GI drugs Flashcards
which layer of the stomach are medicines usually targeted towards?
(1 mark)
mucosa (top layer).
use of villi?
(1 mark)
increase surface area for absorption.
consequences of intestinal damage?
(4 marks)
increased secretions
increased permeability
reduced absorption
reduced villous height.
effect of increased secretions (from damage to villi)?
(2 marks)
cause overproduction of mucus = causes GI issues
effect of increase in permeability (from damage to villi)?
(4 marks)
- epithelial cells that line the villi attached by tight junctions.
- inflammation compromises the integrity of these junctions so large molecules such as proteins can now squeeze through and pass into intestinal tract.
- also loose water and electrolytes as proteins have osmotic pull. they move into intestinal space and lumen.
- bacteria can also move in - possibly pass into blood stream and cause infection spread through body.
effect of reduced absorption (from damage to villi)?
(2 marks)
if inflamed, cannot absorb as many nutrients = deficiency.
effect of reduced villous height (from damage to villi)?
(3 marks)
- reduced turnover of cells
- = no longer making enough cells to keep up with ones being removed.
- causes stunted villous that is smaller in height and impacts absoption.
modes of action?
(6 marks)
mobility agents
secretory agents
absorptive agents
supplements
laxative agents
other
types of mobility agents?
(4 marks)
prokinetics
spasmolytics
emetics
anti-emetics
types of secretory agents?
(2 marks)
pro-secretory
anti-secretory
types of absorptive agents?
(1 mark)
adsorbents
types of supplements?
(2 marks)
prebiotics
probiotics
types of laxative agents?
(5 marks)
emollient
bulk
osmotic
stimulant
irritant
types of other agents?
(3 marks)
anti-inflammatories
protectants
anti-bloat
what is segmentation?
(4 marks)
- segmental contraction of the GI tract.
- points where muscles rhythmically contract.
- this mixes and breaks up contents into smaller boluses.
- mixed with intestinal fluid to ensure soft enough to pass.
what is peristalsis?
(3 marks)
- squeeze faecal matter forwards and propelling it through the GI tract.
- done by using rhythmic muscular contraction behind the bolus.
- once one bit has contracted, the next relaxes.
examples of prokinetics?
(3 marks)
metoclopramide
ranitidine
lidocaine
pharmacodynamics of metoclopramide?
(4 marks)
- stimulates muscarinic ACh receptors / antagonises dopamine.
- increase peristalsis and relaxes pyloric sphincter -
- encourages gastric emptying and movement through upper GIT.
- anti-emetic - prevents V++
metoclopramide licenced in?
(2 marks)
dogs and cats.
can be used off licence in rabbits to treat gut stasis.
pharmacodynamics of ranitidine?
(4 marks)
- stimulates muscarinic ACh receptors -
- generates action potential (anticholinesterase activity) at the neuromuscular junction joining the intestines.
- prokinetic and reduces gastric secretions -
- block histamine which is important for stomach acid.
ranitidine licencing?
(1 mark)
not licenced in animals
pharmacodynamics of lidocaine?
(1 mark)
thought to have direct stimulating effect on smooth muscle.
lidocaine licencing?
(1 mark)
horses - on the cascade to treat gut stasis.
side effect of lidocaine?
(1 mark)
causes prokinetic action.
use of spasmolytics?
(1 mark)
reduce GI motility.
example of spasmolytic?
(1 mark)
butyl scopolamine (Hyoscine)
pharmacodynamics of Butyl scopolamine?
(4 marks)
- inhibits muscarinic ACh receptors -
- reduces contraction of the intestines.
- affects urinary system -
- relaxes nerves and muscles (useful for stones/spasms)
what drug is butyl scopolamine often combined with? + why?
(3 marks)
- metamizole (buscopan)
- doesn’t cross blood-brain barrier so only affects peripheral motor receptors.
- provides additional analgesic and antipyretic effects.
side effect of long term opioid use?
(2 marks)
increases segmental contraction but reduced peristalsis (more mixing in GI tract but not going anywhere).
where is the emetic centre located?
(1 mark)
in the medulla oblongata
what initiates vomiting?
(1 mark)
the chemoreceptor trigger zone relays information to the emetic centre.
reasons vomiting may be initiated?
