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Animal Medicines > GI drugs > Flashcards

GI drugs Flashcards

1
Q

which layer of the stomach are medicines usually targeted towards?

(1 mark)

A

mucosa (top layer).

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2
Q

use of villi?

(1 mark)

A

increase surface area for absorption.

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3
Q

consequences of intestinal damage?

(4 marks)

A

increased secretions
increased permeability
reduced absorption
reduced villous height.

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4
Q

effect of increased secretions (from damage to villi)?

(2 marks)

A

cause overproduction of mucus = causes GI issues

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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.
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6
Q

effect of reduced absorption (from damage to villi)?

(2 marks)

A

if inflamed, cannot absorb as many nutrients = deficiency.

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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.
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8
Q

modes of action?

(6 marks)

A

mobility agents
secretory agents
absorptive agents
supplements
laxative agents
other

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9
Q

types of mobility agents?

(4 marks)

A

prokinetics
spasmolytics
emetics
anti-emetics

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10
Q

types of secretory agents?

(2 marks)

A

pro-secretory
anti-secretory

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11
Q

types of absorptive agents?

(1 mark)

A

adsorbents

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12
Q

types of supplements?

(2 marks)

A

prebiotics
probiotics

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13
Q

types of laxative agents?

(5 marks)

A

emollient
bulk
osmotic
stimulant
irritant

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14
Q

types of other agents?

(3 marks)

A

anti-inflammatories
protectants
anti-bloat

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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.
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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.
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17
Q

examples of prokinetics?

(3 marks)

A

metoclopramide
ranitidine
lidocaine

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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++
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19
Q

metoclopramide licenced in?

(2 marks)

A

dogs and cats.
can be used off licence in rabbits to treat gut stasis.

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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.
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21
Q

ranitidine licencing?

(1 mark)

A

not licenced in animals

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22
Q

pharmacodynamics of lidocaine?

(1 mark)

A

thought to have direct stimulating effect on smooth muscle.

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23
Q

lidocaine licencing?

(1 mark)

A

horses - on the cascade to treat gut stasis.

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24
Q

side effect of lidocaine?

(1 mark)

A

causes prokinetic action.

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25
Q

use of spasmolytics?

(1 mark)

A

reduce GI motility.

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26
Q

example of spasmolytic?

(1 mark)

A

butyl scopolamine (Hyoscine)

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27
Q

pharmacodynamics of Butyl scopolamine?

(4 marks)

A
  • inhibits muscarinic ACh receptors -
  • reduces contraction of the intestines.
  • affects urinary system -
  • relaxes nerves and muscles (useful for stones/spasms)
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28
Q

what drug is butyl scopolamine often combined with? + why?

(3 marks)

A
  • metamizole (buscopan)
  • doesn’t cross blood-brain barrier so only affects peripheral motor receptors.
  • provides additional analgesic and antipyretic effects.
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29
Q

side effect of long term opioid use?

(2 marks)

A

increases segmental contraction but reduced peristalsis (more mixing in GI tract but not going anywhere).

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30
Q

where is the emetic centre located?

(1 mark)

A

in the medulla oblongata

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31
Q

what initiates vomiting?

(1 mark)

A

the chemoreceptor trigger zone relays information to the emetic centre.

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32
Q

reasons vomiting may be initiated?

(5 marks)

A
  • loss of stretch of stomach wall
  • eaten toxin/chemical
  • toxin circulating in blood / CSF
  • sense of balance + vestibular apparatus - motion sickness
  • cerebral cortex - emotions
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33
Q

use of emetics?

(2 marks)

A
  • 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).
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34
Q

examples of emetics?

(3 marks)

A

apomorphine (dogs)
xylazine (cats)
salt/soda crystals

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35
Q

pharmacodynamics of apomorphines?

(1 mark)

A

stimulates dopamine receptors in the chemoreceptor trigger zone.

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36
Q

pharmacodynamics of xylazine?

(1 mark)

A

agonist at a-2 receptors

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37
Q

pharmacodynamics of salt/soda crystals?

(2 mark)

A

direct on pharynx / ingestion of a concentration solution

38
Q

pharmacokinetics of salt/soda crystals?

(1 mark)

A

application directly onto pharynx to stimulate gag

39
Q

why CARE with salt/soda crystals?

(2 mark)

A

risk of salt toxicity / potential for aspiration pneumonia

40
Q

contraindications for emetics?

(6 marks)

A
  • 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
Q

use of anti-emetics?

(3 marks)

A
  • 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
Q

examples of anti-emetics?

(2 marks)

A

maropitant
metoclopramide

43
Q

pharmacodynamics of maropitant?

(2 marks)

A

NK-1 receptor antagonist in emetic centre. long DoA = 24h.

44
Q

benefit of giving maropitant with ACP?

(2 marks)

A

block some vestibular signals = good for motion / travel sickness.

45
Q

pharmacodynamics of metoclopramide?

(4 marks)

A
  • 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
Q

what can happen if metoclopramide is given at high doses?

(1 mark)

A

pyramidal effects (slow, twisting neck movements).

47
Q

what aree 5-HT receptors?

(1 mark)

A

seroronin receptors

48
Q

what cell is important for secretion of acids in the GI tract?

(1 mark)

A

parietal cell

49
Q

why may secretions occur?

(4 marks)

A
  • enterotoxins
  • prostaglandins
  • leukotrienes (inflammation)
  • agents that affect ACh / PSNS
50
Q

what do proton pumps produce?

(1 mark)

A

hydrochloric acid

51
Q

what receptor does histamine stimulate?

(1 mark)

A

H2 histamine receptors

52
Q

what happens when H2 histamine receptors are stimulated?

