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Digestion And Metabolism > GIT Secretions 1 > Flashcards

GIT Secretions 1 Flashcards

1
Q

What is the composition of saliva?

A

Composition:
– From Parotid, Submandibular and Sublingual glands
– 99% water (large volume)
– 1% salts, enzymes (amylase, lipase) and mucins
– Hypotonic

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2
Q

Whhat is the. Function of saliva?

A 
Function :
– Protection
 – Taste
– Lubrication
 – Digestion
  • Control of salivation is mediated almost entirely by nervous system
  • Both Sympathetic and Parasympathetic stimulate secretion
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3
Q

Describe the steps of acinar & ductal modifications

A

Step 1
The acinus produces an initial saliva similar to plasma (isotonic). Contains Na+, K+, Cl-, HCO3-

Step 2
Ducts modify the saliva: absorb Na+, Cl- and secrete K+ and HCO3- (hypotonic)
At low flow rates (basal), contact time allows for reabsorption and secretion. At high flow rates (stimulated) saliva becomes more similar to acinar secretions

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4
Q

Describe acinar secretions

A
  • acinar cells are leaky and secrete digestive enzymes, mucin, electrolytes and water (isotonic NaCl)
  • Cl is co-transported with Na into the cell basolateral
  • Cl diffuses down the gradient into the lumen (apical)
  • channel allows HCO3- to enter the lumen
  • Na+ and H2O follow paracellularly
  • extent of modification depends on flow rate

-isotonic

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5
Q

Describe the ductal modification of the salivon

A

Ductal cells are tight (low water permeability)
Acinar secretion is modified in the duct

  • K+ and HCO3- are actively secreted
  • Na-K ATPase on BL membrane drives active reabsorption of Na+ and K+ secretion
  • anionic exchanger reabsorbs Cl
  • active secretion HCO3- via
anionic exchanger (Cl-
/HCO3-)
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6
Q

Explain regulation of salivary secretion

A 
Both parasympathetic (predominant) and sympathetic ANS regulate release of saliva
• Mechanisms of control
– Ach, VIP and substance P increase intracellular Ca2+, greatest effect on volume of secretion
– NE elevates intracellular cAMP, mainly increasing enzyme and mucous content

• Resting state salivary secretion
– low at 30 ml /hr
– submandibular glands contributing ~ 2/3 resting saliva

• Stimulated glands
– secrete up to 400 ml /hr
– mostly from parotid gland

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7
Q

How does gastric secretions are changed with flow rates?

A

• Composition changes with flow rates

– Cellular mechanism H+ secretion
– Factors that increase and decrease secretion
– Amounts secreted vary during each GI Event:
cephalic, gastric, intestinal phase

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8
Q

Contrast basal secretions and stimulated gastric secretions

A 
Basal Secretion : similar to ECF
• Mainly mucus and water (paracellular diffusion of fluid from ECF and secretions from mucus glands)
• Non-oxyntic component
• Isotonic (high Na+ and Cl-
content)
Stimulated Secretion : change
• Parietal cells secrete HCL 
• Acidic
• Oxyntic component
• Still Isotonic (high H+ and Cl- content)
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9
Q

What are the steps in gastric acid secretion?

A
  1. CO2 + H2O→H+ + HCO3- (catalyst carbonic anhydrase)
  2. H+ is secreted into the lumen via H-K ATPase
  3. K+ can leak back into lumen
  4. Cl- is also secreted
  5. HCO3- produced absorbed into
    the blood stream in exchange for
    Cl- (Cl- - HCO3- exchanger)
  6. alkalinetide:increaseinvenous
    blood pH
  7. Tight junctions prevent
    paracellular transport
  8. 3 stimulants for parietal cells:
    ACh, gastrin and histamine
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10
Q

Summarize gastric acid secretion

A
  • Basal secretion is from non-parietal cells, high Na+ and Cl- (resembles plasma)
  • Stimulation of parietal cells → production of acid secretion
  • Composition now becomes high in H+, K+, and Cl- is also elevated
  • Gastric juice becomes acidic
  • Overall effect of acid secretion is H+ into stomach lumen, and HCO3- into venous blood. pH of venous blood rises: alkaline tide
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11
Q

What is the stimulus of cephalic secretions ?

