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GI > Physiology and drugs of Gastric Secretions > Flashcards

Physiology and drugs of Gastric Secretions Flashcards

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
Q

what is the role of gastrin

A

stimulates HCL secretion

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26
Q

what is the role of somatostatin

A

inhibits HCL secretion

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27
Q

how is HCL made

A

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

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28
Q

what induces the secretion of acid from the gastric parietal cell

A

ACh, gastrin and histamine - work by indirect and direct mechanisms

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29
Q

what signalling pathways does gastrin and ACh act on

A

PLC - IP3

30
Q

what signalling pathway does histamine work on

A

cAMP- PKA

31
Q

what causes the inhibition of secretion of acid (H+)

A

somatostatin and prostaglandins work via cAMP- PKA signalling pathways

32
Q

describe the stimulated state of the parietal cell

A

H+/K+ATPase traffics to the apical membrane taking residence in extended microvilli

33
Q

what is the rare of gastric secretion controlled by

A

stimulatory and inhibitory mechanisms that occur in three overlapping phases (cephalic, gastric and intestinal)

34
Q

what is the cephalic stage

A

before food reaches the stomach preparing it to receive food - driven directly and indirectly by the CNS and vagus nerves

35
Q

what is the gastric phase

A

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
Q

what is the intestinal phase

A

after food has left the stomach - chyme entering the upper small intestine causes weak stimulation of gastric section via neuronal and hormonal mechanisms

37
Q

what are the three phases of gastric acid secretion

A

cephalic phase, gastric phase, intestinal phase

38
Q

how does the vagus nerve drive the cephalic stage

A

stimulates enteric neurones that release ACh, increase secretion of histamine and GRp (Causes release of gastrin) and inhibits D cells

39
Q

what inhibits gastric secretion in the cephalic stage

A

when vagal nerve activity decreases upon cessation of eating/ emptying of the stomach

40
Q

what inhibits gastric secretion in the gastric stage

A

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
Q

what works to inhibit gastric acid secretion in the intestinal phase

A

factors that reduce gastric motility also reduce gastric secretion (neuronal reflexes, enterogastrones)

42
Q

what else can cause a reduction in vagal activity and an increase in symp activity that reduce gastric secretion

A

pain, nausea and negative emotions

43
Q

what drug classes decrease acid secretion

A

muscarinic recptor antagonists (block competitively)

H2 histamine receptor antagonists (blck competitively)

proton- pump inhibitors (block by covalent modification)

44
Q

what drugs increase acid secretion

A

NSAIDs (block irreversibly)

45
Q

how is the mucosa protected from HCL and pepsin

A

locally produced prostaglandins (reduce acid secretion, increase mucous and bicarbonate secretion, increase mucosal blood flow)

46
Q

how does the treatment of peptic ulcers aim to promote healing

A

reducing acid secretion,
increasing mucosal resistance,
eradicating the bacterium H. pyloric (secretes agents that weaken the mucosal barrier)

47
Q

what is a peptic ulcer

A

any ulcer in an area where the mucosa is exposed to HCL and pepsin

48
Q

why do NSAIDs cause peptic ulcers

A

as they reduce prostaglandin formation (COX 1 inhibition) and may:
trigger gastic ulceration and cause bleeding

49
Q

give an example of a NSAID

A

aspirin

50
Q

what can gastric damage due to long term NSAIDs be prevented by

A

with a stable PGE1 analogue (misoprostol)

51
Q

what are the adverse effects of a stable PGE1 anaglogue

A

inhibits basal and and food-stimulated gastric acid formation
maintains (or increases) secretion of mucus and bicarbonate

52
Q

what are drugs that reduce acid secretion used to treat

A

peptic ulcer, gastro-oesophageal reflux disease, acis hypersecretion (zollinger ellison syndrome/ cushing’s ulcers)

53
Q

what is gastro oesophageal reflux disease

A

inappropriate relaxation of lower oesophageal sphincter allowing reflux of acid gastric contents into the oesophagus and subsequent tissue damage – oesophagitis

54
Q

what are the mechanisms used to reduce acid secretion by drugs

A

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
Q

give an example of a proton pump inhibitor

A

omeprazole

56
Q

what do proton pump inhibitors do

A

inhibit the active H+/K+ -dependant ATPase (proton pump)

57
Q

what activates proton pump inhibitors within the body

A

a strongly acidic pH, inactive at neutral pH

58
Q

how are PPIs delivered to the stomach

A

absorved from the GI tract and delivered via the systemic circulation to the stomach

59
Q

why is timing of a PPI dose important

A

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
Q

how do histamine H2 receptor antagonists work to reduce gastric acid secretion

A

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
Q

how are PPIs administered

A

effective orally once daily

62
Q

how are HH2RA administered

A

once/twice daily orally

63
Q

what are HH2RA used to treat

A

peptic ulcers and reflux oesophagitis

64
Q

give two examples of a HH2RA

A

ranitidine and cimetidine

65
Q

give two examples of mucosal strengtheners

A

sucralfate and bismuth chealate

66
Q

how does sucralfate work and how is it administered

A

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
Q

how does bismuth chealate work and how is it administered

A

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
Q

what turns off the secretion of succus entericus

A

fasting

69
Q

where are the digestive enzymes in the small intestine

A

not secreted in succus entericus

sits instead on the apical membrane (brush border)

70
Q

why do CF patients also have problems with both mucous and electrolytes in the small intestines

A

as mucous and chloride are secreted in to the lumen, chlorine secreted by the cystic fibrosis transmembrane conductance regulator channel

71
Q

do alpha amalyses produce glucose

A

no

72
Q

what must glucose be broken down into to be absorbed

A

monomer- monosaccarides

GI (64 decks)

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