Prelims - GIT ORGANIZATION & FUNCTION (Dr. Castro & Dr. Nobleza) Flashcards

1
Q

How much does stomach secrete?

A

2L/day

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2
Q

Secretion of the stomach is

A

ISOTONIC with Plasma

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3
Q

When secretion is SODIUM RICH (by NON PARIETAL CELLS)

A

Basal Secretion

  • No food
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4
Q

When secretion is H+ RICH (PARIETAL CELLS)

A

Stimulated Secretion

  • Thinking of food
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5
Q

Describe CARDIA

A

No Parietal Cells

No Acid Secretion

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6
Q

Other term for PARIETAL CELLS

A

Oxyntic Cells

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7
Q

Other term for CHIEF CELLS

A

Peptic Cells

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8
Q

Parietal cells secrete

A

HCl and Intinsic Factor

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9
Q

Chief cells secrete

A

Pepsinogen

  • it also secretes GASTRIC LIPASE
  • not an acid
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10
Q

pH needed to activate Pepsinogen

A

pH < 3

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11
Q

Usual intraluminal pH range

A

4-6

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12
Q

Describe ANTRUM

A

No Parietal Cells

No Acid Secretion

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13
Q

Endocrine Cells include

A

G Cells

D Cells

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14
Q

G Cells secrete

A

GASTRIN

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15
Q

GASTRIN function

A

Gastric Acid Secretion

Trophic Effect

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16
Q

D Cells secrete

A

SOMATOSTATIN

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17
Q

SOMATOSTATIN function

A

Inhibit Gastrin release and Parietal acid secretion

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18
Q

What secretes HISTAMIN

A

Enterochromaffin-like (ECL) Cells

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19
Q

In Basal State, acid secretion is

A

LOW

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20
Q

Tubulovesicular membrane present in resting non-stimulated parietal cells have what pumps

A

H-K Pump

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21
Q

H-K pump is responsible for

A

Acid Secretion

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22
Q

With stimulation, pH of gastric secretion is

A

<2

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23
Q

Process of ACID SECRETION

A

(1) Stimulation
(2) Tubulovesicular membrane (with H-K Pump) fuse into Cannalicular membrane
(3) Increase surface area of Parietal cells
(4) Insertion of H-K Pumps, Potassium and Chloride channels into Cannalicular membrane
(5) GASTRIC H+ EXTRUDED INTO LUMEN EXCHANGE FOR K
(6) K+ is recycled, Passive moment of Cl- into gland lumen
(7) Active secretion of HCl
(8) Increase in Parietal cell pH
(9) Passive uptake CO2 and H2O; Carbonic Anhydrase convert to H+ and HCO3 (H+ substrate for H-K Pump)

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24
Q

2 Inhibitors of H-K Pump

A

(1) Substituted Benzimidazoles
* not inhibit Na-K pump
(2) Competitive inhibitors of K binding site

