Pharmacology Flashcards

1
Q

Is prednisolone commonly ulcerogenic?

A

Not at normal doses. Unless concurrent gastric hypoxia, hypoperfusion, severe spinal disease, or concurrent use of NSAIDs

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2
Q

When are gastrointestinal protectants indicated?

A

In case of gastrointestinal ulceration or erosion

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3
Q

After initiating GI protectant therapy - when is improvement expected to be noted?

A

After 2-5 days if inciting cause is removed

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4
Q

Drug class - cimetidine, ranitidine, and famotidine

A

Histamine-2 Receptor antagonists (H2 receptor antagonists)

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5
Q

How do H-2 receptor antagonists function?

A

Block histamine receptor on gastric parietal cell - decrease gastric acid secretion

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6
Q

When is peak effect noted with H-2 receptor antagonists?

A

Almost immediately after beginning medication (does not need to build up efficacy)

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7
Q

Which is the most potent H2 receptor antagonist?

A

Famotidine

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8
Q

When should you give cimetidine in relation to food?

A

On an empty stomach - before feeding

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9
Q

Which H-2 receptor antagonists utilize P-450 enzymes?

A

Cimetidine, ranitidine

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10
Q

Which H-2 receptor antagonist utilizes P-450 enzymes and may cause toxic buildup of theophylline, lidocaine, and metronidazole (among others) when administered concurrently?

A

Cimetidine

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11
Q

Which H-2 receptor antagonist causes reduced hepatic blood flow?

A

Cimetidine

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12
Q

How are famotidine and nizatidine excreted from body?

A

Almost unchanged in urine

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13
Q

Which H-2 receptor antagonist may cause vomiting and lethargy if administered IV?

A

Ranitidine

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14
Q

Which H-2 receptor antagonist may cause interference with serum gastrin concentration?

A

Famotidine - causes transient increase in serum gastrin

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15
Q

Drug class - Omeprazole, pantoprazole, esomeprazole

A

Proton pump inhibitors (PPIs)

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16
Q

How do proton pump inhibitors function?

A

Inhibit hydrogen-potassium ATP on parietal cell - stop secretion of hydrogen into gastric lumen

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17
Q

Which PPI has longest duration of effect?

A

Dexlansoprazole

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18
Q

How long does it take for PPIs to reach maximum effect?

A

2-5 days

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19
Q

Where is omeprazole absorbed?

A

In duodenum

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20
Q

When should omeprazole be given in relation to food?

A

On empty stomach - one hour before meal

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21
Q

How are PPIs metabolized?

A

First pass hepatic metabolism

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22
Q

Which PPIs affect P-450 enzymes?

A

Omeprazole and esomeprazole

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23
Q

What are potential risks of alteration of gastric pH?

A

Altered metabolism of some drugs which rely on pH for absorption, potential for admission of some bacteria which would otherwise be destroyed by gastric pH

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24
Q

How does sucralfate function?

A

Locally acting - binds to epithelial cells, especially at erosions and ulcers and protects from pepsin and bile acids

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25
Q

What is sucralfate composed of?

A

Sucrose and aluminum hydroxide

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26
Q

When should sucralfate be administered in relation to antacids?

A

Prior to antacids

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27
Q

Drug class - misoprostol

A

Prostaglandin E1 analog

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28
Q

How does misoprostol function?

A

Antisecretory effect on parietal cells - inhibition of acid secretion, also stimulates secretion of mucus and bicarbonate to increase gastric mucosal blood flow

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29
Q

Where is misoprostol metabolized?

A

First pass metabolism in liver -to active form

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30
Q

Which gastroprotectants are prodrugs?

A

Misoprostol, omeprazole

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31
Q

What are adverse effects of misoprostol

A

Diarrhea (self limiting) and uterine contraction resulting in abortion

32
Q

When are antiemetics indicated?

A

If vomiting makes it difficult to maintain energy, fluid, or electrolyte hemostasis, or when quality of life adversely impacted by nausea. Also indicated if patient at risk of aspiration pneumonia

33
Q

Drug class - maropitant

A

Neurokinin-1 receptor antagonist (NK-1 receptor antagonist)

34
Q

How does maropitant function?

A

Blocks action of substance P in CNS and at peripheral NK-1 receptors in GI

35
Q

How is maropitant metabolized?

A

First pass metabolism in liver

36
Q

Drug class - ondansetron, granisetron, dolasetron

A

5-HT3 receptor antagonists

37
Q

How do 5-HT3 receptor antagonists function?

A

Competitive blocking of 5-HT3 receptors peripherally and centrally

38
Q

How is ondansetron metaboized?

A

Liver

39
Q

How is dolasetron metabolized and then eliminated?

A

Prodrug - metabolized by ubiquitous carbonyl reductase then eliminated by P-450 enzymes

40
Q

What is true of simultaneous administration of ondansetron and tramadol?

A

Ondansetron may reduce efficacy of tramadol

41
Q

How does metoclopramide function?

A

Both antidopaminergic activity and blockade of 5-HT3 receptors - blocks CRTZ

42
Q

Why is metoclopramide less effective in cats?

