GI drugs Flashcards
(92 cards)
1
Q
which layer of the stomach are medicines usually targeted towards?
(1 mark)
A
mucosa (top layer).
2
Q
use of villi?
(1 mark)
A
increase surface area for absorption.
3
Q
consequences of intestinal damage?
(4 marks)
A
increased secretions
increased permeability
reduced absorption
reduced villous height.
4
Q
effect of increased secretions (from damage to villi)?
(2 marks)
A
cause overproduction of mucus = causes GI issues
5
Q
effect of increase in permeability (from damage to villi)?
(4 marks)
A
- 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.
6
Q
effect of reduced absorption (from damage to villi)?
(2 marks)
A
if inflamed, cannot absorb as many nutrients = deficiency.
7
Q
effect of reduced villous height (from damage to villi)?
(3 marks)
A
- 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.
8
Q
modes of action?
(6 marks)
A
mobility agents
secretory agents
absorptive agents
supplements
laxative agents
other
9
Q
types of mobility agents?
(4 marks)
A
prokinetics
spasmolytics
emetics
anti-emetics
10
Q
types of secretory agents?
(2 marks)
A
pro-secretory
anti-secretory
11
Q
types of absorptive agents?
(1 mark)
A
adsorbents
12
Q
types of supplements?
(2 marks)
A
prebiotics
probiotics
13
Q
types of laxative agents?
(5 marks)
A
emollient
bulk
osmotic
stimulant
irritant
14
Q
types of other agents?
(3 marks)
A
anti-inflammatories
protectants
anti-bloat
15
Q
what is segmentation?
(4 marks)
A
- 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.
16
Q
what is peristalsis?
(3 marks)
A
- 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.
17
Q
examples of prokinetics?
(3 marks)
A
metoclopramide
ranitidine
lidocaine
18
Q
pharmacodynamics of metoclopramide?
(4 marks)
A
- stimulates muscarinic ACh receptors / antagonises dopamine.
- increase peristalsis and relaxes pyloric sphincter -
- encourages gastric emptying and movement through upper GIT.
- anti-emetic - prevents V++
19
Q
metoclopramide licenced in?
(2 marks)
A
dogs and cats.
can be used off licence in rabbits to treat gut stasis.
20
Q
pharmacodynamics of ranitidine?
(4 marks)
A
- 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.
21
Q
ranitidine licencing?
(1 mark)
A
not licenced in animals
22
Q
pharmacodynamics of lidocaine?
(1 mark)
A
thought to have direct stimulating effect on smooth muscle.
23
Q
lidocaine licencing?
(1 mark)
A
horses - on the cascade to treat gut stasis.
24
Q
side effect of lidocaine?
(1 mark)
A
causes prokinetic action.
25
use of spasmolytics?
## Footnote
(1 mark)
reduce GI motility.
26
example of spasmolytic?
## Footnote
(1 mark)
butyl scopolamine (Hyoscine)
27
pharmacodynamics of Butyl scopolamine?
## Footnote
(4 marks)
* inhibits muscarinic ACh receptors -
* reduces contraction of the intestines.
* affects urinary system -
* relaxes nerves and muscles (useful for stones/spasms)
28
what drug is butyl scopolamine often combined with? + why?
## Footnote
(3 marks)
* metamizole (buscopan)
* doesn't cross blood-brain barrier so only affects peripheral motor receptors.
* provides additional analgesic and antipyretic effects.
29
side effect of long term opioid use?
## Footnote
(2 marks)
increases segmental contraction but reduced peristalsis (more mixing in GI tract but not going anywhere).
30
where is the emetic centre located?
## Footnote
(1 mark)
in the medulla oblongata
31
what initiates vomiting?
## Footnote
(1 mark)
the chemoreceptor trigger zone relays information to the emetic centre.
32
reasons vomiting may be initiated?
## Footnote
(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
33
use of emetics?
## Footnote
(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).
34
examples of emetics?
## Footnote
(3 marks)
apomorphine (dogs)
xylazine (cats)
salt/soda crystals
35
pharmacodynamics of apomorphines?
## Footnote
(1 mark)
stimulates dopamine receptors in the chemoreceptor trigger zone.
36
pharmacodynamics of xylazine?
## Footnote
(1 mark)
agonist at a-2 receptors
37
pharmacodynamics of salt/soda crystals?
## Footnote
(2 mark)
direct on pharynx / ingestion of a concentration solution
38
pharmacokinetics of salt/soda crystals?
## Footnote
(1 mark)
application directly onto pharynx to stimulate gag
39
why CARE with salt/soda crystals?
## Footnote
(2 mark)
risk of salt toxicity / potential for aspiration pneumonia
40
contraindications for emetics?
## Footnote
(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.
41
use of anti-emetics?
## Footnote
(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.
42
examples of anti-emetics?
## Footnote
(2 marks)
maropitant
metoclopramide
43
pharmacodynamics of maropitant?
## Footnote
(2 marks)
NK-1 receptor antagonist in emetic centre. long DoA = 24h.
44
benefit of giving maropitant with ACP?
## Footnote
(2 marks)
block some vestibular signals = good for motion / travel sickness.
45
pharmacodynamics of metoclopramide?
## Footnote
(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).
46
what can happen if metoclopramide is given at high doses?
## Footnote
(1 mark)
pyramidal effects (slow, twisting neck movements).
47
what aree 5-HT receptors?
## Footnote
(1 mark)
seroronin receptors
48
what cell is important for secretion of acids in the GI tract?
## Footnote
(1 mark)
parietal cell
49
why may secretions occur?
## Footnote
(4 marks)
* enterotoxins
* prostaglandins
* leukotrienes (inflammation)
* agents that affect ACh / PSNS
50
what do proton pumps produce?
