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Alimentary > Pharmacology Of GIT Drugs Reading > Flashcards

Pharmacology Of GIT Drugs Reading Flashcards

0
Q

What happens in nausea? 4

A

Gastric tone reduced, duodenal and proximal jejunal tone is increased, duodenal contents reflux into stomach, depression hyper salivation and repeated swallowing

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1
Q

What are the three stages of vomition?

A

Nausea, retching and vomiting

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2
Q

Differentiate humoral and neural initiation of vomiting

A

Humoral involves stimulation of crtz by blood borne substances whilst neural pathway is through activation of vomiting centre within reticular formation of medulla oblongata.

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3
Q

Can rodents and rabbits vomit?

A

No but they do have a vomiting centre made of the brain stem nuclei and motor systems necessary for emesis but lack the complex synaptic interaction.

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4
Q

Which receptors are important in the vomiting centre?

A

5-HT1a, alpha2 adrenergic and NK1 which are receptors for substance P.

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5
Q

Are opioid receptors involved in vomiting?

A

Their role is confusing. Opioids have emetic action in dogs and cats but acts through s receptors in dogs and u- receptors in cats. Of opioid penetrates the vomiting centre it may cause strong blockade of vomiting. But if it penetrates CRTZ first it will initially cause vomiting before blocking the vomiting centre. Morphine has this dual effect although it may also cause vomiting associated with histamine release.

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6
Q

Are d2-dopamine receptor antagonists such as metro loperamide better anti emetics in dogs or cats?

A

Dogs

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7
Q

What is xylazine?

A

An emetic because it is an alpha2-adrenergic agonist.

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8
Q

What is cytotoxic drug induced emesis mediated by?

A

5HT3 receptors. In CRTZ of cats but in dog visceral. And Vargas after end 5HT3 receptors are activated.

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9
Q

Inappropriate uses of anti-emetics 5

A 
GIT infections
GIT obstruction
GIT toxicity
Systemic hypotension
Epilepsy
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10
Q

What is maropitant used for?

A

Prevention and treatment of general emesis in dogs and prevention of motion sickness in dogs. Significantly more effective in dogs with acute vomiting than metoclopramide

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11
Q

Action of maropitant

A

Selective antagonist of substance p at the NK1 receptor. Inhibits final common pathway so effective against emesis induced by both peripheral and central stimuli.

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12
Q

Adverse effects of maropitant

A

Post dosing emesis in 8% cases at motion sickness dose.

Significant drug interactions are unlikely to occur due to wide safety margin and well characterised pharmacokinetics.

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13
Q

Indications for metoclopramide control of vomiting 4

A

Central or peripheral activation of vomiting
Cancer chemotherapy
Gastroesophageal reflux
Deceased gastric emptying (inflammation, ulcers, neoplasia, autonomic neuropathy, pyloric stenosis, postop GDV, hypokalaemia, abnormal gastric motility)

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14
Q

Mechanism of action of metoclopramide

A

Dopaminergic and 5-HT3 antagonist in CRTZ and peripheral receptors.. Also promotes release of and increases sensitivity of visceral smooth muscle to achetylcholine. Ultimately causes increased gastric emptying and increased small intestinal activity. Doesn’t alter fluid secretion or absorption anywhere.

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15
Q

Contraindications of metoclopramide 3

A

Gastric outlet obstructions, gastric perforations, epileptic patients as may increase frequency of seizures.

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16
Q

Side effects of metoclopramide 4

A

Infrequently may cause mental changes
shouldn’t be given with phenothiazines or narcotic analgesics
Anticholinergic drugs will block effects of metoclopramide on GIT motility
Rarely may cause gastric spasm and actually increase vomiting

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17
Q

Examples of antihistamines 3

A

Diphenhydramine, promethazine, dimenhydrinate

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18
Q

Mechanism of action of antihistamines

A

Acts directly or neural pathways arising in vestibular nucleus so effective against motion sickness and middle ear infections induced emesis but not vomiting induced by other stimuli.

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19
Q

2 side effects of using antihistamines as antiemetics

A

Drowsiness and xerostomia (dry mouth)

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20
Q

Example of a phenothiazine used as an antiemetic

A

Prochlorperazine

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21
Q

Mechanism of action of phenothiazines as antiemetics

A

Block CRTZ at low doses (antidopaminergic) and vomiting centre at higher doses (anticholinergic). Also block peripheral dopamine receptors in stomach. Cannot block visceral afferent (vagal) impulses associated with severe pain and contractions.

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22
Q

Side effect of phenothiazines

A

Arteriolar vasodilation due to alpha adrenergic receptor blocking action.

