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Physiology GIT 206 > GIT Secretion: Stomach > Flashcards

GIT Secretion: Stomach Flashcards

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

A

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

17
Q

pepsin is inactivated by

A

Alkalinity of the duodinum

18
Q

Action of pepsin

A

Incomplete digestion of proteins into various peptides

19
Q

Cells that secrete intrinsic factors

A

parietal cells

20
Q

Action of Intrinsic factors

A

essential for absorption of Vit. B12

21
Q

Explain how Chronic gastritis can cause pernicious anemia

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

A

Neck of Gastric glands in response to vagal stimulation

23
Q

Action of soluble mucous

A

Lubricates food (gastric chyme)

24
Q

Cells secreting Insoluble Mucous

A

Surface epithelium of stomach, mainly in eosophageal and pyloric junctions

25
Q

Actions of Insoluble Mucous

A

protects Gastric mucousa from mechanical friction & corrosivness of Acid

26
Q

Enumerate phases of Gastric Secretion

A
  1. Cephalic Stimulatory phase
  2. Gastric Stimulatory phase
  3. Intestinal Inhibitory phase
27
Q

Difference between conditioned & unconditioned Reflex of Cephalic Stimulatory phase of Gastric Secretion

A
  • Conditioned: Thinking of food, were the signal originates from the brain (Cortex or hypothalamus)
  • Unconditioned: Presence of food in the mouth
28
Q

Mechanism of Cephalic Stimulatory phase

A
  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
Q

mechanism of gastric stimulatory phase

A

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
Q

Mechanism of Intestinal Inhibitory phase

A

When food is present in the deudoenum, gastric secretion decreases by:
* Enterogastric reflex
* Hormones that inhibit gastric secretion (GIP,VIP,CCK,Secretin)

31
Q

Describe Mechanisms of Gastric secretion inhibition

A
  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
Q

Describe how HCL crosses mucosal barrier

A

from parietal cells to lumen through finger like channels, which keeps the flexible gel of insoluble mucous intact

33
Q

Describe how mucosal cells deal with H+ & Na+

A
  • 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
Q

Functions of Prostaglandins in Mucosal Barriers

A

It’s a Vasodilator
* Increase mucosal blood flow, therefore increase Mucous and Bicarbonate secretion
* Inhibts acid secretion
* Strengthens and augemnts Mucosal Barrier

35
Q

Causes of Peptic ulcer originating from breakdown of Mucosal Barrier & Gastric Irritation

A
  • Alcohol
  • Vinegar
  • Bile salts
  • Asprin (NSAIDs) & Corticosteroids: Decrease PG synthesis
  • Helicobacter pylori infection
36
Q

Causes of Peptic Ulcer originating from Excess HCL secretion

A

Zollinger-Ellison syndrome: leading to Hypergastrinemia (abnormal increase in gastrin hormone)

37
Q

Describe how ulcer formed

A
  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
Q

Describe treatement of peptic ulcer

A
  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 (17 decks)

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