(5 marks)
- loss of stretch of stomach wall
- eaten toxin/chemical
- toxin circulating in blood / CSF
- sense of balance + vestibular apparatus - motion sickness
- cerebral cortex - emotions
use of emetics?
(2 marks)
- to make an animal sick that has ingested toxic / poisons / FBs.
- usually want to make them sick within 1-2h so toxin doesn’t reach GI tract (no toxic effect).
examples of emetics?
(3 marks)
apomorphine (dogs)
xylazine (cats)
salt/soda crystals
pharmacodynamics of apomorphines?
(1 mark)
stimulates dopamine receptors in the chemoreceptor trigger zone.
pharmacodynamics of xylazine?
(1 mark)
agonist at a-2 receptors
pharmacodynamics of salt/soda crystals?
(2 mark)
direct on pharynx / ingestion of a concentration solution
pharmacokinetics of salt/soda crystals?
(1 mark)
application directly onto pharynx to stimulate gag
why CARE with salt/soda crystals?
(2 mark)
risk of salt toxicity / potential for aspiration pneumonia
contraindications for emetics?
(6 marks)
- ingestion of a caustic / corrosive substances
- lack of gage reflex (high risk of aspiration pneumonia)
- respiratory depression / hypotension
- reduced consciousness - won’t have normal reflexes to protect airways - aspiration pneumonia
- oily/paraffin containing substances
- sharp objects - don’t want to risk bringing back up as could cause further damage.
use of anti-emetics?
(3 marks)
- used to prevent animal being sick.
- usually animal has disease process that causing it to be sick
- often losing fluids anyway - V++ means further loses.
examples of anti-emetics?
(2 marks)
maropitant
metoclopramide
pharmacodynamics of maropitant?
(2 marks)
NK-1 receptor antagonist in emetic centre. long DoA = 24h.
benefit of giving maropitant with ACP?
(2 marks)
block some vestibular signals = good for motion / travel sickness.
pharmacodynamics of metoclopramide?
(4 marks)
- dopamine antagonist in chemoreceptor trigger zone -
- blocks dopamine binding - no V++.
- acts directly on gut (upper GIT) -
- peristalsis, relaxes pyloric sphincter (bottom of stomach), tightens cardiac sphincter (top of stomach).
what can happen if metoclopramide is given at high doses?
(1 mark)
pyramidal effects (slow, twisting neck movements).
what aree 5-HT receptors?
(1 mark)
seroronin receptors
what cell is important for secretion of acids in the GI tract?
(1 mark)
parietal cell
why may secretions occur?
(4 marks)
- enterotoxins
- prostaglandins
- leukotrienes (inflammation)
- agents that affect ACh / PSNS
what do proton pumps produce?
(1 mark)
hydrochloric acid
what receptor does histamine stimulate?
(1 mark)
H2 histamine receptors
what happens when H2 histamine receptors are stimulated?
(2 marks)
- initites cyclic AMP to be produced
- results in further cascades to get hydrogen ions (which are produced by the pump comining with chloride)
what receptor does acetylcholine stimulate?
(2 marks)
M3 receptors
(via vagus nerve and enteric nervous system)
what happens when M3 receptors are stimulated?
(3 marks)
- increases amount of calcium we have
- chain of events resulting in more hydrogen ions being produced through the pump
- hydrogen ions combine with chloride, producing HCL.
what receptor does gastrin stimulate?
(1 mark)
CCK2 receptors
what happens when CCK2 receptors are stimulated?
(1 mark)
causes histamine secretion (by local ECL cells)
examples of anti-secretory agents?
(3 marks)
- proton pump inhibitors
- H2 blockers
- anti-inflammatories
pharmacodynamics of proton pump inhibitors?
(2 marks)
inhibits ATPase pump = prevent production of hydrogen, therefore hydrogen chloride
example of proton pump inhibitor?
(and theroretical max treatment?)
(2 marks)
omeprazole
(8 weeks)
pharmacodynamics of H2 blockers?
(1 mark)
blocks histamine binding = whole cascade stops
example of H2 blockers?
(and thereotical max treatment?)
(4 marks)
- famotidine >
- ranitidine >
- cimetidine
- (both ran and cim 28 days)
pharmacodynamics of anti-inflammatories?
(in terms of anti-secretory agents)
(2 marks)
inhibit secretions of GIT cells (also anti-motility)
examples of adsorbants?
