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S&F IV: Exam One > Stomach > Flashcards

Flashcards in Stomach Deck (33):
0

Receptive Relaxation

Mediated by a vagovagal reflex, this is the relaxation of the stomach to accommodate to a recently ingested meal

1

Retropulsion

Occurs when peristaltic contractions originating from the pacemaker region in the midstomach reach the pyloric sphincter in cloe it

=>Chyme propelled back into stomach to be further digested

2

Migrating Myoelectric Complex

Contractions occurring in 90 minute intervals during fasting to clear the stomach of any residual food

*Mediated by motilin; hunger pangs will disappear after 3-4 day

3

Order of gastric emptying

Liquids>Carbs>Proteins>Fats

4

Gastric Emptying

Controlled by signals from the duodenum in response to:

Decreased pH
Distention of proximal stomach
Increased fat/protein digestion products

5

Gastroparesis

Impaired emptying of the stomach producing symptoms of fullness, nausea, vomiting

*Most commonly caused by diabetes or anticholinergics

6

Dumping Syndrome

Lower end of S.I. fills to quick w/ undigested food; nausea, vomiting, eventually sweating and dizziness

*Common after stomach surgery

*Symptoms due to hypoglycemia

7

Oxyntic Gland mucosa

Found in the proximal stomach; secrete primarily acid, pepsinogen, intrinsic factor, and mucus

*Mucus neck cells in isthmus serve as stem cell; chief cells and parietal cells also present

8

Pyloric gland mucosa

Found in the distal stomach; secretes primarily gastrin

9

HCl

1. Begins digestion of protein

2. Activates pepsinogen

3. Kills bacteria

10

Pepsin

Released by vagal stimulation and splits interior peptide bonds of proteins

11

Mucus

Soluble: Secreted in active stomach; lubricates chyme

Insoluble: Secreted in inactive stomach to trap HCO3- in layer on mucosa to protect from acidic damage

12

Intrinsic Factor

Binds Vitamin B12 and allows for absorption in the ileum

*Lack of IF=>pernicious anemia

13

Tubulovesicles

Inserted into the luminal membrane of parietal cells when gastric acid is secreted

*Become H+ pumps/K+ antiporter

14

Mechanism of Acid Secretion

Carbonic anhydrase converts CO2 from cell metabolism to H+ and HCO3-

H+ => secreted out of H+/K+ ATPase

HCO3- => Antiported out w/ Cl-; Cl- travels thru membrane channels to the lumen

*K= enters via a Na/K+ ATPase and leaves via a K+ channel to power the H+/K+ ATPase on the luminal side

15

Ionic Composition of Gastric Juices

Low flow => NaCl

High Flow => HCl

*Vomiting may lead to hypokalemia due to high presence of K+ in the lumen

16

Stimulants of Acid Secretion

1. Ach-binds to muscarinic receptors and activates PLC

2. Gastrin- binds to gastrin receptors and activates PLC

3. Histamine- binds to H2 receptors and activates AC

*All eventually raise intercellular Ca2+ and insert H+-pumps in the apical membrane

17

H2 receptor blockers

Blocks the potentiating effects of histamine on gastrin and Ach; effectively lowers the secretion of gastric acid

18

Inhibitors of acid secretion

1. Decreased pH
-pH will drop after initial rise from ingested meal

2. Somatostatin
-released in response to acid in the antrum

3 Chyme in the duodenum
-Neural and hormonal mechanisms inhibit gastrin release

19

Basal secretion phase

Occurs in absence of gastric stimulation; pH is low causing the mucosa to be acidified

20

Cephalic phase of acid secretion

Initiated by the though, taste, smell of food; afferent pathways to vagus nerve stimulate efferent impulses to the stomach

=>Stimulates parietal cell and GRP release

21

Gastric phase of acid secretion

Rise in pH once food enters stomach causes gastrin to be released; stretched mechanoreceptors stimulate local and vagovagal reflexes to secrete acid

*AAs and peptides can also cause release of gastrin from G-cells

*Strongest phase of acid secretion

22

Intestinal phase of secretion

Initiated by presence of protein digestion products in the duodenum

=>Increased gastrin secretion

23

Gastric ulcers

Breakdown of the protective barrier of the stomach

24

Duodenal ulcers

Increased levels of acid/gastrin/pepsin damage the lining of the duodenum

-Pts also have lower HCO3- secretion and defective defensive mechanisms against acid

*Much more common than gastric ulcers and often have H. Pylori infxn

25

H.pylori

Produces urease to neutralize acid in the stomach and corkscrews in thru the mucosa; might even poison nearby cells w/ ammonia

*Inhibits secretion of somatostatins to further cause ulcerations

26

Retching

Involuntary motions of vomiting w/o production

*Includes esophageal dilation, flaccid fundus, abominal contration, closure of soft palate over nasopharynx

27

Vomiting Center

Found in the medulla and activated by:
Tickling throat
Distention of stomach
Vestibular stimulation
Pain
Sights/smell

*Direct activation will cause vomiting w/o nauseas or retching

28

Chemoreceptor Trigger Zone

In area postrema and is activated by radiation, motion sickness, drugs

=>Sends signals to vomiting center and NTS

29

Hyperemesis of Pregnancy

Severe vomiting and nausea causing weight loss during pregnancy

-Baby will come out normal though

30

Effects of protracted vomiting

1. Metabolic alkalosis
2. Dehydration
3. Hypokalemia
4. Hyponatremia

31

Possible inhibitors of gastric emptying

Decreased pH
Increased fat/protein digestion products
Increased distention of the stomach
Increased duodenal pressure

*Inhibits the flow of excess chyme into the SI

32

Treating ulcers

Antibiotics and H+ pump inhibitors