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SUM '20 - Pharm II > Week 2 Antiemetics & GI motility 1 of 4 > Flashcards

Week 2 Antiemetics & GI motility 1 of 4 Flashcards

1
Q

Aspiration Occurrence in adults and children:

A

Adults: 1 in 8,500

<16 yrs: 1:4,400

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2
Q

Incidence of Aspiration undergoing elective surgery:

A

1: 4,500

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3
Q

Incidence of aspiration undergoing emergent surgery:

A

1: 400

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4
Q

What are associated with higher risk of aspiration, associated pulmonary complications, and death?

A
  1. Emergencies

2. ASA 3 or higher

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5
Q

Studies showed that aspiration occurs at what rates and during what?

A
  • 1/3 during intubation
  • 1/3 during extubation
  • 1/3 during procedure
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6
Q

Role of oral antacids is to

A
  • neutralize (remove H ions) from gastric contents

- decrease secretions of HCl into the stomach

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7
Q

Best example of oral antacid:

A

NaHCO3 (sodium bicarbonate)

-combines with HCL to produce NaCl, H2O and CO2

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8
Q

High pH decreases symptoms of

A

gastritis

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9
Q

Consequence of high pH

A

delay digestion of food

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10
Q

Pts with HTN and heart disease may not tolerate the sodium load associated with the chronic use of this drug:

A

NaHCO3 (sodium bicarb)

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11
Q

What can lead to acid rebound?

A

rapid antacid action, such that pH is raised to a neutral value

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12
Q

Name the drug:

  • prompt neutralization of gastric acid.
  • Not assoc. w/acid rebound.
  • Has laxative effect.
  • Systemic absorption may be sufficient to cause neurologic, neuromuscular, and CV impairment in pts with renal dysfunction.
  • Renal dysfunction can also lead to metabolic alkalosis in some pts.
A

Magnesium Hydroxide (MOM)

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13
Q

Name the drug:

  • can produce metabolic alkalosis w/crhonic therapy.
  • symptomatic hypercalcemia may occur w/renal dx.
  • may result in hypophosphatemia.
  • Appendicitis has been reported d/t impact calcium carbonate fecaliths.
A

Calcium Carbonate

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14
Q

What is a fecalith?

A

a stone made of feces. It is a hardening of feces into lumps of varying size and may occur anywhere in the intestinal tract but is typically found in the colon.

It is also called appendicolith when it occurs in the appendix and is sometimes concomitant with appendicitis.

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15
Q

Name the drug:

  • mix. of aluminum hydroxide, aluminum oxide, and some fixed CO2 as carbonate.
  • System absorption may be high in renal dx.
  • Encephalopathy in pts undergoing HD has been attributed to intoxication w/aluminum, especially in pts who ingest solutions containing citrate.
  • Slows gastric emptying and causes constipation.
A

Aluminum Hydroxide

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16
Q

Name the Drug:
-Less likely to cause foreign body reaction if aspirated and mixing with gastric fluid is more complete than with particulate antacids (i.e. Tums, Rolaids)

A

Sodium Citrate (non particulate antacids)

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17
Q

Tums or Rolaids can lead to what if aspirated?

A
  • pneumonitis

- histological changes in lungs

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18
Q

Dosage and admin for Sodium Citrate:

A

dose: 15-30 ml of 0.3 mol/liter
admin: PO, 30 mins before induction of anesthesia

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19
Q

Sodium Citrate is effective in increasing gastric pH in what kind of patients?

A
  • Pregnant

- Non -pregnant

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20
Q

Name 5 Complications associated with Antacid Therapy:

A
  1. Chronic use symptoms
  2. Acid Rebound
  3. Milk-Alkali Syndrome
  4. Phosphorus Depletion
  5. Hypophosphatemia
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21
Q

Symptoms and consequences of Antacid Therapy / Chronic Use -

A
  • alkalized gastric and urine pH resulting in bacterial overgrowth in duodenum and small intestine, and UTI.
  • Increased urine pH > 24hrs after admin - leads to changes in renal elimination of drugs
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22
Q

Symptoms and consequences of Antacid Therapy Milik Alkali Syndrome:

A
  • Hypercalcemia

- Increased BUN and CRT

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23
Q

Acid Rebound is unique to

A

calcium containing acids

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24
Q

System Alkalosis from milk alkali syndrome (marked decrease in renal fxn) is most commonly associated with

A

ingestion of large amounts of calcium cabronate and > 1L milk every day

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25
Q

Ingesting large doses of aluminum salts does what?

A

Binds phosphate ions in the GIT and prevents their absorption.
- can cause phosphorus depletion

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26
Q

Ingesting aluminum salts to induce phosphorus depletion may be helpful for what pts?

A

-Renal patients

b/c it can decrease their plasma phosphate concentration but renal pts may develop toxicity from the aluminum.

