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Mar: Sem 2 - Anes. Pharm (Full) > Lecture 4 - Pre-Op Meds (Exam 1) > Flashcards

Lecture 4 - Pre-Op Meds (Exam 1) Flashcards

1
Q

How does enteric-coated omeprazole (Prilosec) turn into an active form when ingested?

A

It is converted into an active form by protonation in parietal cells.
Slide 17
(Omeprazole is a prodrug)

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2
Q

What is MOA of omeprazole?

A

It inhibits proton pumps that are present.
(so, you have to continually take omeprazole to inhibit the pumps that have been developed at least for about 5 days)
Slide 17

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3
Q

What is the maximum inhibition of proton pumps you can achieve with Omeprazole in about 5 days of taking it?

A

66%
(1/3 of the pumps are still working usually, but still decreases in acid production significantly.)
slide 17

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4
Q

How is Omeprazole metabolized?

A

CYP’s enzyme
(Theoretically, it can inhibit other drug metabolism, but there is no clinical significance that shows it inhibits other drugs)
Slide 17

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5
Q

What is the IV dosage of Prilosec (Omeprazole)?

A

40 mg in 100ml NS over 30 minutes
Slide 17

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6
Q

When do you give PO Omeprazole to the patient who is having surgery?

A

Greater than 3 hours before going to OR
(You need to wait for the medication to convert from prodrug to active form)
Slide 17

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7
Q

What are the 4 most common side effects of H1 antagonists?

A

Blurred vision
Urinary retention
Dry mouth
Drowsiness
Slide 7

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8
Q

What are the side effects of Omeprazole (Prilosec)?

A

HA
Agitation
Confusion (Cross BBB)

Abdominal Pain
N/V
Flatulence
Small bowel bacterial overgrowth (d/t decrease production of acid)

Slide 18

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9
Q

The following drugs block which histamine receptor: Diphenhydramine, Promethazine, Cetirizine, Loratadine?

A

H1
Slide 7

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10
Q

How is Protonix (Pantoprazole) metabolized in our body?

A

CYP metabolism
(No significant drug interactions)
Slide 19

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11
Q

Compared to Prilosec, Protonix has a _______ bioavailability and _________E 1/2 time.

A

Greater, Longer
Slide 19

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12
Q

Diphenhydramine (Benadryl) is mostly used as an …

A

Antipruritic
Slide 8

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13
Q

The elimination half-time for Diphenhydramine is…

A

7-12 hours
Slide 8

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14
Q

When do you give Protonix to the patient who is having surgery?

A

1 hour prior to the OR
(Decreases gastric volume and increases pH, and works as fast as Ranitidine)
Slide 19

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15
Q

Diphenhydramine can inhibit the afferent arc of what reflex?

A

Oculo-emetic reflex
Slide 8

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16
Q

How is domperidone different than metoclopramide?

A

It does not cross the BBB & has no anticholinergic activity
(Slide 27)

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17
Q

What is the dosage of Protonix?

A

40mg in 100ml IVPB over 2-15 minutes.
Slide 19

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18
Q

Benadryl stimulates ventilation and augments the relationship between _______ and ____________ drives

A

Hypoxic and hypercarbic
Slide 8

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19
Q

________ Increases prolactin secretion by pituitary. (To a degree)
(Prolactin: causes the breasts to grow and make milk during pregnancy and after birth; also inhibits testosterone - impotence and gynecomastia)

A

Domperidone
(Slide 27)

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20
Q

What is the dosage of Diphenhydramine?

A

25-50 mg
Slide 8

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21
Q

What is the E 1/2 time for Promethazine?

A

9-16 hours
Slide 9

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22
Q

Which drug is effective as a rescue anti-emetic and can also reduce peripheral pain levels?

A

Promethazine (Phenergan)
Slide 9

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23
Q

What is the dose and onset of Promethazine? (Phenergan)

A

12.5-25 mg
5 minutes
Slide 9

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24
Q

Why is Domperidone no longer FDA approved in the USA?
What country might have it?

A

Because it causes dysrhythmias and sudden death!
You can find it in Mexico OTC. 🇲🇽
You can find it by prescription in Canada.🇨🇦
(Slide 27)

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25
Q

PPI treatment is the DOC for patients who have_____.