(2 marks)

A
  • initites cyclic AMP to be produced
  • results in further cascades to get hydrogen ions (which are produced by the pump comining with chloride)
53
Q

what receptor does acetylcholine stimulate?

(2 marks)

A

M3 receptors
(via vagus nerve and enteric nervous system)

54
Q

what happens when M3 receptors are stimulated?

(3 marks)

A
  • 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
Q

what receptor does gastrin stimulate?

(1 mark)

A

CCK2 receptors

56
Q

what happens when CCK2 receptors are stimulated?

(1 mark)

A

causes histamine secretion (by local ECL cells)

57
Q

examples of anti-secretory agents?

(3 marks)

A
  • proton pump inhibitors
  • H2 blockers
  • anti-inflammatories
58
Q

pharmacodynamics of proton pump inhibitors?

(2 marks)

A

inhibits ATPase pump = prevent production of hydrogen, therefore hydrogen chloride

59
Q

example of proton pump inhibitor?
(and theroretical max treatment?)

(2 marks)

A

omeprazole
(8 weeks)

60
Q

pharmacodynamics of H2 blockers?

(1 mark)

A

blocks histamine binding = whole cascade stops

61
Q

example of H2 blockers?
(and thereotical max treatment?)

(4 marks)

A
  • famotidine >
  • ranitidine >
  • cimetidine
  • (both ran and cim 28 days)
62
Q

pharmacodynamics of anti-inflammatories?

(in terms of anti-secretory agents)

(2 marks)

A

inhibit secretions of GIT cells (also anti-motility)

63
Q

examples of adsorbants?

(1 mark)

A

activated charcoal

64
Q

how do adsorbants work?

(1 mark)

A

bind to substance to prevent absorption

65
Q

pharmacodynamics of activated charcoal?

(3 marks)

A
  • more easily binds to toxins than normal charcoal
  • adsorb toxins
  • increased porosity cf. charcoal
66
Q

other examples of adsorbants?

(not activated charcoal)

(5 marks)

A
  • kaolin
  • pectin
  • bismuth salts
  • calcium carbonate
  • cholestyramine
67
Q

examples of protective agents?

(3 marks)

A
  • sucralfate
  • antacids
  • misoprostol
68
Q

pharmacodynamics of sucralfate?

(4 marks)

A
  • 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
Q

pharmacodynamics of antacids?

(1 mark)

A

inactivates HCL-

70
Q

pharmacodynamics of misoprostol?

(3 marks)

A
  • 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
Q

types of laxatives?

(5 marks)

A
  • emoillent laxatives
  • bulk laxatives
  • osmotic laxatives
  • stimulant laxatives
  • irritant laxatives
72
Q

pharmacodynamics of emoillent laxatives?

(2 marks)

A
  • act locally at site
  • lubricate and soften faecal mass - easier movement through GIT
73
Q

what can long term use of emoillent laxatives cause?

(1 mark)

A

inhibit absorption of fat-soluble vitamins

74
Q

example of emoillent laxatives?

(2 marks)

A
  • mineral oil
  • liquid paraffin
75
Q

pharmacodyamics of bulk laxatives?

(5 marks)

A
  • act locally
  • hydrophillic - absorb water -
  • causes distenstion of GIT to stimulate peristalsis
  • increases faecal bulk
  • MUST ensure adequate water intake - rehydration
76
Q

examples of bulk laxatives?

(2 marks)

A
  • sterculia
  • bran
77
Q

pharmacodynamics of osmotic laxatives?

(3 marks)

A
  • 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
Q

examples of osmotic laxatives?

(3 marks)

A
  • lactulose
  • sodium citrate
  • magnesium sulphate
79
Q

pharmacodynamics of stimulant laxatives?

(4 marks)

A
  • 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
Q

example of stimulant laxatives?

(1 mark)

A

bisacodyl

81
Q

pharmacodynamics of irritant laxatives?

(3 marks)

A
  • irritate mucosa - mucosal secretion -
  • lubricate the faecal mass and push it through
  • not widely used in UK vet med
82
Q

example of irritant laxative?

(1 mark)

A

castor oil

83
Q

what do supplements do?

(1 mark)

A

affect the intestinal flora and enzymes

84
Q

types of supplements?

(5 marks)

A
  • pre-biotics
  • probiotics
  • enzymes
  • vitamins
  • electrolytes
85
Q

difference between prebiotics and probiotics?

(what are they?)

(2 marks)

A

prebiotics:
* nutrients to encourage multiplication of benefical microbes

probiotics:
* formulation of benefical microbes

86
Q

example of prebiotics and probiotics, and a product that contains both?

(3 marks)

A
  • pre = protexin
  • pro = prokolin, yumega-bio
  • both = pro-rumen, canigest
87
Q

examples diseases that require enzymes and vitamins supplementation?

(2 marks)

A
  • exocrine pancreatic insufficiency
  • chronic GI disease
88
Q

what is exocrine pancreatic insufficency? + the enzymes that treat?

(4 marks)

A

pancreas doesnt produce normal enzymes needed for digestion and absroption of food.
* amylase
* lipase
* protease

89
Q

what is chronic GI disease? + enzymes/vitamins to treat?

(3 marks)

A

deficiency of vit b12, etc.
* cobalamin
* vitamin B12

90
Q

how can the body loose electroyltes? + which ones?

(10 marks)

A

D++ = H2O, K+, Na+, HCO3-
V++ = H2O, K+, Na+, H+

91
Q

what can cause the body to loose electrolytes via V++/D++?

(3 marks)

A

acid base imbalance - can lead to metabolic acidosis (D++) / alkalosis (V++)

92
Q

how is acid base imbalance treated?

(1 mark)

A

IVFT

Animal Medicines (20 decks)

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