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27
Q

Symptoms and consequences of Antacid Therapy Phosphorus depletion:

A
  • Osteomalacia
  • Osteoporosis
  • Fractures
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28
Q

If aluminum containing antacids are given chronically, what should we consider supplementing?

A

phosphate

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29
Q

Gastric alkalization increases gastric emptying resulting in

A

faster delivery of drugs into the small intestines

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30
Q

Aluminum hydroxide accelerated absorption and increases bioavailabilty of:

A

Diazepam

*MOA is unknown!

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31
Q

Antacids decrease bioavailability of oral cimetidine by

A

~ 15%

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32
Q

The capacity of some drugs to form complexes with antacids may decrease

A

their bioavailabilty

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33
Q

Antacids containing aluminum and a lesser extent calcium or magnesium interfere with absorption of:

A
  • tetracyclines and possible
  • digoxin

from the gi tract

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34
Q

What interferes with absorption of tetracyclines and possible digoxin from gi tract

A

Antacids containing aluminum and a lesser extent calcium or magnesium

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35
Q

Examples of 1st Gen H1-Receptor Antagonists

A

First generation:

  • Chlorpheniramie
  • Cyproheptadine
  • Diphenhydramine
  • Hydroxyzine
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36
Q

Examples of 2nd Gen. H1-Receptor antagonists

A

Second Generation:

  • Loratadine
  • Acrivastine
  • Azelastine

“LAA” say LAA because you’re not sedated! :D

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37
Q

Histamine Receptor Antagonists 1st generation

A
  • tend to produce sedation

- activate muscarinic, cholinergic, 5-hydroxytryptamine (serotonin), or Alpha-adrenergic receptors

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38
Q

Second Gen. H1 - Histamine Receptor Antagonists Pharmacokinetics

A
  • low water solubility

- not available for parenteral use

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39
Q

H1-Receptor antagonists Clinical Uses:

A
  • most widely used of all medications
  • Prevent allergic rhinoconjunctivitis (sneezing, nasal/ocular itching, rhinorrhea, tearing, etc.)
  • Less effective for nasal congestion characteristic of a delayed allergic reaction
  • may provide some protection against bronchospasm (induced by histamine, exercise, cold dry air)
  • admin w/Epi in the tx of acute anaphylaxis
  • pruritus
  • uricaria
  • angioedema
  • prophyactically for anaphylactoid reactions to radiocontrast dyes
  • Little benefit in the tx of upper RTI
  • no beneift in mgmt of otitis media
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40
Q

First Generation H1-Receptor antagonists SE’s

A

-Tachycardia
-QTc interval prolongation
CNS effects
-somnolence
-slowed reaction time
-cognitive impairment

Muscarinic /anticholinergic effects:

  • dry mouth
  • blurred vision
  • urinary retention
  • impotence
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41
Q

Examples of H2 Receptor Antagonists:

A
  • Cimetidine
  • Famotidine
  • Nizatidine
  • Ranitidine
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42
Q

H2 Receptor Antagonists MOA:

A

competitively and selectively inhibit the binding of Histamine to H2 Receptors

-thereby decreasing the intracellular concentration of cAMP and the subsequent secretion of hydrogen ions by parietal cells.

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43
Q

H2 Receptor Antagonist potency of inhibition of secretion of gastric ions
(least to most)

A

Varies from 20-50 fold:

Cimetidine least potent and famotidine the most potent

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44
Q

H2 Receptor Antagonists Clinical Uses:

A
  • tx duodenal ulcer disease
  • chemoprophylaxis (to increase GI pH prior to induction)
  • decrease risk of acid pneumonitis if inhalation of gastric fluid were to occur in pre-op period
  • decrease gastric fluid volume
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45
Q

H2 Receptor Antagonists Drug Interactions:

A

-most common with Cimetidine
principal type of interaction with Cimetidine is impairment of the hepatic metabolism of another drug bc of the binding of cimetidine to the heme portion of the cytochrome p450 oxidase system.

  • Retards metabolism of propranolol, diazepam
  • may slow metabolism of Lidocaine
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46
Q

H2 Receptor Antagonists SE’s:

A

Interaction with cerebral H2 receptors

  • H/a
  • Somnolence
  • confusion

Interaction with Cardiac H2 receptors

  • bradycardia
  • HB
  • Hypotension
Hyperprolactinemia
Acute pancreatitis
Increased Hepatic transaminase levels
Alcohol dehydrogenase dehydration
Thrombocytopenia
Agranulocytosis
Interstitial nephritis
Interference w/drug metabolism by Cytochrome P450
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47
Q

In some patients with refractory urticaria, concurrent treatment with an H2-receptor antagonist (cimetidine, ranitidine) may enhance

A

relief of pruritus.

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48
Q

H2 receptors account for what % of all histamine receptors in the vasculature?

