Histamine and PONV Flashcards
Exam 1 (382 cards)
1
Q
What is an autocoid?
A
Biological factors that act like local hormones, have a brief duration, and act near the site of synthesis
2
Q
Three defining characteristics of autocoid:
A
1) Act like local hormones
2) Brief duration
3) Act near site of synthesis
3
Q
T/F: Autocoids act distal to the site of synthesis.
A
F: they act close to the site of synthesis.
4
Q
T/F: Autocoids behave similarly to local hormones.
A
True.
5
Q
T/F: Autocoids are characterized by a brief duration.
A
True.
6
Q
What type of autocoid are we focusing on in this lecture specifically?
A
Histamines
7
Q
What is the major difference between autocoids and hormones?
A
Autocoids can be synthesized by almost every cell, while hormones are only synthesized by specific tissues.
8
Q
Is histamine a hormone?
A
No, it is an autocoid, though it behaves similarly to a hormone.
9
Q
What type of autocoid is histamine?
A
Endogenous amine
10
Q
T/F: Histamine is an endogenous amine.
A
True.
11
Q
Histamine is a chemical mediator in what immune response?
A
Inflammatory response
12
Q
What type of role does histamine play in the inflammatory response?
A
It is a chemical mediator in the inflammatory response.
13
Q
What type of cells releases histamine?
A
Mast cells
14
Q
Where can mast cells be found?
A
Skin, lungs, GI tract, basophils
15
Q
What types of tissues are involved in histamine release? By what means?
A
Skin, lungs, GI tract, basophils via mast cell secretion
16
Q
T/F: GI tract tissue releases histamine as part of inflammatory immunoresponse.
A
True.
17
Q
Skin, lungs, GI tract, and basophils all secrete:
A
histamine.
18
Q
Can histamine cross the blood-brain barrier? What about histamine blockers?
A
Histamine cannot cross the blood brain barrier, but histamine blockers can.
19
Q
Histamine causes allergic reaction by what mechanism?
A
Antigen-antibody response
20
Q
The antigen-antibody response of histamine causes what?
A
Allergic reaction
21
Q
Allergic reactions are mediated by what autocoid?
A
Histamine (causes inflammation)
22
Q
How many types of histamine receptors are there?
A
Three.
23
Q
Which histamine receptor is involved in respiratory + GI smooth muscle contraction?
A
H1
24
Q
Which histamine receptor is involved in increased GI secretion of H+?
A
H2
25
Which histamine receptor is involved in pruritis/sneezing?
H1
26
Which histamine receptor is involved in decreased histamine synthesis and release?
H3
27
Which histamine receptor is involved with increased HR/ contractility?
H2
28
Which histamine receptor is involved with nitric oxide release by vascular smooth muscle?
H1
29
Which muscles contract upon activation of H1 receptors?
GI and respiratory smooth muscle
30
H1 receptors are responsible for what three actions?
GI and respiratory smooth muscle contraction
Pruritis/ sneezing
Nitric oxide release by vascular smooth muscle
31
When H1 receptors are stimulated, what is released from vascular smooth muscle?
Nitric oxide
32
Nitric oxide is released from what when H1 receptors are stimulated?
Vascular smooth muscle
33
Which types of muscles are directly affected by stimulation of H1 receptors?
GI + respiratory smooth muscle (contracts)
| Vascular smooth muscle (release nitric oxide)
34
Itchy, watery eyes are mediated by which histamine receptor?
H1 receptor
35
Bronchoconstriction during an asthma attack is caused by activation of which histamine receptor?
H1 receptor
36
Result of activation of H3 receptor?
Decreased histamine synthesis and release
37
T/F: activation of H1 receptors causes releases of nitrous oxide from vascular smooth muscle.
False: causes release of nitric oxide from vascular smooth muscle
38
Activation of H2 receptors cause:
Increased GI secretion of H+
| Increased HR and contractility
39
T/F: activation of H3 receptor is a positive feedback loop that causes increased synthesis and release of histamine.
False; negative feedback loop that causes decreased release and synthesis of histamine
40
Activation of which receptor is responsible for increased HR during allergic reaction?
H2
41
Activation of which receptor is responsible for increased H+ secretion in GI tract?
H2 receptor
42
Which histamine receptors have a direct effect on GI tissues? What are those effects?
H1: increased smooth muscle constriction in GI tract
H2: increased H+ secretion in GI tract
43
If your patient has watery, itchy eyes and is coughing and sneezing, which histamine receptor is activated?
H1
44
What is the effect of NO release by vascular smooth muscle w/ activation of H1 receptors?
