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Physiology and drugs of Gastric Secretions Flashcards

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1
Q

what causes the stomach to relax

A

relaxes receptively- driven by vagus

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2
Q

what is the role of the stomach

A

starting point for digestion of proteins, continues carb digestion, mixes food with gastric secretions to produce chyme, stores food, secrete gastric juice

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3
Q

how absorptive is the stomach

A

limited-except for alcohol

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4
Q

when does the stomach relax

A

in anticipation of food

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5
Q

what works to digest protein in the stomach

A

pepsin and HCL

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6
Q

name three different parts of the stomach

A

fundus, body, antrum

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7
Q

describe the fundus

A

Next to oesophagus
Thin smooth muscle layer
Receives food but little mixing
Little food stored there – usually a pocket of gas

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8
Q

describe the body of the stomach

A

storage aspect of gastric function
Middle section
Thin smooth muscle layer
Little mixing

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9
Q

describe the antrum

A

breaks food down into smaller and smaller particles
Next to duodenum
Thicker smooth muscle layer
Highly contractile
Much mixing of c 30mL at a time with gastric secretions

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10
Q

how is food mixed in the stomach

A

retropulsion- the churning action of gastric smooth muscle against a closed pyloric sphincter

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11
Q

what are the peristaltic contractions driven by

A

supra-threshold gastric slow waves

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12
Q

what determines the escape of chyme through pyloric sphincter

A

strength of antral wave: governed by gastric and duodenal factors

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13
Q

what are the gastric factors that govern the strength of the antral wave

A

volume of chyme in stomach (distension increases motility)

consistency of chyme

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14
Q

how does distention increase motility

A

stretch of smooth muscle- myogenic action

stimulation of intrinsic nerve plexuses (mechano receptors)

increased vagus nerve activity and gastrin release

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15
Q

what is the vagovagal reflex

A

gastrointestinal tract reflex circuits where afferent and efferent fibers of the vagus nerve coordinate responses to gut stimuli via the dorsal vagal complex in the brain. mediated by ANS

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16
Q

how does the duodenum delay emptying

A

Neuronal response: the enterogastric reflex – decreases antral activity by signals from intrinsic nerve plexuses and the ANS

Hormonal response – release of enterogastrones [e.g. secretin and cholecystokinin CCK)] from duodenum inhibits stomach contraction

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17
Q

what stimuli within the duodenum drive the neuronal and hormonal response

A

fat, acid, hypertonicity, distention

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18
Q

what types of cells excrete what in the pyloric gland area (antrum)

A

d cells- somatostatin

G cells- gastrin

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19
Q

what types of cells excrete what in the oxyntic mucosa (fundus and body)

A

Enterochromaffin-
like cell,
Histamine

Parietal cell,
Hydrochloric acid
Intrinsic factor
Gastroferrin

Chief cell
pepsinogen

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20
Q

what is the function of HCL

A

Activates pepsinogen to pepsin
Denatures protein
Kills most (not all) micro-organisms ingested with food

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21
Q

what is the function of pepsinogen

A

Inactive precursor of the peptidase, pepsin. Note: pepsin once formed activates pepsinogen (autocatalytic)

