Physiology GIT 206 > GIT Secretion: Stomach > Flashcards

GIT Secretion: Stomach Flashcards

(38 cards)

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1
Q

Volume of Gastric Secretion

A

2.5 L

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2
Q

pH of Gastric Secretion

A

1 (highly acidic)

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3
Q

Constituents of Gastric Secretion

A

Enzymes:
* Pepsinogen
* Gelatinase
* Lipase

Electrolytes:
* H+
* Cl-

Intrinsic Factors for Absdorption of Vit B12

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4
Q

Enumerate Functions of HCL

A
  1. Activates pepsinogen into pepsin
  2. provide optimum pH for Pepsin Activity
  3. Helps iron & Calcium Absorption
  4. Dissolves food into Chyme
  5. Forms Sterile medium (kills bacteria)
  6. Stimulate bile flow
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5
Q

Cells that secrete HCL

A

Parietal cells (Oxyntic cells)

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6
Q

Describe the Mechanism of Secretion of HCL

A
  1. active transportation of cl- (Chloride) from parietal cells into lumen, which creates negative potential inside the lumen
  2. as a result of the negative potential, K+ (potassium) diffuses passively from cell into lumen
  3. H2O dissociates into OH- & H+

4.The H+ formed by the water dissociation is exchanged with the potassium (K+) in the lumen by** proton pump (H+/K+ ATPase pump) actively**, so H+ increases inside lumen

5.CO2 from metabolism & water (H2O) react by Carbonic anhydrase to form Carbonic acid which splits into H+ and Bicarbonate (HCO3-)

  1. Bicarbonate (HCO3-) diffuses out of the cell into blood/interstitial fluid in** exchange for Cl-**

7.H2O passes into lumen by osmosis

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7
Q

Explain how Alkaline tide occurs

A
  1. The nature of Bicarbonate is Alkaline
  2. So during HCL secretion, Cl- in the blood is exchanged with Bicarbonate (HCO3-) in the parietal cells
  3. causing temporay increase in Blood Bicarbonate level, specifically gastric venous blood
  4. Thus causing increase in pH
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8
Q

Enumerate Stimuli (hormones/ neurotransmitters) of HCL secretion

A
  • Histamine
  • Acetylcholine (vagal stimulation)
  • Gastrin (hormone)
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9
Q

Receptor for Histamine in stimulating HCL secretion

A

H2 receptor

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10
Q

Second messenger for Histamine in stimulating HCL secretion

A

(the strongest) increase intracellular cAMP

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11
Q

Receptors for Acetylcholine in stimulating HCL secretion

A

M3 Muscarinic receptors

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12
Q

Second messenger for Acetylcholine in stimulating HCL secretion

A

Increase in intracellular Ca2+

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13
Q

mechanism of gastrin in stimulating HCL secretion

A
  • Directly activity on Parietal cells: by increasing Intracellular Ca2+
  • Indirect activty: by stimulating **histamine secretion from ECL cells **
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14
Q

Function of Second messengers in stimulating HCL secretion

A

It transfers or facilitates movement of the proton pump (H+/K+ ATpase) from vesicles inside the parietal cells to the plasma membrane, so that they increase in number and facilitate more active transportation of Protons into lumen of stomach

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15
Q

Cells that secrete pepsinogen

A

Chief (peptic) cells

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16
Q

explain positive feedback mechanism of pepsin

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A

Autocatalytic chain reaction:
* The activated pepsin further activates more pepsinogen

17
Q

pepsin is inactivated by

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A

Alkalinity of the duodinum

18
Q

Action of pepsin

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A

Incomplete digestion of proteins into various peptides

19
Q

Cells that secrete intrinsic factors

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A

parietal cells

20
Q

Action of Intrinsic factors

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A

essential for absorption of Vit. B12

21
Q

Explain how Chronic gastritis can cause pernicious anemia

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A

causes damage to parietal cells, thus decrease in Intrinsic factor secretion, therefore causing decrease in Vit. B12 absorption

