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Anesthesia Pharm (Spring '24) - C > Lecture 4 Pre-op Medication Test 1 > Flashcards

Lecture 4 Pre-op Medication Test 1 Flashcards

1
Q

Histamines are endogenous substances that are released from ___________ and _______________.

A

Basophils; Mast Cells

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2
Q

What does histamine do to the airway?

What does histamine do in the stomach?

Histamine causes what NTs to be released in the CNS?

A

Contraction of smooth muscles in the airway.

Acid Secretions in the stomach.

Histamine will cause the release of serotonin, acetylcholine, and norepinephrine in the CNS.

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3
Q

What drugs will induce histamine release?

A

Morphine
Protamine
Mivacurium
Atracurium

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4
Q

When H1 histamine receptors are activated it can activate ______, _________, __________, and ________ receptors.

A

Muscarinic
Cholinergic
5HT3
Alpha-adrenergic

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5
Q

When H2 histamine receptors are activated, it can activate ________ and ________ receptors.

A

5HT3
Beta-1

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6
Q

When histamine binds to an H1-receptor what will be the result?

A

Hyperalgesia and inflammatory pain (insect sting)
Allergic rhino-conjunctivitis symptoms

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7
Q

When histamine binds to an H2-receptor what will be the result?

A

Elevate cAMP (Beta1-like stimulation, tachycardia)
Increase acid and volume production

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8
Q

Activation of both H1 and H2 receptors will result in what symptoms?

A

Prostacyclin Release
Capillary permeability
Tachycardia
Hypotension d/t release of NO
Flushing

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9
Q

What is the most accurate description of an antihistamine?

A

Inverse Agonist
They don’t prevent the release of histamine but responses

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10
Q

What are the effects of H1 receptor antagonists on the following areas?

Vestibular System:
Airway Smooth Muscle:
Cardiac Endothelial:

A

What are the effects of H1 receptor antagonists on the following areas?

Vestibular System: Effective for motion sickness
Airway Smooth Muscle: protection against bronchospasms
Cardiac Endothelial: provide cardiac stability

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11
Q

The first-generation H1 antagonist causes a lot of ____________ as a side effect.

A

sedation

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12
Q

Can you develop tachyphylaxis from H1 receptors?

A

No

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13
Q

What are the side effects of H1 receptor antagonists?

A

Blurred Vision
Urinary Retention
Dry Mouth
Drowsiness/Sedation (first gen)

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14
Q

What are examples of H1 receptor antagonist drugs?

A

Diphenhydramine (Benadryl)
Promethazine (Phenergan)
Cetirizine (Zyrtec)
Loratadine (Claritin)

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15
Q

This H1 receptor drug is mostly used as an antipruritic and pre-treat procedure-related allergy (IVP dye)

A

Benadryl

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16
Q

Diphenhydramine inhibits the afferent arc of the ________________.

A

Oculo-emetic reflex

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17
Q

Diphenhydramine can stimulate ventilation by augmenting the relationship of ____________ and ___________ drive.

A

Hypoxic, Hypercarbic

Only if given as a solo administration

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18
Q

What is the IV dose of Benadryl?

What is the half-time of Benadryl?

A

25-50mg IV

7-12 hours

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19
Q

Which H1 receptor antagonist is a great anti-emetic and is used as a rescue and reduces peripheral pain levels (anti-inflammatory effects).

A

Promethazine

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20
Q

What is the IV dose of Promethazine?

How long does it take to onset?

What is the half-time of Promethazine?

A

12.5-25mg IV (give less to the elderly)

5 minutes for onset

9-16 hours

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21
Q

What were the black box warnings for Phenergan?

A

Can cause death in children under the age of 2.

Can cause extravasation and ischemia to the tissue from IV injection.

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22
Q

H2 receptors antagonist are most commonly used in __________.

How does an H2 receptor antagonist work?

A

Duodenal ulcer disease / GERD

Decrease hypersecretion of gastric fluid (H+) from gastric parietal cells and decrease cAMP, which will decrease gastric volume and increase pH.

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23
Q

H2 receptor antagonist can increase serum creatine by _______% d/t competition for tubular secretion.

A

15%

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24
Q

What are the side effects of H2 receptor antagonists?

