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Physiology > GIT 3 > Flashcards

GIT 3 Flashcards

1
Q

What are the compartments?

A

GIT

  • oral cavity
  • stomach
  • small intestines
  • large intestines

Accessory glands

  • pancreas
  • liver and gall bladder
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2
Q

What is the function of saliva?

A
  • Protection
  • Taste
  • Lubrication
  • Digestion
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3
Q

What glands produce saliva?

A

From Parotid, Submandibular and Sublingual glands

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4
Q

What is the composition of saliva?

A

99% of water

1% salts, enzymes(amylase, lipase) and mucins

Hypotonic

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5
Q

How is saliva secreted?

A

Step 1: the acinus: produces and initial saliva similar to plasma (isotonic). Contains Na+, K+, Cl-, HCO3^-

Step 2:

The ducts: modify the saliva, reabsorb Na+, Cl-; secrete K+ and HCO3^- (hypotonic)

Composition changes with flow rates

Low flow-contact time for Reabsorption and secretion
High flow rates- similar to a acinar secretions

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6
Q

What regulates saliva production ?

A

Mostly regulated by nervous system

Both sympathetic and parasympathetic

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7
Q

What is the function of esophagus?

A

Esophageal glands secrete mucus that lubricates the bolus and reduces friction

When the bolus nears the stomach, the lower esophageal sphincter relaxes, allowing the bolus to pass into the stomach

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8
Q

What are the phases of gastric secretion?

A
  1. Cephalic secretion
  2. Gastric secretion
  3. Intestinal secretion
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9
Q

Explain the cephalic phase of gastric secretion

A

The cephalic phase of gastric secretion begins when you see, smell, taste, or think of food. This phase, which is directed by the CNS, prepares the stomach to receive food. The neural output proceeds by way of the parasympathetic division of the autonomic nervous system, and the vagus nerves innervate the submucosal plexus of the stomach. Next, postganglionic parasympathetic fibers innervate mucous cells, chief cells, parietal cells and G cells of the stomach. In response to stimulation, the production of gastric juice accelerates, reaching rates of about 500 mL/h. This phase generally lasts only minutes

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10
Q

Explain the Gastric phase of gastric secretion

A

The gastric phase begins with the arrival of food in the stomach and builds on the stimulation provided during the cephalic phase. The stimuli that initiate the gastric phase are
1. Distention of the stomach

  1. An increase in the pH of the gastric contents
  2. The presence of undigested materials in the stomach, especially proteins and peptides.

The gastric phase may continue for three to four hours while the acid and enzymes process the ingested materials. During this period, Gastrin stimulates contractions in the muscularis externa of the stomach and intestinal tract. After the first hour, the material in the stomach is churning like clothing in a washing machine. As mixing continues, a large volume of gastric juice is secreted.

The stimulation of stretch receptors and chemoreceptors triggers short reflexes coordinated in the submucosal and myenteric plexuses. This in turn activates the stomach’s secretory cells. The stimulation of the myenteric plexus produces powerful contractions called mixing waves on the muscularis externa

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11
Q

Explain the intestinal phase of gastric secretion

A

The intestinal phase of gastric secretion begins when chyme first enters the small intestine, usually after several hours of mixing contractions. The function of the intestinal phase is controlling the rate of gastric emptying to ensure that the secretory, digestive, and absorptive functions of the small intestine proceed with reasonable efficiency. Although here we consider the intestinal phase as it effects stomach activity, the arrival of chyme in the small intestine also triggers other neural and hormonal events that coordinate the activities of the intestinal tract and the pancreas, liver, and gall bladder

Chyme leaving the stomach decreases the distention in the stomach, thereby reducing the stimulation of stretch receptors. Distention of the duodenum by chyme stimulates stretch receptors and chemoreceptors that trigger the gastric contractions and stimulates the contraction of the pyloric sphincter, which prevents further discharge of chyme. At the same time, local reflexes at the duodenum stimulate mucus production, which helps production, which helps protect the duodenal lining from the arriving acid and enzymes

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12
Q

Summarize the central gastric reflex.

A

Gastroenteric reflex: stimulates motility and secretion along the entire small intestine

Gastroileal reflex: triggers the opening of the ileocecal valve, allowing materials to pass from small intestine into the large intestine

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13
Q

What is the function of atropine in the stomach?

A

Atropine blocks vagal stimulation of parietal cells. Vagal stimulation of G cells is unaffected, as a different transmitter (GRP) is used, not ACh

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14
Q

What does increased Gastrin affect in the stomach?

A

Increases acid secretion primarily through its effects on ECL cells (leading to histamine release) rather than through its direct effect on parietal cells

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15
Q

What is the function of Mucous surface and neck cells in the stomach?

A

They produce alkaline protective mucus

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16
Q

What is the function of the Parietal/Oxyntic cells?

A

The produce HCl and intrinsic factor

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17
Q

What is the function of chief/peptic cells in the stomach ?

