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VETM 443 > Gastrointestinal/Liver > Flashcards

Gastrointestinal/Liver Flashcards

1
Q

list 4 targets for pharm intervention in GI disease? (EMMA)

A

emesis: stimulate or inhibit vomiting
motility: slow or speed it up
mucosal integrity: protect mucosa from damage
appeite: stimulate it

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2
Q

what are 4 different aspects of the body that can activate the vomiting center in the brain?

A
  1. input from the ceebral cortex can activate vomiting center
  2. stimulation of the CRTZ(chemoreceptor trigger zone) activates the vomiting center
  3. input from vestibular system (motion sickness)
  4. afferent inpput from the stomach, esophagus, and pharynx
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3
Q

where is the vomitting center located?

A

in the medulla of the brain

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4
Q

vomiting that is triggered by input from the stomach, esophagus, and pharynx usually occur in response to what?

A

gastric irritation

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5
Q

pharmacological control of vomiting depends on ______

A

receptors and which drugs interact with those receptors

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6
Q

briefly explain the role of the chemoreceptor trigger zone in the stimulation of vomiting (aka normaly physiology)

A

the CRTZ senses blood levels of potentially toxic substances, so if one of these substances if detected, nasuea is experienced and vomiting relfex is initiated before any more of this toxin can be absorbed. This is a safety measure/a failsafe

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7
Q

thw two major neurotransmitters involved in the CRTZ are

A

dopamine and serotonin

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8
Q

briefly explain the role of the vestibular apparatus in the stimulation of vomiting and the main receptors involved

A

it is thought that the vestibular apparatus may have once served as a sensor for certai neurotoxins like alcohol that can produce disequilibrium for the inner ear. it may prevent humans from drinking themselves to death.
main receptors: histamine and acetylcholine

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9
Q

dopamine stimulates the vomiting center, so if a drug is a dopamine receptor antagonist it will have what effect?

A

it will be an antiemetic drug

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10
Q

biefly describe the goal of using an antiemetic drug

A

to stop vomiting associated with motion sickness, chemotherapy, etc. not to be used when vomiting is beneficial to the body

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11
Q

when would we want to use an emetic drug?

A

in toxicity situations where the animal ate something NON cuastic and there is little risk for aspiration penumonia

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12
Q

vomiting usually only removes about _______% of the material in the stomach

A

40-60, MAX 80

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13
Q

which species cannot vomit

A

horses and rabbits

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14
Q

what is the actual drug name for cerenia?

A

maropitant

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15
Q

what kind of drug is meropitant? who is it used for?

A

a neurokinin 1 receptor antagonist
useful in dogs and cats

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16
Q

does meropitant affect nausea as well as vomiting?

A

not really, it is labelled for acute vomiting caused by opiods medications and motion sickness, and based on studies, nausea was still seen even though vomiting stopped

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17
Q

what kind of drug are phenothiazine tranquilizers? list an example of one

A

central dopamine receptor antagonism
ex) acepromazine

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18
Q

what kind of effect do phenothiazine tranquilizers have on the body?

A

they are antiemetic but also have a sedative effect which can cause hypotension (alpha 1 antagonism) so it may be used as a preanesthetic

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19
Q

what is one contraindication of phenothiazine tranquilizers?

A

epileptic patients, the drug can lower seizure threshold

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20
Q

what kind of drug is metoclopramide (emesis)? what are its effects on the body?

A

dopamine receptor antagonist , at high doses also a serotonin receptor antagonist
effects: antiemetic, increases gastro and duodenal emptying (PROKINETIC), used in small animals

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21
Q

what is one contraindication of metoclopramide? list 2 adverse effects of the drug also

A

do not give this drug if GI obstruction is suspected
adverse effects: changes in behavior/mania, especially severe in adult horses

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22
Q

how does metoclopramide increase gut motility?