A

10-15%

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49
Q

Which H1 inhibitor is prescribed as a sedative, antipruritic, and as an antiemetic?

A

diphenhydramine

50
Q

Diphenhydramine, when administered alone, it modestly stimulates ventilation by

A

augmenting the interaction of hypoxic and hypercarbic ventilatory drives

51
Q

Diphenhydramine, when administered in combination with systemic or neuraxial opioids to control nausea and pruritus, there is the risk of

A

depression of ventilation (resp suppression)

*however Diphenhydramine counteracts to some extent the opioid-induced decreases in ventilatory response to CO2 and does not exacerbate the opioid-induced depression of the hypoxic ventilatory response during moderate hypercarbia

52
Q

Does HD remove Second generation H1 antagonists?

A

no

53
Q

what types of patients may be especially prone to adverse cardiovascular effects of H1 antagonists?

A
  • Hepatic dysfunction
  • Cardiac d/o assoc w/QTc prolongation
  • Hypokalemia
  • Hypomagnesemia
54
Q

Dimenhydrinate is a

A

theoclate salt of Diphenhydramine; is an H1 antagonist.

55
Q

Dimenhydrinate has been use to tx motion sickness as well as

A

PONV

56
Q

What drug may attenuate or block the oculocardiac reflex and decrease the incidence of PONV in strabismus surgery?

A

Dimenhydrinate

57
Q

Increased concentrations of cAMP activates the

A

proton pump of gastric parietal cells (as enzyme designated as hydrogen-potassium-ATPase) to secrete hydrogen ions against a large concentration gradient in exchange for Potassium ions.

58
Q

Which H2 blocker does NOT undergo significant hepatic first pass metabolism?

What does this do to its bio-availability after PO admin?

A

Nizatidine

  • bio-availability approaches 100% (all others around 50%)
59
Q

Which H2 blocker does NOT undergo significant hepatic first pass metabolism?

What does this do to its bio-availability after PO admin?

A

Nizatidine

  • bio-availability approaches 100% (all others around 50%)
60
Q

Cimetidine is widely distributed in most organs but no

A

fat

*about 70% of the total body content of cimetidine is found in skeletal muscles.

61
Q

H2 - Volume of distribution in renal disease

A

is not altered

62
Q

H2 - volume of distribution in severe hepatic disease

A

is Increased

63
Q

H2 drugs are present in what?

This means the drugs can:

A

Breastmilk

-Cross the placenta and BBB

64
Q

Cimetidine may need to be decreased in pts with what disease process?

Some reasons why?

A

Hepatic disease

  • Presence of cimetidine in CSF is increased
  • to avoid mental confusion in these pts.
65
Q

H2 volume of distribution in elderly is:

A

decreased about 40% (d/t decreased muscle mass)

66
Q

H2 elimination occurs by

A
  • combination of hepatic metabolism
  • Glomerular filtration
  • renal tubular secretion
67
Q

Principal excretion pathway for H2 blockers:

A

renal

68
Q

All four H2 blockers have an increased elimination half time in pts with

A

renal dysfunction

69
Q

The elimination half-life of ranitidine and famotidine (H2 antagonist) may be increased

A

up to twofold in elderly patients

70
Q

When determining the dose of H2 antagonist what must be considered?

A

increasing age

  • clearance decreases 75% in pts b/w the ages of 20 and 70 yrs. (pg 705)
71
Q

When determining the dose of H2 antagonist what must be considered?

A

increasing age

  • clearance decreases 75% in pts b/w the ages of 20 and 70 yrs. (pg 705)
72
Q

Cimetidine may slow metabolism of Lidocaine and thus

A

increase the possibility of systemic toxicity.

73
Q

What drugs specifically mentioned in Flood are not altered by cimetidine -induced effects on P450 enzyme activity?

A

Benzodiazepines such as oxazepam and lorazepam

74
Q

plasma concentrations of bupivacaine after epidural anesthesia are impacted by cimetidine how?

A

they’re not impacted!

75
Q

Cimetidine may slow metabolism of Lidocaine and thus

A

increase the possibility of systemic toxicity.

76
Q

H2 antagonists competition w/Creatinine, serum CRT levels are increased about what %?

A

15%

77
Q

Famotidine has been reported to interfere with phosphate absorption leading to

A

hypophosphatemia

78
Q

All four H2 antagonists have the potential to alter absorption of some drugs by

A

increasing the gastric fluid pH

79
Q

enhanced absorption of alchohol from teh stomach has been reported with

A

Cimetidine

80
Q

If administered concurrently, the hepatic metabolism of what drug may be enhanced with phenobarbital?

A

Cimetidine

81
Q

If administered concurrently, the hepatic metabolism of what drug may be enhanced with phenobarbital?