A

Less dopamine receptors

43
Q

How is metoclopramide eliminated?

A

Kidneys - use caution in patients with reduced glomerular filtration

44
Q

What can happen with administration of metoclopramide to patients with renal dysfunction?

A

Extrapyramidal signs may occur

45
Q

Drug class - Chlorpromazine, prochlorperazine, acepromazine

A

Promazine derivatives

46
Q

How are the promazine derivatives metabolized?

A

By the liver

47
Q

What is a side effect of the promazine derivitives?

A

Vasodilation, may increase CVP and change HR as well

48
Q

How do the promazine derivatives prevent nausea?

A

Antidopaminergic and antihistaminic effects - block CRTZ and higher doses also block MVC

49
Q

Which anticholinergic is used as an antiemetic in dogs?

A

Aminopentamide

50
Q

Drug class - cisapride

A

5HT4 serotonergic antagonist

51
Q

How is cisapride eliminated?

A

Via first pass metabolism in liver

52
Q

What is the effect of cisapride administration?

A

Enhanced gastric emptying with increased gastroesophageal sphincter pressure

53
Q

How does erythromycin function as a prokinetic?

A

Stimulates motilin receptors

Increases lower esophageal sphincter pressure and peristalsis

54
Q

How do ranitidine, and nizatidine function ans prokinetics?

A

Inhibition of acetylcholinesterase encourages gastric emptying

55
Q

How does bethanechol function as a prokinetic?

A

A true cholinomimetic drug binding to muscarinic receptors - affects motility through GI tract

56
Q

How does misoprostol function as a prokinetic?

A

Enhances colonic motility - used for non-responsive constipation

57
Q

How does capromorelin work?

A

Mimics action of endogenous ghrelin - results in growth hormone secretion and appetite stimulation

58
Q

Where does capromorelin function?

A

Stimulates appetite via hypothalamus and increases IGF-1 in liver and pituitary gland

59
Q

What do beta blockers do?

A

Bind to beta receptors in sympathetic nervous system

Located in heart, vascular system, and bronchioles

60
Q

What does stimulation of the Beta 1 receptors do?

A

Increases heart rate, increase AV nodal conduction velocity, and increases myocardial contraction

61
Q

What does stimulation of the Beta 2 receptors do?

A

Vasodilation of skeletal muscles, bronchodilation

62
Q

Propranolol

A

Beta 1 & 2 blocker
Monitor for bradycardia, lethargy, depression, AV conduction arrhythmias, hypotension, worsening of heart failure, hypoglycemia, bronchospasm

63
Q

Atenolol and metoprolol

A

Beta 1 blocker (high doses block beta 2)

INCREASE hypoglycemic effects of insulin

64
Q

Esmolol

A

Ultra-short acting beta blocker similar to atenolol - used either as CRI or to test efficacy of beta blocker therapy

65
Q

Drugs for supraventricular bradyarrhythmia

A

Atropine or glycopyrrolate
-helps to assess if arrhythmia is vagally induced
Occasionally terbutaline - beta 2 agonist effects

66
Q

Drugs for ventricular bradyarrhythmia

A

Isoproterenol

-Often ventricular bradyarrhytmias are related to 3rd degree AV block and need pacemaker

67
Q

Drugs for supraventricular tachyarrhytmias

A

Calcium channel blockers (amlodipine, diltiazem)

Can also use beta blockers and digitalis glycosides to slow conduction through AV node

68
Q

Drugs for ventricular tachyarrhytmias

A

Class I antiarrythmics - lidocaine, procainamide, quinidine, tocainidine, mexiletine
Class III antiarrythmics - sotalol, amiodarone

69
Q

What is the aerodynamic equivalent diameter size of particles that will be aerosolized into the peripheral airways of the respiratory tree?

A

0.5-5 micrometers

70
Q

What compressor settings are recommended for jet nebulization of inhaled medications?

A

20 - 30 psi, 8-10 LPM

71
Q

Recommended length of time for nebulization via jet nebulizer or ultrasonic nebulizer?

A

5 - 10 minutes

72
Q

How long should an animal be allowed to breathe a dose of metered dose inhaler from the spacer device?

A

1-2 minutes with an average of 7-10 breaths

73
Q

Inhaled bronchodilators

A

Beta-2 adrenergic receptor agonists
Albuterol, salmeterol
Manage bronchoconstriction from inflammatory lower airway disease
Decrease intracellular calcium and thereby cause smooth muscle relaxation of bronchial wall

74
Q

Which type of albuterol is preferred in small animals?

A

R-albuterol (levalbuterol - xopenex) preferred

the S-albuterol (albuterol - ProAir or Ventolin) may cause increased lower airway inflammation

75
Q

Inhaled glucocorticoids

A

Fluticasone, flunisolide
Take two weeks for steady state concentrations of fluticasone so patient needs systemic glucocorticoids
Control airway inflammation with minimal systemic side effects

76
Q

Ipratopium bromide

A

Acetylcholine antagonist that helps relax smooth muscle
Minimal systemic absorption
Used in humans for treatment of bronchitis