A

Thought of food, smell, taste, chewing and swallowing

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12
Q

Describe the pathway of cephalic secretions and stimulus to parietal cell

A

-Vagus nerve to parietal cells and G cells

Stimulus to parietal cell: Ach and gastrin (from G cells)

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13
Q

What is the stimulus of gastric secretions?

A

Stomach distention by food

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14
Q

What is the pathway and stimulus to parietal cells of gastric secretions?

A

Pathway: local ENS reflexes and vagovagal reflexes to parietal cells and G cells

Stimulus to parietal: Ach and Gastrin

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15
Q

What is the stimulus of intestinal secretions?

A

Protein digestion products in duodenum

Distension

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16
Q

What is the pathway and and stimulus to parietal cells for gastric secretions?

A

Pathway:
Amino acids in blood. Intestinal endocrine cell

Stimulus to parietal cell
Amino acids and entero-oxynitin

17
Q

Describe cephalic acid production

A

Food: sight, smell, taste stimulates vagus nucleud—> vagus

Vsgus releases Ach to D cells which decreases somatostatin

Vagus releases ACh to stimukate parietal cells to release HCl

Vagus releases GRP to G cell which then releases gastrin

Gastrin stimukates parietal cell to release HCl and ECL cell to release histodine to release parietal

18
Q

Why is cephalic phase acids necessary?

A

Necessary to inhibit somatostatin since SST normally decreased gastrin

19
Q

Summarize gastric phase acid production

A

Food enters stomach—> neutralizes gastric acid (pH can increase to 6)—>. Gastrin secretion restored—> increased acid secretion

50-60%. Of gastric acid is secreted is secreted during gsstric phase

20
Q

How does stomach stretch lead to acid prpduction?

A

Distention of stomach with food —> stimulate afferents—> long loop vagal reflexes and short ENS reflexes—> ACh

ACh stimulate the G cells of eigestive oroducts and increase gastrin, which increases acid release

21
Q

What phases release their proportional amounts of acid secretion ?

A

Intedigestive ohase- 15%

Cephalic pgase- 30%

Gastric phase- 50%

Intestinal phase- 5%

22
Q

Describe the negative feedback of acid secretion

A

Most gastric acid release ~1hr after meal.
Meal no longer buffers→gastric pH falls

At Stomach pH <3, G cells are inhibited by H+
At low gastric pH, D cells priduce SST (inhibits gastrin)

23
Q

What are enterogastrones?

A

Enterogastrones are enteric Hormones inhibiting gastric acid secretion

24
Q

Give an example 9f an H-K ATPase inhibitor(reduce acid secretion)?

A

Omeprazole

Lanzoprezole

25
Q

Give examples of Histamine receptor blockers (H2-blockers)(acid secretion inhibitors)

A

Cimetidine, Ranitidine

26
Q

Give examples of Muscuranic antagonist (acid secretion inhibitirs)

A

Atropine

27
Q

Give examples of gastrin receptor blockers( acid secretion inhibitors)

A

Benzotript

28
Q

What is the function of the gastrin mucosal barrier?

A

Protects acid damage from gastric acid

Cl- exist into lumen via apical channels—> Creates a lumen negative potential—> Facilitates H+ secretion into lumen—> Trapping H+ in the lumen

29
Q

How does the gastrc mucousal barrier use alkaline uss acid?

A

Bicarbonate is secreted and trapped in mucus gel- neutralizes acid in lumen

Tight junctions prevent back diffusion of H+ and so protect the oxynitic cells against high proton concentration

30
Q

Describe gastro(duodenal) barrier integrity

A

HCO3^-, mucus, blood flow, growth factors, cell renewal, prostaglandins, increased blood flow

Are all counteracted by

H+, pepsins, ethanol, NSAIDs, bile acids, ischemia, smoking, h. Pylori

Ulcers form when there is imbalance between the
digestive effects of the acid and the ability of
gastric and duodenal mucosa to resist

Digestion And Metabolism (57 decks)

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