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22
Q

what is the role of the intrinsic factor and gastroferrin

A

Bind vitamin B12 and Fe2+ respectively, facilitating subsequent absorption

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23
Q

what is the role of histamine

A

stimulates HCL secretion

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24
Q

what is the role of mucus

A

protective

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25
what is the role of gastrin
stimulates HCL secretion
26
what is the role of somatostatin
inhibits HCL secretion
27
how is HCL made
Carbonic acid unstable, dissociates into proton and bicarbonate ions. The process requires potassium which enters the cell Bicarbonate exits cells in exchange for chloride via AE2, which joins with H+ to make HCL in the lumen
28
what induces the secretion of acid from the gastric parietal cell
ACh, gastrin and histamine - work by indirect and direct mechanisms
29
what signalling pathways does gastrin and ACh act on
PLC - IP3
30
what signalling pathway does histamine work on
cAMP- PKA
31
what causes the inhibition of secretion of acid (H+)
somatostatin and prostaglandins work via cAMP- PKA signalling pathways
32
describe the stimulated state of the parietal cell
H+/K+ATPase traffics to the apical membrane taking residence in extended microvilli
33
what is the rare of gastric secretion controlled by
stimulatory and inhibitory mechanisms that occur in three overlapping phases (cephalic, gastric and intestinal)
34
what is the cephalic stage
before food reaches the stomach preparing it to receive food - driven directly and indirectly by the CNS and vagus nerves
35
what is the gastric phase
when the food is in the stomach, involves both physical (distention) and chemical (amino acids stimulate G cells, food buffers (decrease ss inhibition)) mechanisms
36
what is the intestinal phase
after food has left the stomach - chyme entering the upper small intestine causes weak stimulation of gastric section via neuronal and hormonal mechanisms
37
what are the three phases of gastric acid secretion
cephalic phase, gastric phase, intestinal phase
38
how does the vagus nerve drive the cephalic stage
stimulates enteric neurones that release ACh, increase secretion of histamine and GRp (Causes release of gastrin) and inhibits D cells
39
what inhibits gastric secretion in the cephalic stage
when vagal nerve activity decreases upon cessation of eating/ emptying of the stomach
40
what inhibits gastric secretion in the gastric stage
pH falls when food exits stomach (due to decreased buffering of gastric HCl) – release of somatostatin from D cells recommences, decreasing gastrin secretion prostaglandin E2 (PGE2) continually secreted by the gastric mucosa acts locally to reduce histamine- and gastrin-mediated HCl secretion
41
what works to inhibit gastric acid secretion in the intestinal phase
factors that reduce gastric motility also reduce gastric secretion (neuronal reflexes, enterogastrones)
42
what else can cause a reduction in vagal activity and an increase in symp activity that reduce gastric secretion
pain, nausea and negative emotions
43
what drug classes decrease acid secretion
muscarinic recptor antagonists (block competitively) H2 histamine receptor antagonists (blck competitively) proton- pump inhibitors (block by covalent modification)
44
what drugs increase acid secretion
NSAIDs (block irreversibly)
45
how is the mucosa protected from HCL and pepsin
locally produced prostaglandins (reduce acid secretion, increase mucous and bicarbonate secretion, increase mucosal blood flow)
46
how does the treatment of peptic ulcers aim to promote healing
reducing acid secretion, increasing mucosal resistance, eradicating the bacterium H. pyloric (secretes agents that weaken the mucosal barrier)
47
what is a peptic ulcer
any ulcer in an area where the mucosa is exposed to HCL and pepsin
48
why do NSAIDs cause peptic ulcers
as they reduce prostaglandin formation (COX 1 inhibition) and may: trigger gastic ulceration and cause bleeding
49
give an example of a NSAID
aspirin
50
what can gastric damage due to long term NSAIDs be prevented by
with a stable PGE1 analogue (misoprostol)
51
what are the adverse effects of a stable PGE1 anaglogue
inhibits basal and and food-stimulated gastric acid formation maintains (or increases) secretion of mucus and bicarbonate
52
what are drugs that reduce acid secretion used to treat
peptic ulcer, gastro-oesophageal reflux disease, acis hypersecretion (zollinger ellison syndrome/ cushing's ulcers)
53
what is gastro oesophageal reflux disease
inappropriate relaxation of lower oesophageal sphincter allowing reflux of acid gastric contents into the oesophagus and subsequent tissue damage – oesophagitis
54
what are the mechanisms used to reduce acid secretion by drugs
irreversible inhibition of the proton-pump (H+/K+ ATPase) competitive antagonism of histamine H2 receptors competitive antagonism of muscarinic M1 and M3 ACh receptors (mostly obsolete) antagonism of gastrin (CCK2) receptors (not utilized clinically)
55
give an example of a proton pump inhibitor
omeprazole
56
what do proton pump inhibitors do
inhibit the active H+/K+ -dependant ATPase (proton pump)
57
what activates proton pump inhibitors within the body
a strongly acidic pH, inactive at neutral pH
58
how are PPIs delivered to the stomach
absorved from the GI tract and delivered via the systemic circulation to the stomach
59
why is timing of a PPI dose important
inhibition of acid secretion (typically 10-14 hr duration after a single dose before breakfast) greatly exceeds plasma half-life drug must be present in plasma at an effective concentration whilst proton pumps are active
60
how do histamine H2 receptor antagonists work to reduce gastric acid secretion
act as competitive (reversible) antagonists of H2 receptors completely block the histamine-mediated component of acid secretion and reduce secretion evoked by gastrin and ACh
61
how are PPIs administered
effective orally once daily
62
how are HH2RA administered
once/twice daily orally
63
what are HH2RA used to treat
peptic ulcers and reflux oesophagitis
64
give two examples of a HH2RA
ranitidine and cimetidine
65
give two examples of mucosal strengtheners
sucralfate and bismuth chealate
66
how does sucralfate work and how is it administered
requires an acid environment for activation – releases aluminium to acquire a strong negative charge binds to the ulcer base (positively charged proteins) and forms complex gels with mucus – provides a mucosal barrier against acid and pepsin increases mucosal blood flow, mucus, bicarbonate and prostaglandin production administered orally
67
how does bismuth chealate work and how is it administered
has mucosal strengthening actions similar to sucralfate is toxic towards H. pylori - used in combination with antibiotics and histamine H2 antagonists (ranitidine) to promote eradication of the bacterium and ulcer healing administered orally (in combination with ranitidine)
68
what turns off the secretion of succus entericus
fasting
69
where are the digestive enzymes in the small intestine
not secreted in succus entericus | sits instead on the apical membrane (brush border)
70
why do CF patients also have problems with both mucous and electrolytes in the small intestines
as mucous and chloride are secreted in to the lumen, chlorine secreted by the cystic fibrosis transmembrane conductance regulator channel
71
do alpha amalyses produce glucose
no
72
what must glucose be broken down into to be absorbed
monomer- monosaccarides

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