A

it sensitizes he upper GI tract smooth muscle to the stimulatory effects of acetylcholine

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23
Q

list 3 scenarios in which emesis should be induced

A
  1. when an animal has eaten something RECENTLY, within an hour, if asymptomatic
  2. when an animal has eaten something and you don’t know how long it has been since ingestion
  3. when the animal has eatn something that is known to stay in the stomach for long periods of time like grapes, raisins, chocolate, etc
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24
Q

list 4 scenarios in which emesis should NOT be induced

A
  1. if they’ve eaten something corrosive like bleach or battery acid
  2. if they have ingested a hydrocarbon like gasoline or kerosene (aspiration penumonia would be really bad)
  3. in symptomatic pateints (seizuring, termoring, hypoglyceia, weak,etc)
  4. in patients with underlying disease increasing the risk of aspiration penumomia
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25
Q

why do certain emetic drugs work better in dogs vs cats and vice versa?

A

in the CRTZ of dogs, dopamine and histamine receptors predominante, wheras in cats, alpha 2 and serotonin receptors predominante. this means the same drug will not affect a dog and a cat the same way

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26
Q

what kind of drug is Apomorphine? what species responds the best?

A

an emetic, a dopamine receptor agonist
works best on DOGS

27
Q

how is apomorphine best administered?

A

SQ, IV, or in the conjunctival or oral mucosa

28
Q

if you wanna make a cat vomit, what is the best drug type (and specific drug) to choose?

A

alpha 2 agonists
xylazine

29
Q

how do you reverse the vomiting in a cat you just gave xylazine to?

A

give it atipamezole or yohimbine

30
Q

how does hydrogen peroxide induce vomiting?

A

it irritates the esophagus and GI tract leading to afferent signals sent to the vomiting center

31
Q

what spcecies is hydrogen peroxide most effective in? what are some adverse effects?

A

dogs
esophagitis
gastritis

32
Q

the myenteric plexus consists of a chain of neruons that extends the entire length of the gut and it primarily controlls _______

A

gut smooth muscle tone and motility

33
Q

the submucosa plexus controls _____. it regulates processes such as _____,_____, and ______

A

local mucosal function within each segment of the intestinal wall
secretion, absroption, and contraction of small submucosal layers that affect the mucosal folding of the small intestine

34
Q

in general, in the enteric nervous system, _____ is excitatory and _____ is inhibitory

A

acetlycholine, norepinperhine

35
Q

_____ is secreted by M cells in the stomach and it stimulates GI motility

A

motilin

36
Q

what kind of drug is metoclopramide (motility)?

A

a dopamine antagonist, increases sensitivity of enteric smooth muscle to acetylcholine, causes excitment in horses

37
Q

what kind of drug is erythromyocin

A

it is an antimicrobial, but also acts as a prokinetic by binding to motilin receptors and stimulating motilin production

38
Q

why might it be an issue to use erythromyocin as a prokinetic

A

AMR and disruption of the gut microbe, especially since it is given at small doses it may promote the growth of resistant bacteria

39
Q

what is lidocaine used for as a GI drug? What it is used to treat? how is it administered?

A

it is a prokinetic, administered as a CRI in horses after colic surgery. exact mechanism of action is not clear

40
Q

anticholinergics have what effect on the GI system?

A

they are antikinetics (and have other effects too like an increase in heart rate, anything anti parasympathetic)

41
Q

what is hyoscine butyl bromide used for?

A

to treat spasmotic colic in horses (since it is an anticholinergic it slows down GI movement)

42
Q

what effect do opiods have on the GI tract?

A

they have both an anti secretory and anti motility actions by actions on mu and delta receptors of the GI tract. overall they cause constipation

43
Q

what kind of drug is loperamide?

A

an antikinectic opiate (imodium), acting on mu receptors

44
Q

if loperamide is an opiate drug, why is it not a controlled substance?

A

because it has such low bioavailability, esepcially in humans. So it can act on the local receptors in the GI tract without actually being absorbed by the body

45
Q

why is loperamide dangerous for collies or dogs with a mutation in their MDR1 gene?