A
  1. GERD
  2. Gastroduodenal Ulcers
  3. Acute upper GI Hemorrhage (PPI infusion after EGD treatment)
  4. NSAID ulcerations (specifically Omeprazole :)

Slide 20

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26
Q

These drugs are most commonly used in duodenal ulcer disease and GERD

A

H2 receptor antagonists (PPI’s are more effective but $$$)

Slide 10

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27
Q

______ is given for patients who have NSAID ulcerations and NSAIDs are discontinued.

A

Omeprazole (Prilosec) or any PPI :)
Slide 20

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28
Q

___________ was originally developed for schizophrenia and psychosis. (Was given is super high doses)

A

Droperidol (inapsine)
(Slide 28)

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29
Q

Droperidol (inapsine) is a strong D2 antagonist.
T/F?

A

True
(Slide 28)

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30
Q

What are 3 cautions when using Droperidol (inapsine)?

A

*Can cause extrapyramidal symptoms
*Neuroleptic malignant syndrome
*Avoid other CNS depressants: barbiturates, opioids, general anesthetics (:
(Slide 28)

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31
Q

For N/V, ___________ is more effective than metoclopramide/Equally effective to 4mg ondansetron (much cheaper).

A

Droperidol (inapsine)
(Slide 28)

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32
Q

Studies show, H2 blockers are better for patients who have _______.

A
  1. Aspiration Pneumonitis concerns
  2. Intermittent symptoms and cost-effective
    (H2 blockers do not prevent Aspiration Pneumonia but prevent pneumonitis due to decrease acidity of the contents aspirated.)
    Slide 20
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33
Q

Why did Droperidol (inapsine) receive a Black Box Warning in 2001?

A

Because it prolonged QT intervals/torsades with higher doses!!

It also had lots of serious drug interactions with: amiodarone, diuretics, sotalol, mineralocorticoids, calcium channel blockers!!
(Slide 28)

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34
Q

What if a patient forgot to take their PPI before the surgery?

A

Continue to give whatever they were taking at home or, if not available, whatever the facility has.
Slide 20

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35
Q

What is a standard dose for Droperidol (inapsine)?

A

Doses: 0.625-1.25mg IV
(Slide 28)

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36
Q

Why is Ondansetron preferred over Droperidol (inapsine)?

A

Ondansetron works just as well on N/V as Droperidol but it is also has less side effects.
(Slide 28)

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37
Q

What would you give if a patient who has a full stomach needs emergent surgery?

A

H2 blocker works faster to decrease the acidity of the stomach contents. H2 blockers and PPIs do not reduce stomach volume.
Medication that increases gastric emptying should be given like Dopamine Blockers
Slide 20

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38
Q

Antacids are broken down into two groups:

A
  1. Particulate
  2. Non-Particulate
    Slide 21
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39
Q

What are Particulate antacids?

A

Particulate antacids are aluminum or magnesium based.
(example: Maalox/Mylanta)
Slide 21

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40
Q

_________ is released from the chromaffin cells of the small intestine and __________ vagal afferents through the 5HT3 receptors causing __________. (Especially in pregnant people!)

A

Serotonin

Stimulates

vomiting

(Slide 30)

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41
Q

What receptors are ubiquitous meaning that can be found in the kidney, colon, liver, lung, & stomach?

A

Serotonin (5-HT3) RECEPTORS
(Slide 31)

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42
Q

What two locations have a high concentration of Serotonin (5-HT3) RECEPTORS?

A

BRAIN & GI TRACT
(Slide 31)

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43
Q

Why are Particulate antacids are not given to patients who have full stomach?

A

The aspiration of aluminum or magnesium-based antacids is as bad as that of acid.
Slide 21

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44
Q

What are Non-particulate antacids?

A

Non-Particulate antacids are sodium, carbonate, citrate, and bicarbonate based. They neutralize the acid contents in the stomach. Example: Sodium citrate (Bicitra)
(Much safer than particulate antacids if you were to aspirate)
Slide 21

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45
Q

In our bodies, what releases Histamine?

A

Basophils an Mast Cells

(slide 2)

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46
Q

What 3 things does Histamine release induce in our bodies?

A
  1. Contraction of smooth muscles in the airway (bronchoconstriction) & GI tract (semester 1)
  2. Secretion of stomach acid (if we were to aspirate, we would fill our lungs with this acidic fluid)
  3. Release of Neurotransmitters in the CNS

(slide 2)

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47
Q

Histamine induces what 3 neurotransmitters to be released in the CNS?

A

Acetylcholine
Norepinephrine
Serotonin

(slide 2)

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48
Q

What 4 drugs discussed induce Histamine release?

A

Morphine
mivacurium (Mivacron)
Protamine
atracurium (Tracrium)

(slide 3)

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49
Q

Drug induced Histamine release must be treated with what?

