Digestive system Flashcards

1
Q

Digestive system: name components

A
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2
Q

Digestive system: name the components

A
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3
Q

Functions of the digestive system

A
  • Breakdown of ingested matter (eg food) and absorption into the blood.
  • Inactivation of ingested pathogens.
  • Protection of tissues from toxins, undigested food, microbes via mucosal barriers.
  • Control of what passes through the GI epithelium into the tissues via mucus secretions, immune components, special proteins and the microbial community.
  • Detoxification
  • Hormone synthesis
  • Immune function (70-80% of immune system located here - GALT, (MALT), dendritic cells, immunoglobulins, mucus, microbial species, HCL)
  • Neurological activity
  • Synthesis of nutrients - B vitamins, Vitamin K
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4
Q

Roles of Stomach

A
  • Secretion of ‘gastric juices’ (HCL, pepsin, intrinsic factor,gastric lipase), controlled by nerves and hormones, with stimuli in brain, stomach and small intestine. Secretion has three phases: cephalic, gastric and intestinal, although, once initiated they can take place simultaneously.
  • Mechanical breakdown of food into chyme (mixing food, saliva and gastric juices).
  • Start of chemical breakdown; HCL and pepsin initiate protein digestion and release of Intrinsic Factor.
  • Intrinsic factor carries B12 to the ileum – its site of absorption.
  • Controlled release of chyme into the small intestine.
  • Secretes gastrin into the blood.
  • Protected from self-digestion by the mucosal barrier – most secretion from the cardia is of mucus.
  • Lowest microbial population due to effect of HCL
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5
Q

Gastric pit: name its cells and cell secretions

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6
Q

Stomach chemical digestion process: describe secretions and processes

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Once chyme mixed with gastric juice :-

  • salivary amylase inactivated
  • Lingual lipase activated (triglycerides→fatty acids and diglycerides)
  • HCl denatures proteins
  • Pepsinogen secreted by chief cells is converted to pepsin (in presence of HCl)
  • Pepsin (optimum pH2) breaks down proteins to peptide fragments
  • Stomach can also produce gastric lipase (TGs → fatty acids and monoglycerides)
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7
Q

Gastric Secretions: name the location and cells and its secretions

A
  1. Surface mucus cells in the epithelial lining. ○ Secreting protective coat of alkaline mucus
  2. Gastric pits: ○ Mucus secreting cells ○ Parietal cells – produce HCL and Intrinsic Factor ○ Chief cells - pepsin, chymotrypsin
  3. Enteroendocrine cells (mostly pylorus and antrum): ● gastrin – increases gastric secretion & stomach emptying ● serotonin – contracts stomach muscle
  4. Histamine – stimulates HCL production
  5. Ghrelin – stimulates hunger
  6. Somatostatin – restricts gastric secretions
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8
Q

What controls HCL production and describe HCL function

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❏ Parasympathetic stimulation (ACh)

❏ Gastrin from G cells

❏ Histamine released from immune cells within the lamina propria enhances the effects of gastrin and ACh (parietal cells have histamine receptors called H2 receptors)

❏ HCl kills microbes in food, denatures protein and stimulates the release of hormones that promote the flow of bile and pancreatic juice

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9
Q

What nutrients are required for HCL production?

A

● Zinc ○ Required for HCL production (in Zn2+ for for carbonic anhydrase production). ○ Anti-secretory role of Zinc on gastric acid production - Regulates HCL production ○ Lower Gastric pH decreases Zinc absorption.

● Histidine – histamine precursor

● Folate as a histamine regulator

● Protein – gastrin

● Choline – for acetylcholine

● B vitamins

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10
Q

Nutritional Stimulators of HCL

A
  • Lemon juice
  • Apple cider vinegar
  • Bi4er foods eg: – rocket, watercress, chicory, dandelion, radicchio
  • Green leafy vegetables
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11
Q

Small intestine enzymatic secretions: name the cells, enzymes they produce and their function

A
  • M Cells – Motilin stimulates peristalsis, pepsin production and gastric emptying.
  • G Cells – intestinal gastrin.
  • I Cells – CCK, simulating the release of bile and pancreatic enzymes into the SI
  • Goblet cells – peristalsis,
  • Paneth – lysozyme, phagocytosis
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12
Q

Bile acid secretion and release

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❖Made in the liver from cholesterol (at least 1/3 of cholesterol is converted to bile salts. ➢Cholic and chenodeoxycholic acid

❖Conjugated with taurine or glycine to become bile salts (more in glycine form).

