Stomach Flashcards

0
Q

Retropulsion

A

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

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1
Q

Receptive Relaxation

A

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

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2
Q

Migrating Myoelectric Complex

A

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

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3
Q

Order of gastric emptying

A

Liquids>Carbs>Proteins>Fats

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4
Q

Gastric Emptying

A

Controlled by signals from the duodenum in response to:

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

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5
Q

Gastroparesis

A

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

*Most commonly caused by diabetes or anticholinergics

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6
Q

Dumping Syndrome

A

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
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7
Q

Oxyntic Gland mucosa

A

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

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8
Q

Pyloric gland mucosa

A

Found in the distal stomach; secretes primarily gastrin

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9
Q

HCl

A
  1. Begins digestion of protein
  2. Activates pepsinogen
  3. Kills bacteria
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10
Q

Pepsin

A

Released by vagal stimulation and splits interior peptide bonds of proteins

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11
Q

Mucus

A

Soluble: Secreted in active stomach; lubricates chyme

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

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12
Q

Intrinsic Factor

A

Binds Vitamin B12 and allows for absorption in the ileum

*Lack of IF=>pernicious anemia

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13
Q

Tubulovesicles

A

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

*Become H+ pumps/K+ antiporter

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14
Q

Mechanism of Acid Secretion

A

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

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15
Q

Ionic Composition of Gastric Juices

A

Low flow => NaCl

High Flow => HCl

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

16
Q

Stimulants of Acid Secretion

A
  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
Q

H2 receptor blockers

A

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

18
Q

Inhibitors of acid secretion

A
  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
Q

Basal secretion phase

A

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

20
Q

Cephalic phase of acid secretion

A

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
Q

Gastric phase of acid secretion

A

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
Q

Intestinal phase of secretion

A

Initiated by presence of protein digestion products in the duodenum

=>Increased gastrin secretion

23
Q

Gastric ulcers

A

Breakdown of the protective barrier of the stomach

24
Q

Duodenal ulcers

A

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
Q

H.pylori

A

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
Q

Retching

A

Involuntary motions of vomiting w/o production

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

27
Q

Vomiting Center

A
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
Q

Chemoreceptor Trigger Zone

A

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

=>Sends signals to vomiting center and NTS

29
Q

Hyperemesis of Pregnancy

A

Severe vomiting and nausea causing weight loss during pregnancy

-Baby will come out normal though

30
Q

Effects of protracted vomiting

A
  1. Metabolic alkalosis
  2. Dehydration
  3. Hypokalemia
  4. Hyponatremia
31
Q

Possible inhibitors of gastric emptying

A

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
Q

Treating ulcers

A

Antibiotics and H+ pump inhibitors