Vasodilation --> hypotension
45
Hypotension may occur with an allergic reaction because of:
NO release by vascular smooth muscle, caused by activation of H1 receptors
46
Of all three histamine receptors, we are mainly concerned with the effects of:
H1 + H2
47
What are the general cardiovascular effects of histamine release?
```
Decreased BP (d/t NO release, H1)
Increased HR (H2)
Increased capillary permeability (H1)
```
48
T/F: histamine release may result in increased HR and decreased BP.
True
49
T/F: histamine release decreases capillary permeability.
False; increases capillary permeability.
50
How does histamine release affect thee respiratory system? Via which histamine receptor?
It constricts respiratory smooth muscle to cause bronchoconstriction via the H1 receptor.
51
Which receptor is responsible for labored breathing during an allergic reaction?
H1
52
What is the dermal reaction to histamine release?
Classic flare and wheal response
53
The flare and wheal response is what system's reaction to histamine release?
Derma
54
How does NO production (H1) affect the vasculature?
It causes local vasodilation and increased permeability.
55
Which action of histamine release causes local vasodilation?
NO production by vascular smooth muscle
56
What is the immunological affect of histamine release?
Histamine is a mediator of Type I hypersensitive reaction.
57
Histamine is a mediator of what reaction?
Type I hypersensitive
58
Which hypersensitive reaction does histamine mediate?
Type I hypersensitive reaction
59
How does histamine release affect peak airway pressure?
It increases peak airway pressure.
60
If your patient displayed a decreased blood pressure, an increased HR, and high peak pressures, what might you expect?
An allergic reaction--symptoms are caused by histamine release.
61
What four facts must you know about H1 activation?
Occurs at lower concentrations of histamine
Decreased AV node conduction
Coronary artery vasoconstriction
Bronchial smooth muscle constriction
62
What is the effect of H1 activation on bronchial smooth muscle?
Bronchial smooth muscle constriction
63
What is the effect of H1 activation on AV node conduction?
Causes decreased AV node conduction.
64
T/F: Activation of H1 receptors increased conduction at the AV node.
False; it decreases conduction at the AV node.
65
Activation of H1 receptors decreases conduction at what node?
AV node
66
Conduction of AV node is reduced when which histamine receptors are activated?
H1 receptors
67
How does activation of H1 receptors affect the coronary artery?
It causes coronary artery vasoconstriction.
68
Activation of H1 receptors causes constriction of what major blood vessel group?
Coronary arteries
69
Coronary arteries vasoconstrict upon the activation of what histamine receptor?
H1
70
T/F: Activation of H1 receptors occurs at lower concentrations of histamine.
True.
71
How does concentration level of histamine affect H1 receptors?
H1 receptors are activated at lower concentrations of histamine.
72
Which histamine receptor causes CV effects?
H2 receptor
73
Main effects of H2 activation:
CV effects
Catecholamine release
Coronary artery vasodilation
Increased gastric H+ secretion by parietal cells in the stomach
74
What CV effects does activation of H2 receptors have?
Increased HR/ contractility
75
Effect of activation of H2 receptors on coronary artery?
Coronary artery vasodilation
76
Activation of which receptor causes coronary artery vasoconstriction?
Activation of which receptor causes coronary artery vasodilation?
H1
| H2
77
Activation of which histamine receptors results in catecholamine release?
H2
78
What is the main effect of activation of H2 receptors?
Increased gastric H+ secretion by parietal cells in the stomach
79
By what mechanism does activation of H2 receptors cause catecholamine release?
Adrenal gland stimulation
80
H2 activation increases secretion of what by the stomach?
Increases secretion of H+ by parietal cells in stomach.
81
T/F: H2 receptors increase secretion of H+ by parietal cells in the stomach.
True.
82
What is the mechanism behind the skin response to histamine release?
Dilated capillaries in affected area
Edema d/t increased capillary permeability
"Wheal" d/t dilated arterioles around edema
83
Classic mosquito bite/ hives reaction seen in histamine release is d/t what?
Dilated arterioles around edema
84
What causes edema in histamine release?
Increased capillary permeability
85
Effect of histamine release on capillaries?
Causes dilated capillaries w/ increased capillary permeability
86
Dilated arterioles around edema cause what?
Wheals
87
Increased capillary permeability and dilated capillaries cause what?
Edema
88
What two things cause edema in a histamine release reaction?
Dilated capillaries
| Increased capillary permeability
89
Histamine antagonists: what will they block?
Edema + pruitis
90
T/F: histamine antagonists block edema + pruitis.
True.
91
Histamine antagonists: what won't they block? How should you treat instead?
Hypotension d/t NO release in vascular smooth muscle; treat via vasoconstriction
92
T/F: histamine agonists will block edema and pruitis.
False; histamine antagonists block edema + pruitis.