A

HA/Confusion (Elderly)
Bradycardia
Diarrhea
Skeletal Muscle Pain
Weakened Gastric Mucosa
Creatine Increase

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25
Q

Overgrowth of ____________ can increase pulmonary infections d/t weakened gastric mucosa from prolonged administration of H2 antagonist.

A

Candida Albicans

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26
Q

What are examples of H2 receptor antagonists?

A

Cimetidine (Tagamet)
Ranitidine (Zantac)
Famotidine (Pepcid)

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27
Q

How is Cimetidine metabolized?

A

CYP450, hepatic metabolism, renal clearance

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28
Q

Cimetidine strongly inhibits CYP 450 and can affect the metabolism of which drugs?

A

Warfarin
Phenytoin
Lidocaine
Tricyclics
Propranolol (Inderal)
Nifedipine
MEperidine
Diazepam

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29
Q

What are the adverse effects of Cimetidine?

A

Bradycardia
Hypotension (rapid infusion)
Increase Prolactin
Impotence (Inhibits dihydrotestosterone binding to androgen receptors)

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30
Q

What is the dose of cimetidine?

What about renal dosing?

A

150-300mg IV

75-150mg IV

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31
Q

How is Ranitine metabolized?

A

CYP450, hepatic metabolism, renal clearance

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32
Q

What is the dose of Ranitidine?

What about renal dosing?

A

50mg diluted to 20cc given over 2 minutes.

25mg diluted to 20cc given over 2 minutes.

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33
Q

How is Famotidine metabolized?

A

CYP450, hepatic metabolism, renal clearance

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34
Q

What interference is Famotidine involved with?

A

Interferes with phosphate absorption and can result in phosphatemia.

Bone fractures or hips hurting

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35
Q

What is the dosing for famotidine?

What about renal dosing?

What is the half-time for famotidine?

A

20mg IV

10mg IV

2.5-4 hours (most potent and longest of all H2 receptor antagonist)

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36
Q

What group of drugs irreversibly bind to acid secretion pumps and inhibit the movement of protons (H+) across the gastric parietal cells?

A

Proton Pump Inhibitors

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37
Q

How many days does it take for the onset of PPIs?

A

3 to 5 days

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38
Q

What are PPIs most effective against?

A

Controlling gastric acidity
Decreasing Volume

39
Q

PPIs are more effective than H2 receptors in what 4 areas?

A

Healing esophagitis
Healing ulcers
Relieving symptoms of GERD
Best treatment of Zollinger-Ellison Syndrome

40
Q

What are examples of PPI?

A

Omeprazole (Prilosec)
Pantoprazole (Protonix)
Lansoprazole (Prevacid)
Dexlansoprazole (Dexilent)

41
Q

What have PPIs been associated with?

A

Bone Fractures
SLE
Acute Intestinal Nephritis
C-diff
Vitamin B12
Magnesium Deficiency

42
Q

PPI will inhibit ____________ metabolism.

PPI will block enzymes that activate ____________.

A

Warfarin (Warfarin can work too well with PPI, watch the INR)

Clopidogrel (Clopidogrel won’t work as well with PPI)

43
Q

Omeprazole is enteric coated and is a prodrug that protonates in the _____________ to its active form.

Omeprazole only inhibit pumps that are present, acid inhibition increases with repeated dosing, but it only covers about ___________% maximum inhibition.

A

Parietal Cells

66%

44
Q

How is omeprazole metabolized?

A

CYP metabolism

45
Q

What is the dosing of omeprazole?

If given PO, how long before surgery?

A

40mg in 100cc NS given over 30 minutes

PO, at least 3 hours prior to surgery

46
Q

What are the side effects of omeprazole?

A

HA (crosses BBB)
Agitation (crosses BBB)
Confusion (crosses BBB)
Abdominal Pain
N/V
Flatulence
SB bacterial overgrowth

47
Q

How is Protonix metabolized?

Protonix has a greater _____________ and longer ___________ compared to omeprazole.

A

CYP metabolism

Greater bioavailability, and greater half time

48
Q

What is the dose of Protonix?

How long before surgery can you give Protonix?