22
Q

Cells secreting soluble mucous

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A

Neck of Gastric glands in response to vagal stimulation

23
Q

Action of soluble mucous

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A

Lubricates food (gastric chyme)

24
Q

Cells secreting Insoluble Mucous

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A

Surface epithelium of stomach, mainly in eosophageal and pyloric junctions

25
Actions of Insoluble Mucous
protects Gastric mucousa from **mechanical friction** & **corrosivness of Acid**
26
Enumerate phases of Gastric Secretion
1. Cephalic Stimulatory phase 2. Gastric Stimulatory phase 3. Intestinal Inhibitory phase
27
Difference between conditioned & unconditioned Reflex of Cephalic Stimulatory phase of Gastric Secretion
* Conditioned: Thinking of food, were the signal originates from the brain (Cortex or hypothalamus) * Unconditioned: Presence of food in the mouth
28
Mechanism of Cephalic Stimulatory phase
1. Stimulate Dorsal Vagal Nucleus, which stimulates gastric secretion by: * Acetylcholine release * Gastrin releasing peptide (which increases gastric secretion) | it's repsonsible for 1/3 of gastric secretion
29
mechanism of gastric stimulatory phase
when food reaches stomach, gastric secretion occur in 3 ways: 1. Long vago-vagal reflex (like cephalic phase) 2. Submucosal plexus---> Enteric reflex: responding to stretch and chemical stimuli 3. Gastrin secretion | Accounts for 70% of Gastric secretions
30
Mechanism of Intestinal Inhibitory phase
When food is present in the deudoenum, gastric secretion decreases by: * Enterogastric reflex * Hormones that inhibit gastric secretion (GIP,VIP,CCK,Secretin)
31
Describe Mechanisms of Gastric secretion inhibition
1. decrease in **pH below 2** at **deuodenal** and **pyloric** region 2. **Enterogastric** reflex 3. **Hormones** that inhibit gastric secretions (**GIP,VIP,CCK, Secretin**) 4. Emotions or fear **inhibit dorsal vagal Nucleus** 5. **Somatostatin** inhibits **G & ECL** cells & **Secretions of parietal cells**
32
Describe how HCL crosses mucosal barrier
from parietal cells to lumen through finger like channels, which keeps the flexible gel of insoluble mucous intact
33
Describe how mucosal cells deal with H+ & Na+
* Mucosal cells are impermiable to H+ * H+ is pumped actively from mucosal cells out to the lumen * Na+ is pumped actively from mucosal cells into ISF (blood)
34
Functions of Prostaglandins in Mucosal Barriers
It's a Vasodilator * Increase **mucosal blood flow**, therefore increase **Mucous and Bicarbonate** secretion * **Inhibts acid** secretion * Strengthens and augemnts Mucosal Barrier
35
Causes of Peptic ulcer originating from breakdown of Mucosal Barrier & Gastric Irritation
* Alcohol * Vinegar * Bile salts * Asprin (NSAIDs) & Corticosteroids: Decrease PG synthesis * Helicobacter pylori infection
36
Causes of Peptic Ulcer originating from Excess HCL secretion
Zollinger-Ellison syndrome: leading to Hypergastrinemia (abnormal increase in gastrin hormone)
37
Describe how ulcer formed
1. Mucosal Barrier is broken down 2. H+ diffuse from lumen into Mucosal Cells 3. Na+ diffuse from blood (ISF) into mucosal Cells 4. This causes Metabolic dysfunction of Mucosal cells, forming the ulcer
38
Describe treatement of peptic ulcer
1. Inhibition of acid secretion by: * H2 receptor blocker * Proton pump inhibitor 2. Surgical removal of gastrin-secreting Tumours (in Zollinger-ellison syndrome) 3. Stop the usage of Asprin & NSAIDs 4. Eradication of Helicobacter pylori by antibiotics
Physiology GIT 206
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