93
T/F: histamine antagonists will not block hypotension d/t release of NO by vascular smooth muscle cells
True.
94
Principle effects of H2 receptor activation?
Increased H+ secretion in stomach
| Increased HR/contractility
95
Summarize the actions of histamine antagonists:
They will block pruitis and edema caused by histamine release, but they will not treat the hypotension caused by NO release.
96
T/F: to stop a histamine reaction, you must block histamine receptors.
False; it will help the reaction, but it will not stop it.
97
At what receptors do histamine antagonists act?
H1 + H2
98
At what receptors do histamine antagonists not act?
H3
99
What type of antagonists are histamine antagonists?
Competitive inhibitors
100
T/F: histamine antagonists primarily work at H1 + H2 receptors.
True.
101
How do histamine antagonists work?
They do not block the release of histamine. Instead, histamine is still present and an allergic reaction still occurs, but the histamine antagonists block the bad side effects.
102
T/F: histamine antagonists prevent the secretion of histamine.
False.
103
T/F: histamine antagonists aid in diminishing an allergic reaction by blunting the bad side effects of histamine release.
True
104
Do histamine antagonists inhibit the release of histamine?
No.
105
What do histamine antagonists block?
Bad side effects caused by histamine release and activation.
106
By what means do histamine antagonists prevent the bad side effects of histamine release?
Competitive inhibition
107
T/F: histamine antagonists are well absorbed orally.
True
108
Histamine antagonists are especially absorbed when adminisitered in what form?
Oral
109
T/F: histamine receptors work primarily on H1 + H3 receptors.
False: work primarily in H1 and H2 receptors
110
What are the two types of H1 blockers?
First generation + second generation
111
What is the primary difference between first generation and second generation H1 blockers?
H1 receptors blocker tend to cross the BBB more easily.
112
Which type of H1 blocker tends to cross the BBB more readily?
First gen H1
113
T/F: Second generation H1 receptor blockers are falling out of favor because they tend to cross the BBB.
False: first generation
114
Besides H1 receptors, what other receptors do H1 receptor blockers activate?
Muscarinic cholinergic
Serotonin
Alpha
115
Muscarinic cholinergic
Serotonin
Alpha
H1 receptor blockers
What do they have in common?
All blocked by first generation H1 blockers
116
Which type of blocker causes significant sedation?
First generation H1 receptor blocker
117
T/F: First generation H1 receptor blockers cause signficant sedation.
True
118
What receptors do second generation H1 receptor blocker bind w/?
H1 only; no muscarinic cholinergic, alpha, or serotonin
119
At higher doses, second generation H1 receptor blockers are:
non-competitive
120
What is the primary benefit to using second generation H1 receptor blockers instead of first generation?
Much less sedative effect
121
Which type of H1 receptor blockers is non-competitive at higher doses?
Second generation
122
Which type of histamine receptor blocker only affects H1 receptors?
Second generation
123
What are the three first generation H1 receptor blockers you are expected to know?
Diphenhydramine
Dramamine
Promethazine
124
Diphenhydramine is a:
First generation H1 receptor blocker
125
Dramamine is a:
First generation H1 receptor blocker
126
Promethazine is a:
First generation H1 receptor blocker
127
T/F: Diphenhydramine is a second generation H1 receptor blocker.
False: first generation
128
T/F: Dramamine is a first generation H1 receptor blocker.
True.
129
T/F: Promethazine is the same type of H1 receptor blocker as diphenhydramine.
True.
130
Name the second generation H1 receptor blockers that you should know.
Loratadine (Claritin)
| Fexofenadine (Allegra)
131
Another name for Claritin?
Loratadine
132
Another name for Fexofenadine?
Allegra
133
Another name for Loratadine?
Claritin
134
Another name for Allegra?
Fexofenadine
135
Fexofenadine is what type of H1 receptor blocker?
Second generation
136
Loratadine is what type of H1 receptor blocker?
Second generation
137
Which medication tends to cause drowsiness, promethazine or loratadine?
Promethazine
138
Which medication acts on nothing but H1 receptors, Dramamine or Fexofenadine?
Fexofenadine
139
Which medication acts on seratonin receptors, Dramamine or Loratadine?
Dramamine
140
Which antihistamine medications are non-competitive at higher doses?
Loratadine
| Fexofenadine
141
Which antihistamines cause sedation?
Diphenhydramine
Dramamine
Promethazine
142
Promethazine is used to treat what symptoms?
Nausea/ vomiting
143
Which drug is primarily used to treat motion sickness or motion-induced nausea?
Dramamine
144
What is the primary concern w/ second generation antihistamines?
They can prolong QT intervals at high doses.
145
Which has more side effects, first generation or second generation antihistamines? Why?
