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GI lectures > gastric physiology 1 > Flashcards

gastric physiology 1 Flashcards

1
Q

functions of the stomach (9)

A

store and mix food
dissolve and continue digestion
regulate emptying into duodeum
kill microbes
secrete proteases
secrete intrinsic factor
activate proteases
lubricatiin
mucosal protection

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2
Q

what are the key cell types of the stomach (6)

A

mucous cells

parietal cells

chief cells

enterochromaffin-like (ECL) cells

G cells

D cells

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3
Q

what do mucous cells secrete

A

mucous, at entrance to gland

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4
Q

what does mucous do (2)

A
  • lubrication
  • protection of mucosa
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5
Q

what do parietal cells do

A

produce gastric acid (HCL) and intrinsic factor

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6
Q

function of gastric acid / HCL (3)

A
  • digestion
  • activates pepsinogen
  • kills pathogens
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7
Q

function of intrinsic factor

A

absorption of Vitamin B12

– in terminal ileum

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8
Q

what do chief cells do

A

produce pepsinogen

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9
Q

function of pepsinogen

A

converted to pepsin – protease enzyme for digestion

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10
Q

what do enterochromaffin-like (ECL) cells do

A

release histamine

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11
Q

what does histamine do

A

stimulates HCl secretion

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12
Q

what do G cells do

A

release gastrin

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13
Q

what does gastrin do (2)

A
  • stimulates HCl secretion
  • stimulates histamine secretion
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14
Q

what do D cells do

A

release somatostatin

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15
Q

what does somatostatin do

A

inhibits HCl secretion

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16
Q

how much HCL does stomach produce

A

about 2 litres a day

[H+] > 150 mm

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17
Q

pH of HCL

A

2

very strong

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18
Q

how is HCL/gastric acid secretion regulated

A

by neurohumoral regulation

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19
Q

which cells secrete gastric/hcl acid

A

parietal cells
it is energy dependent

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20
Q

what are the 4 stages of gastric acid secretion

A
  1. cephalic stage ON
  2. gastric stage ON
  3. gastric stage OFF
  4. intestinal phase OFF
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21
Q

when does the cephalic stage occur

A

during a meal

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22
Q

when does the gastric stage occur

A

once food has reached the stomach

23
Q

what initiates the gastric phase of turning on parietal cells for gastric acid secretion

A

by gastric distension from the volume of ingested material, presence of peptides and amino acids (released by the digestion of luminal proteins)

24
Q

describe gastric phase of turning on parietal cells for gastric acid secretion

A

gastrin release

gastrin acts directly on parietal cells

gastrin triggers release of histamine

histamine also acts directly on parietal cells

both gastrin & histamine increase the number of H+/K+-ATPase pumps on the
plasma membrane of the parietal cell

net effect = increased acid production

25
Q

why is histamine really important

A

it acts directly but also mediates the effect of gastrin and acetylcholine

amplifies the signal from the vagus nerve

thus can be a good therapeutic target for e.g. acid overproduction etc.

26
Q

what initiates the cephalic phase of turning on parietal cells for gastric acid secretion

A

sight, smell, taste of food and chewing

27
Q

describe the cephalic phase of turning on parietal cells for gastric acid secretion

A

parasympathetic nervous system

acetylcholine release

ACh acts directly on parietal cells

ACh triggers release of gastrin (from G
cells in the pyloric antrum of stomach) and histamine (from ECL cells)

both gastrin & histamine increase the number of H+/K+-ATPase pumps on the
plasma membrane of the parietal cell

net effect = increased acid production

28
Q

how do proteins in the stomach turn on parietal cells for gastric acid secretion

A

proteins in the stomach are a direct stimulus for gastrin release

proteins in the lumen act as a buffer, reducing amount of H+ causing pH to rise :

results in:
- decreased secretion of somatostatin
- more parietal cell activity (lack of inhibition )
- more acid secretion

29
Q

describe gastric phase of turning off parietal cells for gastric acid secretion

A

low luminal pH (high [H+])

  • directly inhibits gastrin secretion so
    indirectly inhibits histamine release (via gastrin)
  • also stimulates somatostatin release which inhibits parietal cell activity
30
Q

what initiates the intestinal phase of turning off parietal cells for gastric acid secretion

A
  • duodenal distension
  • low luminal pH
  • hypertonic luminal contents
  • presence of amino acids and fatty acids
31
Q

describe the intestinal phase of turning off parietal cells for gastric acid secretion

A

in the duodenum

  1. trigger release of enterogastrones ;
  • secretin (inhibits gastrin release, promotors somatostatin release )
  • cholecystokinin (CCK)
  1. also trigger short and long neural pathways, reducing ACh release

net effect = reduced acid secretion

32
Q

how is gastric acid secretion regulated

A

controlled by brain, stomach, duodenum

1 (parasympathetic) neurotransmitter (ACh+)

1 hormone (gastrin +)

2 paracrine factors (produced in stomach) (histamine + , somatostatin-)

2 key enterogastrones (secretin -, CCK-)

33
Q

define ulcer

A

an ulcer is a breach in a mucosal surface

34
Q

most common cause of peptic ulcers

A

helicobacter pylori infection

lives in gastric mucus

35
Q

causes of peptic ulcers

A
  • helicobacter pylori infection
  • drugs - NSAIDS
  • chemical irritants. - alcohol, bile salts, diary factors
  • gastrinoma
36
Q

describe normal stomach defences

A

they are suffiencent to resist attack so no ulcers

37
Q

how do peptic ulcers occur

A

either increased mucosal attack
or
reduced mucosal defence

38
Q

how does the gastric mucosa defend itself (4)