A

Cimetidine

82
Q

PPI are more effective that H2 antagonist for

A

relieving Heart burn

83
Q

What is the cardinal feature of GERD?

A

heart burn

84
Q

H2 antagonists are probably more cost effective than PPI’s for these pts:

A

those w/o esophagitis and infrequent symptoms

85
Q

Omeprazole acts as a

A

prodrug that becomes a PPI

86
Q

is omeprazole a weak acid or base?

A

weak base

87
Q

Omeprazole concentrates in the secretory canaliculi of

A

gastric parietal cells

88
Q

Where is omeprazole pronated to its active form which INHIBITS the enzyme pump?

A

gastric parietal cells

89
Q

Omeprazole only works on the

A

proton pumps that are present

90
Q

As the body generates more proton pumps what is required? (for omeprazole)

A

more omeprazole dosing

91
Q

how long does it take omeprazole to exert maximal inhibitory effect on gastric acid secretion?

A

several days

b/c of new pump generation

92
Q

What PPI provides prolonged inhibition of gastric acid secretion regardless of stimulus; timing or meal acid secretions?

A

omeprazole

93
Q

What heals duodenal and possible gastric ulcers more rapidly than H2 blockers?

A

PPI - Omeprazole

94
Q

Treatment for pts w/ bleeding PUD and signs of recent bleeding?

A

-omeprazole

95
Q

Why is omeprazole first line therapy for bleeding PUD?

A

decreases the rate of bleeding

-decreases the need for surgery

96
Q

Omeprazole as a pre-op med, is effective as it increases _____ and decreases ____.

A

increases pH gastric fluid (less acidic)

decreases gastric fluid volume

97
Q

Onset of gastric anti-secretory effect after a single 20 mg dose of Omeprazole occurs in

A

2-6 hours.

98
Q

Omeprazole Duration of action

A

is prolonged > 24 hours

99
Q

Omeprazole administered the night before surgery, increases gastric fluid pH, whereas

A

administration on day of surgery (up to 3 hours before) fails to improve the environment of gastric fluid

100
Q

prior to anesthesia it is suggested that omeprazole be given

A

> 3 hours prior to anesthesia

101
Q

Can omeprazole cross the BBB?

A

yes

102
Q

Side effects of omeprazole include:

A 
H/A
agitation
confusion
abd. pain
N/V
flatulence
103
Q

does the dose need to be adjusted for PPIs in renal or hepatic dysfunction/

A

no need to adjust

104
Q

pre-op oral dose of omeprazole:

A

20mg

105
Q

the loss of the inhibitory effect of gatric acid results in increased plasma concentration of

A

gastrin

106
Q

esomeprazole is the levoratatory isomer of

A

omeprazole

107
Q

A potent, fast acting PPI is

A

pantoprazole (Protonix)

108
Q

how do pantoprzole and ranitidine given IV, 1 hour before induction compare in effectiveness in decreasing gastric fluid vol and pH?

A

studies have found them equally as effective.

p.710

109
Q

Motility modulating drugs exert their therapeutic effects by:

A
  • increasing LES tone
  • Enhancing peristaltic contractions
  • accelerating gastric emptying
110
Q

Metoclopramide and Domperidone are both what kind of GI motility modulators:

A

Dopamine Blockers

111
Q

Metoclopramide is the only drug FDA approved for the tx of

A

diabetic gastroparesis

112
Q

metoclopramide does not alter:

A

gastric hydrogen ion secretion

113
Q

Domperidone, like metoclopramide, acts as a specific dopamine antagonist that stimulates peristalsis in the GIT, speeds gastric emptying, increases LES tone but is/does not:

A
  • marketed in US
  • cross the BBB easily
  • appear to have any anticholinergic activity
114
Q

Main concern about domperidone that the FDA refused to give approval of sale for:

A
  • prolactin secretion by the pituitary
  • concerns about lactating women using domperidone to increase breast milk production (b/c of increased cardiac risks associated w/use).
115
Q

metoclopramide induced antagonism of dopamine-agonist effects on the chemoreceptor trigger zone (located outside the BBB) contributes to an

A

antiemetic effect

116
Q

Metoclopramide should not be given to pts with known:

A
  • Parkinson disease
  • Restless leg
  • movement disorders r/t dopamine inhibition or depletion
117
Q

Akathisia:

A

a feeling of unease and restlessness in the lower extremities

-may follow IV administration of metoclopramide

118
Q

presentation of what symptom after administration of metoclopramide would result in cancellation of scheduled surgery

A

Akathisia

119
Q

metoclopramide has an inhibitory effect on _____.

Which may explain occasional prolonged responses to succinylcholine and mivacurium in pts receiving these drugs.

A

plasma cholinesterase activity

120
Q

metoclopramide-induced decreases in plasma cholinesterase activity could also slow the metabolism of

A

ester LA’s

SUM '20 - Pharm II (30 decks)

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