A

They produce pepsinogen (in new born and infants produce rennin and gastric lipase)

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18
Q

What is the function of the G cells/D cells in the stomach?

A

They are enteroendocrine cells that produce Gastrin, Somatostatin, histamine and serotonin

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19
Q

How does stomach secretion composition change with flow rates?

A

Cellular mechanism H+ secretion

-Factors that increase and decrease secretion

-Amounts secreted vary during each GI event:
Cephalic, gastric, intestinal phase

20
Q

Describe the basal stomach secretion

A

Similar to ECF

  • mainly mucus and water (paracellular diffusion of fluid from ECF and secretions from mucus glands)
  • Non-oxnitic component
  • isotonic (high Na+ and Cl- content)
21
Q

Describe stimulated secretion of the stomach

A

Parietal cells secrete HCl

  • Acidic
  • Oxynitic component
  • Sill isotonic (high proton and chloride secretion)
22
Q

What are main gastric secretions

A

CO2 and H2O are converted to proton and bicarbonate, catalyzed by carbonic anhydrase

  • proton is secreted into the lumen proton, potassium, ATPase pump
  • Cl- is also secreted
  • Bicarbonate is produced in the cell is absorbed into the blood stream in exchange fo Cl- (Cl- - HCO3^- exchanger)
  • An alkaline tide- change in venous blood pH
  • Parietal cell bear receptors for three stimulators - ACh, Gastrin, Histamine
23
Q

What is the function of oxyntic cells in gastric secretion?

A

Resting oxynitic cells contain tebulovesicles and intracellular canaculi. On stimulation, the tubulovesicles fuse with the canaculi in a dramatic morphological change. Membrane transport proteins and enzymes are also translocated to the luminal cell membrane. These changes together account for the ~10 min delay between stimulating the oxynitic cell and observing acid production

24
Q

How are protons produced in gastric secretions? What is post-prandial alkaline tide?

A

The biochemical steps to produce protons inside the cell are not known, but ultimately they derive from water. The active transporter proton/K+/ATPase is used to pump H+ out of the cell up an immense concentration gradient gradient. The approximately 3 million fold gradient I’d the biggest ion concentration gradient across any membrane in the body!

K+ secretion via a luminal membrane K+ channel provides the K+ needed by the H+/K+/ATPase to pump out of the cell. OH- inside the cell produced along with proton is neutralized by combining it with CO2 to form bicarbonate. Most of the CO2 comes from oxynitic cell metabolism. The HCO3^- produced leaves the cell in such quantity that the gastric venous plasma becomes alkaline. This is known as the post prandial alkaline tide

25
Q

Why are Cl- important to gastric secretion?

A

Cl- enters the cell against its electrochemical gradient, by coupling its entry to the exit of HCO3^- . Cl- is secreted via an ion channel in the luminal membrane. Secretion of Cl- via a channel results in the formation of a large negative electrical potential in the stomach lumen. This is important to reduce the overall electrochemical gradient up which proton needs to be transported. It can be thought of as “trapping” proton in the lumen and thus contributes to the barrier function against acid self-attack of the mucosa

26
Q

How does loss of appetite/ depression reduce gastric secretions?

A

Inhibits Cerebral cortex causes lack of stimulatory impulses to parasympathetic center

27
Q

How does excessive acidity (below pH 2) prevent gastric secretions?

A

Inhibition of G cells which stimulate Gastrin secretion to decline and inhibit stomach secretion declines

28
Q

How does emotional upset prevent gastric secretions?

A

Stimulates Sympathetic nervous system(SNS) activation- overrides parasympathetic controls

29
Q

How does distention of duodenum; presence of fatty, acidic, hypertonic chyme, and/or inherit ants in the duodenum prevent gastric secretions?

A

Inhibits Local reflexes, vagal nuclei in medulla, and pyloric sphincter stimulate entero-gastric reflex

30
Q

How does distention; presence of fatty, acidic, partially digested food in the duodenum reduce gastric secretions?

A

This stimulates release of intestinal hormones (secretin, Gastrin inhibitory peptide, cholecytostokinin, vasoactive intestinal peptide) which inhibits stomach secretory activity

31
Q

How does sight and thought of food stimulate gastric secretions?

A

During the cephalic phase these stimulate cerebral cortex

The conditioned reflex stimulates hypothalamus and medulla oblangata which stimulates the vagus nerve

Increases stomach secretion activity

32
Q

How does taste and smell receptors increase stomach secretions?

A

Stimulates hypothalamus and medulla oblangata which then stimulate the vagus nerve to cause stomach secretions

33
Q

How does stretch receptor stimulation in the stomach increase secretion of stomach activity?

A

Stomach distention activates stretch receptors

Stimulate local reflexes which stimulate stomach secretions

Stimulate vagovagal reflexes which causes the medulla to stimulate the vagus nerve to increase stomach secretion

34
Q

How do food chemicals (especially peptides and caffeine) and rising pH activate chemoreceptors stimulate gastric secretions?