First generation because they act on muscarinic receptors
146
Common side effects of first generation antihistamines?
```
Somnolence
Decreased alertness
Slowed reaction time
Dry mouth
Blurred vision
Urinary retention
Impotence
Tachycardia
Dysrhythmias
```
147
Which symptoms of fist generation antihistamines are primarily d/t their actions on muscarinic receptors?
```
Impotence
Tachycardia
Urinary retention
Dysrhythmias
Dry mouth
Blurred vision
```
148
What are four uses of H1 blockers?
They are primarily used to treat anaphylaxis and anaphylactoid reactions, but they also treat rhinoconjunctivitis, bronchospasm,
and motion sickness.
149
Motion Sickness is treated by what type of histamine receptor blocker?
H1 receptor blocker
150
What should you give a patient to treat rhinoconjunctivitis?
H1 receptor blocker
151
By what means do H1 receptor blockers treat motion sickness?
They decrease vestibular and visual input from the brain.
152
Decreasing vestibular and visual input from the brain assists in treating what issue?
Motion sickness
153
Which histamine receptor blocker treats motion sickness by decreasing vestibular and visual input from the brain?
H1 receptor blocker
154
Any drug that ends in -tidine is what type of histamine receptor blocker?
H2 receptor blocker
155
How can you identify an H2 receptor blocker?
Look for the ending "tidine"
156
What is the main effect of H2 receptor blockers?
They decrease gastric acid secretion.
157
What is the most widely used H2 receptor blocker?
Famotidine (Pepcid)
158
T/F: H2 receptor blockers aid in emptying the gut of gastric acid.
False; they only prevent production of new gastric acid. They do nothing to clear any acid that is already present in the gut.
159
Rank H2 receptor blockers in terms of potency.
C < R = N < F
160
What is the relative potency of cimetidine?
Potency = 1
161
What is the relative potency of famotidine?
Potency = 50
162
What is the relative potency of nizatidine?
Potency = 10
163
What is the relative potency of ranitidine?
Potency = 10
164
T/F: Nizatidine is more potent than ranitidine.
False; they are equally potent.
165
T/F: Cimetidine is less potent than Nizatidine.
True
166
T/F: Ranitidine is more potent than Famotidine.
False; famotidine is the most potent H2 receptor blocker.
167
What is the least potent H2 receptor blocker?
Cimetidine
168
Which type of antihistamine is characterized by extensive first pass metabolism in the liver?
H2 receptor blockers
169
Do H2 antihistamine drugs cross the BBB? What about the placenta?
They cross both; they are not teratogenic, though.
170
T/F: H2 antihistamines are teratogenic.
False.
171
What is the consensus on giving renal failure patients H2 antihistamines?
They are not contraindicated because there are no truly bad side effects, but renal failure will increased the elimination time of these drugs.
172
How does an increase in age affect H2 antihistamine metabolism?
Increasing age doubles half-life.
173
T/F: antihistamines last longer in an elderly patient than a young patient.
True.
174
How are H2 antihistamines best absorbed?
Rapid oral absorption
175
T/F: H2 antihistamines boast rapid oral absorption.
True.
176
What are some reasons to use H2 antihistamines?
Treatment of duodenal ulcers
Allergy prophylaxis
Preop medication (gray area)
177
Which antihistamine is useful for the treatment of duodenal ulcers?
H2 receptor blockers
178
Can you use H2 antihistamines as allergy prophylaxis?
Yes.
179
Effects of H2 receptor blockers on gastric acid already present in belly?
No effect; only prevents new acid secretion
180
Why might you use caution in administering H2 receptor blockers to the elderly?
They cross the BBB, so they may cause confusion at times.
181
What is the issue with long term use of H2 receptor blockers?
They weaken the gastric barrier to bacteria, causing H. pylori to proliferate and weakening the barrier.
182
They stomach is at risk for proliferation of what bacteria under chronic use of H2 receptor blockers?
H. pylori
183
What is a cross reaction that you should keep in mind when administering cimetidine?
Cimetidine inhibits cytochrome p450, resulting in a prolonged duration of propanolol, diazepam, and lidocaine.
184
Cimetidine can prolong duration of propanolol, diazepam, and lidocaine via:
inhibition of cytochrome P450.
185
What H2 receptor blocker may inhibit cytochrome P450 w/ chronic use?
Cimetidine
186
Cimetidine inhibits what w/ chronic use?
Cytochrome p450
187
T/F: Inhibition of cytochrome p450 is a possibility w/ all H2 receptor blockers.
False, only cimetidine
188
H2 antihistamines may interact w/ cerebral H2 receptors, causing what side effects?
Headache
Somnolence
Confusion
189
H2 antihistamines may interact w/ cardiac H2 receptors, causing what side effects?