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23
Q

Mechanism of action of 5-HT3 antagonists

A

Antagonism of peripheral 5-HT3 serotonergic receptors in the gut is principal mechanism.

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24
Q

Examples of anticholinergics

A

Atropine, hyposcine, propanthaline and isopropamide

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25
Q

When are anticholinergic antiemetics effective?

A

When vomiting is due to smooth muscle spasm which is very uncommon.

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27
Q

What should you be aware of when using anticholinergics as antiemetics?

A

They reduce GIT motility which can act as a stimulus for further vomiting. Overuse can cause gastric atony and intestinal ileus. Don’t use in dogs with parvovirus infection as the potential for endotoxaemia is increased

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28
Q

What makes up the gastric protective barrier? 5

A 
Mucous
high epithelial turnover
tight junctions
surface active phospholipids
rich vascular supply prostaglandins
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29
Q

Causes of gastric ulcers 8

A 
drugs (aspirin, PBZ, corticosteroids)
uraemia
liver disease
stress
increased HCL production
hypotension
hypoadrenocorticism
spinal cord disease
30
Q

Outline conseqeuences of damage to mucosal barrier

A

back-diffusion of gastric acid into submucosa –> MC degranulation –> histamine release –> stimulation of acid production by gastric parietal cells –> enhanced oedema and inflammation in submucosa.

31
Q

Examples of anti-ulcer drugs - 5

A 
Histamine receptor antagonists
sucralfate
misoprostol
omeprazol
non-systemic antacids
32
Q

Which gastric ulcers are H-R antagonists effective against?

A

NSAID and uraemia induced. not effective in preventing NSAID-induced ulcers

33
Q

Side effects of histamine-receptor antagonists

A
  • hypoacidity and bacterial overgrowth (chronic use)
  • drug eruption (cimetidine in cats)
  • decrease hepatic metabolism of some drugs
  • may reduce absorption of some drugs that require acid for dissolution and absorption
34
Q

Can you use histamine-receptor antagonists with impaired renal function?

A

Yes but reduce dose by 50%

35
Q

Is sucralfate effective treatment for oral and oesophageal ulcers?

A

Yes

36
Q

What is sucralfate structurally similar to? 2

A

HEPARIN - but doesn’t poses any anticoagulant activity

SURCROSE - but not used as a sugar by the body

37
Q

What does sucralfate protect the ulcer against?

A

hydrogen ion back-diffusion, pepsin and bile and so promotes ulcer healing.

38
Q

Why does sucralfate preferentially adhere to ulcerated tissues?

A

because of electrostatic charges.

39
Q

What are the major drug actions of sucralfate?

A

stimulates mucosal defence and reparative mechanisms (also inactivates pepsin, absorbs bile acids, and is believed to be cytoprotective by stimulating PG synthesis. doesn’t significantly affect gastric acid output and may decrease the rate of gastric emptuing)

40
Q

Does sucralfate interact with any drugs?

A

It may do but none that are clinically important.

41
Q

What is misoprostol? Main use?

A

a synthetic PGE1. most useful in prevention of NSAID-induced ulceration

42
Q

How does misoprostol work?

A 
gastric antisecretory
mucosal protective
inhibits HCL
inhibits gastrin secretion
increases gastric mucous formation
increased mucosal BF --> increases epithelialisation
43
Q

Side effects - misoprostol

A
  • parturition inducer or abortion

- frequently causes diarrhoea, abdominal pain, flatulence and vomiting

44
Q

When should you use omeprazole in practice? 2

A

refractory ulcers or ulcers associated with gastrinomas or mastocytosis

45
Q

How does omeprazole work?

A

it is a proton pump inhibitor that blocks H/K ATPase, thereby blocking gastric acid secretion (in contrast to H2 receptor antagonists, it inhibits gastric acid secretion by any secretagogue).

46
Q

Side effects of omeprazole = ?

A

well tolerated in cats and dogs. Long term therapy may cause reversible gastric hypertrophy in dogs due to the trophic effects of gastrin.

47
Q

Drug interactions of omeprazole

A

inhibition of p450 hepatic enzymes may decrease hepatic clearance of some drugs

reduced absorption of drugs requiring low pH

may exacerbate bone marrow suppression

48
Q

Give some example of non-systemic antacids

A

oral preparations containing aluminium hydroxide, calcium carbonate and magnesium compounds.

49
Q

When are non-systemic antacids most commonly used?

A

in management of uraemia as aluminium hydroxide binds phosphate thus reduces hyperphosphataemia as well as having an antacid effect

50
Q

Explain how non-systemic antacids are administered.

A

must be given orally –> poor owner compliance, must be given at least every 4 hours for 4-6 weeks

51
Q

How do non-systemic antacids work?

