GI Physiology Flashcards

1
Q

Composition of Saliva

A

Hypotonic fluid
Tonicity and composition changes with flow rate
Difficult to have exact list of constituents
99.5% water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Function of Saliva

A

Lubrication and protection (barrier function) - mucins
Buffering action and clearance - bicarbonate
Maintenance of tooth integrity - Ca + Ph
Antibacterial activity - Immunoglobulins (IgA)
Taste and swallowing - libricating food bolus, dissolve molecules for test sensation
Digestion - Amylase begins to act on carbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Stimulation and regulation of Saliva

A

90% of saliva flow is stimulated by chewing and eating.
Almost none when sleeping
Secretion regulated by autonomic nervous system.
Medullary nuclei
Stimulated by mechanical, gustatory and olfactory stimuli -> smell, taste and movement of food.
Both PNS and SNS innervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Goblet cells

A

Secrete Mucous
Alkaline mucous
Lines surface of stomach and protects from HCL and pepsin causing autodigestion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Function of Mucous in stomach

A

Gastroprotection
Lubrication
Bacteriocidal
Secreted by goblet cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Chief Cells

A

Secrete Pepsinogen and gastric lipase
Pepsinogen is converted into pepsin in the low PH stomach environment
Involved in proteolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Parietal Cells

A

HCL + Intrinsic Factor
Located in body and fundus of stomach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pepsinogen

A

Activated to pepsin in presence of H+
Involved in proteolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Function of HCL in stomach

A

Secreted by parietal cells
Provides optimal pH for pepsin function -> Proteolysis
Acidic environment -> Bacteriocidal
Inhibits further gastrin secretion -> neg feedback
Stimulates secretion of bile and pancreatic juices
Facilitates iron absorption in duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Enterochromaffin Cells

A

Secrete Histamine
Histamine stimulates parietal cells to secrete HCL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Function of Histamine in Stomach

A

Stimulates parietal cells to secrete HCL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

G Cells

A

Secrete Gastrin
Gastrin:
- Stimulates parietal cells to secrete HCL (directly and indirectly)
- Increases GI motility
- Stimulates pancreatic secretion and gall bladder contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gastrin function in stomach

A

Stimulates Parietal cells to secrete HCL indirectly and directly - via histamine
Increases GI motility
Stimulates pancreatic secretion and gall bladder contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

D Cells

A

Secrete Somatostatin
Antagonise the stimulatory effect of histamine on acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Intrinsic Factor Function in stomach

A

Co factor - binds vitamin B12, protects B12 from acidic environmentt and facilitates B12 absorption in the terminal ileum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Secretions of Glands in the cardia

A

Mucous mostly
Dominated by Goblet cells

17
Q

Secretions of glads in the fundus

A

oxyntic
Main production is HCL

18
Q

Secretions of glands in the pylorus

A

Mainly Gastrin

19
Q

Function of Gastric Secretions

A
  1. Immune function
    - pH decontaminates bacteria.
    - pH maintained by HCL secretion.
    - HCL secreted by Parietal cells, stimulated by Histamine (ECL cells) and Gastrin (g cells.)
  2. Barrier function.
    - Gastric mucous acts as a barrier and neutralising agent against gastric acid. Prevents auto digestion.
    - Mucous secreted by Goblet Cells.
  3. Macronutrient digestion.
    - Gastric acid
    - proteolytic enzymes begin digestion of protein. Pepsinogen is secreted by Chief cells, and is converted to pepsin by acidic environment. Pepsin = 15% total protein breakdown.
    - Gastric Lipase: Hydrolyses the ester bonds of triglycerides. 30% of total lipid catabolism
  4. Macronutrient digestion
    - Pepsin: ferric iron (Fe3) to more soluble ferrous (FE2)
    - Intrinsic factor: protects B12. Binds B12 creating a complex that can be absorbed in the terminal ileum.
  5. Endocrine and paracrine
    - Gastrin + somatostatin + histamine affect rate of gastric acid secretion.
20
Q