Bradycardia
Hypotension
Heart block
190
T/F: H2 antihistamines can potentiate throbocytopenia.
True.
191
What type of drug is cromolyn?
Mast cell stablizer
192
Name an example of a mast cell stabilizer.
Cromolyn
193
Action of cromolyn?
inhibits antigen-induced release of histamine from mast cells
194
What drug inhibits antigen-induced release of histamine from mast cells?
Cromolyn, a mast cell stabilizer
195
How is cromolyn administered?
Via inhalation
196
What drug is used as prophylaxis for bronchial asthma?
Cromolyn
197
Cromolyn is used as prophylaxis for:
bronchial asthma
198
What type of asthma might you use cromolyn for? How does it help?
Bronchial asthma: prevents histamine release from mast cells, decrease occurance of bronchial smooth muscle constriction (H1-mediated reaction to histamine release)
199
Name three proton pump inhibitors.
Omeprazole
Protonix
Prevacid
200
Omeprazole is what type of drug?
Proton pump inhibitor
201
Protonix is what type of drug?
Proton pump inhibitor
202
Prevacid is what type of drug?
Proton pump inhibitor
203
What do proton pump inhibitors do?
They prolong inhibition of gastric acid secretion for up to 24 hours.
204
How long do PPIs prolong inhibition of gastric acid secretion?
Up to 24 hours
205
Mechanism of action of Omeprazole?
Prolong inhibition of gastric acid secretion for up to 24 hours
206
Which is more effective in preventing further secretion of gastric acid, H2 receptor blockers or PPIs?
PPIs
207
Mechanism of action of Protonix?
Prolongs inhibition of gastric acid secretion for up to 24 hours
208
Which is more effective in preventing gastric acid secretion, Prevacid or Famotidine?
Prevacid
209
What are the benefits to PPIs as a preoperative medicine?
They can increase gastric fluid pH.
They can decrease gastric fluid volume.
They must be given > 3 hours prior to surgery.
210
Effect of PPIs on gastric fluid if given preoperatively?
They can increase gastric pH and decrease gastric volume.
211
In order to be effective, when must PPIs be administered?
> 3 hours prior to surgery
212
What medication class is especially effective at preventing aspiration?
PPIs
213
Why are PPIs given in the ICU to intubated patients?
Patients are NPO for many hours, if not days, but their stomachs continue to produce acid. Without any food to mitigate the acid, it can cause GI ulcers and bleeding.
214
Is serotonin a hormone?
No; like histamine, it is an autocoid, but it has behaviors that are similar to hormones.
215
Serotonin is an:
autocoid
216
Serotonin is oxidized by:
liver and lungs
217
Role of liver and lungs in serotonin levels?
Serotonin is oxidized by the liver and lungs.
218
What part of the body is involved in uptake of serotonin?
Platelets
219
Platelets and serotonin:
Platelets uptake serotonin
220
In addition to being characterized as an autocoid, serotonin is also:
a neurotransmitter in the CNS
221
Where is 90% of serotonin found?
In enterochromaffin cells of the GI tract.
222
Where is 10% of serotonin found?
In CNS and platelets.
223
The majority of serotonin is found in the:
gut.
224
Where are enterochromaffin cells located?
In the GI tract
225
What cells in the GI tract contain the majority of the body's serotonin stores?
Enterochromaffin cells
226
What do enterochromaffin cells store in the gut?
Serotonin
227
How much of serotonin stores are located in the CNS and platelets?
10%
228
What are the sites of action of serotonin?
GI tract
Platelets
CV system
229
Where does serotonin work in the GI tract? What are its effects?
5-HT4 receptor: gastrokinetic effects
| 5-HT3 receptor: drug-induced N/V
230
Which neurotransmitter mediates the N/V reaction to drugs?
Serotonin
231
Via what receptor does serotonin mediate the N/V reaction to drugs?
5-HT3 receptor
232
Via what receptor does serotonin cause gastrokinetic effects?
5-HT4 receptor
233
Serotonin activates the 5-HT4 receptor to cause what effects?
Gastrokinetic effects
234
Serotonin activates the 5-HT3 receptor to cause what effects?
Drug-induced N/V
235
Where are 5-HT3 and 5-HT4 receptors located in the body?
GI tract
236
Serotonin has how many sites of action in the CNS?
15
237
Serotonin mediates what aspects of the CNS?
```
Appetite
Sleep
Cognition
Sensory perception
Motor activity
Temperature regulation
Nociception
Sexual behavior
Hormone secretion
```
238
Appetite, sexual behavior, nociception, temperature regulation, motor activity, hormone secretion, sensory perception, sleep, and cognition are all affected by:
CNS action of serotonin
239
Where are 5HT1 receptors located?