A

an H1 and H2 Antagonist

(slide 3)

50
Q

How many Histamine receptors are there?
Which ones do we discuss in class?

A

H1, H2, H3, H4
(H3 and H4 has no indication for anesthesia)

H1 and H2

(Slide 4)

51
Q

H1 Histamine receptor can also activate which other (4) receptors?

A

Muscarinic
Cholinergic
5-HT3 (Serotonin)
A-adrenergic

(Slide 4)

52
Q

H2 Histamine receptor can also activate which (2) other receptors?

A

5-HT3 (serotonin)
B-1

(slide 4)

53
Q

What are the reactions to Histamine on the H1 receptor?

A

Hyperalgesia and Inflammation (insect stings)
Allergic Rhino-Conjunctivitis (runny nose and weepy eyes)

(slide 4)

54
Q

H2 receptor antagonists decrease hypersecretion of gastric fluid from…

A

Gastric parietal cells
Slide 10

55
Q

H2 receptor antagonists lead to weakened gastric mucosa due to _____

A

Bacteria (overgrowth can occur with a more alkalotic environment.)

Slide 11

56
Q

What are the reactions to Histamine on the H2 receptor?

A

Elevates cAMP (Beta1 stimulation- increased HR/ renin release)
Increases gastric Acid/Volume production

(slide 4)

57
Q

H2 receptor antagonists increase serum creatinine by how much?

A

15%
Slide 11

58
Q

Cimetidine, Ranitidine, and Famotidine are all examples of what drug class?

A

H2 receptor antagonists
Slide 11

59
Q

What is the most common fungus grown when administering H2 receptor antagonists long-term?

A

Candida Albicans
Slide 11

60
Q

H1 and H2 histamine receptor activation causes what clinical reactions in the body? (5 discussed)

A
  1. Hypotension (from the release of Nitric oxide and causes vasodilation)
  2. Capillary Permeability (the “Wheal and Flare triple response from Dr. T)
  3. Flushing
  4. Prostacyclin release (PGI2)
  5. Tachycardia (Beta-1 activation and reflex tachycardia)

(slide 5)

61
Q

Histamine Receptor Antagonists (Antihistamines) are also called: “competitive, reversible, Inverse Agonists” why?

A

Because they do not prevent the release of Histamine, but prevent the response to it.

(slide 5)

62
Q

(1) H1 histamine receptors are located where? (3 places discussed)

A
  1. Vestibular System
    - For the treatment of motion sickness
  2. Airway smooth muscles
    - For the treatment against bronchospasms
  3. Cardiac endothelial cells
    - For the treatment of cardiac stability (tachycardia)

(slide 6)

63
Q

What is a big side effect of 1st generation H1 antagonist?

A

Drowsiness/sedation - crosses the BBB
(don’t take these and drive!)

(slide 6)

64
Q

(For funsies from Dr T’s Lecture:)
What is the Wheal and Flare- “Triple Response” From Histamine release (skin)?

A
  • Microcirculation smooth muscle
  • Capillary endothelium
  • Sensory nerve endings
65
Q

What was the first 5HT3 antagonist that we still use often?

A

Ondansetron (Zofran)

Slide 32

66
Q

What was the original use for ondansetron (zofran)?

A

Chemotherapy & radiation induced N/V.

Slide 32

67
Q

Ondansetron (Zofran) is a _______
drug.
A. Non-competitive antagonist
B. Competitive Antagonist
C. Competitive Agonist

It has almost ____ side effects. It became popular for ____ .

A

B. Competitive Antagonist

No (Side effects)
PONV/ anesthesia related n/v

Slide 32

68
Q

Why are Granisetron (Kytril) & Dolasetron (Anzemet) not used much in clinical practice?

A

‘Alot more work’ for pharmacy to formulate and prepare them & not as effective as Zofran.

Slide 32

69
Q

Does Ondansetron (Zofran) cross the BBB?

Does it affect other receptor sites? (Dopamine, histamine, adrenergic, cholinergic sites)

A

No. (Has no CNS effects)
Nope.

Slide 33

70
Q

The only 3 side effects we worry about for Ondansetron (Zofran) are:

A

HA
Diarrhea
PROLONGED QT (with high doses)

Slide 33

71
Q

Would it be better to give Ondansetron (Zofran) at the beginning or end of the case? Explain.

How much would you give IV?

A

Towards the end bc it’s Plasma 1/2 life is only 4 hours. You want it be effective for the PONV.

