediumforchemicalreactions, Lubricantandshock absorber, Temperatureregulator
28
Q

What is the function of vitamins and what are the 2 types?

A

involved in chemical reactions

  • Vitamins are required in small amounts to act ascoenzymesorcofactors(eg. Vit C as cofactor for synthesis of collagen) for various metabolic reactions They must beacquiredfrom thedietand absorbed by the GI tract.
  • Fatsoluble (vit A, D, E and K)-absorbed just likedietary lipids. Fat-soluble vitamins are incorporated intomicellesand transported to the apical membrane of the intestinal cells. They diffuse across the apical membrane into the cells, are incorporated inchylomicrons,and then are extruded into lymph, which delivers them to the general circulation
  • Watersoluble (B1, B2, B6, B12 and C, biotin, folic acid, nicotinic acid, and pantothenic acid)-mostlyabsorbedvia anNa+ dependent cotransport. Except, the absorption ofvitamin B12(cobalamin)
29
Q

What are the food sources and reference intake for the different vitamins?

A
30
Q

What is the function of minerals?

A

involved in enzyme functions, nerves impulses and bone structure

  • Solid, inorganic substances
  • Not directly used for making energy
31
Q

Define calories

A

A calorie (kilocalories, kcal) is the amount of energy in the form of heat that is required to heat one kilogram of water one degree Celsius

32
Q

Resting energy expenditure REE (kcal/day) =

A

Body Weight (or Fat Free Mass) x kcal/kg
Energy expended lying still at physical and mental rest after an over night fast (>10 hours) with no stimulants in the previous 24 hours

33
Q

Total energy expenditure TEE (kcal/day) =

A

Resting energy expenditure REE x physical activity level PAL

34
Q

What are the NICE recommended nutrient intake ranges?

A
  • 20–35 kcal/kg/day total energy
  • 0.8–1.5 g protein/kg/day
  • 30–35 ml fluid/kg/day
35
Q

Define malnutrition

A

Malnutrition is a state in which deficiency or excess of energy, protein or other nutrients causes measurable adverse effects on tissue/body form and function and clinical outcome

36
Q

What are the main causes of malnutrition in IBD?

A
  1. Poor nutrient intake (avoiding intake)
    • Nausea/vomiting
    • Abdominal pain/discomfort
    • Drugs (sulphasalazine, metronidazole, 5-ASA)
    • diarrhoea is the most prominent symptom
    • ‘Bowel rest’
  2. Increased intestinal protein losses
    • blood and protein loss through the inflamed intestinal mucosa
    • intestinal bacterial overgrowth, abnormalities in the intercellular tight junctions of the mucosal epithelium, and difficulties in the lymphatic drainage of the intestine may contribute to protein loss
  3. Nutrient malabsorption
    • If Crohn’s disease involves the small intestine/surgical resection = malabsorption of various nutrients
    • terminal ileum is extensively diseased or has been resected = Bile-salt malabsorption = fat malabsorption
    • Intestinal bacterial overgrowth = affects carbohydrate and protein absorption and bile-salt metabolism
37
Q

What is refeeding syndrome?

A
  • Refeeding is the process of reintroducing food after malnourishment or starvation
  • As soon as depleted patients are given energy and protein supplements, insulin secretion is stimulated = resulting in increased cellular protein synthesis, and glycogen storage.
  • Enhanced cellular uptake of glucose, phosphorus, and other minerals such as potassium and magnesium.
  • Leads to water and electrolyte disturbances
  • low serum phosphate, potassium and magnesium levels can lead to cardiac arrhythmias or failure, and even death.
    Can occur in any patient, but most common in those enterally or parenterally fed
38
Q

What are the 4 routes of feeding?

A
  • Food First – e.g. Eatwell Guide
  • Oral Nutritional Supplements (ONS)
    • Types: milkshakes, juices, high-energy powders, soup
  • Enteral tube feeding (ETF)
    • Naso-gastric
    • Naso-jejunal
    • Jejunostomy
    • Percutaneous endoscopic gastrostomy
    • Radiologically inserted gastrostomy
  • Parenteral nutrition (PN)
    • Peripheral vein
    • Central vein