❖Bile salts are collected in the gallbladder

❖Release simulated by cholecystokinin (Cps of villae), in response to digestive triggers

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13
Q

Gallstone formation: briefly describe the reasons for its formation

A

Gallstones can form when bile flow is reduced or when cholesterol levels in the bile are greater than the bile salts and lecithin can dissolve.

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14
Q

Factors affecting bile production and flow

A
  • secretion of gastrin, secretin, cholecystokinin-pancreozymins, and glucagon, by increasing the flow of NaCl and bicarbonate solutions.
  • Biliary Kinesia/dyskinesia – CCK – contraction reflex – Sphincter of Oddi motility
  • Bacterial balance – deconjugation of bile salts
  • Liver detoxification
  • Diet – Fibre – Cholagogues
  • beets, • bitter greens • artichokes • Ginger • Turmeric • Apples • Celery
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15
Q

cholecystokinin (CCK): where it is produced and its function?

A

❖ CCK is found in tips of villae and secretion is affected by conditions that cause villous atrophy.

➢ Slows gastric emptying for greater digestion

➢ Stimulates gall-bladder contraction and release of bile

➢ Stimulate pancreatic enzyme secretion.

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16
Q

Cells of the small intestine: its functions/ secretions

A

❖ The small intestine wall consists of folds and columns (called villi) which increase surface area. Types of cells include:

❖ Absorptive cells – digest and absorb nutrients (with microvilli). These constitute the brush border

❖ Brush border is the site of secretion of many enzymes (eg. sucrase, lactase, peptidase)

❖ Goblet cells – secrete mucus

❖ Enteroendocrine cells –

➢ secrete secretin (stimulates the release of pancreatic juice into the intestine),

➢ cholecystokinin (CCK) stimulates the release of digestive enzymes and bile

➢ Secrete GIP (glucose-dependent insulinotropic peptide), thought to induce insulin secretion.

❖ The lamina propria contains a large amount of MALT (mucosa associated lymphoid tissue)

17
Q

Mucosal barrier: nutrients that help to improve its function

A

❖ Vitamin A

❖ Zinc

❖ Essential fatty acids

❖ Sources of sulphur

❖ Glutamine

❖ Short-chain fatty acids

❖ Pre/probiotics

18
Q

Digestion in the Small Intestine - chemical digestion Carbohydrates

A
19
Q

Digestion in the Small Intestine - chemical digestion: Protein

A
20
Q

Digestion in the Small Intestine - chemical digestion: Lipids

A
21
Q

Water absorption in GI

A

● Approx 9.3 litres of fluid enters the small intestine each day (~7l from gastrointestinal secretions; ~2.3l from ingestion of food and drink)

● The majority of fluids is reabsorbed in the small intestine (8.3l) ● Absorption is via osmosis

22
Q

Chemical digestion in the colon

A

Large Intestine – Digestion Chemical via Bacteria

Mucus is secreted by glands, but no enzymes are secreted

Bacteria ferment any remaining carbohydrates, forming hydrogen, CO2 and methane

Bacteria digest fructooligosaccharides into propionic and butyric acid (fuel for colonocytes)

Bacteria putrify the remaining protein to amino acids and then further to indole, skatole, hydrogen sulfide and fatty acids

Some indole and skatole are excreted in faeces, the rest is reabsorbed to the liver # Bacteria break down bilirubin to other pigments, causing the brown colour of faeces

23
Q

What can influence digestive health? Name few examples

A

● Physical eg

○ Dentition

○ The health of the intestinal barrier

○ Structural variation

● Chemical eg

○ Digestive enzyme secretions

○ HCL secretion and appropriate pH

○ Bile acid secretion and delivery ○ Pharmaceuticals/toxins (NSAIDs, heavy metals, OCP

● Environmental eg

○ Stress

○ Diet

○ Microbial

● Immune

● Detoxification system.