(1 mark)
activated charcoal
how do adsorbants work?
(1 mark)
bind to substance to prevent absorption
pharmacodynamics of activated charcoal?
(3 marks)
- more easily binds to toxins than normal charcoal
- adsorb toxins
- increased porosity cf. charcoal
other examples of adsorbants?
(not activated charcoal)
(5 marks)
- kaolin
- pectin
- bismuth salts
- calcium carbonate
- cholestyramine
examples of protective agents?
(3 marks)
- sucralfate
- antacids
- misoprostol
pharmacodynamics of sucralfate?
(4 marks)
- binds to site of ulcer - forms physical barrier (PGE production)
- protects and binds epidermal growth factor -
- (also protect from further damage, loss of proteins from surface of ulcer)
- needs acidic environment
pharmacodynamics of antacids?
(1 mark)
inactivates HCL-
pharmacodynamics of misoprostol?
(3 marks)
- decreases activity of paroetal cells (anti-secretory)
- enhances mucous production as well as mucosal blood flow and epithelialisation (cytoprotectant) -
- promote blood flow and lay down new cells)
types of laxatives?
(5 marks)
- emoillent laxatives
- bulk laxatives
- osmotic laxatives
- stimulant laxatives
- irritant laxatives
pharmacodynamics of emoillent laxatives?
(2 marks)
- act locally at site
- lubricate and soften faecal mass - easier movement through GIT
what can long term use of emoillent laxatives cause?
(1 mark)
inhibit absorption of fat-soluble vitamins
example of emoillent laxatives?
(2 marks)
- mineral oil
- liquid paraffin
pharmacodyamics of bulk laxatives?
(5 marks)
- act locally
- hydrophillic - absorb water -
- causes distenstion of GIT to stimulate peristalsis
- increases faecal bulk
- MUST ensure adequate water intake - rehydration
examples of bulk laxatives?
(2 marks)
- sterculia
- bran
pharmacodynamics of osmotic laxatives?
(3 marks)
- hypertonic solutions -
- higher conc than all surrounding tissues - water moves into solution where it is in GIT with faecal mass
- draw water into intestines - stimulates peristalsis and increase faecal mass
examples of osmotic laxatives?
(3 marks)
- lactulose
- sodium citrate
- magnesium sulphate
pharmacodynamics of stimulant laxatives?
(4 marks)
- precise MoA not clear
- stimulate smooth muscle contraction
- inhibit water absorption
- NOT to be used if any concern re-obstruction (e.g. FB will contract against it and not allow it to pass)
example of stimulant laxatives?
(1 mark)
bisacodyl
pharmacodynamics of irritant laxatives?
(3 marks)
- irritate mucosa - mucosal secretion -
- lubricate the faecal mass and push it through
- not widely used in UK vet med
example of irritant laxative?
(1 mark)
castor oil
what do supplements do?
(1 mark)
affect the intestinal flora and enzymes
types of supplements?
(5 marks)
- pre-biotics
- probiotics
- enzymes
- vitamins
- electrolytes
difference between prebiotics and probiotics?
(what are they?)
(2 marks)
prebiotics:
* nutrients to encourage multiplication of benefical microbes
probiotics:
* formulation of benefical microbes
example of prebiotics and probiotics, and a product that contains both?
(3 marks)
- pre = protexin
- pro = prokolin, yumega-bio
- both = pro-rumen, canigest
examples diseases that require enzymes and vitamins supplementation?
(2 marks)
- exocrine pancreatic insufficiency
- chronic GI disease
what is exocrine pancreatic insufficency? + the enzymes that treat?
(4 marks)
pancreas doesnt produce normal enzymes needed for digestion and absroption of food.
* amylase
* lipase
* protease
what is chronic GI disease? + enzymes/vitamins to treat?
(3 marks)
deficiency of vit b12, etc.
* cobalamin
* vitamin B12
how can the body loose electroyltes? + which ones?
(10 marks)
D++ = H2O, K+, Na+, HCO3-
V++ = H2O, K+, Na+, H+
what can cause the body to loose electrolytes via V++/D++?
(3 marks)
acid base imbalance - can lead to metabolic acidosis (D++) / alkalosis (V++)
how is acid base imbalance treated?
(1 mark)
IVFT