A

neutralise HCl, bind bile acids, decrease pepsin activity, may stimulate local PGE1.

Magnesium increased bowel motility, aluminium decreases bowel motility so the two are usually combined.

52
Q

Side effects of non-systemic antacids = ?

A
  • calcium-containing antacids tend to promote constipation
  • magnesium promotes looser faeces
  • aluminium reduces gastric motility and delays gastric emptying
  • if given infrequently, they may increase gastric acid production
  • may predispose to renal calculi (calcium-containing types)
  • hypophosphataemia and aluminium accumulation (aluminium-containing types)
53
Q

List some examples of motility modifying drugs 4

A

opioid analgesics
anticholinergic drugs
absorbents and protectants
sulphasalazine

54
Q

How are peristalsis and segmental contractions controlled?

A

PERISTALSIS - influenced by the cholinergic system and gut hormones such as motilin
SEGMENTAL - cholingeric dependent

55
Q

Is reducing peristalsis a good thing Why?

A

No this is usually of little clinical benefit and is generally contraindicated so focus on increasing segmental contractions. This is because, in most cases of diarrhoea, the gut is hypomotile not hypermotile and peristalsis and segmental contractions are already reduced.

56
Q

What two groups of agents may modify GIT motility?

A

NARCOTIC ANALGESICS - increase segmental contractions

ANTICHOLINERGIC DRUGS - decrease both segmental contractions and peristalsis.

57
Q

When are opioid analgesics used in veterinary?

A

limited use in practice. acute diarrhoea is usually self-limiting with appropriate symptomatic treatment and chronic diarrhoea doesn’t usually respond to symptomatic therapy.occasionally useful in chronic colitis that can’t be controlled by other means.

58
Q

What are the risks of opioid analgesics? 2

A
  • diarhoea may be beneficial to removing toxins
  • reduced motility may allow enterotoxin-producing organimss to remain in SI thus increasing fluid-loss
  • may facilitate greater time of organism in lumen
59
Q

Mechanism of action of opioid analgesics

A

Opioids increase the amplitude of rhythmic contraction and decrease propulsive contractions. They directly affect intestinal smooth muscle producing both tonic and phasic contractions of the circular muscle. They also act centrally and on synapses to augment segmentation. Opioids either have no effect on longitudinal muscle or they relax it. The net effect of these actions is to inhibit the flow of intestinal contents, delay gastric emptying and increase the tone of the ileocolic valve and anal sphincter.

60
Q

Drug interactions with opioid analgesics = ? 1

A

other CNS depressants

61
Q

Risk of using anti-cholinergic drugs to modify GIT motility?

A

may produce adynamic ileus especially if electrolyte imbalances such as hypokalaemia are also present.

62
Q

When are anti-cholinergics indicated to modify GIT motility?

A

They may be justified in the short
term symptomatic relief of pain and tenesmus associated with large bowel inflammatory
disease. They also may be indicated in stress‐induced colitis where cholinergic mechanisms
might be involved.

63
Q

What are kaolin and pectin, acitvated charcoal and bismuth salicyate examples of?

A

absorbents and protectants

64
Q

What do kaolin and pectin do?

A

soothe irritated GIT mucosa and bind toxins and pathogenic bacteria. Clinical efficacy is unproven.

65
Q

What is activated charcoal used for?

A

treatement of toxicosis - thought to absorb toxic substances and bind bacterial toxins. no controlled studies to evaluate efficacy

66
Q

What is bismuth salicylate used for?

A

treatment and prevention of enterotoxigenic diarrhoea.

67
Q

Clinical indications for sulphasalazine

A

idiopathic ulcerative colitis in dogs and cats. probably only best to use if there is biopsy confirmation of ulcerative colitis and that there has been no response to dietary or other therapy.

68
Q

Define panacea

A

a solution/remedy for all difficulties/diseases

69
Q

Mechanism of action of sulphasalazine

A

Sulphasalazine is a combination of sulpha‐pyridine and 5‐aminosalicylic acid (5‐ASA) which
is cleaved by colonic bacteria resulting in the sulpha component being absorbed and ASA
excreted in faeces. 5‐ASA is probably the active ingredient due to antiprostaglandin and
antileukotriene activity. In addition, it is thought to have oxygen‐free radical scavenging
action, to interfere with phagocytic chemotaxis and function, and to inhibit cytokine and
immunoglobulin production.

70
Q

What is important to remember when using probiotics for dogs and cats?

A

consider the cost: benefit especially in dogs due to lack of current data. Future products may differ in composition as we learn more about gut flora in dogs and cats so they may be better targeted to be of clinical benefit.

Alimentary (37 decks)

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