Factors that Increase Gastric Acid Secretion

A
  1. PSNS Via vagus.
    - Mainly during cephalic phase of digestion.
    - Stimulated by the food bolus entering mouth.
    - mediated by acetylcholine via the M3 receptors
  2. Gastrin
    - during cephalic and gastric phases.
    - Released due to central signals + mechanical effects of food in the stomach.
    - Mediated by binding to gastrin receptors on parietal cells.
    - Also binds CCK-B receptors on enterochromaffin cells = histamine release.
  3. Histamine
    - during cephalic and gastric phases.
    - released due to central signals as well as stimulated by gastrin.
    - Binds to H2 receptors on parietal cells to mediate the release of acid.
  4. Mechanical stretch
    - vago vagal and local smooth muscles stretch reflexes.
  5. Peptides, caffeine, alcohol
    - Sensed by mucosal chemoreceptors of the astral G cells, which then release gastrin.
21
Q

Factors that Decrease gastric acid secretion

A
  1. Somatostatin
    - If luminal pH decreases below 1.5
  2. Small intestine hormones
    - during the intestinal phase of digestion, composition of content entering duodenum is sensed by duodenal chemo and osmoreceptor.
    - Release of inhibitory hormones. Delay gastric emptying.
    - Carbs = release of GIP (gastric inhibitory peptide) = inhibit emptying.
    - Protein degradation products = release CCK (cholesteokinin) = inhibit emptying
    - Fat = Release CCK = Inhibit emptying.
    - Rate (fastest - slowest): Carbs > Protein > fat.
  • Increased H+ = secretin release = inhibit emptying.
  • > Oslolarity = ?unknown mediator = decreased emptying.
  1. Prostaglandins PGE2 and PGI2
    - Promote increased HCO3 and mucus secretion in gastric mucosa
    - these are products of COX 1 activity, the loss of which = ulcers.
22
Q

Function of HCL

A

Secreted by Gastric parietal cells
Aids in protein digestion
optimal pH for pepsin activity
Bactericidal
Facilitates Iron absorption

23
Q

Parietal Cell structure

A

Apical secretory canaliculi which increase the surface area
Numerous vesicles containing proton pump proteins
With stimulation these vesicles fuse with the apical canaliculi to rapidly increase the secretory capacity of these cells.

24
Q

Basal Membrane Ion transport in parietal cells

A

CO2 and water are able to diffuse into parietal cells passively
Carbonic Anhydrase converts the CO2 and H2O into HCO3 and H.
HCO3 is then exchanged for chloride at the basal membrane

25
Q

Apical Membrane ion transport in parietal cells

A

H is exported by an ATP powered H/K proton pump.
Potassium used in the exchange is returned to Gut lumen
Chloride is exported through apical chloride channels.

26
Q

Net effect of parietal cell activity

A

In GUT LUMEN:
- Chloride concentration increases from 120mmol/L up to 180 mmol/L
- pH decreases to 1.5

In Portal circulation
- CA activity consumes CO2, therefor portal venous CO2 = lower than PaCO2.
- this is a negative respiratory quotient.
- this increases the pH of portal venous blood during the cephalic and gastric phases of digestion - alkaline tide.

27
Q

What stimulates acid secretion by the parietal cells during the cephalic and gastric phase

A
  1. Acetylcholine (M3 receptors)
    - during cephalic phase.
    - From Vagal stimulation.
  2. Gastrin (gastrin and CCK-B receptors)
    - during cephalic and gastric phase
    - from G Cells, stimulated by vagal activity.
  3. Histamine (H2 receptors)
    - during cephalic and gastric phase e
28
Q

CCK

A

Released by I Cells in duodenum
Increases SI mobility + pancreatic acid secretions
Stimulated by fat + amino acids + peptides
reduces GI motility and GI secretion

29
Q

Secretin

A

S cells
- released in response to <PH in duodenum
- inhibits gastrin
reduces gastric mobility

30
Q

GIP

A

K Cells in duodenum
- glucose + fat cause secretion
- inhibit gastric secretion nd mobility

31
Q

Motilin

A

Enterochromaffin cells in SI & Stomach
Increases gastric motility
and acid secretion

32
Q

Increasing tone of LES

A

D2 receptor antagonist
Antihistamines
ant acids
Suxamethonium

33
Q

Decreased LES

A

Inhalational
Opioids
cricoid
atropine
dopamine

34
Q

Autonomic pre monitory symptoms

A

Feeling of being about to vomit

35
Q
A