gastrointestinal Flashcards
how is the enteric system controlled neuronally and hormonally
neuronal control:
myenteric plexus
meissners plexus
pns
sns
hormonal:
gastrin/somatostatin
histamine
prostoglandins e2 and i2
what is gastric juice made of
juice:
pepsinogens
acid (HCL)
intrinsic factor
what cells are in da stomach lining
cells:
parietal cells: gastric acid
peptic cells (chief): pepsinogen (protease precursor)
mucous cells: mucus and bicarbonate to protect stomach lining
D cells: produces somatostatin (inhibits acid secretion)
G cells: produces gastrin (stimulates acid secretion)
describe the mechanism of parietal cell acid secretion
Co2 from blood capillaries react with h2o to produce H2CO3 and this reaction is catalysed by carbonic anhydrase
H2CO3 then ionizes into H+ and HCO3-.
H+ cells are secreted by H+-K+ ATPase transporter (k+ into cell H+ out)
Hco3- is absorbed back into the blood via the HCO3- CL- antiporter (HCO3- into blood Cl- into cell)
cl- is effluxed into the stomach lumen to combine with H+ to make HCL
some KCl and NaCl is also produced
parietal cells can respond to gastrin (cck2 receptors), histamine (H2 receptors), acH (m3) (enhances acid secretion)
and prostoglandins E2 and I2 (inhibits acid secretion)
differentiate between direct and indirect pathway of parietal cell stimulation
direct: acH gastrin and histamine stimulate triggering H+ release into lumen
indirect: Ach and gastrin stimulate enterochromaffin like (ecl) cells leading them to release histamine which acts on parietal cells
what are the causes of dyspepsia (indigestion)
- Peptic ulceration
due to Helicobacter pylori infection or long use of NSAID’s - Gastro-oesophageal Reflux disease (GERD)
Bile secretions into stomach - Zollinger Ellison Syndrome (gastrin secreting tumour)
4.Gastritis (Inflammation) (can lead to ulcers)
Spicy foods
Alcohol
what can ulcers lead to
Can lead to erosion of mucous lining (duodenal gastric or oesophageal)
Damage the protective layers
Leads to excessive bleeding
describe the use of antacids and alginates for dyspepsia
symptom relief.
antiacids Increase gastric pH >4 and inhibits action of pepsin ex: aluminium hydroxide and magnesium hydroxide
sodium bicarbonate aluminium bicarbonate
mg bicarbonate
side effx: Nausea, Vomiting, Hypophosphatemia, Chalky taste, Constipation, Abdominal cramping. Diarrhoea, Electrolyte imbalance
alginates: Alginic acid combines with saliva to form a viscous foam
Floats on gastric contents and protects oesophagus
describe the use of antibiotics for dyspepsia
2 antibiotics given with PPI or H2 antagonist for eradication if H. pylori present (amoxicillin/clarithromycin/metronidazole)
describe the use of H2 antagonists for dyspepsia
symptom relief
H2 antagonists ex: ranitidine
Block Histamine activation of H2 receptors on parietal cells
H2 receptors are coupled to cAMP to activate proton pump action
Reduce gastric acid secretion
side effects:Headache, Anxiety, Depression, Dizziness, Cardiovascular effects, Thromocytopenia
describe the use of PPI for dyspepsia
symtpom relief.
ppi (irreversibly inhibit H+/k+ atpase)
Activated in acidic environments
Inhibition of >90% HCl secretion: can lead to achlordiya (absence of acid)
ex: omeprazole lansoprazole
side effects: Headaches, Abdominal pain, Diarrhoea, Nausea, Vomiting, Constipation, Flatulence, Vitamin B12 deficiency, Osteoporosis
describe the use of potassium competitive agents for dyspepsia
symptom relief
Potassium competitive acid blockers (binds to potassium H+/k+ is symporter needs both to bind) ex: vanoprazan
side effects: Naopharyngitis, Fall, Confusion, Diarrhoea, Upper Respiratory tract inflammation, Eczema, Constipation, Back pain
describe the use of cytoprotective agents for dyspepsia
symtpom relief
cytoprotective agents (stimulate mucus production and enhance blood flow to lining of GI) ex: Misoprostol Sucralfate
side efx: Diarrhoea, abdominal pain, headache, constipation
list emetic stimulti and what drugs can be used
Bacterial or viral infection
Pregnancy : 5HT3 antagonist in CTZ and GI ex: ondansteron granisteron metoclopramide
Chemicals in blood ex: toxins/drugs
from things like chemo : 5HT3 antagonist (CTZ GI) ex: ondansteron granisteron metoclopramide
D2 dopamine antagonist (CTZ GI) ex: prochloroperazine, tiethylperazine, domepridone, metoclopramide, phentothiazines
NK1 antagonist (GI) ex: aprepitant
cannabinoid agonist (vomitting center) ex: dronabinol (unclear mechanism)
from drugs: D2 dopamine antagonist (CTZ GI)
ex: prochloroperazine, tiethylperazine, domepridone, metoclopramide, phentothiazines
Motion sickness: antihistamine H1 antagonist acts on vestibular nuclei
ex: diphenhydramine dimenhydrinate /cinnarizine, cyclizine, promethazine
some histamine analogues are H1 partial agonists h3 antagonists used in vertigo ex: betahistine (increases blood flow to ear?)
chronic idiopathic nausea and cyclic vomitting: tricyclic antidepressant
ex: amitriptyline and nortriptyline
also: anti muscarinic ex: hyoscine
Act on vomiting centre and vestibular apparatus
Highly effective but adverse side effects limit their usefulness
How do NSAID’s cause damage to stomach
NSAID’s inhibit both COX-1 and 2. Cox 1 enzyme produces prostanoids that have gastric protective effects and COX 2 enzyme produces prostanoids that have a role in inflammation.
to prevent this damaging side effect NSAID can be given with cytoprotective agents such as misoprostol which bind to prostanoid receptors that block gastric H+ secretions