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Pharmacology Final > Gastrointestinal Drugs > Flashcards

Gastrointestinal Drugs Flashcards

1
Q

why do significant knowledge gaps remain in the pharmacology of GI drugs, particularly in pts <1yr?

A

many of the drugs commonly used to tx GI conditions in infants have not been throughly studied- especially in the use of off-patent drugs

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2
Q

in what population are antiemetics used?

A

not typically prescribed for NI patients, usually only for post surgical patients

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3
Q

how is vomiting controlled?

A

vomiting is controlled by the vomiting center of the medulla and has input from at least four sources: chemoreceptor trigger zone, cortex, vestibular apparatus and the GIT

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4
Q

what antiemetic agent has a long history of use in the neonate population?

A

promethazine (phenergan), most commonly prescribed antiemetic in US

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5
Q

what are the side effects of promethazine?

A

sedation, extrapyramidal effects, hallucinations, sz, tachycardia and HTN

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6
Q

what are the side effects of metrocopramide?

A

(reglan)- sedation, anticholinergic effects and extrapyramidal symptoms

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7
Q

what are the indications for antacids in children?

A

gastritis, esophagitis, peptic ulcer dz and GERD

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8
Q

why aren’t antacids prescribed as much now?

A

r/t dosing irregularity and safety concerns

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9
Q

what are the current recommendations r/t antacids as prophylaxis for stress ulcers?

A

replaced by other acid modifying drugs (H2 receptor antagonists, protein pump inhibitors)

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10
Q

what are the 4 type of antacid products?

A

sodium bicarbonate, calcium carbonate, magnesium- containing and aluminum-containing

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11
Q

what antacid products are the most potent?

A

those containing Na and Ca, they are also rapid acting

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12
Q

what side effects are a/w chronic use of sodium bicarbonate?

A

fluid retention, stomach alkalosis and milk-alkali syndrome

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13
Q

what are the advantages and disadvantages of Calcium carbonate?

A

has a longer duration of effect than sodium bicarb but has been a/w adverse events including: hyperCa, hypercalciurea, renal Ca deposits, compromised renal fx and gastric acid hyper secretion

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14
Q

what side effects are a/w magnesium-containing products?

A

diarrhea, hypermagnesiumia, especially in pts with compromised renal fx

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15
Q

what side effects are a/w aluminum-containing products?

A

constipations, hypcalcemia and hypophosphatemia

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16
Q

what actions should be taken with patients who are prescribed antacids in addition to other medications?

A

concomitant use with other medications may decrease drug absorption due to alteration in the gastric pH; administering 2 hours after other drugs may help to avoid this interaction

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17
Q

when should antacids be taken with relation to meal times?

A

administering 1 hour after meals has been shown to be effective in reducing gastric acidity

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18
Q

what special considerations should be taken with pediatric patients requiring long term therapy?

A

should be closely monitored for adverse effects

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19
Q

why are prokinetic agents prescribed?

A

to improve gastric motility

20
Q

what are examples of prokinetic agents?

A

metoclopramide, cisapride and erythromycin

21
Q

what is the most common prokinetic agent used in the US?

A

metoclopramide

22
Q

what is the mechanism of action for metoclopramide?

A

a combination of central and peripheral dopamine antagonism; augments acetylcholine release from postganglionic nerve terminals (the likely cause of the drugs effect on GI smooth muscle.)

23
Q

what are the intended effects of metoclopramide?

A

DOES NOT increase gastric secretion, endogenous gastrin release or salivation; DOES promote the coordination of gastric, pyloric and duodenal motor fx- accelerated gastric emptying by increasing gastric tone

24
Q

some studies demonstrate improvement in the treatment of what diagnoses (off label use)

A

GERD and reflux symtpoms

25
Q

what are the adverse effects of metoclopramide?

A

drowsiness, restlessness, dry mouth, light headedness, diarrhea and extrapyramidal effects

26
Q

how frequently are side effects seen with relation to metoclopramide?

A

appear to be dose related and in only 20% of pts

27
Q

where is cisapride still prescribed?

A

removed from the US and Canadian markets due to safety conerns; still widely used throughout the world

28
Q

what were the safety concerns a/w cisapride use?

A

prolonged QT interval with assoc ventricular arrhythmias, underlying cardiac dz, eletrolyte disturbances, renal insufficiency, hepatic dysfx and concurrent treatment with medications known to alter cardiac conduction intervals

29
Q

what is the dose of erythromycin intended for prokinetic activity?

A

much smaller than what is required for antimicrobial activity

30
Q

what is the intended effect of erythromycin?

A

similar to the polypeptide hormone motilin- stimulates migrating motor complexes in the GIT and promotes the movement of nutrient

31
Q

what is the suspected mechanism of action of erythromycin?

A

thought to increase LES tone and the duration but NOT the amplitude of contraction of the distal esophagus (in adults with GERD)

32
Q

what is of concern with chronic administration of erythromycin in patients?

A

the development of infantile hypertrophic stenosis (after the widespread use of EES for pertussis prophylaxis, there was nearly a 7 fold increase in the rate of pyloric stenosis) low doses have not been a/w subsequent devpt of dz

33
Q

how many H2 receptor antagonists are available for clinical use in children?

A

only four agnts are available, only 2 are used in children: ratinidine and famotide

34
Q

what are the indications for H2 receptor administration in children?

A

reflux, tx of gastric/ duodenal ulcers and tx/prophylaxis against GI hemorrhage

35
Q

what is the mechanism of action of the H2 receptor antagonist class?

A

reduces gastric acid secretion by acting as a competitive, reversible inhibitor of histamine at the histamine H2 receptor site; decreases the acid-secretory response of the parietal cells to stimulated acide secretion from cholinergic agents, gastrin, food and vagal stim

36
Q

when are H2 receptor agonists particularly effective?

A

in suppressing nocturnal acid production (important especially for those at risk for duodenal ulcers)

37
Q

what are the side effects of H2 antagonist receptors?

A

GI symptoms, rash, dizziness- most common; mania, sz, galactorrhea, impotence, possible decrease in permatogenesis, thrombocytopenia and agranulocytosis

38
Q

why has routine use of H2 receptor antagonists been questioned?

A

due to concerns in the alteration of the gastric pH which might allow for the overgrowth of pathogenic bacteria. Additionally, the use of VLBW infants may increase the risk of NEC. (larger scale studies are needed to analyze the assoc)

39
Q

How many proton pump inhibitors are approved for clinical use in the US?

A

4; none of the PPIs have been approved for administration to pts <1 yr old

40
Q

what is the mechanism of action for lansoprazole?

A

prevacid; inhibition of the hydrogen/potassium atpase- the enzyme responsible for the final step in the secretion of HCl acid from the parietal cells, the proton pump.

41
Q

what are the indications for the administration of lansoprazole?

A

tx of reflux esophagitis

42
Q

what is the onset of action of lansoprazole?

A

within 1 hour

43
Q

what is the onset of maximal effect of lansoprazole?

A

at 1.5 hours

44
Q

how is lansoprazole metabolized?

A

hepatically

45
Q

what is the average elimination time of lansoprazole?

A

avg half life is 11.5 hours

46
Q

what are the side effects of lansoprazole?

A

headache, nausea and diarrhea

47
Q

what is associated with lansoprazole and VLBW infants?

A

questionable association between VLBW infants and late-onset gram negative sepsis

Pharmacology Final (5 decks)

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