A

the drug uses P-glycoprotein as a substrate and if there is a mutation in this gene that makes this protein, this drug can be toxic for these dogs and affect their central nervous system

46
Q

which cell in the stomach produces gastric acid?

A

pareital cells

47
Q

what is the role of histamine in gastric acid production?

A

histamine binds to H2 receptors which trigers translocation of the proton pump to the luminal surface of the cell, allowing release of H+ ions into the stomach lumen

48
Q

gastrin both stimulates ______ and ______

A

acid production by pareital cells
stimulates histamine release by enterochromaffin like cells

49
Q

what role does acetylcholine play in gastric acid production?

A

acetylcholine stimulation will increase gastric acid production

50
Q

drugs that reduce gastric acid production will act on either the ____ or the _____

A

H2 receptor
proton pump

51
Q

how do antiacids and protectants work?

A

they neutralize acid in the stomach lumen and protectants coat the gastic mucosa with a protective physical barrier to help prevent ulceration

52
Q

explain how H 2 blockers work and list an example of one

A

they are competitive histamine receptor antagonists and therefore reduce gastric acid secretion
example: ranitidine

53
Q

how is ranitidine usually given?

A

IV or PO in dogs, cats, and horses (less common in ruminants)

54
Q

explain how protein pump inhibitors work and list an example of one

A

they are irreversible inhibitors of the proton pump itself
example: omeprazole

55
Q

proton pump inhibitors such as omeprazole are prone to ______ which means the plasma concentration cannot be used to predict efficacy

A

ion trapped (weak bases become trapped in an acidic environment of parietal cells)

56
Q

why does it take a few days to seethe effects of omeprazole?

A

because previously dormant parietal cells are activated as acid secretion is inhibited (drug is administered, pareital cells stop making acid, the dormant cells begin producind acid, they eventually sto, this whole process takes a few days)

57
Q

give an example of a protectant. what is the goal of this drug? what is one possible side effect?

A

sucralfate
provides physical barrier that sticks to ulcerated mucosa and it increases mucosal synthesis of prostaglandins which protect the mucosa also
the drug is not absorbed so the only adverse effect is maybe constipation

58
Q

what kind of drug is activated charcoal and how does it work?

A

it is an adsorbent, it binds to toxins, poisons, and drugs and prevents their absorption. because of this reason they can interact wither other drugs you’re attempting to give

59
Q

what kind of drug is mirtazapine? what is it often used for? how does it work?

A

an appetite stimulant and antiemetic , often used for cats in chronic kidney disease
it is a serotonin receptor antagonist and a H1 receptor antagonist. response takes 8-36 hours

60
Q

what drug is commonly used to treat hepatic encephalopathy? explain how this drug works

A

lactulose
it is a galactose/fructose disaccharide that is not really absorbed by the body, they are metabolized by bacteria in the colon to produce lactic acid which draws water into the colon ultimately causing a laxative effect. it also acidifys the colon contents which draws ammonia into the colon so it can be excreted (so it reduced blood ammonia levels). this works well to treat hepatic encephalopathy because patients with thise disease will have high levels of ammonia in the blood and in the brain especially

61
Q

what kind of drug is Ursodiol? what is it used to treat? what does this drug do?

A

an orally administered bile acid
is it used to treat cholestasis
the drug reduced hepatic synthesis, secretion, and intestinal absroption of cholesterol. very little reaches systemic circulation

62
Q

ursodiol is contraindicated in what animals?

A

horses and rabbits (hind gut fermenters)

63
Q

what is the drug SAMe and what is it used for?

A

it promotes hepatocellular function. it is a compound normally produced by the liver but may be decreased in animals with a failing liver. it is an essential part of metabolic pathways (making gluthione which is an antioxidant the liver uses in detox reactions) so it acts like a supplement (exogenous substrate) to improve hepatocellular health. it has few adverse effects and it is expensive

VETM 443 (18 decks)

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