A

40mg in 100cc given over 2-15 minutes

1 hour before to decrease gastric volume and increase pH (works as fast as ranitidine)

49
Q

PPI’s are the treatment of choice for ______, _______, and _______.

A

GERD
Gastroduodenal Ulcers
Acute upper GI Hemorrhage (post EGD treatment)

50
Q

What is given to treat NSAID ulceration?

A

Omeprazole

51
Q

What will protect the acidity of aspiration pneumonitis and be the most cost-effective for intermittent symptoms?

A

H2 antagonist

52
Q

What is a particulate antacid?

What is a non-particulate antacid?

A

Particulate antacids are Aluminum or Magnesium based. Aspiration equals acid aspiration.

Non-Particulate antacids are Sodium, Carbonate, Citrate, or Bicarb base. Neutralize Acid.

53
Q

What are long-term effects of all antacids?

A

If pH is too high, acid breakdown of food will be inhibited and acid rebound can occur.

54
Q

What are the long-term effects of magnesium-based antacids?

What are the long-term effects of calcium-based antacids?

What are the long-term effects of sodium-based antacids?

A

Magnesium-based: Osmotic diarrhea, neurological/neuromuscular impairment

Calcium-based: Hypercalcemia, Kidney stones

Sodium-based: Hypertension

55
Q

How does sodium citrate (Bicitra) neutralizes acid?

A

The Bicitra and acid are combined to make salt, CO2, and water, resulting in neutralization.

56
Q

Sodium citrate increases __________.

A

Intra-gastric volume

57
Q

What is the dose of sodium citrate?

When does it lose its effectiveness?

A

15-30 mL

After 30-60 minutes

58
Q

Pregnancies are considered full stomach after _________ weeks.

A

12 weeks

59
Q

What types of drugs are known for stimulating gastric motility (prokinetic)?

These drugs will increase lower esophageal _____________.
Stimulate _______________.
Relax ____________ and ____________ for the gastric emptying of intestinal transit.

A

Dopamine-blocking drugs for full stomachs

Lower Esophageal Sphincter tone.
Stimulate Peristalsis.
Relax Pylorus and Duodeum.

60
Q

Who is contraindicated by dopamine blockers?

A

Individuals who are dopamine depleted (Parkinson’s).

61
Q

What are the side effects of dopamine blockers?

A

Extrapyramidal reactions (easily crosses BBB)
Orthostatic Hypotension
Can affect the chemoreceptor trigger zone (antiemetic effect).
No change in gastric pH

62
Q

What are examples of dopamine blockers?

A

Metoclopramide (Reglan)
Domperidone - not available in the US
Droperidol (Inapsine)

63
Q

What is the FDA-cleared drug for diabetic gastroparesis?

A

Metoclopramide (Reglan)

64
Q

What are the side effects of Reglan?

A

Abdominal cramps from the rapid infusion
Muscle Spasm
Hypotension
Sedation
Increase Prolactin Release
Neuroleptic malignant syndrome
Decrease plasma cholinesterase levels - slow metabolism of succinylcholine, mivacurium, and ester local anesthetics.

65
Q

What is the dose of Reglan?

When do give before induction?

A

10-20mg given over 3 to 5 minutes

15 to 30 minutes before induction

66
Q

Unlike Reglan, _____________ does not cross the BBB and has no anticholinergic activity.

It also increases __________ secretion by the pituitary to a greater degree.

This is not FDA-approved due to _________ and __________ but is available outside the country.

A

Domperidone

Prolactin

Dysrhythmias and Sudden Death

67
Q

What drug was initially developed for schizophrenia and psychosis?

Like Reglan, this drug can cause __________and __________ as adverse side effects.

A

Droperidol (Inapsine)

Extrapyramidal syndrome and Neuroleptic Malignant Syndrome

68
Q

What CNS depressants do you want to avoid with droperidol?

A

Barbituates
Opioids
General Anesthesia (lol)

69
Q

Droperidol is more effective than ______________ for N/V.

Droperidol is equally effective to ____ mg of ____________ for N/V.

A

Reglan

4 mg of Zofran

70
Q

What is the black box warning for Droperidol?