A

During the gastric phase :Stimulate G cells which increase Gastrin release to blood increase stomach secretory activity

35
Q

How does presence of low pH and partially digested foods in duodenum when stomach begins to empty stimulate stomach secretions?

A

In the intestinal phase: presence of low pH and partially digested foods in duodenum when stomach begins to empty.

This causes intestinal (enteric)Gastrin release to blood

This increases stomach secretion

36
Q

Summarize the negative feedback of stomach acid secretion

A

Ingestion of meal- gastric acid is greatest at 1 hr

Meal no longer buffers so gastric pH starts to fall

At stomach pH below 3, g cells are inhibited by protons

At low gastric pH, D cells produce SST which inhibits Gastrin release

37
Q

Describe Gastro(duodenal) barrier integrity

A

Prostaglandins important in protecting mucosa: they inhibit acid secretion, stimulate HCO3 and mucous production, increase mucosal blood flow and modify the local inflammatory mediators. These mediators cause a local vasodilation and the tissue re-heals when the injury is not too severe. With more severe damage then inflammatory mediators are produced reducing blood flow and resulting in further tissue damage

Breakdown of the superficial mucosa not involving the submucosa is called a erosion. Damage to the muscularis mucosa and deeper layers is called ulceration. H pylori, a gram -ve bacillus, colonists the antral mucosa and secretes urease which converts urea into NH3. The ammonia buffers stomach acid and protects H. Pylori from the acidity. The increase in gastric acid secretion that occurs often in patients with DU’s may result from H. Pylori antral inflammation inhibiting somatostatin release by the antral D cells and this would result in loss of the inhibition of Gastrin. Inhibition of acid secretion heals but doesn’t cure H. Pylori peptic ulcers. Antibiotics are needed to eradicate

38
Q

Why is the inhibition of secretion in the small intestine important?

A
  1. Secretion of acid is only important during the digestion of food.
  2. Excess acid causes mucosal damage. After a meal the proteins in the food buffer the acidity and the pH is usually >3 . If the protein buffering capacity is exceeded, or the stomach is empty, pH falls more than 3 and the G cell is directly inhibited by proton. Falling pH also stimulates D cells in the antrum to release somatostatin, which inhibits Gastrin. Low pH also inhibits oxynitic cells
39
Q

How is stomach pH the most sensitive regulator of acid secretion.

A

Somatostatin released by gastric D cells in the antrum is the central mechanism of inhibition of acid secretion. Somatostatin inhibits gastric acid secretion by both direct and indirect pathways. Direct pathway: somatostatin binds directly to the parietal cell.

The source of this SST can be paracrine, D cells in the corpus or endocrine D cells in the antrum. Indirect pathways (both paracrine): In the corpus D cells release SST, which inhibits the release of Gastrin from G cells

During the imdigestive period the stomach only secretes a few mls of almost entirely non oxynitic fluid composed mostly of mucous, with little pepsin, and pH can range from 3 to 7. The pH of the fluid in the empty(fasted) stomach is usually below 2 because of the basal proton secretion and the absence of food that would otherwise buffer the secreted acid.

40
Q

What is the function of the pancreas?

A
  • digestion
  • protection
  • neutralizes the acidity of the contents leaving the stomach
  • Optimal pH for enzyme activity
41
Q

What is the composition of pancreatic secretions?

A
  • high volume
  • same Na+ and K+ as plasma
  • HIGH HCO3^- concentrations
  • Low Cl-
  • isotonicity
  • Enzymes- lipase, amylase and proteases

Low flow rates: isotonic- mostly Na+ Cl-
High flow rates: isotonic - mostly Na+HCO3^-

42
Q

Describe the formation of pancreatic secretions

A

Acinar cells: small volume, mainly NaCl

Ductal cells: modifies; absorbing Cl-, secreting HCO3^- exchanger

Pancreatic ductal cells are permeable to water

43
Q

Explain secretin function

A

Secreted from S cells of duodenum in response to proton in duodenal lumen this increases bicarbonate ion secretion

44
Q

Explain the function of CCK

A

Secreted from I cells of duodenum in response to small peptides, amino acids, fatty acids in duodenal lumen

Increases enzyme secretion, increases potentates bicarbonate secretion

45
Q

Explain the function of ACh

A

Secreted from Vagovagal in response to protons, small peptides, amino acids, fatty acids

Increased enzyme secretion and potentates bicarbonate secretion

46
Q

Describe the composition of liver and gall bladder

A

Organic: bile salts, phospholipids, cholesterol, bile pigments (bilirubin)

Bicarbonate

47
Q

What are the functions of liver and gall bladder ?

A

Amphipathic nature helps with micelleformation for the emulsification of fats

  • Detergent action
  • neutralize acidic chyme

Physiology (36 decks)

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