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25
Mechanism of GASTRIN
(1) CCK 2 (2) Ga(q) (3) PLC (4) IP3 (5) Ca and Activation of PKC * Gastrin is from G Cells * CCK 1 - attached to CCK CCK 2 - equal affinity for CCK 2 and Gastrin
26
Mechanism of HISTAMIN
(1) H2 Receptor (2) Ga(s) (3) Adenylyl Cyclase (4) CAMP (5) PKC (6) Phosphorylation of H-K pump * Histamine released from ECL cells
27
Mechanism of Ach
(1) M3 Receptor (2) Ga(q) (3) PLC (4) Converts IP2 to IP3 (increases calcium release) & DAG (PKC) * Ach released from Vagal stimulation
28
Histamine/H2 receptor blockers example
Histidine * can be direct or indirect
29
ACID SECRETION by PARIETAL CELLS
(1) Water in Parietal cell dissociates into H+ and OH- (2) H+ active secretion in exchange with K+ (H-K ATPase) (3) K+ ions in Basolateral side leak into lumen (BUT RECYCLED) (4) Basolateral pump creates low IC Na = Low Na+; REABSORPTION (5) K+ and Na+ in cannaliculus is reabsorbed in CYTOPLASM; H+ in CANNALICULUS (6) Increase OH- to accumulate; Form HCO3 from CO2 Carbonic Anhydrase (7) HCO3 out across basolateral membrane into ECF; Exchange Cl (8) Increase HCl in cannaliculus (9) HCl secreted outside the lumen
30
ACID SECRETIONS Direct and Indirect Example
DIRECT: Gastrin, Histamine and Ach INDIRECT: Gastrin and Ach stimulate ECL cells to secrete Histamine and act on parietal cells
31
What secretes pepsinogen
Chief cells and Mucus cells
32
What initiates hydrolysis of ingested protein in the stomach
Pepsin
33
Group 1 Pepsinogen are secreted from
BASE OF GLANDS in Corpus of Stomach
34
Group II Pepsinogens are secreted from
CHIEF CELLS and MUCUS NECK CELLS of Cardia, Corpus and Antral Area
35
Basal secretion of Pepsinogen
20% of Maximal Secretion after stimulation
36
Pepsinogen is released through
Compound Exocytosis * Allows RAPID SECRETION and SUSTAINED release
37
Pattern of Pepsinogen release
INITIAL PEAK followed by PERSISTENT LOWER RATE of secretion
38
STIMULATION of CHIEF CELLS
(1) Agonists via CAMP (2) Activate CAMP (3) Increase secretion of Pepsinogen (1) M3 receptors for Ach/Gastrin/CCK 1 ``` PATH 1 (2) Increase Ca release from intracellular stores by IP3 and increase Ca ``` PATH 2 (2) Ach release due to vessel stimulation (3) Release pepsinogen; stimulate Parietal cell to secrete acid (4) STOMACH: Dec pH, stimulate chief cells = Pepsinogen release DUODENUM: Acid = release Secretin from S Cells; Chief cells release more Pepsinogen
39
Barrier that prevents acid from destroying own cells
Mucous Bicarbonate Barrier
40
In the Mucous Bicarbonate Barrier, HCl passes througn one pathway which is
Viscous Fingering
41
Describe G-17
More Active; ANTRAL G cells
42
Describe G-34
Slower degradation; DUODONENAL G Cells
43
G-34 released from
Duodenal G Cells
44
G-17 released from
Antral G Cells
45
GASTRIN major effect on GI cells
> Stimulation of Acid Secretion by parietal cells > Release of Histamine by ECL cells > Regulation of mucosal growth (TROPHIC effect) on Corpus, SI and LI
46
What releases SOMATOSTATIN
D cells
47
What triggers D Cells Corpus
Neural and Hormonal Mechanism * endocrine
48
What triggers D cells Antrum
Low intraluminal pH * Paracrine
49
This D cell is stimulated by low intraluminal pH
D cells Antrum (PARACRINE)
50
This D cell is triggered by Neural and Hormonal mechanism
D Cell Corpus (ENDOCRINE)
51
SOMATOSTATIN 3 Mechanisms
(1) Bind to Ga(1) coupled receptor SST ---> inhibit adenylyl cyclase ---> antagonize stimulatory effect on Histamine (2) CORPUS of stomach ---> inhibit release of Histamine from ECL cells ---> reduce gastric acid secretion (3) ANTRUM of stomach ---> inhibit release of Gastrin from G cells ---> reduce gastric acid secretion
52
Most potent inhibitor of gastric acid secretions
Lipid
53
SECRETIN is released from
S Cells of Small Intestine/Duodenum
54
SECRETIN functions
> Inhibition of release of GASTRIN from Antrum > Stimulation of SOMATOSTATIN release > Direct down regulation of PARIETAL H release
55
GASTRIC INHIBITORY PEPTIDE (GIP) is released from
K Cells in the duodenum and jejunum
56
Cholecystokinin (CCK) is released from
I Cells of duodenum/jejunum
57
GASTRIC INHIBITORY PEPTIDE (GIP) function
> (directly) inhibit PARIETAL CELL ACID SECRETION | > (indirectly) inhibit ANTRAL GASTRIN RELEASE
58
CHOLECYSTOKININ (CCK) function
> (feedback inhibition): directly reduces GASTRIC ACID secretion by PARIETAL CELLS
59
Inhibit Histamine activation
Prostaglandin (PGE2)
60
PARTS OF STOMACH and specific ENZYMES they secrete
CARDIA - Mucous Cells ``` FUNDUS - Parietal Cells (HCl) Chief Cells (Pepsin) ``` BODY/CORPUS ``` ANTRUM - Mucous Cells G Cells (Gastrin) ``` PYLORUS
61
3 Phases of Gastric Acid Secretion
(1) Cephalic - 30% of total acid (2) Gastric - 50-60% of total acid (3) Intestinal - 5-10% of total acid
62
Explain CEPHALIC PHASE
(1) Sight, smell, taste or thought and swallowing of food (2) Mediated by VAGUS NERVE of (Medulla Oblongata) (3) Parasympathetic stimulation (4) - Release of Ach: Parietal cell H+ secretion - BODY of stomach Ach trigger Histamine release - ANTRUM GRP induce Gastrin release - ANTRUM and BODY inhibit D cells - reduce Somatostatin and background inhibition of Gastrin release
63
Explain GASTRIC PHASE
(1) DISTENTION of Proximal Part of stomach (VASOVAGAL REFLEX), partially digested proteins stimulate Antral G cells (2) Send impulse to medulla oblongata; Parasympathetic stimulation (3) Active parietal cell; Increase Gastric Acid secretion (4) Mixing of food and Gastric juices: CHYME
64
Explain INTESTINAL PHASE
(1) Chyme in DUODENUM (2) Decrease pH (3) Inhibition of Gastric Acid (4) - Signal Medulla Oblongata inhibition of PS stimulation - DISTENTION results to stimulation of reflex: decrease secretion - Release of Secretin, GIP and CCK
65
Contact of food with the Epithelium Stimulates Secretion - Function of ENS
(1) Tactile stimulation (2) Chemical irritation (3) Distention of the gut wall
66
SYMPATHETIC STIMULATION has a dual effect
SYMPATHETIC - Slight increase in secretion SYMPATHETIC plus PARASYMPATHETIC - with vasoconstriction = dec. blood supply ---> decrease secretion
67
TRUE or FALSE Small increase in volume DOES increase intragastric pressue
FALSE * does not
68
MECHANICAL ACTIONS of STOMACH
(1) PROPULSION - waves move from fundus to pylorus (Pyloric valve closed) (2) GRINDING - most vigorous grinding and mixing occur close to pylorus (Pyloric valve closed) (3) RETROPULSION - the pyloric end acts as pump that delivers small amounts of chyme into duodenum, simultaneously forcing most of its contents backward into the stomach (Pyloric valve slightly opened)
69
Emptying of LIQUIDS
Function on SMOOTH MUSCLE (Proximal Part)
70
Emptying of SOLIDS
Function of SMOOTH MUSCLE (Antral Part)
71
Function on SMOOTH MUSCLE (Proximal Part)
Emptying of Liquids
72
Function of SMOOTH MUSCLE (Antral Part)
Emptying of Solids