4 or 8mg IV

Slide 33

72
Q

What is the proposed MOA on how corticosteroids inhibit PONV?

A

-Centrally inhibit prostaglandin synthesis & control endorphin release.

-Increase effectiveness for 5HT3 antagonist (Ondansetron/Zofran) & Droperidol/ Inaspine (D2 Antagonist)
*You may see steroid given in addition to zofran or droperidol.

-Anti-inflammatory = less P/O pain = less opioid use (induces n/v)

Slide 34

73
Q

Your patient is on long-term steroid therapy. You need to give a stress-dose steroid, Solumedrol, for sx.

Would you give an additional dose of Dexamethasone (Decadron) in addition to the Solumedrol to cover your PONV?
Explain.

A

No, you can use your stress-dose steroid as your PONV steroid in this instance.

Slide 34

74
Q

Your case is expected to last 2hrs. When would you give your Dexamethasone (Decadron)? Why?

Your next case is expected to last 6hrs. When would you give your Decadron?
Why?

A

2hr case: At the start of the case.
*Decadron has a delayed onset of 2hrs (efficacious for 24hr)

6hr case: ~4 hrs into the case - to allow it to be adequately effective p/o.

Slide 35

75
Q

You give 4mg of Dexamethasone (Decadron) in preop & your patient screams, “Woah! My butthole feels spicy!!!”

What caused this?

A

You pushed your Decadron too fast, silly.

Slide 35

76
Q

You give your diabetic patient 4mg of Dexamethasone (Decadron).
The pre-op RN asks if you want an additional sugar check and you say ‘nah.’
Why did you say ‘Nah’?

When would you say ‘Yeh’?

A

Studies show that just 1 small dose (4mg) of Decadron for N/V does not really affect sugar levels.

If you needed to give an additional dose or larger dose, maybe check a sugar.

Slide 35

77
Q

What are the traditional IV doses of Decadron?

When would you give more?

A

4mg or 8mg

-Difficult or multiple attempted intubation, used a scope. Basically anytime you cause trauma to the airway to prevent swelling.
(you get n/v coverage too:)

Slide 35

78
Q

Scopalamine is a ______ antagonist of ACh.
It causes _____ because it crosses the blood-brain barrier.
It comes in the form of a _____ that that needs to be placed behind the ear ~____ hrs before surgery and stay on for ~____ hrs.

A

Competitive, muscarinic antagonist
Sedation
Patch
~4hrs before surgery
24-72hrs (Kane says 48hrs & by 72, not as effective; but PPT and book say 72)

Slide 36

79
Q

What are the side effects of Scopalamine?

A

Mydriasis (dialted pupils)
Sedation

Slide 36

80
Q

Scopalimine patches have a ‘sustained-release’ effect.
What is the priming dose of the patch?
The maintenance?

When would it peak?

A

Priming dose of 140mcg
Maintenance - 1.5mg over the next 72hrs

Peaks @ 24hrs

Slide 36

81
Q

Scopalamine, compared to Atropine or Robinul, does not cause much tachycardia or smooth muscle relaxation.

True or False?

A

True.

Slide 36

82
Q

What are the risks associated with long-term use of antacids (particulate or non-particulate)?

A
  • increased pH
  • alteration in microbiome (potentially overgrowth of bad bacteria)
  • acid breakdown of food is inhibited
  • acid rebound with abrupt cessation of antacids (why’s it spicy?!)

(slide 22)

83
Q

Your buddy Joe Schmo says he’s going to start taking Maalox and/or Mylanta for his heartburn. You, as a distinguished SRNA, decide to warn him of possible risks with taking said meds.

What is the base component of these antacids and what side effects are associated with them?

A

Base component: Magnesium (or as Kane says, “Magnaaaysium”) & aluminum

S/E: osmotic diarrhea; neurologic and neuromuscular impairment

(slide 22)

84
Q

Joe Schmo didn’t believe you after warning him and took too much Mylanta which gave him the skitters (diarrhea) AND heartburn. So now he’s popping TUMS like they’re PEZ candy. You attempt to warn him about what?

A

Watch out for Hypercalcemia, bro. May cause you to develop some serious kidney stones

(slide 22)

85
Q

Joe Schmo expired d/t severe nepholithiasis secondary to excessive consumption of TUMS. His grieving wife, Janice Schmo, also suffers from heartburn and asks your opinion on taking Sodium Citrate. What do you tell her?