CNS
240
How many 5HT1 receptor subtypes does serotonin act on?
5: 5HT1a-f
241
Serotonin acts on 5HT1 receptors to cause
cerebral vasoconstriction
242
By what means does serotonin cause cerebral vasoconstriction?
It acts on 5HT1 receptors in the brain.
243
What serotonin agonist reverses middle cerebral artery vasodilation to improve migraine and cluster headaches?
Sumatriptan
244
Sumatriptan is what type of drug?
Serotonin agonist
245
Action of sumatriptan?
Reverses middle cerebral artery vasodilation to improve migraine and cluster headaches.
246
What type of headaches does sumatriptan relieve?
Migraines and cluster headaches
247
Why does reversal of vasodilation in the middle cerebral artery improve headaches?
A reduction of BF in the head reduces ICP, and that reduces headache incidence.
248
Sumatriptan is related to what receptor in the brain?
5HT1
249
Serotonin activates 5HT3 receptors in the gut to cause:
N/V, appetite, addiction, pain and anxiety
250
N/V, appetite, addiction, pain and anxiety are all mediated by what receptor in the gut?
5HT3 receptors
251
The "setrons" are antagonists to what type of serotonin-mediated receptor?
5-HT3 receptors in the gut
252
T/F: Ondansetron is an antagonist to 5-HT3 receptors in the gut.
True.
253
5-HT3 receptors mediate what type of symptoms?
N/V
Pain and anxiety
Appetite
Addiction
254
First clinical use of Ondansetron?
Treatment of chemo-induced nausea
255
T/F: Ondansetron is structurally related to serotonin.
True.
256
Major side effects of ondansetron include:
Headaches, diarrhea, and increased liver enyzmes
257
Your patient arrives to POHA complaining of nausea. Will ondansetron help you?
It is of little assistance in the midst of nausea--more effective as prophylaxis.
258
Options for Ondansetron administration:
Sublingual
PO
IV
259
T/F: Zofran is not approved for morning sickness.
False; Zofran is effective as a prophylactic measure against morning sickness.
260
Action of antacids?
Neutralized or remove acid from gastric contents
261
Which class of medication neutralizes or removes acid from gastric contents?
Antacids
262
How do antacids neutralize or remove acid from gastric contents?
They increase the pH of the stomach to inactivate pepsin and increase gastric motility
263
At what pH is gastrin inactivated?
pH > 5
264
At what pH is gastric motility increased?
pH > 5
265
When antacids increase the pH of the stomach to >5, what is the result?
Pepsin is inactivated and gastric motility increases.
266
T/F: gastric motility is higher with lower pH.
False; gastric motility is higher with higher pH.
267
What are the main benefits to using antacids prophylactically?
They are inexpensive, they promote healing, and they are fast-acting.
268
Name some types of antacids.
Sodium bicarbonate (Tums)
Magnesium hydroxide
Calcium Carbonate
Aluminum Hydroxide
269
What is the overall structural pattern of an antacid?
Metal + neutralizing base
270
Benefits to sodium bicarbonate include:
Highly soluble
Rapid action in stomach
Brief duration
271
How do we administer sodium bicarbonate to our patients? Why?
30 mL shot SB; we don't have our patients chew TUMS prior to surgery for the fact that they could aspirate on the chewed particles.
272
What antacids can cause metabolic alkalosis?
Sodium bicarbonate
| Calcium carbonate
273
Milk of Magnesia is also known as:
Magnesium hydroxide
274
Which antacid may have a laxative effect?
Magnesium hydroxide
275
What is the problem with giving high doses of magnesium hydroxide?
It may cause hypermagnesemia.
276
What is the major benefit of giving magnesium hydroxide to your patient as opposed to other antacids?
No acid rebound
277
Which antacid has a risk list that includes hypercalcemia, acid rebound, and metabolic alkalosis w/ chronic use?
Calcium carbonate
278
What are the defining characteristics of aluminum hydroxide?
Minimal absorption
Phosphate depletion
Decreased gastric emptying
279
Name two major drug interactions of antacids:
Increases delivery of PO drugs
| Decreases bioavailability
280
The drug effects of antacids depends on the drug's specific:
pKA
281
Why might administration of sodium citrate give you pause?
It may cause an increase of citric acid in the stomach.
282
What is sucralfate?
It is a stomach coat that treats duodenal or gastric ulcers by protecting them from stomach acid
283
What drug is known as a viscous suspension?
Sucralfate
284
What drug protects the stomach lining from inflammatory effects of gastric acid?
Sucralfate
285
What are the effects of prokinetics?
They increase LES tone.
They increase peristalsis.
They increase gastric emptying.