A

Prolonged QT intervals
Torsades with higher doses
Serious Drug Interactions: Amio, Diuretics, Beta Blockers, CCB, Steroids

71
Q

What is the dose for droperidol?

A

0.625 to 1.25mg IV

72
Q

____________ is released from the chromaffin cells of the small intestine and stimulates _______________ through 5HT3 receptors that cause __________.

A

Serotonin
Vagal Afferents
Vomiting

73
Q

Serotonin 5HT3 receptors are ubiquitous they are in the kidneys, lungs, colon, liver, and stomach. There is a large concentration of 5HT3 receptors in the ________ and __________.

A

Brain and GI Tract

74
Q

What group of drug that was originally used in chemo and radiation therapy related to N/V is now used for PONV? It is a competitive antagonist with almost no side effects.

A

5HT3 antagonist

75
Q

What is 5HT3 not effective against?

A

Motion sickness and vestibular stimulation

76
Q

What are examples of 5HT3 antagonists?

A

Ondansetron (Zofran)
Granisetron (Kytril)
Dolasetron (Anzemet)

77
Q

Which drug is the first 5HT3 antagonist and does not cross the BBB.

A

Ondansetron (Zofran)

78
Q

What are the side effects of Zofran?

A

HA
Diarrhea
Slight QT prolongation

79
Q

What is the dose of Zofran?

What is the plasma half-life?

A

4 or 8mg IV

4 hours (Give Zofran at the end of the case)

80
Q

The exact mechanism of this group of drug is unknown for N/V, but it centrally inhibits prostaglandin synthesis and control endorphin release.

There is also increased effectiveness for 5HT3 antagonist and droperidol.

This group of drugs also has an anti-inflammatory effect resulting in less post-op pain, and less opioid use.

A

Corticosteroids

81
Q

What is the diabetic risk of Decadron?

What is another side effect of Decadron?

A

Perioperative Hyperglycemia (minimal side effect with one dose)

Perineal Burning/Itching (rapid IV push)

82
Q

What is the dose of Decadron?

What is the delay in onset?

How long does the efficacy of decadron persist?

A

4mg or 8mg

2 hours (Give Decadron at the beginning of the case)

24 hours

83
Q

When will you consider giving an increased dose of decadron?

A

Airway trauma d/t multiple intubation attempts (12 or 16 mg)

84
Q

What are Scopolamine patches used for?

A

They are muscarinic antagonists (anticholinergic) for nausea and vomiting.

They have both central and peripheral effects (crosses the BBB, sedation)

85
Q

What are the side effects of Scopolamine patches?

A

Dilated pupils
Sedation

86
Q

Peak concentration hours for Scopolamine patches are between _________ and __________ hours.

How long does it take the patch to work?

A

8 to 24 hours

4 hours for onset of action.

87
Q

What is the priming dose of Scopolamine?

How much scopolamine will be given over the next 72 hours?

Where will the patch be placed?

A

140 mcg

1.5mg

Post-auricular

88
Q

What group of drugs is similar to epinephrine that stimulates the G-proteins, activates cAMP which will decrease Ca2+ entry, and relax smooth muscles in the airway?

A

Beta-receptor agonists (Bronchodilators)

89
Q

Bronchodilators can reduce inflammatory cell activation, directly relax smooth muscles, and increase FEV1 by _________% within ______ minutes (2 puffs).

A

15% improvement in 6 minutes

90
Q

How do you deliver an inhaled SABA?

A

Discharge inhaler while taking a slow deep breath over 5-6 seconds.
Hold your breath at max inspiration for 5-6 seconds.

91
Q

What percentage of the inhaled SABA reaches the lungs?

What percentage of the inhaled SABA is delivered to the lungs through mechanical ventilation?

How often are inhaled SABAs given?

A

12%

50-70%

Every 4 hours

92
Q

What are the side effects of beta agonists?

A

Tremor
Tachycardia
Transient Decrease in arterial oxygenation
Hyperglycemia

93
Q

What are examples of bronchodilators?

A

Albuterol (Proventil)
Levo-albuterol (Xopenex)

94
Q

What are ways to deliver SABA?

A
  1. Inhaler
  2. Puff piece nebulizer
  3. Syringe

Anesthesia Pharm (Spring '24) - C (20 decks)

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