A

Establish if Janice has Hypertension or Congestive Heart Failure. If she does have either of these dx’s then tell her that Sodium-based antacids are contraindicated for her issues. Also tell her to go see her damn PCP and maybe get some grief counseling

(slide 22)

86
Q

Which antacid protects against aspiration pneumonia (not specifically aspiration itself) by making the gastric acid more alkalotic?

A

Sodium Citrate (Bicitra)

(slide 23)

87
Q

Sodium Citrate (Bicitra) also causes _________ which actually increases the risk of aspiration, especially in pts who ate/drank just prior to the procedure

A

Increased intragastric volume; if pt has been compliant and NPO, then we only increase intragastric volume by ~15-30 mls

(slide 23)

88
Q

How does Sodium Citrate neutralize stomach acid?

A

converts gastric acid into salt, CO2, and water; so it neutralizes both the acid and base

(slide 23)

89
Q

Scene: You (CRNA) arrive to your hospital and prepare for your first case for the day. The first case is a planned Cesarian-section and you want to treat preoperatively. The designated OR is prepped and the case is expected to proceed soon so you give Sodium Citrate. Shortly after, Dr. Fuknutz (the intended surgeon) calls in and says he lost his car keys and won’t make it to the hospital for another 90 mins. Why is this a problem?

A

Sodium Citrate (Bicitra) works fast but looses its effectiveness in 30-60 mins

ALSO: remember that Bicitra is commonly used in C-sections**

(slide 23)

90
Q

Standard dose(s) of Sodium Citrate (Bicitra)

A

15-30 mls PO

(slide 23)

91
Q

Any pregnant pts after 12 weeks gestation are ALWAYS considered _____ _______ when planning their anesthesia care plan.

A

Full Stomach

Question: “But what if they’re NPO for >12 hours?”
Medicosis Perfectionalis: shut up, it doesn’t matter, they’re ALWAYS considered a Full stomach

(- Kane remarks on this on slide 24)

92
Q

Dopamine Blockers are known for?

What are the Pharmacodynamics?

A

Stimulating Gastric Motility: (aka Prokinetics)
- increases lower esophageal sphincter tone
- stimulates peristalsis
- relaxes pylorus and duodenum

All these effects result in Gastric Emptying and Intestinal Transit

(slide 25)

93
Q

Since Dopamine Blockers antagonize dopamine receptors, we avoid using these meds in which pt population?

Why?

A

Pts with dopamine depletion or inhibition (Parkinson’s)

Parkinson’s pts already have depleted dopamine neurons to begin with secondary to it’s disease process. So we don’t want to block dopamine receptors when they already receive so little.

(slide 25)

94
Q

Dopamine Blockers can pass the blood-brain barrier: True or false?

A

True

(slide 25)

95
Q

So Dopamine Blockers can cross the BBB. What sort of side effects do we monitor for as a result?

A

Extrapyrimidal reactions: dystonias, parkinsonism, and akathisia

Can also get anxious and pick at things (Janice, stop messing with your damn IV!)

ORTHOSTATIC HYPOTENSION

And neuroleptic malignant syndrome

(slide 25)

96
Q

The best place to place a scopolamine patch on the body is where?

A

Behind the ear. In general, thinner areas of skin that will remain unbothered, not exposed to elements. (Slide 37)

97
Q

Mechanism of action for beta agonist bronchodilators?

A

Stimulate G proteins —> activate cAMP. Activated cAMP in lungs will decrease Ca++ entry into smooth muscle and also decrease contractile protein sensitivity to Ca++.

G protein —> cAMP —> ⬇️ Ca++ —> ⬇️ contraction —> nice open airway

(Slide 39)

98
Q

Dopamine Blockers are great for which statuses?

A

Some effects on the Chemoreceptor Trigger Zone for Chemo Induced N/V (CINV) and post-op C-section

But apparently Zofran is still a better choice…so yeah

(slide 25)

99
Q

Beta bronchodilator intended effects/action?

A

Reduce inflammation, relax smooth muscle of airways (slide 39).

100
Q

2 puffs of an inhaler can increase your expiratory volume by what percentage? You will see this effect in ___ min.

A

FEV increases by 15% by 6 minutes. (Slide 39)

101
Q

How do you use an inhaler?

A

Squeeze inhaler and take in deep breath over 5 - 6 seconds. Hold breath for 5 - 6 seconds. (Slide 40)

102
Q

What percentage of bronchodilator drug actually reaches the lungs when you use an inhaler? How much reaches the lungs when administered through an ETT?