286
T/F: prokinetics increase gastric emptying.
True.
287
T/F: prokinetics serve to relax the LES.
False; they increase the LES tone.
288
What is the most clinically useful prokinetic?
Metoclopramide
289
What parts of the GI tract does Metoclopramide relax? When?
It relaxes the pylorus and the duodenum when the stomach contracts.
290
Major effects of Metoclopramide?
Increased gastric emptying
Increased LES
Relaxes pylorus and duodenum when the stomach contracts
291
In addition to being a prokinetic, what type of antagonist is metoclopramide?
Dopamine antagonist
292
What are some side effects of metoclopramide as a dopamine antagonsit?
May cause sedation, agitation, and dysphoria
293
What drug may cause dysphoria, agitation, and sedation when it interacts with dopamine receptors?
Metoclopramide
294
In what patient population shoudl you avoid giving Metoclopramide?
Parkinsons patients
295
Parkinsons patients should not receive what prokinetic? Why?
Parkinsons is caused by a depletion of dopamine in the brain, and metoclopramide is a dopamine antagonist that will exacerbate the situation.
296
How should you administer metoclopramide?
Administer slowly to avoid dysphoria and agitation in patients.
297
If you adminsiter Metoclopramide to quickly, what can occur?
It can cause dysphoria and agitation in patients.
298
How is metoclopramide absorbed?
Oral absorption
299
How is metoclopramide eliminated?
Renal elimination
300
What organs eliminate metoclopramide from the body?
Kidneys
301
What is the dosage of metoclopramide as a preop adjunct?
10-20 mg over 3-5 minutes, 15-30 minutes prior to induction
302
When should you give metoclopramide in a preop setting?
15-30 minutes prior to induction
303
Over what time period should you give metoclopramide?
Over 3-5 minutes
304
How much is an appropriate preoperative dose of Metoclopramide?
10-20 mg
305
Does Metoclopramide alter gastric pH?
No.
306
T/F: Metoclopramide lowers gastric pH.
False; it increases LES tone, increases gastric emptying, and relaxes the pylorus and duodenum upon contraction of stomach.
307
T/F: Reglan is a powerful anti-emetic.
False; there is no data to show that.
308
Metoclopramide is used chronically to treat:
Gastroparesis and GERD
309
What patients should receive metoclopramide prior to surgery?
```
Trauma
Full Stomach
Obese
Diabetic
Pregnant
```
310
Besides trauma and emergency patients that come in with a full stomach, what population groups are known for decreased gastric emptying that would benefit from Metoclopramide prior to surgery?
Obese
Diabetic
Pregnant
311
The fact that metoclopramide is a dopamine antagonist doesn't only affect Parkinson's patients. What is a negative effect seen across patient pouplations?
Dysrhythmias: extrapyramidal effect
312
Main side effects of Metoclopramide?
Abdominal cramping
Dysrhythmias
Dry mouth
313
Rare side effects of chronic metoclopramide therapy include:
Hirsuitism
| Maculopapular rash
314
What kind of rash may occur on patients that are tacking metoclopramide chronically?
Maculopapular rash, a raised and red rash that occurs all over the body
315
What type of prokinetic may cause hyperprolactinemia? What are the effects?
Metoclopramide
| Can cause breast enlargement and menstrual irregularities
316
Why might chronic metoclopramide use cause breast enlargement and irregular menstrual cycles?
Can cause hyperprolactinemia
317
What are the fetal effects of Reglan?
No real effects
318
Besides dopamine-depleted patients, what patients should not receive Metoclopramide?
Patients with GI obstruction because the blockage prevents the forward movement of food
319
If your patient has a GI obstruction, avoid giving them:
Metoclopramide
320
What type of drug is domperidone?
Prokinetic
321
Domperidone is a
Prokinetic
322
Main effects of domperidone as a prokinetic?
Increases peristalsis
Increases LES tone
Increases stomach emptying
323
Is domperiodone a dopamine antagonist?
Yes.
324
How does domperidone differ from metoclopramide in terms of side effects?
Domperidone doesn't have cholinergic or central effects.
325
T/F: domperidone has widespread cholinergic effects.
False; no cholinergic activity
326
Does domperidone have central effects?
No, but metoclopramide does.
327
What type of drug is cisapride?
Prokinetic
328
Cisapride is a
Prokinetic
329
Are all prokinetics dopamine antagonists?
No, cisapride is not a dopamine antagonist.
330
Name a prokinetic that is not a dopamine antagonist.
Cisapride
331
How does cisapride work?
It increases Ach in the gut to increase parasympathetic drive and increase gastric emptying.
332
What prokinetic increases Ach in the gut to increase parasympathetic drive and therefore increases gastric emptying?
