Week 5 Flashcards
(100 cards)
Describe the neuronal control of the GIT
Parasympathetic from vagus:
- cholinergic and excitatory
Sympathetic fibres are post-ganglionic to:
- BVs
- smooth muscle
- glands
- inhibit acetyl choline release from plexuses
Describe the GIT hormonal control
What are gastric secretion made of
acid
bicarbonate (base to neutralise acid)
mucus (protects lining os stomach)
How can gastric secretions be modified & give examples
neutralisation
- e.g. magnesium hydroxide & trisilicate
mucosal protection
- e.g. sucralfate (coats lining of stomach)
absorbents
- e.g. activated charcoal (binds bacteria & toxins)
histamine antagonist
- e.g. cimetidine
proton pump inhibitors
- e.g. omeprazole
Misoprostol (protects lining & prevents ulcers)
Why might we want to neutralise gastric secretions
ruminal acidosis
gastritis
oesophagitis
What is the effect of histamine antagonists on gastric secretion
Inhibits gastrin, histamine and acetylcholine stimulated secretion
Pepsin secretion falls (less volume of fluid)
Get a rebound increase on withdrawal
What is the effect of proton pump inhibitors on gastric secretion
highly effective
irreversible binding to ATPase
basal & stimulated release is inhibited
What is the effect of Misoprostol on gastric secretion
stable analogue of PGE1
inhibits acid secretion
increases mucosal blood flow
increases uterine contraction
What are the 2 centres that control emetics
chemo receptor trigger zone
- chemical stimuli
- BBB permeable
- also involved in motion sickness
- impulses pass to vomiting centre
vomiting centre in brainstem:
- coordinates & integrates vomiting
Describe the pathophysiology of vomiting
Impulse to vomiting centre via central, peripheral pathways or vestibular apparatus
substance P (neurotransmitter) binds to NK-1 receptors at cell membrane
signal travels via vagus nerve to abdominal muscles + diaphragm => vomiting
How can vomiting be induced (emetic examples)
apomorphine (dopamine agonist)
- IV or mucosa
- rapid effect
alpha2 agonists
- e.g. xylazine
syrup of Ipecac
- direct irritant
- cardiotoxicity in high doses
What are some anti-emetics
Dopamine antagonists
Cerenia (maropitant)
Anti-histamines
Anticholinergics
Cannabinoids
Describe the action of metaclopramide and domperidone (dopamine antogonists) as anti-emetics
Short action so need to infuse IV
Metaclopramide - centrally acting (CRTZ)
Domperidone - peripherally acting
Increase gastric emptying and increased motility
Do not use if vomiting due to obstruction (sends obstruction further down GIT)
What are some dopamine antagonists (anti-emetics)
phenothiazine derivatives
metaclopramide and domperidone
Describe the action of Cerenia as an anti-emetic
NK1 antagonist
competes with substance P
How is diarrhoea managed
maintenance of fluid balance:
- IV fluid therapy (Hartmann’s solution)
- oral fluids
- anti-infectives e.g., zinc = immune stimulant
why may you want to modify intestinal motility in cases of diarrhoea
reduce pain
increase transit time and reabsorption window
What are the 2 main classes of antimotility (spasmolytics) drugs
opiates
- increase contractions but decrease propulsion –> increased large intestinal tone –> constipation
- e.g. morphine, loperamide
muscarinic antagonists
- inhibit acetylcholine stimulatory effects from vagus nerve
- e.g. hyoscine (buscopan)
What drugs improve gut motility
laxatives
- saline & hyperosmotic agents
- irritants to stimulate movement
- bulk producing agents
prokinetics
How does bulk (a laxative) improve gut motility
e.g. agar bran
polysaccharide polymers that are not easily digested
form hydrates bulk in gut
hold water
promote peristalsis
How do osmotic laxatives aid intestinal motility?
Poorly absorbed solutes
Lactulose - broken down to lactic acid => lower pH => traps ammonia and water in gut => softens faeces => eases motility
What drugs are used in idiopathic inflammatory bowel disease?
anti-inflammatory
- steroids such as prednisolone
- sulphasalazine (pro-drug = broken down into active substance in liver)
What are antifoaming agents used for and give an example
Define catabolism and anabolism