A

alkaline mucus on luminal surface

tight junctions between epithelial cells

replacement of damaged cells - stem cells at the base of pits to produce new cells

feedback loops

39
Q

what does helicobacter pylori do

A

lives in the gastric mucus

secretes urease, splitting urea into carbon dioxide and ammonia

ammonia + H+ = ammonium

Ammonium is toxic to gastric mucosa resulting in less mucous produced

secreted proteases, phospholipase & vacuolating cytotoxin A can then begin
attacking the gastric epithelium further reducing mucous production

results in an inflammatory response and less mucosal defence

40
Q

what are NSAIDs

A

non-steroidal anti-inflammatory drugs

41
Q

how do NSAIDs cause peptic ulcers

A

non steroidal anti inflammatory drugs

mucus secretion is stimulated by prostaglandins

(in inflamed tissue, prostaglandin
triggers inflammatory response thus inhibition = less inflammation)

cyclo- oxygenase 1 needed for prostaglandin synthesis

NSAIDs inhibit cyclo-oxygenase 1

reduced mucosal defence

42
Q

how do bile salts cause peptic ulcers

A

duodeno- gastric reflux

regurgitated bile strips away mucus layer

reduced mucosal defence

43
Q

how to treat peptic ulcer disease caused by helicobacter pylori

A

kill the organism

use triple therapy

1 proton pump inhibitor - (inhibits
pump pumping H+ ions into stomach lumen thereby increasing gastric pH making conditions inhospitable for helicobacter pylori)

2 antibiotics
- clarithromycin
- amoxicillin
- tetracycline
- metronidazole

44
Q

describe the epithelium of the stomach

A

the epithelial layer lining the stomach invaginates into the mucosa,

forming many tubular glands

simple columnar

45
Q

describe the upper portion of the stomach

A

it is thin
contains glands that :

contain mucous cells
- secrete mucuous

contains parietal cells
- secrete HCL

contains chief cells
- secrete the enzyme precursor pepsinogen

46
Q

describe the lower portion of the stomach

A

has a much thicker layer of smooth
muscle

is called the antrum

is responsible for mixing the stomach contents -
the glands in this region of the stomach secrete little acid but contain the endocrine cells that secrete the hormone gastrin (G cells)

47
Q

describe the process of gastric acid secretion

A
  1. H2O in the parietal cell breaks down into OH- and H+
  2. The origin of the H+ ions is CO2
  3. CO2 & H2O from respiration are converted into bicarbonate (H2CO3) via the enzyme carbonic anhydrase
  4. H2CO3 rapidly disassociates into HCO3- and H+
  5. The H+ ions produced can then react with the OH- ions from the breakdown of H2O to regenerate H2O
  6. The H+ ions from the break down of H2O are then pumped into the stomach lumen via H+/K+ ATPase pumps in the luminal membrane of parietal cells
  7. they pump 1 K+ ion into the parietal cell for every 1 H+ ion they pump out into the stomach (so as to ensure there is no change in polarity of the cell) - these pumps require ATP to function
  8. the K+ ions pumped in can then diffuse back out into the stomach via K+ channels on the plasma membrane of parietal cells
  9. the HCO3- from the breakdown of H2CO3 is secreted into the capillary for the exchange of Cl- ions

10.Cl- ions can then enter the stomach by diffusing through Cl- channels in the plasma membrane of the parietal cell

  1. then in the stomach, the H+ ions and Cl- ions can react to form HCl
  2. removal of the end products of this reaction enhance the forward rate of reaction - in this way production and secretion of H+ are coupled
  3. increased acid secretion stimulated by the factors mentioned below, results from the migration of H+/K+ - ATPase protein in the membranes membranes of intracellular vesicles in the parietal cell to the plasma membrane by fusion of these vesicles with the membrane thereby increasing the number of pump protein in the plasma membrane meaning more H+ can be pumped in = more acid
48
Q

how to treat peptic ulcers caused by NSAIDs

A

use prostaglandin analogues (mimic effect of prostaglandins)

e.g. misoprostol and reduce acid secretion

49
Q

how do chemical irritants cause peptic ulcers

A

alcohol, bile salts

secreted into duodenum but can reflux into stomach and wash way protective mucous lining

duodenal-gastric reflux causes bile to enter stomach, alkaline bile strips away
gastric mucous layer of stomach resulting in reduced mucosal defence

50
Q

what is gastrinoma

A

rare tumours of parietal cells = excessive gastrin release =
increase in gastric acid =
increased attack on gastric mucosa = ulcer

51
Q

what are the synthetic ways to reduce gastric acid secretion

A
  1. proton pump inhibitors
  2. H2 receptor agonists
52
Q

what do proton pump inhibitors do

A

inhibit pumps pumping H+ into stomach lumen,
they only block pumps NOT the activators

e.g. gastrin, examples include; omeprazole, lansoprazole & esomeprazole (all have varied side effects)

53
Q

what do H2 receptor agonists do

A

block receptors for histamine thereby reducing acid secretion,

examples include; cimetidine & ranitidine

GI lectures (9 decks)

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