A

Inhaler = 12%. ETT 50 -70%. (Slide 40)

103
Q

Do Dopamine Blockers cause any changes to gastric pH?
If so then what are the changes?

A

No
LESS likely to cause aspiration d/t decreased gastric volume (prokinetic)

(slide 25)

104
Q

Name 3 examples of Dopamine Blockers

A

Metaclopramide (Reglan)
Domperidone
Droperidol (Inapsine)

(slide 25)

105
Q

What side effects does a Beta agonist bronchodilator have? (Hint, think of what B1, B2, and B3 receptors do)

A

Tachycardia (B1), tremors (B2 in skeletal muscle), hyperglycemia (B3 breaking down fats).

May also see a transient decrease in arterial oxygenation. (Slide 41)

106
Q

What is the dose range for Cimetidine?

A

150-300mg IV
Half the dose in renal impairment.

Slide 12

107
Q

1 DOC (drug of choice) for diabetic gastroparesis

A

Metaclopramide

(slide 26)

108
Q

Why is a transient decrease in arterial oxygenation seen with administration of a bronchodilator?

A

Bronchodilator is given —> airways that were not open/perfused are now open/perfused.

Lungs need to adjust to ventilating and perfusing more area, which is where we see the initial decrease in oxygenation. Lungs rebound quickly, and are able to get in more oxygen overall with the extra airways that are now open.

(Slide 41)

109
Q

2 examples of beta bronchodilators mentioned in class?

A

Albuterol (Proventil)
&
Levo - albuterol (Xopenex, also the L isomer of albuterol)

(slide 41)

110
Q

What are the adverse effects of Cimetidine mentioned in lecture?

A

1.) Bradycardia and hypotensions from interacting with Cardiac H2 receptors (most common with rapid infusions)

2.) Increased plasma levels of prolactin

3.)Inhibits dihydrotestosterone binding to androgen receptors (impotence).

Slide 12

111
Q

Metoclopramide’s (Reglan) common side effects: name 5

A

abdominal cramping (if rapid IV)
muscle spasms
hypotension (eeeeeeeekkk)
sedation
increased prolactin release

(slide 26)

112
Q

What is the dose for Ranitidine (Zantac)?

A

50mg diluted in 20ml and given over 2 minutes.

Half dose for renal impairment.

Slide 13

113
Q

What are two SEVERE adverse rxn’s of Metoclopramide (Reglan) & the side effects seen?

A

Neuroleptic Malignant Syndrome
- as noted by sudden fever, muscle rigidity, tachycardia, and confusion

Decreases Plasma Cholinesterase
- SLOWS metabolism of Succ’s, Mivacurium, and Ester-based LA

(slide 26)

114
Q

4 methods for administering bronchodilators mentioned in lecture (1 method is for everyone, 1 method probably saw at bedside, 2 methods seem very Macgyver Anesthesia)

A

1) Inhaler
2) Nebulizer
3) Take cannister out of inhaler, attach to syringe, push syringe to push medication into patient.
4) Take cannister out of inhaler, attach to syringe, ???, attach syringe to elbow piece of ETT, magically administer medication with ventilator. (Slide 42)

115
Q

So you’ve established there’s no c/d to giving Metaclopramide (Reglan) for a particular case.
What administration methods and dosing are important to know?

A

Dose: 10-20 mg IV given slowwwwwwwwwwwwly (over 3-5 mins) to avoid abdominal cramping.

This dopamine blocker takes some time to reach its peak effect so make sure to give it 15-30 mins PRIOR to induction.

(slide 26)

116
Q

A patient is on long-term phenytoin (Dilantin). What H2 antagonist would be most appropriate?
(Dilantin is to help control SZ)

A

Famotadine (Pepcid)
Does not interfere with P450 enzymes

Slide 14

117
Q

What is the most potent H2 antagonist and also interferes with phosphate absorbtion?

A

Famotidine (Pepcid)

Slide 14

118
Q

Dose for Famotidine (Pepcid)

A

20mg IV
Half dose for renal impairment

Slide 14

119
Q

What conditions, mentioning in lecture, are more effectively treated with PPI’s than H2 Antagonists?

A

Esophagitis
Ulcers
GERD symptoms
Zollinger-Ellison Syndrome

Slide 15

120
Q

PPI’s inhibit ______ metabolism and block the enzyme that activates _______.

A

warfarin
clopidogrel

Slide 16

121
Q

What do the 4 examples of PPI’s end with?

A

-prazole

Mar: Sem 2 - Anes. Pharm (Full) (20 decks)

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