## Footnote
(1 mark)
hydrochloric acid
51
what receptor does histamine stimulate?
## Footnote
(1 mark)
H2 histamine receptors
52
what happens when H2 histamine receptors are stimulated?
## Footnote
(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)
53
what receptor does acetylcholine stimulate?
## Footnote
(2 marks)
M3 receptors
(via vagus nerve and enteric nervous system)
54
what happens when M3 receptors are stimulated?
## Footnote
(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.
55
what receptor does gastrin stimulate?
## Footnote
(1 mark)
CCK2 receptors
56
what happens when CCK2 receptors are stimulated?
## Footnote
(1 mark)
causes histamine secretion (by local ECL cells)
57
examples of anti-secretory agents?
## Footnote
(3 marks)
* proton pump inhibitors
* H2 blockers
* anti-inflammatories
58
pharmacodynamics of proton pump inhibitors?
## Footnote
(2 marks)
inhibits ATPase pump = prevent production of hydrogen, therefore hydrogen chloride
59
example of proton pump inhibitor?
(and theroretical max treatment?)
## Footnote
(2 marks)
omeprazole
(8 weeks)
60
pharmacodynamics of H2 blockers?
## Footnote
(1 mark)
blocks histamine binding = whole cascade stops
61
example of H2 blockers?
(and thereotical max treatment?)
## Footnote
(4 marks)
* famotidine >
* ranitidine >
* cimetidine
* (both ran and cim 28 days)
62
pharmacodynamics of anti-inflammatories?
| (in terms of anti-secretory agents)
## Footnote
(2 marks)
inhibit secretions of GIT cells (also anti-motility)
63
examples of adsorbants?
## Footnote
(1 mark)
activated charcoal
64
how do adsorbants work?
## Footnote
(1 mark)
bind to substance to prevent absorption
65
pharmacodynamics of activated charcoal?
## Footnote
(3 marks)
* more easily binds to toxins than normal charcoal
* adsorb toxins
* increased porosity cf. charcoal
66
other examples of adsorbants?
| (not activated charcoal)
## Footnote
(5 marks)
* kaolin
* pectin
* bismuth salts
* calcium carbonate
* cholestyramine
67
examples of protective agents?
## Footnote
(3 marks)
* sucralfate
* antacids
* misoprostol
68
pharmacodynamics of sucralfate?
## Footnote
(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
69
pharmacodynamics of antacids?
## Footnote
(1 mark)
inactivates HCL-
70
pharmacodynamics of misoprostol?
## Footnote
(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)
71
types of laxatives?
## Footnote
(5 marks)
* emoillent laxatives
* bulk laxatives
* osmotic laxatives
* stimulant laxatives
* irritant laxatives
72
pharmacodynamics of emoillent laxatives?
## Footnote
(2 marks)
* act locally at site
* lubricate and soften faecal mass - easier movement through GIT
73
what can long term use of emoillent laxatives cause?
## Footnote
(1 mark)
inhibit absorption of fat-soluble vitamins
74
example of emoillent laxatives?
## Footnote
(2 marks)
* mineral oil
* liquid paraffin
75
pharmacodyamics of bulk laxatives?
## Footnote
(5 marks)
* act locally
* hydrophillic - absorb water -
* causes distenstion of GIT to stimulate peristalsis
* increases faecal bulk
* MUST ensure adequate water intake - rehydration
76
examples of bulk laxatives?
## Footnote
(2 marks)
* sterculia
* bran
77
pharmacodynamics of osmotic laxatives?
## Footnote
(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
78
examples of osmotic laxatives?
## Footnote
(3 marks)
* lactulose
* sodium citrate
* magnesium sulphate
79
pharmacodynamics of stimulant laxatives?
## Footnote
(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)
80
example of stimulant laxatives?
## Footnote
(1 mark)
bisacodyl
81
pharmacodynamics of irritant laxatives?
## Footnote
(3 marks)
* irritate mucosa - mucosal secretion -
* lubricate the faecal mass and push it through
* not widely used in UK vet med
82
example of irritant laxative?
## Footnote
(1 mark)
castor oil
83
what do supplements do?
## Footnote
(1 mark)
affect the intestinal flora and enzymes
84
types of supplements?
## Footnote
(5 marks)
* pre-biotics
* probiotics
* enzymes
* vitamins
* electrolytes
85
difference between prebiotics and probiotics?
| (what are they?)
## Footnote
(2 marks)
prebiotics:
* nutrients to encourage multiplication of benefical microbes
probiotics:
* formulation of benefical microbes
86
example of prebiotics and probiotics, and a product that contains both?
## Footnote
(3 marks)
* pre = protexin
* pro = prokolin, yumega-bio
* both = pro-rumen, canigest
87
examples diseases that require enzymes and vitamins supplementation?
## Footnote
(2 marks)
* exocrine pancreatic insufficiency
* chronic GI disease
88
what is exocrine pancreatic insufficency? + the enzymes that treat?
## Footnote
(4 marks)
pancreas doesnt produce normal enzymes needed for digestion and absroption of food.
* amylase
* lipase
* protease
89
what is chronic GI disease? + enzymes/vitamins to treat?
## Footnote
(3 marks)
deficiency of vit b12, etc.
* cobalamin
* vitamin B12
90
how can the body loose electroyltes? + which ones?
## Footnote
(10 marks)
D++ = H2O, K+, Na+, HCO3-
V++ = H2O, K+, Na+, H+
91
what can cause the body to loose electrolytes via V++/D++?
## Footnote
(3 marks)
acid base imbalance - can lead to metabolic acidosis (D++) / alkalosis (V++)
92
how is acid base imbalance treated?
## Footnote
(1 mark)
IVFT