● Microbiome

24
Q

Effect of the ANS on the ENS

A

Parasympathetic innervation generally causes an increase in motility and GI secretions (remember ‘rest and digest’) #

Sympathetic innervation generally causes a decrease in motility and GI secretions (digestion not a priority when needing to fight or flee)

❖ Neuronal communication

➢ Vagus nerve

❖ Systemic communication

➢ HPA Axis

➢ Neurotransmitters

➢ Bacterial metabolites

➢ Cytokines

25
Q

Microbiome function

A

● Home to trillions of micro-organisms, collectively known as the microbiome (bacteria, viruses, yeasts).

● Largest microbial content of the intestinal tract – 1,000,000,000/ml 1014. Many times more microbes in this part of the GI over the SI.

● Over a kg in weight.

● 60% of faeces is made up of bacteria

● Ferment undigested food

● Release nutrients from the fibre

● Regulate immune function through immune/bacterial cross-talk.

26
Q

Roles of the microbiome

A

• RegulaCon of inflammaCon
• ProtecCon of mucosal barrier
• communication with the immune system
• Communication with CNS
• Digestion of food components and release of
nutrients
• production of butyrate for epithelium.

27
Q

Hormonal Control of Appetite

A

❖ Hypothalamus is the key centre of appetite control
➢ Lateral Hypothalmic area (feeding centre)
➢ Ventromedial hypothalamus (satiety centre)

❖ Appetite control is a homeostatic process

❖ Regulated by the arcuate nucleus, located at the base of the region.

❖ Gut hormone receptors located in neurons within the ARC
➢ Partly accessible to circulating appetite modulating neurons due to incomplete isolation from BBB

❖ Two distinct populations of neurons
➢ Pro-opiomelanocortin (POMC), which is anorexigenic
➢ Neuropeptide Y (NPY) and Agouti-related peptide (AgRP), which are orexigenic.

❖ Peripheral signals change the relative activity of these and their relative neuropeptide release.

28
Q

Leptin: where it is released, its function, its action and dysfunctional patterns

A

● Expressed and secreted by white adipose tissue (WAT)

● Decreases food intake

● leptin has been shown to inhibit the orexigenic NPY/AgRP co-expressing neurons and to stimulate
the anorexigenic POMC-expressing neurons, within the hypothalamic ARC.

● Individuals with leptin deficiency are obese

● and decreased leptin production from white adipose tissue has been demonstrated to contribute to a
plethora of metabolic abnormalities associated with visceral obesity.2

● Leptin resistance - circulating levels of leptin can be raised in obese individuals (impaired transport
across BBB)?

29
Q

Insulin: where it is released, its function and dysfunctional patterns

A

● Insulin levels rise rapidly after a meal and are involved in depressing appetite at this time.
● Insulin levels are related to adiposity
● Some cross-talk with leptin
● Insulin resistance - increased WAT (white adipose tissue) can lead to a decrease in insulin sensitivity.
● Adiposity may be a consequence of insulin resistance.

30
Q

Ghrelin: where it is released, its function and dysfunctional pattern

A

Produced in the stomach
Only orexigenic hormone.
Stimulates appetite regardless of adiposity status.
Circulating ghrelin levels do not fall as much after meals in the obese

31
Q

Hormones related to appetite control. Explain their actions

A

Leptin, Ghrelin, Insulin

❖ GLP 1
➢ Released from L cells of the small and large intestine in response to caloric intake.
➢ Anorexigenic
➢ Obese individuals may have lower circulating levels

❖ Peptide YY -
➢ Produced from L cells of GI tract
➢ Influenced by meal composition and calorific content.
➢ Rise within 1 hour of eating, suppressing appetite

❖ Pancreatic polypeptide
➢ Released from the endocrine pancreas and a little from colon and rectum
➢ Reduces appetite and food intake in both lean and obese individuals

❖ CCK
➢ Released from duodenum and jejunum
➢ Reduces appetite within 15 minutes of starting a meal
➢ Inhibits gastric emptying