Cisapride
333
What type of drug is dexamethasone?
Glucocorticoid
334
How is dexamethasone effective as an antiemetic?
It is a glucocorticoid that inhibits prostaglandin synthesi.
335
What drug acts as an anti-emetic by inhibiting prostaglandin synthesis?
Dexamethasone
336
When is dexamethasone administered?
At induction
337
Effective dose of dexamethasone?
4 mg
338
What is the half-life of dexamethasone? Why is that significant?
Half-life is 36 hours, making it a good choice for outpatient procedures.
339
Why should you avoid high doses of dexamethasone?
At high doses, dexamethasone will increase sugar production in diabetics without increasing anti-emetic benefit.
340
What type of drug is droperidol?
Butyrophenone
341
Which antiemetics are a butyrophenone?
Droperidol, haloperidol
342
T/F: droperidol is a dopamine antagonist.
True.
343
Besides metoclopramide and domperidone, name a dopamine antagonist.
Droperidol
344
Why is droperidol rarely used anymore?
It has a black box warning because it can cause QT elongation, leading to Torsades de Pointes (ventricular dysrhythmia d/t anti-dopamine activity).
345
How much droperidol must you give your patient to see QT-prolonging effects?
How much to provide effective anti-emesis?
QT prolongation seen at 12 mg doses
| Anti-emetic dose = 0.625 mg
346
What type of drug is haloperidol?
Butyrophenone
347
If you see "-idol," think:
Butyrophenone
348
Does haloperidol have anti-dopamine effects?
Yes; affinity for D2 receptors
349
When should you use haloperidol?
As a rescue drug for PONV
350
Effective dose of haloperidol?
1 mg
351
When is the optimal time to done a scopalamine patch?
Night before, but morning of will suffice
352
What type of drug is scopolamine?
Anticholinergic
353
A signficant side effect of scopolamine can be:
Dry mouth d/t anticholinergic effects
354
Why should patients wash their hands after removing their scopolamine patch?
Scopolamine is very lipophilic, and it can get into eyes and cause pupil dilation d/t anticholinergic effects.
355
Why should you use caution in giving scopolamine to elderly populations?
Can cause dysphoria or even a cholinergic crisis
356
What is the dose of a scopolamine transdermal patch?
1.5 mg
357
What is a rescue drug for patients who are already nauseous and vomiting?
Promethazine (Phenergan)
| H2 antihistamine
358
What two antihistamines are considered antiemetics?
Promethazine
| Diphenhydramine
359
What illegal drug is often used to treat nausea due to chemotherapy?
Cannaboids
360
T/F: ephedrine has anti-emetic effects.
True.
361
What type of drug is aprepitant?
NK1 antagonist
362
Name an NK1 antagonist that is primarily used to treat N/V d/t chemotherapy.
Aprepitant
363
What type of antagonist is aprepitant?
NK1 antagonist
364
What is the main ligand of NK1 receptors? Where are they found?
Main ligand = substance P
| Found in vomiting center of brain in high concentrations
365
NK1 receptors are highly concentrated in which part of the brain?
Vomiting center of brain
366
How should you administer Aprepitant as an anti-emetic?
Give preoperatively PO to prevent PONV.
367
Why is aprepitant not widely used as an anti-emetic?
It is extremely expensive.
368
What parts of the CNS are involved in PONV?
Cortex
Thalamus
Hypothalamus
Meninges
369
Which receptors in the vestibular system are involved in PONV?
H1 receptors are possibly involved, and M1 receptors are definitely involved.
370
What cranial nerve(s) controls input to the GI tract and heart?
CN IX and CN X
371
What receptors in the GI tract and the heart are involved in PONV?
Mechanorecetpors
Chemoreceptors
5-HT3 receptor
372
Where is the vomiting center of the brain located?
Medulla oblongata
373
What receptors are involved in the vomiting center of the brain?
H1 receptor
M1 receptor
NK1 receptor
5-HT3 receptor
374
Where are D2 receptors located?
In the chemoreceptor trigger zone (area postrema)
375
A 32 year old female prevents for first c-section. She feels very nauseated after epidural placement. What should you give her?
Give her fluids; she is nauseated after epidural placement because it caused hypotension.
376
When you see "Heller myotomy," you should automatically think:
Achalasia
377
Effective dose of droperidol?
0.625 - 1.25 mg
378
Effective dose of Zofran?
4 mg (0.1 mg/kg)
379
Effective dose of graniestron?
0.01 mg/kg
380
Effective dose of dolasetron?
12.5 mg (0.35 mg/kg)
381
Effective dose of metoclopramide?
10 mg (0.15 mg/kg)
382
Effective dose of dexamethasone?
4-10 mg (0.1 mg/kg)
